Interventional Spine: An Algorithmic Approach

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List of Contributors

Arjang Abbasi DO Attending Physician Interventional Pain Management and Spine Rehabilitation Long Island Spine Specialists Commack NY USA Elsayed Abdel-Moty PhD Research Associate Professor Department of Neurological Surgery The Rosomoff Comprehensive Pain and Rehabilitation Center Miami Beach FL USA Salahadin Abdi MD, PhD Professor of Clinical Anesthesiology Chief, Division of Pain Medicine University of Miami Pain Center LM Miller School of Medicine Miami FL USA David R. Adin DO Spine and Sports Fellow Department of Physiatry Hospital for Special Surgery New York NY USA Sang-Ho Ahn MD, PhD Associate Professor of Rehabilitation Medicine and Spine Center Yeungnam University College of Medicine Daegu Republic of Korea Venu Akuthota MD Director The Spine Center and Associate Professor Department of Rehabilitation Medicine University of Colorado School of Medicine Aurora CO USA William A. Ante MD Attending Physiatrist Physical Medicine and Rehabilitation Tri-State Orthopaedic Surgeons, Inc. Evansville IN USA

Alvin K. Antony MD, FABPM&R, FABPM Director, Physiatry and Pain Management Advanced Centers for Orthopedic Surgery and Sports Medicine Clinical Instructor, Department of PM&R Johns Hopkins University Medical Center Baltimore MD USA Charles N. Aprill MD Clinical Professor Physical Medicine and Rehabilitation Interventional Spine Specialists Louisiana State University Health Science Center Kenner LA USA Madhuri Are MD, BA Assistant Professor, Cancer Pain Management Department of Anesthesiology and Pain Medicine MD Anderson Cancer Center University of Texas Houston TX USA Joshua D. Auerbach MD Resident Department of Orthopaedic Surgery University of Pennsylvania Philadelphia PA USA Giancarlo Barolat MD Director and CEO The Barolat Institute Lone Tree CO USA Katrien Bartholomeeusen PT MSc Manual Therapy, Dip ManipTher, MSc Sport PT Head of Private Practice for Manipulative PT and Sports PT Faculty of Physical Education and Physiotherapy Lier Belgium

Lisa M. Bartoli DO, MS, FAAPMR Adjunct Clinical Assistant Professor Head Team Physician USA Rugby Women’s National Team Center for Health and Healing Department of Orthopedics Beth Israel Medical Center New York NY USA Bonnie Lee Bermas MD Associate Rheumatologist Robert B. Brigham Arthritis Center Brigham and Women’s Hospital Boston MA USA Sarjoo M. Bhagia MD, MSc (Orth) Interventional Physiatrist Department of Orthopedics and Rehabilitation Miller Orthopaedic Clinic Charlotte NC USA Amit S. Bhargava MD, MS Physician Interventional Spine, EMG, Arthritis, Pain and Sports Medicine Physical Medicine and Rehabilitation Owings Mills MD USA Atul L. Bhat MD Clinical Instructor Department of Physical Medicine and Rehabilitation Tufts University School of Medicine Nashua NH USA Klaus Birnbaum Priv.-Doz. Physician Orthopädie Hennef Hennef Germany Nikolai Bogduk BSc(Med), MBBS, PhD, MD, DSc, Dip Anat, MMed (Pain Management) FAFRM, FAFMM, FFDM (ANZCA) Conjoint Professor of Pain Medicine Department of Clinical Research The Newcastle Bone and Joint Institute University of Newcastle Newcastle Australia

Donatella Bonaiuti MD Physiatrist Chief of Rehabilitation Medicine Department S. Gerardo Hospital Milan Italy Guiseppe Bonaldi MD Director, Neuroradiology Department Department of Neuroradiology Riuniti Hospital Bergamo Italy Joanne Borg-Stein MD Assistant Professor of Physical Medicine and Rehabilitation Department of Physical Medicine and Rehabilitation, Harvard Medical School Medical Director, Spaulding Wellesley Rehabilitation Center Wellesley MA USA Kenneth P. Botwin MD Fellowship Director Florida Spine Institute Clearwater FL USA Craig D. Brigham MD Physician OrthoCarolina Charlotte NC USA Oleg Bronov MD Clinical Instructor in Radiology Department of Radiology/Neuroradiology Division University of Pennsylvania Medical Center Philadelphia PA USA Lee Ann Brown DO Physical Medicine and Rehabilitation Florida Spine Institute Clearwater FL USA

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List of Contributors Mark D. Brown MD, PhD Professor and Emeritus Chairman Department of Orthopaedics and Rehabilitation University of Miami School of Medicine Miami FL USA Thomas N. Bryce MD Assistant Professor Department of Rehabilitation Medicine Mount Sinai Medical Center New York NY USA Allen W. Burton MD Associate Professor Department of Anesthesiology and Pain Medicine University of Texas MD Anderson Cancer Center Houston TX USA John A. Carrino MD, MPH Assistant Professor of Radiology Harvard Medical School Department of Radiology Brigham and Women’s Hopsital Boston MA USA Bojun Chen MD, PhD Clinical Instructor Department of Rehabilitation Medicine Mount Sinai Medical Center New York NY USA Yung Chuan Chen MD Physical Medicine and Rehabilitation Specialist, Pain Physician, Physiatrist Physical Medicine and Rehabilitation Spinal Diagnostics and Treatment Center Daly City CA USA Cynthia Chin MD Associate Professor of Clinical Radiology Department of Radiology University of California, San Francisco San Francisco CA USA Kingsley R. Chin MD Assistant Professor of Orthopaedic Surgery Division of Spine Surgery Hospital of the University of Pennsylvania Philadelphia PA USA

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Larry H. Chou MD Medical Director, Sports and Spine Rehabilitation Division Premier Orthopaedic and Sports Medicine Associates, LTD Clinical Associate Professor of Physical Medicine and Rehabilitation University of Pennsylvania Health System Philadelphia PA USA David W. Chow MD Medical Director California Spine Center Walnut Creek CA USA Yung Chuan Chen MD Physical Medicine and Rehabilitation Specialist, Pain Physician Physical Medicine and Rehabilitation Spinal Diagnostics and Treatment Center Daly City CA USA Gianluca Cinotti MD Registrar Orthopaedic Surgery Clinical Orthopedics Universita of Rome Italy Steven P. Cohen MD Associate Professor Department of Anesthesiology and Critical Care Medicine John Hopkins School of Medicine Baltimore MD USA Paul Cooke MD, FABPM&R Assistant Attending Physiatrist Hospital for Special Surgery Attending Physician, The Medical Center of Princeton Princeton, NJ USA Anthony R. Cucuzzella MD Medical Staff Christiana Care Health System Christiana Spine Center Newark NJ USA Richard J. Daniels MD Staff Interventional Radiologist University Hospital Pennsylvania Philadelphia PA USA Kenny S. David MS(Orth) Consultant Department of Orthopaedic Surgery Christian Medical College Vellore India

Gregory Day FRACS (Orth) Associate Professor Department of Surgery School of Medicine Bond University Queensland Australia

Omar El-Abd MD Clinical Instructor, Interventional Physiatrist Spaulding Rehabilitation Hospital Harvard Medical School Wellesley MA USA

Miles Day MD, FIPP, DABPM Associate Professor Department of Anesthesiology and Pain Medicine Texas Tech University Health Sciences Center Lubbock TX USA

Mark I. Ellen MD, FAAPM&R Medical Director and Section Chief Physical Medicine and Rehabilitation Service Birmingham Veterans Administration Medical Center Birmingham AL USA

Rick B. Delamarter MD Medical Director The Spine Institute Santa Monica CA USA

Dawn M. Elliott PhD Associate Professor Department of Orthopaedic Surgery and Department of Bioengineering University of Pennsylvania Philadelphia PA USA

Michael J. DePalma MD Associate Professor Director, VCU Spine Center Physical Medicine and Rehabilitation Virginia Commonwealth University Richmond VA USA Richard Derby MD Medical Director Spinal Diagnostics and Treatment Center Adjunct Clinical Associate Professor Division of Physical Medicine and Rehabilitation Stanford University Medical Center Daly City CA USA Timothy R. Dillingham MD, MS Professor and Chairman Dept of Physical Medicine and Rehabilitation The Medical College of Wisconsin Brookfield WI USA Carol A. Dolinskas MD, FACR Clinical Associate Professor of Radiology University of Pennsylvania Philadelphia PA USA Jonathan A. Drezner MD Associate Professor, Team Physician Associate Director, Sports Medicine Fellowship Department of Family Medicine Hall Health Sports Medicine University of Washington Seattle WA USA Thomas Edrich MD, PhD Instructor of Anesthesia Department of Anesthesiology Brigham and Women’s Hospital Boston MA USA

Clifford R. Everett MD, MPH Assistant Professor of Orthopaedics Physical Medicine and Rehabilitation Department of Orthopaedics University of Rochester Rochester NY USA Amir H. Fayyazi Assistant Professor Department of Orthopedics Institute for Spine Care Syracuse NY USA Claudio A. Feler MD, FACS Semmes-Murphey Neurologic and Spine Institute Associate Professor Department of Neurosurgery University of Tennessee Health Science Center Memphis TN USA Julius Fernandez MD Semmes-Murphey Neurologic and Spine Institute Assistant Professor Department of Neurosurgery University of Tennessee Health Science Center Memphis TN USA Robert Ferrari MD, FRCPC, FACP Clinical Professor University of Alberta Hospital Edmonton AB Canada Jeffrey S. Fischgrund MD Attending Orthopaedic Surgeon William Beaumont Hospital Royal Oak MI USA

List of Contributors David A. Fishbain MD, BSc (Hon), MSc, FAPA Professor of Psychiatry and Adjunct Professor of Neurological Surgery University of Miami Rosomoff Pain Center Miami Beach FL USA Colleen M. Fitzgerald MD Medical Director, Women’s Health Rehabilitation Rehabilitation Institute of Chicago Assistant Professor Physical Medicine and Rehabilitation Northwestern University Feinberg School of Medicine Chicago IL USA Yizhar Floman MD Professor of Orthopedic Surgery Israel Spine Center Assuta Hospital Tel Aviv Israel Edward J. Fox MD Assistant Professor of Orthopaedic Surgery Division of Orthopaedic Oncology Hospital of the University of Pennsylvania Philadelphia PA USA Michael B. Furman MD, MS Clinical Assistant Professor Department of Physical Medicine and Rehabilitation Temple University School of Medicine Philadelphia PA USA Rollin M. Gallagher MD, MPH, DABPM Director of Pain Management Department of Anesthesiology Philadelphia Veterans Affairs Medical Center Philadelphia PA USA Steven R. Garfin MD Professor and Chair Department of Orthopedics University of California San Diego San Diego CA USA Timothy A. Garvey MD Staff Surgeon Twin Cities Spine Center Minneapolis MN USA

Robert J. Gatchel PhD, ABPP Professor and Chairman Department of Psychology College of Science, University of Texas at Arlington Arlington TX USA Peter Gerner MD Assistant Professor of Anesthesiology Department of Anesthesiology Brigham and Women’s Hospital Boston MA USA Peter C. Gerszten MD, MPH, FACS Associate Professor of Neurological Surgery Department of Neurological Surgery Presbyterian University Hospital Pittsburgh PA USA Russell V. Gilchrist DO Assistant Professor Department of Physical Medicine and Rehabilitation University of Pittsburgh Medical Center Pittsburgh PA USA Robert S. Gotlin DO, FAAPMR Director, Orthopaedic and Sports Rehabilitation Assistant Professor, Rehabilitation Medicine Albert Einstein College of Medicine at Yeshiva University Department of Orthopaedic Surgery Continuum Center for Health and Healing New York NY USA M. Sean Grady MD Professor and Chairman Department of Neurosurgery University of Pennsylvania School of Medicine Philadelphia PA USA Richard D. Guyer MD Associate Clinical Professor Department of Orthopedics University of Texas PlanoTX USA Andrew J. Haig MD, FAAEM, FAAPMR Associate Professor Physical Medicine and Rehabilitation and Orthopedic Surgery University of Michigan Ann Arbor MI USA

Stephen Hanks MD Assistant Professor of Clinical Orthopaedic Surgery Department of Orthopaedic Surgery University of Arizona Health Sciences Center Pittsburgh PA USA Matthew Hannibal MD Orthopedic Surgeon San Francisco Orthopedic Surgeons San Francisco CA USA Mouchir Harb MD Attending Physician Spring Valley Hospital Las Vegas NV USA Donal F. Harney MD, Dip Pain Med, CARCSI, FCARCSI Department of Anesthesiology Pain Management and Research Center University Hospital Maastricht Maastricht The Netherlands Mark A. Harrast MD Clinical Associate Professor of Rehabilitation Medicine and Orthopaedics and Sports Medicine University of Washington Seattle WA USA Syed Anees Hasan MD Spine Fellow Penn Spine Center, HUP University of Pennsylvania Health System Philadelphia PA USA Sara Ruth Sanne Haspeslagh, MD, FIPP Anesthesiologist, Pain Specialist Department of Anesthesiology AZ Sint-Augustinus Hospital Wilrijk Belgium James Heavner PhD, DVM Professor Department of Anesthesiology Texas Tech University Health Sciences Center Lubbock TX United States Johannes Hellinger MD Professor of Orthopaedics, Spine Surgeon Department of Orthopaedics Isar Klinik Munich Munich Germany

Stefan Hellinger MD Orthopaedic Surgeon, Spine Surgeon Department of Orthopaedics Isar Klinik Munich Munich Germany Steven Helper MD Physiatrist Penn Spine Fellow University of Pennsylvania Philadelphia PA USA Harry N. Herkowitz MD Chairman Department of Orthopaedic Surgery William Beaumont Hospital Royal Oak MI USA Harish S. Hosalkar, MD, MBMS(Orth), FCPS (Orth), DNB (Orth) Pediatric Orthopedic Surgeon Department of Orthopedic Surgery University of Pennsylvania Philadelphia PA USA Kenneth Hsu MD Attending Orthopaedic Surgeon Spine Center St. Mary’s Hospital and Medical Center San Francisco CA USA Raymond D. Hubbard MD Pre-doctoral Fellow Department of Bioengineering University of Pennsylvania Philadelphia PA USA Christopher W. Huston MD Consultant to Phoenix Suns, Mercury and Arizona Rattlers The Orthopedic Clinic Association Phoenix AZ USA Victor W. Isaac MD, FAAPMR Associate Director Center for Spine, Joint and Neuromuscular Rehabilitation Brentwood TN USA Zacharia Isaac MD Instructor Physical Medicine and Rehabilitation Harvard Medical School Chestnut Hill MA USA

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List of Contributors James D. Kang MD Professor of Orthopaedic and Neurological Surgery Department of Orthopaedic Surgery University of Pittsburgh School of Medicine Pittsburgh PA USA

Daniel H. Kim MD, FACS Assistant Clinical Professor Department of Orthopaedic Surgery The Boston Spine Group Boston MA USA

Joseph M. Lane MD Professor Orthopaedic Surgeon Orthopaedic Surgery Hospital for Special Surgery New York NY USA

Brinda S. Kantha DO Attending Physician New Jersey Institute of Minimally Invasive Spine Surgery West Orange NJ USA

David H. Kim MD Assistant Clinical Professor Department of Orthopaedic Surgery Tufts University Medical School New England Baptist Hospital The Boston Spine Group Boston MA USA

Hoang N. Le MD Clinical Instructor in Neurosurgery Department of Neurosurgery Stanford Medical Center Palo Alto CA USA

Frederick S. Kaplan MD Isaac and Rose Nassau Professor of Orthopaedic Molecular Medicine Department of Orthopaedic Surgery University of Pennsylvania School of Medicine Philadelphia PA USA

Mark A. Knaub MD Assistant Professor of Orthopaedics and Rehabilitation Penn State Milton S. Hershey Medical Center Penn State College of Medicine Hershey PA USA

Jaro Karppinen MD, PhD, BSc Professor of Physical and Rehabilitation Medicine Department of Occupational Medicine Finnish Institute of Occupational Health Oulu Helsinki Finland

Brian J. Krabak MD, MBA Clinical Associate Professor Department of Rehabilitation Medicine University of Washington Seattle WA USA

Yoshiharu Kawaguchi MD, PhD Assistant Professor Department of Orthopaedic Surgery Toyama Medical and Pharmaceutical University Toyama Japan Christina Kerger Hynes MD Attending Physician, Women’s Health Rehabilitation Rehabilitation Institute of Chicago Instructor, Physical Medicine and Rehabilitation Northwestern University Feinberg School of Medicine Chicago IL USA Byung-Jo Kim MD, PhD Associate Professor of Neurology Department of Neurology Korea University College of Medicine Seongbuk-Gu Seoul Korea Choll W. Kim MD, PhD Assistant Professor, Minimally Invasive Orthopaedic Surgery Department of Orthopaedic Surgery University of California San Diego CA USA xii

Elliot S. Krames MD Medical Director Department of Anesthesiology Pacific Pain Treatment Centers San Francisco CA USA

Kathryn E. Lee Pre-doctoral Fellow Department of Bioengineering University of Pennsylvania Philadelphia PA USA Sang-Heon Lee MD, PhD Physiatrist Research Physician Spinal Diagnostics and Treatment Center Daly City CA USA David A. Lenrow MD, JD Vice Chair of Clinical Affairs Associate Professor Department of Physical Medicine and Rehabilitation Hospital of the University of Pennsylvania Philadephia PA USA

Per O. J. Kristiansson MD, PhD Associate Professor of General Practice Department of Public Health and Caring Sciences Uppsala University Uppsala Sweden

Paul H. Lento MD Assistant Professor, Northwestern Medical School and Attending Physician, Center for Spine, Sports and Occupational Rehabilitation Rehabilitation Institute of Chicago Chicago IL USA

Jukka-Pekka Kouri MD Specialist in Physical Medicine and Rehabilitation Pain Specialist Helsinki Finland

Isador H. Lieberman BSc, MD, MBA, FRCS(C) Professor of Surgery Spine Institute Cleveland Clinic Cleveland OH USA

Richard D. Lackman MD, FACS Associate Professor and Chairman Department of Orthopaedic Surgery Hospital of the University of Pennsylvania Philadelphia PA USA Francis P. Lagattuta MD Fellowship Director LAGS Spine and Sportscare Medical Center, Inc. Santa Maria CA USA

Julie T. Lin Assistant Professor Department of Rehabilitation Medicine Weill Medical College of Cornell University New York NY USA Jason S. Lipetz MD Assistant Professor Department of Rehabilitation Medicine Albert Einstein College of Medicine East Meadow NY USA

Donald Liss MD Assistant Clinical Professor of Rehabilitation Medicine Columbia University College of Physicians and Surgeons New York NY and Attending Physician The Physical Medicine and Rehabilitation Center Englewood NJ USA Howard Liss MD Assistant Clinical Professor of Rehabilitation Medicine Columbia University College of Physicians and Surgeons New York NY and Attending Physician The Physical Medicine and Rehabilitation Center Englewood NJ USA Steven M. Lobel MD Fellow Georgia Pain Physicians Training Program Atlanta GA USA Carmen E López-Acevedo MD Associate Professor Department of Physical Medicine, Rehabilitation and Sports Medicine University of Puerto Rico School of Medicine San Juan Puerto Rico Susan M. Lord BMedSc, BMed, PhD, FANZCA, FFPMANZCA Staff Specialist, Pain Medicine Division of Anaesthesia, Intensive Care & Pain Management John Hunter Hospital New Lambton Heights NSW Australia William W. Lu PhD, MHKIE Associate Professor Department of Orthopaedics and Traumatology The University of Hong Kong Hong Kong China Keith D. K. Luk Professor of Orthopaedic Surgery Department of Orthopedic Surgery Duchess of Kent Children’s Hospital University of Hong Kong Hong Kong China Gregory E. Lutz MD Physiatrist-in-Chief Hospital for Special Surgery New York NY USA

List of Contributors Jean-Yves Maigne MD Head, Department of Physical Medicine Hôtel-Dieu Hospital Paris France

Ian Bruce McPhee FRACS (ortho) Associate Professor Orthopaedics Division of Orthopaedics The University of Queensland Queensland Australia

Gerard A. Malanga MD Director, New Jersey Sports Institute New Jersey Medical School West Orange NJ USA

Samir Mehta MD Resident Department of Orthopaedic Surgery University of Pennsylvania Philadelphia PA USA

Julie Marley PT, Dip MDT Physical Therapist Spine Center Christiana Spine Center Newark NJ USA Richard Materson MD Clinical Professor, Physical Medicine and Rehabilitation Baylor College of Medicine and University of Texas Medical School and Chairman of the Board, Institute for Religion and Health Texas Medical Center Houston TX USA Christopher J. Mattern MD Orthopaedic Resident Hospital for Special Surgery New York NY USA Eric A.K. Mayer MD Physician Productive Rehabilitation Institute of Dallas for Ergonomics Dallas TX USA Tom G. Mayer MD Medical Director, Productive Rehabilitation Institute of Dassas for Ergonomics Clinical Professor of Orthopedic Surgery University of Texas Southwestern Medical Center Dallas TX USA Frank McCabe MPT Cert. MDT Physical Therapist Physical Therapy Wallace, Glick and McCabe Physical Therapy and Fitness Montgomery PA USA Colleen McLaughlin BSRT Radiology Technologist Penn Spine Center University of Pennsylvania Health System Philadelphia PA USA

Renée S. Melfi MD Physician Physical Medicine and Rehabilitation Orthopaedic Associates of Central New York Syracuse NY USA Thomas Metkus BS Associate Professor Department of Neurosurgery University of Pennsylvania School of Medicine Philadelphia PA USA Mathew Michaels MD Consultant Georgia Pain Physicians, PC Atlanta GA USA William F. Micheo MD Chairman and Professor Department of Physical Medicine, Rehabilitation and Sports Medicine University of Puerto Rico School of Medicine San Juan USA

Michael Ray Moore MD Clinical Assistant Professor of Surgery The Bone and Joint Center The University of North Dakota School of Medicine and Health Sciences Bismarck ND USA Michael H. Moskowitz MD MPH Assistant Clinical Professor Anesthesiology and Pain Medicine University of California Davis Sacramento CA and Bay Area Pain Medical Associates Mill Valley CA USA S. Ali Mostoufi MD Interventional Physiatrist MGH Spine Center MGH Pain Clinic Boston MA USA Scott F. Nadler DO Formerly, Professor Physical Medicine and Rehabilitation Randolph NJ USA Stefano Negrini MD Scientific Director Italian Scientific Spine Institute (ISICO) Milan Italy Markus Niederwanger MD Fellow Georgia Pain Physicians Training Program Atlanta GA USA

Evan R. Minkoff DO Physician Desert Pain and Rehabilitation Associates Palm Desert CA USA

Conor W. O’Neill MD Comprehensive Spine Diagnostics Medical Group, Inc Daly City CA USA

Peter J. Moley MD Assistant Attending Physiatrist HSS Affiliated Physician’s Office Old Greenwich CT USA

Donna D. Ohnmeiss Dr.Med President Texas Back Institute Research Foundation Plano TX USA

Marco Monticone MD Researcher Italian Scientific Spine Institute Milan Italy Gul Moonis MD Assistant Professor of Radiology Department of Radiology/Neuroradilgy Division University of Pennsylvania Medical Center Philadelphia PA USA

Raymond W.J.G Ostelo PhD, PT Doctor of Epidemiology Institute for Research in Extramural Medicine (EMGO) Institute VU Medical Centre Amsterdam The Netherlands Jeffrey Ostrowski PT Physical Therapist Excel Physical Therapy Philadelphia PA USA

Ashley Lewis Park MD, FACP Clinical Assistant Professor of Medicine Department of Internal Medicine Division of Rehabilitation University of Tennesee College of Medicine Staff Physician, Campbell Orthopaedic Clinic Germantown TN USA Vikram Parmar MD Physician Opelousas General Health System Opelousas LA USA Rajeev K. Patel MD Assistant Professor Orthopaedics Department of Orthopaedics University Orthopaedic Associates Pittsford NY USA Andrew Perry MD Orthopaedic Resident University of California San Diego San Diego CA USA Frank M. Phillips MD Professor of Orthopaedic Surgery Rush University Medical Center Chicago IL USA Robert J. Pignolo MD, PhD Assistant Professor of Medicine Department of Medicine Division of Geriatric Medicine University of Pennsylvania School of Medicine Philadelphia PA USA Christopher T. Plastaras MD Assistant Professor Physical Medicine and Rehabilitation Feinberg Northwestern School of Medicine Chicago IL USA Franco Postacchini MD Professor of Orthopaedic Surgery Clinical Orthopedics University of Rome ‘La Sapienza’ Rome Italy Roberto Postacchini MD Professor of Orthopaedic Surgery Clinica Ortopedica University of Rome ‘La Sapienza’ Rome Italy Ben B. Pradhan MD, MSE Director of Clinical Research The Spine Institute Santa Monica CA USA xiii

List of Contributors Joshua P. Prager MD, MS, DABPM Director Department of Anesthesiology and Internal Medicine UCLA Pain Medicine Center Los Angeles CA USA Heidi Prather DO Associate Professor Chief, Section of Physical Medicine and Rehabilitation Department of Orthopedics Washington University School of Medicine St Louis MO USA Adriana S. Prawak DO Attending Physician and Partner Sports and Spine Rehabilitation Division Premier Orthopaedic and Sports Medicine Associates, LTD Havertown PA USA Joel M. Press MD Attending Physician Spine and Sports Rehabilitation Center, Rehabilitation Institute of Chicago and Associate Professor Department of Physical Medicine and Rehabilitation Northwestern University Feinberg School of Medicine Chicago IL USA G. X. Qiu MD Professor of Orthopaedic Surgery Department of Orthopaedic Surgery Peking Union Medical College Hospital Beijing PR China Gabor B. Racz MD, DABA, FIPP, ABMP, ABIPP Professor and Chair Department of Anesthesiology and Pain Management Texas Tech University Lubbock TX USA Kristjan T. Ragnarsson MD Professor and Chairman Department of Rehabilitation Medicine Mount Sinai Medical Center New York NY USA Raj D. Rao MD Director of Spine Surgery Department of Orthopedic Surgery Medical College of Wisconsin Milwaukee WI USA

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Ryan S. Reeves MD Medical Director, Spine Team Texas Attending Physiatrist, Spine Team Texas Southlake TX USA

Terry C. Sawchuk MD Adjunct Professor Intermountain Spine Institute University of Utah Salt Lake City UT USA

Ramnik Singh MD Attending Physician Institute for Spinal Disorders Cedars-Sinai Medical Center Los Angeles CA USA

Luke Rigolosi MD Physical Medicine and Rehabilitation New Jersey Medical School University of Medicine and Dentistry of New Jersey University Hospital Newark NJ USA

Jerome Schofferman MD Director of Research and Education Spine Care Medical Group San Francisco Spine Institute Daly City CA USA

Clayton D Skaggs DC Associate Professor of Research Logan University Adjunct Instructor Department of Obstetrics Washington University St Louis MO USA

James Schuster MD, PhD Assistant Professor Department of Neurosurgery The Hospital of the University of Pennsylvania Philadelphia PA USA

Jan Slezak MD Medical Director of Northeast Pain Research Center Interventional Spine Medicine Barrington NH USA

Eric D. Schwartz Associate Professor of Radiology Department of Radiology/Neuroradiology Division University of Pittsburgh Medical Center Pittsburgh PA USA

Curtis W. Slipman MD Director, Penn Spine Center Associate Professor of Physical Medicine and Rehabilitation University of Pennsylvania Health System Philadelphia PA USA

Rinoo Vasant Shah MD, DABPMR, DABPMR (Pain), DABPM Assistant Professor Department of Anesthesiology Guthrie Clinic Horseheads NY USA

Wesley L. Smeal MD Attending Physician, Spine and Sports Rehabilitation Center Rehabilitation Institute of Chicago Instructor, Department of Physical Medicine and Rehabilitation Northwestern University – Feinberg School of Medicine Chicago IL USA

Hubert L. Rosomoff MD, DMedSc, FAAPM Medical Director The Rosomoff Comprehensive Pain and Rehabilitation Center Miami Jewish Home and Hospital at Douglas Gardens Miami Beach FL USA Renee Steele Rosomoff RN, BSN, MBA Program Director The Rosomoff Comprehensive Pain and Rehabilitation Center Miami Beach FL USA Sarah M. Rothman Pre-doctoral Fellow Department of Bioengineering University of Pennsylvania Philadelphia PA USA Anthony S. Russell MA, MBBChir, FRCP, FRCPC, FACP Professor of Medicine University of Alberta Edmonton AB Canada Bjorn Rydevik MD, PhD Professor of Orthopaedic Surgery Department of Orthopaedics Salgrenska University Hospital Gothenburg Sweden Durgadas Sakalkale MD Clinical Instructor Department of Orthopaedics and Rehabilitation Yale University School of Medicine New Haven CT USA Robert Savarese DO Physician Jacksonville Orthopedic Institute Jacksonville FL USA

Parag Sheth MD Assistant Professor of Medicine Department of Rehabilitation Medicine Mount Sinai School of Medicine New York NY USA Frederick A. Simeone MD, FACS Emeritus Professor of Neurosurgery University of Pennsylvania School of Medicine Philadelphia PA USA Alexander C. Simotas MD Assistant Professor of Rehabilitation Medicine Physical and Rehabilitative Medicine Weill Medical College of Cornell University New York NY USA Gurkirpal Singh BS, MBBS, MD Adjunct Clinical Professor of Medicine Division of Gastroenterology and Hepatology Stanford University School of Medicine Stanford CA USA

Jennifer L. Solomon MD Clinical Instructor Physical Medicine and Rehabilitation Weill Medical College of Cornell University New York NY USA Hillel M. Sommer MD, FRCPC, CSPQ, Dip. Sport Med Associate Professor Physical Medicine and Rehabilitation University of Manitoba Winnipeg MB Canada Brad Sorosky MD Clinical Instructor Department of Physical Medicine and Rehabilitation Northwestern Feinberg School of Medicine Chicago IL USA

List of Contributors Daniel Southern MD Danbury Orthopedic Associates Danbury CT USA Gwendolyn A. Sowa MD, PhD Assistant Professor of Physical Medicine and Rehabilitation Center for Sports, Spine and Occupational Rehabilitation Pittsburgh PA USA Milan P. Stojanovic PhD Director, Interventional Pain Program HMS Anaesthesia Massachusetts General Hospital Boston MA USA William J. Sullivan MD Assistant Professor Department of Physical Medicine and Rehabilitation University of Colorado at Denver and Health Sciences Centre Aurora CO USA Gul Koknel Talu MD Associate Professor of Anesthesiology Department of Algology Medical Faculty of Istanbul University Istanbul Turkey Andrea Tarquinio RN Head Nurse Penn Spine Center Hospital of the University of Pennsylvania Philadelphia PA USA Philip Tasca MD Assistant Clinical Professor of Rehabilitation Medicine Columbia University Medical Center New York NY and Interventional Physiatrist The Physical Medicine and Rehabilitation Center, PA Englewood NJ USA Santhosh A. Thomas DO, FAAPM&R Medical Director, Spine Center Co-Director, Medical Spine Fellowship Cleveland Clinic Foundation Westlake OH USA Issada Thongtrangan MD Department of Neurosurgery Stanford University Medical Center Palo Alto CA USA

Carlos F. Tirado MD Clinical Research Fellow in Addiction University of Pennsylvania Treatment Research Centre Philadelphia PA USA John E. Tobey MD Clinical Instructor, Department of Physical Medicine and Rehabilitation University of Colorado Health Sciences Center Boulder CO USA

Christophe Van de Wiele MD, PhD Department of Nuclear Medicine University Hospital Gent Gent Belgium

Douglas S. Won MD Attending Spine Surgeon Southwest Spine Institute Irving TX USA

Maarten van Kleef Head of Department of Anesthesiology and Pain Management Pain Management and Research Center University Hospital Maastricht Maastricht The Netherlands

Kirkham Wood MD Associate Professor Department of Orthopaedics Massachusetts General Hospital Boston MA USA

Daisuke Togawa MD, PhD Adjunct Staff Spine Centre Hakodate Central General Hospital Hakodate City Hokkaido Japan

Jan Van Zundert MD, PhD, FIPP Head of Multidisciplinary Pain Centre Anesthesiologist, Department of Anesthesiology, Pain Management and Research Centre, University Hospital Maastricht Maastricht The Netherlands

Jesse T. Torbert MD, MS Orthopaedic Tumour Post-Doctoral Research Fellow Pennsylvania Hospital Philadelphia PA USA

Kamen Vlassakov MD Director, Division of Orthopaedic and Regional Anesthesia Brigham and Women’s Hospital Boston MA USA

Carlo Trevisan MD Medical Specialist Surgeon in Orthopedics Clinical Orthopedics University of Milan–Bicocca Monza Italy John J. Triano DC, PhD, FCCS(C) Director Chiropractic Division Texas Back Institute Plano TX USA Mark D. Tyburski MD Physiatrist Department of Physical Medicine and Rehabilitation Spine Clinic Roseville CA USA Mohammad N. Uddin MD Pain Management Physician APAC Centers for Pain Management Chicago IL USA Alexander Vaccaro MD, FACS Professor and Co-chief, Spine Division Department of Orthopaedic Surgery Rothman Institute Philadelphia PA USA Vijay B. Vad MD Assistant Professor Department of Rehabilitation Medicine Weill Medical College of Cornell University New York NY USA

John B. Weigele MD, PhD Assistant Professor of Radiology Department of Radiology Hospital of the University of Pennsylvania Philadelphia PA USA William C. Welch MD Chief of Neurosurgery, Pennsylvania Hospital Professor of Neurosurgery Clinical Practices of the University of Pennsylvenia University of Pennsylvania Health System Philadelphia PA USA C. Y. Wen MMedSc MBBS Department of Orthopaedics and Traumatology Clinical Science Building Prince of Wales Hospital Hong Kong China Robert E. Windsor MD FAAPMR FAAPM FAAEM President Georgia Pain Physicians, PC Atlanta GA USA

Chandra S Yerramalli PhD Department of Orthopaedic Surgery McKay Orthopaedic Research Laboratory University of Pennsylvania Philadelphia PA USA Anthony T. Yeung MD Orthopedic Surgeon Arizona Institute for Minimally Invasive Spine Care Arizona Orthopedic Surgeons Phoenix AZ USA Christopher Alan Yeung MD Voluntary Clinical Instructor Department of Orthopedic Surgery University of California San Diego School of Medicine Phoenix AZ USA Way Yin MD Medical Director Spinal Diagnostics; Interventional Pain Management Interventional Medical Associates of Bellingham, PC Bellingham WA USA Faisel M. Zaman MD, FAAPMR&ABPM Interventional Physiatrist Intermountain Spine Institute Affiliate Faculty, University of Utah Division of Physical Medicine and Rehabilitation Salt Lake City UT USA James F. Zucherman MD Medical Director Orthopedic Spine Surgeon St Mary’s Spine Center San Francisco CA USA

Beth A. Winklestein PhD Assistant Professor of Bioengineering and Neurosurgery Department of Bioengineering University of Pennsylvania Philadelphia PA USA xv

Preface

Two decades ago, the notion that the variety of disciplines that practice spine care would universally embrace the concept of a comprehensive algorithmic approach was an anathema. While this methodical, stepwise approach had been practiced by the spine surgical community the other specialties treating patients with spinal disorders have had a haphazard orientation. Some disciplines offered a singular technique, which was used to treat all painful conditions, while others used ‘a little of this, and a little of that’. As the years passed, a variety of influences have irrevocably changed the perspective that conservative care cannot be appropriately integrated with the surgical approach. Among the propelling factors have been cohort and randomized studies of patients undergoing medical rehabilitation and interventional spine care; an explosion in the number of physicians who practice interventional spine/pain medicine; education of the lay community, which has been accelerated by the internet, and their desire to pursue the least aggressive treatment available; and malpractice lawsuits predicated on surgery having been performed without adequate conservative treatment. This book represents the culmination of the growth and development of the diagnosis and treatment of patients with spinal pain. Indeed, the composition of editors underscores the importance this integrated approach has taken. Our focus has been to write about algorithmic approaches for a variety of conditions. A basic premise and a central theme of this text is that certain disorders require immediate surgery, but most

can be managed with medications, therapy and possibly injection or other percutaneous procedures. We want the reader to understand when surgery can be delayed, when it should be avoided, and when it is required. It is also our hope that this text will provide a stepwise approach for those patients that have disorders that fall under the former two situations. Some of our algorithms are universally accepted, while others represent the idiosyncratic approach of the author. In fact, there are several instances in which the same problem is attacked in a different way by two authors. Since the science of medical rehabilitation and interventional spine care is evolving, it is no surprise that spine practitioners may have different views regarding which tests to request, the order of diagnostic and treatment interventions and which therapeutic alternatives are best. However, within that expected and reasonable diversity of opinion a central belief should be conveyed to the reader. Patients deserve the least aggressive care feasible, but the alternatives must be chosen by the individual spine practitioners’ interpretation of the literature and their clinical experience. When this is accomplished, an algorithmic approach can be offered that adequately balances the potential outcomes and known side effects or complications. As our understanding of painful spinal disorders evolves we should expect that most patients with a particular disorder will be treated in a similar fashion and we believe this textbook places us closer to this penultimate goal. Curtis W. Slipman 2007

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Acknowledgments

The development and production of a textbook of this scope is an enormous task and requires the assistance of numerous individuals. My appreciative comments begin with my residency at Columbia Presbyterian Medical Center and its residency director, Erwin Gonzalez. During the past 24 years he has served as a mentor and enthusiastic supporter. In 1992 when I was recruited to develop the Penn Spine Center, it was Alfred Fishman who had the vision, political prowess and guidance to insure that interventional physiatry would thrive in an academic setting. Concurrently, Ron Wisneski, whose tenure of chief of orthopedic spine surgery temporarily overlapped with my presence at The University of Pennsylvania, helped formulate the idea of an algorithmic approach to neck and back pain. Since my arrival at Penn an exponential growth in my education of spine care occurred. Richard Herzog provided the foundation and nuances for the interpretation of radiological studies, Ron Wisneski and Ed Vresilovic shared the surgical perspective and were open to learning and employing a Physiatric perspective. Of course there were and remain many physicians with whom I have practiced that have a played a key role in my understanding of spinal disorders. Among them are Lori Loevner, Evan Siegelman, Robert Grossman, Murray Dalinka, Robert Hurst, Paul Marcotte, David Lenrow, Fred Kaplan, Mark Ellen, Larry Chou, Dawn Elliot, and Beth Winklestein. Several physicians who practiced outside of Penn were instrumental in the growth of the Penn Spine Center and in my spine education including Fred Simeone and Giancarlo Barolat. Perhaps the single most valuable contribution to my understanding of spine care comes from the Penn Spine Center Fellows; Elliot Sterenfeld, Chris Huston, David DeDanious, Randy Palmitier, Jason Lipetz, Howard

Jackson, Zac Isaac, Atul Bhat, Russell Gilchrist, Mike Frey, Phil Tasca, Sarjoo Bhaggia, Omar el Abd, Michael DePalma, Raj Patel, David Chow, Frank Bender, Carl Shin, Amit Bhargava, Aleya Salem, Victor Isaac, Faisel Zaman, Serge Menkin, Steven Helper, and Paul Singh. Their enthusiasm, intellect and hard work have created the opportunity to see a large volume of patients, conduct research and refine my views on interventional spine care. There have been a few individuals who as medical students shared their time, enthusiasm and intellect who deserve recognition, Larry Chou, Chris Plastaras, Alfred Campbell, Catherine Loveland-Jones and Jason Berke. My current chairman, Richard Salcido, and a number of staff members at the Penn Spine Center were particularly supportive of the time and effort I needed to devote to the writing and editing of this text including Andrea Tarquinio, Colleen McLaughlin and Lynette Rundgren. The editorial staff at Elsevier, Joanne Scott, Amy Head, Cecilia Murphy, Susan Pioli, Dolores Meloni and Rolla Couchman deserve enormous thanks for their dedication, attention to detail and perseverance. Without their effort and guidance this book would not exist. I want to thank the physicians who have been the pioneers and leaders in interventional spine for the last two decades. These individuals created the opportunity all of us are now enjoying. Join me in extending appreciative thoughts to Scott Nadler, Rick Derby, Nic Bogduk, Jeff Saal, Stan Herring, Joel Press, Charles Aprill, Guisseppe Bonaldi, Paul Dreyfus, and Stu Weinstein. Finally a deep heartfelt thanks to the co-editors of this text, Rick Derby, Fred Simeone, Tom Mayer, David Lenrow, Kingsley Chin, Salahadin Abdi and Larry Chou. Their input has been invaluable and their energy irreplaceable. Curtis W. Slipman 2007

xix

To Jared

PART 1

GENERAL PRINCIPLES

Section 1

Introduction

CHAPTER

Past, Present, and Future of Interventional Physiatry

1

Richard Materson

THE PAST One might inquire what a history and philosophical chapter is doing in an evidence-based clinical textbook. Interventional spine procedures by physiatrists at first glance seem simply to be an outgrowth of physical medicine, a clinical right turn justified by new information similar to other changes in medical practice such as interventional cardiology. But the role of the practitioner is so fundamentally changed from previous roles that a deeper inquiry is invited. How do such striking ‘about-faces’ occur in medicine? What and who promotes these changes and how are they accomplished? After all, a hospital-based practitioner can’t simply announce one day that he or she is going to have entry to a surgical suite or intervention room and do new procedures. The author is grateful to the many early members of the Physiatric Association of Spine Sport and Occupational Rehabilitation (PASSOR) who were willing to e-mail to the author their observations regarding how they became involved is this movement, who influenced them, and in which directions they believe we are evolving. Most of organized medicine, including its Boards, Academies and educational hierarchy, justify their existence by including words such as ‘in the public interest …’ in their constitution or bylaws preamble. None should believe that such baser needs such as ego, power, control, and economic well-being and keeping a practice away from ‘the other guy’ do not play a role as well. The trick to good organizational management and maintenance of the voluntary system of medical accreditation is to be sure the balance favors public good a great deal more than the practitioner benefit. The development of interventional physiatry represents a model study of how change is reasonably brought about in medical practice. If one reviews the history of the practice of medicine in the United States since Flexner’s report,1 the complex story of organized medicine is found to be the string in the supersaturated sugar solution (the great mix of knowledge, attitudes, and practices) allowing the formation of rock candy (the roles of the various medical and surgical specialties). An approach through organized medical channels is the ‘way’ to get desired changes. Change does not occur quickly, nor particularly smoothly; however, the system seems to work. Perseverance pays. Such has been the case for interventional physiatry. Osler in medicine, and Halstead and others in surgery are names known by every internist and surgeon. These pioneers opined that 4 years of matriculation through even the best medical school curriculum was inadequate to teach the volume and complexity of knowledge, skills, and behaviors required to properly care for patients with significant illness. Postgraduate medical education at the bedside was required, and the development of a capacity for life-long professional learning. During the first 20 years of the twentieth century there was no such thing as a physical medicine and rehabilitation doctor. World

War One, however, produced sufficient casualties, many with musculoskeletal injuries, that would become chronic and which seemed to improve when treated with physical modalities including hydrotherapy and therapeutic exercise and newly harnessed portions of the electromagnetic spectrum. With the lead of the American Medical Association in the 1915–21 time frame, a group of physical modality experts were called together to see how more physicians might learn about and put to use these procedures. The AMA Board of Trustees approved this group, called the American Congress of Physical Therapy, in September 1921. It was not to be the start of a new specialty, but rather a task force to enhance knowledge and skills. It consisted of physicians from medicine, most of whom were attached to academic centers and who had studied and advocated for these methods. The AMA had previously and subsequently stimulated and assisted the creation of the American College of Surgeons (ACS) and the American College of Physicians (ACP) and several surgical and medical specialty organizations. With the American Association of Medical Colleges (AAMC) and the Association of Teaching Hospitals, the AMA, ACP, and ACS, the idea of credentialing individuals who were willing to subject themselves to additional postgraduate education, training, and experience and who were willing to put their knowledge and skills to a test, thereby identifying properly trained ‘specialists’ for the public. The medical schools came under the supervision of the Liaison Council for Medical Education (LCME), the residencies under residency review committees (RRCs) appointed jointly by the AMA section councils and specialty societies and supervised by the Accreditation Council on Graduate Medical Education (ACGME) and the American Board of Medical Specialties (ABMS), continuing education led by the Council on Medical Specialty Societies (CMSS). The various liaison groups had representation from practitioners, academicians, hospitals, boards, and medical and surgical academies. When federal dollars became prominent in support of medical education and practice, government representatives were added, but control was always in the hands of physician volunteers who were either elected by or appointed by their peers to represent them. In its earliest days practitioners of physical medicine often shared an interest in the newly developed area of ionizing radiation. In 1923, the American College of Radiology and Physiotherapy became the first physical medicine society. As radiology established itself as a separate discipline, the organization’s name was changed to drop radiology; however, the first journal was titled the Archives of Physical Therapy, X-ray and Radium. In 1930, the organization became the American Congress of Physical Therapy and in 1945, as the practice of physical therapy became its own discipline, the name changed to the American Congress of Physical Medicine. By 1954, the World War Two-developed team concept of care, espoused by Howard Rusk and George Deaver, caused another name change to Physical Medicine 1

Part 1: General Principles

and Rehabilitation. By 1967, the ‘team concept of rehabilitation’ devotees were of sufficient number to cause the name to change to the American Congress of Rehabilitation Medicine. Their journal became the Archives of Physical Medicine and Rehabilitation. Upon action from an AMA advisory council on medical specialties, on June 6, 1947, eleven physiatrists became the first American Board of Physical Medicine with Krusen as its first chairman and Zeiter as vice-chairman. A few physiatrists were ‘grandfathered’ and a total of 103 became the first listed Board Diplomats. In 1949 the board name was changed to the American Board of Physical Medicine and Rehabilitation following the trend towards rehabilitation. The group that was to become the American Academy of Physical Medicine and Rehabilitation (PM&R) began in 1938–39 as an invitation-only membership of 42 physical therapy physicians with an intent of limiting membership to 100 physicians. After 1952, all Diplomats of the American Board of Physical Medicine and Rehabilitation were invited to become members. In 1957, a conference was held to determine the proper roles of the Academy versus the American Congress. The Congress was to control the journal, to provide interdisciplinary rehabilitation education, and to reach out to nonphysiatrist physicians interested in the field. The Academy was to bring their member physiatrists into closer collaboration with other physician peers and concentrate on physiatric education and policy. The Academy was to represent the field in the AMA House of Delegates. Later, after considerable negotiation, the Archives of PM&R ownership were split by the Congress with the Academy for a purchase price of ‘$1.00 and considerations.’ Editorial Boards represented each organization under an editor-in-chief. As the Academy grew, and as the various allied professions became more independent with policy interests different at times from physicians, physiatric membership in the Congress declined. Several attempts were made to work out ways to stay allied and share a common central office but a split was inevitable. The Congress now is independent of the Academy, smaller in membership and has refocused itself to interdisciplinary rehabilitation research. The Council of Academic Societies (CAS) of the Association of American Medical Colleges in 1967 rejected the American Academy of Physical Medicine and Rehabilitation as too broadly based to be a constituent member but at the same time recognized the newly formed Association of Academic Physiatrists (AAP) to represent undergraduate and graduate medical education interests and academic policy. The history of the specialty of Physical Medicine and Rehabilitation is covered in detail elsewhere and should be reviewed for a more complete story.2–6 Elkins, Knapp, Bennett, Bierman, Kovacs, Molander, Coulter, Zeiter, Krusen Ewerhardt and others were among the originators of the field followed by Rusk, Deaver, Johnson, Lehman, Kottke, Stillwell and many more than can be mentioned here. Review will be rewarding to observe how a small group of dedicated physicians gave much volunteer time and attention to the multiple facets necessary for growth of a medical specialty. One should appreciate that what began as a ‘physical medicine’oriented body of knowledge transitioned to a medical rehabilitation orientation over time. Physical medicine was never ‘lost;’ it was simply less visible with the overriding mass appeal of rehabilitation as popularized by Rusk.7 New York philanthropist Bernard Baruch played a major role in stimulating development of 12 departments that matriculated nearly 60 early physiatric pioneers. Baruch convinced President Truman of the field’s contribution to the war and postwar effort. The President ordered military medical authorities to embrace the field. Civilian interest followed. Large infusions of federal dollars from the Medicare program followed. During the DeBakey era, heart disease and stroke held the top-tiered research support position. This funding resulted in increased medical rehabilitation demands and 2

funding at a time of virtual nonfunding for musculoskeletal disorders and research. These currents influenced the practitioners and their representatives in the American Academy of Physical Medicine and Rehabilitation. Those physicians with a more physical medicine orientation often complained of inadequate attention and resource sharing in the Academy. In general, the physical medicine oriented physiatrists gravitated towards care of more acute neuro-musculo-skeletal disorders including ever more ubiquitous spine related pain. In the military, the training programs focused on physical medicine, with rehabilitation to occur in the Veterans Administration system. In this setting, and in the growing private musculoskeletal practice setting, the physiatrist saw acute patients and often provided full diagnostic and therapeutic care, referring to other specialties as was appropriate. This conflicted with the rehabilitation model in which practitioners were describing their domain as ‘the third phase of medicine after preventive medicine and acute care.’ In the latter paradigm, the physiatrist did not have access to the patient except upon referral from a physician or surgeon who were the primary practitioners. In preparation of this chapter, a call was sent to founding PASSOR members to identify the influences upon them to become members. Perhaps the most frequently cited was the desire to become a primary practitioner for musculoskeletal patients. They were influenced by orthopedists such as James Cyriax, Arthur White, John Fromoyer, Malcolm Pope, W.H. Kirkaldy-Willis, and Alf Nachemson and sometimes encouraged to become ‘nonoperative orthopedists’ in lieu of physiatrists. They were also influenced by independent minded physiatrists whose credentials in physical medicine were rich and who were expert in use of modalities and therapeutic exercise, clinical kinesiology, and the newly developing field of electrodiagnostic medicine such as V. Lieberson, Carl Granger, Justus Lehman, Ernest Johnson, Myron Laban, Erwin Gonzalez, Ian MacLean, Joe Honet and others. Henry Betts was identified as a facilitator sympathetic to growth in this arena. Newer generations of PASSOR members were greatly influenced by Jeffrey and Joel Saal and their associate Stan Herring. These physiatrists were often themselves sportsmen whose interests gravitated in this direction. To this group add those physiatrists whose practices included large numbers of injured workmen. Many of these patients suffered spine-related pain disorders. The musculoskeletal physiatrists included also those who followed the work of Janet Travell and Dave Simons in dealing with the clinical entity of myofascial pain syndrome and those whose interests gravitated to arthritis and related disorders. Many of these physicians tended to feel that the Archives of Physical Medicine and Rehabilitation, especially those issues sponsored by the American Congress of Rehabilitation Medicine, did not adequately represent their spine and musculoskeletal interests and did not believe the Archives was well regarded by spine and sports peers in medicine. The policy issues facing the main field of rehabilitation, which were primarily government regulatory-related, were of little concern to the physical medicine practitioner who was not practicing in rehabilitation facilities but was more often office or clinic based. Furthermore, the educational offerings of the Academy were felt to slight the need for both basic and advanced material from the musculoskeletal area, especially spine and sport, and not to pay adequate attention to the office practice needs of these physiatrists. The earliest and common practice model, which continues today, was for the physiatrist to associate with an orthopedist or orthopedic group practice, becoming the member who did not perform surgery, but attended to diagnostics and postoperative care. Government and insurance bodies tended to ‘bundle’ preoperative care, surgery, and limited postoperative care into one standard surgical fee. The surgeon now had a financial incentive to pass on care to another specialist. Furthermoe, additional members in a group practice made investment in practice-owned diagnostic

Section 1: Introduction

imaging equipment and laboratories inviting and increased the frequency of use of the equipment. As physiatrists became competent in interventional spine procedures, more struck out on their own or became part of single-specialty (physiatric spine medicine) practice groups. Several academic programs became involved. Orthopedists and family practitioners laid claim to sports medicine, although several physiatrists have become professional and school team physicians and are highly regarded for their work. Physiatrists have become increasingly attractive to insurers and re-insurers as the physicians of choice for industrial musculoskeletal injuries and post-trauma soft tissue injuries. These physicians offer thorough history and physical examination, astute diagnostic capabilities, nonsurgical (read less expensive) remediative and rehabilitative care, ability to collaborate when surgery is indicated, and disability evaluation and management all in one place. The capacity to perform electromyography and diagnostic and therapeutic blocks in carefully selected patients was an added benefit. During the 1980s the Academy of PM&R attempted to address these musculoskeletal and related issues by permitting the development of special interest groups (SIGs) which became responsible for developing education appropriate to their interest and promoting policy concerns to Academy Board attention. During the annual meeting, the Academy met the first part of a week, the Congress the second part, with the middle weekday for supposed integrated blend. Time and organizational collaboration was inadequate to meet the needs of either party and disenchantment grew. There was even consideration of development of a new group outside of the Academy of PM&R to represent the interests of these musculoskeletal-oriented physiatrists. At the same time, the Academy Board, and in fact much of organized medicine, was involved in a great debate regarding subspecialization and the credentialing of subspecialists. To the degree that groups identified special added competence, the issues of territoriality appeared, i.e. limitation to one kind of practitioner or open to members of vorious Boards of Specialty. Added to this were issues of curriculum content definition and development of a critical mass of expert educators and clinical facilities to achieve the educational standards. Would specialization prevent the general Diplomat from practice in the defined area? Would that in effect drive out competition and be inflationary? Would subspecialty educational offerings be available to all (generally making the offerings entry level) or be at advanced level, good for the specialist but beyond benefit to the generalist? Would an added credential become a requirement for hospitals and certifying organizations to allow privileges or access to practitioners or for courts to recognize expertise? The Academy (and medicine) resolved these issues differently in various areas such as pediatric rehabilitation, electrodiagnostic medicine, spinal cord injury, and head injury rehabilitation. There was waxing and waning of support for the musculoskeletal specialization at the Academy Board level depending on the relative representation of rehabilitation primary versus physical medicine primary practitioners on the Board. Quick fixes allowing SIGs greater access to program content met with resistance from program committee members who felt their control and ability to meet their responsibilities challenged. At the same time, division over ownership and editorial control of the Archives of PM&R raged on at a time when the two organizations were growing ever more apart in their aspirations and needs. In 1983, the Richard and Hinda Rosenthal Foundation indicated its wish to identify physiatrists less than 50 years of age who would be outstanding leaders in the clinical nonoperative care of low back pain. An AAPM&R Rosenthal Lectureship was created with Myron M. LaBan, MD, as the first recipient and Jeffery A Saal, MD, as the

second. Both of these physiatrists were strongly identified with the movement to enhance the place of spine, sports and occupational rehabilitation in the field. The Rosenthal award served not only to recognize outstanding and innovative practitioners such as the two mentioned and those Rosenthal awardees who followed, but indicated real interest on the part of the many physiatrists who overflowed the meeting rooms to hear these lectures. The Academy leadership had to be impressed with the quality of the presentations and the professionalism of those who were listening. This was not simply some start-up group of malcontents, but rather a real wave of practitioners with like clinical interests. Jeff Saal, MD, became the first physician at Stanford University to begin facet and image-guided epidural spinal injections. By 1987, he, together with his brother Joel and associate Stanley Herring, MD, began to teach two-day spinal injection courses which attracted a larger number of applicants than could be accommodated. This type of course was integrated into Academy offerings. Short courses were recognized to be inadequate to gain competency but served as an introduction and facilitated the need for curricular design and Fellowship development. In 1989, the Saal brothers again made a major contribution to understanding the rationale for antiinflammatory use in disc disease by describing disc disease treatment with epidural steroids and stabilization exercises and elaborating on the inflammatory enzymes involved (PLA2). This attracted great additional interest in interventional physiatry. The new data were particularly welcome in an era of ‘low back losers’ and Nachemsen’s articles regarding the great divergence of surgical rates between the United States and Sweden and describing the long-term natural course of disc disease. By now the journal Spine was becoming well recognized as a place to publish spine-related material. From 1983, a succession of Academy of PM&R Presidents (Grant, Kraft, LaBan, Materson, Gonzalez, MacLean) were particularly impressed with the need to reach out to their colleagues, pressing this movement, and were themselves interested in musculoskeletal medicine practice. Drs Opitz, de Lateur, Christopher, and Demopoulos were interspersed with these others and, while personally more rehabilitation medicine oriented or balanced, paved the way for ascendancy of this area from a SIG to a higher-level entity within the Academy.

THE PRESENT With the urging of LaBan, Honet and Gonzalez, Saal and others, the concept of making this group an official body of the Academy with the ability to raise dues, put on educational offerings, and self-govern became real with the official creation of the Physiatric Association of Spine, Sports and Industrial Rehabilitation (PASSOR) in 1993 with Jeff Saal, MD, as its first president. A three-year probationary period for new councils was defined in the Academy Bylaws. PASSOR Founding members and Charter members are listed in Table 1.1 and Table 1.2. The Founding members in particular all played important roles in getting the organization established, supported the educational programs and special courses as organizers and faculty, took leadership in the definition of a Fellowship curriculum, contributed to definitions for proper billing and procedure codes for this subspecialty, and represented the subspecialty to outside organizations and journals. They also contributed to the writing of the PASSOR Constitution and Bylaws. Worried that feisty PASSOR leaders might lead a movement to ‘jump ship’ from the Academy if their needs were not immediately met, the then Academy president appointed Joe Honet and Dick Materson, former Academy presidents, to an Advisory Board for PASSOR and Myron LaBan as a Board Liaison. Their job was to see that ‘cooler heads’ prevailed and that PASSOR was given good information on the best strategies to assure its needs were met. As an 3

Part 1: General Principles

Table 1.1: PASSOR Founding Members

Table 1.2: PASSOR Charter Members

Jeffrey A. Saal, MD, Founding Chairman

Terence P. Braden, III, DO

Richard P. Bonfiglio, MD

Mark Steven Carducci, DO

Robert S. Gamburg, MD

James P. Foydel, MD

Steve R. Geiringer, MD

Michael Fredericson, MD

Erwin G. Gonzalez, MD

Kenneth W. Gentilezza, MD

Peter A. Grant, MD

Michael C. Geraci, Jr., MD

Andrew J. Haig, MD

Jerel H. Glassman, MPH, DO

Stanley A. Herring, MD

Richard A. Goldberg, DO

Gerald P. Keane, MD

Robert S. Gotlin, DO

Francis P. Lagattuta, MD

Robert Iskowitz, MD

Edward R. Laskowski, MD

John Keun-Sang Lee, MD

Joel M. Press, MD

Aaron M. Levine, MD

Joel S. Saal, MD

Howard I. Levy, MD

Curtis W. Slipman, MD

Donald Liss, MD

Barry S. Smith, MD

Howard Liss, MD William James Pesce, DO Bernard M. Portner, MD

attendee at a majority of the subsequent board meetings, this author will testify as to the maturity, wisdom, professionalism, and dedication of the founding officers and those leaders who have followed to this date. With Jeff Saal, MD, as Founding President of PASSOR and Erwin Gonzalez his successor, administration of PASSOR and its transition to a fully functioning academic organization proceeded at a remarkable pace, withstanding the trials and tribulations of meeting the individual desires of its well ego-defined Board personalities. A dues structure was necessary in order to put on programs, develop and disseminate academic and marketing materials, enhance membership, promote research, and reward visiting faculty for contributions. An initial dues of US$300 per member per annum was agreed upon to which would be added the revenues from the successful and oversubscribed cadaver courses on injection techniques (now named the PASSOR Spinal Procedures Workshop Series) and annual meetings fees. Disputes regarding the size of the economic commitment of membership and its effect on both PASSOR membership and Academy membership numbers, and access of PASSOR materials and educational events to non-PASSOR Academy members caused animated debate but were resolved. AAPM&R Bylaws stated Councils could self-govern; however, all policy and procedure were required to be consistent with Academy policy and subject to their overall approval. The PASSOR Board controlled finances, but dues were collected and finances reviewed and approved at Academy Board levels. Subsequent PASSOR presidents (see Table 1.3, PASSOR past presidents) each identified major areas of emphasis for their presidential years. As frequently happens in similar organizations, discussion began to consider lengthening the presidential term to 2 years to allow task completion, as presidents discovered the tasks were great and the time short. (A single-year term prevailed, encouraging presidential efficiency). As PASSOR members demonstrated their ability to plan and conduct highly valued educational offerings for the annual AAPM&R session, they were allocated additional program time and responsibility, evolving towards greater control of all musculoskeletal offerings. Aside from standard lectures and symposia, clinical demonstrations were scheduled and some (such as joint examination) videotaped for future use. Topics were purposefully varied so that sports 4

Stephen R. Ribaudo, MD Robert D. Rondinelli, MD, PhD Sridhar V. Vasudevan, MD John C. Vidoloff, MD

medicine and industrial medicine topics could be interspersed with those dealing with the spine (which was always highlighted by the Rosenthal Lecture presentation). Typical of similar organizations, a committee structure was seen as desirable. Committees dealing with Constitution and Bylaws; Nominations and Membership were first, followed by Education and Program, Research, Marketing and Communication, Medical Practice, and Information Systems. Unlike too many other organizational committees, PASSOR members served faithfully and enthusiastically, with appropriate and timely reports requiring careful management of board meetings to remain on course and on time. The presidents rose to the occasion so that motions were acted upon, either being

Table 1.3: PASSOR Past Presidents Jeffrey A. Saal, MD

1993–1994

Erwin G. Gonzalez, MD

1994–1995

Joel S. Saal, MD

1995–1996

Joel M. Press, MD

1996–1997

Robert E. Windsor, MD

1997–1998

Andrew J. Cole, MD

1998–1999

Barry S. Smith, MD

1999–2000

Gerard A. Malanga, MD

2000–2001

William F. Micheo, MD

2001–2002

Bruce E. Becker, MD

2002–2003

Section 1: Introduction

approved, disapproved, or tabled, and with meaningful but limited debate encouraged. This was carried out efficiently and with good humor, with a minimum of bruised egos, which can be a part of such undertakings. A review of the board meeting minutes, minutes of telephone conferences, annual meetings, and reports to members demonstrate a continued thread of progress of important PASSOR business. This was facilitated by outstanding administrative support in the person of Dawn M. Levreau, staff liaison assigned by Academy Executive Director Ronald A. Henrichs, CAE. Ms. Levreau was an Illinois State University graduate with a BS in economics and a minor in Speech Communication who began work at the Academy in April, 1994. Her educational background, and 12 years of experience in association management, made her an invaluable contributor to PASSOR growth. Those who serve in volunteer medical organization roles recognize just how important good staffing is to an organization’s success. Board and Committee and Task Force packets were prepared in orderly fashion, agendas planned, meetings, speakers, meeting and exhibit space planned and carried out with flexibility and positive attitude. The Academy board, other councils, committees, and staff developed a pride in their work with PASSOR and sparked member enthusiasm with benefits. Rarely do members speak up when things go well in organizations; rather, their loud protests are heard if someone is perceived to ‘muck up.’ In PASSOR’s history, praise for leadership and staff assistance has been a constant. PASSOR members became interested in defining a model musculoskeletal curriculum and muscuoskeletal physical examination competencies for use in Fellowships and generally in postgraduate PM&R training programs. Evidence of a generally unsatisfactory low level of history taking and physical examination skills observed at Fellowship entry has propelled this into a major project. Plans to educate the instructors, identified in collaboration with the Association for Academic Physiatrists, were seen as a precursor to organizing curricula and instructional materials. A traveling Fellowship was proposed and is being explored so that a Fellow might gain from the varied strengths of more than one teaching program. So as not to tread on prerogatives of credentialing bodies, RRC, and Boards, these materials were seen as approaches or guidelines rather than requirements for certification. Since fellowships were not formally defined, Dr. Slipman, in his capacity of Chair of the Education Committee of PASSOR, developed the concept that a single credible reference source was necessary for residents who wished to seek elective fellowships of value. Together with committee member Terry Sawchuk he produced the first resident’s Fellowship Guide. Rob Windsor subsequently recognized the need to differentiate between Fellowships PASSOR recognized and those which it did not. Modest criteria for PASSOR recognition were set but the idea was set in motion that all Fellowships were not created equal. More recently, Jason Lipetz, in his role as Education Committee Chair, further raised the bar, as the entry requirement includes scholarly criteria (publications and scientific presentations). These materials were developed and disseminated and have become a valuable resource for trainees. PASSOR promulgated its criteria for Fellowship Directors and model curricular content of fellowships. Programs could voluntarily supply information for the guide but PASSOR found itself incapable of policing the accuracy of the data even if it were desirable to do this. Nevertheless, the guide has been highly valued by residents exploring such programs and informal truth-telling networks developed by resident’s ‘circuits’ complemented the guides. Issues of practice privileges at hospitals and institutions began to develop, with some physiatrists denied privileges. This spurred investigation of formal subspecialization credentials through the RRCs, the Boards, and the ABMS. Subspecialization is a complex issue as previously alluded to in this chapter dealing with

curriculum, capacity, means of credentialing, and its effect on others and the public. Further pursuit by PASSOR members is active, especially in the sports medicine arena. Confusion over the meaning of, pronunciation of, and marketing usefulness of the term physiatrist has come up recurrently. A ‘naming’ organization was hired to study the issue and present choices for new name consideration and adoption. Observations of member’s practices and member interviews and polls were carried out with no real consensus. Older members preferred to stay with ‘physiatrist,’ younger members wished a name change. ‘Externist,’ ‘orthomyologist,’ ‘orthologist’ and others were discussed. The name was to apply to muscuolskeletal-interested physiatrists, not replace ‘physiatrist.’ The PASSOR board agreed that 90% of the members should favor a change and polls were taken. Response was never adequate to be determinative, and in the interim, marketing could not be delayed. With time and exposure, more members seemed to be comfortable with ‘physiatrist.’ The AAPM&R Board decided to dip into reserves and launch a major marketing program for the field. After considerable discussion the PASSOR Board decided also to invade reserves and make a major financial and creativity contribution to the effort. The Academy Marketing and Communication staff was geared up for the effort and PASSOR members made outstanding contributions to brochure development, newspaper inserts, speaker bureaus, and development of desktop office marketing materials aimed at patients, medical colleagues, insurance companies, and adjusters. A USA Today insert was highly regarded. The program was a remarkable success. The PASSOR goal was to identify the physiatrist as the physician of choice (experts) for functional musculoskeletal rehabilitation. Drs K Ragnarsson and Joel Press played major roles. Education has always been a mainstay of PASSOR. Officers and members generously gave of their time to produce AAPM&R annual meeting muscuoskeletal programs and demonstrations. Mid-year advanced-level courses were offered with varied success in attracting attendance despite the high order of materials and lecturers. An exception was the PASSOR Spinal Procedures Workshops Series that was sufficiently popular to be offered at or about the time of the Annual AAPM&R meeting and at mid-year on a regional basis. Joel Press started the idea of a special bibliography with a sports topic while he chaired the first education committee. The work continued through Curtis Slipman’s chair of the committee and the two served as the editors of the final product. Following Brian A Casazza, MD, and Jason Lipetz and others, the medical education committee saw to the development of bibliographies regarding major musculoskeletal topics including Lower Extremity, Lumbar Spine, and Cervical Spine as the initial three. All Fellowship Chairs are to review and contribute to these documents. The bibliographies were placed in the PASSOR website as the new millennium brought PASSOR to the cyber-education age. Musculoskeletal and EMG case studies were added after the pioneering contributions of Ian C. MacLean, MD, to make the EMG case studies available for this methodology. These continue to be contributed by Jason Lipetz, MD, and his medical education committee members who have also attempted to add a cyber journal club to the offerings. The Fellowship Guide and other references were also made available online. Informally, PASSOR members contributed to the Academy’s cyclic Study Guide sections promulgated through the Academy of PM&R’s Medical Education Committee (MEC). They also contributed to the Resident and Practitioner Self-Assessment materials published by the Academy’s MEC subcommittee on self-assessment (SAE-R and SAE-P). Earlier, some papers authored by PASSOR members were developed and distributed as educational mini- monographs; however, this has been discontinued. PASSOR Educational Guidelines for the 5

Part 1: General Principles

Performance of Spinal Injection Procedures was produced and additional education guides are planned. Promulgation of ‘practice guidelines’ was considered and rejected for a myriad of reasons including copyright and legal issues as well as an inability to keep such papers current. Collaboration with the information steering function of the Agency for Health Care Research and Quality (AHRQ – formally the Agency for Health Care Policy Research [AHCPR] of the Department of Health and Human Services) and other organizations such as the American Association of Electrodiagnostic Medicine and The American Academy of Neurology was considered more appropriate for practice guidelines. Several coalitions of spine and musculoskeletal societies developed including the National Association of Spine Societies (NASS), the Council of Spine Societies (COSS), and the Joint Commission on Sports Medicine. PASSOR members regularly contributed in ever increasing numbers to the peer-reviewed medical literature in the Archives of Physical Medicine and Rehabilitation and other journals. After considerable investigation and debate a formal affiliation with and sponsorship of the Clinical Journal of Sports Medicine began with Stuart Weinstein, MD, as Senior Editor. However this affiliation was dropped at the end of the first contract term in 2003. PASSOR paid the subscription price for its members during the contract. The PASSOR Spinal Procedure Workshop Series and the musculoskeletal and sports education courses were the paradigm of PASSOR members giving extraordinarily generously of their time and personal

expertise to take learners through a well-devised curriculum and practical clinical demonstrations and experience. These courses were organized and carried out by PASSOR members with the capable assistance of Academy staff. Professional meetings companies expert in the delicate arrangements for such courses helped arrange the cadaver courses. Space does not permit listing all of these outstanding educators; however, a few are mentioned here: Curtis Slipman, Jeff and Joel Saal, Robert Windsor, Andrew Haig, Andrew Cole, Gerard Malanga, William Micheo, Francis Lagattuta, Paul Dreyfuss, Jeffrey Young, Stanley Herring, Stuart Weinstein, Scott Nadler, Heidi Prather, Jeff Pavell, Anthony Cucuzzella, Bruce Becker, Joel Press, Michael Furman, David Bagnall, Jay Smith, Sheila Dugan, Barry Smith, Ann Zeni, Venu Akuthota, Lori Wasserburger, Kurt Hoppe, Susan Dreyer, Terry Sawchuk, Frederick McAdam, Erwin Gonzalez, Jerrold Rosenberg, Krystal Chambers, Christopher Huston, Edward Rachlin, James Atchison, and Joseph Feinberg. Research was recognized as the key to successful incorporation of this subspecialty into accepted practice. This needed to be evidencebased, primarily clinical, research. PASSOR elected to support the newly reformatted Foundation for Physical Medicine with a significant donation from reserves and personal commitment to a challenge grant by all Board members. PASSOR tightened its criteria for award of the Rosenthal Awardees (Table 1.4 – Rosenthal Lecturers). Recently, the Saal Family Foundation has announced its sponsorship of spine research. A PASSOR Research Grant Award for US$10 000

Table 1.4: Richard and Hinda Rosenthal Foundation Lecturers The Richard and Hinda Rosenthal Foundation Lecture is presented by a young physiatrist who has demonstrated noteworthy advancement in the nonsurgical care of low back pain. This prestigious lectureship was established through the generosity of the Richard and Hinda Rosenthal Foundation. Lecturer

Year

Rosenthal Lecture Title

Scott F. Nadler, DO

2003

Core Strength: What is it all about?

Stuart M. Weinstein, MD

2001

The 21st Century Physiatrist: Seasoned Veteran or Rookie Sensation. Cancelled due to 9/11

Joseph D. Fortin, DO

2000

Interventional Physiatry: The ‘Cardiology’ Approach to Musculoskeletal Medicine

Curtis W. Slipman, MD

1999

Controlling Our Future: Managing the Dilemmas Facing Physiatry

Susan J. Dreyer, MD

1998

The Forgotten Spinal Epidemics: Osteoporosis

Andrew J. Cole, MD

1997

Education and Mentoring: Physiatric Core Values

Paul H. Dreyfuss, MD

1996

Diagnosis Driven Spine Care in the 21st Century

Joel M. Press, MD

1995

The Future of Physiatric Low Back Care

Andrew J. Haig, MD

1994

New Job for an Old Test: Needle Electromyography of the Paraspinal Muscles

James Rainville, MD

1993

Uncoupling Pain and Impairment – Maximizing the Potential of Chronic Low Back Pain in Patients

Maury Ellenberg, MD

1992

Radiculopathy Secondary to Disc Herniation: Does it Require Surgery?

Nicolas E. Walsh, MD

1991

Research Design in Low Back Pain

Joel S. Saal, MD

1990

The Biochemistry and Pathophysiology of Lumbar Degenerative Disc Disease: A Rationale for Non-Operative Care

Stanley A. Herring, MD

1989

Stanley A. Herring, MD The Physiatrist as the Primary Spine Care Specialist, Implications for Training and Education

Avital Fast, MD

1988

Low Back Pain in Pregnancy

Irina Barkan, MD

1987

Lumbar Outlet Syndrome and Myofascial Back Syndrome: Diagnosis and Treatment

Patricia E. Wongsam, MD

1986

Biomechanics of the Lumbar Spine: Some Recent Advances

Jeffery A. Saal, MD

1985

Advances in Conservative Care in the Lumbar Spine: Correlation of SNR Block and Clinical EMG Findings

Myron M. LaBan, MD

1983

Vesper’s Curse’ Night Pain – The Bank of Hypnosis

Note that Dr. Nadler passed away in December 2004.

6

Section 1: Introduction

Table 1.5: PASSOR Research Grant Recipients 2004

Jay Smith, MD

Electromyographic Activity in the Immobilized Shoulder Girdle Musculature during Ipsilateral and Contralateral Upper Limb Motions

2003

Julie Lin, MD

Functional Impact of the Posture Training Support in Elderly Osteoporotic Patients

2002

Michael Fredericson, MD

The Effect of Running on Bone Density and Bone Structure in Elite Athletes

2001

Heidi Prather, DO

Vertebral Compression Fractures Related to Cancer Patients and Treatment with Vertebroplasty

2000

Anne I. Zeni, DO PT

Does Athletic Amenorrhea Induce Cardiovascular Changes?

1999

Gregory E. Lutz, MD

The Biomechanical and Histological Analysis of Intradisc Electrothermal Therapy on Interventional Discs

1998

Thierry H.M. Dahan, MD

Double blind randomized clinical trial examining the efficacy of modified Bupivacaine suprascapular nerve blocks in the treatment of chronic refractory painful subacromial impingement syndrome

‘seed money’ Research Award was created. (See Table 1.5 for awardees and topics.) Organizations Awards highlight PASSOR values. Aside from the Presidential awards, Research Grant Award, and Rosenthal Lectureships, the PASSOR Board created the PASSOR Distinguished Clinician Award to honor members who have achieved distinction on the basis of their outstanding performance in musculoskeletal patient care, their scholarly level of teaching, and who have contributed significantly to the advancement of the specialty through participation in PASSOR activities (see Table 1.6 – Distinguished Clinician Awardees). A Distinguished PASSOR Member Award was also created to honor PASSOR members who have provided invaluable services to the specialty through participation in PASSOR activities (see Table 1.7). These awards were to be directed to members who were not serving on the Board in the three years prior to the award.

THE FUTURE PASSOR has had a recent strategic plan which redefines its mission, goals, and objectives and which seeks to reintegrate PASSOR into the mainstream of the Academy of PM&R. This would eliminate distinct dues or meeting fees and necessitate creative ways to maintain funding and momentum. It remains to be seen if this is not simply another change in the flow of organizational makeup and if the good will and resources necessary to meet the needs of all members is present. A number of members have opined that simply being a nonoperative orthopedist eschews the valuable education, training, and experience of general physiatrist rehabilitation training. The proper value of team care and methodologies, and attention to psychosocial, vocational and disablement issues for selected patients

Table 1.6: PASSOR Distinguished Clinician Award Recipients The PASSOR Distinguished Clinician Award honors PASSOR members who have achieved distinction on the basis of their outstanding performance in musculoskeletal patient care, their scholarly level of teaching, and have contributed significantly to the advancement of the specialty through participation in PASSOR activities.

must be appreciated and not shunned. Some members opine that there is often no need for ancillary assistance when a skilled physiatrist can ‘provide it all,’ and state that physical therapists, chiropractors, and others do not truly represent competition if physiatrists are good at all that they lay claim to be good at. This author is in agreement with colleague Bernie Portner, MD,8 who observes, ‘… that much of what is done today is way off mark. There is, in the book on the History of Medicine, a chapter entitled ‘blood letting, the four humors, the hypothymic syndrome and other nonsensical, yet commonly held, tomfoolery of days gone by …’ and then gives his personal opinion of some of today’s practices. Each of us could make a list of those things that we do which may not be adequately supported by evidence-based research, or which appear to have greater physician emollient benefit than good patent outcome. Often, procedures are promulgated with much greater enthusiasm than for which evidence of their long-term success exists. Polls of spines surgeons have indicated that financial incentives alone for doing added procedures, not careful medical individualization, have made laminectomy without fusion relatively rare. We must support and utilize evidence-based medical literature, starting with this textbook, and look for carefully done outcomes research. Despite the requirement for resource constraint considerations and cost–benefit analysis, as a profession we must guard against primarily economic-driven clinical decision-making, or the public will demand diminishment of medical autonomy and substitution of creativity-stifling regulation. To this end, NIH, NIDRR, and other recognized funders of research (including private endowments) must support bona fide musculoskeletal clinical and research models. Regarding progress in academia, Curtis Slipman founded the first interdisciplinary academic spine program at the university of Pennsylvania in 1992 at a time when physiatrists were being blocked by anesthesia and orthopedics. His program included direct participation of ortho spine, neurosurg spine, and radiology, and all saw patients in the same facility, and created the first academic

Table 1.7: Distinguished PASSOR Member Award Recipients

2003

PASSOR members who have provided invaluable service to the specialty through participation in PASSOR activities.

Francis P. Lagattuta, MD

2002

Erwin G. Gonzalez, MD

2002

Paul H. Dreyfuss, MD

2001

Jeffrey A. Saal, MD

2001

Jeffrey L. Young, MD

2000

Robert E. Windsor, MD

2000

Robert E. Windsor, MD

7

Part 1: General Principles

interventional physiatric fellowship in 1993. Slipman’s emphasis had also been on developing leaders of interventional physiatry that could go on to develop academic programs with top-notch fellowships. He has been able to place a group of incredibly productive young physiatrists in academic centers. These physiatrists include: Zacharia Isaac at Harvard, Omar el Abd at Harvard, Jason Lipetz at Einstein in NY, Michael dePalma at the Medical College of Virginia, Raj Patel at the University of Rochester, David deDanious at the Medical College of Wisconsin, Russell Gilchrist at the University of Pittsburgh, and Amit Bhargavia at the University of Maryland. The University of Michigan program was founded by Andrew Haig, MD, and emphasized the critical importance of research to this field. Another prediction that has been observed to be coming true is that young women physiatrists who were themselves athletes during their school years have become attracted to this arena and see opportunity in the hands-on approach to interventional spine treatment, and welcome the opportunity to contribute to the medical literature dealing specifically with women’s issues Physiatry will continue to evolve as science warrants and practitioners are willing. Organizations such as PASSOR, collaborating with organized medicine, will facilitate the needed changes as new young

8

leaders act today to create the history of tomorrow. Congratulations colleagues, you’ve produced an enviable history.

References 1.

Flexner A. Medical education in the United States and Canada: A report to the Carnegie Foundation for the advancement of teaching. Bulletin No 4. New York: Carnegie Foundation for the Advancement of Teaching; 1910.

2.

Materson R. Introduction. In: Grabois M, Garrison S, Hart K, Lehmkuhl D, eds. Physical medicine and rehabilitation. The complete approach. Malden, Mass: Blackwell Science; 2000:1–16.

3.

Kottke F, Knapp ME. The development of physiatry before 1950. Arch Phys Med Rehab 1988; 69:4–14.

4.

Krusen FH. Historical development in physical medicine and rehabilitation during the last forty years. Arch Phys Med Rehab 1969; 50:1–5.

5.

Martin GM, Opitz J, eds. The first 50 years: The American Board of Physical Medicine and Rehabilitation. Arch Phys Med Rehab 1997; 78(supp 2):1–68.

6.

Opitz J, ed. Fifty years of physiatry; the forging of the chain. Arch Phys Med Rehab 1988; 69: 1–3.

7.

Rusk HA. A world to care for. New York: Random House; 1972.

8.

Porner B. e-mail communication to Materson. May 2004.

PART 1

GENERAL PRINCIPLES

Section 1

Introduction

CHAPTER

Epidemiology

2

David A. Lenrow

INTRODUCTION Epidemiology is the branch of medicine that deals with the study of the causes, distribution, and control of disease in populations.1 Epidemiology of spine pain provides insight into the scope of the problem and allows us to evaluate the impact of various treatment methods and preventative strategies. Without reliable epidemiologic data it is impossible to evaluate treatment or prevention with any accuracy. In reviewing the literature on the epidemiology of spine pain, it quickly becomes evident that there are significant gaps in our knowledge which require sound evidence-based medicine for resolution. Until we have reproducible data with set criteria for spine pain, in general and specific populations, we will be unable to accurately define its natural history or the benefit of selected treatments. Historically, the medical profession has held a variety of opinions on the cause of spine pain with associated treatments. This led to the teaching of treatments without any clear scientific evidence and has propagated potentially ineffectual approaches to ill-defined causes of spine problems. The long history of opinion-based clinical medicine and medical education is coming to a close. In this era of evidencebased medicine it is essential to determine the epidemiology of spine problems so we can proceed to focusing on effective treatment and prevention. Understanding the epidemiology of spine pain will establish the extent of the problem in the population, and its natural history. The next level of studies should be aimed at determining the relationship between specific factors, both external and internal, which are associated with spine pain. It is likely that this will vary with specific etiologies of spine pain, so the studies of causation will be intimately linked with research aimed at determining the pain generators in specific syndromes. Only when we have reached this level of understanding will researchers be able to systematically develop methods of treatment and prevention which elevate the care of these patients from opinion-based to evidence-based medicine. The terms often used in studying the effect of spine pain on populations are incidence and prevalence. Prevalence is the percentage of a population that is affected with a particular disease or symptoms at a given time or during a specific set time interval. There are many factors contributing to prevalence including, but not limited to, the number of new cases, the duration of symptoms, and individuals with spine pain moving in or out of the study population.2 The determination of prevalence only requires sampling at one time point. A cross-section of the population of interest should be sampled to ensure that the data will be generalizable to the population as a whole. The study population must reflect the population to which the information will be applied or the information will have little or no utility. Point prevalence is thought to be fairly accurate when obtained in surveys, whereas prevalence over long periods of time or an individual’s lifetime is often less accurate. Memory fades with time, particularly if pain has resolved.

Incidence is the rate of occurrence of spine pain or a specific subset of spine pain in the population being studied. Incidence is always in relation to a defined period of time. It refers to new episodes or occurrences. To determine incidence in a specific population it is necessary to sample an appropriate cross-section of the population when they are symptom free and then to follow them for occurrence of symptoms over a specific time period. Prevalence and incidence of spine pain allow us to better define the scope of the problem. They also allow for the formulation of theories of etiology by analysis of associated factors. They do not determine causation.3 The estimates of costs to society further define the problem and include economic, medical, and disability-related costs.

CHALLENGES The collection of epidemiologic data on spine pain presents difficulties on several levels. The inclusion criteria for an episode of spine pain vary. Without clear and standardized criteria for an episode of spine pain, or a specific syndrome, it is not possible to generalize or combine the data from studies. An example is an attempt to compare point prevalence across studies that define episodes of spine pain as having a duration of at least 2 weeks to studies which count any episode of spine pain, even fleeting pain. These studies are not comparable and the information in each is at best only generalizable to the specific population of the study. Consistency among studies with clearly defined criteria for an episode of spine pain would allow for comparison and pooling of data. Fleeting, transient, mild neck pain should not be evaluated in the same category as severe, intense, disabling, chronic neck pain. The study should include the question used and how it was administered. The length of the particular questions used and the method of administration can alter the responses obtained. The prevalence period must be defined. Only the same prevalence periods should be compared. Point prevalence represents the most reliable information to obtain in survey studies since memory is not required. The longer the recall period the more this is apt to be affected by memory.4 This can cause errors in both directions. Memory may fade with time or events may be remembered as occurring more recently than they actually occurred.5,6 Point prevalence avoids this issue. Self-reporting of spine pain has been criticized for being subjective and not as reliable as direct observation or examination. With pain, and specifically spine pain, there is no objective test to determine the existence of symptomatic pain. When assessing the outcomes of a treatment, we rely substantially on our patients’ reported symptoms, and perhaps in research that is also our best tool with the least misperception. What has been called a weakness of many studies may be its strength. 9

Part 1: General Principles

Generalizability of the information from a study population is frequently the goal. To allow for the extrapolation of findings from the sampled population to the larger population requires that the sample population be representative of the group as a whole. It is essential that the study population be a random sample of the target population. It is important to define the population prior to sampling so the outcome is relevant. It is time to standardize the methodology of performing epidemiologic studies for spine pain. We need widespread use of standardized scales for data collection, appropriate population samples and valid, reliable outcome measures. If the measures used have not been validated, the data are of questionable value at best.

Scope of the problem Spine pain is nearly ubiquitous in industrial societies. It is among the most common medical problems in developed countries. It is present in rural workers and in sedentary through heavy-duty occupations. In the majority of cases causation remains muddled. The often repeated causal factors including obesity, heavy work, leg length discrepancy, and others have not been proven. The data for low back pain vary but the lifetime prevalence in industrial nations is high, 50–85% or greater.7,8 The annual incidence is approximately 5% with some reports up to 15%.8 Back pain accounted for 15 million physician visits in 1990 in the US.9 It is a major factor in lost work days and the first or second most common cause of disability.10 In people under 45 year of age it is the most common cause of disability in the US.10 The societal costs are enormous. The prognosis for a single episode of back pain is excellent, with 90–95% of acute episodes resolving fully. Resolution of symptoms usually occurs within 3 months. The patients who do not recover are often noted to be the major cost in disability and medical care. It is becoming evident that there is a significant recurrence rate for acute back pain with an associated progression to chronic pain. With surveys, participants have been found to forget up to 25% of episodes of back pain for which they sought medical attention, making recurrence rates difficult to determine. The epidemiology of neck pain is much less often the target of studies, but it appears to be nearly as prevalent as back pain.

History Back pain has been present since the earliest of recorded time. In the Edwin Smith papyrus circa 1500 BCE there is a description of back pain, including the examination and diagnosis. Neanderthal skeletons and Egyptian mummies revealed degenerative spine changes. Hypocrites (460–370 BC) noted that back pain with sciatic pain lasted about 40 days and affected men 40–60 years old.11 Historically, chronic back pain was not thought to be secondary to injury until the mid nineteenth century. This was the time of the industrial revolution and the building of the railways. It was called railway spine and thought to be related to work, or even travel on the railroad, even if there was no identifiable injury.12 This led to the acceptance of spine pain as an occupational injury.

STATISTICS

North America

Europe

National Health and Nutrition Examination Survey-CDC (NHANES 1999–2000) found the prevalence of low back pain (LBP) within the past 3 months to be 37.44% with a sample size of 4880.24 Neck pain over the previous 3 months lasting at least 1 day revealed a prevalence of 18.46%. Deyo analyzed the NHANES II data (1976–1980) with a survey population of 27 801 and found a lifetime prevalence in the US of LBP of 13.8% and prevalence in the previous year of 10.3%.25 In the Deyo study an episode of LBP was defined as lasting at least 2 weeks.

In Britain, a study in the general population with 4515 respondents from three general practices determined the prevalence of neck and back pain.13 An episode of spine pain was defined as lasting at least 1 week in duration. The 1-month prevalence of all spinal pain was 29%. The prevalence for back pain was 24.5% for women and 21.3% for men. For neck pain the prevalence was 16.5% for women and 10.7% for men. Of the total spine pain, 40% was disabling. 10

A British study with 12 907 respondents to a survey found a 1-year prevalence of 34% and a weekly prevalence of 20% for neck pain.14 Of the total respondents, 11% reported neck pain within the past year that interfered with their normal activities. An episode was defined as pain lasting 1 day or longer. In one of the few prospective studies the lifetime and annual prevalence of low back pain in the UK was 59% and 42%, respectively.15 This was a mailed survey with 1455 respondents. An incidence rate of 4% was found. Age was associated with increased prevalence. An episode of back pain was defined as lasting longer than 1 day and not associated with menstrual cycle, pregnancy, or febrile illness. Guez, in a Swedish study of 4392 adults, found an 18% prevalence of chronic neck pain with continuous pain lasting longer than 6 months.16 Of the subjects with neck pain, 30% had a history of trauma. No data were reported on the interval between trauma and neck pain. The definition of neck injury was injury that was severe enough to lead to a physician visit. In another Swedish population study with 6000 respondents, 48% of men and 38% of women reported neck pain on a self-administered questionnaire.17 The prevalence as a whole was 43% with women having a significantly higher prevalence than men. Chronic neck pain defined as lasting greater than 6 months was reported in 22% of women and 16% of men. A history of head or neck trauma was present in 25% of the subjects who developed chronic neck pain. Linton, in a Swedish study, surveyed 3000 persons and found a 2-year prevalence of 73% for low back pain.18 Of these, 17% utilized sick time and another 14% had been off work but did not use sick time. In the Mini-Finland Health Survey 8000 people were interviewed and examined.19 Lifetime prevalence of neck pain was 71%. Chronic neck pain was diagnosed in 9.5% of the men and 13.5% of the women. An association was found between neck pain and history of injury and mental and physical stress at work. In a survey study of 10 000 Norwegians, the 1-year prevalence rate of neck pain was 34.4%.20 Neck pain lasting for more than 6 months had a prevalence of 13.8%. In a telephone survey of 1964 participants in Catalonia, Spain, the 6-month prevalence of low back pain was 50.9%.21 Back pain was more common in women, manual workers and less-educated respondents. Back pain limited the daily activities in 36.7% and was responsible for time off work in 17% and disability pension in 6.5%. In a Belgian study of 618 blue collar workers in the steel industry, lifetime prevalence was 66%, 1-year prevalence was 53%, and 1-week prevalence was 25%.22 An episode was any ‘problem in the low back.’ Most of these episodes were mild and categorized as fatigue or common low back pain. Only 17% sought medical advice and only 11% were limited in their occupational or domestic activities. In the Netherlands in a survey with 3664 respondents, low back pain had a prevalence of 26.9% and neck pain 20.6%. Low back pain was the most common musculoskeletal pain and neck pain was the third most common.23

Section 1: Introduction

Canada has been the site for many epidemiologic studies for both lumbar and cervical ailments. Cassidy et al., with 1131 respondents to a mailed survey in Saskatchewan, found 28.4% point prevalence and 84.1% lifetime prevalence of back pain.26 The 6-month prevalence was graded into five intensities and disability categories. This was an attempt to stratify the prevalence so that transient nondisabling pain could be differentiated from disabling back pain. Low intensity/ low disability back pain accounted for 48.9% of the population that had back pain in the previous 6 months. High intensity/high disability back pain was reported by 10.7% of this population. The remaining 12.3% of the subjects in the 6-month prevalence group reported high intensity/low disability back pain. Women were twice as likely as men to report severe disabling back pain; low intensity was equal between genders. The authors conclude that general prevalence is not terribly useful information since the majority of responders who had episodes of back pain had low intensity/nondisabling episodes of back pain. Cote et al. looked at the prevalence of neck pain in the same random survey of the Saskatchewan population.27 The lifetime prevalence of neck pain was 66.7% and point prevalence was 22.2%. Neck pain was defined as any pain between the occiput and third thoracic vertebrae as detailed on a mannequin diagram. Subjects were stratified by intensity of pain and disability in a fashion similar to the study on back pain. Women experienced more neck pain than men in all severity groups. Women had a 58.8% 6-month prevalence and men had a 47.2% 6-month prevalence. The 6-month prevalence of low intensity/low disability neck pain was 39.75% and 10.1% for high intensity/low disability neck pain. A total of 4.6% of the surveyed population reported highly disabling neck pain for the previous 6-month period. Interestingly, low intensity/low disability neck pain was found to decrease with age. High disability neck pain was more prevalent in women than in men. Kopec et al., in a longitudinal study of households in 10 provinces in Canada, were able to determine the incidence of back pain.10 The interval of the two surveys was 2 years and the sample size was 11 063 subjects age 18 years or older. An episode of back pain was defined as lasting longer than or equal to 6 months in duration or expected duration. The 2-year incidence in females was 9.0% and in males was 8.1%. Of note is that this was a self-administered survey but the question was ‘Have you been diagnosed by a health professional with back problems, excluding arthritis?’ One could envision several potential biases of this longitudinal prospective study. The question asked is not defined in terms of intensity but only duration. The duration maybe 6 months or longer or in the alternative be expected to last 6 months or longer. This opinion on expected duration is that of the subjects. The diagnosis of back problems by health professionals is being self-reported by the subject and not by health professionals or their records. The validity of this second-hand information is unclear. George, in another Canadian survey with 1131 respondents, showed an 8% 6-month incidence of clinically significant low back pain by the Chronic Pain Questionnaire.28 The prevalence of low back pain in North America, as elsewhere, varies by study. In an attempt to reconcile the variability and determine reliable prevalence rates a methodological review of the literature was performed to identify acceptable studies and compare prevalence rates.29 They found 13 studies from 1981–1998 methodologically acceptable, but with variable assessments and definitions of an episode of back pain. The range of point prevalence in the studies varied from 4.4% to 33.0%. One-year prevalence rates ranged from 3.9 to 63%. The explanation for the variability is partially blamed on the differing durations of back pain required to constitute a reportable episode.

Asia In a cross-sectional study of garment workers, battery/kiln workers, and teachers in Shanghai, People’s Republic of China, the overall yearly prevalence of back pain was 50%.30 The number of subjects in this study was 383. This was self-reported back pain with symptoms lasting a minimum 24 hours. Garment workers had the highest yearly prevalence of 74% while teachers had a prevalence of 40%. The 7-day prevalence was 45% for garment workers and 22% for teachers. The different occupations were thought to account for the variation in prevalence. In a study of 800 workers in Russia, the lifetime prevalence was 48.2%, point prevalence was 11.5%, and the 1-year prevalence was 31.5%. The vast majority (88.2%) had pain for less then 2 weeks. Only 1.8% had pain for longer than 12 weeks.31

Low-income countries Studies to determine statistics for spine pain in low-income countries are much less common than in wealthy industrialized nations. The literature on back pain is primarily from high-income countries accounting for less then 15% of the world population. In an attempt to test the hypothesis that in low-income countries, since physical labor is more common, back pain should have a higher prevalence, a systematic review of the literature for lowincome countries was performed.5 The point prevalence was the benchmark and used for comparison. Interestingly, high-income countries had 2–4 times the point prevalence found in rural, lowincome countries. The variation within both the high-income and low-income groups was twofold. This large disparity within categories of countries puts the methodology and therefore strength of the study into question. Notwithstanding the methodologic issues, manual labor does not appear to correlate with back pain. Perhaps physical activity is protective or even serves as treatment. This study in a general way lends evidentiary support to exercise as a treatment modality. Harlow found a 29.8% prevalence of low back pain, a 38.3% prevalence of upper back pain, and a 26.4% prevalence of neck pain in women in Tijuana, Mexico. 32 In a study in urban Zimbabwe of 10 839 respondents, back pain was the second most disabling condition after headaches.33 Omokhodion, in 840 Southwest Nigerian office workers, found a 12-month prevalence of low back pain of 38% and point prevalence of 20%.34 The overall rate of disability was 5.6%. In a cross-sectional study in rural Tibet with n=499, the point prevalence of low back pain was 34.1%, the 12-month prevalence was 41.9%. 35 Subjects also reported functional disability related to their pain. In rural China 36 the prevalence was found to be 12.1% and in Nepal 37 18.4% for low back pain. Sharma reported that 23% of patients seen for medical care in outdoor rural India were seen for back pain.38 The information from rural nations may be helpful in our understanding of the factors important in developing spine pain and its prevention. The prevalence and incidence of spine pain is a large problem internationally regardless of compensation systems and culture. The variability both in the same populations and across populations is substantial. Even with this large variation in prevalence and methodology the statistics remain staggering. Before we hypothesize on why these variations are found, both in different groups of subjects and in time, we must determine the value of the data we are comparing. The methodology and generalizability of the individual studies must be sound and comparable before there is any value in formulating reasons for the differences noted. 11

Part 1: General Principles

COST The cost of back pain to various societies is hard to quantify. This is due to the lack of central data collection and variation in methodology. Extrapolating data from worker’s compensation claims in the US and then projecting to the population as a whole reveals staggering costs.39 In 1988 the estimate was 22.4 million cases of back pain with 149.1 million lost work days. This loss of workdays alone is estimated to cost more than US$13.3 billion. This does not take into account health care, personal expenses, and insurance costs. Estimates of total cost in the US range from US$50 to US$100 billion per year. A Swedish study found that 6% of sufferers accounted for over 50% of the costs.18 In Australia the cost is estimated at US$10 billion per year with a lifetime prevalence of 80%.40 In the Netherlands back pain is the most common cause of lost days at work and disability. In 1991 the direct costs of medical care for back pain in the Netherlands was US$367.6 million and the indirect costs were US$4.6 billion.41 In a 2003 study in the US, back pain was the second most common pain condition resulting in lost time from work after headache.42 Out of the total work force, 3.2% lost time from work as a result of back pain. Pain-related loss of productive work time cost an estimated US$61.2 billion. The majority was because of decreased productivity while at work and not due to absence from work.

FACTORS The cause of most episodes of spine pain is uncertain. The purported risk factors are numerous. Heavy lifting, particularly on a repetitive basis, has often been suggested as an inciting event. Age, gender, and psychological distress have all been implicated, but not consistently. Cigarette smoking and obesity have been related to back pain in some studies.43–46 Socioeconomic status has been identified as a risk factor in some studies43,47 but not all studies.10 Before leaping from associated factors to causation and postulated mechanisms, we must have better data for prevalence and incidence so the significance of these potentially inconsequential associations can be adequately evaluated. Cote et al. analyzed the Saskatchewan Health and Back Pain Survey data to determine the factors associated with neck pain and disability.48 In the sample population, 15.9% reported prior neck injury in a motor vehicle accident. This history and headaches were strongly associated with all grades of neck pain. Subjects with cardiovascular or digestive problems had a higher 6-month prevalence of disabling neck pain but not milder neck pain. There was an association between low back pain and neck pain. The Mini-Finland Health Survey found chronic neck pain strongly associated with back pain and shoulder disorders, but only weakly associated with osteoarthritis, cardiovascular, and mental disorders.19 Trauma to the neck or low back was associated with chronic neck pain. Kopec et al., in a prospective study, tried to identify factors in the development of back pain in the general population.10 General health and psychosocial factors were important in both sexes. Other factors in men were age, usual activity pattern, lack of gardening, and height. For women the other factors were self-reported arthritis or rheumatism and a history of psychological trauma. If a woman has none of these identified factors her risk of developing back pain in a 2-year period is 6%. For a woman who has activity restriction, has been diagnosed with arthritis or rheumatism, has two or more traumatic events in childhood, and reports a high level of personal stress, her risk of developing back pain is 32% in a 2-year period. General health was a strong predictor of back pain in a study in the UK by Croft et al.49 They studied 2715 individuals from two general

12

practices in Manchester. The relative risk was 1.5 for men and 2.2 for women who had poor general health.

Weight Weight has often been cited as a risk factor in spine pain, most often in low back pain. Webb found an association between obesity and back pain with disability but not with neck pain or low-intensity back pain.13 Kopec et al. found no significance but weight was close to significant as a factor in women.10 Croft found weight to be a significant factor for women but not men.49 Gyntelberg, in a study of Danish men, found an association between height and low back pain but not weight.50

Occupation In a British survey with 12 907 respondents, no association for neck pain was found for lifting, vibratory tool use, or professional driving.14 There was an association found with above-the-shoulder activity for >1 hr/day. Stronger associations were found with tiredness or frequent stress. Occupations with the highest prevalence were, in descending order; construction workers, nurses, armed services members, and the unemployed. No association was found between physical workload, postures, or exposure to vibration and low back pain in steel workers.22 In a study in the Netherlands, scaffolders had a 60% 12-month back pain prevalence.51 Supervisors had similar rates for back pain and perceived disability but less severe back pain and lower absence rates than scaffolders. Ehrlich opines that most spine pain is not related to work activities but may be related to psychosocial factors.52 Job dissatisfaction, stress, the system of compensation, and hiring a lawyer are all reported to decrease return-to-work rates. Hadler states how back pain is dealt with determines if it is disabling or not; secondary gain such as workers’ compensation increases the morbidity.53

Secondary gain There is a long-standing controversy regarding the role of secondary gain in spine pain and disability. Disability from spine pain was not a significant problem until the industrial revolution. Cassidy et al. analyzed the effect of compensation on whiplash injury in Saskatchewan.54 On January 1, 1995, the tort compensation system for traffic injuries was changed to a no-fault system eliminating recovery for pain and suffering. This provided natural data collection points. It is important to note that Saskatchewan was the only insurer for motor vehicle injuries in the Province and all residents benefit from state health insurance. For the last 6 months of the tort claim system the 6-month cumulative incidence was 417 per 100 000 persons compared to 302 and 296 per 100 000 in the first and second 6-month periods of the no-fault system. This equates to a 28% decrease in claims for whiplash injury. The time from the date of injury to claim closure decreased from 409 days to 194 days in the same time interval. During this same period there was an increase in the number of vehicle-damage claims and distance driven.

Psychological The development of back pain has often been associated with psychological factors.55–57 In the Manchester study, psychological factors were found to be predictive of low back pain.57 This was a prospective study of 4501 surveyed subjects. Subjects with no back pain but high scores for psychological distress were more likely to develop back pain than individuals with low scores.

Section 1: Introduction

Perez found an association prospectively between psychological factors and back pain in healthy workers.56 The only factors related to back pain in that study were age, depression, and general stress. Kopec et al. found general stress to be a factor in men and personal stress (a subset of general stress) a factor in women, as well as a history of psychological trauma in women.10 In a Finnish study, an association between depression and neck and back pain was found in both men and women.58 Power, in a British cohort study looking at early life variables, found psychological distress at age 23 to be the strongest predictor of low back pain.59 This doubled the risk of back pain later in life. In rural India 67%, of patients seen for low back pain had psychosocial issues, and 38% were dissatisfied with their current job.38

Smoking Smoking has be implicated as a factor in developing spine pain.45,59 The Manchester study,49 Kopec et al.10 and Guez et al.16 among others did not find an association between spine pain and smoking. In a systematic review of the literature for 1976–1997 an association between smoking and non-specific back pain was found.45 The results revealed an association between smoking and back pain in men in 18 of 26 studies and in 18 of 20 studies in women. It is not clear if smoking preceded back pain or if there is a close relationship. The finding of a positive association does not imply causation.

Age The highest prevalence of low back pain occurs between 40 and 60 years of age. Kopec et al., in one of the few studies looking at incidence and age, showed a peak incidence at 45–64 years of age.10 Rates of back pain seem to increase during adult life until age 65 and then they decrease. Predicting back pain by knowing the causation and associated factors would allow for an intelligent, scientific approach to prevention. The data currently available are often contradictory and difficult to explain. In one study, gardening is associated with a lower risk of low back pain.10 In other studies sports and nonoccupational home improvement increased the risk.49 Is gardening really associated with lower incidence of back pain or do people prone to back pain not garden? We must ask the right questions to determine the association between risk factors and the development of spine pain. Perhaps these are just chance associations. Without precise methodology, reproducibility, and multiple studies in agreement, the true associated factors remain uncertain and true causation beyond our reach.

respondents reporting persistent annual low back pain.15 Acute episodes recurred and in some patients turned into chronic, constant pain.

DISABILITY Spine pain is a major cause of disability. It has been estimated that 1% of the population is disabled by back pain. It is the leading cause of disability in the US for the population under 45 years old and the second cause for those 45–65 years old.46 Back pain accounts for approximately one-fourth of worker’s compensation claims in the US. In a survey of 30 074 respondents 5256 subjects, or about 17.5%, self-reported back pain lasting at least 1 week.39 Construction workers in males and nurses aides in females had the highest prevalence rates of 22.6% and 18.8%, respectively. Subjects reported missing work or changing jobs in 12.1% of those with reported pain. Extrapolating this to national estimates yields staggering numbers of cases of back pain and lost work days. There is little known about the extent of the disability spine pain produces in less-industrialized nations. In Nigerian office workers, only 5% of those surveyed reported lost days due to back pain, with a mean of 4.7 days per year.34 The incidence of back pain was similar to that in industrialized nations but the absence from work was not as significant. The history of spine pain and disability helps illuminate some of the factors that transform spine pain, as an accepted part of life, into a disabling condition. Allan and Waddell review the history of back pain and disability.11 There was very little written about spine pain causing disability until the industrial revolution. Early reports of spine disability in railway workers led to much more frequent spine disability in the early twentieth century. This was coupled with the concept of compensation for work-related injury. During WWI the US draft board rejected recruits that had static problems of the spine to avoid backache. Recruits still developed backache, but could be made fit for service by special training battalions. This suggested that back pain might be a fitness problem and not a medical problem. In the British armed forces there was a fivefold increase in withdrawal from duty for back pain between WWI and WWII. In Britain in 1911 and the US in 1949, workers were covered for injury by Workman’s Compensation Insurance. As the breadth of compensation increased so did the extent of disability for back pain. The author’s concluded that disability is not a natural sequelae of back pain, but is secondary to how we compensate, manage, and treat patients with these aliments.

CONCLUSION RECURRENCE The traditional notion that the great majority of episodes of nonspecific back pain resolve has come under scrutiny. There is good evidence that a substantial fraction of back problems have recurrent symptoms. Miedema found that 28% of patients with an episode of back pain, for which they consulted their physician, went on to develop chronic back pain.41 Only 1 in 5 people with back pain consult their physician. In a review of the literature the 1-year recurrence rate for low back pain was 20–44%.8 Lifetime recurrence rates were up to 72%. These studies were prospective studies for occupational back pain. Nurses and drivers had the highest recurrence rates while white collar workers had the lowest recurrence rates. In general, men had higher rates of recurrence than women. In a longitudinal cross-sectional study in the UK there was a 59% lifetime prevalence, with 42% of those

Spine pain is a widely prevalent condition. Spine disorders account for a tremendous cost both in lost productivity and medical care to industrial societies. Back pain is one of the top two reasons persons seek medical care, superceded only at times by respiratory infection. The prevalence is variable across studies but there is no standardized methodology to study spine pain. Definitions of spine problems vary greatly as do methods of obtaining data. These variables make it impossible to compare statistics across studies even if the populations were identical. Spine pain is not a specific disease or one etiology of pain, which makes it difficult to address. It is most often of non-specific cause, or more accurately an as yet unidentified cause. The rate of surgery varies by regions and by country with up to a 15fold variation within the US. The use of various treatments including COX-2 antiinflamatory drugs, spinal injections, IDET and percutaneous discectomies, just to name a few treatments, vary greatly by geographic area. Treatment trends have changed throughout the history

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Part 1: General Principles

of medicine. The factors driving these shifts are, unfortunately, not always scientific in basis or in the patient’s best interest. This is perhaps driven more in the US by reimbursement trends and patients desire for specific treatments. The lay press and insurance industry fuel this, and not necessarily scientific evidence. Once these treatment modalities become common and patients ask for them, it is very difficult to study their effectiveness. The first step to evidence-based medicine in the treatment of spine pain is the collection of valid, consistent, epidemiologic data. This will serve as the foundation on which to build rational treatment in the future. The study of the epidemiology of spine pain is essential to understanding the scope of the problem, factors implicated in causation, and the natural history. The next step is to control causative factors or comorbid conditions with possible etiologic associations, to see if the incidence of these conditions can be altered. Basing our treatment of spine disorders on poor epidemiologic studies amounts to opinionbased medicine rather than rational treatment with evidence as its foundation. The charge to this generation of researchers and medical professionals is to base treatment on scientific evidence. To do so, we must first focus on accurate epidemiology with consistent definitions of episodes of spine pain and durations that are significant.

References 1. Pickett JP, et al. The american heritage dictionary of the English language. 4th edn. Boston: Houghton Mifflin Company; 2000. 2. Looney P, Stratford P. The prevalence of low back pain in adults: A methodological review of the literature. Physical Therapy April 1999; 79(4):384. 3. Spitzer WO. In: Troidl H, Spitzer WO, McPeek B, et al. eds. Principles and practice of research: Strategies for surgical investigators. New York: Springer-Verlag; 1986. 4. Leboiuf-yde C, Lauritsen JM. The prevalence of low back pain in the literature: A structured review of 26 Nordic studies from 1954 to 1993. Spine 1995; 20:2112– 2118. 5. Volinn E. The epidemiology of low back pain in the rest of the world: A review of surveys in low and middle-income countries. Spine 1997; 22:1747–1754. 6. Carey TS, Garrett J, Jackman A, et al. Reporting of acute low back pain in a telephone interview: Identification of potential biases. Spine 1995; 20:787–790.

20. Bovim G, Schrader H, Sand T. Neck pain in the general population. Spine 1994; 19:1307–9. 21. Bassols A, Bosch F, Campillo M, et al. Back pain in the general population of Catalonia (Spain). Prevalence, characteristics and therapeutic behavior. Gac Sanit 2003; 17(2):97–107. 22. Masset D, Malchaire J. Low back pain, epidemiologic aspects and work-related factors in the steel industry. Spine 1994: 19(2):143–146. 23. Picavet HSJ, Schouten JSAG. Musculoskeletal pain in the Netherlands: prevalences, consequences and risk groups, the DMC3-study. Pain 2003; 102:167–178. 24. http://www.cdc.gov/nchs/about/major/nhanes/frequency/mpq.htm 25. Deyo RA, Tsui-Wu YJ. Descriptive epidemiology of low back pain and its related medical care in the United States. Spine 1987; 12:264–268. 26. Cassidy JD, Carroll LJ, Cote P. The Saskatchewan health and back pain survey: The prevalence of low back pain and related disability in Saskatchewan adults. Spine 1998; 23(17):1860–1866. 27. Cote P, Cassidy JD, Carroll L. The Saskatchewan health and back pain survey: The prevalence of neck pain and related disability in Saskatchewan Adults. Spine 1998; 23(15):1689–1698. 28. George C. The six-month incidence of clinically significant low back pain in the Saskatchewan adult population. Spine 2002; 27(16):1778–1782. 29. Loney PL, Stratford PW. The prevalence of low back pain in adults: A methodological review of the literature. Physical Therapy 1999; 79:384–396. 30. Jin K, Sorock GS, Courtney TK. Prevalence of low back pain in three occupational groups in Shanghai, People’s Republic of China. J Safety Res 2004; 35:23–28. 31. Toroptsova N, Benevolenskaya L, Karyakin A, et al. Cross-sectional study of low back pain among workers at an industrial enterprise in Russia. Spine 1995; 20(3):328–332. 32. Harlow SD, Becceril LA, Scholten JN, et al. The prevalence of musculoskeletal complaints among women in Tijuana, Mexico: sociodemographic and occupational risk factors. Int J Occup Environ Health 1999; 5(4):267–275. 33. Jelsma J, Mielke J, Powell G, et al. Disability in an urban black community in Zimbabwe. Disabil Rehabil 2002; 24:851–859. 34. Omokhodion FO, Sanya AO. Risk factors for low back pain among office workers in Ibadan, Southwest Nigeria. Occup Med (Lond) 2003; 53(4):287–289. 35. Hoy D, Toole MJ, Morgan D, et al. Low back pain in rural Tibet. Lancet 2003; 362(9353):225–226.

7. Anderson GBJ. Epidemiology of low back pain. Acta Orthop Scand 1998; 69(suppl):28–31.

36. Wigley RD, Zhang NC, Zeng QY, et al. Rheumatic disease in China: ILAR-China Study comparing the prevalence of rheumatic symptoms in northern and southern rural populations. J Rheumatol 1994; 21:1484–1490.

8. Andersson GBJ. Epidemiological features of chronic low-back pain. Lancet 1999; 354:581–585.

37. Anderson RT. An orthopedic ethnography in rural Nepal. Med Anthropol 1984; 8:46–58.

9. Hart GL, Deyo RA, Cherkin DC. Physician office visits for low back pain. Spine 1995; 20:11–19.

38. Sharma SC, Singh R, Sharma AK, et al. Incidence of low back pain in work age adults in rural North India. Indian J Med Sci 2003; 57(4):145–147.

10. Kopec JA, Sayre EC, Esdaile JM. Predictors of back pain in a general population cohort. Spine 2003; 29:70–78.

39. Guo HR, Tanaka S, Cameron LL, et al. Back pain among workers in the United States: national estimates and workers at high risk. Am J Industrial Med 1995; 28:591–602.

11. Allan DB, Waddell G. An historical perspective on low back pain and disability. Acta Orthop Scand 1989; 60(Suppl 234):1–23. 12. Harrington R. On the tracks of trauma: railway spine reconsidered. Soc Hist Med. 2003 Aug 16(2):209–223. 13. Webb RT, Lunt M, Urwin M, et al. Prevalence and predictors of intense, chronic, and disabling neck and back pain in the UK general population. Spine 2003; 28:1195–1202. 14. Palmer KT, Walker-Bone K, Griffin MJ, et al. Prevalence and occupational associations of neck pain in the British population. Scand J Work Environ Health 2001; 27:49–56. 15. Waxman R, Tennant A, Helliwell P. A prospective follow-up study of low back pain in the community. Spine: 2000; 25(16):2085–2090. 16. Guez M, Hildingsson C, Stegmayr B, et al. Chronic neck pain of traumatic and nontraumatic origin: a population-based study. Acta Orthop Scand 2003; 74:576–579. 17. Guez M, Hildingsson C, Nilsson M, et al. The prevalence of neck pain: A population-based study from northern Sweden. Acta Orthop Scand 2002; 73:455–459. 18. Linton SJ, Ryberg M. Do epidemiological results replicate? The prevalence and health-economic consequences of neck and back pain in the general population. Eur J Pain 2000; 4(4):347–354.

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19. Makela M, Heliovaara M, Sievers K, et al. Prevalence, determinants and consequences of chronic neck pain in Finland. Am J Epidemiol 1991; 134:1356–1367.

40. Frymoyer JW, Cats-Baril WL. An overview of the incidences and costs of low back pain. Orthop Clin North Am 1991; 22:263–271. 41. Miedema A, Chorus AM, Wevers CW, et al. Chronicity of back problems during working life. Spine 1998; 23(18):2021–2028. 42. Stewart WF, Ricci JA, Chee E, et al. Lost productive time and cost due to common pain conditions in the US workforce. JAMA 2003: 290(18):2443–2454. 43. Burdorf A, Sorock G. Positive and negative evidence of risk factors for back disorders. Scand J Work Environ Health 1977; 23:243–256. 44. Skovron ML. Epidemiology of low back pain. Baillieres Clin Rheumatol 1992; 6:559–573. 45. Goldberg MS, Scott SC, Mayo NE, et al. A review of the association between cigarette smoking and the development of nonspecific back pain and related outcomes. Spine 2000; 25:995–1014. 46. Frank JW, Kerr MS, Brooker AS, et al. Disability resulting from occupational low back pain: I. What do we know about primary prevention? A review of the scientific evidence on prevention before disability begins. Spine 1996; 21:2908–2917. 47. Houtman IL, Bongers PM, Smulders P, et al. Psychosocial stressors at work and musculoskeletal problems. Scand J Work Environ Health 1994; 20:139–145.

Section 1: Introduction 48. Cote P, Cassidy D, Carroll L. The factors associated with neck pain and its related disability in the Saskatchewan population. Spine 2000; 25(9):1109–1117. 49. Croft PR, Papageorgiou AC, Thomas E, et al. Short-term physical risk factors for new episodes of low back pain: Prospective evidence from the South Manchester Back Pain Study. Spine 1999; 24:1559–1561. 50. Gyntelberg F. One-year incidence of low back pain among male residents of Copenhagen aged 40–59. Dan Med Bull 1974; 21:30–36. 51. Elders L, Heinrich J, Burdorf A. Risk factors for sickness absence because of low back pain among scaffolders: A 3-year follow-up study. 2003; 28(12):1340–1346.

54. Cassidy JD, Carroll LJ, Cote P, et al. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 2000; 342:1179–1186. 55. Bigos S, Battie MC, Spengler DM, et al. A prospective study of work perceptions and psychological factors affecting the report of back injury. Spine 1991; 16:1–6. 56. Perez CE. Chronic back problems among workers. Health Rep 2000; 12:42. 57. Croft PR, Papageorgiou AC, Ferry S, et al. Psychologic distress and low back pain: evidence from a prospective study in the general population. Spine 1995; 20:2731–2737.

52. Ehrlich GE. Back pain. J Rheumatol 2003; 30 (suppl 67):26–31.

58. Rajala U, Keinanen-Kiukaanniemi S, Uusimaki A, et al. Musculoskeletal pains and depression in middle-aged Finnish population. Pain 1995; 61:451–457.

53. Hadler NM. Occupational musculoskeletal disorders. Philadelphia: Lippincott Williams and Wilkins; 1999.

59. Power C, Frank J, Hertzman C, et al. Predictors of low back pain onset in a prospective British Study. Am J Public Health 2001; 91:1671–1678.

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PART 1

GENERAL PRINCIPLES

Section 2

Spinal Pain

CHAPTER

Inflammatory Basis of Spinal Pain

3

James D. Kang and Stephen Hanks

INTRODUCTION Low back pain with or without radiculopathy continues to be a significant clinical entity causing major disability in patients. However, the etiology of low back pain and the exact pathophysiology remains elusive. Intervertebral disc degeneration has been implicated as one of the key factors associated with low back pain. The intervertebral disc continues to be a structure of great interest because its degeneration or failure may influence a variety of structures in processes believed to play a role in low back pain. There has been a large body of recent work focusing on the interaction between biomechanics and the biochemistry of disc degeneration and their seemingly coupled interaction. Low back pain is undoubtedly one of the largest health problems affecting society, both individually and as a whole. It is the second most common reason listed for a doctor’s office visit and the lifetime prevalence is estimated at 91%. Of the total Workmen’s Compensation expenditure nationwide, it accounts for somewhere between 70% and 90%. It is the second leading cause of disability worldwide and its incidence is increasing disproportionately to the population growth and other disabling conditions. For these important reasons, characterizing the underlying causes of low back pain has become more important in the scientific literature in the last 7–10 years.

THE INTERVERTEBRAL DISC The intervertebral disc has many functions including stabilization of the spine by attaching vertebral bodies together and allowing movement between these bodies giving the spine its flexibility. With the facet joints, the spine bears the entire compressive load to which the trunk of the body is exposed. Discs within the lumbar spine are exposed to three times or more the weight of the trunk while in the sitting position and this number can double during certain activities such as jumping, lifting out of position, or trauma. Changes within the disc as humans age affects the ability of the spine to respond to the loads to which it is subjected.

Disc structure The intervertebral disc is composed of four concentrically arranged layers including (1) the outer anulus fibrosus, (2) the fibrocartilaginous inner anulus fibrosus, (3) the transition zone between the anulus fibrosus and the nucleus pulposus, and (4) the nucleus pulposus. The outer anulus is composed of approximately ninety collagen sheaths bonded together in concentric laminated bands within which the fibers are arranged in the helicoid manner. These sheaths are oriented at about 30° to the disc plane and at about 120° therefore in alternate bands. This orientation is important

in resisting the high pressure of the nucleus, as well as maintaining stability against rotational forces. Cutting all fibers of the same orientation, while preserving fibers of the other direction, results in a greater increase in the axial rotation of the isolated motion segments than does removal of both facet joints. The inner anulus fibers attach directly to the cartilaginous endplate whereas the outer fibers attach directly to the vertebral body via Sharpey’s fibers. The nucleus pulposus is centrally located and consists of a relatively random network of collagen and hydrated proteoglycans. The lumbar nucleus occupies 30–50% of the total disc area in cross-section. Water content varies from 70% to 90%, is highest at birth, and decreases with advances in age as the concentration of proteoglycans also decreases. The intervertebral disc is composed of a collection of macromolecules that include mostly collagen and proteoglycan. The matrix of the outer anulus consists of approximately 80% of type I collagens and small amounts of type V collagen. Inside the outer anulus, the concentrations of type II collagen and proteoglycan become progressively greater toward the center of the disc as the concentration of type I collagen decreases. Inside the nucleus, the concentration of type II collagen approaches 80% while type I is absent. Type II fibers are more hydrophilic than type I fibers and therefore are 25% more hydrated. Most of the data on the mechanical behavior of discs have been obtained from in vitro studies of spine specimens obtained at autopsy. There is evidence that the hydration in discs changes quickly after death, including transfer of water from the outer to inner anulus, and this may affect testing results in research using cadavers. The presence of degenerative discs, as mentioned, is nearly universal as humans age. All disc tissue ages from birth to death, with the most marked changes occurring in the nucleus pulposus where the proteoglycan concentration, water content, and the number of viable cells all decrease. These changes are accompanied by fragmentation of the aggregating proteoglycans. Although all discs eventually show these same changes, the rate at which they show them varies not only from person to person, but within discs from the same individual.

Disc biomechanics In general, tissue failure occurs because the loads to which they are exposed as stresses generated exceed the strength of the tissue. These can be tensile, compressive, or shear forces contributing to the damage. Stokes and Greenapple demonstrated strains of 6–10% during extremes of flexion and axial rotation in lumbar disc fibers.1 The strains were greater in the posterolateral areas than in the anterior regions. While pure axial compression, even in testing at very high loads, does not cause herniation of the nucleus pulposus, cyclic loading can cause annular tears that may eventually lead to disc herniation. Discs are known to exhibit creep, relaxation, and hysteresis. In these studies, the amount of hysteresis was shown to increase with 17

Part 1: General Principles

load and decrease with age. These studies also demonstrate that nondegenerative discs creep less slowly than degenerative discs. This may indicate that there is less physiologic elasticity in degenerative discs. Finite element analysis has effectively modeled the functional spinal unit (FSU). It has been shown that in compression the load is transferred from one vertebra to another through the endplates via the nucleus pulposus and the anulus fibrosus. The application of a load causes pressure to develop within the disc, pushing fibers out and away from the center of the disc. Rupture of the annular fibers was seen posterolaterally in the innermost layer during progressive failure analysis in compression and in shear loads at various rotations. The rupture progressed toward the periphery, with increased loads up to the maximum used in the analysis. These structural changes to the disc and functional spinal unit can be readily seen with modern imaging techniques. However, mechanical phenomena or biomechanical changes are inadequate to explain some of the clinical observations made in the patients who have low back pain or radiculopathy. These include clinical improvement after treatment with powerful antiinflammatory medications, clinical improvement in the absence of a change in the pathologic anatomy of the disc, and the lack of correlation between symptoms or neurologic signs and the size of the disc herniation.

INFLAMMATION Acute inflammation is a response of living tissue to damage and it has three functions. The inflammatory exudates formed carry protein and fluid in cells from blood vessels to the damaged area to mediate local defenses. It also helps eliminate any infective agent that is present in the area, and helps break down damaged tissue, facilitating its removal from the site of the damage. Acute inflammation may result from physical damage, chemical substances, microorganisms, or other agents. The response results in changes in local blood flow and increased permeability of blood vessels that facilitates the escape of proinflammatory cells from the blood into the tissues. These changes are essentially the same whatever the cause and wherever the site. Usually, acute inflammation is a short-lasting process. However, the length of the process is probably dependent on the inciting cause. Hypersensitivity reactions are another cause of acute inflammation, as are physical agents such as tissue damage from trauma, ultraviolet or ionizing radiation, burns, or frostbite. Irritants and corrosive chemicals can cause inflammation and tissue necrosis. Lack of oxygen or necrosis is another mechanism by which acute inflammation can propagate. In this particular cause, the reduction of oxygen and nutrients resulting from inadequate blood flow or infarction is a potent inflammatory stimulus. Celsus described the four principal effects of acute inflammation nearly 2000 years ago (Table 3.1). These include redness from acute dilatation of small blood vessels within the area. Heat, or warmth, is usually seen only in the peripheral parts of the body such as the skin. It is also due to the increased blood flow or hyperemia through the

Table 3.1: Celsus’s original description of the characteristic signs of inflammation Erythema (rubor) Warmth (calor) Pain (dolor) (Loss of function was added by Virchow)

18

region from vascular dilatation. Swelling results from edema which is the accumulation of fluid in the extravascular space and from the physical mass of the inflammatory cells migrating to the area. Pain is one of the best-known features of acute inflammation and it results partly from the stretching and distortion of tissues due to the edema in the area. Chemical mediators of acute inflammation including bradykinin, the prostaglandins, and serotonin are also known to induce pain. Loss of function is a well-known consequence of inflammation added by Virchow to the list originated by Celsus. Movement of an inflamed area is consciously and reflexively inhibited by pain, while severe swelling or local muscle spasm may limit movement of the area. The acute inflammatory response involves three changes or processes. Changes in the vessel size and flow, increased vascular permeability and the formation of the fluid exudate, and migration or de-margination of polymorphonuclear leukocytes (PML) into the extravascular space are characteristic processes of acute inflammation. Briefly, these early stages involve small blood vessels adjacent to the area of the tissue damage, which become dilated with increased blood flow. As blood flow begins to slow, the endothelial cells swell and partially retract so that they form a leaky continuum within the blood vessel. The vessels become leaky, which permits the passage of water, salts, and small proteins into the damaged area. One of the main proteins to leak out during this period is fibrinogen. Circulating PMLs initially adhere to the swollen endothelial cells and then migrate through these channels created by the retracted endothelial cells and through the basement membrane, passing into the area of tissue damage. Later on, blood monocytes (macrophages) migrate in a similar way. The microcirculation consists of a network of small capillaries that lie between the arterioles. These microcapillaries initially experience an increased blood flow following the initial phase of arteriolar constriction, which is transient. Blood flow to the injured area may increase up to tenfold during this time, but then blood flow begins to slow down, allowing the leukocytes to de-marginate into the area. The slowing of this blood flow, which follows the phase of hyperemia, is due to increased vascular permeability and allows plasma to escape into the tissues while blood cells stay within the blood vessels. Blood viscosity is therefore relatively increased as the percentage of red cells relative to white cells and other proteins increases. The increased vascular permeability increases capillary hydrostatic pressure as well as allowing the escape of plasma proteins in the extravascular space. Instead of the usual return of fluid into the vascular space, however, proteins act to increase the colloid osmotic pressure in the extravascular space. Consequently, more fluid leaves the vessel than comes back and the net escape of protein rich fluid is called exudation. Experimental work has demonstrated three patterns of increased vascular permeability. There is an immediate response that is transient, lasting 30–60 minutes, mediated by histamine acting on the endothelium directly. A delayed response starts 2–3 hours after injury and may last for up to 8 hours. This is mediated by factors synthesized by local cells such as bradykinin or factors from the complement cascade, or those released from dead neutrophils in the exudate. A third response that can be prolonged for more than 24 hours is seen if there is a direct necrosis of the endothelium. In the later stages of acute inflammation where movement of neutrophils becomes important, experimental evidence has shown purposeful migration of neutrophils along a concentration gradient. This movement appears to be mediated by substances known as chemotactic factors diffusing from the area of damage. The main neutrophil chemotactic factors are C5a, LTB4, and bacterial components. These factors, when bound to the receptor on the surface of a neutrophil, activate secondary messenger systems stimulating increased cytosolic calcium with the assembly of cytoskeletal specializations that are involved in their ability to move.

Section 2: Spinal Pain

The spread of the inflammatory response following injury to a small area of tissue suggests that chemical substances are released from the injured tissues spreading out to uninjured areas. These chemicals are called endogenous mediators and contribute to the vasodilatation, de-margination of neutrophils, chemotaxis, and increased vascular permeability. Chemical mediators released from the cells include histamine, which is probably the best-known chemical mediator in acute inflammation. It causes vascular dilatation in the immediate transient phase of increased vascular permeability. This substance is stored in mast cells, basophils and eosinophils, as well as platelets. Histamine released from those sites is stimulated by complement components C3a and C5a, and by lysosomal proteins released from neutrophils. Lysosomal compounds are released from neutrophils and include cationic proteins that may increase vascular permeability and neutral proteases, which may activate complement. Prostaglandins are a group of long-chain fatty acids derived from arachidonic acid and synthesized by many cell types. Some prostaglandins potentiate the increase in vascular permeability caused by other compounds. Part of the antiinflammatory activity of drugs such as aspirin and nonsteroidal antiinflammatory drugs (NSAIDs) is attributable to inhibition of one of the enzymes involved in prostaglandin synthesis. Leukotrienes are also synthesized from arachidonic acid, especially in neutrophils, and appear to have vasoactive properties. SRS-A (slow-reacting substance of anaphylaxis) involved in type I hypersensitivity is a mixture of leukotrienes. Serotonin (5-hydroxytryptamine) is present in high concentration in mast cells and platelets and is a potent vasoconstrictor. Lymphokines are a family of chemical messengers released by lymphocytes. Aside from their major role in type IV sensitivity, lymphokines also have vasoactive or chemotactic properties. Within the plasma are four enzymatic cascade systems including the complement system, the kinins, the coagulation factors, and the fibrinolytic system, which are interrelated and produce various inflammatory mediators. The complement system is a cascade system of enzymatic proteins and can be activated during the acute inflammatory reaction in various ways. In tissue necrosis, enzymes capable of activating complement are released from dying cells. During infection, the formation of antigen–antibody complexes can activate complement via the classical pathway, while endotoxins of Gram-negative bacteria activate complement via the alternative pathway. Products of the kinin, coagulation, and fibrinolytic systems can also activate complement. The products of complement activation that are most important in acute inflammation include C5a, which is chemotactic for neutrophils, increases vascular permeability, and releases histamine from mast cells. C3a has similar properties to those of C5a, but is less active. C5, 6, and 7 are all chemotactic for neutrophils and, in combination with 8 and 9, have additional cytolytic activity. Finally, C4b, C2a, and C3b are all important in the opsonization of bacteria, which facilitates phagocytosis by macrophages. The kinin system includes the kinins, which are peptides of 9 to 11 amino acids that are important in increasing vascular permeability. The most important of these is bradykinin. The kinin system is activated by coagulation factor XII. Bradykinin is also an important chemical mediator of pain, which is a cardinal feature of acute inflammation. Within the coagulation system, factor XII, once it has been activated by contact with extracellular materials, will activate the coagulation, kinin, and fibrinolytic systems directly. This system is responsible for the conversion of soluble fibrinogen into fibrin, which is the major component of the acute inflammatory exudate. These fibrin degradation products result from the lysis of fibrin in the presence of plasmin. Within the fibrinolytic system, the fibrin degradation products have effects on local vascular permeability.

The PML is the characteristic cell in acute inflammation. Its ability to move in a response to a concentration gradient of chemotactic factors has been well demonstrated and is mediated by cytosolic calcium. Neutrophils are able to bind to bacterial components via their Fc receptor and are able to phagocytose various particles or organisms and partially liquefy them with toxic compounds contained within lysosomes. Following tissue damage or loss from any cause, including damage due to the inflammatory process, there may be resolution, regeneration, or repair. All of these processes may occur in the same tissue or begin as soon as there is significant tissue damage. Healing does not wait for inflammation or other mechanisms to subside, but usually takes place concurrently. The outcome depends on which of these three processes predominate and on a number of factors. Resolution tends to occur when there is little tissue destruction as well as a limited period of inflammation and short, successful treatment. Regeneration occurs when lost tissue is replaced by a proliferation of cells of the same type reconstructing the normal architecture. Regeneration proceeds based on cell type, and cells are usually classified into three groups based on their ability to regenerate. Labile cells are those that are normally associated with high rate of loss and replacement and therefore have a high capacity for regeneration. Stable cells do not normally proliferate to a significant extent but can be stimulated to do so after they have been damaged. Permanent cells are unable to divide after their initial development and therefore cannot regenerate when lost (i.e. neurons). Tissue architecture is also important. Simple structures are easier to reconstruct following damage than complex ones. An imperfect attempt at regeneration can have important clinical consequences such as the cirrhosis that results after damage to the liver and the resulting abnormal nodular architecture from the repair. This process is also dependent on the amount of tissue loss. There must be cells left in the area to regenerate, as well as a reasonable volume to regenerate prior to scar formation. In repair, the process results in formation of a fibrous scar from the granulation tissue. Following the acute inflammation and phagocytosis of necrotic debris and other foreign material, blood vessels proliferate and fibroblasts assemble at the edge of the damaged area. As the endothelial cells and fibroblasts grow into the damaged area, vascularization also proceeds. Fibroblasts continue to proliferate, producing collagen and giving the tissue mechanical strength; eventually a scar consisting of dense collagen results. Factors influencing healing include the rate of healing, the presence of foreign material or of continuing inflammation, inadequate blood supply, abnormal motion, or certain medications that inhibit this process. Systemically, the healing process becomes less effective and slower with increasing age. Nutritional deficiencies play an important role as well as metabolic diseases such as renal failure or diabetes mellitus. Some patients with ongoing malignancies are actually in a catabolic state and unable to heal even simple wounds. Additionally, corticosteroids are important systemic inhibitors of wound healing.

The process of inflammation Inflammation is a complex, stereotypical reaction of the body in response to damage of cells in vascularized tissues. In avascular tissue such as the normal cornea or within the disc space, true inflammation does not occur. The cardinal signs of inflammation presented earlier, including redness, swelling, heat, pain and deranged function, have been known for thousands of years. The inflammatory response can be divided temporally into hyperacute, acute, subacute, and chronic inflammation. The response can be based on the degree of tissue damage, such as superficial or profound, or on 19

Part 1: General Principles

the immunopathological mechanisms such as allergic, or inflammation mediated by cytotoxic antibodies, or inflammation mediated by immune complexes, or delayed-type hypersensitivity reactions. As presented earlier, the development of inflammatory reactions is controlled by cytokines, by products of the plasma enzyme systems (complement, the coagulation system, the kinin and fibrinolytic pathways), by lipid mediators (prostaglandins and leukotrienes) released from different cells, and by vasoactive mediators released from mast cells, basophils, and platelets. These inflammatory mediators controlling different types of reactions differ from one another. Fast-acting mediators such as the vasoactive amines and the products of the kinin system modulate the immediate response. Later, newly synthesized mediators such as leukotrienes are involved in the accumulation and activation of other cells. Once the leukocytes have arrived at the site of inflammation, they release mediators that control the later accumulation and activation of other cells. However, it is important to realize that in inflammatory reactions initiated by the immune system the ultimate control is exerted by the antigen itself, in the same way as it controls the immune response itself. For this reason, the cellular accumulation at the site of a chronic infection or in an autoimmune reaction is quite different from that at sites where the antigenic stimulus is rapidly cleared. Inflammation can become chronic. In certain settings, the acute process, characterized by neutrophil infiltration and edema, gives way to a predominance of mononuclear phagocytes and lymphocytes. This probably occurs to some degree with the normal healing process that becomes exaggerated and chronic when there is an effective elimination of foreign material as in some infections, or introduction of foreign bodies, or deposition of crystals, or persistent inflammatory product secretions such as disc herniations.

Inflammatory cells Mast cells and basophils Mast cells and basophils play a central role in inflammation and immediate allergic reactions. They are able to release potent inflammatory mediators such as histamine, proteases, chemotactic factors, cytokines, and metabolites of arachidonic acid that act on the vasculature, smooth muscle, connective tissue, mucous glands, and inflammatory cells. Mast cells settle in the connective tissue and usually are not circulating in the bloodstream. Basophils are the smaller circulating granulocytes that settle into the tissues upon stimulation. Both these types of cells contain special cytoplasmic granules which store these mediators of inflammation. The release of these mediators is known as degranulation and can be induced by physical destruction such as mechanical trauma, or chemical substances such as proteases, or endogenous mediators including tissue proteases or cationic proteins derived from eosinophils and neutrophils, or immune mechanisms which may be IgE dependent or IgE independent. Neutral proteases, which account for the vast majority of the granule protein, serve as markers of mast cells and different types of mast cells. The newly generated mediators, often absent in resting mast cells, are typically produced during IgE-mediated activation and consist of arachidonic acid metabolites, principally leukotriene C4 (LPC4), and prostaglandin D2 (PGD2), and cytokines. Of particular interest in humans is the production of tumor necrosis factor (TNF-αγ, IL-4, IL-5, and IL-6). In the cytoplasm of both mastocytes and macrophages are special granules called lipid bodies where metabolism of arachidonic acid occurs and where their products, including leukotrienes, may be stored.

20

Eosinophils Eosinophils are terminally differentiated end-stage leukocytes that reside predominantly in submucosal tissue and are recruited at the sites of specific immune reactions including allergic diseases. Like other granulocytes, they possess a polymorphous nucleus, although with only two lobes and no nucleus. The eosinophil cytoplasm contains large ellipsoid granules. Recently, it has been recognized that eosinophils are capable of elaborating cytokines that include those with potential growth factor activities and those with potential roles in acute and chronic inflammatory responses. Cytokines produced by human eosinophils that have activity in acute and chronic inflammatory responses include IL-1α, IL-6, IL-8, TNF-α, and both transforming growth factors TGF-α and TGF-β. In addition to the acute release of protein, cytokine, and lipid mediators of inflammation, eosinophils likely contribute to chronic inflammation including the development of fibrosis. Additional roles for the eosinophil modulating extracellular matrix deposition and remodeling are suggested by studies of normal wound healing. During dermal wound healing, eosinophils infiltrate into the wound site and sequentially express TGF-α early and TGF-β later during wound healing.

Neutrophils Neutrophils, also known as polymorphonuclear leukocytes, represent 50–60% of the total circulating leukocytes and constitute the first line of defense. Once an inflammatory response is initiated, neutrophils are the first cells to be recruited. Neutrophils contain granules which contain antimicrobial or cytotoxic substances, neutral proteinases, acid hydrolases, and a pool of cytoplasmic membrane receptors. The granules contain, in addition to other substances, serine proteases such as elastase and cathepsin-G, which hydrolyze protein in cell envelopes. Substrates of granulocyte elastase include collagen crosslinks and proteoglycans, as well as elastin components of blood vessels, ligaments, and cartilage. Cathepsin-G cleaves cartilage proteoglycans while granulocyte collagenases are active against type I, and to a lesser degree type III collagen from bone, cartilage, and tendon. Collagen breakdown products have chemotactic activity for neutrophils, monocytes, and fibroblasts. Although neutrophils are essential to host defense, they have also been implicated in the pathology of many chronic inflammatory conditions and ischemia– reperfusion injury. This may be triggered by substances released from damaged host cells or as a consequence of superoxide generation through xanthine oxidase. Neutrophils, macrophages, endothelial, and other cells produce two types of free radicals. The first type is represented by reactive oxygen intermediates that are formed in neutrophils by the activity of NADPH oxidase. The second type includes reactive nitrogen intermediates such as nitric oxide. Reactive nitrogen intermediates have been of some interest in low back-associated pain. These are sometimes called reactive oxynitrogen intermediates. The pathway by which they are originated is an oxidative process in which short-lived nitric oxide is derived from the guanidino nitrogen in the conversion of L-arginine to L-citrulline. This reaction is catalyzed by nitric oxide synthase (NOS) and, like the respiratory burst, it involves oxygen uptake. Three distinct isoforms of nitric oxide synthase representing three distinct gene products have been isolated and purified. The three isoforms vary considerably in their subcellular location, structure, kinetics, regulation, and hence functional roles. Two of the enzymes are constantly present and termed constitutive NOS (cNOS). The endothelial cNOS is mostly membrane bound and formed only in endothelial cells. The neuronal cNOS was identified in cytosol or central and peripheral neurons. The third isoform is an

Section 2: Spinal Pain

inducible form that is not present in resting cells. Cytokines are a potent stimulus for iNOS production or suppression. Those with an apparent stimulating effect include IFN-γ, IL-1, IL-6, TGF-α, GMCSF, and PAF (platelet activating factor) while suppression has been observed by IL-4, IL-8, IL-10, TGF-β, PDGF (platelet derived growth factor), and MDF (macrophage deactivating factor). Cytokines are basic regulators of all neutrophil functions. Many of them, including somatesthetic growth factors and pyogens, have shown to be potent neutrophil priming agents. Neutrophils are also capable of de novo synthesis and secretion of small amounts of some cytokines including IL-1, IL-6, IL-8, TNF-α and GM-CSF. Bioactive lipids originate mainly from arachidonic acid which is an abundant constituent of neutrophil membranes. Arachidonic acid is metabolized to prostaglandins, leukotrienes, and lipoxins. LTB4 is a strong neutrophil chemoattractant that may play a role in the priming process. Vasoactive leukotrienes LTC4, LTB4, and LTE4 increase microvascular permeability and may contribute to ischemia–reperfusion injury. In contrast to leukotrienes, prostaglandins suppress most neutrophil functions, possibly through their ability to elevate intracellular cyclic AMP.

Macrophages Macrophages can be divided into normal and inflammatory macrophages. A macrophage population in a particular tissue may be maintained by three mechanisms: the influx of monocytes from the circulating blood, local proliferation, and biologic turnover. Under normal steady-state conditions, the renewal of tissue macrophages occurs through local proliferation of progenitor cells and not by monocyte influx. Inflammatory macrophages are present in various exudates. Very specific markers such as peroxidase activity may characterize them and, since they are derived exclusively from monocytes, they share similar properties. Macrophages are generally a population of ubiquitously distributed mononuclear phagocytes responsible for numerous homeostatic, immunologic, and inflammatory processes. Their wide tissue distribution make these cells well suited to provide an immediate defense against foreign elements prior to leukocyte immigration. Macrophages display a wide range of functional and morphologic phenotypes. The term activated macrophages is reserved for macrophages possessing specifically increased functional activity. There are two stages of macrophage activation. The first is a prime stage in which macrophages exhibit enhanced MHC class II expression, antigen presentation, and oxygen consumption, but reduced proliferation. The agent that primes macrophages for activation is IFN-γ, a product of stimulated TH1 and TH0 cells. Other factors including IFN-α, IFN-β, IL-3, M-CSF, GM-CSF, and TNF-α can also prime macrophages for select functions. Primed macrophages respond to secondary stimuli to become fully activated, the stage defined by their inability to proliferate, high oxygen consumption, killing of facultative and intercellular parasites, tumor cell lysis and maximal secretion of the mediators in inflammation including TNF-α, PGE2, IL-1, IL-6, and reactive oxygen species of nitric oxide production by iNOS. Macrophages are important producers of arachidonic acid and its metabolites. Upon phagocytosis, macrophages release up to 50% of their arachidonic acid for membranous esterified glycerol phospholipid. It is immediately metabolized into different types of prostanoids. From them, prostaglandins, especially PGE2 and prostacyclin (PGI2), are characterized as proinflammatory agents. They induce vasodilation, act synergetically with complement components C5a and LTB4, and mediate myalgia response to IL-1. In combination with

bradykinin and histamine, they contribute to edema and pain induction. Thromboxane (TXA2) is considered an inflammatory mediator that facilitates platelet aggregation and triggers vasoconstriction. Neovascularization is an important component of inflammatory reactions and subsequent repair and remodeling processes. Some diseases such as arthritis are maintained by persistent neovascularization. Macrophages are very important to this process. The angiogenic activity of macrophages is associated with their secretory activity in an active state. Macrophages become angiogenic when exposed to low oxygen conditions or to wound-like concentrations of lactate, pyruvate, or hydrogen ions. They can also be activated by cytokines such as IFN-γ, GM-CSF, PAF, or MCP (monocyte chemoattractant protein).

Mediators of inflammation In addition to the previously mentioned cell types, there are several chemical mediators of inflammation. There is considerable redundancy of these mediators. The most important vasoactive mediators stored in mast cells and basophil granules are histamine and serotonin. These are both also present in human platelets. Histamine has diverse functions including dilation of small vessels, locally increased vascular permeability by endothelial cell contraction, chemotaxis for eosinophils, and blocking of key T-lymphocyte function. Serotonin is also capable of increasing vascular permeability, dilating capillaries, and producing contractions of nonvascular smooth muscle.

Lipid mediators The major constituents of cell membranes are phospholipids. Cellular phospholipase, especially phospholipase A2 and C, are activated during inflammation and degrade phospholipids to arachidonic acid. Arachidonic acid has a short half-life and can be metabolized by two major routes, the cyclooxygenase and the lipoxygenase pathways. The cyclooxygenase pathway produces prostaglandins, prostacyclins, and thromboxanes. The lipoxygenase pathway produces either leukotrienes or lipoxins. The prostaglandins are a family of lipid-soluble hormone-like molecules produced by different cell types in the body. For example, macrophages and monocytes are large producers of both PGE2 and PGF2. Neutrophils produce moderate amounts of PGE2, and mast cells produce PGD2. PGE2 enhances vascular permeability, is pyrogenic, and increases sensitivity to pain. Prostaglandins must be synthesized and released in response to an appropriate stimulus and do not exist free in tissues. Thromboxin A2 is produced by monocytes and macrophages as well as platelets. It causes platelets to aggregate and vasoconstriction. These effects are somewhat opposed by the action of prostacyclin which is a potent vasodilator. Leukotrienes LTD4 and 5-hydroxyeicosatetranoate (5-HETE) cause the chemotaxis and chemokinesis of several cell types including neutrophils. They are spasmogenic and cause contraction of smooth muscle and have effects on mucous secretion. Lipoxins LXA4 and LXB4 stimulate changes in microcirculation.

Products of the complement system Complement is a complex system containing more than 30 different glycoproteins present in the serum in the form of components, factors, or other regulators, and on the surface of different cells in the form of receptors. The components of the classical pathway are numbered 1–9 and in prefix by the letter ‘C.’ All these pathways use C5–C9

21

Part 1: General Principles

that form the membrane attack complex (MAC). Activation of each of the components results from the proteolytic cleavage event in a cascade mechanism. The complement system influences the activity of numerous cells, tissues, and physiologic mechanism of the body. The result of cytotoxic complement reaction may be beneficial or harmful to the body. The complement system is a potent mechanism for initiating and amplifying inflammation. This is mediated through fragments of complement components. Tissue injury following ischemic infarction may also cause complement activation and abundant deposition of membrane attack complex may be readily seen in tissue following ischemic injury.

Cytokines mediating inflammatory functions Cytokines are soluble glycoproteins that act nonenzymatically through specific receptors to regulate cell functions. Cytokines make up the fourth major class of soluble intercellular signaling molecules with neurotransmitters, endocrine hormones, and autocoids. Cytokines are synthesized, stored, and transported by many different cell types. Lymphokines are cytokines that are secreted mainly by activated T lymphocytes and monokines are produced by activated macrophages and monocytes. In order to unify the terminology of these factors, the term interleukin was accepted. Besides the term expressing their origin, cytokines can also be named according to their function as are interferons and others. Cytokines are directly responsible for the temporal amplitude and duration of the immune response as well as tissue remodeling. Individual cytokines can have widely varying responses and functions depending on cell type, concentration, and the synergistic or modulating effects of other cytokines. The information that an individual cytokine conveys depends on a pattern of regulators to which a cell is exposed and not on just a single cytokine. There is no doubt that cytokines contribute to the signs, symptoms, and pathology of inflammatory, infectious, autoimmune, and malignant diseases. TNF-α is an excellent example. Locally, it has important regulatory and antitumor activities but when TNF-α circulates in higher concentrations it may be involved in the pathogenesis of endotoxic shock, cachexia, and other serious diseases. Inflammation is dependent on both pro- and antiinflammatory cytokines. Proinflammatory cytokines are produced predominantly by activated macrophages and are involved in the upregulation of inflammatory reactions. Antiinflammatory cytokines belong to the T-cell-derived cytokines and are involved in the downregulation of inflammatory reactions. The central role in inflammatory responses involves IL-1 and TNFα. Antagonists to IL-1 (IL-1ra) and TNF-α may become important clinically in the treatment of some rheumatologic conditions such as ankylosing spondylitis and rheumatoid arthritis. IL-1 and TNF-α with IL-6 serve as endogenous pyrogens. The upregulation of inflammatory reactions is also performed by IL-11, IFN-α, IFN-β, and especially by the members of the chemokines superfamily. On the other hand, antiinflammatory cytokines (IL-4, IL-10, and IL-13) are responsible for the downregulation of the inflammatory response. The production of most lymphokines and monokines such as IL-1, IL-6, and TNF-α is also inhibited by TGF-β. However, TGF-β has a number of proinflammatory activities including chemoattractant effects on neutrophils, T lymphocytes, and nonactivated monocytes. TGF-β has been demonstrated to have in vivo immunosuppressive and antiinflammatory effects, as well as proinflammatory and selected immunoenhancing activities. When administered systemically, TGF-β acts as an inhibitor, but if given locally it can promote inflammation. Generally, TGF-β stimulates neovascularization and the proliferation and activities of connective tissue cells, and is a pivotal factor in scar formation and wound healing. But TGF-β has antiproliferative effects on most 22

other cells including epithelial cells, endothelial cells, smooth muscle cells, myeloid, erythroid, and lymphoid cells.

Chemokines Chemokines represent a superfamily of chemotactic cytokines acting as initiators and potentiators of antiinflammatory reactions. They are active over a high concentration range, and are produced by a wide variety of cell types. Exogenous irritants and endogenous mediators such as IL-1, TNF-α, PDGF and IFN-γ induce the production of chemokines, and because they bind to specific cell surface receptors they are considered second-order cytokines. Additionally, most chemokine molecules share structural similarities and function, and are attractants for many different types of cells.

BIOCHEMISTRY OF DISC DEGENERATION The biochemical events that occur with intervertebral disc degeneration and, in particular, the role of biochemical mediators of inflammation and tissue degradation, have received more attention in the literature over the last 10 years. Matrix metalloproteinases (MMPs), prostaglandin E2 (PGE2), and a variety of cytokines have been shown to play a role in the degradation of articular cartilage. Nitric oxide is another mediator. The clinical presentation of acute lumbar radiculopathy is most often attributed to a compressed lumbar nerve root by a herniated intervertebral disc. It is well-known and something of a paradox that some patients with large herniations have no radicular symptoms and, in contrast, some patients with no evidence of disc herniations have severe radiculopathy. While the mechanics of nerve root compression undoubtedly play a role in the pain, it probably only partially explains the exact pathophysiology of the radiculopathy.

MMPs, cytokines, and nitrous oxide Matrix metalloproteinases (MMPs) are thought to be responsible for the turnover of the extracellular matrix within the nucleus pulposus and anulus fibrosus. Their activity is controlled on at least three levels. First, they are upregulated by cytokines such as interleukin-1 via gene expression, and also by TNF-αγ. Next, MMPs are latent in their proform, requiring activation prior to reaching their full degradative potential. And lastly, MMPs are inhibited in connective tissue by a number of TIMPs (tissue inhibitors of metalloproteinases). MMPs come in several different varieties. The most commonly investigated ones in terms of intervertebral disc degeneration have been MMP2 (gelatinase-α) and MMP3 (stromelysin). Kang investigated stromelysin production as well as production of nitric oxide IL-6 and PGE2, comparing 18 herniated lumbar discs with 8 control discs obtained from patients undergoing anterior surgery for scoliosis and burst fractures.2 Kang examined gelatinase, stromelysin, as well as collagenase activity. His group found a nearly sixfold increase in gelatinase among the herniated disc samples compared to the controls. Collagenase production was absent in the control subjects and nonsignificantly elevated in the herniated discs. Caseinase (or stromelysin – MMP3) showed an approximately fourfold increase in the herniated samples compared with the control discs. This early finding and the activity of MMPs in herniated disc samples was interesting, especially in the case of caseinase (stromelysin) which is known to degrade the core protein of cartilage proteoglycans. The progressive loss of these proteoglycans within the nucleus pulposus is believed to be one of the central reasons behind its desiccation and failure to retain its water content. The high levels found in the herniated discs probably repre-

Section 2: Spinal Pain

sent the levels found in the degenerative discs compared to the lower level of MMP activity in the normal discs. It is likely that the smaller or lower activity of the MMPs in the normal discs reflects a basal amount of MMP activity responsible for ongoing remodeling of the disc architecture. The high MMP production in the herniated discs is likely a result of the increased inflammatory mediators produced within the discs or in the immediate area of the discs because of the inflammation. IL-1 is known to have a positive modulating response on the MMPs. In the presence of a high IL-1 concentration and a low or relatively low TIMP concentration, the degradative enzymes may be expected to flourish. In a follow-up study to this article, Kang et al. reported on the effect of interleukin-1β on control and herniated discs using samples from the lumbar and cervical spine.3 They showed significantly elevated MMP production in the form of gelatinase and stromelysin by normal nondegenerated disc specimens after the addition of IL-1β. The basal levels of gelatinase and stromelysin were already increased in the lumbar and cervical degenerative disc specimens and the addition of IL-1β to these cultures did not significantly increase them. Collagenase activity was not detected. An interesting control in this last study was the use of L-NMA (nmonomethyl-L-arginine) to block endogenously produced NO. Cells were cultured (control and diseased) in the presence of L-NMA in order to study the effects of endogenously produced nitrous oxide on the other mediators. When L-NMA was added to the nondegenerate control specimens that had been stimulated with IL-1β, the production of gelatinase was significantly decreased, but not the production of stromelysin. When this same effect was studied in herniated lumbar discs that were stimulated with IL-lβ, both gelatinase and stromelysin were significantly reduced. Interestingly, the same study done on the herniated cervical discs stimulated with IL-1β had no significant effect on gelatinase or stromelysin.3 Several other authors have studied MMPs and their association with intervertebral disc degeneration. Fujita et al. studied autopsy specimens of degenerative discs.4 They first discovered serine elastases with high activity in the endplate and nucleus pulposus of degenerative discs. Another group using a monoclonal antibody against MMP3, found the MMP3-positive cell ratio was significantly correlated with the magnetic resonance imaging grade of intervertebral disc degeneration. The MMP3-positive cell ratio observed in prolapsed lumbar

intervertebral discs was significantly higher than in nonprolapsed discs. The same study used an anti-TIMP1 monoclonal antibody to demonstrate the normal presence of MMP3 and TIMP1 together in the degenerative intervertebral discs and hypothesized that an imbalance between MMP3 and TIMP may induce degeneration. IL-1 is a known mediator of mesenchymal cells and probably has a central role in disc degeneration. It is one of the key inflammatory mediators and it has been found in mononuclear cells responding to disc herniations. The studies on human disc tissue have had difficulty demonstrating IL-1β in the intervertebral disc tissues, but when disc cells were stimulated with lipopolysaccharide, elevated levels of IL1β were found. Both MMP2 (gelatinase) and MMP3 (stromelysin) respond to IL-1. In an experiment using ovine disc cells, Shen et al. demonstrated the ability of IL-1 to enhance the in vitro production of MMP2 and MMP3 by cells of the nucleus pulposus.5 However, the active form of MMP3 predominated over the active form of MMP2 in this model of IL-1 activation. This suggests that, in the presence of IL-1 as an inflammatory mediator, MMP3 may be more intimately involved with ongoing intervertebral disc degeneration than is MMP2. Therefore, the MMPs appear to be key factors in disc degeneration (Fig. 3.1). 3. They are the active form of the enzymes that they produce, and are capable of degrading constituents of the extracellular matrix and basement membrane at physiologic pH values. Substrates for these MMPs are present in abundance in the disc: collagens II and III are substrates for MMP1, MMP8 and MMP13, as well as their proteoglycans and other minor collagens which are substrates for MMP2 and MMP9. Compared with healthy discs, degenerative discs have been noted to have higher activities of not only MMP3 and MMP7, but also TIMP1. MMP3 activity has been correlated to the size of osteophytes present in disc degeneration. Inhibitors of MMPs have been found in low levels and are constitutively expressed. TIMP2 appears to be released by most cell types within the discs, whereas TIMP1 appears to be exclusively overexpressed in discs with degenerative disease. These expressions of MMPs and TIMPs have also been measured in spines with presumed abnormal biomechanical loading characteristics such as those with scoliosis. Handa et al. showed that proteoglycans and inhibitors of MMPs were produced in increased amounts under hydrostatic conditions when loads were increased to within a normal range.6 Taking these loads to abnormally high pressures resulted in decreased proteoglycan production and an increased production of MMP3.

Resident chondrocytes

TNF-α

Macrophage infiltration of disc tissue

Neurovascularization

Nerve conduction velocity reduction

Factories for production of inflammatory mediators (TNF-α, IL-1, IL-6, NO)

Nerve ingrowth

Nerve sensitization DRG sensitization

Back pain

Radiculopathy

Nitric oxide

↓

MCP-1 IL-8

MMP3/TIMP

Matrix degradation response to abnormal loading

Disc degeneration

↓

Upregulation

MMP-7 TNF-α

IL-1 (Many sources)

MMP2/MMP3

Nitric oxide

Matrix degradation

Nerve effects

Back pain

IL-6/PGE2

Radiculopathy

Fig. 3.1 MMPs as key factors in disc degeneration. 23

Part 1: General Principles

Much of the work involving the study of MMP activation and measurement has been done using tissue obtained from patients operated on for herniated discs. Therefore, many of these publications include the fact that the assay was done on disc tissue that had been presumably exposed to some type of a burst of inflammation after exposure to the epidural space. It has been proposed that patients with herniated, sequestered, or noncontained herniations may have a more severe inflammatory reaction and pain response. Nygaard et al. looked at 37 patients undergoing surgery for lumbar disc herniation.7 They divided the patients into those who had a bulging disc, a contained or incomplete herniation, or a noncontained or sequestered free disc fragment. Unfortunately, they were unable to recruit enough patients with bulging discs to investigate this phenomenon statistically. In looking at the two groups with the largest number of patients, including the contained herniation group which had 25 members and the noncontained herniation group which had 9 members, there was a significant difference in the mean concentrations of LTB4, with the noncontained group having almost double the concentration versus the contained herniation group. As well, thromboxane B2 was significantly higher in the noncontained versus the contained herniation group. Although the measured concentration of these two proinflammatory cytokines was lower in the bulging disc, their numbers were too small to be included in the statistical analysis. This study seems to support the theory that there are different inflammatory characteristics of different degrees of disc herniations. One of the other paradoxes in the delineation of an inflammatory response for disc herniation has to do with the atypical cellular response when compared to inflammation occurring at other places in the body. Neutrophils are the sine qua non of acute inflammation; however, they have really only been found in noncontained or sequestered disc fragments where neovascularization may be occurring. Most of the cellular elements that have been identified and are proposed to be the source or factories for most of the inflammatory cytokines are macrophages. Gronblad,8 Nojara,9 Yasuma,10 and Haro11 have identified macrophages as well as vascular proliferation in the granulation tissue of herniated discs. Haro additionally found that inflammatory cells were more abundant in the noncontained group of disc herniations than in the contained group. Inflammatory cells are known to act in an autocrine or paracrine type fashion with regard to their effect on resident cells in the inflammatory process. This must also be true for the degenerative disc. The intervertebral disc, which is normally nourished through diffusion, can become neovascularized to some extent after exposure to the epidural space. These discs display granulation tissue with macrophage and T-lymphocyte infiltration not observed in healthy discs. Haro et al. have proposed that the natural resorption of a herniated disc appears to occur by a vascularization-mediated process and is correlated with macrophage infiltration. It is also known that chondrocytes replace proteoglycans within the nucleus pulposus and these cells have been proposed to play a very important role in the inflammatory process in regards to production of abnormal types of collagen as well as MMPs and TIMPs in response to abnormal loading characteristics. Haro et al. reported their results in a co-culture system of chondrocytes and macrophages and demonstrated a marked upregulation of MMP3 by disc chondrocytes with the addition of macrophages to the culture system. This resulted in eventual resorption of the disc through macrophage action. They further used MMP-null mice to determine that the production of MMP3 by the chondrocytes was required for macrophage infiltration in disc resorption. In a more recent study, this same group has shown that the production of MMP7 by macrophages was found to be required for infiltration into disc tissue through a mechanism involving the release of soluble TNF-α.12 24

The support for macrophage-mediated cellular response in herniated disc tissue is also supported by another study by Haro. While macrophage invasion appears to accompany and participate in the inflammatory response, the likely end to this is reabsorption of the herniated disc tissue. Groups have proposed neovascularization of these disc tissues as the means by which this happens. Previous studies have shown that resorption may be mediated by neovascularization as measured through Gd-DTPA MRI. Komori showed that the tendency of these herniated disc tissues to spontaneously resorb was proportional to the degree of Gd-DTPA enhancement, which suggests that the resorption was mediated by a vascular event.13 Haro and his group have shown that, in an in vitro co-culture system they have used previously, an increase in macrophage VEGF protein (vascular endothelial growth factor) and mRNA expression was observed after they exposed disc tissue to the co-culture.14 They found TNF-α was required for induction of VEGF protein and conclude that this may be one mechanism for resorption for herniated disc tissue. Further evidence for the involvement of the macrophage and its importance is shown in the paper by Burke et al.15 This group studied the production of monocyte chemoattractant protein-1 (MCP1) and interleukin-8 (IL-8) by intervertebral discs removed after surgery. Burke found that MCP1 and IL-8 were detected in both the control and herniated disc specimens and that the noncontained herniated samples contained higher levels of these chemokines than those with an intact anulus. They proposed that the MCP1 production attracts the macrophages while IL-8 may influence the angiogenesis or the neovascularization that is seen in these samples. Although the stimulus for MCP1 in this in vitro experiment was not investigated and is as yet unknown, this may represent a physiologic mechanism for initiation of macrophage infiltration after disc prolapse and the process of disc resorption. IL-8 was also strongly influenced by the noncontained morphology of these samples. In addition to the angiogenic properties of IL-8, it is also chemotactic for T cells that have been identified in the chronic inflammatory filtrate around disc herniations. In addition to TNF activation of or paracrine/autocrine effects governing MMP production, TNF-αγ has long been regarded to be a key player in mediating the sensitization of nerve roots by material from the nucleus pulposus, and other effects such as edema, intervascular coagulation, reduction in blood flow, and the splitting of myelin. TNF-αγ is known to be released from the chondrocyte resident cells in the nucleus pulposus. In a local application of TNF-αγ, it induced a reduction in nerve conduction velocity in a porcine experiment done by Aoki et al.16 In this study, applications of interleukin-1β and interferon-γ induced a very small reduction of nerve velocity compared with epidural fat. In a follow-up study to this, Olmarker and Rydevik demonstrated that local blockers to TNF-αγ prevented the reduction of nerve conduction velocity and seemed to limit the nerve fiber injury and intercapillary thrombus formation, as well as the intraneural edema seen in the absence of the inhibitor.17 These authors have suggested that TNF-αγ inhibitors may be important therapeutically in the future. Presently, synthesis of TNF-αγ can be blocked with systemic corticosteroids, IL-10, TGF-βγ or by other drugs such as chlorpromazine, pentoxifylline, or ciclosporin. However, these drugs are non-specific inhibitors and may result in side effects that would be undesirable. Presently, there are anti-TNF agents being used in the treatment of rheumatoid arthritis. The first of these, infliximab (Remicade), was quickly followed by etanercept (Enbrel). Recently, a monoclonal antibody against TNF-αγ, adalimumab (Humira), has been released. These agents are not presently approved for treatment of sciatic pain, but have given sufferers of rheumatoid arthritis a further dimension for their treatment. Another potent inflammatory mediator that is also induced by TNF-αγ is nitric oxide. Nitric oxide is a particularly interesting

Section 2: Spinal Pain

Table 3.2: Temporal relationships in disc degeneration Pre-adolescence

Adolescence

Early Adulthood

Middle Adulthood

Late Adulthood

Matrix remodeling for ‘slow growth’

Highest period of weightbearing linear growth

Continued matrix imbalance

Continued structural imbalances

Structural loss of height stable

No inflammogenic changes

Matrix remodeling imbalances

Collagen isotype switch ↑chondrocyte nests

Chronic and acute on chronic inflammation

In vivo collapse and autofusion or

Loss of proteoglycan

Inflammogenic events (e.g. injury, abnormal motion)

Desiccation and breakdown of anulus

In vivo collapse with facet joint incompetence and instability

Onset of early degeneration

Structural changes – loss of height

compound in that it has been shown to act in various ways depending on the tissues that in which it resides. In bone, mechanical stress affects intracellular cyclic AMP, calcium, and PGE2 levels, as well as having effects on matrix synthesis. It has been demonstrated that nitric oxide is a key mediator of these processes. Articular chondrocytes have been shown to produce large amounts of nitric oxide. As described in the preceding sections introducing the inflammatory process, nitric oxide is produced in several forms including the inducible form that is present in chondrocytes. Kang et al. first showed the spontaneous production of nitric oxide from human lumbar discs and that this production was higher in herniated discs than normals.2 In a follow-up study, Kang et al. examined the effects of IL-1β on normal and herniated disc tissue. They found that the addition of IL-1βγ caused a significant increase in the production of nitric oxide as well as IL-6 and PGE2.3 While these inflammatory mediators were sharply increased in both normal and herniated disc tissue, the interesting point to this paper was that MMP production did not change in the herniation disc material, while the normal disc showed a sharp increase in the production of MMPs. It is also noted by this group that endogenously produced nitric oxide had a large inhibitory effect on IL-6.

PUTTING IT ALL TOGETHER The inflammatory basis for intervertebral disc degeneration likely begins at or around the time of puberty when linear growth accelerates. It is possible that the rapid growth rate seen during this time outstrips the ability of the intervertebral disc to remodel effectively, leading to imbalances in MMP and TIMP concentrations. This may be further enhanced by increased diffusional demands for nutrition and a less than desirable pH balance within the disc (Table 3.2). As the process continues, changes in collagen isotype and loss of proteoglycan support occur and nests of chondrocytes replace normally aggregating proteoglycans. These chondrocytes likely become the factories for continued MMP and TIMP production as well as the source for inflammatory mediators. As the changes progress outward toward the disc anulus and involve the ability of the disc to respond to loads, chondrocyte proliferation continues and collagen fragmentation secondary to abnormal loading initiates an inflammatory response within the disc. As the process continues toward the periphery, the anulus begins to fail under the increased stiffness of the FSU and the inflammatory cascade promulgates. Macrophages are recruited and produce multiple inflammatory mediators. Granulation tissue around the disc containing these cells is a source for continuing inflammation

Changes contributing to DJD or stenosis

as well as the neovascularization that both potentiates the response and serves as a nidus for nerve invasion of the outer anulus. Inflammatory mediators such as bradykinin, nitric oxide, and TNF-αγ may directly affect local nerves having effects on conduction velocity and sensitizing nerve endings to normally benign motion. As well, the effect on perineural vascularity and edema is pronounced in the presence of these mediators. These proinflammatory contributors may help explain the previously mentioned paradox concerning a lack of evidence supporting compression per se in causing spinal nerve pain. Researchers continue to unravel the temporal relationships as well as new ways of treating this common entity. Solution of the a priori ‘first cause’ for degenerative disc disease will probably await our ability to genetically replace damaged discs. Such research is ongoing in several centers and deserves support.

References 1. Stokes I, Greenapple DM. Measurement of surface deformation of soft tissue. J Biomech 1985; 18:107. 2. Kang JD, Georgescu HI, McIntyre-Larkin L, et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 1996; 21(3):271–277. 3. Kang JD, Stefanovic-Racic M, McIntyre LA, et al. Toward a biochemical understanding of human intervertebral disc degeneration and herniation: contributions of nitric oxide, interleukins, prostaglandin E2, and matrix metalloproteinases. Spine 1997; 22(10):1065–1073. 4. Fujita K, Nakagawa T, Hirabayashi K, et al. Neutral proteinases in human intervertebral disc: role in degeneration and probable origin. Spine 1993;1 8(13):1766–1773. 5. Shen B, Melrose J, Ghosh P, et al. Induction of matrix metalloproteinase-2 and -3 activity in ovine nucleus aragose gel culture by interleukin-1β: a potential pathway of disc degeneration. Eur Spine J 2003; 12:66–75. 6. Handa T, Ishihara H, Ohshima H, et al. Effects of hydrostatic pressure on matrix synthesis and matrix metalloproteinase production in the human lumbar intervertebral disc. Spine 1997; 22(10):1085–1091. 7. Nygaard ØP, Mellgren SI, Østerud B. The inflammatory properties of contained and noncontained lumbar disc herniation. Spine 1997; 22(21):2484–2488. 8. Gronblad M, Virri J, Ronkko S, et al. Type (group II) phospholipase A2 and inflammatory cells in macroscopically normal, degenerated, and herniated human lumbar disc tissues. Spine 1996; 21(22):2531–2538. 9. Nojara. Marseilles: ISSLS Presentation; 1993. 10. Yasuma T, Arai K, Yamauchi Y. The histology of lumbar intervertebral disc herniation. The significance of small blood vessels in the extruded tissue. Spine 1993; 18(13):1761–1765. 11. Haro H, Shinomiya K, Komori H, et al. Upregulated expression of chemokines in herniated nucleus pulposus resorption. Spine 1996; 21:1647–1652.

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Part 1: General Principles 12. Haro H, Crawford HC, Fingleton B, et al. Matrix metalloproteinase-7-dependent release of tumor necrosis-αγ in a model of herniated disc resorption. J Clin Invest 2000; 105(2):143–150. 13. Komori H, Okawa A, Haro H, et al. Contrast-enhanced magnetic resonance imaging in conservative management lumbar disc herniation. Spine 1998; 23(1):67–73. 14. Haro H, Kato T, Komori H, et al. Vascular endothelial growth factor (VEGF)-induced angiogenesis in herniated disc resorption. J Orthop Res 2002; 20(3):409–415. 15. Burke JG, Watson RWG, McCormack D, et al. Spontaneous production of monocyte chemoattractant protein-1 and interleukin-8 by the human lumbar intervertebral disc. Spine 2002; 27(13):1402–1407. 16. Aoki Y, Rydevik B, Kikuchi S, et al. Local application of disc-related cytokines on spinal nerve roots. Spine 2002; 27(15):1614–1617.

Franson RC, Saal, JS, Saal JA. Human disc phospholipase A2 is inflammatory. Spine 1992; 17(6S):S129–S132. Freemont AJ, Peacock TE, Goupille P, et al. Nerve ingrowth into diseased intervertebral disc in chronic back pain. Lancet 1997; 350(9072):178–181. Freemont AJ, Watkins A, Maitre CL, et al. Current understanding of cellular and molecular events in intervertebral disc degeneration: implications for therapy. J Pathol 2002; 196(4):374–379. Gaetani P, Rodriguez y Baena R, Riva C, et al. Collagenase-1 and stromelysin distribution in fresh human herniated intervertebral disc: a possible link to the in vivo inflammatory reactions. Neurol Res 1999; 21(7):677–681.

17. Olmarker K, Rydevik B. Selective inhibition of tumor necrosis factor-α prevents nucleus pulposus-induced thrombus formation, intraneural edema, and reduction of nerve conduction velocity. Spine 2001; 26(8):863–869.

Goupille P, Jayson MIV, Valat JP, et al. Matrix metalloproteinases: the clue to intervertebral disc degeneration. Spine 1998; 23(14):1612–1626.

Further reading

Grabowski PS, Wright PK, Van’t Hof RJ, et al. Immunolocalization of inducible nitric oxide synthase in synovium and cartilage in rheumatoid arthritis and osteoarthritis. Br J Rheumatol 1997; 36:651–655.

Adams MA, Hutton WC. 1981 Volvo Award in Basic Science. Prolapsed intervertebral disc. A hyperflexion injury. Spine 1982; 7(3):184–191. Ahn SH, Cho YW, Ahn MW, et al. mRNA expression of cytokines and chemokines in herniated lumbar intervertebral discs. Spine 2002; 27(9):911–917.

Goupille P, Jayson MIV, Valat JP, et al. The role of inflammation in disk herniation-associated radiculopathy. Semin Arthritis Rheum 1998; 28(1):60–71.

Grange L, Gaudin P, Trocme C, et al. Intervertebral disk degeneration and herniation: the role of metalloproteinases and cytokines. Joint Bone Spine 2001; 68(6): 547–553.

An HS, Thonar EJ-MA, Masuda K. Biological repair of intervertebral disc. Spine 2003; 28(15):S86–S92.

Habtemariam A, Gronblad M, Virri J, et al. A comparative immunohistochemical study of inflammatory cells in acute-stage and chronic-stage disc herniations. Spine 1998; 23(20):2159–2165.

Baggiolini M, Dewald B, Moser B. Interleukin-8 and related chemotactic cytokines-CXC and CC chemokines. Adv Immunol 1994; 55:97–179.

Hashizume H, Kawakami M, Nishi H, et al. Histochemical demonstration of nitric oxide in herniated lumbar discs. Spine 1997; 22(10):1080–1084.

Brisby H, Byröd G, Olmarker K, et al. Nitric oxide as a mediator of nucleus pulposusinduced effects on spinal nerve roots. J Orthop Res 2000; 18(5):815–820.

Häuselmann HJ, Oppliger L, Michel BA, et al. FEBS Letts 1994; 352:361–364.

Burke JG, Watson RWG, McCormack D, et al. Intervertebral discs which cause low back pain secrete high levels of proinflammatory mediators. J Bone Joint Surg Br 2002; 84(2):196–201. Burke JG, Watson RWG, Conhyea D, et al. Human nucleus pulposus can respond to a pro-inflammatory stimulus. Spine 2003; 28(24):2685–2693. Caron JP, Fernandes JC, Martel-Pelletier J, et al. Chondroprotective effect of intraarticular injections of interleukin-1 receptor antagonist in experimental osteoarthritis. Suppression of collagenase-1 expression. Arthritis Rheum 1996; 39(9): 1535–1544.

Horwitz AL, Hance AJ, Crystal RG. Granulocyte collagenase: selective digestion of type I relative to type III collagen. Proc Natl Acad Sci USA 1977; 74(3):897–901. Igarashi T, Kikuchi S, Shubayev V, et al. 2000 Volvo Award Winner in Basic Science Studies. Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Spine 2000; 25(23):2975–2980. Kääpä E, Han X, Holm S, et al. Collagen synthesis and types I, III, IV, and VI collagens in an animal model of disc degeneration. Spine 1995; 20(1):59–66. Kanemoto M, Hakuda S, Komiya Y, et al. Immunohistochemical study of matrix metalloproteinase-3 and tissue inhibitor of metalloproteinase-1 human intervertebral discs. Spine 1996; 21(1):1–8.

Collier S, Ghosh P. The role of plasminogen in interleukin-1 mediated cartilage degradation. J Rheumatol 1988; 15(7):1129–1137.

Kanerva A, Kommonen B, Gronblad M, et al. Inflammatory cells in experimental intervertebral disc injury. Spine 1997; 22(23):2711–2715.

Cooper RG, Freemont AJ, Hoyland JA, et al. Herniated intervertebral disc-associated periradicular fibrosis and vascular abnormalities occur without inflammatory cell infiltration. Spine 1995; 20(5):591–598.

Koch H, Reinecke JA, Meijer H, et al. Spontaneous secretion of interleukin 1 receptor antagonist (IL-1Ra) by cells isolated from herniated lumbar discal tissue after discectomy. Cytokine 1998; 10(9):703–705.

Coppes MH, Marani E, Thomeer RTWM, et al. Innervation of ‘painful’ lumbar discs. Spine 1997; 22(20):2342–2350.

Kokkonen SM, Kurunlahti M, Tervonen O, et al. Endplate degeneration observed on magnetic resonance imaging of the lumbar spine. Spine 2002; 27(20):2273–2278.

Dayer JM, de Rochemonteix B, Burrus B, et al. Human recombinant interleukin-1 stimulates collagenase and prostaglandin E2 production by human synovial cells. J Clin Invest 1986; 77:645–648.

Lefebvre V, Peeters-Joris C, Vaes G. Modulation by interleukin 1 and tumor necrosis factor-α of production of collagenase, tissue inhibitor of metalloproteinases and collagen types in differentiated and dedifferentiated articular chondrocytes. Biochim Biophys Acta 1990; 1052:366–378.

Dean DD, Martel-Pelletier J, Pelletier JP, et al. Evidence for metalloproteinase and metalloproteinase inhibitor imbalance in human osteoarthritic cartilage. J Clin Invest 1989; 84:678–685. DiPasquale G, Caccese R, Pasternak R, et al. Proteoglycan- and collagen-degrading enzymes from human interleukin 1-stimulated chondrocytes from several species: proteoglycanase and collagenase inhibitors as potentially new disease-modifying antiarthritic agents (42416). Proc Soc Exp Biol Med 1986; 183(2):262–267.

26

Fox SW, Chambers TJ, Chow JW. Nitric oxide is an early mediator of the increase in bone formation by mechanical stimulation. Am J Physiol 1996; 270:E955–E960.

Liu GZ, Ishihara H, Osada R, et al. Nitric oxide mediates the change of proteoglycan synthesis in the human lumbar intervertebral disc in response to hydrostatic pressure. Spine 2001; 26(2):134–141. Liu J, Roughley PJ, Mort JS. Identification of human intervertebral disc stromelysis and its involvement in matrix degradation. J Orthop Res 1991; 9(4):568–575.

Doers TM, Kang JD. The biomechanics and biochemistry of disc degeneration. Curr Opin Orthop 1999; 10:117–121.

Lotz M, Guerne PA. Interleukin-6 induces the synthesis of tissue inhibitor of metalloproteinases-1/erythroid potentiating activity (TIMP-1/EPA). J Biol Chem 1991; 266(4):2017–2020.

Doita M, Kanatani T, Ozaki T, et al. Influence of macrophage infiltration of herniated disc tissue on the production of matrix metalloproteinases leading to disc resorption. Spine 2001; 26(14):1522–1527.

Maroudas A, Stockwell A, Nachemson A, et al. Factors involved in the nutrition of the human lumbar intervertebral disc: cellularity and diffusion of glucose in vitro. J Anat 1975; 120(1):113–130.

Edwards DR, Murphy G, Reynolds JJ, et al. Transforming growth factor beta modulates the expression of collagenase and metalloproteinase inhibitor. EMBO J 1987; 6(7):1899–1904.

Martel-Pelletier J, McCollum R, Fujimoto N, et al. Excess of metalloproteases over tissue inhibitor of metalloprotease may contribute to cartilage degradation in osteoarthritis and rheumatoid arthritis. Lab Invest 1994; 79(6):807–815.

Evans CH, Watkins SC, Stefanovic-Racic M. Nitric oxide and cartilage metabolism. Methods Enzymol 1996; 269:75–88.

Matrisian LM. Metalloproteinases and their inhibitor in matrix remodeling. Trends Genet 1990; 6(4):121–125.

Eyre DR, Muir H. Types I and II collagens in intervertebral disc. Interchanging radial distributions in anulus fibrosus. Biochem J 1976; 157:267–270.

Meachim G, Cornah MS. Fine structure of juvenile human nucleus pulposus. J Anat 1970; 107(2):337–350.

Eyre DR, Muir H. Quantitative analysis of types I and II collagens in human intervertebral discs at various ages. Biochim Biophys Acta 1977; 492:29–42.

Melrose J, Ghosh J, Taylor TKF. Neutral proteinases of the human intervertebral disc. Biochim Biophys Acta 1987; 923:483–495.

Section 2: Spinal Pain Melrose J, Ghosh J, Taylor TKF, et al. The serine proteinase inhibitory proteins of the human intervertebral disc: their isolation, characterization and variation with aging and degeneration. Matrix 1992; 12:456–470.

Roberts S, Menage J, Duance V, et al. 1991 Volvo Award in Basic Sciences. Collagen types around the cells of the intervertebral disc and cartilage end plate: an immunolocalization study. Spine 1991; 16(9):1030–1038.

Miyamoto H, Saura R, Harada T, et al. The role of cyclooxygenase-2 and inflammatory cytokines in pain induction of herniated lumbar intervertebral disc. Kobe J Med Sci 2000; 46:13–28.

Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990; 15(7):674–678.

Mort JS, Dodge GR, Roughley PJ, et al. Direct evidence for active metalloproteinases mediating matrix degradation in interleukin 1-stimulated human articular cartilage. Matrix 1993; 13:95–102. Nagano T, Yonenobu K, Miyamoto S, et al. Distribution of the basic fibroblast growth factor and its receptor gene expression in normal and degenerated rat intervertebral discs. Spine 1995; 20(18):1972–1978.

Sakurai H, Kohsaka H, Liu MF, et al. Nitric oxide production and inducible nitric oxide synthase expression in inflammatory arthritides. J Clin Invest 1995; 96:2357– 2363. Sedowofia KA, Tomlinson IW, Weiss JB, et al. Collagenolytic enzyme systems in human intervertebral disc. Their control, mechanism, and their possible role in the initiation of biomechanical failure. Spine 1982; 7(3):213–222.

Ng SCS, Weiss JB, Quennel R, et al. Abnormal connective tissue degrading enzyme patterns in prolapsed intervertebral discs. Spine 1986; 11(7):695–701.

Shinmei M, Kikuchi T, Yamagishi M, et al. The role of interleukin-1 on proteoglycan metabolism of rabbit anulus fibrosus cells cultured in vitro. Spine 1988; 13(11):1284– 1290.

Olmarker K, Larsson K. Tumor necrosis factor alpha and nucleus pulposus-induced nerve root injury. Spine 1998; 23(23):2538–2544.

Specchia N, Pagnotta A, Toesca A, et al. Cytokines and growth factors in the protruded intervertebral disc of the lumbar spine. Eur Spine J 2002; 11(2):145–151.

Özaktay AC, Cavanaugh JM, Asik I, et al. Dorsal root sensitivity to interleukin-1 beta, interleukin-6 and tumor necrosis factor in rats. Eur Spine J 2002; 11(5): 467–475.

Stadler J, Stefanovic-Racic M, Billiar TR, et al. Articular chondrocytes synthesize nitric oxide in response to cytokines and lipopolysaccharide. J Immunol 1991; 147:3915– 3920.

Park JB, Kim KW, Han CW, et al. Expression of Fas receptor on disc cells in herniated lumbar disc tissue. Spine 2001; 26(2):142–146. Park JB, Chang H, Kim YS. The pattern of interleukin-12 and T-helper types 1 and 2 cytokine expression in herniated lumbar disc tissue. Spine 2002; 27(19):2125–2128. Pearce RH, Mathieson JM, Mort JS, et al. Effect of age on the abundance and fragmentation of link protein of the human intervertebral disc. J Orthop Res 1989; 7(6):861–867. Pendás AM, Knäuper V, Puente XS, et al. Identification and characterization of a novel human matrix metalloproteinase with unique structural characteristics, chromosomal location, and tissue distribution. J Biol Chem 1997; 272(7):4281–4286.

Takahashi H, Suguro T, Okazima Y, et al. Inflammatory cytokines in the herniated disc of the lumbar spine. Spine 1996; 21(2):218–224. Tengblad A, Pearce RH, Grimmer BJ. Demonstration of link protein in proteoglycan aggregates from human intervertebral disc. Biochem J 1984; 222(1):85–92. Tolonen J, Grönblad M, Virri J, et al. Oncoprotein c-Fos and c-Jun immunopositive cells and cell clusters in herniated intervertebral disc tissue. Eur Spine J 2002; 11(5):452–458. Willburger RE, Wittenberg RH. Prostaglandin release from lumbar disc and facet joint tissue. Spine 1994; 19(18):2068–2070.

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PART 1

GENERAL PRINCIPLES

Section 2

Spinal Pain

CHAPTER

Transduction, Transmission and Perception of Pain

4

Sarah M. Rothman, Raymond D. Hubbard, Kathryn E. Lee and Beth A. Winkelstein

Painful spinal disorders are common problems in society, affecting an estimated 50 million Americans. The societal costs (including litigation, work lost, treatment, and disability) for such disorders of the spine are staggering. For example, the cost of low back pain alone has been estimated at US$40–50 billion annually.1,2 Chronic neck pain has a similarly high cost of nearly US$30 billion in health-related expenses.3 Until a better understanding of the pathomechanisms of pain and the injuries which produce them are defined, the effective prevention and treatment of these disorders and their symptoms will remain elusive. Further, distinguishing those physiologic mechanisms which lead to persistent pain from those which differentially produce only transient symptoms is also important in understanding and managing these syndromes. It is the intent of this chapter to highlight traditional and emerging theories of pain detection and transmission in the context of spine-related syndromes. A brief discussion of the neurophysiology of pain highlights concepts of local responses, pain transduction, signal transmission, and processing and is integrated with more recent hypotheses of the central nervous system’s (CNS) neuroimmunologic involvement in persistent pain. This chapter focuses on the sensory system, presenting the general anatomy of the spinal cord, nerve roots, and nerves. There are many physiologic mechanisms by which pain is detected and through which they can elicit nociception and ultimately the perception of pain. Mechanisms of pain detection are presented with specific points related to transmission of pain signals. In persistent pain, CNS changes can produce hypersensitivity or central sensitization. In addition to the electrophysiologic changes leading to central sensitization, the spinal cord and brain mount a series of neuroimmune responses which may further contribute to sensitization and persistent pain symptoms. Findings related to neuroimmunity are briefly reviewed here to form a basis for discussing more recent views of mechanisms of persistent pain. Physiologic mechanisms, together with neurochemical responses, are addressed and discussed in the context of findings from animal models of persistent pain in which behavioral hypersensitivity is produced. In particular, studies examining mechanical injuries to different anatomical structures of the spine and which lead to persistent pain symptoms are used here to provide a comparative discussion of pain detection and transmission and perception, in the context of factors for consideration in the spine. As such, findings with radiculopathy models of nerve root compression are presented and compared for discussion of potential differences in mechanisms of transient and persistent sensitivity (pain). In addition, findings from the cervical radiculopathy model are directly compared to those behavioral responses for a facet-mediated distraction pain model in the cervical spine. These behavioral studies provide a platform for exploring similarities and differences in pain responses for different types of tissue injuries. Measures of injury responses are presented for these

models, including behavioral sensitivity, local structural changes, and cellular and molecular changes in the CNS, as they provide insight into understanding pain mechanisms. It is important to define, at the outset, relevant distinctions in terminology. ‘Pain’ is a complex perception that is influenced by prior experience and by the context within which the noxious stimulus occurs. Likewise, ‘nociception’ is the physiologic response to tissue damage or prior tissue damage. Similarly, for discussion in this chapter, ‘hyperalgesia’ is defined as enhanced pain to a noxious stimulus.4 Strictly speaking, this is a leftward shift of the stimulus–response function relating pain to intensity. The corresponding pain threshold is lowered and there is enhanced response to a given stimulus. Hyperalgesia is mediated by nociceptor sensitization, where ‘sensitization’ describes a corresponding shift in the neural response curve for stimulation. Sensitization is characterized by a decrease in threshold, an increased response to suprathreshold stimulus, and spontaneous neural activity. For this chapter, many of the examples are drawn from painful injuries related to the cervical or lumbar spine. These include both low back and neck pain from radiculopathy and facet-mediated injury. While it is recognized that these examples are by no means allinclusive of pain related to the spine, they do provide an ideal context for discussing many of the broader mechanisms presented here.

RELEVANT NEURAL ANATOMY Before presenting and discussing pain mechanisms, it is first necessary to describe the relevant anatomical structures, biological connections, and relationships of neural sensory and processing components. These are reviewed only briefly here to provide appropriate context; a more detailed presentation can be found in texts specifically focused in neural science and pain.4,5 The primary afferents, which relay pain signals from injured or stimulated tissues, terminate in the dorsal horn of the spinal cord. At each level in the spinal cord, the dorsal nerve roots carry sensory information from the periphery into the spinal cord. Dorsal roots contain sensory neurons, whose cell bodies make up the enlarged dorsal root ganglion (DRG) (Fig. 4.1). In contrast, the ventral root contains the axons of neurons whose cell bodies are within the ventral horn of the spinal cord and transmits efferent signals. At each spinal level, the dorsal and ventral nerve roots come together, outside of the spinal column and distal to the DRG, and combine to form the nerve which communicates with the peripheral nervous system. The spinal nerves further branch into smaller nerves in the periphery and innervate bones, ligaments, joints, discs, muscles, organs, and many other tissue types. Structurally, three protective layers surround the spinal cord, which are themselves extensions of the cranial meninges: the dura mater 29

Part 1: General Principles

Fig. 4.1 Axial section of dorsal and ventral C7 nerve root stained with osmium tetroxide. Small- and large-diameter fibers are apparent in the dorsal root (bottom), as well as cell bodies of the dorsal root ganglion. Scale bar is 100 μm.

(outermost), the arachnoid mater, and the pia mater (innermost layer closest to the spinal cord). Within the spinal column, the lumbar dorsal and ventral nerve roots extend below the spinal cord and this neural tissue, collectively called cauda equina, fills the sacral spinal column. The spinal cord is anatomically composed of two regions (Fig. 4.2). These are distinguished by their appearance, function, and

Dorsal root (primary afferents)

Tract of Lissauer

Dorsal column

I II X

Gray matter Dorsal horn

Lateral column

TRANSDUCTION

Ventrolateral column

Ventral root

Central canal

White matter

Fig. 4.2 Schematic illustration of the spinal nerve roots, spinal cord, and its regions of gray and white matter. Also indicated are columns of the neuronal tracts in the white matter. Those regions of the gray matter (laminae) of particular relevance to pain sensation and transmission are indicated. 30

cell populations. The gray matter, which has a darker appearance, contains the cell bodies of spinal neurons and makes up the central region of the spinal cord. It is surrounded by the white matter which contains the axons of the spinal neurons. The columnar tracts of the spinal cord are regionally specialized according to information they carry (see Fig. 4.2). The lateral column contains motor neurons; the dorsal column carries information related to mechanoreception; and the ventrolateral column houses neurons which communicate information regarding pain, temperature, and motor signals. In general, the sensory system ascending pathway comprises the dorsal portion of the spinal cord, while the descending pathway of the motor control system comprises the ventral aspect of the cord. Afferents of the dorsal nerve root enter the spinal cord dorsolaterally and branch in the white matter, with collaterals which terminate in the gray matter. Nerve fibers mediating pain pass through the tract of Lissauer and have branches which terminate in the most superficial regions of the dorsal horn, laminae I and II. Neurons in these laminae synapse on secondary neurons in laminae IV–VI of the dorsal horn and these secondary neurons cross the midline before ascending to the brain contralaterally in the anterolateral region of the cord. Lamina X, which is located in the gray matter region closest to the central canal, also receives sensory inputs related to pain. The neurons of the substantia gelatinosa receive information from Aδ and C fibers; Aβ afferents terminate in the deeper laminae. After injury, it is believed that Aβ afferents sprout from the deeper lamina into the dorsal horn where they make synaptic contacts with neurons.6,7 Nociceptive information is transmitted from the spinal cord to supraspinal sites, primarily in the pons, medulla and thalamus. The anterolateral ascending system has three tracts: spinothalamic, spinoreticular, and spinomesencephalic. The spinothalamic is the most prominent of the tracts. Briefly, the spinothalamic and spinoreticular tracts mediate noxious sensations, with axons terminating on neurons in the reticular formation of the medulla and pons. From there, signals are relayed to the thalamus, and then, neurons project to the somatosensory cortex. Each regional level of the spinal cord receives sensory information from specific regions of the body, known as dermatomes. Typically, nerves from approximately two spinal levels innervate any given region of the skin’s surface. These surfaces have been divided into discrete regions, providing a dermatomal map relating each region of the skin to a corresponding spinal level.8 Clinically, dermatomal maps are used to identify the origin of painful symptoms. However, nerve endings which innervate internal organs can also produce cutaneous sensation. This ‘referred pain’ sensation is experienced at sites other than its source and is due to the fact that nearly all spinal neurons that innervate internal organs also are associated with cutaneous sensation.

Nociceptive afferents are specific for sensing different noxious stimuli: thermal, mechanical, and chemical stimuli. Some nociceptors are polymodal and sense all types of stimuli. Broadly, sensory nerve fibers range in diameter from <0.05 μm to 20 μm. These fibers are either unmyelinated or myelated with thick or thin myelin sheathes enclosing them. Their conduction velocities can range from 0.5 m/s to 120 m/s, depending on their axon diameter and/or the presence of myelination. A fibers are myelinated and can evoke sharp and pricking pain sensation; they can also convey sensations of aching pain. The largest, myelinated sensory axons, Aβ, are generally classified as mechanoreceptive. Aβ fibers are primarily proprioceptive (sensing mechanical movement in joints and muscles). Their diameters are approximately 10 μm; these fibers have slower conduction velocities

Section 2: Spinal Pain

than Aδ fibers. The smallest myelinated fibers are Aγ fibers, which primarily mediate pin-prick, itching, and other mechanical sensations of pain. Unmyelinated C fibers mediate thermal sensation, in addition to mechanical pain. Stimulation of C fibers can also induce a burning sensation. C and some A fibers are the primary high-threshold noceiceptors. The A fibers exhibit greater response frequencies than C fibers and have more communications to the spinal cord. Pain results most often from direct tissue injury or from inflammation which alters the local peripheral chemical milieu. For a given insult, local nociceptors become activated; this occurs when the nerve endings of the Aδ and C fibers are stimulated. Conduction velocities of Aδ fibers are approximately 10 times those of C fibers (5–30 m/s and 0.5–2 m/s, respectively) due to the saltatory conduction mediated by their myelin sheathing. As a consequence of this difference in conduction velocity, a sharp pain is first detected in response to a stimulus, followed by a longer-lasting, dull and burning pain, which is mediated by the C fibers. Pain detection and signaling begin at the injury site where Aδ and C fibers are activated by thermal, chemical, mechanical, and/or electrical stimuli. These nociceptors can become sensitized, lowering their thresholds for firing and increasing their firing rates when stimulated.9 Further, damaged cells at the site of injury release ATP and free protons. Briefly, a complex series of reactions also occur, including altered blood flow, release of neuropeptides from the afferent fiber itself, and a generalized host of biochemical and cellular responses typical of an immune response. For painful tissue injuries, inflammation is induced in an effort to promote healing and recovery. In this process, inflammatory mediators such as prostaglandin E, serotonin, bradykinin, and histamine, among others, can alter fiber responses. These and other mediators directly activate nociceptors or can sensitize those nociceptors which are already responding to stimuli. This further induces increased neuronal activity. Specifically, bradykinin, serotonin, excitatory amino acids, and hydrogen ions are all responsible for directly activating afferents.9,10 Similarly, prostaglandins, serotonin, noradrenaline, adenosine, nitric oxide, and nerve growth factors can sensitize nociceptors. In addition to altered electrical activity, and the local synthesis and release of inflammatory mediators that induce inflammation and

edema as part of the healing process, these same immune processes that provide healing also sensitize nociceptors and recruit new nociceptors that enhance pain.11,12 In particular, cytokines are released in the periphery in association with tissue injury and inflammation. These small proteins, in turn, contribute to the local inflammatory response, while further modulating electrophysiologic responses of nerve fibers and altering nociception. Additional details regarding specific biochemical mediators of pain and their mechanisms of action throughout the pain signaling pathway (i.e. injury site and spinal cord) are provided in a later section specifically addressing biochemical mediators of pain.

TRANSMISSION In general, injury to a variety of tissues, including muscle, disc, ligament, and neural tissue, can induce many cascades and physiological signals which lead to pain transmission (Fig.4.3). During this process, neuroplasticity and subsequent CNS sensitization responses produce altered functions of chemical, electrophysiological, and pharmacological systems throughout the periphery and central systems.4,13–17 This cascade of biochemical and molecular reactions causes changes in gene transcription, post-translational modifications, and culminates with the transmission of pain.18 The interplay of these system responses involves complicated cross-system effects between injury and changes in both the peripheral and central nervous systems. The integration of multiple physiologic systems, as occurs with pain transmission (see Fig. 4.3), contributes to the overall challenges in preventing such syndromes since a given insult may initiate a host of different responses which can be established and maintained remote from the actual site of injury. Regardless, there is a generalized series of responses which occurs following a painful injury in the periphery. A chemical insult in the periphery causes direct activation of sensory neurons; voltage-gated sodium channels are integral for initiating and propagating pain signals in these sensory neurons. Two separate types of such channels have been designated as SNS and SNS-2, respectively. The SNS subtype is present on both C and some A fibers; SNS-2 channels are exclusively present on unmyelinated

Pain

Afferent fibers

Injury

Local site of injury/pathology Structural and material responses Edema

CNS Electrophysiologic signalling

Dorsal horn excitability Decreased threshold, Increased response to stimuli, Ongoing spontaneous activity

Inflammation and immune responses Neuromodulator release

Neuroimmune activation and inflammation Glial activation, Cytokine and chemokine upregulation/release, Altered synaptic transmission Algesic mediator induction and release SP, CGRP, prostaglandins, glutamate, NO

Fig. 4.3 Schematic diagram detailing the broad collection of physiologic mechanisms which initiate and contribute to pain. While the schematic suggests a simple linear cascade (from left to right) of events which lead to pain, these responses are quite dynamic in nature and involve aspects of electrophysiology, immunology, and their interplay. The degree to which these alterations occur is variable and dependent on both the nature of the injury and the type of response. Moreover, many of these individual responses affect each other (small arrows) and are themselves directly altered by confounding physiologic, anatomical, and mechanical factors. 31

Part 1: General Principles

neurons. The vanilloid receptor (VR1) is spatially co-localized with these channels. Calcium concentrations play a critical role in mediating pain in the central nervous system by controlling and regulating levels of nitric oxide synthase (NOS), prostaglandins, and changes in their gene transcription.19 An increase in calcium causes enhanced release of neurotransmitters, as well as an increase in activity of neuronal nitric oxide synthase. Because changes in intracellular calcium occur through the actions of several different channel types, it is possible to isolate the effects of calcium based on which channel opened. For example, in striatal neurons, the population of calcium that activates nNOS is derived from opening of a voltage-gated calcium channel. In addition, increases in intracellular calcium via NMDA receptor influx causes increases in arachidonic acid which can enable COX and prostaglandin production. This process sensitizes neurons of the dorsal horn by a protein kinase C pathway; this second messenger can induce neurons to release substance P and glutamate and provide nociceptive transmission. Primary afferents communicate with spinal neurons via synaptic transmission. A variety of neurotransmitters (i.e. glutamate, NMDA, substance P) modulate postsynaptic responses, with further transmission to postsynaptic spinal neurons and supraspinal sites via the ascending pathways.9 Peripheral signals of injury pain generate increased neuronal excitability in the spinal cord.17 Associated with this sensitization are a decreased activation threshold, increased response magnitude, and increased recruitment of receptive fields.4 The continuous input from nociceptive afferents can drive spinal circuits and lead to central sensitization, maintaining a chronic pain state.15 These neuroplastic changes are accompanied by other electrophysiological manifestations that cause neurons to fire with increased frequency and even to fire spontaneously.16 Spinal processing is further directly altered by descending inhibitory and facilitory pathways that can provide additional modulation of spinal interneurons.20 Ultimately, persistent pain results from the sensitization of the central nervous system. While the exact mechanism by which the spinal cord reaches a ‘hyperexcitable’ state of sensitization is not fully known, many hypotheses have emerged. Here, only highlights of these theories are provided as an overview. More extensive and detailed discussions can be found elsewhere in the literature.17,21–23 Central hyperexcitability is characterized by a ‘wind-up’ response of repetitive C fiber stimulation, expanding receptive field areas, and spinal neurons taking on properties of wide dynamic-range neurons.24 Low threshold Aβ afferents, which normally do not transmit pain, begin to signal spontaneous and movement-induced pain.22 Aβ fibers stimulate postsynaptic neurons to transmit pain, where these Aβ fibers previously had no effect. This plasticity of neuronal function in the spinal cord contributes to central sensitization.

BIOCHEMICAL MEDIATORS OF PAIN Many chemical mediators are involved in the transduction and transmission of pain, including local sensory terminals, synaptic transmitters, afferent sensitizers in the periphery, neuronal activators and modulators, and mediators of spinal cord signaling. Many of these mediators are endogenous; some are inducible. In addition, many of these chemicals are directly involved in pain, while some are primarily inflammatory with secondary actions of nociception. Their properties and interactions are eloquently detailed in the previous chapter.4 A brief synopsis of the primary mediators affecting nociception is provided to create context for understanding the complexities of pain signaling. Nitric oxide (NO) is a pleiotropic pronociceptive messenger, with both intracellular and extracellular mechanisms of action. It can also serve directly as a neurotransmitter. NO is formed when L-arginine is catabolized to L-citrulline, by nitric oxide synthase (NOS). NOS 32

is constitutively expressed by both neurons and endothelial cells. Of note with regard to pain signaling, neuronal NOS (nNOS) is particularly potent due to its activity being enhanced in the presence of intracellular calcium (see above). While the main source of NO in the CNS is through the activity of neurons in pathological states such as inflammation and/or pain, microglia and inflammation can also produce NO. While nitric oxide acts primarily at the site of its synthesis, it can also serve as a neurotransmitter, having direct influence on transmission of painful stimuli. Dorsal horn neurons can respond to NO signaling in pain, directly initiating phosphorylation of membrane proteins and changes in gene transcription within these neurons. In the dorsal horn, NO can feed back to the presynaptic terminals of primary afferents where it promotes the release of glutamate and substance P. This action accentuates nociceptive signaling. As well, NO can stimulate glial cells to produce prostaglandins and cytokines, which leads to nociception. Bradykinin is a hormone intimately involved in inflammation and vascular responses that also contributes to pain signaling. This protein works through a series of transmembrane G protein-coupled receptors: bradykinin B1 is implicated in chronic pain and bradykinin B2 is involved in acute inflammation and pain.25 Both receptors are expressed on primary sensory neurons where they can directly participate in the primary effects of nociception. Bradykinin sensitizes nociceptors, which produces hyperalgesia. While the B2 receptor is constitutively expressed, the B1 receptor is induced in tissue that is damaged by either infection, disease, or injury. For example, as early as 48 hours after a peripheral nerve injury, B2 receptor mRNA increases, while B1 expression does not reach similar levels until 14 days later.25 B2 receptor kinetics are comparatively fast relative to B1, including the processes of ligand binding, release, and internalization. Through the B2 receptor, bradykinin causes the release of substance P and calcitonin gene-related peptide from primary sensory neurons. This release is further increased in the presence of prostaglandins, which are upregulated at the site of insult. Prostanoids are a class of pronociceptive molecules such as prostaglandin E2 that are produced when arachidonic acid is metabolized by the COX enzyme, which exists in isoforms COX-1 and COX-2. Specifically, the COX-2 isoform is dramatically upregulated in the spinal cord after injury in the periphery. The release of prostaglandin E2 which occurs in response to the upregulation of that enzyme causes a shift in the peripheral terminal of the nociceptor, lowering its threshold and increasing its excitability. There is a host of other inflammatory-related mediators which have direct and indirect effects on pain and nociception. Serotonin is released from platelets downstream from mast cell degranulation, as occurs during inflammation. Serotonin directly modulates pain by activating primary afferents and also enhances sensitivity of sensory responses to bradykinin. Leukotriene B4 is a neutrophil attractant that can sensitize afferents. Substance P is a pronociceptive neurotransmitter, which is released in the periphery following afferent activation. It mediates inflammation by causing vasodilation and the release of prostaglandin E2 and cytokines. These actions impact local inflammation, directly modulating nociception. Substance P can cause a release of calcium from intracellular stores and lead to NO production, neuronal excitability, and long-term sensitization.26,19 Substance P has been shown to have a role in pain in the central nervous system. Administration of antagonists to the substance P receptor, neurokinin-1 (NK-1), can induce antinociception in the central nervous system following chronic painful mechanical nerve constriction.28 Calcitonin gene-related peptide (CGRP), a neuropeptide often colocalized with substance P in the spinal cord, contributes to sensiti-

Section 2: Spinal Pain

zation. It regulates nociceptive responses by promoting the release of substance P and glutamate from primary afferents, while impeding the metabolism of substance P.28,29 CGRP alone causes a slow membrane depolarization in sensory neurons and an influx of calcium through voltage-gated calcium channels. These actions enhance sensitization and promote NK-1 and NMDA activation.19 Antibodies to substance P and CGRP can attenuate pain symptoms in inflammatory models of carageenan-induced hyperalgesia and painful nerve injury;26,30 these studies strongly implicate both such neuropeptides in pain transmission. Excitatory amino acids, such as glutamate, have potent roles in pain, both at the site of injury and in the central nervous system. Indeed, both non-neuronal and neuronal cells in the periphery produce glutamate. Both of these sources act on primary afferents by activating them when bound to any of the NMDA, kainite, AMPA, or metabotropic glutamate receptors.4 Certainly, this positive feedback mechanism of nociceptor excitation leads to peripheral sensitization and to altered afferent signaling into the spinal cord. Glutamate receptors are expressed in dorsal root ganglion cells,30 suggesting its direct involvement in afferent signaling to the cord. As the NMDA glutamate receptor has a key role in regulating synaptic efficacy, there is also a direct role for this receptor in the spinal plasticity changes associated with central sensitization and persistent pain. In a normal resting state, NMDA receptors are blocked by the presence of a magnesium ion, and glutamate is free to bind only to low-affinity AMPA receptors. For a neuronal depolarization, the magnesium ion blocking the NMDA receptor becomes liberated, which allows glutamate to bind in its place. This binding activates a complicated cascade, allowing an influx of a host of ions, including calcium. These events, in turn, activate a kinase cascade. Each NMDA receptor is composed of two subunits: the NR1 subunit and the NR2 subunit. The NR2B subunit has been specifically implicated in pain transmission via research findings from a variety of knockout studies,31 and its ability to be more readily phosphorylated than the other NR subunits. NMDA receptors are found both post- and presynaptically. Presynaptic NMDA receptor activation causes the release of substance P from small-diameter primary afferent fibers. The opening of the NMDA receptor also increases the synaptic strength of neurons in the dorsal horn by activating the kinase cascade. These events, which can directly potentiate neuronal fiber sensitization, produce the ‘wind-up’ responses described for dorsal horn neurons.17,24,32 However, despite the known involvement of the NMDA receptor in pain signaling, little clinical success has been demonstrated for NMDA antagonists in ameliorating pain, due to profound side effects such as memory or coordination deficits. Cytokines can directly and indirectly regulate biochemical cascades leading to the transmission and modulation of pain. Broadly, cytokines include both proinflammatory and antiinflammatory proteins, both of which are upregulated in painful injuries.33–37 In particular, in models of neural injury either distal (peripheral injury) or proximal (nerve root injury) to the DRG, spinal IL-1β, IL-6, IL-10, and TNF-mRNA have all been observed to be significantly elevated for persistent pain.38 Not all of these factors are proinflammatory. For example, IL-10 has been shown to suppress NO production in cultured astrocytes and also suppress proliferation in macrophages,39 which in turn has antiinflammatory effects. The presence of cytokines can further stimulate their own production, as demonstrated by IL-1 stimulating its own production.36 Cytokines mediate cellular processes through the production or suppression of nitric oxide. NO has an immunoregulatory role in the central nervous system. Its production leads directly to hyperalgesia, as previously mentioned. Cytokines regulate NO by interfering with the production of NOS. Astrocytes produce each of the two main forms of NOS, inducible

(iNOS) and constitutive (cNOS), whereas microglia are only responsible for inducible NOS.39 TNF-α and IL-1β control the stimulation of iNOS in both astrocytes and glia, therefore inducing the production of NO from those cell types. Alternatively, TGF-β suppresses NO production in both astrocytes and microglia whereas IL-10 only affects NO production in astrocytes.

CNS NEUROIMMUNE RESPONSES IN PAIN While central sensitization contributes to nociceptive mechanisms of persistent pain in the CNS, recent research has demonstrated the potent role of spinal neuroimmune responses in the generation of chronic pain.40 CNS immune changes have been demonstrated to occur in the setting of persistent pain.33,36–38,41,42 Among the disorders in which this phenomena has been observed are radiculopathy, neuropathy, diabetes, and HIV. These immunological alterations provide evidence that implicates a role for centrally produced proinflammatory cytokines, glial activation, and leukocyte trafficking in rodent pain models of lumbar radiculopathy.38,43–46 From this body of work, a cascade of events in the CNS has been proposed following injury.14,40 Glial cells and neurons become activated and can produce and release cytokines, which in turn can lead to increased activation of these cell types. As well, they lead to increased release of pain mediators.33,34,36 Glial and/or neuronal proinflammatory cytokines can sensitize peripheral nociceptive fields47 and cells in the dorsal root ganglia.48 Events that induce behavioral hypersensitivity also activate central and peripheral immune cells that mediate chronic pain.25,34,36,49,50 Cytokines and growth factors have been strongly implicated in the generation of pathological pain states throughout the nervous system. Specifically, proinflammatory cytokines, such as IL-1, IL-6, and TNF, are upregulated both locally and in the spinal cord.32,33,35 Immune activation with cytokine production may indirectly induce the expression of many pain mediators such as glutamate, nitric oxide, and prostaglandins in the CNS. In conjunction with this neuroimmune activation, neuroinflammatory actions, in which immune cells migrate from the periphery into the CNS in association with pain, occur.14,40,45 Such infiltration may lead to further nociceptive changes in the CNS and potentially to central sensitization. Infiltrating immune cells alter and compound neuronal activation, and promote algesic mediator release, further perpetuating the maintained excitability and sensitization in the CNS, leading to pain and behavioral sensitivity in the case of in vivo models. The spinal immune response of nociception has many facets, forming a complicated cascade of events leading to pain (see Fig. 4.3). It is important to recognize, though, that while quite potent, these immune responses are only one aspect of nociception and the effects of these cellular and chemical sequelae can themselves directly modulate many other potent pathways of pain signaling in the CNS.

INJURY AND BIOMECHANICAL FACTORS MODULATING NOCICEPTION AND PAIN PERCEPTION Electrophysiologic and neuroimmune responses of the CNS likely work together to affect pain for spinal syndromes, with local biomechanics at the site of an injury modulating both such responses. Low back pain is an ideal syndrome to use as an illustrative example for discussing these mechanisms and cellular response cascades of pain. In this discussion, injury conditions are presented as examples of how mechanical loading modulates nociception in low back pain, with particular emphasis on nerve root injury (i.e. radiculopathy). In addition, 33

Part 1: General Principles

throughout the following text comments will be made where applicable to other spinal regions such as the cervical spine. In vivo studies of animal models of pain report altered electrophysiologic and cellular function for graded cauda equina compression. Applied compression increases endoneurial pressure locally in the rat sciatic nerve and DRG in proportion to the degree of mechanical loading.51,52 It has been shown that edema patterns and intensity are modulated by the nature of the mechanical insult.52–55 Loading to the nerve root can produce changes in electrical impulse propagation and conduction velocity56–58 and repetitive neuronal firing in the dorsal horn of the spinal cord,57,59 which are physiologic correlates leading to spinal sensitization and, consequently, persistent pain. This collective body of research suggests an electrophysiological and neuronal mechanism of spinal cord plasticity and central sensitization for mechanical injuries. It is only inferential for understanding the production and maintenance of pain symptoms. Imaging techniques have been used in a rodent model of painful lumbar radiculopathy to quantify nerve root tissue deformation for an applied root ligation. In that study, Winkelstein et al. examined the injury parameter of tissue deformation in the context of pain (behavioral hypersensitivity).60,61 Local injury mechanics were found to modulate pain behaviors. There was a significant positive correlation in that pain model between behavioral sensitivity and the amount of tissue compression.60 This observation led to a mechanical compressive deformation threshold for pain behaviors and hypersensitivity that were defined based on the amount of nerve root compression.27 More recent work examining cervical nerve root compression magnitude and behavioral sensitivity in the forepaw suggests that a force-based threshold may be more sensitive than deformation for predicting pain symptoms. It has been suggested that a load below 10 g may be sufficient to elicit persistent pain for cervical dorsal nerve root compression.49 Interestingly, while work in the cervical spine suggests that tissue loading may more directly influence pain symptoms, neural tissue is a very soft material and, as such, can undergo extreme tissue deformations before establishing any perceivable load. Continued research is needed to fully define those exact mechanisms through which direct mechanical loading/deformation of the cervical root can be transduced to produce persistent pain. Nonetheless, recent findings of evidence of neuronal degeneration local to the insult (Fig. 4.4) suggest that local changes in the region of injury are robust and occur as early as 1 day after direct insult. Together, mechanical parameters defining painful injuries provide added utility for clinicians in diagnosing painful injuries, directly linking the injury event to the likelihood of pain symptoms. Moreover, in the future, it will hopefully provide insight into predicting clinical outcomes for this class of injuries. While defining the relationship between spinal tissue insult and pain is necessary for understanding the clinical context of painful pathologies, understanding the specific and relevant nociceptive responses is crucial for characterizing the central mechanisms of persistent spine pain. Using RNase Protection Assays to detect spinal mRNA of a panel of cytokines (TNF-α, IL-1αβ, IL-6, IL-10) in lumbar radiculopathy, a statistically significant correlation was found between mRNA levels at postoperative day 7 and the degree of tissue deformation for lumbar root compression.60 This observation suggests a modulatory effect of injury magnitude on one aspect of spinal nociception. IL-1β has been reported to depend on nerve root compression intensity.44 This observation suggests preservation of these changes at both the message and protein level spinal cytokines involved in chronic low back pain. In comparative models of cervical nerve root injury created by either compression or transection, spinal IL-6 protein at day 1 following radicular injury was elevated, implying a potential relationship to hypersensitivity on the day of assay.35 While continued research into these and other cytokine responses is needed for understanding cervi34

A

B

Fig. 4.4 Fluoro jade-B staining of nerve root and DRG for control (A) and injured (B) conditions demonstrating the lack of degeneration in the control sample where there is no fluorescence. In contrast, the image on the right is a DRG 1 day following a painful compression to the root. The noticeable dots in the DRG indicate degenerating cells and may suggest a mechanism of pain symptoms in this model.

cal nerve root injuries and pain mechanisms, findings suggest similar cytokine responses may be evident throughout the spine (i.e. lumbar versus cervical injuries). Spinal microglial activation has been demonstrated to be more intense for greater nerve root deformation at injury in lumbar injuries,44,62 which is consistent with the graded behavioral responses and spinal cytokine expression according to injury severity.44,60,61 Interestingly, in these same studies, astrocytic activation did not follow injury magnitude, suggesting that biomechanics at injury in lumbar radiculopathy models may differentially modulate some neuroimmune responses and not others.62 Recent work from the authors’ laboratory has examined these same spinal glial responses in two different cervical spine injuries.49,50 In these studies of nerve root compression and facet joint tension different astrocytic responses were observed. In the nerve root compression model spinal astrocytic expression was elevated compared to sham and followed the behavioral hypersensitivity patterns.49 Astrocytic activation did not show a dependence on mechanical force magnitude. In our facet-mediated

Section 2: Spinal Pain

SUMMARY It is recognized that the pathologies presented are by no means the only chronically painful syndromes of the spine. As such, it should be noted that many of the theories described above may assist with developing a more broad understanding in the context of pain in the spine. While many factors modulate electrical signaling patterns (amplitude, frequency) and local tissue changes (edema, pressure), and the neuroimmune cascade for painful radiculopathy, their effects for other painful syndromes may be similar. Continued integration of

Dorsal

Dorsal root

Increased allodynia (sensitivity) = “more pain” 10 9 Facet joint injury Facet sham 10g root injury Root sham

8 # of paw withdrawals

painful injury model spinal astrocytic activation did demonstrate a significant correlation with injury magnitude and behavioral sensitivity.50 This finding may suggest that different spinal immune cascades exist for mechanical injuries to different tissue types. In a study directly comparing behavioral hypersensitivity produced for these nerve root compressions and facet-mediated injuries, no differences were observed (Fig. 4.5). Both insults produced symptoms immediately that were sustained for almost 5 weeks depending on the insult. Moreover, within the first 2 weeks following injury, there was no difference in symptom intensity between the two scenarios. However, for this pilot study, the joint-mediated pain appeared to be sustained for a longer duration than the neural tissue injury. Together with the CNS glial findings for these two models of neck pain, these behavioral outcomes suggest that pain symptoms (perception) may be mediated differently depending on the source of the insult or signaling. This comparative work from the authors’ lab suggests that for injuries in the cervical spine direct damage to neural tissue may be perceived the same as for a nondestructive ligament loading scenario.63 These observations and suppositions highlight the need for continued integrative research to identify common and different physiologic mechanisms for injuries within the musculoskeletal system.

7 6 5 4 3 2 1 0 10

0

20 Post-operative time (days)

30

40

Fig. 4.5 Mechanical allodynia (behavioral sensitivity) produced in the ipsilateral forepaw for cervical radicular (10 g root) and facet distraction (facet joint) injuries. Both injuries produce immediate increases in allodynia compared to sham procedures. The increased sensitivity (pain) is sustained for almost 3 weeks and even longer for the facet injury.

multidisciplinary approaches will help define nociceptive responses in these and other spinal disorders. In the typical response of an acutely painful episode for spinal conditions, the balance of injury, repair, and healing is achieved and the cascade of electrophysiologic and chemical events resolves following inflammation and injury. However, for persistent pain, the local, spinal, and even supraspinal, responses are undoubtedly altered from that described above (Fig. 4.6). Based on the discussion presented here regarding persistent pain, a comprehensive picture is emerging for spinal injuries and CNS responses of nociception: spinal cytokine

Injury or insult

Dorsal root ganglion (DRG) Spinal nerve

Ventral root Ventral Local root responses

Spinal responses Neuropeptide expression Altered electrophysiology Immune changes – glial cell activation – cytokine release Central sensitization

Persistent pain?

DRG responses

Axonal injury Altered electrophysiology Neuronal degeneration Myelin disruption/breakdown Altered fiber caliber Local glia responses – debris removal – cytokine release

Neuronal degeneration ↑ membrane permeability Altered Na+ channels Neuropeptide expression Local glia plasticity −growth factor release −neuropeptide release −cytokine release

Acute pain?

Fig. 4.6 Nociceptive responses are complicated and involve a host of changes both locally and in the central nervous system. Some responses are self-regulating and can promote healing processes which produce resolving pain, while other changes occur both at the site of injury and in the spinal cord and CNS and can be sustained, leading to persistent pain symptoms.

35

Part 1: General Principles

upregulation, microglial and astrocytic activation, altered neuronal–glial interactions, cellular adhesion molecule upregulation, and immune cell infiltration into the spinal cord.14,36,40,46,64 These aspects of neuroimmune activation induce the expression and release of pain mediators (substance P, glutamate, nitric oxide) and also lead to neuronal hypersensitivity. Many of these may be locally and centrally mediated (see Fig. 4.6). In this context, it is important to consider novel methods for preventing and treating painful injuries. Clinical emphasis has largely been focused on local interventions at the injury site. However, the previous discussion points to the spinal cord physiology as having equal, if not stronger, contribution for maintenance of pain (see Fig. 4.6). Continued understanding of spinal mechanisms of central sensitization can hopefully provide valuable contributions to this understanding. It was the intent of this chapter to highlight existing theories of persistent pain and illuminate interesting new work within the study of pain, highlighting the complications and intricacies of its nature. The extremely complicated mechanisms of pain detection and signaling and their extensive integration with each other point to an equally complicated clinical presentation.

16. Waxman S, Dib-Hajj S, Cummins T, et al. Sodium channels and pain. Proc Nat Acad Sci USA 1999; 96:7635–7639.

Acknowledgments

26. Ma W, Eisenach J. Intraplantar injection of a cyclooxygenase inhibitor ketorolac reduces immunoreactivities of substance P, calcitonin gene-related peptide, and dynorphin in the dorsal horn of rats with nerve injury or inflammation. Neuroscience 2003; 121:681–690.

The authors gratefully acknowledge the following for financial support: National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR47564), the Whitaker Foundation, and the Catharine Sharpe Foundation.

References 1. Frymoyer J, Cats-Baril W. An overview of the incidences and costs of low back pain. Orthoped Clin N Am 1991; 22:263–271. 2. Frymoyer J, Durett C. The economics of spinal disorders. In: Frymoyer JW, ed. The adult spine: principles and practice. Philadelphia: Lippincott-Raven; 1997. 3. Kivioja J, Rinaldi L, Ozenci V, et al. Chemokines and their receptors in whiplash injury: elevated RANTES and CCR-5. J Clin Immunol 2001; 21:272–277. 4. Wall P, Melzack R. Textbook of pain. 3rd Edn. London: Churchill Livingstone; 1994. 5. Kandel ER, Schwartz JH, Jessell TM. Principles of neural science. 3rd Edn. New York: Elsevier; 1991. 6. Furue H, Katafuchi T, Yoshimura M. Sensory processing and functional reorganization of sensory transmission under pathological conditions in the spinal dorsal horn. Neurosci Res 2004; 48:361–368.

18. Costigan M, Woolf C. Pain: molecular mechanisms. J Pain 2000; 1:35–44. 19. Millan M. The induction of pain: An integrative review. Progress Neurobiol 1999; 57:1–164. 20. Vanderah TW, Ossipov MH, Lai J, et al. Mechanisms of opioid-induced pain and antinociceptive tolerance: descending facilitation and spinal dynorphin. Pain 2001; 92:5–9. 21. Coderre TJ, Katz J, Vaccarino A, et al. Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence. Pain 1993; 52: 259–285. 22. Devor M. Pain arising from the nerve root and the dorsal root ganglion. In: Weinstein J, Gordon S, eds. Low back pain: a scientific and clinical overview. Rosemont, IL: AAOS; 1986:187–208. 23. Dubner R, Basbaum AI. Spinal dorsal horn plasticity following tissue or nerve injury. In: Wall PD, Melzak R, eds. Textbook of pain. Edinburgh: Churchill-Livingstone; 1994:225–241. 24. Cook AJ, Woolf CJ, Wall PD, et al. Dynamic receptive field plasticity in rat spinal cord dorsal horn following C-primary afferent input. Nature 1987; 325:151–153. 25. Couture R, Harrisson M, Vianna RM, et al. Kinin receptors in pain and inflammation. Eur J Pharmacol 2001; 429:161–176.

27. Winkelstein BA, DeLeo JA. Mechanical thresholds for initiation and persistence of pain following nerve root injury: Mechanical and chemical contributions at injury. J Biomech Engineer 2004; 126:258–263. 28. Meert T, Vissers K, Geenan F, et al. Functional role of exogenous administration of substance P in chronic constriction injury model of neuropathic pain in gerbils. Pharmacol Biochem Behav 2003; 76(1):17–25. 29. Allen B, Li J, Menning P, et al. Primary afferent fibers that contribute to increased substance P receptor internalization in the spinal cord after injury. J Neurophysiol 1999; 81(3):1379–1390. 30. Satoh M, Kuraishi Y, Kawamura M. Effects of intrathecal antibodies to substance P, calcitonin gene-related peptide and galanin on repeated cold stress-induced hyperalgesia: comparison with carrageenan-induced hyperalgesia. Pain 1992; 49 (2):273–278. 31. Bursztajn S, Rutkowski M, Deleo J. The role of the N-methyl-D-aspartate receptor NR1 subunit in peripheral nerve injury-induced mechanical allodynia, glial activation and chemokine expression in the mouse. Neuroscience 2004; 125:269–275. 32. Woolf C, Safieh-Garabedian B, Ma Q, et al. Nerve growth factor contributes to the generation of inflammatory sensory hypersensitivity. Neuroscience 1994; 62: 277–331.

7. Kohno T, Moore K, Baba H, et al. Peripheral nerve injury alters excitatory synaptic transmission in lamina II of the rat dorsal horn. J Physiol 2003; 548:131–138.

33. DeLeo J, Colburn R. The role of cytokines in nociception and chronic pain. In: Weinstein J, Gordon S, eds. Low back pain: a scientific and clinical overview. Rosemont, IL: AAOS; 1986:163–185.

8. Slipman C, Plastaras C, Palmitier R, et al. Symptom provocation of fluoroscopically guided cervical nerve root stimulation. Are dynatomal maps identical to dermatomal maps? Spine 1998; 23:2235–2242.

34. DeLeo J, Colburn R, Nichols M, et al. Interleukin (IL)-6 mediated hyperalgesia/ allodynia and increased spinal IL-6 in two distinct mononeuropathy models in the rat. J Interferon Cytokine Res 1996; 16:695–700.

9. Cavanaugh JM. Neurophysiology and neuroanatomy of neck pain. In: Yoganandan N, Pintar FA, eds. Frontiers in whiplash trauma: clinical and biomechanical. Amsterdam: IOS Press, 2000; 79–96.

35. Hubbard R, Rothman S, Winkelstein B. Mechanisms of persistent neck pain following nerve root compression injury: understanding behavioral hypersensitivity in the context of spinal cytokine responses and tissue biomechanics. North American Spine Society 19th Annual Meeting, #P49, Chicago, IL, October, 2004.

10. Kawakami M, Weinstein JN. Associated neurogenic and nonneurogenic pain mediators that probably are activated and responsible for nociceptive input. In: Weinstein J, Gordon S, eds. Low back pain: a scientific and clinical overview. Rosemont, IL: AAOS; 1986:265–273.

36. Watkins L, Maier S, Goehler L. Immune activation: the role of pro-inflammatory cytokines in inflammation, illness responses, and pathological pain states. Pain 1995; 63:289–302.

11. Dray A, Perkins M. Bradykinin and inflammatory pain. Trends Neurosci 1993; 16(3):99–104.

37. Watkins L, Wiertelak E, Goehler L, et al. Characterization of cytokine-induced hyperalgesia. Brain Res 1994; 654:15–26.

12. Dubner R, Hargreaves KM. The neurobiology of pain and its modulation. Clin J Pain 1989; S2:S1–S6.

38. Winkelstein B, Rutkowski M, Sweitzer S, et al. Nerve injury proximal or distal to the DRG induces florid spinal neuroimmune activation related to enhanced behavioral sensitivity. J Comparative Neurol 2001; 439:127–139.

13. Black J, Langworthy K, Hinson A, et al. NGF has opposing effects on Na+ channel III and SNS gene expression in spinal sensory neurons. Neuroreport 1997; 8:2331– 2335.

36

17. Woolf CJ. Evidence for a central component of post-injury pain hypersensitivity. Nature 1983; 306:686–688.

39. Xiao BG, Link H. Immune regulation within the central nervous system. J Neurol Sci 1998; 157:1–12.

14. DeLeo J, Winkelstein B. Physiology of chronic spinal pain syndromes: From animal models to biomechanics. Spine 2002; 27(22):2526–2537.

40. DeLeo JA, Yezierski RP. The role of neuroinflammation and neuroimmune activation in persistent pain. Pain 2001; 91:1–6.

15. Devor M. Neuropathic pain and injured nerve: peripheral mechanisms. Br Med Bull 1991; 47:619–630.

41. Rutkowski M, Pahl J, Sweitzer S, et al. Limited role of macrophages in generation of nerve injury-induced mechanical allodynia. Physiol Behav 2000; 71:225–235.

Section 2: Spinal Pain 42. Sweitzer S, Martin D, DeLeo J. IL-1ra and sTNFr reduces mechanical allodynia and spinal cytokine expression in a model of neuropathic pain. Neuroscience 2001; 103:529–539. 43. Colburn R, Rickman A, DeLeo J. The effect of site and type of nerve injury on spinal glial activation and neuropathic pain behavior. Exper Neurol 1999; 157:289–304. 44. Hashizume H, DeLeo J, Colburn R, et al. Spinal glial activation and cytokine expression following lumbar root injury in the rat. Spine 2000; 25:1206–1217. 45. Rutkowski MD, Winkelstein BA, Hickey WF, et al. Lumbar nerve root injury induces CNS neuroimmune activation and neuroinflammation in the rat: Relationship to painful radiculopathy. Spine 2002; 27(15):1604–1613. 46. Sweitzer S, Arruda J, DeLeo J. The cytokine challenge: methods for the detection of central cytokines in rodent models of persistent pain. In: Kruger L, ed. Methods in pain research. Boca Raton: CRC Press; 2001;109–132.

with special reference to differences in effects between rapid and slow onset of compression. Spine 1989; 14:569–573. 55. Pedowitz R, Garfin S, Massie J, et al. Effects of magnitude and duration of compression on spinal nerve root conduction. Spine 1992; 17:194–199. 56. Cornefjord M, Sato K, Olmarker K, et al. A model for chronic nerve root compression studies. Presentation of a porcine model for controlled slow-onset compression with analyses of anatomic aspects, compression onset rate, and morphologic and neurophysiologic effects. Spine 1997; 22:946–957. 57. Hanai F, Matsui N, Hongo N. Changes in responses of wide dynamic range neurons in the spinal dorsal horn after dorsal root or dorsal root ganglion compression. Spine 1996; 21:1408–1415.

47. Junger H, Sorkin LS. Nociceptive and inflammatory effects of subcutaneous TNF alpha. Pain 2000; 85(1–2):145–151.

58. Skouen J, Brisby H, Otami K, et al. Protein markers in cerebrospinal fluid experimental nerve root injury. A study of slow-onset chronic compression effects or the biochemical effects of nucleus pulposus on sacral nerve roots. Spine 1999; 24:2195–2200.

48. Ozaktay AC, Cavanaugh JM, Asik I, et al. Dorsal root sensitivity to interleukin-1 beta, interleukin-6 and tumor necrosis factor in rats. Eur Spine J 2002; 11(5):467–475.

59. Yoshizawa H, Kobayashi S, Kubota K. Effects of compression on intraradicular blood flow in dogs. Spine 1989; 14:1220–1225.

49. Hubbard RD, Winkelstein BA. Transient cervical nerve root compression in the rat induces bilateral forepaw allodynia and spinal glial activation: mechanical factors in painful neck injuries. Spine 2005; 30(17):1924–1932.

60. Winkelstein B, Rutkowski M, Weinstein J, et al. Quantification of neural tissue injury in a rat radiculopathy model: comparison of local deformation, behavioral outcomes, and spinal cytokine mRNA for two surgeons. J Neurosci Methods 2001; 111:49–57.

50. Lee K, Davis M, Mejilla R, et al. In vivo cervical facet capsule distraction: mechanical implications for whiplash and neck pain. Proceedings of 48th Stapp Car Crash Conference, Paper #2004-22-0016, 48:373-393, 2004.

61. Winkelstein B, Weinstein J, DeLeo J. Local biomechanical factors in lumbar radiculopathy: An in vivo model approach. Spine 2001; 27:27–33.

51. Lundborg G, Myers R, Powell H. Nerve compression injury and increased endoneurial fluid pressure: a ‘miniature compartment syndrome.’ J Neurol Neurosurg Psychiatry 1983; 46:1119–1124.

62. Winkelstein BA, DeLeo JA. Nerve root tissue injury severity differentially modulates spinal glial activation in a rat lumbar radiculopathy model: Considerations for persistent pain. Brain Res 2002; 956(2):294–301.

52. Rydevik B, Myers R, Powell H. Pressure increase in the dorsal root ganglion following mechanical compression. Closed compartment syndrome in nerve roots. Spine 1989; 14:574–576.

63. Lee K, Thinnes J, Gokhin D, et al. A novel rodent neck pain model of facet-mediated behavioral hypersensitivity: implications for persistent pain and whiplash injury. J Neurosci Methods 2004; 137:151–159.

53. Olmarker K, Holm S, Rydevik B. Importance of compression onset rate for the degree of impairment of impulse propagation in experimental compression injury of the porcine cauda equina. Spine 1990; 15:416–419.

64. Sweitzer S, White KA, Dutta C, et al. The differential role of spinal MHC class II and cellular adhesion molecules in peripheral inflammatory versus neuropathic pain in rodents. J Neuroimmunol 2002; 125(1-2):82–93.

54. Olmarker K, Rydevik B, Holm S. Edema formation in spinal nerve roots induced by experimental, graded compression. An experimental study on the pig cauda equina

37

PART 1

GENERAL PRINCIPLES

Section 2

Spinal Pain

CHAPTER

Central Influences on Pain

5

Michael H. Moskowitz

INTRODUCTION Understanding central influences on pain is crucial if acute pain is to be prevented from becoming chronic and chronic pain is to be brought under effective control. Central influences on pain exemplify neuroplasticity and, as such, help distinguish between pain as a disease and pain as a symptom. One cannot fully grasp the concepts of central pain influences without detailing the contribution of peripheral pain processes to their development and perpetuation. While they are most often tied in to structural changes in the peripheral (PNS) or central nervous system (CNS), central changes that occur in chronic pain establish it as a separate, but connected, process to the structural injury. Despite our focus in pain research on spinal cord action in development of neuroplasticity, brain nuclei responsible for the manufacture and axonal transport of neurotransmitters and membrane placement of neuroreceptors place the brain in the command position for regulating central pain. Appreciation of the brain’s adaptation to afferent signals altered at the dorsal horn and the synergism of brain-based, top-down modulation of these spinal cord events represents the next frontier of therapeutic targets, especially as our understanding of the genome’s effect upon the proteome matures. Finally, it is through the common pathways and common neuroplastic events of centrally maintained pain and major affective disorder that the link between chronic pain and chronic affective disorder can be established at a molecular level.

CENTRAL INFLUENCES ON PAIN Perhaps the best place to begin is to look at what is meant by central influences on pain. Although the definition in the literature has ranged from specific damage to brain or spinal cord to intracellular processes that occur in the CNS, for the purpose of this chapter central influences involve the reaction of the CNS to acute and chronic pain of any origin. While central influences on acute pain must be understood to explain the maladaptive processes involved in chronicity, this chapter will focus on the type of reorganization that occurs in the CNS at the anatomic, neurophysiologic, intracellular, and molecular levels, as influenced by chronic activation of the nociceptive system. Research into the anatomy of the spinal cord and the brain over the last several decades has revealed an increasing awareness of the complexity of the perception of pain as an unpleasant physical and emotional experience. Not only are we progressively more aware of the built-in areas of pain processing, but also of the interconnections of the circuits that run to and from these regions. The result is that we have a much better idea of how the brain and spinal cord work together to control nociception and how this process breaks down in chronic pain disorders. We also have a clearer understanding of where to target treatment and why effective treatment of peripheral stimulus is not always successful in resolving pain problems. Increasingly, our therapeutic targets of long-term treatment of chronic pain are directed toward the intercellular mechanisms that occur at the inter-

face of neurons and their synapses. This has been a trend in neurology and psychiatry, as well as in pain research. As a result of this research we have an ever more precise grasp of neurotransmitters, neuroreceptors, positive and negative feedback loops, excitatory and inhibitory influences, and modulation of these processes by second messengers and comodulating neurotransmitters. More recent discoveries about neuroglia, microglia, and the specialized cells of the blood–brain barrier focus upon far more complex processes than passive support and protection. More sophisticated understanding of downstream events addresses intracellular processes and how the genome is influenced to create changes in the proteome. This provides us with the basic building blocks of neuroplasticity and a refocus of our traditional understanding of pharmaceutical targets and effects. This new understanding of intracellular mechanisms also allows for development of specific therapeutics aimed at influencing the genome for more pinpoint treatment, opening up a new potential for managing neuroplastic events in specific anatomical areas and precise synaptic targets. Ultimately, if we can change the ways that specific cells in specific areas turn on and turn off production of neurotransmitters, neuroreceptors, nerve growth factors, enzymes, and neurohormones, we will be able to realize the dream of getting the runaway process of chronic pain back into its normal physiologic harness.

NEUROPLASTICITY AND THE DISEASE OF PAIN It is important for physician and patient alike to distinguish pain as a symptom from pain as a disease. The symptom of pain is an essential fact of life and helps guide us to immobilize an injured part of the body, seek help, and direct care. Pain is one of the most common symptoms aiding physicians in diagnosis and treatment. It is also disturbing enough for most people who have it to require some action, usually a cessation of activity. Successful treatment aimed at the source of the pain often eliminates it. In fact, the body has physiologic mechanisms designed to diminish pain quickly after most tissue injuries. The disease of pain, however, is quite different. It is the underlying condition and the extensive pathology of that condition distinguishes the disease of pain from the symptom of pain. Although there are definitions of pain becoming a chronic problem based upon duration of injury, nerve damage, or frequency of flare-ups, the best definition views the disease process from the standpoints of phenomenology and neurophysiology. Phenomenologically, the disease of pain represents a concatenation of biological, psychological, and social events that disrupt the life of the patient. Cascades that occur in each area result in the experience of chronic pain. When people experience pain, there is an expectation that it will eventually stop as the body heals. If this fails to occur there are consequences that occur throughout the individual’s life. Mersky and Bogduk define pain in the following manner: 39

Part 1: General Principles

‘Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.’1 The reason that this definition stands the test of time is that it succinctly reflects the ambiguity of pain and unifies the physical and the emotional, actual injury and potential damage, expectations and experience, while highlighting the unpleasantness of pain. What it fails to take into account is the distinction of the symptom of acute pain and the disease of chronic pain. Donald Price describes acute pain as a two-staged event of desire to avoid harm and expectation that harm will be avoided. Price points out that when a person is injured, immediate concern about tissue damage is replaced with anxiety about healing and ‘threat to the self.’2 He describes fear and anger as emotional aspects of acute pain and despair, frustration, hopelessness and depression as common affective experiences of persistent pain. While this expands the understanding of pain from the IASP definition it still lacks the necessary social perspective. For this we must turn to the biopsychosocial model developed by George Engel. Engel’s view of the biomedical model was that it ignored anything beyond reductionistic science and did not consider patients in the context of their psychology or as a larger part of society. In his paper, ‘Clinical Application of the Biopsychosocial Model,’ Engel stated, ‘The biomedical model can make provision for neither the person as a whole nor for data of a psychological or social nature . . . The triumphs of the biomedical model all have been in the areas for which the model has provided a suitable framework for scientific study. The biopsychosocial model extends that framework to heretofore neglected areas.’3 To integrate the ideas of Price and Engel with those of Bogduk and Mersky it makes more sense to view persistent pain as an unpleasant emotional and sensory experience associated with actual or potential threat to the integrity of one’s entire life and described in terms of that threat. Why is it important to understand phenomenology in a textbook on interventional spine and what is this doing in a chapter entitled Central Influences on Pain? Patients do not present to pain specialists with declarations about discs or nerves or neuroplasticity, but do come with descriptions of the disruptive nature of their pain to their ability to be comfortable, to be happy, to relate to others, to work, and to play. Understanding central influences on pain requires that physicians distill the biopsychosocial information brought in by the patient down to the molecular changes occurring in the central nervous system, with the goal of crafting a plan to address these central neuroplastic changes in order to reestablish homeostasis in the patient’s life. Neuroplasticity develops in response to injury. This is usually a temporary state aimed at reestablishing the homeostatic balance of both the PNS and CNS. Peripherally, the immune system responds to injured tissue with release of inflammatory chemicals, such as bradykinins, prostaglandins, and histamines to isolate the injury from healthy tissue and increase the number, availability, and activation of peripheral opioid receptors.4 When this works well, healing occurs and the CNS and PNS quickly remodel to normal molecular, physiologic, and anatomic status. When there is unrelenting peripheral stimulation or a breakdown in adaptive function, neuroplastic changes that occur at the peripheral injury, dorsal horn of the spinal cord, and the brain result in the disease of pain, also known as maldynia.5 This is very different from the symptom of pain, eudynia. In maldynia pathological processes developing at the site of the peripheral injury, and discussed in much greater detail in Chapters 3 and 4, include excessive activity of sodium and calcium channels, ectopy through the alteration of neurotransmission from orderly ion channel transductions to rapid-fire stimulus encoding, and recruitment of non-nociceptors proximal and distal to the site of injury.6 At the dorsal horn of the spinal cord, excessive activity of excitatory amino 40

acids results in wind-up pain, driven by the extreme peripheral and central input. Wind-up appears to be the direct product of activation of N-methyl D-aspartate (NMDA) receptors in the superficial dorsal horn neurons.7 After nerve injury, reorganization directed by the dorsal root ganglion (DRG) results in dorsal horn atrophy of nociceptive (Aδ and C-fibers) end-terminals, as well as phenotypic changes in non-nociceptors (Aβ fibers) so that they produce nociceptive neurotransmitters and grow and reconnect into areas that are normally populated by nociceptive (C-fiber) nerve terminals.8 The brain itself goes through major changes at both a molecular and anatomic level. Actual apoptosis occurs in the brain in different regions for different chronic pain states, resulting in nerve cell loss and dendritic pruning.9 Functional MRI and MR spectroscopy in complex regional pain syndrome (CRPS) and in chronic low back pain have demonstrated this phenomenon.10

ACUTE PAIN Acute pain is pain that is of recent origin, is related to specific injury or illness, is of short duration, and is accompanied by time-limited, if any, disability. Acute pain is an important indicator that alerts us to the presence of a problem and tells us to stop using the injured body part to avoid further injury and allow healing. It is caused by normal activation of pain nerve receptors, known as nociceptors. These specialized nerve endings are embedded throughout the body and respond to penetrating wounds, chemical irritations or burns, heat, cold, pressure, nerve injury, inflammation, muscle spasm, fractures, infections, edema, expansion or rupture of visceral tissue, ischemia, overuse, erosion, and degeneration. This covers almost all of the pain conditions that present medically, and, in fact, pain is one of, if not the most common presenting medical complaint to primary care physicians’ practices. Pain is often the symptom that helps us pinpoint the pathology, or at least helps us to begin to develop a differential diagnosis. At the same time, pain can be quite confounding both for diagnosis and treatment. It is not an uncommon experience to find the underlying pathology, treat it effectively, and still be left with residual pain complaints. Although this occurs less frequently with acute pain, and more often when that pain becomes chronic, it may point to misdiagnosis and a revision of treatment plans in acute pain problems. Although most acute pain clears up with treatment of the underlying condition, it is important to treat the pain concomitantly with the healing of the structural and physiologic pathology. Treating acute pain decreases the unpleasantness of the experience, which if left activated can have serious consequences to psychological and neurotransmitter homeostasis. Additionally, when the pain does not clear up, more aggressive means should be employed, to prevent that pain from becoming chronic. Once chronicity sets in, the pain is much more difficult to treat. When a peripheral nociceptor is activated an action potential is generated and sent down the axon to cell bodies in the dorsal root ganglion. The incoming signal results in the DNA encoding the messenger RNA to instruct ribosomes in the cytoplasm to manufacture substance-P (SP), a neurotransmitter and calcitonin gene related peptide (CGRP), a neuropeptide. SP is constantly being manufactured at the ribosome in response to pain signals. It is then sent to nerve terminals where it is released. It is important to remember that the pain signal’s effect upon the nerve cell body causes the manufacture of more SP. SP is released at nerve endings synapsing on second-order nociresponsive neurons within the spinal cord. There it activates neurokinin-1 receptors (NK-1R) in the spinal cord dorsal horn cells and a new action potential is generated.11 In acute pain the signal at these dorsal horn neurons is typically equivalent in strength to the signal

Section 2: Spinal Pain

Fig. 5.1 In acute pain the incoming pain signal is passed on unaltered at the dorsal horn and is further passed to arousal, emotional, neuroendocrine, somatosensory, and autonomic centers, resulting in activation of descending pathways from many of the same centers. This countersignal is sent down to the dorsal horn, where the incoming signal is downwardly modulated.

coming into the CNS. This signal is then passed predominantly to either the neospinothalamic tract or the paleospinothalamic tract and sent to midbrain, thalamic, hypothalamic, and limbic structures in the brain. These are passed further to other deep and cortical structures in multiple regions of the brain resulting in a broad stimulation of pain sensation, arousal, autonomic pathways, somatosensory centers, and neuroendocrine pathways. This allows for a response to a painful stimulus, which is sensory and emotional and produces physiologic activity that is orchestrated through the interplay of far-flung areas of the brain and culminates in a countersignal from other widespread regions of the brain via descending pathways to dampen and ultimately to help to extinguish the incoming signals (Fig. 5.1).12

CHRONIC PAIN Chronic pain is best thought of as persistent pain that has no significant chance of being altered by usual treatment modalities or natural healing. This is pain that often has been amplified by the severity of pain signals reaching the CNS and causing a wind-up phenomenon at the dorsal horn of the spinal cord.13 It may even involve rapid depolarization and ectopy at the site of injury or the cell bodies in the dorsal root ganglia. Sympathetic coupling, antidromic neurogenic inflammation, CNS immune cell mediated inflammation, limbic kindling, activation of the neuromatrix, or other forms of central sensitization may also be involved.9 Finally, anxiety, depression, or other psychosocial factors are influenced by and influence pain perception.14 The result is pain that is physiologically amplified and often psychologically augmented, while conversely activating psychological responses. The patient experiences pain that feels overwhelming and represents an unwelcome change in life. When a peripheral nociceptor is chronically activated, SP, CGRP, and adenosine triphosphate (ATP), which targets the P2X3 subtype purinergic receptor, are released from the nociceptor and in turn activate non-nociceptive touch, movement, position, temperature and mechanical receptors. Action potentials are generated and sent down the axon to their cell bodies in the dorsal root ganglion. The incoming signal results in the DNA encoding the messenger RNA to instruct ribosomes in the cytoplasm to make SP in cells that normally do not produce this neuropeptide. In particular, SP is released at the dendritic end-terminals into the synapses between the dendritic tree

and the dorsal horn interneurons. On the interneuron membranes SP activates NK-1R in the spinal cord dorsal horn cells and new action potentials are generated. At the dorsal horn the SP/NK-1R complex is incorporated into the cytoplasm of the neuron, where it is ultimately broken down into its constituent components and recirculated. The action of the SP/NK-1R complex also depolarizes the membrane wall of the neuron and causes the removal of magnesium ions from NMDA receptors. Magnesium ions normally block these receptors, keeping them inactive. This results in activation of normally dormant NMDA receptors via reception of the ubiquitous excitatory neurotransmitter, glutamate, which in turn allows calcium ions to pass into the interneuron cytoplasm, causing the signal to be amplified in frequency and duration (wind-up).15 This amplified signal is then passed through Lissauer’s tracts to the neospinothalamic tract and/or the paleospinothalamic tract and sent to brain stem, midbrain, thalamic, hypothalamic, and limbic structures in the brain. To complicate matters further, other pathways engaged in chronic pain by unknown, but documented, mechanisms augment these classical spinal cord tracts.16 These signals are passed further to other deep and cortical structures in multiple regions of the brain resulting in a broad stimulation of pain sensation, arousal, autonomic responses, somatosensory activation, and neuroendocrine alteration. This results in an extreme response to a painful stimulus, which is sensory and emotional and produces physiologic activity that is modulated by sensory input from multiple areas of the brain.17 The brain’s attempt to diminish this signal is thwarted due to the ongoing process of windup pain at the dorsal horn of the spinal cord (Fig. 5.2).

CENTRAL PAIN Trauma to specific areas of the central nervous system can result in severe pain that may be immediate or delayed for months to years after the damage occurs. The term often used for this is central pain, and although many central pain processes drive this type of pain, the name actually describes the location of pain in the CNS. Central pain can be a problem in a number of different pathological CNS processes. Strokes in areas of the brain that involve ascending or descending pain pathways or the thalamus itself are frequently marked by severe and unrelenting pain. Demyelinating illnesses may cause central 41

Part 1: General Principles

Fig. 5.2 In chronic pain the incoming pain signal winds up and increases in frequency, resulting in a more intense signal at the dorsal horn and is further passed to arousal, emotional, neuroendocrine, somatosensory, and autonomic centers. As with acute pain, descending pathways are activated. This countersignal is sent down to the dorsal horn, where it cannot downwardly modulate the incoming stimulus, due to continued windup in dorsal horn neurons. The result is continued broad, intense, and relentless stimulation of brain centers.

pain. Trauma to the spinal cord can also result in chronic pain. This type of pain is subject to the same problems noted in centralization of peripheral pain, including neurotransmitter, neurocircuit, and neuroreceptor plasticity. Central pain of this type can be rather difficult to treat due to limited utility of a number of medications. Different studies show that after injury to the spinal cord, anywhere from 18% to 94% (with an average of 69%) of patients will develop chronic pain disorders and that chronic pain ranks high on the list for patients with difficult post-traumatic sequelae of spinal cord injury, right behind paralysis, sexual dysfunction, and incontinence. Recent studies show that about one-third of patients who develop postspinal cord injury pain will suffer from severe pain.18 Syringomyelia is an example of central pain that develops slowly over time due to deafferentation, a physiologic interruption of input to CNS neurons resulting in loss of excitation, inhibition, and modulation of information to the receptive neurons. In syringomyelia more than 90% of patients will develop pain disorders, but the time of onset averages 4–9 years after development of the syrinx.19 This delay in symptoms can obfuscate the etiology of the pain and has led to the incorrect conclusion by some researchers that syringomyelia is rarely painful. Studies done over time on patients with syrinx show that development of chronic pain is a common phenomenon. Melzak’s latest theory views deafferentation pain as a problem of hypervigilant brain function, via a concept he labels the neuromatrix. Deafferentation occurs when the normal input to central nociceptors is interrupted. This brain-based matrix consists of neurons, circuits, and dendrites in the thalamus, cortex, and limbic system, constantly cycling signals, allowing the brain to generate body image with or without sensory input. Interruption of normal peripheral input forces these centers of the brain to provide information to other areas of the brain. When consistent input to the matrix is interrupted, it works to reestablish balance by approximating output consistent with that previous input. Melzak further theorizes that a second output neuromatrix sends information to the PNS and its innervations, resulting in perception of movement, spasm, and pain even if these sites are denervated (spinal root avulsion) or amputated. At the same time, the output neuromatrix sends signals to the emotional centers of the brain, evoking emotional response to pain. The neuromatrix preserves the image of self at the cost of unrelenting pain. Thus, the failure of brain-based homeostatic mechanisms leads to central pain.20 42

WIND-UP PAIN Wind-up pain is one of the main features of central pain plasticity that distinguishes chronic pain from acute pain as a disease process rather than a symptom. Wind-up is a highly complex problem related to activation of NMDA receptors in second order neurons in the dorsal horn of the spinal cord and third-, fourth-, and fifth-order neurons in the brain. The activation of NMDA receptors results in a pain signal amplification through several processes culminating in hypersensitivity of the NMDA receptor-activated neuron to even minimal input from presynaptic sites. The process of wind-up pain is driven by the peripheral stimulus, but can continue independently even if the peripheral stimulus is well controlled. Activation of central processes caused by wind-up pain can maintain high pain levels. This is another reason why extinction of peripheral processes via various medication and invasive procedures may not extinguish or even diminish severe pain perception caused by peripheral injury. Normally, NMDA receptors are located on all CNS neurons, but are in an inactive state due to a magnesium block. They serve the purpose of destroying dying nerve cells by apoptosis to promote removal of cells and pruning back of dendrites to make room for cell replacement with new cells and rearborization of the dendritic tree. Apoptosis is best understood as programmed cell death and consists of complex intracellular process that lead to activation of NMDA receptors on the cell membrane and influx of calcium into the cytosome, resulting in pinpoint neuronal death, dendritic pruning, and ultimate replacement with new neurons, arborization, and synaptogenesis. It is this way that the CNS makes new connections, new pathways, and reduces dead and redundant cells and circuits. Without this process, the vibrant interplay of anatomic, physiologic, emotional, and experiential events could neither be sustained nor adaptively altered.21 To understand wind-up pain it is essential to understand the role of neurocircuits at the junction of the PNS to the dorsal horn, tracts from the spinal cord to the brain, intracranial connections, and pathways from the brain back to the dorsal horn. Furthermore, the role of neurotransmitters and neuromodulators must also be appreciated, as the combination of ubiquitous compounds with more focal substances results in the picture of adaptive processes gone wrong. Ultimately, intracellular processes that result in exertion of genomic shifts in

Section 2: Spinal Pain

the proteome determine when and where neurotransmitters, neuroreceptors, neuropeptides, and neurohormones will be dispatched. The dorsal horn is organized in lamina with second-order neurons serving as receptors for incoming signals from PNS nerve terminals. There are ten lamina identified as part of the organization of the spinal cord with lamina I–VI as part of the dorsal horn.22 Lamina I, II, IV, and V are the main nociceptive regions of the spinal cord.11 Fast excitatory postsynaptic potentials are produced by excitatory amino acid neurotransmitters and slow excitatory postsynaptic potentials are produced by neuropeptides (Fig. 5.3).23 Information from these terminals is passed to the several different nerve tracts that course through the white matter of the spinal cord, with the most significant nociceptive tracts being the paleospinothalamic tract and the neospinothalamic tract. In the dorsal horn there are nociceptive-specific (NS) neurons and wide dynamic range (WDR) neurons. As indicated by their names, the former are activated only by lightly myelinated Aδ fiber (first pain) and unmyelinated C-fiber (second pain) input, while the latter receive A-δ fiber, C-fiber, and heavily myelinated Aβ fiber (mechanoreceptor) input. Additionally, WDR neurons are capable of increasing response to increasing input. In turn, both NS and WDR neurons send axons to multiple brainbased sites, including brainstem and midbrain reticular formation, the superior colliculus, the periaquaductal gray, parabrachial nuclei, hypothalamus, ventrolateral, and medial thalamus. In turn, these deep brain structures send further connections to the insula, anterior cingulate cortex, supplementary motor area, somatosensory cortex, posterior parietal cortex, posterior cingulate cortex, and prefrontal cortex.24 Even this complex set of connections and inputs is an oversimplification made more complex by variable collateral branching to other brain regions, afferent and efferent two-way connections between brain nuclei, modulating negative feedback loops, excitatory, inhibitory and comodulating neurotransmitters, activation of brain-based apoptosis and regeneration, dendritic pruning and rearborization, and dynamic shifts in blood–brain barrier permeability.25

Supplementary motor cortex Anterior cingulate cortex

Insula

Frontal cortex

Amygdala Ventromedial posterior complex Hypothalamus Medial dorsal nucleus: ventrocaudal part

I IV

III

II

V VI VII X IIX VIII IX

IX IX

Fig. 5.3 Lamina I, II, IV, and V of the dorsal horn of the spinal cord are the main nociceptive receiving and transmitting levels. It is in lamina I and II where C-fibers and Aδ fibers terminate, while terminations of C, Aδ and Aβ fibers occur in lamina IV and V. These lamina are not only the anatomical source of normal CNS pain processes, but it is here where wind-up from peripheral stimulus occurs.

This complexity of anatomy, physiology, cellular mechanisms, genetic processes, and constant remodeling determines the complexity of the pain experience and pain behaviors (Fig. 5.4). Afferent pain systems tell only part of the story. These must be placed into the context of the activity of efferent pathways as well. Once pain enters the CNS, it does not become cut off from the PNS any more than the brain and spinal cord function in isolation. The experience of pain unpleasantness requires a multitude of responses including reflexive recoil, voluntary motor responses, conscious

Posterior cingulate cortex 1st somatosensory cortex 2nd somatosensory cortex

Posterior parietal complex

Fig. 5.4 Various regions of the brain and Ventroposterior their connections to the paleospinothalamic lateral nucleus tract (PST) and neospinothalamic tract (NST), demonstrating the complexity of the afferent CNS connections of major pain Periaquaductal gray processing pathways. It must be noted that Parabrachial nucleus in chronic pain disorders, other spinal tracts are recruited to pass on nociceptive signals. (VPL, ventroposterior lateral nucleus; PAG, periaquaductal gray matter; AMYG, amygdala; HYP, hypothalamus; VMpo, ventromedial Paleospinothalamic tract posterior complex; ACC, anterior cingulate Neospinothalamic tract cortex; SMA, supplementary motor cortex; MDvc, medial dorsal nucleus: ventrocaudal part; S1, first somatosensory cortex; S2, second somatosensory cortex; PPC, posterior parietal cortex; PCC, posterior cingulate cortex; PB, parabrachial nucleus) 43

Part 1: General Principles

avoidance, emotional awareness, and intellectual assessment and planning. The brain mounts a counteroffensive against the incoming activation of nociceptors in an attempt to turn the excessive activity down in a process of synergy that involves dampening of output from peripheral dendritic terminals, release of nociceptive neurotransmitters synapsing on dorsal horn neurons, and hyperpolarization of dorsal horn membrane potentials.26 Anatomically, pain-modulating pathways in the brain originate in the cerebral cortex, amygdala, and hypothalamus and synapse in the periaquaductal and periventricular gray nuclei. These converge to other synaptic connections in the rostroventral medulla and from there course down bulbospinal tracts to synapse with presynaptic primary end-terminals and dorsal horn second order neurons.27 Additionally interneurons in the dorsal horn play an important role in modulation of pain (Fig. 5.5). Wind-up pain occurs with constant stimulation of C-fiber afferents resulting in increased dorsal horn receptive field size due to activation of NMDA receptors, loss of Aβ fiber inhibition of nociception, phenotypic Aβ terminal change to SP production and release and neuropathy induced sprouting of Aβ fibers into more superficial levels of the dorsal horn.28 Although constant input is needed to start this process, very little, if any input is needed to maintain it, thus creating a nightmare of positive feedback with minimal or even absent peripheral stimulus. It is the unrelenting bombardment of the dorsal horn neurons that perverts the adaptive function of NMDA receptor activation into a maladaptive disease process. The release of SP and glutamate from presynaptic nerve endings arising from peripheral, primary-order neurons results in activation of NK-1 receptors and non-NMDA (AMPA and kainate) glutamate receptors. The normal restraining influence of gamma aminobutyric acid (GABA) and the endorphin systems is overwhelmed. Without this brake upon the activity of glutamate, NK-1 receptors are stimulated excessively and cause depolarization of cell membranes of NS and WDR neurons, rich in dormant NMDA receptor populations. In turn, this process activates NMDA receptors by causing them to release their magnesium block due to the migration

of magnesium from membrane depolarization and glutamate attaches to external and internal sites in the NMDA receptor, promoting the influx of calcium into the cell. Calcium activates L-argenine to break down to nitric oxide (NO). This diffuses across the synapse and stimulates the release of more SP and glutamate, perpetuating this vicious cycle. The action of intracellular calcium also results in the breakdown of prostanoids to arachidonic acid, resulting in activation CNS inflammation (Fig. 5.6).15,29 Recent research has shown that a very similar, but brain-based process occurs in chronic affective disorder, including bipolar disorder, major depressive disorder, generalized anxiety disorder, panic disorder, and post-traumatic stress disorder.30 Most of this research has been done independently of pain research, but converges on the same basic processes in the CNS for this set of disorders. Primary dementia also has been examined from the standpoint of NMDA receptor activation and apoptosis, with treatment for memory loss being focused increasingly upon NMDA receptor blockade. Additionally long-term mu opioid stimulation of PK-C production and activation appears to be a major process involved in the development of tolerance to opioid medications and as such presents us with a possible strategy for improving pain control by decreasing tolerance.

MOLECULAR PAIN PROCESSES As with any bodily process, pain transmission occurs due to molecular processes. We know far more about molecular pain processes than we have in the past, but unraveling this mystery is still in its early stages and there is far more to understand. What we do know is that molecular changes in cell function occur with nociceptive and neuropathic injury and that these changes may go on to further changes common in chronic intractable pain. Some of the neurotransmitters involved are SP and glutamate, but also include dopamine, norepinephrine, serotonin, histamine, and acetylcholine. Other molecules brought into play are nerve growth factors, calcium, sodium, potassium, and chloride ions, μ-opioid receptors, protein kinase-C (PK-C), c-fos

Supplementary motor cortex

Periventricular gray

Frontal cortex

Periaqueductal gray

Amygdala Hypothalamus

44

Rostroventral medulla

Fig. 5.5 Descending pathways from the brain modulate pain signals coming into the CNS from the PNS. Many of the same areas involved in ascending pathways are involved in top-down modulation of pain. The spinal bulbar tract runs from the brain down to the dorsal horn. (SMA, supplementary motor cortex; HYP, hypothalamus; PAG, periaquaductal gray matter; PVG, periventicular gray matter; RMV, rostroventral medulla; AMYG, amygdala)

Section 2: Spinal Pain

Substance-P

Ca Mg

Glutamate

P

Glutamate

P Ca Ca

P

P

P

P

Activated NMDA receptor

P

P Mg

P

Mg

NMDA receptors

AMPA receptors

Ca NK-1 receptors

Mg

Ca Mg

Ca Mg

Activated AMPA receptors

Released magnesium

MU-opioid receptor (post-synaptic)

A

P

P

Substance-P Activated NK-1 receptors

B

P P P

PP

P P

P

P P

PP

P

Ca

P

P

P

Ca

Ca Ca

PKC

Ca++ activated PKC

Ca

PKC

PKC PKC

C

P

P

Ca PKC influenced mRNA mRNA New NMDA receptors

PKC

D

Fig. 5.6 (A) Presynaptic terminals release glutamate and SP into synapse. Postsynaptic nerve cells show magnesium-blocked NMDA receptors, AMPA, and NK-1 receptors. (B) Glutamate attaches to AMPA receptors and SP attaches to NK-1 receptors. Long-term depolarization of cell membrane causes the magnesium block to be removed from the NMDA receptor. Glutamate attaches to external and internal sites resulting in calcium influx to the cytosome. (C) Inactive PKC is activated by calcium. (D) Activated PKC influences mRNA to instruct the proteome to create more NMDA receptors, which are sent to the cell membrane. (Continues)

45

Part 1: General Principles

Nitric oxide

Glutamate NO NO P P P

PP

P

P

Induced and activated NMDA receptors

P P

P

Ca

NO Ca Ca Ca NO Ca Ca

Ca

P

Nitric oxide Ca Ca

mRNA

Ca

P

P

P

Activated Activated AMPA PKC NK-1 receptors receptors Ca Ca Ca Ca

P

P

Substance-P

Ca

mRNA

PKC

P

P P

PKC

F

E

Fig. 5.6—cont’d (E) Intracellular PK-C causes magnesium blocks to be removed from NMDA receptors, activating them. More calcium flows into the cytosome. Calcium transforms cytosomal L-argenine via nitric oxide. (F) NO diffuses across the synapse to the presynaptic cytosome, causing release of SP and glutamate. This results in increased pain and perpetuation of the vicious cycle of wind-up.

protein, prostanoids, arachidonic acid, interleukin-1, tumor necrosis factor-α (TNF-α), peripheral and central bradykinins and brainderived neurotrophic factor (BDNF). Holding the whole excitatory process back is GABA (Table 5.1). In nerve injury, excessive sodium and calcium channel activity leads to a markedly increased production of SP in DRG neurons and massive release of SP at dendritic terminals. Interestingly, neuron morphology in the DRG neurons changes, but there is almost no cell death, due to production of nerve growth factors, especially BDNF by these cells after axotomy.31 A more startling development is that cells in the dorsal horn replace C-fiber nociceptors with Aβ fiber non-nociceptors, which in turn make new synaptic connections in the superficial lamina of the dorsal horn.32 We know that A-beta nerve fibers do produce SP and CGRP after nerve injury. It is likely that activation of synapses by phenotypically changed Aβ fibers leads to allodynia and involves nerve growth factors to establish these synaptic reconnections. Central neuroplasticity in chronic intractable pain disorders is not only complex, but serves to confound many interventions, as well as diminish effectiveness of successful treatment over time. The

centerpiece of this process is activation of NMDA receptors in the dorsal horn and the brain. The process is described elsewhere in this chapter. What is important to understand is that NMDA activation is a process that actually leads to several other intracellular processes that develop into manufacture, membrane placement, and constant turnover of newly activated NMDA receptors. Thus, a vicious cycle leads to ongoing production and replacement of postsynaptic NMDA receptors. These cause an incoming pain signal to become relentless, constant, and self-perpetuated, even absent significant ongoing peripheral stimulus. In a further piece of biological irony, the endogenous opioid receptors that serve best to regulate pain become contributors to wind-up through this same NMDA receptor activation and turnover, because opioid action on μ-opioid receptors in the spinal cord and brain results in further processes that keep sequencing this vicious cycle. We are faced with the paradox of SP/NK-1 receptor-bound complexes causing activation and proliferation of NMDA receptors resulting in increased production and release of presynaptic SP and glutamate and the primary treatment to prevent SP release and attachment to NK-1 receptors, exogenous opioids and endogenous opioid (endorphin) release, also perpetuating the same

Table 5.1: Some of the Major Molecules Involved in Nociception Amino acids

Brain Amines

Nerve Growth Factors

Ions

Inflammatory Mediators

Others

Glutamate

Norepinephrine

NGF-1, 2, 3

Sodium

Prostanoids

Substance-P (neurokinen)

GABA

Serotonin

Brain derived neurotropic factor

Potassium

Arachidonic acid

c-fos protein (gene)

Dopamine

Calcium

Interleukin

μ-opioid receptor

Histamine

Chloride

Tumor necrosis factor-α

Protein kinase-C (enzyme)

Acetylcholine

46

Bradykinins

Section 2: Spinal Pain

changes at the NMDA receptor.33 This then is at least a partial molecular explanation of opioid tolerance, i.e. NMDA receptor activation and turnover. In fact, several animal studies have demonstrated the activation of NMDA receptors with ongoing opioid treatment.34–36 At this point we need to step back from the physiologic process of wind-up pain and look at the neurotransmitters and neuromodulators that play roles in its occurrence. It is here also that one sees the molecular interplay of pain and chronic affective disorder due to the action of many of these very same molecules, especially when viewed through the perspective of the aforementioned phenomenology and anatomy of pain and affective centers. The CNS is dominated by two neurotransmitters, glutamate and GABA, although the latter is more classically seen as a neuromodulator. These two molecules make up 90% of neurotransmitters in the CNS. They are collocated in all areas, although usually on different neurons. They are involved in homeostasis of excitatory and inhibitory neurotransmission, respectively. GABA is almost entirely synthesized from glutamate via the enzymatic action of glutamate decarboxylase. Glutamate and GABA also have the most extensive distribution of any neurotransmitters in the CNS. While there are other excitatory and inhibitory neurotransmitters (e.g. aspartate and glycine), glutamate and GABA should be viewed as the molecular heavyweights of CNS neurotransmitter homeostasis, with all other neurotransmitters aimed at fine tuning their activity.37 Glutamate is an excitatory amino acid that is released at synaptic end terminals and in turn activates several types of postsynaptic receptors. These include ionotropic AMPA (α-amino-3-hydroxy-5methylisoxazole-4-proprionic acid), kainate, and NMDA, as well as metabatropic receptors. Ionotropic receptors regulate ion flow into and out of the cytosome through activated receptor channels. Metabatropic receptors work by activating second messengers in the cytosome that effect long-term changes in the proteome through complex intracellular and intranuclear activity. Glutamate’s role in acute pain is unclear, but it likely has a significant effect upon this via excitatory activity on AMPA and kainate receptor types, due to the fast component of excitatory postsynaptic potentials (EPSP) upon stimulation by glutamate. AMPA receptors are distributed on the same neurons as NMDA receptors. Magnesium ions serve to functionally block activation of NMDA receptors. Once the magnesium block is removed from NMDA receptors, they can become activated by glutamate, resulting in the slow component of EPSP and establishment of the gateway to neuroplasticity.38 Evidence-based animal and human studies have established the activation of NMDA receptors as central to development and maintenance of chronic pain and opioid tolerance in the CNS, whether or not peripheral stimuli persist.39,40 An obvious question is that of what purpose these receptors play in normal CNS function. Researchers believe that the NMDA receptor is essential to normal neurodevelopment, through molecular, physiologic, and anatomic remodeling throughout the life an organism. Humans are born with two to three times the number of brain-based nerve cells we will end up with during adulthood. The circuits connecting these neurons are rudimentary and expand through processes such as intellectual stimulation, emotional experience, developmental task mastery, establishment of relationships, new learning, and motor skill development. These neurocircuits connecting neuron centers with neuron targets are generally completed during the first 10 to 15 years of life, followed by a period of apoptosis and dendritic pruning over the next decade or two, resulting in the framework of neurons, neurocircuits, and neuroreceptors we will use for the rest of our lives.41 These, in turn, must die and be replenished to continue to allow further development and maintain life.42 NMDA receptors play a central role in the pruning process. When internal cellular processes signal a need to destroy or replace a cell, NMDA receptors

are activated allowing for orderly apoptosis and related dendritic tree pruning. Thus, the individual’s life experience and internal brain development remain connected and interactive.43 Additionally, activation of NMDA receptors throughout the life of an individual allows for apoptotic activity with dying nerve cells, ultimately culminating in removal and replacement with new neurons. It also appears that activation of NMDA receptors leads to long-term potentiation, which appears critical to development and laying down of new memory.44 It is the abnormal activation of these NMDA receptors and the damage caused by excitatory glutamate to the cells affected that lead to chronic pain, chronic affective disorders, primary dementia, and opioid tolerance. The most important restraint to both the PNS and CNS is the activity of GABA upon peripheral nerve terminals interfacing with dorsal horn second-order neurons, as well as multiple sites in the brain. GABA is the second most ubiquitous neurotransmitter in the CNS and is released at dorsal horn sites in balance with glutamate release. It acts as the brake upon CNS activation from glutamate. On the presynaptic nociceptor terminal it prevents excessive release of glutamate and SP. In the CNS, GABA serves to oppose excitation of brain neurons activated in pain, chronic stress, depression, and anxiety. It also restrains the release of glutamate and SP from presynaptic terminals. Three types of GABA receptors are known GABA-a, GABA-b and GABA-c. Little is known of GABA-c, but it appears that GABA-a receptors are mostly located in the brain and GABA-b mostly in the dorsal horn of the spinal cord. Over 150 000 subtypes of GABA receptors have been identified. Some GABA neurons are excitatory because they inhibit other inhibitory pathways, so the picture can be quite complicated.45 This is the process that appears to be at work in the sleep center of the hypothalamus. When histaminic wake promoter neurons activate neighboring GABAergic pathways, this results in inhibition of sleep promoter neurons which leads to GABAergic inhibition of wake promoter neurons resulting in sleep.46 This process goes awry in chronic pain disorders, and increased sleep latency, decreased sleep time, and decreased deep stage 3 and 4 sleep are hallmarks of chronic pain. Insomnia is considered a comorbid condition at best and a contributor to chronic pain and chronic affective disorders at worst.47 As the main inhibitory neuromodulator of glutamate and SP release, GABA inhibits A-delta fibers (first pain mixed nociceptors), C-fibers (second pain nociceptors), and Aβ fibers (phenotypically altered nociceptors). Apparently, GABA plays a key role in preventing hyperalgesia and allodynia, but it also appears that when NMDA receptors are pathologically activated, the ability of GABA to keep excitatory processes in check becomes compromised (Fig. 5.7).48 The neuropeptide SP has been implicated as one of the main neurotransmitters involved in the experience of pain for several decades. SP is synthesized in the DRG with 80% being sent down axons to the periphery and 20% to the end-terminals for release to targets in the dorsal horn. The highest prevalence of SP is in hypothalamus, substantia nigra, dorsal horn of spinal cord, spinal ganglia, autonomic nerves, and the sympathetic trunk. SP is a neurokinin and binds preferentially to NK-1R, but also binds to NK-2R and NK-3R. SP/NK-1R binding is associated with pain, emesis, depression, and anxiety. In the PNS, SP is associated with antidromic neurogenic inflammation. The amygdala, locus ceruleus, hypothalamus, substantia nigra, and peduncular nuclei all stain intensively for SP. Moderate staining occurs in caudate putamen, nucleus accumbens, raphe nuclei, and lamina 1 of the spinal cord, with low levels in cerebral cortex, cerebellum, and hippocampus. Even in areas of high density, SP is limited to 5% or less of neurons. SP localizes to synapses, released by dendrites and cell bodies. The distribution of NK-1 roughly corresponds to that of SP. Rapid binding of SP occurs with closely apposed NK-1R and 47

Part 1: General Principles

GABA vesicle GABA neuron

GABA

Activity of opioids at the μ receptor increases PK-C in its inactive form. This is activated by intracellular calcium, leading to increased production and activation of NMDA receptors

GABA

GABA neuron

P P P

P P P P

Mg

Mg

Mg

NMDA receptors

Opioids AMPA receptors

NK-1 receptors

Ca Opioids

Ca Fig. 5.7 Under normal physiologic conditions GABA restrains the excitatory influence of glutamate. They are neurotransmitters in harmony with one another, resulting in homeostatic CNS activity. The activity of GABA on presynaptic glutamate and SP-containing neurons is to balance the release and reuptake of each by its own action and reuptake on interneurons and neurons from central command centers.

subsequent internalization to cell within 5 minutes via the action of endosomes. Scientists have observed basolateral amygdala internalization in rats experiencing maternal separation. The degree of SP release and SP/NK-1R internalization is directly proportional to the intensity and duration of stressors. Previous exposure to painful or stressful stimuli results in a more robust release of SP. Repeated or more intense stimuli result in diffusion of SP to distant sites with up to 3–5 times activation of NK-1 receptors. Several animal models show increased anxiety in SP agonist stimulation.49 Ablation of NK-1 neurons with the potent neurotoxin saporin bound to SP in the dorsal horn resulted in markedly decreased nociception.50 Animal models using SP antagonists or genetically altered SP knockout mice show decreased anxious correlates to rodent behavior. There is high colocalization of SP and NK1 in emetic and emotional centers of brain, as well the superficial lamina of the dorsal horn.49 The intracellular compound PK-C serves as a second messenger system in central nervous system hyperalgesia.51 PK-C is activated after NMDA receptors in the dorsal horn and the brain are turned on by incorporation of the SP/NK-1R transmitter/receptor complex into the cytosol. As described earlier in this chapter, this results in depolarization of the cell membrane and loss of affinity of the magnesium block for the dormant NMDA receptor. After magnesium migrates into the cytosol, the NMDA receptor is activated. Once PKC is activated it migrates from the cytosol to the cell membrane, where PK-C further sensitizes NMDA receptors and more calcium is transported through these open NMDA channels into the cell.52 It is the action of glutamate upon these newly activated NMDA channels that causes inwardly generated currents to produce wind-up pain.53 The action of opioids on μ-opioid receptors also increases the activation of PK-C resulting in more sensitization of NMDA receptors and more calcium influx into the cytosol. This appears to play a critical step in the intracellular development of tolerance to opioids, as blocking these receptors with NMDA receptor antagonists reverses opioid tolerance (Fig. 5.8).54 Prostanoids present another problem of CNS hyperalgesia. When inflammation occurs in the periphery, prostaglandin E2 (PGE2) attaches to prostanoid (EP) comorbid receptors. This causes hyperalgesia and widens the nociceptive field in dorsal horn neurons. There 48

P

Ca

Fig. 5.8 Opioid activation of PK-C at the μ-receptor.

are four types of EP receptors, EP1–4. EP1, EP2, and EP4 receptors are stimulated by spinal cord release of PGE2, resulting in central sensitization. It also appears that once this process has occurred PGE2 attaching to a subtype of EP3 receptors (EP3α receptors) decreases central hyperalgesia.55 Serotonin, norepinephrine, and dopamine in brain pathways ascend into the cortical, limbic, hypothalamic, and basal ganglia/cerebellar centers from the medulla and pons, regulating mood, wakefulness, vegetative function, executive function, and pleasure. Serotonergic and noradrenergic pathways descend to the spinal cord from the medulla and regulate painful stimuli. Serotonergic downward modulating circuits may have positive or negative effects on pain processing in the dorsal horn, but noradrenergic stimulation of α2 receptors clearly down-modulates painful stimuli.56 Normal function of serotonin and norepinephrine in the brain promotes genome production of BDNF. Current research indicates that BDNF production and dissemination is most likely the common denominator between the positive effect upon depression by such varied approaches as serotonergic and noradrenergic antidepressants, valproic acid, lithium, and electroconvulsive therapy (ECT).30 Increased systemic circulation of glucocorticoids has been detected in pain disorders and chronic affective disorders. Excessive serum glucocorticoid activity causes overactivity of glutamate in the hippocampus, amygdala, hypothalamus, and brainstem. It appears that BDNF reverses this excessive and destructive activity of glutamate on NMDA, AMPA, and kainate receptors. It has been demonstrated that SSRIs, valproic acid, lithium carbonate, and ECT are neuroprotective and neurotrophic, actually growing back damaged neurons and promoting dendritic branching, through activation and release of BDNF. The ascending reticular activating system (ARAS) is one of the major components of normal executive function. This system is made up of noradrenergic, serotonergic, dopaminergic, and cholinergic neurons and their common circuits coursing to the frontal lobes. This system works via release of these neurotransmitters in the frontal

Section 2: Spinal Pain

cerebral cortex and should be seen on a direct continuum with the amount of neurotransmitters released. Low release results in depression, anxiety, poor concentration and attention, and diminished executive function. Normal release results in euthymia and normal attention concentration and executive function. High release results in fight or flight response, panic, and hypervigilance. One of the major problems in both chronic affective disorders and chronic pain disorders is that of poor sleep. Sleep is negatively affected in length and architecture, exhibiting insomnia, hypersomnolence, and various dyssomnias. While this relates in part to dysfunction of the ARAS, histaminic neurons in the tuberomamillary region of the hypothalamus are also involved. Unlike the variable response ARAS neurons, histaminic neurons function as a threshold system that is either on or off. These two systems must work together to promote proper initiation and maintenance of sleep (Fig. 5.9).57 Molecular cross-talk plays another role in connections between the pain and emotional systems, as well as between inflammation and neuroendocrine mediators. Dopamine is a neurotransmitter involved in mood control, executive function, cognitive processes, pleasure, energy, and movement. It appears that much of this effect is controlled via dopaminergic control of glutamate action in several different brain regions via several different mechanisms. There is evidence for dopamine effects synaptically and extrasynaptically in prefrontal cortex neurons. This region also shows control of glutamate by dopamine’s activation of GABAergic restraint on glutamate release. Glutamate neurons from the prefrontal cortex innervate populations of dopamine neurons in their originating sites in the brainstem tegmentum. Finally, dopamine and glutamate neurons send convergent dendrites to synaptic and extrasynaptic sites in basal ganglia, prefrontal cortex and amygdala.58 The high level of neuromodulation that occurs between dopamine and glutamate suggests potential problem areas of neuroplasticity, which will require further study, but also opens possibilities for therapeutic intercession.

Histamine Ascending Dopamine reticular Serotonin activating Acetyl choline system Norepinephrine Fig. 5.9 Ascending reticular activating system (ARAS) neurons consist of neuron centers in the medulla and pons. Among other areas of the brain, these neurons send tracts to the frontal cortex and release their neurotransmitters at these sites. The ARAS tracts run parallel with a tract from histaminic neuron centers in the tuberomamillary region of the hypothalamus. The action of dopamine, serotonin, norepinephrine, acetylcholine, and histamine allow for normal executive function, including normal energy, problem solving, and creativity. If these neurotransmitter levels are low, patients experience fatigue, depression, loss of motivation. If the neurotransmitters are too high, problems occur with panic, fear, and external vigilance.

Reactive gliosis occurs when brain microglia release cytokines in response to anatomic, physiologic, molecular, or genetic insult. Immune cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) enhance glucocorticoid activity in the pituitary. In turn, this induction of glucocorticoids reduces apoptosis from TNF-α.59 Since circulating glucocorticoid elevations can result in NMDA-induced apoptosis in the limbic system in chronic affective disorder, theoretically one problem of this neuroinflammatory/neuroendocrine induction could occur when chronic CNS inflammation results in chronically elevated CNS glucocorticoid levels. The point is that these normally adaptive processes may lead to maladaptive secondary responses if chronicity sets in and is not curbed. The pain responsive molecular systems also have other built-in peripheral and central restraints. Ultimately, these can be exploited. There are peripheral opioid receptors that respond to endorphins, which are endogenous opioids. They are synthesized in the DRG and transported down axons to the peripheral nociceptors. Peripheral opioid receptors are increased in number during inflammation. Inflammation increases cyclic AMP, which decreases nociceptor excitability via opioid receptor stimulation. Peripheral nociceptor sprouting increases in inflammation, creating more opioid sites. Activation of peripheral opioid, sites leads to decreased excitability, decreased release of excitatory neuropeptides and decreased nerve firing. It also appears that local immune cells, activated by inflammation, produce endogenous opioids. corticotrophin releasing factor and IL-1, increased in inflammation, stimulate endorphin release and attachment to receptors in inflamed nociceptors, but not to normal tissue. Inflammatory chemicals also increase permeability of the perineurium so that endorphins can attach to receptors on nociceptors and their axons.60 Endogenous opioids are also of benefit in the CNS. Endogenous opioids are released and activated in the dorsal horn of the spinal cord with nociceptive and neuropathic pain. They are sent to the area of excessive stimulation and attach to μ-, δ-, and κ-opioid receptors.56,61 Rapid deactivation is also considered a hallmark of endogenous opioid effects and limits their benefit in chronic pain states. If medication can be found to extend the activity of endorphins, these endogenous molecules might have greater utility in the treatment of chronic pain disorders. Another endogenous antinociceptive process that controls pain peripherally and centrally is the stimulation of α2 adrenergic receptors by endogenous norepinephrine. This occurs at the junction of peripheral nerve terminal interface with the dorsal horn of the spinal cord. Norepinephrine release in the brainstem can cover several different areas of the brain, but also is sent to the dorsal horn of the spinal cord. It has its effect on nociception at the presynaptic terminal and the dorsal horn NS and WDR neuron. When norepinephrine attaches to α2 adrenoreceptors at the peripheral nerve terminals, it prevents the release of SP and glutamate, diminishing their stimulation of NK-1 and NMDA receptors in the dorsal horn of the spinal cord. Furthermore, when norepinephrine stimulates α2 receptors on the dorsal horn neurons, potassium ions are released from the intracellular space to the extracellular space, resulting in hyperpolarization and limited firing of NS and WDR neurons (Fig. 5.10).62 One of the notions that has fallen out of favor is the old idea of neurotransmission of one transmitter for one specific target neuron. We now know that diffusion of neurotransmitters occurs to targets distant from the intended cells, as in the massive release of SP in patients with neuropathic pain. The result is that of both a precise and a diffuse effect of neurotransmitters. Additionally, it is also known that neurotransmitters have a greater effect upon the biology of the cell than we understood previously. The action of neurotransmitters on membrane-located neuroreceptors is not only related 49

Part 1: General Principles Norepinephrine releases from descending neurons from medulla and attaches to alpha-2 receptors. Calcium influx is blocked and release of substance-P and glutamate is inhibited

Norepinephrine attaches to alpha-2a receptors on interneuron and Potassium egress occurs, hyperpolarizing cell. Neurotransmission is prevented.

K+ K+ K+

K+ + K+ K K+ K+

A

B

Fig. 5.10 (A) Presynaptic action of α2 agonism blocks release of SP and glutamate. (B) Postsynaptic action of α2 agonism hyperpolarizes neuron via potassium (K) efflux.

to propagation of action potentials, but also results in neuroplastic change by affecting cytoplasmic RNA. This results in coding of nuclear mRNA by DNA. Subsequently, mRNA instructs cytoplasmic ribosomes to manufacture neurotransmitters, neuroreceptors, nerve growth factors, neurokinins, and neuromodulators. DNA coding of the mRNA also directs these new substances to various deployment sites on the cell membrane, in the cytoplasm of the neuron or at nerve terminals or peripheral nociceptors.63 None of this is orchestrated randomly. Peripheral injury to nerve tissue and inflammatory activation of nociception results in changes in CNS transcription factors, such as c-jun, and sequence-specific binding factor nuclear factor-κB in the nuclei of neurons, with subsequent neuropeptide changes occurring over the next 5–7 days.7 Other neurotransmitters, neuropeptides, second messengers, and neuromodulators are known to take part in this incredibly complex orchestration of neuroplasticity in the CNS. Adding to the complexity of neuronal information processing is the emerging knowledge we are gaining about the function of glial cells, the other 90% of brain and spinal cord cells. Long known to serve supportive, insulating, and nutritional function, we now are beginning to unravel the far more complex function of glia in neurotransmission. It has become apparent in the last 15 years of research of glia that they communicate with each other through calcium imbibition responsive to neuronal firing. Glial cells then feed back to neuronal networks by releasing increased neurotransmitters to increase synaptic strength and the number of new synaptic connections. Furthermore, 50

this information can be passed to distant sites via still unknown glial mechanisms resulting in alteration of neurons that are not physically connected to each other. It appears that glia communicate chemically by secreting substances that are only picked up by other glia, ultimately influencing these distant sites. This slow form of information processing allows for adjustments to synaptic strength, blood–brain barrier permeability, and neuronal apoptosis and replenishment.64 We have far more to learn and it is inevitable that our emerging knowledge of the human genome will reveal a treasure trove of information about these processes. Through unraveling the information in the genome we will gain accuracy in developing therapeutics to alter processes in a precise and temporally controlled fashion.

CONCLUSION Central influences on pain are best understood in terms of adaptive systems that allow peripheral stimuli to alert us to ‘an unpleasant physical and emotional experience,’ and to respond to that experience by reestablishing homeostasis. While in the vast majority of cases this system performs its task well, when CNS-mediated wind-up pain leads to hyperalgesia and allodynia, the adaptability of this system goes awry, shifting to maladaptive consequences that reverberate throughout the CNS. This chapter attempts to describe some of the important breakthroughs in our understanding of these processes. Research in this field is still in its infancy and ranges outside the area of pain medicine to neurology, psychiatry, basic neuroscience, and genetics.

Section 2: Spinal Pain

One of the shortcomings of pain medicine in evaluating central influences on pain has been the limited focus of looking beyond the spinal cord to the brain and this chapter endeavors to correct this by delineating the anatomy, physiology, and molecular biology of brain-based pain, emotion, behavior, adaptation, and maladaptation. There is also a preliminary attempt to look at the burgeoning field of pain genetics, which will doubtless play an increasingly important role both in our understanding of central pain influences and in targets aimed at altering the proteome to reverse pain cascades. The complexities are staggering, and we are only beginning to grasp some of the possibilities. What we are finding is that greater connections are being made to explain the relationship of the PNS and CNS to acute and chronic pain. This expanding knowledge allows us to understand why current interventions are effective and to consider novel combination strategies to tip the balance toward adaptive responses. While many of our interventional targets are in the PNS, all that we do as practitioners of pain and spine medicine is ultimately determined as success or failure by how we control these central processes.

21. Freeman R. The cell cycle and neuronal cell death. In: Koliatsos V, Ratan R, eds. Cell death and diseases of the nervous system. Totowa: Humana Press Inc.; 1999:103–179.

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PART 1

GENERAL PRINCIPLES

Section 3

General Diagnostic Technique

CHAPTER

Radiology

6

John B. Weigele, Eric D. Schwartz, Oleg Bronov and Gul Moonis

INTRODUCTION

Disadvantages

Remarkable advances in diagnostic imaging of the spine have occurred over the last several decades. Since magnetic resonance imaging (MRI) was introduced into clinical practice in the mid 1980s it has rapidly assumed the preeminent role in spinal imaging as a result of its abilities to display exquisite anatomic images and to accurately characterize a broad spectrum of diseases encompassing degenerative, inflammatory, infectious, traumatic, neoplastic, and congenital disorders.1–3 Nonetheless, MRI has limitations. Conventional radiographs (plain films), computed tomography (CT), and myelography combined with postmyelography computed tomography (myelo CT) also play important roles in the evaluation of spine pathology.4 In this chapter the roles, advantages, disadvantages, and techniques for each of these imaging modalities will be discussed, followed by considerations of imaging the normal spine and a number of spinal disorders commonly evaluated and treated by the spine interventionist.

Plain films have intrinsically poor contrast resolution. Only materials with markedly different X-ray attenuations such as metal, bone, soft tissue/water, fat, and air can be distinguished. Conventional radiographs cannot discriminate among various soft tissue structures, discs, ligaments and cerebrospinal fluid (CSF). As a result, many disorders such as herniated discs, tumors, and myelopathies are not visible. In addition, conventional radiographs represent a two-dimensional projection of the anatomy. Three-dimensional relationships are not demonstrated as they are on multiplanar tomographic CT and MRI images. This lack of multiplanar tomographic imaging limits the assessment of many clinical questions. Plain films are obtained with ionizing radiation.

IMAGING MODALITIES Conventional radiographs (plain films, X-rays) Roles Diagnostic imaging of the spine usually begins with conventional radiographs. Plain films provide an inexpensive and rapid screening of skeletal anatomy and potential abnormalities to guide further clinical evaluation and imaging. Primary care patients with low back pain who were screened with plain films and rapid MRI had nearly identical clinical outcomes, and plain film screening was less expensive.5 The spinal segments are readily counted and the alignment, size and shape of the vertebral bodies are easily assessed. Plain films screen for degenerative disease that can be demonstrated by disc interspace narrowing, osteophytes, and endplate sclerosis. Grossly destructive neoplastic or infectious/inflammatory processes can be diagnosed by cortical bone destruction or vertebral collapse. Plain films of the lumbar spine readily depict pars defects (spondylolysis) and spondylolisthesis. Conventional radiographs provide rapid and cost effective evaluation of skeletal spine trauma although CT is assuming an increasingly important role.6,7 Flexion and extension plain films evaluate spinal stability in trauma and postsurgical cases. For the interventionist this study is particularly important for patients who experience pain during extension or show evidence of spondylolisthesis with plain films. Conventional radiographs provide intraoperative guidance and postoperative assessment of surgical hardware, bone grafts, alignment, and stability.

Advantages Conventional radiographs have high spatial resolution and are widely available, rapidly and inexpensively obtained. Flexion–extension views to evaluate spinal stability are easy to acquire.

Technique A standard complete cervical spine radiographic examination includes anteroposterior (AP), lateral, bilateral oblique, and open mouth views. A ‘swimmers’ lateral with one shoulder elevated and the other depressed is used for trauma if C6 and C7 are not well visualized on the conventional lateral view. For thoracic spine evaluation AP and lateral views are usually sufficient. Lumbar spine radiographs are tailored to the indication. A full examination consists of AP, both oblique, and lateral views. The oblique view provides the ‘Scotty dog’ image that is most useful to evaluate the pars interarticularis for a defect (spondylolysis) and the facet joints (Fig. 6.1). In some, cases such as for surgical guidance or for a postoperative assessment, one or two views may suffice.

Magnetic resonance imaging Roles MRI has become the most valuable method to image the spine. After screening plain films, MRI is the next imaging study of the spine usually obtained. It is considered the most useful modality for the evaluation of myelopathy, radiculopathy, and back pain requiring advance imaging. CT and CT-myelography are usually reserved for patients with a contraindication to MRI or for the investigation of specific questions raised or remaining unanswered by the MRI.

Advantages The superior contrast resolution of MRI depicts the soft tissue anatomy of the spine better than plain films and CT. MRI is comparable to CT and bone scans for most pathologic processes causing neurological compromise and is better than CT for the detection of systemic diseases.1 The spinal cord, nerve roots, CSF, vertebrae, discs, and ligaments can be exquisitely resolved and distinctly visualized.6 Multiplanar tomographic imaging optimally 53

Part 1: General Principles

Fig. 6.1 Pars defect. Oblique plain film of the lumbosacral spine demonstrates a L5 pars defect (arrow), and a normal L4 pars interarticularis (arrowhead) for comparison.

displays three-dimensional anatomic relationships. MRI is able to reveal inflammatory, traumatic, and infectious processes using image acquisitions that are sensitive to edema such as fat-suppressed T2-weighted fast spin echo (FSE) and short tau inversion recovery (STIR) pulse sequences.6 Gadolinium-enhanced images display inflammatory processes (with fat-suppression) (Fig. 6.2), tumors, and distinguish scar from disc in postoperative patients. Ionizing radiation is not used. There are no known risks of MRI for patients without a contraindication except for exceedingly rare allergic reactions to gadolinium injections.

Disadvantages MRI is expensive and the examination time is longer than for plain films and CT scans. MRI may not display bony pathology such as cervical foraminal stenosis as well as CT (Fig. 6.3).6 Access to the

Fig. 6.2 Discitis and osteomyelitis. Fat suppressed contrastenhanced T1-weighted thoracic spine MRI image reveals marked enhancement of two adjacent vertebrae (arrows) with destruction of the intervening disc and endplates (arrowheads). 54

A

B

Fig. 6.3 Bony neural foraminal stenosis. Axial cervical spine bone window CT image (A) and T2-weighted gradient-echo MRI image (B) demonstrate bony neural foraminal stenosis (arrows).

patient in the scanner is limited and the introduction of ferromagnetic objects into the strong magnetic field can be hazardous. This makes a MRI examination of unstable and critically ill patients more difficult. Rapid patient access and resuscitation can be compromised. Some individuals experience severe claustrophobia inside the bore of the magnet. It is dangerous to place patients with cardiac pacemakers and ferromagnetic implants into the strong magnetic field of the MRI scanner. Most cochlear implants, ocular implants, and neurostimulators as well as some aneurysm clips are not MRI compatible. Most of the orthopedic hardware, surgical clips, and staples currently in use are safe. Cardiac valve prosthesis, vascular stents, wires, and coils are usually MRI compatible but require different amount of time after placement before the patient can be safely placed in the magnetic field. In general, a published resource such as the ‘Reference Manual for Magnetic Resonance Safety, Implants and Devices’ or the manufacturer should be consulted if the patient reports any implanted medical device or retained metallic foreign body. Knowledge of the exact name and manufacture of a device is necessary to determine its safety; if this information is not available, it is recommended that the patient not undergo MRI scanning.8 Images in the region of surgical hardware may be nondiagnostic.9 There is limited experience with dynamic studies of the spine and studies with physiological spine loading, and these examinations are not readily available at most centers.

Technique Lumbar spine MRI exams typically include both sagittal and axial acquisitions using T1- and T2-weighted pulse sequences. Sagittal images should be carried from one neural foramen to the other neural foramen with thin slices and a minimal interslice gap. Sagittal and axial T1-weighted spin echo images are useful to evaluate the

Section 3: General Diagnostic Technique

It can also image skeletal anatomy not adequately visualized on plain films in trauma patients, in particular the C1–2 and C6–7 regions. CT can be used to as a less expensive alternative to MRI to screen patients with lumbar radiculopathy. CT is routinely used to characterize bony tumors of the spine due to its exquisite depiction of bony detail and ability to display calcifications, osseous and cartilaginous matrix. Fig. 6.4 Normal cervical foraminal nerve roots. Axial 3-D T2-weighted gradient echo cervical spine MRI image demonstrates normal nerve roots in the neural foramina (arrows) surrounded by bright CSF in the nerve root sleeves.

vertebral body marrow, epidural, and foraminal fat. T2-weighted fast spin echo (FSE) images evaluate the disc space, nerve roots, and facets. CSF is brighter than discs, nerve roots, cartilage, bone, and ligaments on a T2-weighted FSE acquisition. Axial 3–5 mm images are angled parallel to the disc interspace to optimally evaluate disc morphology. The images are carried from the pedicle above the disc interspace to the pedicle below to look for migrated free fragments. Since fat is relatively bright on T2-weighted FSE images, the sagittal T2-weighted FSE images can be obtained with fat-suppression to evaluate the vertebrae for edema associated with trauma, infection, or inflammation. Postgadolinium (contrast enhanced) axial and sagittal T1-weighted images are obtained for specific indications, including postoperative evaluations to distinguish a disc herniation from scar tissue, possible infection/inflammation, and tumors. MRI pulse sequences for cervical spine imaging typically include sagittal and axial T1-weighted, axial and sagittal T2-weighted FSE, and axial three-dimensional T2-weighted gradient echo images. T1weighted sagittal images assess the vertebrae for size, shape, and alignment and for marrow signal intensity. T2-weighted axial and sagittal FSE images evaluate the spinal cord, nerve roots, and facets. Thin section (e.g. 1.5 mm) axial three-dimensional T2-weighted gradient echo images are valuable in the cervical spine. On these images, the disc is variably moderate in intensity, CSF is very bright, and bone is dark. The nerve root sleeves containing CSF in the neural foramina are optimally visualized (Fig. 6.4). This is important since T1-weighted images are not as useful to evaluate the cervical neural foramina as for the lumbar spine because there is less fat. Compression of the nerve roots or spinal cord by osteophytes or disc herniations is demonstrated with high sensitivity. Gradient echo images, however, can artifactually accentuate the apparent degree of bony stenosis due to susceptibility effects. The FSE images are less sensitive to susceptibility effects; therefore, the degree of bony central canal stenosis is best estimated on sagittal T2-weighted FSE images. Sagittal short tau inversion recovery (STIR) images are valuable to evaluate the soft tissues, especially the ligaments, in trauma cases.10

Computed tomography (noncontrast) Roles Noncontrast CT may answer important clinical questions not answered by MRI, particularly about bony detail such as the integrity of the posterior vertebral body cortical bone in a patient with a malignant compression fracture being evaluated for vertebroplasty. Bony stenoses of the neural foramina in the cervical spine are depicted more accurately than on MRI.6 Noncontrast CT often depicts subtle fractures and displacements such as facet jumps better than plain films.7

Advantages CT provides high-resolution detail of trabecular and cortical bone and is able to differentiate soft tissue, disc, CSF, and fat. Images acquired in the axial plane on modern helical CT scanners can be reconstructed in other planes. Exquisite three-dimensional models of the bony anatomy can be reconstructed for surgical planning. CT is less severely degraded by imaging artifact from surgical hardware than MRI. In the cervical spine, CT provides a more accurate representation of bony stenoses of the central canal and neural foramina than MRI. A CT scan takes less time than a MRI examination. The patient is more accessible within the scanner, facilitating the study of uncooperative, critically ill, and unstable individuals. Patients are less likely to be claustrophobic in a CT scanner than in the typical highfield MRI gantry. Obese patients who cannot fit in the MRI bore and those with pacemakers and other MRI-incompatible hardware can be successfully imaged on the typical CT scanner. CT is also very useful for guiding spinal interventions.

Disadvantages CT cannot distinguish soft tissues with very similar X-ray attenuations. CT is therefore much less sensitive than MRI in detecting pathologic processes such as infection and tumor. MRI is also much more sensitive to intrinsic spinal cord pathology. Scar, disc material, and other soft tissue can have similar attenuation values on unenhanced CT scans and can be difficult to distinguish. Spinal cord, nerve roots, and CSF cannot be distinguished without intrathecal contrast. Patients are exposed to ionizing radiation.

Technique Spiral CT of the spine is currently performed with 1–3 mm collimation depending on the region being evaluated and the specifications of the CT scanner. In the cervical spine 1–1.5 mm collimation is routinely used on multislice row detectors. Images are reviewed in both soft tissue and bone windows. Sagittal and coronal reconstructions are obtained when indicated. Computed tomography utilizes a highly collimated X-ray beam, which is registered by the detector after passing through the patient. The original CT developed by Godfrey Hounsfield in 1972 had one X-ray source and one detector rotating around the patient. Current CT scanners have many rotating X-ray tubes and detectors that acquire data as the patient is continuously advanced through the bore of the scanner (helical or spiral scanning). X-ray sources and detectors can be aligned in several rows, which allow simultaneous image acquisition at several levels. This configuration can obtain thinner slices in a shorter time. Attenuation values of the X-ray beam passing through the tissue at many various angles are computed using a projection reconstruction technique and a number is assigned to every pixel (picture element); these calculated values of relative attenuation are called Hounsfield units. By one convention, 0 is the Hounsfield number of water and 1000 is the Hounsfield number for air. Materials such as bone and metal that attenuate more of the X-ray beam are assigned higher numbers. Assigning each pixel a grayscale value based on its Hounsfield number creates images. Window level refers to the Hounsfield number at the middle of the grayscale range and window width refers to the number of Hounsfield 55

Part 1: General Principles

units that span the grayscale range from black to white. If the window width is large, there is less contrast between tissues with relatively close attenuation values, but many different tissues with a wide range of attenuation parameters will be shown in different grades of gray. A narrow window helps to demonstrate even small differences in tissue attenuation within the chosen window, but all of the tissues with Hounsfield units above or below the window limits will be completely white or black. Specific windowing protocols vary among scanners and manufacturers. A typical soft tissue window level is 50 and window width is 450, while a typical bone window level is 350 and window width is 2000. Different mathematical reconstruction algorithms can be applied to increase contrast between structures. A bone algorithm is particularly helpful to accentuate bony margins and interfaces of bone with air and soft tissues.

Standard myelogram films include AP, oblique, and lateral views. Standing, flexion, and extension images may be useful. The postmyelogram lumbar CT is obtained with the patient prone if tolerated to allow the contrast to pool in the ventral thecal sac and in the nerve root sleeves. Thin section images are obtained parallel to each disc interspace from the pedicle above to the pedicle below so a free fragment will not be missed. In the cervical spine, contiguous thin-section CT images are obtained. Images are reviewed in soft tissue and bone windows.

Myelography and postmyelography CT

Discography is reviewed in Chapter 25.

Roles Myelography and postmyelography CT are used to study patients with surgical hardware that renders MRI images nondiagnostic, and as problem solving tool for patients with equivocal or discordant findings on MRI, and for patients with a contraindication to having a MRI examination. Myelography and postmyelography CT provides additional information to that obtained from a MRI in exam 33% of patients with lumbar degenerative disease.11 It is often the definitive imaging study for cervical myelopathy and radiculopathy since it is the gold standard for detecting osteophytic impingement on cervical nerve roots. Myelography and postmyelography CT can be useful to detect small tumor implants on nerve roots and also arachnoiditis.

Advantages Postmyelography CT provides the definitive assessment of central stenosis and the degree of cord compression in the cervical spine. Myelography and postmyelography CT can demonstrate herniated discs in the cervical spine neural foramina missed on MRI. Subtle compression of nerve roots in the lumbar lateral recesses is demonstrated better on myelography than postmyelography CT or MRI.12 Myelography and postmyelography CT provide better assessment of the spinal canal and nerve roots than MRI in the region of surgical hardware. Myelographic films can be obtained with the patient standing and during flexion and extension to evaluate dynamic abnormalities during physiologic loading.13

Disadvantages Myelography and postmyelography CT require puncture of the thecal sac with a spinal needle (usually lower lumbar, occasionally at C1–2) and instillation of nonionic iodinated contrast into the subarachnoid space. Although complications are uncommon, they include headache (occasionally due to a CSF leak requiring a blood patch), contrast reaction, seizure, infection, and hemorrhage. The procedures and recovery period is lengthy. Patients are exposed to ionizing radiation.

Technique The patient typically lies prone and a standard lumbar puncture is performed with a 22–25-gauge spinal needle. Nonionic iodinated contrast is instilled into the subarachnoid space during fluoroscopic monitoring to confirm the correct needle position. Twelve to 15 cc of Omnipaque 180 is instilled for lumbar myelography and 10–12 cc of Omnipaque 300 is instilled for cervical myelography. For a cervical myelogram, the patient is briefly tilted head-down on the table to facilitate the gravitydependent flow of the contrast into the cervical subarachnoid space. 56

Nuclear medicine Nuclear medicine imaging of the spine is discussed in Chapter 7.

Discography

IMAGING OF THE NORMAL SPINE Spinal cord and nerve roots The spinal cord extends from the caudal aspect of the medulla oblongata at the upper border of the first cervical vertebra (C1) to its inferior termination as the conus medullaris occurring variably from the twelfth thoracic vertebra (T12) to the second lumbar vertebra (L2). The filum terminale is a fibrous cord that extends caudally from the tip of the conus. It initially travels intradurally and then merges with the dura to insert in the coccyx. The nerve roots extending inferior to the conus are called the cauda equina. The sacral roots are positioned centrally and posteriorly within the thecal sac; the lumbar roots are located anterolaterally.14 There are two regions of normal spinal cord expansion, one in the lower cervical cord extending approximately from C4 to T1 and the other in the lower thoracic cord extending approximately from T9 to T12. These normal regions of cord enlargement supply the brachial and lumbosacral plexuses, and should not be misinterpreted as pathologic.14 The spinal cord gives rise to 31 paired sets of spinal nerves: 8 cervical, 12 thoracic, 5 lumbar, and 5 sacral, and 1 coccygeal. The first cervical spinal nerve is purely sensory and exits the spinal canal above the ring of C1; the second spinal nerve exits into the C1–2 neural foramen above the C2 pedicle, and so on to the seventh cervical spinal nerve exiting into the C6–7 neural foramen. The eighth cervical spinal nerve exits into the C7–T1 neural foramen. In the cervical region the nerve roots occupy the lower portion of the foramen at the same level as the disc interspace. Each thoracic and lumbar spinal nerve exits the canal beneath its like-numbered pedicle so that the first thoracic spinal nerve exits beneath the T1 pedicle into the T1–2 neural foramen, the first lumbar spinal nerve exits beneath the L1 pedicle into the L1–2 neural foramen, and so on. Sensory (dorsal) and motor (ventral) nerve roots arising from the spinal cord join to form the spinal nerves. The dorsal root ganglion contains the sensory nerve cell bodies and lies in the neural foramen near the junction of the dorsal and ventral roots. A conjoined root consists of two nerve roots traveling in the same dural sleeve; it is a normal anatomic variant occurring in approximately 5% of patients. The conjoined roots may exit through the same or different neural foramina.14 In the lumbar spine each nerve exits the thecal sac enclosed in a root sleeve of variable length entering the lateral recess (subarticular space) bounded by the vertebral body anteriorly, the pedicle laterally, and the superior articular process posteriorly (Fig. 6.5).14 The minimum normal diameter of the lateral recess is 3–4 mm. The lateral recesses are best imaged on axial CT and MRI images. The nerve root passes inferiorly and laterally into the upper portion of the neural

Section 3: General Diagnostic Technique

Vertebrae

Fig. 6.5 Normal lumbar lateral recesses. Axial CT demonstrates normal L4–5 lateral recesses (arrows).

foramen above the level of the disc interspace surrounded by fat. The neural foramen is keyhole-shaped and widest superiorly (Fig. 6.6).15 The neural foramen is optimally examined on sagittal MRI, reconstructed sagittal CT, and oblique plain films. On T1-weighted MRI the spinal cord and nerve roots have a uniform intermediate signal intensity that is brighter than the surrounding relatively low signal intensity CSF (Fig. 6.7A). On T2-weighted images, the spinal cord and intrathecal nerve roots are extremely well visualized as relatively hypointense structures bathed in bright surrounding CSF (Fig. 6.7B). The nerve roots in the cervical foramina are best seen on high-resolution three-dimensional T2-weighted axial images outlined by surrounding bright CSF in their nerve root sleeves (see Fig. 6.4). In the lumbar foramina the nerve roots are visualized best on axial and especially sagittal T1-weighted images surrounded by the hyperintense fat within the foramen (see Fig. 6.6).16 The spinal cord normally does not enhance; however, enhancement of normal spinal nerve roots has been reported. Extensive nerve root enhancement, thickening, and nodularity are abnormal. On CT images the spinal cord and nerve roots are difficult to distinguish from surrounding CSF unless intrathecal contrast is used (Fig. 6.8). The spinal cord and nerve roots are silhouetted by intrathecal contrast on myelogram radiographs.

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The spine contains 7 cervical, 12 thoracic, and 5 lumbar vertebrae, the sacrum (consisting of 5 fused elements), and the coccyx. Except for the uniquely shaped first and second cervical vertebrae, the vertebrae have a generic shape that consists of an anterior cylindrically shaped vertebral body and the posterior elements consisting of the pedicles, transverse processes, superior and inferior facets, lamina, and spinous process.14 There are important regional variations in the morphology and size of the vertebrae. The first and second cervical vertebrae have unique shapes. The first cervical vertebra (the atlas) does not have a discrete body; it consists of a ring comprised of anterior and posterior arches connected by lateral masses that articulate with the occipital condyles above and the second cervical vertebra below. The axis, the second cervical vertebra, has a unique superior projection (dens) extending from the C2 vertebral body to articulate with the anterior arch of C1, secured by the transverse and subsidiary ligaments.14 The distance between the posterior border of the anterior arch of C1 and the anterior border of the dens should be 3 mm or less in an adult and 5 mm or less in a child. The cervical vertebrae from C3 to C7 are conventionally shaped and increase in size progressing caudally. They have unique uncinate processes that extend superiorly from the lateral aspects of the vertebral bodies to articulate with the vertebra above forming the uncovertebral joints (joints of Luschka). Spurs extending from the uncinate processes may compromise the nearby neural foramen. The superior and inferior facets are fused into the articular pillars. The vertebral arteries pass through foramina in the transverse processes of C1 to C6.14 The central canal of the cervical spine is triangular, measuring a minimum AP diameter of 15 mm at C1–2 and 12 mm in the lower cervical region. The 12 conventionally shaped thoracic vertebrae are larger than the cervical vertebrae and increase in size from T1 to T12. The interpedicular distance decreases to T6, and then increases to T12. The transverse processes of the thoracic vertebrae articulate with the ribs. The 5 lumbar vertebrae are the largest. The lumbar spinal canal usually is triangular in shape; less frequently it may be oval. The minimal normal AP diameter of the lumbar spinal canal is 11.5 mm and

Fig. 6.6 Normal lumbar neural foramen. Sagittal T1-weighted lumbar spine MRI image (A) demonstrates the typical keyhole-shaped L4–5 neural foramen containing the L4 nerve superior to the disc level and surrounded by hyperintense fat (arrow). Sagittal lumbar CT image in bone window (B) demonstrates the L3–4 neural foramen (arrow) and the L3 articular facets (arrowheads) 57

Part 1: General Principles

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the minimal cross-sectional area is 1.45 mm2 (Fig. 6.9). The interpedicular distance increases slightly from L1 to L5. The MRI appearance of the vertebrae is age dependent.17 The vertebral marrow is normally red (hematopoietic) during childhood,

Fig. 6.8 Cervical nerve root avulsions. Coronal cervical myelogram CT demonstrates normal left-sided cervical nerve roots (arrows). The right-sided cervical nerve roots were traumatically avulsed. 58

Fig. 6.7 Normal cervical spine. Sagittal T1-weighted (A) and T2-weighted (B) cervical spine MRI images reveal normal vertebrae, disc interspaces, spinal canal, and spinal cord. The normal cervical enlargement serving the brachial plexus is evident. CSF is hypointense on T1- and hyperintense on T2-weighted images. The cerebellar tonsils are in normal position.

gradually converting to yellow (nonhematopoietic) by adolescence.17 Normal adult yellow bone marrow is relatively hyperintense on T1weighted images due to the fat, and should always be brighter than the intervertebral discs. Marrow fat distribution can be heterogeneous, so some mild signal heterogeneity on the T1-weighted images is common. The vertebrae are hypointense on conventional T2-weighted spin echo sequences; the normal intervertebral discs are brighter. On fast spin echo (FSE) T2-weighted sequences the marrow is more hyperintense and lesions causing bone edema may be obscured unless fat suppression is used. The vertebrae display mild homogeneous enhancement after gadolinium administration. Since there are few mobile protons to provide MRI signal in the cortical bone, it appears as a thin, uniform, dark line outlining the bone marrow.

Fig. 6.9 Normal lumbar spinal canal. Sagittal helical CT image of the lumbar spine in the midline reveals normal alignment, vertebral body heights, lordosis, and spinal canal.

Section 3: General Diagnostic Technique

Intervertebral discs, anterior and posterior longitudinal ligaments The discovertebral complex consists of the cartilaginous endplate, anulus fibrosus, and nucleus pulposus. The well-hydrated nucleus pulposus is a fibrocartilage remnant of the primitive notocord. It is less well structured than the outer anulus fibrosus, occupies a large portion of the disc during childhood, and is bright on T2-weighted images (Fig. 6.10). With progression though adolescence into early adulthood, a horizontal low signal band develops in the center of the nucleus on T2-weighted images that corresponds to the development of higher collagen concentration in the equatorial region. This is called the intranuclear cleft and is a part of normal maturation (Fig. 6.11). The surrounding anulus fibrosus consists of multilayered (up to 15) dense parallel fibrous bands. The outer ring of the anulus fibrous contains peripheral lamellae that insert into the bony ring apophysis (Sharpey’s fibers) (see Fig. 6.10A). The outer anulus is relatively dark on T1- and T2-weighted images. The inner ring of the anulus is brighter on T2-weighted images and gradually merges with the nucleus. Both the nucleus and anulus have similar signal intensities on T1-weighted images and are difficult to distinguish. The nucleus is eccentrically located toward the posterior aspect of the disc. The posterior anular fibers are thinner and smaller in number. The outer annular fibers merge with the anterior and posterior longitudinal ligaments. The lumbar intervertebral discs increase in width from L1–2 to L4–5. The L5–S1 disc thickness is variable and may be less. The thoracic discs are uniformly thinner than the lumbar discs. The cervical discs are more wide anteriorly than posteriorly.14 Cervical discs have a less well-defined nucleus and anulus with less of a discrete posterior anulus. The anterior (ALL) and posterior (PLL) longitudinal ligaments are dense fibrous bands that are low signal intensity on T1- and T2weighted MRI images. The ALL lies adjacent to the anterior surface of the vertebral bodies and intervertebral discs. It forms a layer that is attached to the outer anulus and provides some fibers that attach to the vertebral body. The PLL merges with the outer anulus at the disc interspace (Fig. 6.12). The PLL is separated from the posterior surface of the vertebral body by the venous plexus in the

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Fig. 6.11 Intranuclear cleft. Sagittal T2-weighted lumbar spine MRI image demonstrates a normal T2 hypointense L5–S1 intranuclear cleft (arrow).

ventral epidural space and lies just anterior (ventral) to the thecal sac (Fig. 6.12). A midline septum attaches the PLL to the periosteum of the posterior vertebral body and serves to compartmentalize the ventral epidural space.18 The cartilaginous endplate is composed of hyaline cartilage that covers the bony endplate of the vertebral body and is bound to it by multiple fibrous attachments. The margin of the cartilaginous endplate attaches to the ring apophysis. The osseous endplate has perforations and numerous vascular channels to the disc interspace.

Posterior elements The pars interarticularis and the facet joints are well demonstrated on oblique plain films, sagittal and axial MRI, and CT images. The articular cartilage is best seen on sagittal MRI. The posterior ligamentous complex (interspinous ligaments, ligamentum flavum, facet joint capsules) is imaged best with MRI.

Fig. 6.10 Normal lumbar disc. Sagittal (A) and axial (B) T2-weighted MRI images of a lumbar disc demonstrate the hyperintense central nucleus pulposus (arrowheads) surrounded by the hypointense peripheral anulus fibrosus (arrows).

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Part 1: General Principles

Fig. 6.12 Normal posterior longitudinal ligament. Sagittal T2-weighted lumbar spine MRI image demonstrates the thin, linear hypointense posterior longitudinal ligament (arrows) separated from the posterior vertebral bodies by the epidural venous plexus and attached to the outer aspects of the anulus fibrosus.

IMAGING OF THE ABNORMAL SPINE Degenerative disease Nomenclature The use of ambiguous terminology to describe findings on spine imaging has interfered with clear and precise communication between radiologists and clinicians. To address this significant problem, cooperative multispecialty task forces of the North American Spine Society, American Society of Spine Radiology, and the American Society of Neuroradiology have proposed standardized nomenclature for lumbar disc pathology.19 These recommendations have been endorsed by the parent societies of the task forces, the Joint Section on Disorders of the Spine and Peripheral Nerves of the American Association of Neurological Surgeons, and the Congress of Neurological Surgeons, and the CPT and ICD coding Committee of the American Academy of Orthopedic Surgeons.19 The definitions recommended by the task forces are based on anatomy and pathology and are not intended to imply etiology or clinical significance. Although these definitions were developed specifically for lumbar disc pathology, it seems logical to extrapolate the use of these terms to the thoracic and cervical spine.19 The lumbar disc is classified into the following general diagnostic categories: normal, congenital/developmental variation, degenerative/traumatic, infectious/inflammatory, neoplastic, and morphologic variant of uncertain significance.19 The normal category includes a morphologically normal disc in a young adult and does not include degenerative, developmental, and adaptive changes that may be considered clinically normal, such as the changes typically associated with aging.19 The congenital/developmental variation category includes congenitally abnormal discs and adaptive disc changes in response to abnormal biomechanical forces, for example, morphological disc changes due to scoliosis or spondylolisthesis.19 The degenerative/traumatic category includes the subcategories of annular tear, herniation, and degeneration. This category includes degenerative changes that may be part of normal aging and not necessarily pathologic. Degenerative changes considered pathologic are also included. 60

Within the degenerative/traumatic subcategories, a number of more specific terms are defined.19 Annular tears (annular fissures) are separations between annular fibers, avulsion of fibers from vertebral attachments, or breaks in the fibers that extend radially, transversely, or horizontally through the lamellae.19 Herniation is defined as a localized displacement of disc material (any combination of nucleus, anulus, endplate, cartilage, or bony ring apophysis) beyond the limits of the disc interspace involving less than 50% of the disc circumference. The disc interspace is defined craniocaudally by the edges of the vertebral endplates and laterally by the outer margins of the ring apophyses, without the inclusion of osteophytes. Herniations are further described as focal (involving <25% of the disc circumference) or broad-based (involving 25–50% of the disc circumference). Generalized disc displacements involving >50% of the disc circumference are called bulges.19 Despite the obvious utility of standardized nomenclature, experienced interpreters demonstrate significant interobserver variability describing lumbar spine disc disease.20 A herniation can be subcategorized as a protrusion or extrusion on the basis of its shape. A herniation is defined as a protrusion if the distance between the edges of disc material beyond the interspace is always less than the distance between the edges of the base of the herniation in the same plane. A herniation is called an extrusion if any distance between the edges of the disc material beyond the interspace is greater than the distance between the edges of the base of the herniation in the same plane. Protrusion and extrusion are defined solely on a morphological basis; the terms do not refer to whether or not the anulus is intact.19 A sequestration (free fragment) is a subtype of an extrusion where the displaced disc material has lost continuity with the parent disc. Migration refers to displacement of the disc material away from the site of the extrusion, whether or not it is sequestrated. Craniocaudal disc herniations through the vertebral body endplate are called intervertebral herniations (Schmorl’s nodes). Disc herniations are contained if covered by an intact anulus and uncontained if not covered. MRI frequently cannot distinguish contained from uncontained herniations. Discography can demonstrate an uncontained herniation.19 Standard bony landmarks can be used to define the location of a disc herniation. In the axial plane, the following zones can be defined from medial to lateral: central – between the medial edges of the articular facets; subarticular – from the medial edge of the articular facets to the medial edge of the pedicle; foraminal – from the medial edge of the pedicle to the lateral edge of the pedicle; and extraforaminal (far lateral) – lateral to the lateral edge of the pedicle. In the sagittal plane, herniation location can be described to be discal, infrapedicular, suprapedicular, and pedicular. The volume of the herniation can be categorized on the axial image showing the most significant impact on the canal. Compromise of less than one- third of the canal is defined as mild, compromise of onethird to two-thirds of the canal is moderate, and compromise of more than two-thirds of the canal is severe.19 The description of a disc herniation can include the following: morphology (protrusion, extrusion, broad-based, focal), status of containment (by the outer anulus), continuity (sequestered or free), relationship with the PLL (subligamentous), volume (spinal canal or foraminal compromise), composition (disc, cartilage, bone, and ligament), and location.19 Some consider a recurrent disc contained if it is limited by scar tissue. The term degeneration includes the findings of disc desiccation, fibrosis, and narrowing, numerous annular tears, mucinous annular degeneration, endplate sclerosis, and osteophytes. Two distinct degenerative patterns have been described. The first pattern, spondylosis deformans, affects the anulus fibrosus and adjacent ring apophysis. It is believed to be a consequence of normal aging with

Section 3: General Diagnostic Technique

findings that include anterior and lateral osteophytes, disc dehydration without disc interspace narrowing, small transverse and concentric annular tears, and small amounts of gas in the annular entheses. Posterior osteophytes are not considered to be an element of spondylosis deformans. The second pattern, intervertebral osteochondrosis, affects the nucleus pulposus and the endplates. It is considered pathologic, not due to normal aging. Intervertebral osteochondrosis may or may not be symptomatic. It includes desiccation and narrowing of the disc, extensive gas in the disc, disc bulging, posterior osteophytes that can narrow the spinal canal and neural foramina, endplate sclerosis and erosions, and chronic bone marrow changes adjacent to the disc interspaces.19 The other categories are inflammatory/infection, neoplasia, and morphologic variant of unknown significance. The inflammation/ infection category includes infection, inflammatory discitis, and inflammatory spondylitis. Modic type 1 changes are included in this category. The neoplasia category includes morphologic disc changes due to primary or metastatic tumor. Structural abnormalities of the disc without sufficient data to define are placed in the category of morphologic variant of unknown significance.19

Spondylosis deformans Spondylosis deformans refers to degenerative changes that are associated with the normal aging process, including small concentric and transverse annular tears, decreased hydration of the disc, anterior and lateral osteophytes, and small amounts of gas in the annular entheses. Concentric tears have fluid or mucoid material that is bright on T2-weighted images between lamellar layers. Transverse tears occur at the insertion of the anulus into the ring apophysis, and may contain fluid that is bright on T2-weighted images or gas that is visible on plain films or CT. The discs have decreased water content due content to a decreased glycosaminoglycan/collagen ratio and are moderately less bright on T2-weighted images without a loss in height of the disc interspace. Osteophytes are dark on both T1- and T2-weighted images.19

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Intervertebral osteochondrosis Intervertebral osteochondrosis refers to degenerative changes that are considered pathologic and not due to normal aging, including desiccation and narrowing of the disc, extensive gas in the disc, disc bulging, radial annular tears, posterior osteophytes, endplate sclerosis and erosions, and chronic bone marrow changes adjacent to the disc interspaces. Radial annular tears are failures of multiple annular layers. They are bright on T2-weighted images and may enhance (Fig. 6.13). Such high-intensity zones on MRI have a high specificity for painful annular tears on discography; however, the sensitivity is low.21 Disc desiccation and loss of water content causes decreased disc height and decreased signal intensity on T2-weighted images. Juxtaendplate changes (Modic types 1–3) may be present (Fig. 6.14). Modic type 1 corresponds to increased vascularity in the juxta-endplate vertebra. Its MRI appearance reflects increased water content: dark on T1-weighted images and bright on T2-weighted images (Fig. 6.14A, B). Modic type 2 represents increased fatty marrow: bright on T1-weighted and dark on fat-suppressed T2-weighted FSE images (Fig. 6.14C, D). Modic type 3 denotes sclerotic changes: dark on both T1- and T2-weighted images (Fig. 6.14E, F).22 Posterior osteophytes are also dark on both T1- and T2-weighted images and can narrow the spinal canal and neural foramina. Extensive gas in the disc (vacuum disc) can be seen on plain films and CT, and sometimes seen on MRI.19

Disc herniations On CT, disc herniations are similar to the density of the parent disc and are higher density than the CSF. On myelogram radiographs, disc herniations are diagnosed by effacement of a nerve root sleeve or by compression of the thecal sac (extradural defect). Myelography is relatively insensitive to lateral (foraminal) disc herniations and also central herniations at L5–S1 since the thecal sac is farther from the disc interspace. Postmyelography CT detects small disc herniations and herniations at L5–S1 missed on myelography.23

Fig. 6.13 Annular tear. Sagittal (A) and axial (B) T2weighted MRI images reveal a peripheral annular tear (arrow). 61

Part 1: General Principles

On T1-weighted MRI images, lumbar spine disc herniations are usually iso- to slightly hyperintense relative to the parent disc (Fig. 6.15A, B). Disc herniation signal intensity on T2-weighted FSE images is variable; the herniation is often iso- to hypointense to the parent disc (Fig. 6.15C, D). Posterior disc herniations are often contiguous with a radial tear. Anterior disc herniations are less common and more frequently asymptomatic. Posterior and posterolateral disc herniations usually affect the descending nerve root in the lateral recess, e.g. the L4 nerve root is affected by a L3–4 disc herniation (Fig. 6.15) whereas lateral (foraminal) herniations affect the exiting nerve root, e.g. the L3 nerve root is affected at L3–4 (Fig. 6.16). A prominent localized venous plexus of epidural veins can look similar to a disc herniation on MRI and can cause radicular symptoms.24 MRI anatomically characterizes foraminal and extraforaminal herniations best.25 Effacement of foraminal fat on the sagittal T1-weighted

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images is an important sign (Fig. 6.16). Sagittal T2-weighted images demonstrate loss of continuity of a sequestered lumbar disc herniation with its parent disc (Fig. 6.17).26 MRI cannot reliably distinguish supraligamentous from subligamentous lumbar disc herniations.27 Thoracic disc herniations are quite rare, representing less than 1% of all disc herniations (Fig. 6.18). They present insidiously with myelopathy, back pain, or radiculopathy.28 Myelopathy occurs more commonly than radiculopathy because of the lordotic curve in the thoracic spine. Calcified thoracic disc herniations may be difficult to diagnose on MRI. Myelo-CT may be more definitive in this setting. Cervical disc herniations occur most frequently at C5–6 and at C6–7 (Fig. 6.19).29,30 Lateral cervical disc herniations are rare because the uncovertebral joints (joints of Luschka) block the herniation from extending in this direction. The nomenclature designed for lumbar disc pathology also can be used to describe cervical disc disease.

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Fig. 6.14 Juxta-endplate changes. Sagittal T1-weighted and T2-weighted MRI images display Modic type 1 (A, B) and Modic type 2 (C, D) changes (arrows). Sagittal T1-weighted MRI image (E) and sagittal CT image (F) display Modic type 3 changes (arrows). 62

Section 3: General Diagnostic Technique

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The natural history of disc herniations is varied. Disc herniations clearly can decrease over time with conservative management and clinical improvement can be seen. The mechanisms for this are unknown. Possible factors include disc fragmentation, shrinkage, and phagocytosis. Inflammation and neovascularity around the disc margin may promote resorption.31,32

Spinal stenosis Spinal stenosis is the term for clinically symptomatic narrowing of the spinal canal or neural foramen. These symptoms include radiculopathy, myelopathy, and neurogenic claudication due to nerve root compression.33–35 There are a number of causes of spinal stenosis. In children and young adults these include achondroplasia, mucopolysaccharidoses, congenitally short pedicles, spondylolisthesis, congenital spinal lipomas, and disc herniations. Degenerative disease is the most common cause of spinal stenosis in older adults. The typical degenerative lumbar spine with spinal stenosis has varied combinations of degenerative bulges/herniations, osteophytes that form from stresses exerted on the ring apophysis by the disc after Sharpey’s fibers have torn, facet hypertrophy due to osteoarthritis of the synovial facet joint, and hypertrophy of the ligamentum flavum. The degree of canal compromise may be accentuated by the presence of congenitally short pedicles or spinal lipomatosis. In the lumbar spine, there are three zones to consider: the central spinal canal, the lateral recesses, and the neural foramina.34,35 Suggested values in the literature for the normal measurements of these regions vary; the subjective evaluation of the images by an

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Fig. 6.15 Lumbar disc herniation. Sagittal (A) and axial (B) T1weighted, sagittal (C), and axial (D) T2weighted MRI images demonstrate an L5–S1 disc extrusion (arrow) impinging on the S1 nerve root in the lateral recess.

experienced interpreter may provide the most useful correlation with the clinical presentation. As general guidelines, lumbar central canal is considered abnormal if the area is less than 1.5 cm2 or the AP diameter is less than 11.5 mm. The narrowed lower lumbar canal often has a trefoil or ‘T’ shape from posterior spurs, disc bulges, facet hypertrophy, and thickened ligamentum flavum. The trefoil shape is accentuated by congenitally short pedicles. The lateral recess is narrowed if it is less than 4 mm in AP diameter. Hypertrophy of the superior articular facet frequently narrows the lateral recess. Lateral recess narrowing may compress the exiting nerve root. The normal ligamentum flavum is 2–4 mm in thickness. Thicker than 5 mm it is considered hypertrophied. Lumbar spinal stenosis is frequently evaluated with MRI. Both sagittal and axial planes, and both T1- and T2-weighted pulse sequences provide valuable information. Axial-loaded MRI can reveal more severe central canal stenosis and modify the treatment plan.36 The lumbar neural foramen is best evaluated on sagittal T1-weighted images.37 Sagittal images display the foramen in optimal profile. The lumbar foramen is predominately filled with bright fat that contrasts well with surrounding disc, ligament, and bone. The normal foramen has a ‘key-hole’ shape; the superior aspect of the foramen is larger than the inferior aspect. The inferior aspect of the foramen usually narrows first (Fig. 6.20). The superior portion of the foramen containing the nerve root usually narrows later. Positional MRI of the lumbar spine with patients seated and imaged in flexion and extension demonstrates minor neural foraminal compromise better than conventional supine MRI and correlates with positional pain differences.38 There is still an important role for conventional myelography in the evaluation of patients with lumbar radiculopathy. Lumbar root 63

Part 1: General Principles

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Fig. 6.16 Foraminal lumbar disc herniation. Sagittal (A) and axial (B) T1-weighted and axial T2-weighted (C) MRI images reveal a foraminal (lateral) lumbar disc herniation (arrow) impinging on the nerve root and ganglion, and obliterating the foraminal fat.

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Fig. 6.17 Free disc fragment. Sagittal T2-weighted (A), axial T1-weighted (B), and axial T2-weighted (C) MRI images demonstrate a disc sequestration (arrow) impinging on the thecal sac and nerve root in the lateral recess. 64

Section 3: General Diagnostic Technique

Fig. 6.20 Bony lumbar foraminal stenosis. Sagittal T1-weighted MRI image reveals bony foraminal encroachment at multiple levels (arrows).

Fig. 6.18 Thoracic disc herniation. Sagittal T2-weighted MRI image displays a thoracic disc herniation (arrow).

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compression in the lateral recess caused by degenerative changes is demonstrated by myelography with greater sensitivity than postmyelography CT or MRI. Surgically confirmed nerve root compression in the lumbar lateral recess was missed on MRI in 28%, missed on postmyelography CT in 38%, but only missed on conventional myelography in 6%.12 Causes of cervical spinal canal narrowing include osteophytes, ligamentous thickening (posterior longitudinal ligament and ligamentum flavum), disc herniations, and bulges. The cervical spine canal is considered narrow if the anteroposterior diameter measures less than 11 mm. On MRI, this is most accurately determined on sagittal T2-weighted images. MRI can overestimate the degree of stenosis compared to postmyelography CT.39 Kinematic MRI demonstrates that spinal stenosis and cervical cord impingement increases in flexion and extension as degenerative disease progresses.40 Bony stenosis of the cervical neural foramina is displayed best by CT (Fig. 6.21).

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Fig. 6.19 Cervical disc herniation. Sagittal (A) and axial (B) T2-weighted fast spin echo MRI images and an axial T2-weighted gradient echo MRI image (C) demonstrate a cervical disc herniation (arrow) impinging on the exiting nerve root. 65

Part 1: General Principles

consideration. There is an increased incidence of juxta-articular cysts in spondylolisthesis. CT facet arthrography can be useful to confirm the diagnosis in some cases.44 Rare thoracic and cervical juxta-articular cysts have been reported.6,45,46 Synovial cysts can also be caused by calcium pyrophosphate deposition disease.47 Fig. 6.21 Bony cervical foraminal stenosis. Axial bone window CT image demonstrates marked foraminal stenosis caused by uncinate process (arrowhead) and facet (arrow) hypertrophy.

Spinal cord myelopathy caused by spinal stenosis is bright on T2weighted images (Fig. 6.22). Different patterns have been described and correlated with surgical outcomes. Well-defined and intense intramedullary high signal on T2-weighted images is associated with a poor surgical prognosis.41

Juxta-articular cysts Juxta-articular cysts are associated with degenerative disease and occur in a characteristic location, extending anteromedially into the canal from the lumbar facet joint forming a round posterolateral extradural mass.42,43 The majority is true synovial cysts; however, a few are ganglion cysts and contain a connective tissue capsule. Juxta-articular cysts most commonly occur at L4–5 and at L5–S1, more often on the right side. They may present with radicular pain and neurological deficits. The juxta-articular cyst is diagnosed by its characteristic position in the posterolateral aspect of the spinal canal abutting the anterior aspect of the facet joint and by associated degenerative changes in the facet joint including joint space narrowing, sclerosis, and osteophytes. The imaging appearance can vary. The contents may have characteristics of fluid or blood with varied MRI signal intensities (Fig. 6.23). The periphery can calcify and enhance. A posterolateral disc extrusion is the primary differential diagnostic

Fig. 6.22 Spinal stenosis-induced myelopathy. Sagittal T2-weighted cervical spine MRI image demonstrates spinal stenosis and myelopathy (arrow). 66

Correlation of imaging and clinical evaluation It is exceedingly important that careful correlation is carried out between the imaging findings and the presenting symptoms and signs before causality is assumed. A positive correlation between imaging findings and the clinical presentation of patients with back pain is often absent. In addition, morphologic abnormalities are frequently detected on imaging studies of clinically asymptomatic individuals.48–52 Lumbar disc bulges and protrusions but not extrusions are found on MRI in many asymptomatic individuals. Annular tears, Schmorl’s nodes, and facet arthropathy are also common.52,53 Therefore, the imaging abnormalities found in patients with back pain may be coincidental and unrelated to the pain. In addition, asymptomatic people with lumbar spine abnormalities on MRI do not have a higher probability of developing back pain in the future.54 Cervical spine abnormalities are also frequently found in asymptomatic individuals.50

Failed back syndrome Failed back syndrome refers to continued or recurrent back pain after spinal surgery. It has been variably reported to occur in 5–40% postoperative patients. The pain can be caused by scar tissue, residual or recurrent disc herniation, insufficient decompression with central or foraminal stenosis, instability, spondylolisthesis, hematoma, postoperative fluid collection, operation at the wrong level, CSF leak, infection, and arachnoiditis.55–60 The MRI appearance of the postoperative spine evolves over time. In the first week after surgery, there is usually more mass effect visible at the operated level than before the procedure. The degree of mass effect does not correlate with the eventual clinical outcome and the mass effect typically begins to decrease after the first week. Granulation tissue, the instrumented disc, and the adjacent vertebrae all normally enhance after surgery. Surgicel placed for hemostasis can markedly compress the posterior thecal sac in the immediate postoperative period in patients who are clinically doing well.61 The imaging diagnosis of a residual or recurrent disc is therefore difficult in the immediate postoperative period.60,62 After the immediate postoperative period, gadolinium-enhanced MRI reliably differentiates postoperative epidural scar from a residual or recurrent disc herniation (Figs 6.24, 6.25). On nonenhanced T1weighted images, scar and disc are indistinguishable (Fig. 6.25A, B). On T2-weighted images, epidural scar may be slightly brighter than disc material.63 On gadolinium-enhanced T1-weighted images performed immediately after the contrast injection, postoperative scar enhances avidly and homogeneously, while disc material does not (Fig. 6.25C, D).64 In patients who are studied more than 6 weeks after surgery, MRI is 96% accurate in differentiating scar tissue and disc herniation.64 Fat suppression is useful because both enhancing epidural scar and fat are bright on nonfat-suppressed T1-weighted images.65 The periphery of a disc herniation can enhance immediately following injection, but the central portion does not. Severely fragmented discs can display rapid diffuse enhancement similar to epidural scar. A recurrent disc may exert mass effect on a nerve root but epidural scar usually does not. On delayed imaging after injection, contrast can diffuse into a disc herniation causing it to be confused with enhancing scar tissue. Interestingly, one recent study has suggested contrast-enhanced MRI imaging does not improve diagnostic accuracy in patients with prior lumbar surgery.66

Section 3: General Diagnostic Technique

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Fig. 6.23 Synovial cyst. Sagittal T1-weighted (A) and T2-weighted (B) lumbar spine MRI images, and an axial T2-weighted MRI image (C) display a left-sided L4–5 synovial cyst (arrow).

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Postoperative nerve root enhancement may be a marker of active neural inflammation associated with radiculopathy.67 Lumbar nerve roots, however, can enhance in patients that have not had surgery and there is no correlation with radiculopathy.68 Postoperative discitis and osteomyelitis are difficult to diagnose on MRI in the first 6 months after back surgery. Asymptomatic patients can have an imaging appearance identical to infection with a disc and adjacent vertebrae that are dark on T1-weighted images, are bright on T2-weighted images, and demonstrating diffuse enhancement.

Vertebral compression fractures Vertebral compression fractures are defined by a loss of more than 15% of normal vertebral body height. Osteoporosis is the most common cause of compression fractures and occurs most often in post-

Fig. 6.24 Postoperative epidural scar. Axial pre(A) and postgadolinium (B) T1-weighted MRI images demonstrate enhancing epidural scar tissue surrounding the nerve root in the lateral recess (arrow).

menopausal women. Additional causes include metastases, multiple myeloma, leukemia, lymphoma, malignant and benign primary vertebral neoplasms, trauma, osteomyelitis, osteomalacia, osteitis cystica, and hemochromatosis. The World Health Organization defines osteoporosis as bone mineral density more than 2.5 standard deviations below the mean in a normal young adult population. Osteoporosis may be primary (associated with aging) or secondary to corticosteroids, hyperthyroidism, multiple myeloma, oophorectomy, male hypogonadism, paralysis, anticonvulsants, and alcoholism. Thirty percent of postmenopausal white women in the United States are estimated to have osteoporosis; this is associated with bone fragility and an increased risk of fractures. The cumulative lifetime risk of developing a symptomatic vertebral compression fracture is 16% in white women and 5% in white men.69,70 67

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The clinical presentation and course of osteoporotic compression fractures is quite varied. Although spine imaging often detects incidental, asymptomatic compression fractures in elderly people, painful compression fractures are quite common. It is estimated there more than 700 000 symptomatic osteoporotic compression fractures occur each year in the United States associated with 115 000 hospital admissions, 161 000 physician visits and five million days of restricted activity.71 The pain associated with osteoporotic compression fractures usually lasts 2 weeks to 3 months, but may persist indefinitely and can significantly impair physical, functional, and psychosocial performance. Many compression fractures are associated with severe pain that is refractory to conventional forms of therapy such as immobilization, bracing, and analgesics. Patients commonly experience a profoundly negative impact on the quality of their lives, and potentially life-threatening secondary medical problems can develop such as deep venous thrombosis, pulmonary embolism, pneumonia, constipation, decubitus ulcers, and depression. Vertebral compression fractures associated with benign and malignant tumors also frequently cause severe pain and disability that is refractory to conventional therapies. Percutaneous vertebroplasty is a relatively new and effective minimally invasive technique to treat painful compression fractures. The procedure was first performed in France in 1984; it consists of the percutaneous insertion of a relatively large-gauge bone needle into a vertebral body and the injection of a viscous liquid mixture of polymethyl methacrylate cement under fluoroscopic guidance. The procedure is usually performed for pain relief, but may also mechani68

Fig. 6.25 Postoperative disc herniation. Sagittal and axial T1-weighted MRI images pre- (A, B) and postgadolinium (C, D) demonstrate a postoperative disc herniation. The disc herniation (arrow in C and D) is surrounded by enhancing scar/granulation tissue (arrowheads in C) and impinges on the nerve root (arrowhead in D) in the lateral recess.

cally reinforce the pathologically weakened vertebra. Cement polymerization strengthens and stabilizes the vertebral body. Mechanical stabilization is thought be the primary mechanism for pain relief; however, neurotoxic effects from the methylmethacrylate monomer and heat from the exothermic polymerization reaction may also contribute by destroying nociceptive receptors and nerves. Vertebroplasty has successfully treated painful vertebral compression fractures caused by osteoporosis, hemangiomas, metastases, multiple myeloma, and lymphoma.72 Patients are typically screened with plain films to identify the presence, number, and positions of the vertebral compression fractures. If there are serial examinations, the interval development of new compression fractures can be determined and correlated with the clinical history. MRI usually is obtained next, to obtain more information about the age and etiology of the compression fractures, and also to exclude other causes for the patient’s symptoms. CT and bone scans are obtained in selected cases to answer specific questions. The MRI appearance of osteoporotic compression fractures varies with time. The bone marrow in a vertebra with an acute benign compression fracture has edema and inflammation that is dark on T1-weighted images and bright on STIR and T2-weighted images. This bone edema usually resolves in 4–6 weeks. The bone marrow signal intensity returns to normal with resolution of the bone edema and is bright on T1-weighted images reflecting fatty marrow.73,74 This return to normal-appearing bone marrow is diagnostic of a benign cause and excludes a malignant compression fracture.

Section 3: General Diagnostic Technique

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Fig. 6.26 Malignant compression fracture. T1-weighted (A), fat-suppressed T2-weighted (B), and fat-suppressed contrast-enhanced T1-weighted (C) sagittal lumbar spine MRI images demonstrate a malignant L4 compression fracture (arrows).

A malignant vertebral compression fracture is also dark on T1-weighted images and variably bright on T2-weighted images (Fig. 6.26). Unlike a benign compression fracture, the low signal intensity on T1-weighted images will only return to normal following radiation therapy. Benign and malignant compression fractures can look identical on MRI, and definitive diagnosis may require a biopsy; however, there are some distinguishing characteristics. As previously noted, the benign compression fracture marrow signal intensity usually returns to normal in about 6 weeks, while the malignant compression fracture marrow does not. A malignant compression fracture often has abnormal signal throughout the vertebra, and can have abnormal signal in the pedicles and the rest of the posterior elements. The abnormal signal in benign compression fractures usually does not involve the entire vertebral body or the posterior elements. Large paravertebral or epidural masses are common with malignant and uncommon with benign compression fractures.73,74 Patients who are referred for vertebroplasty often have multiple osteoporotic compression fractures of indeterminate ages with nonlocalizing physical examinations. Identifying the compression fractures that are responsible for the pain that will respond to vertebroplasty can be difficult. The presence of increased uptake on a bone scan in an osteoporotic compression fracture is a good predictor for a positive clinical response to vertebroplasty. Of 27 patients with 35 osteoporotic compression fractures that demonstrated increased activity on bone scan, 93% had a significant decrease in pain following vertebroplasty.75 All of the 14 patients evaluated for mobility had a significant improvement after vertebroplasty. The presence of bone edema on MRI can distinguish painful acute/subacute from asymptomatic chronic osteoporotic compression fractures and correlates with a clinical benefit from vertebroplasty.76 The sagittal STIR pulse sequence detects bone edema with the greatest sensitivity. T2-weighted FSE images are almost as sensitive. MRI can also demonstrate the fluid-filled cavity within a vertebra seen in Kümmel’s disease (vertebral body osteonecrosis) (Fig. 6.27), which responds well to vertebroplasty.77,78 Although CT is not used as commonly as plain films and MRI for the evaluation of vertebroplasty patients, it has roles. CT is useful to evaluate the integrity of the posterior bony cortex of a vertebra with a malig-

nant compression fracture. Large regions of posterior cortical destruction (Fig. 6.28) increase the risk of cement extravasation causing spinal cord or nerve root compression and are associated with higher vertebroplasty complication rates. Such cortical destruction is rare in osteoporotic compression fractures and occurs more commonly in cases of malignant compression fractures due to metastases. If the CT demonstrates this type of destruction the vertebroplasty technique can be modified or the procedure might not be performed. CT is the most accurate method to evaluate the distribution of the polymethyl methacrylate cement after a vertebroplasty, especially important in a patient with a new radiculopathy or myelopathy that may be due to extravasated cement.79

Arachnoiditis Arachnoiditis is a result of leptomeningeal inflammation that may be caused by any source of subarachnoid blood (surgery, trauma, ruptured arteriovenous malformation, and aneurysm), infection (tuberculous and bacterial meningitis), and other inflammatory disorders. Arachnoiditis used to be common following myelography with Pantopaque (iophendylate) but is rare with currently used nonionic contrast agents.80 Arachnoiditis can be the source of significant back pain and has been reported to cause 6–16% of the cases of failed back syndrome.81 The findings of arachnoiditis are variable and well seen on sagittal and axial T2-weighted FSE images, myelogram films, and postmyelography CT images. Obliteration of nerve root sleeves is an early finding. More severe cases display irregular clumping of the nerve roots (Fig. 6.29), distortion of the thecal sac and adhesion of the nerve roots to the thecal sac giving the ‘empty sac’ sign. Thoracic arachnoid cysts can occur. Enhancement is variable. Tuberculous arachnoiditis has a distinctive pattern with leptomeningeal thickening and nodules on the spinal cord and nerve roots (differential diagnosis: metastases, sarcoid).

Dural ectasia Dural ectasia is abnormal enlargement of the thecal sac or nerve root sleeves at any level but most commonly in the lumbosacral region. Causes include Marfan syndrome, Ehlers-Danlos syndrome, neurofibromatosis, and ankylosing spondylitis.82 Findings include scalloping 69

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Fig. 6.28 Posterior cortical destruction. Axial lumbar spine CT in bone window demonstrates a vertebral body metastasis with posterior cortical destruction (arrows).

of the posterior vertebral bodies (Fig. 6.30A), increased interpediculate distances (Fig. 6.30B), widened neural foramina, thinning of the cortex of the pedicles and lamina, and meningoceles.

Infection Spine infections, including discitis, osteomyelitis, and epidural abscess, are best detected and characterized by MRI.6 Bacteria that cause discitis are most often spread by hematogenous dissemination, followed by direct introduction during surgical procedures. The most common organism is Staphylococcus aureus. Pneumonia and urinary tract infections are typical sources. The infection spreads from the endplate into the disc and adjacent subchondral vertebral marrow. The clinical presentation is varied; an acute infection may cause severe back pain and fever, while an indolent infection may cause remarkably subtle symptoms. The lumbar spine is the most common site. Spinal cord and nerve root dysfunction may evolve as the infection progresses from either direct compression or septic thrombophlebitis. An elevated erythrocyte sedimentation rate and an elevated white blood cell count are usually present. Bacterial discitis and vertebral osteomyelitis is detected on MRI with 96% sensitivity, 93% sensitivity, and 94% accuracy.83 On MRI, the disc interspace and the adjacent vertebrae are dark on T1-weighted images, bright on T2-weighted images and enhance due to 70

Fig. 6.27 Avascular necrosis. Sagittal helical CT image (A) and sagittal fat-suppressed T2-weighted MRI image (B) demonstrate an air- and fluid-filled subchondral cavity (arrows) in the L4 vertebral body.

Fig. 6.29 Arachnoiditis. Axial CT-myelogram demonstrates clumping of the lumbar nerve roots (arrow) and a laminectomy defect.

edema and inflammation (Fig. 6.31).83,84 An enhancing paravertebral mass (phlegmon) or frank abscess may be present. Renal spondyloarthropathy can look similar but there is usually less edema and no clinical evidence of infection. Destruction of the endplates on plain films is an insensitive but relatively specific sign of infection. CT often demonstrates endplate irregularities and bony juxta-endplate sclerosis. The MRI findings can persist long after successful antibiotic therapy and do not reflect therapeutic failure. The MRI appearance of tuberculous osteomyelitis is variable and may be more suggestive of tumor than infection.85 Epidural abscesses are caused by direct extension of discitis/osteomyelitis and also by hematogenous dissemination. Intravenous drug abuse, immunosuppression, AIDS, endocarditis, pneumonia, and urinary tract infections are common settings. Patients present with fever, back pain, and tenderness. Neurological deficits can be due to mass effect or septic thrombophlebitis. On MRI, an epidural abscess is dark on T1-weighted images and bright on T2-weighted images. Enhancement can be diffuse (phlegmon) or peripheral (pus surrounded by an enhancing pseudocapsule) (Fig. 6.32). The abscess is positioned more frequently in the posterior epidural space than anterior. Facet synovitis may be sterile (inflammatory) or infectious. MRI can accurately diagnose pyogenic facet joint infection.86 Staphylococcus

Section 3: General Diagnostic Technique

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aureus is the most common organism. Most occur in the lumbar spine. An epidural abscess is associated in 25%. It is best seen on sagittal images. Fat-suppressed T2-weighted FSE images may show fluid in the synovial joint space and edema in the adjacent subcortical bone. The joint space may enhance on postgadolinium fat-suppressed T1weighted images. Biopsy may be necessary for definitive diagnosis.87

Rheumatoid arthritis Rheumatoid arthritis typically involves multiple joints in the upper and lower extremities. Involvement of the cervical spine is not uncommon; however, the thoracic and lumber spine are rarely affected. The craniocervical junction is the most vulnerable area of the spine

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Fig. 6.30 Dural ectasia associated with neurofibromatosis type 1. Sagittal T2-weighted thoracic spine MRI image (A) shows scalloping of posterior vertebral bodies (arrows). Anteroposterior thoracic spine plain film (B) demonstrates widening of the interpediculate distances (arrows).

and its involvement can range from virtually asymptomatic to disabling, which may require urgent surgery due to progressing neurological deficits and instability. Rheumatoid arthritis can cause atlantoaxial subluxation due to transverse ligament laxity as a result of synovial inflammation. The synovitis may evolve from a joint effusion into a fibrous pannus. Odontoid erosions occur frequently due to synovial inflammation between the dens and the atlas. Conventional radiographs are relatively insensitive to rheumatoid arthritis of the cervical spine. Bony erosions can be seen in atlas and axis. Atlantoaxial subluxation manifests as increase of anterior atlanto-odontoid distance, which is due to laxity and/or disruption of transverse ligament. Vertical and lateral subluxation is more difficult to detect on plain radiographs.88

Fig. 6.31 Discitis and osteomyelitis. Sagittal T2-weighted (A) and fat-suppressed contrastenhanced T1-weighted (B) thoracic spine MRI images demonstrate a destroyed, fluid-filled disc interspace with peripheral enhancement (arrows) as well as marked bone edema and enhancement in the adjacent vertebrae. 71

Part 1: General Principles

Fig. 6.32 Epidural abscess. Sagittal contrast-enhanced T1-weighted cervical spine MRI reveals a peripherally enhancing ventral epidural abscess (arrows) and prevertebral inflammation (arrowheads).

CT is the test of choice to evaluate for bony changes in rheumatoid arthritis of the cervical spine (Fig. 6.33). Imaging of rheumatoid arthritis reveals disc space narrowing, osseous irregularities, and erosions without osteophytes. Even small erosions can be seen with thin-section spiral CT. C1 and C2 are routinely involved (see Fig. 6.33A, B). The odontoid process is affected in 14–35% of patients with rheumatoid arthritis. Subchondral erosions can also be seen at other levels of the cervical spine involving the endplates and facet joints. Erosion and/or destruction of the spinous processes also can be present. Inflammatory facet arthropathy is not uncommonly seen. Osteophytes are not a feature of rheumatoid arthritis, although in elderly individuals rheumatoid arthritis and osteoarthritis often coexist. Sagittal and coronal reformatted images are useful to evaluate for vertical and lateral dislocation at the craniocervical junction, and can also demonstrate subluxations at lower levels, particularly at C3–4 and C4–5. Rheumatoid arthritis can cause significant narrowing of the spinal canal by pannus (Fig. 6.33C). Detection of pannus on CT can be augmented by the use of intravenous contrast, although the soft tissues are now usually evaluated by MRI.89 MRI is the best imaging test for visualization of inflammatory changes in the soft tissues, including the ligaments and the synovium. MRI signal characteristics and enhancement pattern can reliably distinguish different stages of pannus formation.

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Fig. 6.33 Rheumatoid arthritis. Sagittal (A) and axial (B) bone window CT images demonstrate erosions of the odontoid and anterior arch of C1. Axial soft tissue window CT image (C) demonstrates pannus (arrowheads) narrowing the spinal canal.

Section 3: General Diagnostic Technique

Hypervascular pannus is hyperintense on T2-weighted images, vividly enhances with gadolinium, and retains enhancement over 5–10 minutes. Hypovascular pannus demonstrates intermediate T2 signal and has moderate enhancement that mildly decreases over 5–10 minutes. Fibrous pannus is usually hypointense on T2-weighted images and demonstrates mild or absent enhancement. Nonenhanced T1-weighted images are not helpful as all types of pannus are hypointense.90 MRI also reveals mass effect on the spinal cord and medullocervical junction, including spinal canal stenosis and cord compression.

Ankylosing spondylitis Ankylosing spondylitis is an inflammatory spondyloarthropathy with a reported incidence of 1.4%; it occurs in young adults with a strong male predominance (4:1). More than 97% of patients are HLA-B27 positive. An inflammatory infiltrate of plasma cells and lymphocytes causes vascularization and ossification of ligamentous attachments to bone (enthesopathy) and inflammation of synovial and cartilaginous articulations. The sacroiliac joints are universally involved. This process in the outer anulus, ALL, and PLL results in multilevel vertebral fusion and ossification (syndesmophytes). The plain film appearance is called the ‘bamboo spine’ (Fig. 6.34A, B). The

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Fig. 6.34 Ankylosing spondylitis. AP (A) and lateral (B) plain films demonstrate a bamboo spine with syndesmophytes. A sagittal T1weighted MRI image (C), and sagittal (D), and axial (E) T2-weighted MRI images reveal abnormal marrow, dural ectasia, and arachnoiditis with the empty sac sign and clumping of nerve roots (arrows). 73

Part 1: General Principles

vertebrae lose their normal anterior convexity and appear squared. The upper and lower corners of the anterior vertebral body become sclerotic. Calcification of the discs is common. There is fusion of the facet and sacroiliac joints. On MRI, the vertebral bodies are dark on T1-weighted images, bright on T2-weighted images, and enhance (Fig. 6.34C, D). Calcified discs can be dark or bright on T1-weighted images. Spinal fractures, deformity, subluxation, rotatory instability, and stenosis occur.91,92 Stress fractures through the disc interspace with nonunion cause an unstable pseudoarthrosis. Destruction of the disc interspace with adjacent zones of bony sclerosis is evident. Ankylosing spondylitis is associated with arachnoiditis and dural ectasia (Fig. 6.34D, E).

Ossification of the posterior longitudinal ligament and diffuse idiopathic skeletal hyperostosis Ossification of the posterior longitudinal ligament (OPLL) is an inflammatory degenerative process associated with cervical spine degenerative disease that affects both men and women, usually in middle age.93 OPLL occurs in 50% of patients with diffuse idiopathic skeletal hyperostosis (DISH). OPLL can cause central spinal canal stenosis, compress the spinal cord, and cause myelopathy. CT with sagittal reconstructions accurately displays the extent and severity of the process (Fig. 6.35A, B). OPLL can be difficult to diagnose on MRI since the ossified ligament is dark on both T1- and T2-weighted images (Fig. 6.35C). OPLL may contain bone marrow that will change its MRI appearance. Deformity and compression of the spinal cord on sagittal T2-weighted images may suggest the diagnosis. The differential diagnosis of OPLL includes posterior osteophytes, calcified discs, and meningiomas. Differentiation of OPLL from posterior osteophytes is usually straightforward since osteophytes occur focally

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at the disc interspaces while OPLL is a continuous process along the posterior longitudinal ligament. Diffuse idiopathic skeletal hyperostosis (DISH), also known as Forestier disease, demonstrates exuberant calcification of the ALL without significant disc disease or ankylosis of the facet joints. Bony bridging of at least four contiguous vertebrae is characteristic. Hyperostosis also occurs at ligamentous and tendonous insertions, and juxta-articular ossifications are present.

Spondylolysis and spondylolisthesis Spondylolysis is defined as a fracture through the pars interarticularis (pars defect). The etiology of spondylolysis is unknown; stress fractures and congenital defects are considered possible causes. Spondylolysis is a common source of chronic back pain in children and young adults. Pars defects are readily demonstrated on plain films as a fracture through the neck of the ‘Scotty dog’ on the oblique view (see Fig. 6.1) and on CT on both axial and reconstructed sagittal images (Fig. 6.36A, B). Diagnosis of pars defects on MRI is more difficult.94 On sagittal T1-weighted images, a break in the bony cortex or the marrow signal of the pars interarticularis can be seen;95 however, 25% of pars defects are missed on MRI (Fig. 6.36C, D). Spondylolisthesis is anterior or posterior displacement (translation) of a vertebra relative to an adjacent vertebra. Anterolisthesis refers to anterior displacement of a vertebra relative to the adjacent caudal (inferior) vertebra while retrolisthesis refers to posterior displacement. Severity is graded by the percentage of the vertebral body that is displaced. Grade I is less than 25%, grade II is 25–50%, grade III is 50–75%, and grade IV is greater than 75%. A number of conditions that destabilize the posterior column can cause spondylolisthesis. These include congenital disorders (dysplastic and misoriented articular processes, kyphosis, spina bifida), spondylolisthesis,

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Fig. 6.35 OPLL. Sagittal (A) and axial (B) CT images and a sagittal T2-weighted MRI image (C) demonstrate ossification of the posterior longitudinal ligament (arrows). 74

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Fig. 6.36 Spondylolysis and spondylolisthesis. Sagittal (A) and axial (B) CT images, sagittal T1-weighted (C), and axial T2-weighted (D) MRI images demonstrate pars defects (arrows) and grade I anterolisthesis of L5 on S1.

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degenerative facet arthropathy, the surgically fused spine, trauma (pedicle fractures), and destructive processes (tumor, infection, osteoporosis, osteopetrosis). Spondylolisthesis frequently causes neural foraminal narrowing best evaluated on reconstructed sagittal CT images and sagittal T1weighted MRI images. The normal shape of the neural foramen is altered; the longest axis of the foramen changes from vertical to horizontal. The sagittal MRI can demonstrate foraminal stenosis, obliteration of foraminal fat, and nerve root compression and/or kinking. A fibrocartilaginous mass may be seen around the nonhealed pars fracture. A disc herniation is more common at the level above the spondylolisthesis than at the same level. The anterior displacement of the upper vertebra relative to the disc confers the artifactual appearance of a disc bulge or herniation (pseudobulge or herniation). Neither isthmic nor degenerative spondylolisthesis appears to be associated with instability or hypermobility when studied with kinematic MRI.96

Neoplastic disease

side. The mass forms a well-defined meniscus with the subarachnoid contrast on the myelogram radiographs. Intradural–intramedullary masses originate within the spinal cord. The spinal cord is expanded and the subarachnoid space is circumferentially narrowed. These include tumor (astrocytoma, ependymoma, metastases), syringohydromyelia, infection, and inflammatory/demyelinating lesions. The superior soft tissue contrast resolution of MRI has markedly enhanced the detection and characterization of neoplastic disease of the spinal cord and canal.2,6 The use of i.v. gadolinium contrast is essential since the large majority of tumors enhance while many inflammatory/demyelinating lesions do not.

Intramedullary neoplasms Intramedullary neoplasms usually expand the spinal cord, are of high signal intensity on T2-weighted images, and enhance. Ependymomas and astrocytomas are the most common primary spinal cord tumors.97,98

Technique

Ependymoma

Prior to MRI, myelography was the primary method to evaluate masses involving the spinal canal and spinal cord. On myelography, masses are differentiated into extradural, intradural–extramedullary, and intradural–intramedullary locations. Extradural masses arise from the disc (herniation), epidural space (infection, tumor), or vertebral body (osteophytes, benign and malignant tumors, retropulsed fracture fragments). The thecal sac and spinal cord are displaced away from the mass. Intradural–extramedullary masses arise within the thecal sac and outside the spinal cord. Meningiomas and nerve sheath tumors (neurofibroma and schwannoma) are the most common intradural–extramedullary masses. These enlarge the ipsilateral subarachnoid space and displace the spinal cord to the opposite

Ependymomas represent approximately one-half of spinal cord tumors and are the most common intramedullary tumor in adults, usually occurring in the third to fifth decade of life. They arise from the ependymal cells of the central canal. They are unencapsulated, benign, well-circumscribed, slowly growing tumors. Cervical and cervical–thoracic locations are most common. Ependymoma is the most common primary spinal cord neoplasm of the distal spinal cord, conus medullaris, and filum terminale (6.5% of all ependymomas) (Fig. 6.37). Myxopapillary ependymoma is a particular histological variant occurring in this region. These are mucin-containing tumors that can calcify or hemorrhage. These are often hyperintense on T1weighted images, likely due to a high mucin content.99 Ependymomas 75

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typically are iso- to hypointense on T1-weighted images, and hyperintense on T2-weighted images, usually with multinodular high signal intensity throughout the cord that may be focal (over several vertebrae) or diffuse (up to 15 vertebrae). They frequently hemorrhage and may contain dark areas on T2-weighted images representing hemosiderin from old bleeds. Sharply marginated regions of enhancement are typically seen; however, enhancement patterns can be quite varied.99 Most ependymomas have associated cysts that are usually not tumoral.

Astrocytoma Astrocytomas comprise approximately 40% of spinal cord tumors. They are the most common intramedullary tumor in children. In children, the tumors are grade I pilocytic astrocytomas with a good prognosis. Astrocytomas also occur in adults with a mean age of 29 years and are more common in men. In adults the tumors are usually lowgrade infiltrative astrocytomas with a poorer prognosis, and generally not resectable. The tumors extend on average over 7 vertebrae. They occur most commonly in the thoracic spinal cord. The tumors are iso- to hypointense on T1-weighted images, and hyperintense on T2weighted images (Fig. 6.38A). Uneven enhancement is usually present (Fig. 6.38B). Cysts (usually tumoral) and syrinxs can be associated.

Hemangioblastoma Hemangioblastoma is the third most common intramedullary tumor (1–7%). It is a vascular tumor that usually has solid and cystic components; however, 25% are entirely solid. The solid component typically enhances intensely. There is usually associated edema. The tumors can be eccentric and can appear extramedullary. Hemorrhage is common. Prominent vascular flow voids can be seen. Approximately one-third of patients with hemangiomas have von Hippel-Lindau syndrome. The hemangiomas can be multiple in these patients.

Cavernous malformation Spinal cord cavernous malformations are uncommon neoplastic vascular lesions. They have a strong female predominance, and usually 76

Fig. 6.37 Conus medullaris ependymoma. Sagittal T2-weighted (A) and contrast-enhanced T1-weighted (B) lumbar spine MRI images demonstrate a heterogeneous T2-hyperintense, contrast-enhancing conus mass.

present acutely in the fourth to sixth decade due to hemorrhage. MRI is the most sensitive diagnostic imaging study. The lesions appear similar to cavernous malformations in the brain and are typically rounded in shape with a mixed signal intensity core containing regions of T1 and T2 high signal intensity due to methemoglobin surrounded by a T2 low signal intensity rim of hemosiderin (Fig. 6.39). They are typically not visualized on spinal angiography (angiographically occult vascular malformation) although occasionally late pooling of contrast or abnormal draining veins can be demonstrated. Histologically proven intramedullary arteriovenous malformations can have the same clinical presentation and imaging characteristics.100

Other uncommon intramedullary tumors Less common intramedullary tumors include ganglioglioma/gangliocytoma and metastases. Ganglioglioma/gangliocytoma usually occurs in children and adolescents. The cervical spinal cord is the most common location. They typically display mixed signal intensity on T1-weighted images, high signal intensity on T2-weighted images, and patchy peripheral enhancement. A minority does not enhance. Prominent tumoral cysts are common. Intramedullary metastases are usually dark on T1-weighted images, bright on T2-weighted images, and demonstrate intense, homogeneous enhancement. There is usually marked edema surrounding the tumor.

Intradural–extramedullary neoplasms Meningioma Intradural–extramedullary neoplasms typically compress and displace the cord away from the tumor and enlarge the ipsilateral subarachnoid space next to the mass (Fig. 6.40). Meningiomas represent about 25% of spinal canal tumors. There is an association with neurofibromatosis type 2. They occur more frequently in women than men, most often in the thoracic spine. Meningiomas are well circumscribed and dural based. They are usually iso- to slightly hypointense on T1-weighted images and may be heterogeneous. The tumors are similar intensity or slightly hyperintense to the spinal cord on

Section 3: General Diagnostic Technique

A

Fig. 6.38 Spinal cord astrocytoma. Sagittal T2-weighted (A) and contrast-enhanced T1weighted (B) cervical spine MRI images reveal marked spinal cord expansion, pathologic heterogeneous T2 hyperintensity, and enhancement (arrows).

B

T2-weighted images. Intense, homogeneous enhancement is characteristic. Calcification can occur.

Nerve sheath tumors Nerve sheath tumors (schwannoma and neurofibroma) may be intradural–extramedullary, both intradural and extradural, or completely extradural. Schwannomas are associated with neurofibromatosis type 2. Neurofibromas are associated with neurofibromatosis type 1. Both types of tumors are usually isointense on T1-weighted images and hyperintense on T2-weighted images, and enhance. Combined intradural–extradural tumors often enlarge the neural foramen (Fig. 6.41) and can display a characteristic dumbbell shape.

Fig. 6.39 Spinal cord cavernoma. Axial T2-weighted gradient echo MRI image of the cervical spine reveals a typical peripherally T2-hypointense lesion with susceptibility effects caused by hemosiderin (arrow).

Schwannoma and neurofibroma are indistinguishable by MRI appearance, although solitary lesions are usually schwannomas, and schwannomas are more commonly associated with vascular changes, hemorrhage, cysts, and fatty degeneration.

Extradural tumors Metastatic disease The vertebrae are the most common location of metastatic disease in the spine. Most metastases begin in the vertebral body but they may grow through the pedicles into the posterior elements. The most common primary sources of vertebral metastases are breast, lung, renal, and prostate carcinomas. Leukemia, lymphoma, multiple myeloma, melanoma, and sarcomas also commonly involve the spine. Plain films and CT are relatively insensitive for the early detection of spine metastases. Most metastases are osteolytic and eventually cause a radiolucent geographic defect or a combined osteolytic and osteoblastic lesion. A relatively specific, but insensitive plain film finding is loss of a pedicle. Common osteoblastic metastases include prostate, breast, ovarian, and transitional cell carcinoma, lymphoma, and carcinoid. MRI is more sensitive than plain films and CT in detecting spinal metastatic disease.2,6 The T1-weighted acquisition is the most sensitive MRI pulse sequence. Tumor deposits are usually well circumscribed and darker than the normally bright adult fatty marrow on T1-weighted images see (Fig. 6.26A). On postgadolinium T1-weighted images, enhancing tumor can be equally bright as the 77

Part 1: General Principles

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surrounding normal fatty marrow and may be obscured.65 This pitfall can be avoided by obtaining nonenhanced T1-weighted images. Fat suppression on the postgadolinium images is also helpful (see Fig. 6.26C).65 Tumor contains more water than fatty marrow and usually is relatively bright on fat-suppressed T2-weighted images (see Fig. 6.26B). On non-fat suppressed T2-weighted images tumor and fatty marrow can have very similar signal intensities and can be difficult to distinguish. Osteoblastic metastases are dark on both T1- and T2-weighted images. Several criteria have been described for MRI and CT findings to distinguish benign and malignant compression fractures. Osteoporotic compression fractures are low signal intensity on T1-weighted images in the acute phase, but typically return to normal over the course of 4–6 weeks. Malignant compression fractures remain low signal intensity indefinitely unless treated with radiation therapy. Malignant compression fractures are more likely to have abnormal signal throughout the entire vertebra and the posterior elements are more commonly involved. Epidural masses are common with malignant and uncommon with benign compression fractures. Paravertebral masses are more

Fig. 6.41 Schwannoma. Axial cervical spine MRI image demonstrates an expansile hyperintense mass in the neural foramen (arrow).

78

Fig. 6.40 Meningioma. Sagittal T2-weighted (A) and contrast-enhanced T1-weighted (B) thoracic spine MRI images demonstrate a mildly T2 hyperintense, mildly enhancing intradural extramedullary mass (arrows).

common and typically larger with malignant compression fractures. On CT, benign compression fractures typically are not associated with cortical bone destruction while malignant compression fractures may be associated with destruction of a pedicle, cortical, or cancellous bone. Biopsy may be necessary for definitive diagnosis. CSF dissemination of tumor to the leptomeninges occurs in a number of childhood and adult malignancies. The leptomeningeal spread can be from drop metastases from a primary central nervous system (CNS) malignancy or from systemic metastatic disease. Diagnosis can be made both with MRI and myelography and postmyelography CT. On MRI the pial surface of the spinal cord can display nodular or linear enhancement and the contour of the cord can be irregular. Extensive covering of the pial surface has been called ‘sugar-coating’ (Fig. 6.42). Tumor nodules can be seen on nerve roots (‘Christmas balls’). Contrast-enhanced MRI detects leptomeningeal metastases in 50% of high-risk patients with initially negative CSF serology.101

Vertebral body hemangioma The vertebral body hemangioma is the most common benign tumor of the osseous spine. It is present in approximately 11% of population and multiple in 4%.102 The tumor is composed of adult-type blood vessels and is often an incidental finding on a CT or MRI scan performed for unrelated reasons. The tumor may be a focal lesion or fill the entire vertebral body and extend into the posterior elements. On plain films the typical incidental hemangioma has a characteristic radiographic appearance of prominent vertical striations within in vertebra that represent thickened bony trabeculae. These thickened bony trabeculae have a characteristic spotted appearance on axial CT images. The bony cortex is usually intact. MRI detects even small hemangiomas with great sensitivity. The typical hemangioma is bright on both T1- and T2-weighted images due to increased fat and water content. There is variable enhancement after gadolinium administration. A fat-suppressed T2-weighted image will differentiate a hemangioma from focal fatty replacement. An occasional hemangioma can appear hypointense on T1-weighted images and might be confused with another tumor such as a metastasis. In case of uncertainty, a CT can demonstrate the characteristic features of a hemangioma (Fig. 6.43C).

Section 3: General Diagnostic Technique

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Most symptomatic or aggressive hemangiomas are located in the thoracic spine.103 Neurological deficits are produced by large tumors that have epidural extension causing spinal canal stenosis or neural foraminal narrowing with resultant spinal cord or nerve root compression (Fig. 6.43A, B). The epidural component usually has low signal intensity on T1-weighted images and enhances with gadolinium (Fig. 6.43B). Hemangiomas also cause painful compression fractures (Fig. 6.43A, C). Painful compression fractures due to ver-

A

Fig. 6.42 Drop metastases from glioblastoma multiforme. Sagittal T2-weighted lumbar spine MRI image (A) demonstrates nodular tumor deposits in the cauda equina (arrows). Contrastenhanced T1-weighted lumbar spine image (B) shows diffuse, thickened enhancement of the pial surface of the conus (arrowheads), linear and nodular enhancement of the cauda equina, and thickened, enhancing lumbar nerve roots (arrows).

B

tebral hemangiomas have been successfully treated with percutaneous vertebroplasty.79 Aggressive hemangiomas have been successfully treated with percutaneous alcohol sclerotherapy.104

Osteochondroma Osteochondromas are relatively rare in the spine in comparison to the long tubular bones. They commonly involve the lumbar or thoracic spine; the cervical spine is least often affected.105 These benign tumors

C

Fig. 6.43 Aggressive spinal hemangioma. Sagittal fat-suppressed T2-weighted MRI image (A) demonstrates a hyperintense vertebral and epidural mass (arrows) and a superior endplate fracture. The vertebral, epidural (arrow), and paravertebral (arrowheads) mass enhances on an axial postgadolinium T1-weighted MRI image (B). Sagittal helical CT image (C) demonstrates a superior endplate fracture and thickened, vertically oriented trabeculae. 79

Part 1: General Principles

usually originate from the posterior elements, most commonly from the spinous process. A vertebral body origin is quite unusual. Symptoms are usually related to mass effect and compression of adjacent structures. Conventional radiographs demonstrate an exophytic lesion that has direct contiguity with cortex of the native bone with a broad or pedunculate attachment. CT shows similar findings but can delineate fibrous cap to better advantage. The lesion has a heterogeneous MRI appearance due to it mixed bony and cartilaginous content. The cartilaginous components are bright on T2-weighted images. The ossified components are dark on all pulse sequences. MRI can be useful to assess mass effect in cases of spinal canal compromise. An osteochondroma may occasionally undergo malignant degeneration into a chondrosarcoma. This is much more common in individuals with multiple lesions due to multiple hereditary exostosis disease. Features suspicious for malignant degeneration include new pain, rapid growth, lytic changes, and disappearance of calcifications that were previously present.106

Osteoid osteoma The spine is the second most common location for this benign lesion following the metaphyses of long tubular bones. Osteoid osteomas occur most often in the lumbar spine. They occur half as often in the cervical spine and rarely in the thoracic spine. The lesion is confined to the posterior elements 75% of the time. The lamina, articular processes, and pedicles represent the most typical sites of involvement.107 There is a 2:1 to 4:1 male to female predominance. They occur in adolescents and young adults, and are rarely seen after 30 years of age. Pain is the usual presenting symptom, classically described as occurring at night and relieved by aspirin. Unexplained focal pain in the region of the spine in a young individual without prior trauma should raise the possibility of an osteoid osteoma. Plain films can demonstrate a lytic lesion that can contain calcifications surrounded by sclerosis. Due to superimposition of different structures on plain films, a small lesion can easily be overlooked. In case of high clinical suspicion, a nuclear bone scan with SPECT imaging is a sensitive and cost-efficient way to make the diagnosis. If a focal area of increased radiotracer uptake is detected in the bony spine, targeted CT is performed to better characterize this finding. The CT typically reveals a well-defined focal hypodensity in the posterior elements measuring less than 1.5 cm in diameter representing the nidus. The nidus may contain internal calcifications and is usually surrounded by bony sclerosis. Administration of intravenous contrast results in avid, prompt enhancement due to hypervascularity within the nidus.108 MRI usually is not required, but if performed it demonstrates a heterogeneous, well-defined lesion. Hypointense foci on both T1- and T2-weighted sequences may be seen if calcifications are present. Marked enhancement with gadolinium defines the nidus.

Chordoma The chordoma is an uncommon, slowly growing, locally invasive bone tumor arising from primitive notochord cells. The tumor occurs most often in the clivus and the sacrum. The cervical spine is the next most common location. There is 2:1 male to female predominance. A chordoma can present at any age and there is no characteristic age peak.111 Although the chordoma is histologically benign, it may behave in a malignant fashion and can even metastasize. Metastases are uncommon in clival and sacral tumors, but are seen more often in vertebral chordomas. Conventional radiographs demonstrate a destructive osseous lesion with amorphous calcifications, which involves more then one vertebra in almost 50% of cases. CT is superior in demonstrating the bone destruction and calcified matrix.112 MRI is less sensitive for the bony details but can accurately depict epidural and paravertebral extension. MRI signal characteristics are non-specific. The tumor is usually hypo- or isointense on T1-weighted images and hyperintense on T2-weighted images. Heterogeneity of signal may be due to calcifications, cystic changes, and prior hemorrhage.113

Giant cell tumor Giant cell tumor rarely occurs in the spine except for the sacrum. On plain films the tumor appears as a lytic, expansile mass with a thinned bony cortex. CT is non-specific and reveals an expansile, hypodense mass usually lacking internal calcifications. The MRI findings are also non-specific. The tumor typically is hypointense on T1-weighted images, hyperintense on T2-weighted images, and enhances with gadolinium. Occasionally, the tumor may aggressively invade the surrounding soft tissues, mimicking a malignant neoplasm. MRI is the preferable imaging modality to assess extension into the soft tissues.114

Aneurysmal bone cyst Aneurysmal bone cyst (ABC) is a benign osseous lesion usually diagnosed before 20 years of age. There is no clear sex predilection. The spine is a relatively common location. The typical presenting complaint is pain. On occasion, patients present with findings caused by spinal cord or nerve root compression. The posterior elements are involved in the majority of cases; however, involvement of the vertebral body is also common (Fig. 6.44). Less than 25% of the lesions extend into paraspinal soft tissues. Plain films show an expansile lytic lesion with a thinned cortex; sometimes septations can be detected.

Osteoblastoma The osteoblastoma is histologically similar to osteoid osteoma but is larger in size; the tumor nidus measures more than 1.5 cm in diameter. It is a rare benign bone lesion with clear predilection for the spine where it routinely involves the posterior elements, most commonly the spinous process.108 It may occur in infants to the elderly with a 2:1 male to female predominance. Plain films usually demonstrate an expansile, well-defined lytic mass causing thinning of the cortex. Cortical destruction occurs fairly often. Dense sclerotic margins can occasionally be seen. Radiographic features suggest malignancy in 12% of the cases. The primary differential diagnosis is osteosarcoma.109,110 CT will show similar findings. MRI signal characteristics are non-specific. Heterogeneous signal intensity is usually observed due to the presence of calcifications and intratumoral blood products. Tumor extension within the spinal canal and paraspinal soft tissues is better defined on MRI. 80

Fig. 6.44 Aneurysmal bone cyst. Sagittal T2-weighted thoracic spine MRI reveals a multiloculated, hyperintense, expansile mass in the posterior elements and in the vertebral body.

Section 3: General Diagnostic Technique

CT demonstrates the same findings but can also demonstrate any soft tissue extension. Septations and a multilocular appearance may be evident on CT; fluid levels sometimes can be seen in several compartments, which is highly suggestive of an ABC. MRI more readily demonstrates the septations and multiple fluid levels of different signal intensities due to presence of blood products of different age. These findings correlate well with the histopathologic composition, which consists of several cavernous spaces filled with blood products. MRI often demonstrates a thin, dark rim around the lesion on T1-weighted images. Enhancement of the septae after gadolinium administration is generally seen.115

Osteosarcoma Primary osteosarcoma of the spine is rare; although overall it is the most common primary malignant neoplasm of the bone. It is usually diagnosed in adolescents and young adults. There is approximately a 2:1 male predilection.116 Osteosarcoma of the spine has non-specific appearances on all imaging studies. Plain radiographs show a lytic or mixed lytic/sclerotic lesion sometimes with disruption of cortex. CT can better delineate bony changes including cortical interruption as well as calcified bony matrix and periosteal reaction if present.117 MRI usually demonstrates a heterogeneous mass that is hypointense on T1weighted and predominantly hyperintense on T2-weighted images. The tumor enhances after gadolinium administration. Extension into the spinal canal and paravertebral soft tissues can be appreciated on MRI.118 Metastatic disease to the spine from osteosarcoma elsewhere in the body is much more common than primary vertebral osteosarcoma.

Chondrosarcoma Chondrosarcoma is a malignant bone neoplasm arising from cartilage. The majority of cases involve middle-aged individuals. Males are involved two times more often than females. Chondrosarcoma can arise as primary lesion or as a result of malignant transformation of a benign cartilage-containing tumor such as an osteochondroma or enchondroma. The spine is rarely a primary site of chondrosarcoma. The cervical spine and cervicothoracic junction are involved in about 40% of cases. Conventional radiographs show a lytic destructive lesion often containing calcified matrix. Radiographic differentiation from osteosarcoma can be difficult. CT is excellent for depiction of bony details, cortical breakthrough, and nature of the calcifications. Soft tissue extension can be seen on CT, but MRI is the best imaging modality to assess paraspinal and epidural involvement. The tumor usually appears as a heterogeneous mass predominantly hypointense on T1-weighted and hyperintense on T2-weighted images. Intratumoral calcifications and blood products from prior hemorrhage contribute to heterogeneity. Enhancement with gadolinium is commonly present.

Ewing’s sarcoma Ewing’s sarcoma is a primary bone malignancy predominantly affecting children and young adults. Spine involvement is rare, but spinal metastases from the distant tumor in the long or flat bones are quite common.119,120 Plain radiographs demonstrate lytic changes, often permiative destruction, and cortical disruption. Periosteal reaction is commonly present, sometimes with characteristic ‘onion peel’ appearance. CT can show the same findings to better advantage plus presence of soft tissue mass. MRI can excellently demonstrate extent of the tumor within the bone and surrounding soft tissues as well as epidural disease, but signal characteristics are quite non-specific: hypointense on T1-weighted images and heterogeneous but predomi-

nantly hyperintense on T2-weighted images with enhancement after gadolinium administration.121

Leukemia Leukemia is the most common malignancy in children; however, adults of different ages are also commonly affected. Acute lymphoblastic leukemia is predominant in children and constitutes about 80% of all cases.122 Imaging studies, plain radiographs, and CT demonstrate osteopenia/osteoporosis throughout the spine, sometimes with compression fractures. Extreme compression deformity of the vertebral body (vertebra plana) sometimes can be seen. Lucent bands within the vertebrae may be present. Sclerotic foci occasionally can be noted.123 MRI clearly demonstrates diffuse bone marrow signal abnormality, dark on T1- and bright on T2-weighted images, due to the replacement of fatty bone marrow by leukemic cells. Enhancement with gadolinium is a common feature.124 An unusual presentation of myelogenous leukemia (chloroma) can occur in the spine as an expansile mass often extending into the soft tissues and typically isointense on T1-weighted images.

Lymphoma Primary non-Hodgkin’s lymphoma can involve the spine, but metastatic lesions from primary lymphoma elsewhere in the body are much more common. Non-Hodgkin’s lymphoma most commonly occurs in middle-aged and elderly patients. It is two times more common in men. In primary spinal lymphoma plain radiographs usually demonstrate lytic or permiative bone destruction, though occasionally sclerotic areas may be seen. CT findings are concordant with plain films. MRI typically shows T1 hypointensity within the involved bone marrow. The T2-weighted images can demonstrate slightly hyperintense, isointense, or even hypointense signal characteristics as in other hypercellular tumors.125

Ganglioneuroma, ganglioneuroblastoma and neuroblastoma Ganglioneuroma, ganglioneuroblastoma, and neuroblastoma constitute a group of tumors originating from primitive neural crest tumors and differ by degree of cell differentiation, ganglioneuroma being the most benign. These tumors are seen almost exclusively in children. Adrenal origin is most common, followed by paraspinal tumors arising from the sympathetic chain ganglia. The cervical spine is affected much less commonly than lumbar and thoracic spine.126 Because of their paraspinal location, these tumors can grow through the neural foramina into the spinal canal, causing impingement on the thecal sac, and sometimes grow into the epidural space. Plain radiographs can demonstrate a paraspinal mass. Several radiographic features are suggestive of tumor extension into the spinal canal through a neural foramen, including widening of the neural foramen, erosion of the pedicle, and widening of the spinal canal. Other radiographic findings include thinning and scalloping of the ribs, widening of the intercostal distance, and scalloping of the vertebral body. CT provides additional information regarding the bony changes and also demonstrates the tumor and its relationship with adjacent structures. Extension of the tumor into the spinal canal can be seen on CT, but differentiation of the tumor from spinal cord can be difficult. MRI is best to evaluate for tumor extension into the spinal canal and epidural space and is crucial for surgical planning. Neuroblastoma is usually of low signal intensity on T1-weighted images and low to intermediate signal intensity on T2-weighted images because of its hypercellularity and low water content. Heterogeneity may be seen due to areas of necrosis, hemorrhage, and intratumoral calcifications. These tumors usually enhance after gadolinium administration. The spinal cord 81

Part 1: General Principles

may have abnormal signal when compressed by tumor within the spinal canal.127

based on the clinical course of disease. ADEM is a monophasic illness while MS typically has recurrent episodes.

Multiple sclerosis

Sarcoidosis

Multiple sclerosis (MS) is a demyelinating disease of the CNS that most commonly affects young to middle-aged adults with a female predominance, but it can occur at any age and occasionally develops in children and in the elderly. The brain is the most commonly affected site, often accompanied by spinal lesions. Isolated involvement of the spinal cord occurs in 5–24% of cases.128–130 There is no direct correlation between the radiographic appearance of MS and the clinical condition of the patient. More then 50% of detected spinal cord lesions are located in the cervical spine. A single lesion is visualized more commonly than multiple plaques.131 The typical MS plaque in the spinal cord is peripherally located, involves both gray and white matter and spans less then 2 vertebral bodies in its vertical extent. Expansion or atrophy of the spinal cord is seen in minority of cases. T2-weighted sequences are superior for detection of MS lesions. Unenhanced T1-weighted sequences are not sensitive for MS plaques and usually appear normal. T2-weighted images demonstrated a hyperintense lesion eccentrically located within the cord (Fig. 6.45A). An FSE T2-weighted pulse sequence is almost as sensitive as a conventional T2-weighted spin echo sequence.132 Fast STIR images can sometimes detect additional lesions not clearly seen other sequences.133 Approximately 56% of spinal cord plaques seen on MRI enhance after gadolinium contrast administration (Fig. 6.45B).131

Acute disseminated encephalomyelitis Acute disseminated encephalomyelitis (ADEM) is an acute monophasic CNS inflammatory demyelinating process that usually follows a viral infection or a vaccination, although sometimes the underlying etiology (possibly a subclinical infection) cannot be identified. The brain is affected much more commonly than the spinal cord. Spinal cord symptoms usually manifest as an acute transverse myelitis. On MRI, the spinal cord lesions are undistinguishable from MS plaques. The lesions are bright on T2-weighted images, commonly enhance with gadolinium, and can cause cord expansion. T1-weighted images usually are normal.134 Differentiation between MS and ADEM is

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B

Sarcoidosis is granulomatous disease of unknown etiology, which can affect almost any organ or system. The lungs are the most commonly affected sites, although patients often remain asymptomatic when lung involvement is detected on a chest X-ray performed for unrelated reasons. CNS involvement (neurosarcoidosis) is present in approximately 5% of patients. Neurosarcoidosis is a great mimicker, as it can involve both the brain and its coverings with different radiographic presentations. Primary involvement of the spinal cord is rare.135 Only 6–8% of patients with neurosarcoidosis have spinal cord involvement, most commonly in the cervical region. Nodules may be present on the pial surface mimicking tumor deposits. Intramedullary lesions are usually bright on T2-weighted images with patchy enhancement postgadolinium and commonly associated with focal expansion of the cord. Pial enhancement is often present and in the appropriate clinical setting can help establish a diagnosis.136

Behçet’s syndrome Behçet’s syndrome is uncommon disease characterized by recurrent ulcerations of the oral and genital mucosa, uveitis, and iridocyclitis. Involvement of CNS is present in less then 50% of cases and occasionally can be the only manifestation of disease. Involvement of spinal cord is less common than the brain and usually demonstrates non-specific T2-hyperintense intramedullary lesions that are not visible on T1-weighted images; some lesions may enhance with gadolinium. Focal cord expansion or atrophy can be present depending on chronicity of the process.137

Systemic lupus erythematosus Systemic lupus erythematosus (SLE) can affect almost any organ or system and the CNS is not an exception. SLE is 8 times more common in females. Transverse myelitis is a rare complication of SLE. Transverse myelitis usually occurs in patients with positive antiphospholipid antibodies. Radiologic findings in SLE-induced transverse myelitis are non-specific and include bright signal abnormality within the spinal cord on T2-weighted sequences with possible cord expansion and enhancement.138

Fig. 6.45 Spinal cord multiple sclerosis. Sagittal T2-weighted (A) and contrast-enhanced T1-weighted (B) cervical spine MRI images reveal an eccentric T2 hyperintense MS plaque with peripheral curvilinear enhancement (arrows).

Section 3: General Diagnostic Technique

Radiation myelopathy Radiation myelopathy is an uncommon complication of radiation therapy. It usually occurs when a significant radiation dose is delivered to the structures adjacent to the spinal cord, and the spinal cord cannot be excluded from the radiation port; the most typical example is a radiation therapy for a nasopharyngeal carcinoma. There are two distinctive time peaks for development of radiation myelopathy, 12–14 months and 24–28 months after the radiation treatment. A larger radiation dose leads to earlier development of clinical symptoms.139 There are distinct histologic categories of radiation-induced spinal cord abnormalities, including white matter parenchymal lesions (type 1), primary vascular lesions (type 2), and a combination of both (type 3). White matter abnormalities unusually demonstrate demyelination, while vascular lesions are characterized by hyalinization or fibrinoid necrosis of vessel walls.140 In the acute phase of postradiation myelopathy there is spinal cord edema, which appears hypointense on T1-weighted and hyperintense on T2-weighted images. Areas of necrosis may be seen in severe radiation injury. Spinal cord expansion and enhancement with gadolinium may be present that sometimes has an appearance of intramedullary neoplasm. Occasionally there is extension of the signal abnormality above and below the level of radiation exposure, which may be related to propagation of extravasated fluid along the white matter tracts. In the chronic phase the signal abnormalities may reverse and be replaced by cord atrophy.139

Gout The spine is much less commonly involved with gout than the appendicular skeleton. Spinal involvement usually occurs in long-standing disease. Any area of the spine can be affected. Plain films are not sensitive for detecting gout in the spine. CT can demonstrate bony changes including erosions and soft tissue calcifications. MRI better visualizes gouty tophi. The tophi are low to intermediate signal intensity on T1-weighted images and heterogeneous, predominantly hyperintense signal intensity on T2-weighted images. The tophi contain small, discrete, dark areas on all pulse sequences. Diffuse or peripheral enhancement is seen. The tophi are typically juxtaarticular in location associated with joint erosions.141

Syringohydromyelia Syringohydromyelia refers to CSF-filled cavities within the spinal cord (Fig. 6.46). Cystic dilatation of the central canal is called hydromyelia, whereas fluid cavities within the cord parenchyma are called syringomyelia. Since it is often difficult to make this distinction on the basis of the imaging appearance, the general term syringohydromyelia (syrinx) is often used to include all CSF-containing cystic cavities within the spinal cord. Hydromyelia most commonly occurs in association with congenital malformations, most commonly the Chiari malformations. Other causes include narrowing of the foramen magnum secondary to achondroplasia and tumor. Syringomyelia can be caused by intramedullary tumors, trauma, ischemia, and arachnoiditis or may be idiopathic. On MRI, syringohydromyelia appears as a cystic intramedullary collection that usually has CSF signal intensity on all pulse sequences (Fig. 6.46). A high protein concentration can increase the signal intensity on T1-weighted images. Benign syringes are typically fusiform in shape, with tapered proximal and distal margins. Tumor syringes are frequently more rounded or oval in shape. The cavities can be multiple and can be incompletely septated, appearing beaded (Fig. 6.46). Gliotic changes may be present at the ends of the syrinx. Gadoliniumenhanced images are essential to look for any underlying tumor.142

Fig. 6.46 Syringohydromyelia. Sagittal T2-weighted thoracic spine MRI reveals extensive syringohydromyelia.

Neurenteric cyst The neurenteric cyst (enterogenous cyst) is caused by inclusion of endodermal elements in the spinal canal during embryogenesis. Most are intradural-extramedullary in location although rare intramedullary neurenteric cysts occur. They are typically positioned ventral or ventrolateral to the spinal cord with variable dural attachment. There may be communication with an extraspinal component. Vertebral anomalies are often associated. On MRI, a smooth unilocular CSF signal intensity cyst is typically seen ventral to the cord, possibly displacing and compressing it. High protein concentration in the cyst may increase the signal on T1-weighted images. The neurenteric cyst does not enhance, distinguishing it from a neoplasm.143

Arachnoid cyst Spinal arachnoid cysts are rare causes of spinal cord or nerve root compression. The cysts may be intradural or extradural in location; intradural cysts are less common. Both forms can present with back pain, sensory changes, weakness, and bowel or bladder dysfunction. The severity of symptoms often varies dramatically with changes in posture. A fluctuating clinical course with remissions and exacerbations is common, and can be confused with multiple sclerosis.144,145 Intradural spinal arachnoid cysts affect men and women equally, usually presenting in the third to fifth decade. The majority (80%) 83

Part 1: General Principles

are located in the thoracic spine, typically posterior to the spinal cord. They may be single or multiple. A number of etiologies have been proposed, including congenital, inflammation (arachnoiditis), and previous surgery or trauma. Plain films are usually normal. On myelography and postmyelography CT the cysts may demonstrate immediate filling with contrast, delayed filling (12–24 hours), or may never fill. Cysts that fill immediately may be difficult to visualize. On MRI, the cysts are isointense to CSF on all pulse sequences and can be difficult to discriminate from the normal subarachnoid space. Absence of pulsation artifact within the cyst may help identify it. Sagittal views can show anterior displacement of the spinal cord with possible flattening, and widening of the posterior CSF space (Fig. 6.47).144 Extradural arachnoid cysts are the result of a congenital defect in the dura through which the arachnoid membrane herniates. These cysts have a connection (pedicle) with the subarachnoid space. They occur most often in the mid- to lower thoracic spine and less commonly in the lumbar spine lying posterior or posterolateral to the thecal sac. There is a 2:1 male predominance; they usually present in the second decade. Plain films typically show widening and erosion of the spinal canal, erosion of pedicles, foraminal enlargement, and vertebral body scalloping. On myelography and postmyelography CT there is an extradural mass that fills with contrast. If the connecting pedicle is narrow the filling may be delayed. MRI demonstrates an extradural mass posterior or posterolateral to the thecal sac that is isointense to CSF on all pulse sequences. The thecal sac is displaced anteriorly and compressed. The cyst abuts the epidural fat at the cranial and caudal margins.145

Dermoid and epidermoid cysts Dermoid and epidermoid cysts are rare spinal tumors that result from inclusion of ectodermal cells during neural tube closure between the third and fifth weeks of embryogenesis. They can also result from implantation of cells during lumbar puncture and surgery. Epidermal cells line the wall of epidermoid cysts while dermoids also contain

other dermal components including hair follicles, sebaceous and sweat glands. Most of these cysts are intradural-extramedullary in location; they occur most commonly in the lumbar spine. Their MRI appearance is variable. Dermoids typically are bright on T1-weighted images due to fatty elements and are heterogeneous in appearance. Epidermoids are often iso- to hyperintense to CSF on T1-weighted images and are variably iso- to hyperintense to CSF on T2-weighted images. MRI cannot reliably differentiate between dermoid and epidermoid cysts.142,146

Tarlov (perineural) cysts Tarlov or perineural cysts are nerve root lesions that occur most frequently in the sacrum. Tarlov first described them in 1938. The cysts arise from the junction of the dorsal ganglion and nerve root between the endoneurium and perineurium. Possible etiologies include increased hydrostatic pressure and trauma. Most are asymptomatic and are incidentally detected, although symptomatic Tarlov cysts occur rarely. On myelography and postmyelography CT there is delayed filling of the cyst with contrast reflecting the absence of a direct connection with the subarachnoid space; this delayed filling differentiates the Tarlov cyst from a meningeal diverticulum. Sacral foramina are enlarged on plain films and CT. The cysts are isointense to CSF on all MRI pulse sequences. Patients with neurological deficits related to Tarlov cysts larger than 1.5 cm in diameter may benefit from surgical resection of the cyst wall.147

Transdural spinal cord herniation Transdural spinal cord herniation is rare and may occur spontaneously, after surgery, or following trauma. Patients can present with myelopathy, radiculopathy, sensory deficits, and Brown-Sequard syndrome. MRI demonstrates a locally displaced spinal cord with a dilated subarachnoid space opposite the herniation. Associated intramedullary high signal on T2-weighted images, a vertebral body nuclear trail sign, and syringohydromyelia have been reported.148 The imaging appearance of a transdural spinal cord herniation can be confused with an arachnoid cyst.

Spinal vascular lesions

Fig. 6.47 Spinal arachnoid cyst. Sagittal T2-weighted thoracic spine MRI images demonstrate a CSF intensity expansile cystic mass dorsal to the spinal cord remodeling the posterior elements. 84

Spinal vascular lesions can be categorized into vascular neoplasms (hemangioblastoma, cavernous malformation), aneurysms, and arteriovenous lesions. Varied nomenclatures for arteriovenous lesions have been proposed. Spinal vascular malformations have been divided into type I (spinal dural arteriovenous fistula), type II (intramedullary arteriovenous malformation), type III (combined intradural and extradural or juvenile arteriovenous malformation), and type IV (spinal cord arteriovenous fistula). A more recent modified classification scheme divides these arteriovenous lesions into arteriovenous fistulas (direct arteriovenous connection without an intervening nidus) and arteriovenous malformations (containing a vascular nidus), with subdivisions of these broad categories. Arteriovenous fistulas are subdivided into extradural, intradural-ventral, and intradural-dorsal types. Arteriovenous malformations are subdivided into extradural-intradural and intradural types. The intradural arteriovenous malformations are further categorized as intramedullary compact, intramedullary diffuse and conus medullaris arteriovenous malformations.149 The spinal dural arteriovenous fistula (type I arteriovenous malformation, intradural dorsal arteriovenous fistula) is the most common spinal vascular malformation and most controversial in terms of etiology, pathophysiology, diagnosis, and treatment.149 A fistula forms in a spinal dural nerve root sleeve supplied by a branch of the corresponding radiculomedullary artery with arterialized venous drainage into the coronal venous plexus surrounding the spinal cord. Lower thoracic

Section 3: General Diagnostic Technique

and upper lumbar nerve root sleeves are the most common locations, although the fistula can form in any spinal nerve root sleeve. Multiple feeding arteries can occur. This lesion typically presents in the fifth to sixth decade of life with a strong (>5:1) male predominance and is often associated with intervertebral osteochondrosis, suggesting it is acquired. Venous hypertension induced in the coronal venous plexus induces progressive myelopathy (spinal cord edema, ischemia, and eventual infarction) known as the Foix-Alajouanine syndrome. Clinically, these patients typically present with an insidious, slowly progressive myelopathy that results in severe disability if not treated by endovascular or surgical obliteration. Neurological deterioration is usually not reversible, so an expedient diagnosis is essential. This diagnosis can be challenging since the clinical presentation can mimic other spine disorders such as degenerative disc disease and the imaging findings can be subtle. On MRI, the spinal cord can be normal in size or enlarged. Intramedullary high signal intensity on T2-weighted images is typically but not invariably visible (Fig. 6.48A). Peripheral T2-weighted hypointensity in the spinal cord can be seen and may increase the specificity for the diagnosis of venous hypertension.150 Prominent vessels along the dorsal aspect of the spinal cord are usually but not always visible (Fig. 6.48A, B). These vessels and the spinal cord can enhance (Fig. 6.48B). All patients with an otherwise unexplained progressive myelopathy and any suggestive MRI findings should undergo a comprehensive spinal angiogram that includes all intercostal and lumbar segmental arteries, and the subclavian, vertebral, thyrocervical, costocervical, median sacral, and internal iliac arteries.

A

B

Intramedullary spinal cord arteriovenous malformations (type II arteriovenous malformations) are supplied by branches of the anterior and posterior spinal arteries.149 There is an intraparenchymal nidus (compact or diffuse) drained by the spinal veins. The angioarchitecture is similar to brain arteriovenous malformations. Intranidal or feeding artery aneurysms may be present. These lesions usually present acutely secondary to intraparenchymal hemorrhage. Compression-induced myelopathy and progressive myelopathy due to vascular steal also occur. Diagnosis on MRI is usually straightforward. Prominent, tortuous feeding and draining vessels and a vascular nidus that contain flow voids and enhancement are visible. Conventional angiography is usually necessary for complete characterization. Extradural-intradural arteriovenous malformations (juvenile, metameric, type III arteriovenous malformations) are rare lesions that do not respect tissue boundaries and typically involve the spinal cord, vertebral body, and extraspinal structures.149 They usually become symptomatic during childhood or adolescence and require a multidisciplinary approach to treatment, and have a poor prognosis. Extensive involvement of the spinal cord, spine, and surrounding structures is typically seen on MRI. The spinal cord arteriovenous fistula (type IV arteriovenous malformation) is an intradural ventral arteriovenous fistula located on the anterior pial surface comprised of a direct arteriovenous connection involving the anterior spinal artery and an enlarged venous network.149 Clinical presentations include progressive myelopathy and acute subarachnoid hemorrhage. MRI demonstrates prominent pial vessels with flow voids without a parenchymal nidus.

Fig. 6.48 Spinal dural fistula. Sagittal T2-weighted (A) and contrast-enhanced T1-weighted (B) thoracic spine MRI images demonstrate multiple serpiginous tubular T2 flow voids with enhancement dorsal to the spinal cord consistent with pathologically enlarged perimedullary veins (arrows), and thoracic spinal cord T2-hyerintensity and enhancement caused by venous hypertension and interstitial edema (arrowheads). 85

Part 1: General Principles

SUMMARY MRI is the preeminent imaging modality for evaluation of spinal disorders; however, there remain important roles for plain films, CT, and myelography with postmyelography CT. Standardized nomenclature promises to improve communications between the physicians interpreting imaging examinations and those caring for the patients. Correlation of the imaging findings with the clinical presentation is essential.

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138. Campi A, Filippi M, Comi G, et al. Recurrent acute transverse myelopathy associated with anticardiolipin antibodies. Am J Neuroradiol 1998; 19(4):781–786. 139. Wang PY, Shen WC, Jan JS. MR imaging in radiation myelopathy. Am J Neuroradiol 1992; 13(4):1049–1055; discussion 1056–1058. 140. Schultheiss TE, Stephens LC, Maor MH. Analysis of the histopathology of radiation myelopathy. Int J Radiat Oncol Biol Phys 1988; 14(1):27–32. 141. Hsu CY, Shih TT, Huang KM, et al. Tophaceous gout of the spine: MR imaging features. Clin Radiol 2002; 57(10):919–925. 142. Evans A, Stoodley N, Halpin S. Magnetic resonance imaging of intraspinal cystic lesions: a pictorial review. Current Problems in Diagnostic Radiology 2002; 31(3):79–94. 143. Brooks BS, Duvall ER, el Gammal T, et al. Neuroimaging features of neurenteric cysts: analysis of nine cases and review of the literature. Am J Neuroradiol 1993; 14(3):735–746. 144. Abou-Fakhr FS, Kanaan SV, Youness FM, et al. Thoracic spinal intradural arachnoid cyst: report of two cases and review of literature. Eur Radiol 2002; 12(4):877– 882.

124. Daffner RH, Lupetin AR, Dash N, et al. MRI in the detection of malignant infiltration of bone marrow. Am J Roentgenol 1986; 146(2):353–358.

145. Rimmelin A, Clouet PL, Salatino S, et al. Imaging of thoracic and lumbar spinal extradural arachnoid cysts: report of two cases. Neuroradiology 1997; 39(3):203– 206.

125. Weaver GR, Sandler MP. Increased sensitivity of magnetic resonance imaging compared to radionuclide bone scintigraphy in the detection of lymphoma of the spine. Clin Nuclear Med 1987; 12(4):333–334.

146. Gupta S, Gupta RK, Gujral RB, et al. Signal intensity patterns in intraspinal dermoids and epidermoids on MR imaging. Clin Radiol 1993; 48(6):405–413.

126. Punt J, Pritchard J, Pincott JR, et al. Neuroblastoma: a review of 21 cases presenting with spinal cord compression. Cancer 1980; 45(12):3095–3101.

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137. Morrissey SP, Miller DH, Kendall BE, et al. The significance of brain magnetic resonance imaging abnormalities at presentation with clinically isolated syndromes suggestive of multiple sclerosis. A 5-year follow-up study. Brain 1993; 116(Pt 1):135–146.

147. Voyadzis JM, Bhargava P, Henderson FC. Tarlov cysts: a study of 10 cases with review of the literature [see comment]. J Neurosurg 2001; 95(1 Suppl):25–32.

127. Siegel MJ, Jamroz GA, Glazer HS, et al. MR imaging of intraspinal extension of neuroblastoma. JComput Assist Tomogr 1986; 10(4):593–595.

148. Watters MR, Stears JC, Osborn AG, et al. Transdural spinal cord herniation: imaging and clinical spectra [see comment]. Am J Neuroradiol 1998; 19(7):1337– 1344.

128. Honig LS, Sheremata WA. Magnetic resonance imaging of spinal cord lesions in multiple sclerosis. J Neurol Neurosurg Psychiatr 1989; 52(4):459–466.

149. Spetzler RF, Detwiler PW, Riina HA, et al. Modified classification of spinal cord vascular lesions [see comment]. J Neurosurg 2002; 96(2 Suppl):145–156.

129. Tartaglino LM, Friedman DP, Flanders AE, et al. Multiple sclerosis in the spinal cord: MR appearance and correlation with clinical parameters. Radiology 1995; 195(3):725–732.

150. Hurst RW, Grossman RI. Peripheral spinal cord hypointensity on T2-weighted MR images: a reliable imaging sign of venous hypertensive myelopathy [see comment]. Am J Neuroradiol 2000; 21(4):781–786.

PART 1

GENERAL PRINCIPLES

Section 3

General Diagnostic Technique

CHAPTER

Nuclear Medicine Imaging With an Emphasis on Spinal Infections

7

Christophe Van de Wiele

INTRODUCTION Nuclear medicine imaging assesses pathophysiologic processes such as regional perfusion, permeability, accumulation of white blood cells, bone turnover, etc. These processes precede morphological changes as assessed by radiologic imaging. As such, it accounts for the high sensitivity of nuclear medicine procedures, but also for the low specificity in differential diagnosis of different diseases with similar pathophysiologic characteristics. As an established infectionimaging modality, nuclear medicine plays a vital healthcare role in the diagnosis and subsequent effective treatment of infection of the spine. Various radiopharmaceuticals have been shown to significantly aid diagnosis of infection of the spine: single photon emitting agents for single photon emission computerized tomography (SPECT), bone scanning agents, 111In-oxine-, 99mTc-hexamethylpropyleneamine oxime-, and 99mTc-stannous fluoride colloid-labeled leukocytes, 99mTcFanolesmab and 67Ga-citrate; and more recently 18fluorodeoxyglucose (FDG) for positron emission tomography (PET). This chapter describes and evaluates available data on FDG PET for assessment of infection of the spine as opposed to SPECT and radiologic examinations. First, technical aspects of PET and SPECT are described followed by a brief overview of routinely available radiopharmaceuticals of relevance for imaging infection of the spine. Subsequently, results obtained in clinical studies are described.

PET AND SPECT The gamma camera or SPECT camera is a camera that is able to detect scintillations (flashes of light) produced when gamma rays, resulting from radioactive decay of single photon emitting radioisotopes, interact with a sodium iodide crystal at the front of the camera. The scintillations are detected by photomultiplier tubes, and while the areas of crystal seen by tubes overlap, the location of each scintillation can be computed from the relative response in each tube.1 The energy of each scintillation is also measured from the response of the tubes, and the electrical signal to the imaging computer consists of the location and photon energy. In front of the crystal resides a collimator which is made of lead and usually manufactured with multiple elongated holes (parallel-hole collimator). The holes allow only gamma rays that are traveling perpendicularly to the crystal face to enter. The gamma photons absorbed by the crystal therefore form an image of the distribution of the radiopharmaceutical distribution in front of the camera. By rotating the camera around the patient and acquiring images at different angles, tomographic images, or SPECT images, can be generated through the use of specific reconstruction algorithms.2 As with SPECT, PET relies on computerized reconstruction procedures to produce tomographic images, but by means of indirectly detecting positron emission.3 Positrons, when emitted by radioac-

tive nuclei, will combine with an electron from the surroundings and annihilate it. Upon annihilation, both the positron and the electron are then converted to electromagnetic radiation in the form of two high-energy photons which are emitted 180 degrees away from each other. It is this annihilation radiation that can be detected externally and is used to measure both the quantity and the location of the positron emitter. Simultaneous detection of two of these photons by detectors on opposite sides of an object places the site of the annihilation on or about a line connecting the centers of the two opposing detectors. At this point, mapping the distribution of annihilations by computer is conducted. If the annihilation originates outside the volume between the two detectors, only one of the photons can be detected, and since the detection of a single photon does not satisfy the coincidence condition, the event is rejected. Since radioisotopes suitable for PET have a short half-life (e.g. 110 min for 18F), an on-site cyclotron is needed for production of such isotopes.4 Special radiosynthesis facilities are required, restricting the availability of noncommercially available PET radiopharmaceuticals to specialized centers. In contrast to PET, the synthesis of SPECT radiopharmaceuticals is much less expensive. As the half-lifes of the isotopes used in SPECT are longer than those of isotopes used in PET (hours versus minutes), longer acquisition times are possible in SPECT. On the other hand, the resolution of a conventional PET camera is twice as good as that of a conventional gamma camera and PET allows for more accurate quantification when compared to SPECT.

RADIOPHARMACEUTICALS AND METHODOLOGY Tc-MDP/HDP

99m

Bone scintigraphy makes use of 99mTc-labeled organic analogues of pyrophoshate which are characterized by P-C-P bonds and predominantly absorb at kinks and dislocation sites on the surface of hydroxyapatite crystals. The most commonly used diphosphonate agents are 99mTc hydroxyethylene diphosphonate (99mTc HDP) and 99mTc methylene diphosphonate (99mTc MDP). The major physiologic determinants of bone uptake of these phosphate agents are the rate of bone turnover and blood flow, and the bone surface area involved.5 When performed for osteomyelitis, the study is usually done in three or four phases. Three-phase bone imaging consists of a dynamic imaging sequence, the flow or perfusion phase, followed immediately by static images of the region of interest, which is the blood-pool or soft-tissue phase. The third, or bone phase, consists of planar static images of the area of interest, acquired 2–4 h later. SPECT is performed when deemed necessary by the nuclear medicine physician. The usual injected dose for adults is 740–925 MBq (20–25 mCi) of 99mTc-MDP. The nor89

Part 1: General Principles

mal distribution of this tracer, by 3–4 h after injection, includes the skeleton, genitourinary tract, and soft tissues.6

Ga

67 67

Ga-citrate has been used for localizing infection for more than three decades. 67Ga, which is cyclotron produced, emits 4 principal rays suitable for imaging: 93, 184, 296, and 388 keV. Several factors govern uptake of this tracer in inflammation and infection. When injected intravenously, 67Ga binds primarily to transferrin a β-globulin responsible for transporting iron. Increased blood flow and increased vascular membrane permeability associated with inflammation/infection result in increased delivery and accumulation of transferrin-bound 67 Ga at inflammatory foci. At the site of infection or inflammation, 67 Ga can then bind to lactoferrin, which is present in high concentrations in inflammatory foci, attach to leukocytes, or may be directly taken up by bacteria. Siderophores, low molecular weight chelates produced by bacteria, have a high affinity for 67Ga. The siderophore– 67 Ga complex is presumably transported into the bacterium, where it remains until phagocytosed by macrophages.7 Imaging is usually performed 18–72 h after injection of 185–370 MBq of 67Ga-citrate. The normal biodistribution of 67Ga, which can be variable, includes bone, bone marrow, liver, genitourinary and gastrointestinal tracts, and soft tissues.7

IgG1 (Granuloscint; CISBio International) that binds to non-specific cross-reactive antigen-95 present on neutrophils. Studies generally become positive by 6 h after injection; delayed imaging at 24 h may increase lesion detection.11 Another agent that has been investigated is a murine monoclonal antibody fragment of the IgG1 class that binds to normal cross-reactive antigen-90 present on leukocytes (LeukoScan; Immunomedics). Sensitivity and specificity of this agent range from 76% to 100% and from 67% to 100%, respectively.12 18

F FDG

18

Fluorodeoxyglucose is a fluorinated glucose analogue that, like glucose, passes through the cell membrane. Following subsequent phosphorylation by glucose-6-hexokinase it is trapped within the cell.13–15 Although FDG PET is reported to be a sensitive and specific technique in oncological imaging, it is well known that inflammatory and infectious lesions can cause false-positive results.16 Various types of inflammatory cells such as macrophages, lymphocytes, and neutrophil granulocytes as well as fibroblasts have been shown to avidly take up FDG, especially under conditions of activation. It even appears that on autoradiography, the FDG distribution in certain tumors is highest in the reactive inflammatory tissue, i.e. the activated macrophages and leukocytes surrounding the neoplastic cells.7,8

INFECTION OF THE SPINE Radiolabeled leukocytes Neutrophils concentrate in large numbers, up to 10% of the total number of neutrophils per day, at sites of infection. Their accumulation is stimulated by the presence of lactoferrin, local neutrophil secretions, and chemotactic peptides. Several techniques for in vitro radiolabeling of isolated leukocytes have been reported; the most commonly used procedures make use of the lipophilic compounds 111Inoxyquinoline (oxine) and 99mTc hexamethyl propyleneamine oxine (HMPAO).8 The lipophilic oxine binds bi- and trivalent ions such as 111In. Following diffusion of 111In-oxine across the cell membrane, 111 In is released from oxine, which leaves the cell and binds intracellularly. HMPAO forms a small neutral lipophilic complex with 99mTc that readily crosses the cell membrane and changes into a secondary hydrophilic complex that is trapped in cells. The radiolabeling procedure takes about 2–3 h. The usual dose of 111In-labeled leukocytes is 10–18.5 MBq (300–500 μCi); the usual dose of 99mTc-HMPAOlabeled leukocytes is 185–370 MBq (5–10 mCi). A total white count of at least 2000/mm3 is needed to obtain satisfactory images. Usually, the majority of leukocytes labeled are neutrophils, and hence the procedure is most useful for identifying neutrophil-mediated inflammatory processes, such as bacterial infections. The procedure is less useful for those illnesses in which the predominant cellular response is other than neutrophilic, such as tuberculosis.9 At 24 h after injection, the usual imaging time for 111In-labeled leukocytes, the normal distribution of activity is limited to the liver, spleen, and bone marrow. The normal biodistribution of 99mTc-HMPAO-labeled leukocytes is more variable. In addition to the reticuloendothelial system, activity is also normally present in the genitourinary tract, large bowel (within 4 h after injection), blood pool, and occasionally the gallbladder.10 The interval between injection of 99mTc-HMPAO-labeled leukocytes and imaging varies with the indication; in general, imaging is usually performed within a few hours after injection. 99m

Tc-labelled antibodies

Considerable effort has been devoted to developing in vivo methods of labeling leukocytes using peptides and antigranulocyte antibodies/ antibody fragments. One method makes use of a murine monoclonal 90

Vertebral infection represents 2–4% of all cases of osteomyelitis and its incidence is increasing.17 In order to prevent clinically significant consequences which include neural compromise and late spinal deformities, early diagnosis and prompt treatment are essential. Causative pyogenic microorganisms in decreasing order of frequency are Staphylococcus aureus, Streptococcus and Pneumococcus and Gram-negative bacteria.18 Tuberculous spondylitis is an important form of nonpyogenic granulomatous infection. The routes of spinal infection include hematogenous spread, postoperative infections, direct implantation during spinal punctures, and spread from a contiguous focus.

Acute osteomyelitis and spondylodiscitis The combination of physical examination and biochemical alterations in combination with three-phase bone scanning, and especially MRI, have a high sensitivity (>90%) for the detection of acute osteomyelitis and spondylodiscitis.19–21 Accordingly, in the absence of complicating factors, the added value of scintigraphic imaging techniques will be limited. Nevertheless, FDG PET especially may have a role in doubtful cases, albeit rarely. For instance, it may play a role in differentiating spondylodiscitis from erosive degenerative disc disease, a condition occasionally displaying a false-positive MRI and bone scan findings.20,22–24 When confronted with a negative PET scan in this clinical situation, infection can be excluded.

Chronic osteomyelitis Patients with chronic osteomyelitis may present with a variety of symptoms, including localized bone and joint pain, erythema, swelling, fevers, night sweats, etc. Laboratory tests, such as leukocyte count, estimated sedimentation rate, and C-reactive protein can be helpful in diagnosis but lack sensitivity and specificity in low-grade infections.25–28 C-reactive protein is also useful for gauging response to therapy. Many imaging modalities have been proposed for the noninvasive evaluation of chronic osteomyelitis.29 Radiographs are helpful in the diagnosis and staging of the patient. However, changes are

Section 3: General Diagnostic Technique

often subtle. Conventional radionuclide scans can also be useful in the diagnosis but do not aid in preoperative planning of resection. Combined three-phase bone scintigraphy and leukocyte scan has a good clinical accuracy (79–100%) when considering the peripheral skeleton;19,30–35 however, its accuracy decreases (1) in low-grade chronic infections(lower sensitivity);25,27 (2) in the presence of periskeletal soft tissue infection due to the limited resolution of conventional nuclear imaging (lower sensitivity and specificity); (3) in the central skeleton due to the presence of normal bone marrow and the possibility of so-called ‘cold lesions’ (lower sensitivity and specificity);24,31–35 and (4) after trauma or surgery due to the presence of ectopic hematopoietic bone marrow (lower specificity). To avoid false-positive studies due to ectopic bone marrow, the combination of leukocyte scanning with bone marrow scanning (99mtechnetium sulfur colloid) has been proposed.36 Congruency between leukocyte and bone marrow scanning indicates the presence of bone marrow, while the presence of a positive leukocyte scan and negative marrow scan suggests the presence of infection. Using this technique, diagnostic accuracy of up to 96% has been reported. In the vertebral column, a combination of bone and gallium scan has been proposed to improve both sensitivity and specificity.37 However, the need for two or even three (bone scan/leukocyte scan/bone marrow scan or bone scan/gallium scan) techniques is not practical, adds to the cost and patient radiation dose, and is time consuming. Computed tomography is used to identify a sequestered infection and for preoperative resection planning. Similarly, MRI is useful for surgical planning because it delineates intraosseous and extraosseous involvement. CT and MRI are, however, of limited value in the presence of metallic implants as well as for discriminating between edema and active infection after surgery.21,29,30 Overall, in spite of the available armamentarium of imaging modalities, clinicians are often confronted with an indeterminate diagnosis and the clinical strategy adopted is often limited to a ‘wait and see’ policy or empirical antibiotic treatment.25,38,39 Accordingly, novel imaging modalities with a very high accuracy for identification of sites of chronic osteomyelitis are of major interest. Several authors have addressed the value of FDG PET for this purpose. Guhlman et al. studied 51 patients suspected of having chronic osteomyelitis in the peripheral (n=36) or central (n=15) skeleton prospectively with static FDG PET imaging and combined 99mTc-antigranulocyte Ab/99m Tc-methylene diphosphonate bone scanning within 5 days.40 Obtained images were evaluated in a blinded and independent manner by visual interpretation, which was graded on a five-point scale of two observers’ confident diagnosis of osteomyelitis. Receiver operating characteristic (ROC) curve analysis was performed for both imaging modalities. The final diagnosis was established by means of bacteriologic culture of surgical specimens and histopathologic analysis (n=31) or by biopsy and clinical follow-up over 2 years (n=20). Of 51 patients, 28 had osteomyelitis and 23 did not. According to the unanimous evaluation of both readers, FDG PET correctly identified 27 of the 28 positives and 22 of the 23 negatives (IS identified 15 of 28 positives and 17 of 23 negatives, respectively). On the basis of ROC analysis, the overall accuracy of FDG PET and immunoscintigraphy in the detection of chronic osteomyelitis were 96%/96% and 82%/88%, respectively. Kälicke et al. evaluated the clinical usefulness of fluorine-18 fluorodeoxyglucose positron emission tomography (FDG PET) in acute and chronic osteomyelitis and inflammatory spondylitis.41 The study population comprised 21 patients suspected of having acute or chronic osteomyelitis or inflammatory spondylitis. Fifteen of these patients subsequently underwent surgery. FDG PET results were correlated with histopathological findings. The remaining six patients, who underwent conservative therapy, were excluded from any further

evaluation due to the lack of histopathological data. The histopathological findings revealed osteomyelitis or inflammatory spondylitis in all 15 patients: seven patients had acute osteomyelitis and eight patients had chronic osteomyelitis or inflammatory spondylitis. FDG PET yielded 15 true-positive results. However, the absence of negative findings in this series may raise questions concerning selection criteria. De Winter et al. reported on 60 patients suffering from a variety of suspected chronic orthopedic infections.42 In this prospective study, the presence or absence of infection was determined by surgical exploration in 15 patients and long-term clinical follow-up in 28 patients. As opposed to the study by Guhlmann et al., patients with recent surgery were not excluded. Considering only those patients with suspected chronic osteomyelitis, FDG PET was correct in 40 of 43 patients. There were three false-positive findings, 17 true-negative findings, and no false-negative findings. This resulted in a sensitivity of 100%, a specificity of 85%, and an accuracy of 93%. Two of three false-positive findings occurred in patients who had been operated on recently (6 weeks and 4 months, respectively). Zhuang et al. studied the accuracy of FDG PET for the diagnosis of chronic osteomyelitis.43 Twenty-two patients with possible osteomyelitis (5 in the tibia, 5 in the spine, 4 in the proximal femur, 4 in the pelvis, 2 in the maxilla, and 2 in the feet) that underwent FDG PET imaging and in whom operative or clinical follow-up data were available were included for analysis. The final diagnosis was made by surgical exploration or clinical follow-up during a 1-year period. FDG PET correctly diagnosed the presence or absence of chronic osteomyelitis in 20 of 22 patients but produced two false-positive results, respectively two cases of recent osteotomies, resulting in a sensitivity of 100%, a specificity of 87.5%, and an accuracy of 90.9%. It is, however, unclear from their report in how many patients histopathologic or microbiologic studies were available. Chako et al. retrospectively analyzed the accuracy of FDG PET for diagnosing infection in a large population of patients and in a variety of clinical circumstances, including suspicion of chronic osteomyelitis in 56 patients.44 Final diagnosis was made on the basis of surgical pathology and clinical follow-up for a minimum of 6 months. Among the patients suspected of having chronic osteomyelitis, the accuracy was 91.2%.

CONCLUSION Although limited, available data on FDG PET for imaging of the spine are promising, displaying a higher accuracy for diagnosing osteomyelitis when compared to other imaging modalities for this purpose, including conventional nuclear medicine examinations. For instance, in the study by Guhlman et al., comparing the combination of bone scan and leukocyte scan with FDG PET, the latter proved significantly more accurate for the diagnosis of osteomyelitis in the central skeleton. The fact that FDG PET is not disturbed by the presence of metallic implants and is able to differentiate between scar tissue and active inflammation constitutes a major advantage when compared to CT and MRI. As opposed to radiolabeled leukocytes or radiolabeled antibodies, FDG is likely to penetrate easier and faster in lesions than cellular tracers or antibodies.45 Aside from the potential for higher sensitivity, taking into account available data, a negative PET scan virtually rules out osteomyelitis.42,44 Initially, it was thought that the specificity of FDG PET for detection of infection of the spine may be limited by the fact that this tracer also accumulates in benign lesions and tumors. More recent papers, however, focusing on fractures, hemangioma, Paget’s disease, and endplate abnormalities of and in the spine, tend to contradict this hypothesis. Following traumatic fracture or surgical intervention, 91

Part 1: General Principles

bone scintigraphy reveals a positive result for an extended period of time, up to 2 years post-fracture, posing a challenge when evaluating patients for superimposed infection or for possible malignancy. Similarly, acute fracture or recent surgical intervention of the bone may cause increased FDG accumulation. However, available results suggest that FDG uptake patterns following fracture differ amongst various bones. In a series of 17 patients by Schmitz et al., MRI demonstrated a vertebral compression fracture generating from osteoporosis in 13 cases.46 In 12 of these 13 cases, PET scans were categorized as true negative. Comparable results were obtained by Zhuang et al. in a retrospective study assessing the pattern and time course of abnormal FDG uptake following traumatic or surgical fracture.47 Out of 10 patients with a documented fracture of the spine (interval between confirmation of the fracture and time of PET scanning, 24 days and 45 months), none displayed increased FDG uptake. Importantly, in other bone structures, if positive, uptake proved normal by a maximum of 3 months after fracture or surgical intervention of the bone. Accordingly, based on currently available data, there should be normal FDG uptake at spine fractures either initially or by a maximum of 3 months post-fracture. Bhargava et al. reported on a case of vertebral Paget’s disease showing normal FDG uptake and intense osteoblastic activity on the bone scan.48 Bybel et al. performed FDG PET to stage a nasopharyngeal carcinoma and found hypometabolic regions in multiple thoracic vertebrae.49 These corresponded to multiple hemangiomas as evidenced by MRI. These findings are in sharp contrast to those reported by Hatayama et al. in 16 patients with histopathologically documented hemangiomas of the extremities.50 In these authors’ experience, all 16 lesions examined by PET displayed FDG accumulation with standardized uptake values ranging from 0.7 to 1.67. Stumpe et al. performed prospectively FDG PET in 30 consecutive patients with substantial endplate abnormalities found during MR imaging of the lumbar spine.51 The sensitivity and specificity for differentiation of degenerative from infectious endplate abnormalities were 50% and 96% for MRI versus 100% and 100% for FDG PET. Finally, in most patients, a thorough medical history makes the presence of tumor unlikely, and sterile inflammations such as chronic polyarthritis, vasculitis, and tumors often appear at sites or show distribution patterns that are suggestive of these diseases. To conclude, based on available data, FDG PET has potential to become the imaging gold standard for detection of infection in the spine.

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Section 3: General Diagnostic Technique 39. Spangehl MJ, Younger ASE, Masri BA, et al. Diagnosis of infection following total hip arthroplasty. Am J Bone Joint Surg 1998; 79A:1578–1588.

45. Chianelli M, Mather SJ, Martin-Comin J, et al. Radiopharmaceuticals for the study of inflammatory processes: a review. Nucl Med Commun 1997; 18:437–455.

40. Guhlmann A, Brecht-Krauss D, Suger G, et al. Fluorine-18-FDG PET and technetium-99m antigranulocyte antibody scintigraphy in chronic osteomyelitis. J Nucl Med 1998; 39:2145–2152.

46. Schmitz A, Risse JH, Textor J, et al. FDG-PET findings of vertebral compression fractures in osteoporosis: preliminary results. Osteoporos Int 2002; 13:755–761.

41. Kälicke T, Schmitz A, Risse JH, et al. Fluorine-18 fluorodeoxyglucose PET in infectious bone diseases: results of histologically confirmed cases. Eur J Nucl Med 2000; 27:524–528. 42. De Winter F, Van de Wiele C, Vogelaers D, et al. F-18 Fluorodeoxyglucose positron emission tomography: a highly accurate imaging modality for the diagnosis of chronic musculoskeletal infections. Am J Bone Joint Surg 2001; 83A:651–660.

47. Zhuang H, Sam JW, Chacko TK, et al. Rapid normalization of osseous FDG uptake following traumatic or surgical fractures. Eur J Nucl Med Mol Imaging 2003; 30:1096–1103. 48. Bhargava P, Naydich M, Ghesani M. Normal F-18 FDG vertebral uptake in Paget’s disease on PET scanning. Clin Nucl Med 2005; 30:191–192. 49. Bybel B, Raja S. Vertebral hemangiomas on FDG PET scan. Clin Nucl Med 2003; 28:522–523.

43. Zhuang H, Duarte PS, Pourdehand M, et al. Exclusion of chronic osteomyelitis with F-18 fluorodeoxyglucose positron emission tomography. Clin Nucl Med 2000; 25:281–284.

50. Hatayama K, Watanabe H, Ahmed AR, et al. Evaluation of hemangioma by positron emission tomography: role in a multimodality approach. J Comput Assist Tomogr 2003; 27:70–77.

44. Chacko TK, Zhuang H, Stevenson K, et al. The importance of the location of fluorodeoxyglucose uptake in periprosthetic infection in painful hip prostheses. Nucl Med Commun 2002; 23: 851–855.

51. Stumpe KD, Zanetti M, Weishaupt D, et al. FDG positron emission tomography for differentiation of degenerative and infectious endplate abnormalities in the lumbar spine detected on MR imaging. Am J Roentgenol 2002; 179:1151–1157.

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PART 1

GENERAL PRINCIPLES

Section 3

General Diagnostic Technique

CHAPTER

Electrodiagnostic Approach to Patients with Suspected Radiculopathy

8

Timothy R. Dillingham

INTRODUCTION Cervical and lumbosacral radiculopathies are conditions involving a pathological process affecting the spinal nerve root. Commonly, this is a herniated nucleus pulposus that anatomically compresses a nerve root within the spinal canal. Another common etiology for radiculopathy is spinal stenosis resulting from a combination of degenerative spondylosis, ligament hypertrophy, and spondylolisthesis. Inflammatory radiculitis is another pathophysiological process that can cause radicular pain and/or radiculopathy. It is important to remember, however, that other more ominous processes such as malignancy and infection can present with the same symptoms and signs of radiculopathy as the more common causes. This chapter deals with the clinical approach used in an electrodiagnostic laboratory to evaluate a person with neck pain, lumbar spine pain, or limb symptoms which are suggestive of radiculopathy. The indications for referring for testing as well as the limitations of testing are discussed to give a greater understanding of this important diagnostic procedure. This is not intended to be a basic chapter dealing with how to perform electrodiagnostic studies. Given the extensive differential diagnosis for limb and spine symptoms, it is important for electrodiagnosticians to develop a conceptual framework for evaluating these referrals with a standard focused history and physical examination and a tailored electrodiagnostic approach. Accurately identifying radiculopathy by electrodiagnosis whenever possible, provides valuable information that helps guide treatment and minimizes other invasive and expensive diagnostic and therapeutic procedures.

SPINE AND NERVE ROOT ANATOMY: DEVIATIONS FROM THE EXPECTED Spinal anatomy is discussed in detail in Chapters 46 and 80 by Russell Gilchrist and will not be emphasized here. From an electrodiagnostic perspective, however, there are several specific anatomical issues that merit further discussion. At all levels the dorsal root ganglion (DRG) lies in the intervertebral foramen. This anatomical arrangement has implications for clinical electrodiagnosis of radiculopathy, namely that sensory nerve action potentials (SNAPs) are preserved in most radiculopathies as the nerve root is affected proximal to the DRG. Regarding the cervical nerve roots and the brachial plexus, there are many anatomic variations. Perneczky1 described an anatomic study of 40 cadavers. In all cases, there were deviations from accepted cervical root and brachial plexus anatomy. Levin, Maggiano, and Wilbourn2 examined the pattern of abnormalities on electromyography (EMG) in 50 cases of surgically proven cervical root lesions. A range of needle EMG patterns was found with EMG demonstrating less specificity for the C6 root level, but more specificity and consistent patterns for

C8, C7, and C5 radiculopathies. In subjects with C6 radiculopathies, half the patients showed findings similar to those with C5 radiculopathies and the other half demonstrated C7 patterns. This surgical group was more severely affected than patients who do not require surgical interventions, and this pattern may not hold for less symptomatic patients. In the lumbar spinal region dorsal and ventral roots exit the spinal cord at about the T11–L1 boney level and travel in the lumbar canal as a group of nerve roots in the dural sac. This is termed the ‘horse’s tail’ or cauda equina. This poses challenges and limitations to the EMG examination. A destructive intramedullary (spinal cord) lesion at T11 can produce EMG findings in muscles innervated by any of the lumbosacral nerve roots and manifest the precise findings on needle EMG as those seen with a herniated nucleus pulposus at any of the lumbar disc levels. For this reason, the electromyographer cannot precisely determine the anatomic location of a lumbar intraspinal lesion producing distal muscle EMG findings in the lower limbs. The needle EMG examination can only identify the root or roots that are physiologically involved, but not the precise anatomic site of pathology in the lumbar spinal canal. This is an important limitation requiring correlation with imaging findings to determine which anatomic location is most likely the offending site. This can be difficult in elderly persons with foraminal stenosis as well as moderate central canal stenosis at more than one site. In a prospective study of 100 patients with lumbosacral radiculopathy who underwent lumbar laminectomy, EMG precisely identified the involved root level 84% of the time.3 Needle EMG failed to accurately identify the compressed root in 16%. However, at least half of the failures were attributable to anomalies of innervation. Another component to this study involved stimulating the nerve roots intraoperatively with simultaneous recording of muscle activity in the lower limb using surface electrodes. These investigators demonstrated variations in root innervation, such as the L5 root innervating the soleus and medial gastrocnemius, in 16% of a sample of 50 patients. Most subjects demonstrated dual innervation for most muscles.3 These findings underscore the limitations of precise localization for root lesions with EMG. The electrodiagnostician should maintain an appreciation of these anatomic variations to better convey the level of certainty with respect to diagnostic conclusions.

PHYSICAL EXAMINATION The electrodiagnostic examination is an extension of the standard clinical examination. The history and physical examination are vital initial steps in determining what conditions may be causing the presenting symptoms. Most radiculopathies present with symptoms in one limb. Multiple radiculopathies such as are seen in cervical spinal stenosis or lumbar stenosis may cause symptoms in more than one limb. A focused neuromuscular examination that assesses strength, 95

Part 1: General Principles

reflexes, and sensation in the affected limb and the contralateral limb is important, providing a framework for electrodiagnostic assessment. An algorithmic approach to utilizing physical examination and symptom information to tailor the electrodiagnostic evaluation is shown in Figure 8.1. In this approach, symptoms and physical examination signs create a conceptual framework for approaching these sometimes daunting problems. Admittedly, there are many exceptions to this approach with considerable overlap in medical disorders which might fall within multiple categories. Radiculopathies and entrapment neuropathies are examples of such conditions with a variety of clinical presentations and physical examination findings, such that they are included in both focal symptom categories with and without sensory loss. In the case of a person with lumbosacral radiculopathy, a positive straight leg raise test may be noted in the absence of motor, reflex, or sensory changes. Conditions such as myopathies and polyneuropathies better fit this algorithmic approach, given that symptoms and physical examination signs are more specific. Figure 8.1 also contains musculoskeletal disorders and denotes how they fall into this conceptual framework. The electrodiagnostician must be willing to modify the electrodiagnostic examination in response to nerve conduction and EMG findings and adjust the focus of the examination in light of new information. The implications of symptoms and signs on electrodiagnostic findings were investigated by Lauder and colleagues for suspected cervical and lumbosacral radiculopathies.4,5 Even though physical examination findings were better at predicting who would have a radiculopathy, many patients with normal examinations had abnor-

mal electrodiagnostic studies, indicating that clinicians should not curtail electrodiagnostic testing simply because the physical examination is normal. For lower limb symptoms, loss of a reflex or weakness dramatically increased the likelihood of having a radiculopathy by EMG. Losing the Achilles reflex, for instance, resulted in an odds ratio of 8.4 (p<0.01), in other words eight times the likelihood of having a radiculopathy by EMG with this physical examination finding compared to someone without loss of this reflex.4 Similar findings were noted for upper limb symptoms; if a reflex was lost or weakness was noted the likelihood of having a cervical radiculopathy confirmed by EMG was many times greater.5 Combinations of findings, particularly weakness plus sensory loss or plus reflex changes, resulted in a ninefold greater likelihood of cervical radiculopathy and two to three times greater likelihood of lumbosacral radiculopathy.4,5

The American Association of Neuromuscular and Electrodiagnostic Medicine Guidelines for Radiculopathy Evaluation The American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) guidelines recommend that for an optimal evaluation of a patient with suspected radiculopathy, a needle EMG screen of a sufficient number of muscles and at least one motor and one sensory nerve conduction study should be performed in the involved limb.6 The nerve conduction studies are necessary to exclude polyneuropathy. The sufficiency of the EMG screen and a recommended number of muscles is discussed in detail below. An EMG study is considered diagnostic for a radiculopathy if EMG abnormalities are

Fig. 8.1 Algorithmic approach to structuring the electrodiagnostic examination based upon physical examination signs and the location of the patient’s symptoms. Focal symptoms refer to single limb symptoms whereas generalized symptoms are present when the patient complains of symptoms affecting more than one limb. 96

Section 3: General Diagnostic Technique

found in two or more muscles innervated by the same nerve root, and different peripheral nerves, yet muscles innervated by adjacent nerve roots are normal.7 This assumes, of course, that other generalized conditions such as polyneuropathy are not present. It is often necessary to study bilateral limbs, particularly if a single limb shows EMG findings suggestive of radiculopathy and the patient has symptoms in both the studied and the contralateral limb. If bilateral limbs are involved, the electrodiagnostician should have a low threshold for studying selected muscles in an upper limb (if the lower limbs are abnormal on EMG) or a lower limb (if both upper limbs are abnormal) to exclude a generalized process such as polyneuropathy or motor neuron disease. Likewise, additional nerve conduction studies are appropriate to exclude other suspected conditions and the electrodiagnostician should have a low threshold for expanding the study.

H-REFLEXES, F-WAVES, AND NERVE CONDUCTION Nerve conduction studies, H-reflexes, and F-waves are not very useful for confirming radiculopathy. They are useful, however, to exclude polyneuropathy or mononeuropathies.

H-reflexes H-reflexes have commonly been used to determine whether a radiculopathy demonstrates S1 involvement.7 It is a monosynaptic reflex that is an S1-mediated response and can differentiate to some extent L5 from S1 radiculopathy. Many researchers have evaluated their sensitivity and specificity with respect to lumbosacral radiculopathies and generally found a range of sensitivities from 32% to 88%.7–12 However, many of these studies suffered from lack of a control group, imprecise inclusion criteria, or small sample sizes. Marin et al.12 prospectively examined the H-reflex and the extensor digitorum brevis reflex in 53 normals, 17 patients with L5, and 18 patients with S1 radiculopathy. Patients included in the study had all of the following: (1) radiating low back pain into the leg, (2) reduced sensation or weakness or positive straight leg raise test, and (3) either EMG evidence of radiculopathy or structural causes of radiculopathy on magnetic resonance imaging (MRI) or computed tomography (CT) imaging. The maximal (2 SD) value for the H-reflex side-toside latency difference was 1.8 ms as derived from the normal group. They analyzed the sensitivity of the H-reflex for side-to-side differences greater than 1.8 ms or a unilaterally absent H-reflex on the affected side. The H-reflex only demonstrated a 50% sensitivity for S1 radiculopathy, 6% for L5 radiculopathy, but had a 91% specificity. Amplitudes were not assessed in this study. These results suggest that the H-reflex has a low sensitivity for S1 root level involvement. H-reflexes may be useful to identify subtle S1 radiculopathy, yet there are a number of shortcomings related to these responses. They can be normal with radiculopathies12 and, because they are mediated over such a long physiological pathway, they can be abnormal due to polyneuropathy, sciatic neuropathy, or plexopathy.7 They are most useful in the assessment for polyneuropathy. In order to interpret a latency or amplitude value and render a judgment as to the probability that it is abnormal, precise population-based normative values encompassing a large age range of normal subjects must be available for comparison of these nerve conduction findings. Falco et al.13 demonstrated in a group of healthy elderly subjects (60–88 years old) that the tibial H-reflex was present and recorded bilaterally in 92%. Most elderly are expected to have normal H-reflex studies and, when abnormalities are found in these persons, the electrodiagnostician should critically evaluate these findings

and the clinical scenario before attributing H-reflex abnormalities to the aging process. In patients with upper limb symptoms suggestive of cervical radiculopathy, H-reflexes and F-waves are not useful in diagnosis but rather help exclude polyneuropathy as an underlying cause of symptoms. One study by Miller and colleagues14 examined the H-reflexes in the upper limb in a set of patients defined by a combination of clinical criteria (no imaging or EMG studies) as having definite or probable cervical radiculopathy. They tested the H-reflex for the FCR, the ECR, the APB, and the biceps heteronymous reflex. The later reflex is derived by stimulating the median nerve in the cubital fossa and recording over the biceps brachii muscle, averaging 40–100 trials. These reflex studies had a 72% sensitivity overall for the group with 100% for the subset of patients with definite cervical radiculopathy. In contrast, needle EMG demonstrated 90% sensitivity for the definite group. Although these findings suggest a possible role for these upper limb H-reflexes, they are highly specialized, time consuming, and difficult to consistently elicit. They may have a role in sensory radiculopathies where needle EMG will not be positive and imaging findings are equivocal. Further studies are necessary to clarify whether the findings of Miller et al.14 can be duplicated at other centers.

F-waves F-waves are late responses involving the motor axons and axonal pool at the spinal cord level. They can be assessed and classified by using the minimal latency, mean latency, and chronodispersion or scatter.7 As in the case of H-reflexes, they demonstrate low sensitivities and are not specific for radiculopathy; rather, they are a better screen for polyneuropathy. Published sensitivities range from 13% to 69%; however, these studies suffer from many of the same shortcomings that are found in the H-reflex studies.8,15,16 London and England17 reported two cases of persons with neurogenic claudication from lumbosacral spinal stenosis. They demonstrated that the F-wave responses could be reversibly changed after 15 minutes of ambulation, which provoked symptoms. This suggested an ischemia-induced conduction block in proximal motor neurons. A larger-scale study of this type might find a use for F-waves in the identification of lumbosacral spinal stenosis and assist with the delineation of neurogenic from vascular claudication.

Motor and sensory nerve conduction studies Standard motor and sensory nerve conduction studies are not helpful in identifying a cervical or lumbosacral radiculopathy. However, they should be performed to screen for polyneuropathy and exclude common entrapment neuropathies if the patient’s symptoms could be explained by a focal entrapment. Remember that based upon the anatomy of the dorsal root ganglion, sensory responses should be normal in most radiculopathies. If they are absent, this should raise suspicion for another diagnosis such as polyneuropathy, plexopathy, or mononeuropathy. Plexopathies often pose a diagnostic challenge as they are similar to radiculopathies in symptoms and signs. In order to distinguish plexopathy from radiculopathy, sensory responses which are accessible in a limb should be tested. In plexopathy, they are likely to be reduced in amplitude, whereas in radiculopathy they are generally normal. If substantial axonal loss has occurred at the root level, the compound muscle action potential recorded in muscles innervated by that root may be reduced in both plexopathies and radiculopathies. This is usually when severe axonal loss has occurred such as with cauda equina lesions or penetrating trauma that severely injures a nerve root. The distal motor latencies and conduction velocities are usually preserved as they reflect the fastest conducting nerve fibers.7 97

Part 1: General Principles

SOMATOSENSORY EVOKED POTENTIALS, DERMATOMAL SOMATOSENSORY EVOKED POTENTIALS, AND MAGNETIC EVOKED POTENTIALS The AANEM guidelines recently examined the literature and concluded that somatosensory evoked potentials (SEPs) may be useful for cervical spondylosis with cord compression. Likewise, in lumbosacral spinal stenosis, dermatomal somatosensory evoked potentials (DSEPs) may be useful in defining levels of deficits.6 These tests are not necessary for electrodiagnostic testing for persons with suspected radiculopathies and their usefulness is limited to special circumstances. These tests are not recommended for the routine evaluation of persons with suspected radiculopathy. DSEPs can document physiological evidence of multiple or single root involvement in lumbosacral spinal stenosis and may be useful in the case where spinal canal narrowing is minimal and the patient has symptoms. This testing also complements standard needle EMG. Snowden et al.18 found that for single and multilevel lumbosacral spinal stenosis, DSEPs revealed 78% sensitivity relative to spinal imaging. In this well-designed prospective study, DSEP criteria as well as inclusion criteria were precisely defined. The predictive value for a positive test was 93%. Yiannikas, Shahani, and Young19 demonstrated that SEPs may be useful for cervical myelopathy. In this study of 10 patients with clinical signs of myelopathy, all 10 had abnormal peroneal SEPs and seven had abnormal median SEPs. Maertens de Noordhout et al.20 examined motor and SEPs in 55 persons with unequivocal signs and symptoms of cervical spinal myelopathy. In this group 87% showed gait disturbances, and 82% showed hyperreflexia. MRI was not the diagnostic standard as these authors felt that MRI was prone to overdiagnosis; rather, metrizamide myelography showed unequivocal signs of cervical cord compression for all of these patients. Magnetic stimulation of the cortex was performed and the responses measured with surface electrodes. In these subjects 89% demonstrated abnormalities in magnetic evoked potential (MEP) to the first dorsal interosseus muscle and 93% had one MEP abnormality. At least one SEP abnormality was noted in 73%. Tavy et al.21 examined whether MEPs or SEPs assisted in identifying persons with radiological evidence of cervical cord compression but who were without clinical markers for myelopathy. All patients had clinical symptoms of cervical radiculopathy, but not myelopathy. In this group, MEPs were normal in 92% and SEPs were normal in 96%. These investigators concluded that MEPs and SEPs are normal in most cases of persons with asymptomatic cervical stenosis. This indicates that abnormal MEPs and SEPs are likely to be true-positive findings and not false positives related to mild asymptomatic cord compression. It is important to remember that cervical spondylosis is a process that causes a continuum of problems including both radiculopathy and myelopathy. The inherent variability and difficulty in determinations of what constitutes normal SEPs prompted investigation. Dumitru and colleagues22 examined the variations in latencies with SEPs. In 29 normal subjects, they examined the ipsilateral intertrial variations, arithmetic mean side-to-side differences, and maximum potential side-to-side differences with stimulation of the superficial peroneal sensory nerve, sural nerve, and L5 and S1 dermatomes with respect to P1 and N1 latencies and peak-to-peak amplitudes. Considerable ipsilateral intertrial variation was observed and side-to-side comparisons revealed a further increase in this inherent variation regarding the above measured parameters. They suggested an additional parameter with which to evaluate SEPs: the maximum side-to-side latency difference.

98

Dumitru and colleagues,23 in a study involving persons with unilateral and unilevel L5 and S1 radiculopathies, evaluated DSEPs and segmental SEPs. History, physical examination, imaging studies, and electrodiagnostic medicine evaluations clearly defined patients with unilateral/unilevel L5 or S1 nerve root compromise. Regression equation analysis for cortical P1 latencies evaluating age and height based on comparable patient and control reference populations revealed segmental and dermatomal sensitivities for L5 radiculopathies to be 70% and 50%, respectively, at 90% confidence intervals. Similar sensitivities were obtained for 2 standard deviation mean cortical P1 latencies. Side-to-side cortical P1 latency difference data revealed segmental and dermatomal sensitivities for S1 radiculopathies to be 50% and 10%, respectively, at 2 standard deviations. These investigators questioned the clinical utility of both segmental and dermatomal SEPs in the evaluation of patients with suspected unilateral/unilevel L5 and S1 nerve root compromise, finding little utility for these tests in persons with single-level lumbosacral radiculopathy.

PURPOSE OF ELECTRODIAGNOSTIC TESTING Electrodiagnostic testing is expensive and uncomfortable for patients and so it is important to understand why it is performed and the expected outcomes. Electrodiagnostic testing serves several important purposes: (1) It effectively excludes other conditions that mimic radiculopathy such as polyneuropathy or entrapment neuropathy. Haig and colleagues24 demonstrated that the referring diagnostic impression is often altered with electrodiagnostic testing. (2) Electrodiagnostic testing can, to some extent, suggest severity or extent of the disorder beyond clinical symptoms. Involvement of other extremities can be delineated or the involvement of multiple roots may be demonstrated, such as in the case of lumbosacral spinal stenosis. (3) There is utility in solidifying a diagnosis. An unequivocal radiculopathy on EMG in an elderly patient with non-specific or mild lumbar spondylosis or stenosis on MRI reduces diagnostic uncertainty and identifies avenues of management such as lumbar steroid injections or decompression surgery in certain situations. (4) Outcome prediction may be possible. If surgical intervention is planned for a lumbosacral radiculopathy, a positive EMG preoperatively improves the likelihood of a successful outcome postoperatively (see below). This is an area that deserves more research attention.

USEFULNESS OF ELECTRODIAGNOSTIC TESTING The value of any test depends upon the a priori certainty of the diagnosis in question and this principle applies to electrodiagnostic testing. For a condition or diagnosis for which there is great certainty before additional testing, the results of the subsequent tests are of limited value. This concept, diminishing returns on the road to diagnostic certainty, is important. For instance, in a patient with acute-onset sciatica while lifting, L5 muscle weakness, a positive straight leg raise, and an MRI showing a large extruded L4–5 nucleus pulposus, an EMG test will be of limited value in confirming the diagnosis of radiculopathy. In contrast, an elderly diabetic patient with sciatica, limited physical examination findings, and equivocal or age-related MRI changes presents an unclear picture. In this case electrodiagnostic testing is of high value, placing in perspective the imaging findings and excluding diabetic polyneuropathy as a confounding condition.

Section 3: General Diagnostic Technique

ELECTROMYOGRAPHY AND DIAGNOSTIC SENSITIVITIES The need for EMG, particularly in relationship to imaging of the spine, has been recently highlighted.25 Needle EMG is particularly helpful in view of the fact that the false-positive rates for MRI of the lumbar spine are high, with 27% of normals having a disc protrusion.26 For the cervical spine, the false-positive rate for MRI is much lower, with 19% of subjects demonstrating an abnormality, but only 10% showing a herniated or bulging disc.27 Radiculopathies can occur without structural findings on MRI, and likewise without EMG findings. The EMG only evaluates motor axonal loss or motor axon conduction block and for these reasons a radiculopathy effecting the sensory root will not yield abnormalities by EMG. If the rate of denervation is balanced by reinnervation in the muscle, then spontaneous activity is less likely to occur. The sensitivity of EMG for cervical and lumbosacral radiculopathies has been examined in a number of studies. The results of some of these studies are displayed in Table 8.1, which lists the ‘gold standards’ against which these EMG findings were compared. Studies using a clinical standard may reflect a less severe group, whereas those using a surgical confirmation may indicate a more severely involved group. The sensitivity for EMG is unimpressive, ranging from 49% to 92% in these studies. Electromyography is not a sensitive test, yet likely has higher specificity. The issue of specificity and its value in electrodiag-

nosis was underscored by Robinson.25 It is apparent that EMG is not a very good screening test. In terms of screening tests, MRI is better for identifying subtle structural abnormalities, with EMG to assess their clinical relevance and to exclude other disorders.

PARASPINAL MUSCLE EXAMINATION Several reports suggested high rates of false-positive fibrillations in lumbar paraspinal muscles.28,29 Dumitru, Diaz, and King30 conducted a well-designed study to examine whether or not fibrillations are found in the lumbar paraspinal muscles of normal asymptomatic volunteers. These investigators examined lumbosacral paraspinal muscles and intrinsic foot muscles with monopolar EMG and recorded potentials for analysis. Regular firing rate was required in order for classification as fibrillation potentials. They found many irregularly firing potentials with similar waveform characteristics as fibrillations and positive sharp waves (PSW). By excluding these irregularly firing potentials (atypical endplate spikes) they found much lower false-positive paraspinal fibrillation prevalences than other investigators. Only 4% of these normal subjects had lumbar fibrillations or PSW potentials by EMG testing. The investigators felt that the higher prevalences of spontaneous activity reported by other investigators28,29 were due to not fully appreciating the similarity between innervated and denervated spontaneous single muscle fiber discharges. This well-designed quantitative study underscores the need to assess both firing rate

Table 8.1: Selected studies evaluating the sensitivity of EMG relative to various ‘gold standards’ Study

Sample Size

Gold Standard

EMG Sensitivity

Lumbosacral radiculopathy Weber and Albert59

42

Clinical + imaging HNP

60%

Nardin et al.

47

Clinical

55%

29

Kuruoglu et al.

100

Clinical

86%

95

Clinical

64%

Tonzola et al.61

57

Clinical

49%

Schoedinger62

100

Surgically proven

56%

Knutsson

206

Surgically proven

79%

100

Clinical and imaging

84%a

19

Myelography and CT

78%

8

Khatri et al.60

46

Young et al.

3

Linden and Berlit10 Lumbosacral spinal stenosis Hall et al.48

68

Clinical + myelogram

92%

Johnsson et al.63

64

Clinical + myelogram

88%b

Cervical radiculopathy Berger et al.64

18

Clinical

61%

65

77

Intraoperative

67%

Leblhuber et al.

24

Clinical + myelogram

67%

14

Clinical

71%

20

Clinical and/or radiographic

50%

20

Clinical

95%

108

Clinical

51%

Partanen et al.

9

So et al.66 Yiannikas et al.

19

Tackman and Radu.

16

Hong et al.67 a

Both fibrillations or large motor units >8 mV were considered positive. This study assessed EMG parameters and used quantitative EMG with a unique grading scale not used in clinical practice. Fibrillations were infrequent. This limits the generalizability of this otherwise strong study. Unless otherwise stated the EMG parameters used in sensitivity calculations were fibrillation potentials. b

99

Part 1: General Principles

and rhythm as well as discharge morphology when evaluating for fibrillations and positive waves in the lumbar paraspinal muscles. Electrodiagnosticians should take care not to overcall fibrillations in lumbosacral paraspinal muscles by mistaking irregularly firing endplate spikes for fibrillations. Paraspinal muscles may be abnormal in patients with spinal cancers31–33 or amyotrophic lateral sclerosis,34 and following spinal surgery35 or lumbar puncture.36 In fact, fibrillations can be found years after lumbar laminectomy.35 The absence of paraspinal muscle fibrillations in such patients is helpful, but finding fibrillations in someone after laminectomy is of uncertain relevance as these fibrillations may be residual from the previous muscle damage or relatively new denervation. Investigations over the last decade have provided insights into better quantification and examination of lumbosacral paraspinal muscles. The lumbar paraspinal muscle examination has been refined through investigations that used a grading scale for the findings.37–40 The ‘mini PM’ score provides a quantitative means of deriving the degree of paraspinal muscle denervation.40 It distinguishes normal findings from persons with radiculopathy. This novel and quantitative technique may prove useful to identify subtle radiculopathies or spinal stenosis with greater precision. Cervical and lumbar paraspinal muscles should only be examined for insertional activity and spontaneous activity while at rest. Recruitment findings and motor unit morphology for these muscles has not been established and consequently we do not know for sure what constitutes normal. Examiners should not overcall radiculopathies based upon ‘reduced recruitment’ or ‘increased polyphasicity’ in the paraspinal muscles. Paraspinal muscles either show spontaneous activity and therefore localize the lesion to the root level or they do not. There is considerable overlap in paraspinal muscles with single roots innervating fibers above and below their anatomic levels. For this reason, the level of radiculopathy cannot be delineated by paraspinal EMG alone, but rather is based upon the root level that best explains the distribution of muscles demonstrating fibrillations.

IDENTIFICATION AS A SEPARATE CONCEPT FROM SENSITIVITY Electrodiagnostic testing is uncomfortable and expensive. Because electrodiagnosis is a composite assessment composed of various tests, a fundamental question is; when has the point of diminishing returns been reached? Some radiculopathies cannot be confirmed by needle EMG, even though the signs and symptoms along with imaging results suggest that radiculopathy is present. A screening EMG study involves determining whether or not a radiculopathy, if present, can be confirmed by EMG. If the radiculopathy cannot be confirmed, then presumably no number of muscles can identify the radiculopathy. If it can be confirmed, then the screen should identify this possibility with a high probability. The process of identification can be conceptualized as a conditional probability: given that a radiculopathy can be confirmed by needle EMG, what is the minimum number of muscles which must be examined in order to confidently recognize or exclude this possibility? This is a fundamentally different concept from sensitivity. It involves understanding and defining the limitations of a composite test (group of muscles).

HOW MANY AND WHICH MUSCLES TO STUDY The concept of a screening EMG encompasses identifying the possibility of an electrodiagnostically confirmable radiculopathy. If one of the muscles in the screen is abnormal, the screen must be expanded to exclude other diagnoses, and to fully delineate the radiculopathy 100

level. Because of the screening nature of the EMG exam, electrodiagnosticians with experience should look for more subtle signs of denervation and, if present in the screening muscles, then expand the study to determine if these findings are limited to a single myotome or peripheral nerve distribution. If they are limited to a single muscle, the clinical significance is uncertain.

The cervical radiculopathy screen Dillingham et al.41 conducted a prospective multicenter study evaluating patients referred to participating electrodiagnostic laboratories with suspected cervical radiculopathy. A standard set of muscles were examined by needle EMG for all patients. Those with electrodiagnostically confirmed cervical radiculopathies, based upon EMG findings, were selected for analysis. The EMG findings in this prospective study also encompassed other neuropathic findings: (1) positive sharp waves, (2) fibrillation potentials, (3)complex repetitive discharges (CRD), (4) high-amplitude, long-duration motor unit action potentials, (5) increased polyphasic motor unit action potentials, or (6) reduced recruitment. There were 101 patients with electrodiagnostically confirmed cervical radiculopathies representing all cervical root levels. When paraspinal muscles were one of the screening muscles, five-muscle screens identified 90–98% of radiculopathies, six-muscle screens identified 94–99%, and seven-muscle screens identified 96–100% (Tables 8.2 and 8.3). When paraspinal muscles were not part of the screen, eight distal limb muscles recognized 92–95% of radiculopathies. Six-muscle screens, including paraspinal muscles, yielded consistently high identification rates, and studying additional muscles lead to only marginal increases in identification. Individual screens useful to the electromyographer are listed in Tables 8.2 and 8.3. In some instances a particular muscle cannot be studied due to wounds, skin grafts, dressings, or infections. In such cases the electromyographer can use an alternative screen with equally high identification. These findings were consistent with those derived from a large retrospective study.42

The lumbosacral radiculopathy screen A similar prospective multicenter study was conducted at five institutions by Dillingham et al.43 Patients referred to participating electrodiagnostic laboratories with suspected lumbosacral radiculopathy were recruited and a standard set of muscles examined by needle EMG. Patients with electrodiagnostically confirmed lumbosacral radiculopathies, based upon EMG findings, were selected for analysis. As described above for the prospective cervical study, neuropathic findings were analyzed along with spontaneous activity. There were 102 patients with lumbosacral radiculopathies representing all lumbosacral root levels. When paraspinal muscles were one of the screening muscles, four-muscle screens identified 88–97%, five-muscle screens identified 94–98%, and six-muscle screens 98–100% (Tables 8.4–8.6). When paraspinal muscles were not part of the screen, identification rates were lower for all screens and eight distal muscles were necessary to identify 90%. If only four muscles can be tested due to limited patient tolerance, as seen in Table 8.4, and if one of these muscles are the paraspinals, few electrodiagnostically confirmable radiculopathies will be missed. A large retrospective study noted consistent findings, concluding that five muscles identified most electrodiagnostically confirmable radiculopathies.44 Dillingham and Dasher45 re-analyzed data from a study published by Knutsson almost 40 years earlier.46 In this detailed study, 206 patients with sciatica underwent lumbar surgical exploration. All subjects underwent standard EMG by the author (Knutsson) with a standard set of 14 muscles using concentric needles. The examiner was blinded to other test results and physical examination findings. In addition to

Section 3: General Diagnostic Technique

Table 8.2: Five-muscle screen identifications of patients with cervical radiculopathies

Table 8.3: Six-muscle screen identifications of the patients with cervical radiculopathies

Muscle screen

Muscle Screen

Neuropathic

Spontaneous activity

Without paraspinals Deltoid, APB, FCU

92%

65%

85%

54%

84%

58%

91%

60%

80%

55%

Deltoid, triceps

89%

64%

Biceps, triceps, EDC

94%

64%

Deltoid, triceps, PT

99%

83%

96%

75%

94%

77%

98%

79%

APB, EDC, PSM 95%

73%

FDI, PSM

Biceps, triceps, EDC FDI, FCU, PSM

90%

73%

PSM, FCU Biceps, FCR, APB

87%

With paraspinals 98%

APB, PSM

Deltoid, EDC, FDI

Biceps, triceps, FCU

PT, APB, FCU

With paraspinals

Biceps, triceps, EDC

66%

EDC, FDI, FCR, PT

PT, APB, FCU Deltoid, triceps, PT

93%

EDC, FCR, FDI

EDC, FDI, FCR Biceps, triceps

Deltoid, APB, FCU Triceps, PT, FCR

EDC, FCR, FDI Deltoid, triceps

Spontaneous Activity

Without paraspinals

Triceps, PT Biceps, triceps

Neuropathic

Deltoid, EDC, FDI PSM, FCU, triceps

95%

77%

Biceps, FCR, APB

PT, PSM

PT, PSM, triceps

The screen detected the patient with cervical radiculopathy if any muscle in the screen was one of the muscles which were abnormal for that patient. Neuropathic findings for nonparaspinal muscles included positive waves, fibrillations, increased polyphasic potentials, neuropathic recruitment, increased insertional activity, CRDs, or large amplitude/long duration motor unit action potentials. For paraspinal muscles the neuropathic category included fibrillations, increased insertional activity, positive waves, or CRDs. Spontaneous activity referred only to fibrillations or positive sharp waves. APB, abductor pollicis brevis; FCU, flexor carpi ulnaris; FCR, flexor carpi radialis; PSM, cervical paraspinal muscles; FDI, first dorsal interosseous; PT, pronator teres, supra-supraspinatus, infra-infraspinatus; EDC, extensor digitorum communis. Adapted with permission, Dillingham et al.41

Muscle abbreviations, identification criteria, and definitions are described in Table 8.2.

the EMG and surgical information, myelogram and physical examination data were derived. In this contemporary re-analysis, screens of four muscles with one being the PSM yielded an identification rate of 100%, a 92% sensitivity with respect to the intraoperative anatomical nerve root compressions, and an 89% sensitivity with respect to the clinical inclusion criteria.45 This study, using data from four decades ago, confirmed that four-muscle screening examinations provide high identification. These findings are consistent with contemporary work showing that screens with relatively few muscles (six) are optimal. As described above, these research efforts were undertaken to refine and streamline the EMG examination. The strongest studies, contemporary prospective multicenter investigations, provide the best estimates for a sufficient number of muscles.41,43 In summary, for both cervical and lumbosacral radiculopathy screens the optimal number of muscles appears to be six muscles, including the paraspinal muscles and muscles that represent all root level innervations. When paraspinal muscles are not reliable, then eight nonparaspinal muscles must be examined. Another way to think of this: ‘To minimize harm, six in the leg and six in the arm’

LUMBAR SPINAL STENOSIS With the aging population in the United States and the increasing prevalence of lumbar spinal stenosis that occurs in the elderly, this condition takes on greater public health significance. In fact, an entire edition of the Physical Medicine and Rehabilitation Clinics of North America was recently dedicated to this complex topic.47 There are few studies involving spinal stenosis and electromyography. For lumbosacral spinal stenosis, Hall and colleagues48 showed that 92% of persons with imaging-confirmed stenosis had a positive EMG. They also underscored the fact that 46% of persons with a positive EMG study did not demonstrate paraspinal muscle abnormalities, only distal muscle findings. In 76%, the EMG showed bilateral myotomal involvement.48 These results suggest that in such patients, distal limb findings may be the most prominent and electromyographers should not expect fibrillations in lumbosacral paraspinal muscles. In the United States, diabetes is on the increase, with increasing prevalence and incidence.49 Diabetes often confounds accurate diagnosis of radiculopathy and spinal stenosis.50,51 Inaccurate recognition of sensory polyneuropathy, diabetic amyotrophy, or mononeuropathy can lead to unnecessary surgical interventions. In a recent prospective study by Adamova and colleagues,50 the value of electrodiagnostic testing was assessed. There were three groups; one group composed of 29 persons with imaging confirmed clinically mild lumbar spinal stenosis, 24 subjects with both diabetes and polyneuropathy, and 25 healthy age-matched volunteers served as control subjects. In this well-designed study, sural sensory amplitudes distinguished the diabetic polyneuropathy group (an amplitude of 4.2 microvolts or less was found in 47% of diabetic patients and only 17% of stenosis patients). The ulnar F-wave was prolonged in polyneuropathy patients and not lumbar stenosis 101

Part 1: General Principles

Table 8.4:

Four-muscle screen identifications of patients with lumbosacral radiculopathies

Screen

Neuropathic

Spontaneous Activity

Four muscles without paraspinals

Screen

Neuropathic

Spontaneous Activity

Six muscles without paraspinals

ATIB, PTIB, MGAS, RFEM

85%

75%

ATIB, PTIB, MGAS, RFEM, SHBF, LGAS

89%

78%

VMED, TFL, LGAS, PTIB

75%

58%

VMED, TFL, LGAS, PTIB, ADD, MGAS

83%

70%

VLAT, SHBF, LGAS, ADD

52%

35%

VLAT, SHBF, LGAS, ADD, TFL, PTIB

79%

62%

ADD, TFL, MGAS, PTIB

80%

67%

ADD, TFL, MGAS, PTIB, ATIB, LGAS

88%

79%

97%

90%

ATIB, PTIB, MGAS, PSM, VMED, TFL

99%

93%

Four muscles with paraspinals ATIB, PTIB, MGAS, PSM

Six muscles with paraspinals

VMED, LGAS, PTIB, PSM

91%

81%

VMED, LGAS, PTIB, PSM, SHBF, MGAS

99%

87%

VLAT, TFL, LGAS, PSM

88%

77%

VLAT, TFL, LGAS, PSM, ATIB, SHBF

98%

87%

ADD, MGAS, PTIB, PSM

94%

86%

ADD, MGAS, PTIB, PSM, VLAT, SHBF

99%

89%

VMED, ATIB, PTIB, PSM, SHBF, MGAS

100%

92%

99%

91%

The screen identified the patient if any muscle in the screen was abnormal for that patient. The muscle either demonstrated neuropathic findings or spontaneous activity. Neuropathic findings for nonparaspinal muscles included positive waves, fibrillations, increased polyphasic potentials, neuropathic recruitment, increased insertional activity, CRDs, or large amplitude long duration motor unit action potentials. Spontaneous activity referred only to fibrillations or positive sharp waves. For paraspinal muscles the neuropathic category included fibrillations, increased insertional activity, positive waves, or CRDs. PSM, lumbosacral paraspinal muscles; PTIB, posterior tibialis; ATIB, anterior tibialis; MGAS, medial gastrocnemius, LGAS, lateral gastrocnemius, TFL, tensor fascia lata, SHBF, short head biceps femoris; VMED, vastus medialis; VLAT, vastus lateralis; RFEM, rectus femoris; ADD, adductor longus. Adapted from Dillingham, et al.43, with permission.

patients and the radial SNAP was similarly reduced in the group with polyneuropathy.50 These findings underscore the value of performing sensory testing in the involved extremity as well as an upper limb to fully recognize diabetic polyneuropathy when pres-

Table 8.5: Five-muscle screen identifications of patients with lumbosacral radiculopathies Screen

Neuropathic

Spontaneous activity

ATIB, PTIB, MGAS, RFEM, SHBF

88%

77%

VMED, TFL, LGAS, PTIB, ADD

76%

59%

VLAT, SHBF, LGAS, ADD, TFL

68%

50%

ADD, TFL, MGAS, PTIB, ATIB

86%

78%

ATIB, PTIB, MGAS, PSM, VMED

98%

91%

VMED, LGAS, PTIB, PSM, SHBF

97%

84%

VLAT, TFL, LGAS, PSM, ATIB

97%

86%

ADD, MGAS, PTIB, PSM, VLAT

94%

86%

Five muscles without paraspinals

Five muscles with paraspinals

Abbreviations and definitions of muscle abnormalities are the same as in Table 8.4.

102

Table 8.6 Six-muscle screen identifications of patients with lumbosacral radiculopathies

VMED, TFL, LGAS, PSM, ATIB, PTIB ADD, MGAS, PTIB, PSM, ATIB, SHBF

Abbreviations and definitions of muscle abnormalities are the same as in Table 8.4.

ent and differentiate this condition from lumbar spinal stenosis or radiculopathy.

LIMITATIONS OF THE EMG SCREEN These cervical and lumbosacral muscle screens should not substitute for a clinical evaluation and differential diagnosis formulation by the electrodiagnostic consultant. Rather, information from investigations described above allows the electrodiagnostician to streamline the EMG evaluation and make better-informed clinical decisions regarding the probability of missing an electrodiagnostically confirmable radiculopathy when a given set of muscles are studied. Performing a focused history and physical examination is essential, and these screens should not supplant such clinical assessment or a more detailed electrodiagnostic study when circumstances dictate. If one of the six muscles studied in the screen is positive, there is the possibility of confirming electrodiagnostically that a radiculopathy is present. In this case, the examiner must study additional muscles to determine the radiculopathy level and to exclude a mononeuropathy. If the findings are found in only a single muscle, they remain inconclusive and of uncertain clinical relevance. If none of the six muscles are abnormal, the examiner can be confident of not missing the opportunity to confirm by EMG that a radiculopathy is present, and can curtail the painful needle examination. The patient may still have a radiculopathy, but other tests such as MRI will be necessary to confirm this clinical suspicion. This logic is illustrated in Figure 8.2. It is important to remember that the EMG screens for cervical and lumbosacral radiculopathies were validated in a group of patients with limb symptoms suggestive of radiculopathies. These screens will not provide sufficient screening power if a brachial plexopathy is present or if a focal mononeuropathy such as a suprascapular neuropathy is the cause of the patient’s symptoms. The electrodiagnostician should always perform EMG on weak muscles to increase the diagnostic yield. These screens do not sufficiently screen for myopathies or motor neuron disease. It is incumbent upon the electrodiagnostician to formulate a differential diagnosis and methodically evaluate for the likely diagnostic possibilities, further refining the examination as data are acquired.

Section 3: General Diagnostic Technique Suspected radiculopathy

Six muscles (with PSM)-lumbar screen Six muscles (with PSM)-cervical screen

If one muscle is positive, expand study

If all muscles negative, stop EMG exam in this limb

Determine if EMG reflects 1 radiculopathy (which level), 2 entrapment neuropathy, 3 generalized condition, or 4 findings that are of uncertain relevance.

The patient will not have an electrodiagnostically confirmable radiculopathy. They may 1 not have radiculopathy, or 2 have a radiculopathy but you will not confirm this with EMG. Other diagnostic tests must be utilized such as MRI or SNRB .

Fig. 8.2 Implications of a positive EMG screening evaluation.

SYMPTOM DURATION AND THE PROBABILITY OF FIBRILLATIONS In the past, a well-defined temporal course of events was thought to occur with radiculopathies despite the absence of studies supporting such a relationship. It was a commonly held notion that in acute lumbosacral radiculopathies, the paraspinal muscles denervated first, followed by distal muscles, and that reinnervation started with paraspinal muscles and then the distal muscles. This paradigm was recently addressed with a series of investigations.52–55 For both lumbosacral and cervical radiculopathies, symptom duration had no significant relationship to the probability of finding spontaneous activity in paraspinal or limb muscles. There is no evidence to support a relationship between the duration of a patient’s symptoms and the probability of finding fibrillations in paraspinal or limb muscles. This simplistic explanation, although widely quoted in the older literature, does not explain the complex pathophysiology of radiculopathies. Electrodiagnosticians should not invoke this relationship to explain the absence or presence of fibrillations in a particular muscle.

IMPLICATIONS OF AN ELECTRODIAGNOSTICALLY CONFIRMED RADICULOPATHY It is important that the electrodiagnostician not forget that EMG does not indicate the exact cause of the symptoms, only that motor axonal loss is taking place. A spine tumor, herniated disc, bony spinal stenosis, chemical radiculitis, or severe spondylolisthesis can all yield the same EMG findings. This underscores the need to image the spine with MRI to assess for significant structural causes of electrodiagnostically confirmed radiculopathy. A negative EMG test should not curtail obtaining an MRI if clinical suspicion for radiculopathy is high. Given the low sensitivities of needle EMG, it is not an optimal screening test, but rather a confirmatory test.

There are few studies that examine outcomes and the usefulness of electrodiagnosis in predicting treatment success, the exception being surgical outcomes for lumbar discectomy in patients with herniated nucleus pulposus. Tullberg et al.56 evaluated 20 patients with lumbosacral radicular syndromes who underwent unilevel surgery for disc herniations. They evaluated these patients before surgery and 1 year later with lower limb EMG, nerve conduction studies, F-waves, and SEPs. They showed that the electrodiagnostic findings did not correlate with the level defined by CT for 15 patients. However, those patients in whom electrodiagnostic testing preoperatively was normal were significantly more likely to have a poor surgical outcome (p<0.01). In spite of the fact that the sample size in this study was small, the significant correlation of a normal electrodiagnostic study with poor surgical outcome suggests that this may be a true relationship. Spengler and Freeman57 described an objective approach to the assessment of patients preoperatively for laminectomy and discectomy for lumbosacral radiculopathy. Spengler et al.58 confirmed and underscored these previous findings regarding objective methods to assess the probability of surgical success preoperatively. In this preoperative screening evaluation, the EMG findings were combined with imaging, clinical, and psychological assessments. The EMG findings figured prominently (one-quarter of the scale): those patients with positive EMGs were more likely to have a better surgical outcome. This was particularly true when the EMG findings correlated with the spinal imaging findings, in a person without psychological or dysfunctional personality issues.

SUMMARY This chapter reviews electrodiagnostic testing for patients with suspected radiculopathies. The expected sensitivities for different electrodiagnostic tests were discussed. One cannot minimize the importance of the clinical evaluation and differential diagnosis formulation by the electrodiagnostician to guide testing. The needle EMG examination is the most useful electrodiagnostic test but is limited in sensitivity. EMG screening examinations using six muscles are possible, optimizing identification yet minimizing patient discomfort. Electrodiagnosticians should understand the strengths and limitations of electrodiagnostic testing in order to effectively use this important diagnostic tool when evaluating patients with suspected radiculopathy.

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PART 1

GENERAL PRINCIPLES

Section 3

General Diagnostic Technique

CHAPTER

The Psychiatric and Psychological Evaluation of the Chronic Pain Patient: An Algorithmic Approach

9

David A. Fishbain INTRODUCTION The goals of psychiatric and psychological assessment of the chronic pain patient (CPP) are:1 (1) diagnosis of psychiatric pathology, (2) prediction of behavior, (3) decision-making for treatment planning, (4) prediction of response to treatment, and (5) evaluation of change of symptoms (outcome). Of these goals, the most important is that of decision-making for treatment planning. This goal, however, cannot be accomplished without a clear delineation of the current psychiatric and psychological problems of the CPP. It is unfortunate that the above goals do not lend themselves readily to the formulation of a problem list out of which a problemoriented psychiatric and psychological treatment plan can be readily developed. The usual chapter on the psychiatric and psychological evaluation of the CPP ignores this issue. Generally, a generic global approach to the evaluation of the CPP is touted and presented rather than the problem-oriented approach. It is therefore the goal of this chapter to present a problem-oriented approach to the psychiatric and psychological evaluation of the CPP, utilizing the concept of ‘comorbidity.’ In addition, as there is very little information on the psychiatric and psychological evaluation of the patient with acute or subacute pain, these areas will not be addressed in this chapter. Finally, some chapters on the psychiatric and psychological evaluation of the CPP include the evaluation of pain and function. As these two topics are huge in scope, they will not be addressed in this chapter.

PSYCHIATRIC, PSYCHOLOGICAL, AND SOMATIC COMORBIDITIES ASSOCIATED WITH CHRONIC PAIN A ‘comorbidity’ has been defined as any distinct clinical entity that exists or occurs during the clinical course or treatment of the index disease.2 In this case, the index disease is chronic pain. Treatment of the index disease can be complicated by the comorbid disease or condition, which can interfere with or increase the difficulty of treatment, resulting in worse prognosis for the index disease.3 Thus, ‘comorbidity’ can lead to spurious medical outcomes and false research information in reference to the index disease. Comorbidity is a psychiatric concept because it has been noted for years that psychiatric illnesses are comorbidly associated with each other.3 However, it is only recently that the ‘comorbidity’ concept was applied to CPPs.4–10 Thirty years of research and clinical experience have crystallized into a body of knowledge, which can, with relative certainty, delineate which ‘comorbidities’ are found in the ‘usual’ chronic pain patient (CPP). This issue is important because it then simplifies the psychiatric and psychological examination of the CPP. Screening questions can be asked

for the comorbidities usually found and/or specific tests can be given to measure these comorbidities. Application of the comorbidities concept also facilitates a ‘problem-focused’ approach to the treatment of the CPP. Three major groups of comorbidities are usually associated with chronic pain (CP): (1) psychiatric problems meeting the threshold for diagnosis utilizing the Psychiatric Diagnosis And Statistical Manual of Mental Disorders, 4th edition (DSM-IV);11 (2) psychological problems which may not meet the threshold for diagnosis according to the DSM-IV, or which are not diagnosable by the DSM-IV system, e.g. conflicts over abuse (sexual or physical), etc.; and (3) somatic comorbidities, which may or not have a behavioral component. CPPs usually demonstrate significant psychiatric comorbidity. In an early study, Fishbain et al.12 reported that in a large group of CPPs treated at a pain facility, only 5.2% had no DSM-III (the system used at that time) diagnosis on Axis I where state diagnoses, such as anxiety and depression, are coded. Thirty-four point nine percent had one diagnosis, but 59.9% had more than one diagnosis on Axis I.12 Thus, overall, 94.8% had psychiatric comorbidity, while approximately 60% had complex comorbidity (more than one diagnosis). The most common/frequent comorbidities usually found in CPPs are presented in Table 9.1 in order of decreasing frequency. Psychological comorbidities are also frequently associated with chronic pain (CP). These behavioral comorbidities develop because of the environmental response of the patient developing CP and are situation dependent. For example, the usual CPP finds himself/ herself with what he/she perceives as a medical problem for which physicians cannot make an appropriate diagnosis and/or develop a cure.16 Meanwhile, this illness is associated with significant disability, which has tremendous impact on the CPP’s life, yet physicians are not able to assign an appropriate impairment which matches the disability.17 The CPP is often suspected or accused of having a drug problem, or faking,18,19 or having a psychiatric problem in order to try to assign an explanation for the mismatch between the observed medical impairment and the disability.9,20 As a result, the CPP gets into conflict with the insurance and medical systems and winds up in litigation. The litigation process is extremely stressful, often leading to economic uncertainty for the CPP until settlement. All of these diverse environmental problems can increase stress, and in fragile individuals leads to psychiatric comorbidity. The psychological comorbidities usually found in CPPs are presented in Table 9.2. This table is subdivided into 12 major areas which will be discussed below. The somatic comorbidities usually found in CPPs are presented in Table 9.3. Studies of fatigue, headache, sleep, and memory/concentration problems indicate that these comorbidities are extremely common within CPPs.4,30 Because the group of comorbidities usually present as symptoms and signs which interfere with function, the presence of any of these increases the difficulty in rehabilitating 105

Part 1: General Principles

Table 9.1: Psychiatric Comorbidities on Axis I of the DSM-IV Usually Found in CPPs in Order of Frequency4,5,7,10,12–15 1. Affective disorders (major depression, dysthymia, adjustment disorder with anxious mood) plus or minus suicidal ideation/attempt. 2. Psychoactive substance use disorders (e.g. opioid dependence/abuse, alcohol dependence/abuse, etc.). 3. Somatoform disorders (pain disorder, conversion disorder). 4. Anxiety syndromes (panic disorder, generalized anxiety disorder, agoraphobia, post-traumatic stress disorder, adjustment disorder with anxious mood, social phobia, obsessive compulsive disorder). 5. Intermittent explosive disorder (anger/irritability) with or without threatened/actual violence.

Table 9.2: Psychological Comorbidities Usually Found in CPPs4,21–29 I. Associated with injury circumstances Anger or grief over employer/ or other individual negligent in injury II. Associated with medical circumstances Organic diagnoses elusive Confusion over conflicting diagnoses and recommendation Search for a clue/desire to be the same / unrealistic expectations of treatment Dissatisfaction with medical care for failure to diagnose/cure Hostility/anger at physician for failure to diagnose/cure or for perceived incorrect input into the legal system III. Associated with difficulties with insurance carriers Perception of worsening medical condition because of non-authorization of perceived needed medical care and/or medications Anger at carrier for above or for late payment of benefits IV. Financial issues related to disability status Loss of home Loss of vehicle Loss of credit status V. Return to work issues Perception of pre-injury job stress Fear of re-injury VI. Effect of patient’s disability on leisure/sports/family activities Concern/grief over loss of ability to participate in these activities Loss of self-esteem secondary to the above Frustration/anger with self for the above VII. Effect of patient’s disability on others Spousal depression Perceived non-support or rejection by spouse Non-belief of spouse in patient’s pain as a disability Spousal oversolicitousness VIII. Childhood/adolescence issues Childhood victimization IX. Coping with pain Poor coping strategies X. Pain Fear of pain Pain beliefs XI. Personality assessment Pre-pain personality

the CPP.30 Some of the comorbidities fall under the rubric of medically unexplained symptoms. As such, they become the purview of the psychiatrist or psychologist. Because these comorbidities are usually not evaluated by the psychiatrist or psychologist, they are only presented here for the sake of completeness. The comorbidities presented in Tables 9.1 and 9.2 will be utilized below in a problem-oriented fashion to suggest an approach to the psychiatric and psychological evaluation of the CPP. This in turn lends itself to the algorithmic approach. 106

PAPER AND PENCIL TESTS TO BE UTILIZED TO COMPLEMENT THE PSYCHIATRIC OR PSYCHOLOGICAL PAIN INTERVIEW Rating scales, multiaxial inventories or personality tests At the present time, the pain clinician is confronted by a bewildering choice of paper and pencil tests alleged to measure some behavioral

Section 3: General Diagnostic Technique

Table 9.3: Somatic Comorbidities Usually Found in CPPs4,8,30–39,40,41 Headache Fatigue Sleep Sexual dysfunction Memory/concentration problems Irritable bowel syndrome Symptoms: Autonomic disturbances (dizziness, increased sweating, nausea, low blood pressure/high blood pressure, vomiting) Nonorganic physical findings Somatization Greater disability versus medical impairment

aspect which may be important to pain treatment. Before a choice can be made, however, that clinician should understand the concept of State and Trait and the differences between paper/pencil tests in reference to the concept of State–Trait. State psychiatric disorders have the following characteristics:42 they are a result of plasticity in the biobehavioral systems which allows for reversibility; they are time limited and usually respond to medications or other somatic treatments; examples of these disorders are depression and anxiety; and these disorders are coded on Axis I of the DSM-IV. On the other hand, Trait psychiatric disorders have the following characteristics:42 they are a function of plasticity which is organization and therefore does not allow for much reversibility; Trait disorders are dysfunctional personality qualities which individuals tend to develop and carry throughout life and which manifest as predictable patterns of interaction and response to stress; these disorders respond better to psychosocial treatment rather than medications; and they are coded on Axis II of the DSM-IV. Presently, the available behavioral paper/pencil tests can be divided into three rough groupings: rating scales, multiaxial inventories, and personality tests. Characteristics of each type of test are presented in Table 9.4. It is to be noted from Table 9.4 that rating scales usually measure State conditions and are therefore designed to measure change (outcome), while personality tests are designed to measure Traits and are therefore not designed to change, as it is expected that personality structure will not change. Multiaxial inventories, on the other hand, usually are a mixture of questions for State–Trait prob-

lems, and as such it is unclear whether the measurement of change is an intended consequence of the development of the test. It is to be noted that this mixing of State and Trait items in some test instruments has been described by some psychologists as ‘leading to results which are confusing and difficult to interpret.’43 Recently, however, another problem has been noted in reference to the State–Trait measurement issue and pain. Pain can be considered to be a very powerful State problem. It appears that there is significant evidence44 that the presence of pain as a State phenomenon affects the measurement of Trait (personality characteristics). In other words, the personality structure of the individual as measured by some personality tests can appear to be more pathological in the presence of pain. This finding is less clear for the multiaxial inventories,44 but because of their nature can still be a problem. What is the purpose of the above discussion? These observations would lead one to conclude that in trying to measure behavioral issues, one should utilize behavioral tests that are oriented toward measuring State problems, can measure change, and that may not be confounded by the presence of pain. As such, if possible, rating scales should be utilized. Thus, when available, rating scales have been chosen for the behavior measurements (described below).

SCREENING QUESTIONS AND MEASUREMENT APPROACHES FOR THE PSYCHIATRIC COMORBIDITIES Table 9.5 presents a series of screening questions for the psychiatric comorbidities frequently found in CPPs. In addition, this table presents what are currently thought to be the most useful paper/ pencil tests for these comorbidities. The paper and pencil tests can be administered if the CPP answers affirmatively to the screening question. As an alternate approach, the pain clinician can request a psychiatric or psychological consultation if the screening questions are answered in the affirmative. Some of the suggested tests in Table 9.5 deserve comment (below). Characteristics of these tests in reference to chronic pain will be found in Table 9.6. The Beck depression inventory (BDI) is a 21-item, self-report questionnaire relating to depression.46,47 It was developed for psychiatric patients, but has been utilized and written about extensively in reference to CPPs. As it is a rating scale, it is an excellent tool to measure improvement. Unfortunately, because of its focus on somatic symptoms (fatigue, sleep, concentration), which are frequently found in CPPs (Table 9.3), it will overestimate the severity of depression. As an example, the cutoff score for being depressed in physically healthy individuals is 10. A recent study exploring the predictive validity of the Beck in CPPs found the optimal cutoff score to be

Table 9.4: Differences Between Rating Scales, Multiaxial Inventories, and Personality Tests Rating Scales

Multiaxial Inventories

Personality Tests

Measure what?

Usually one target symptom, e.g. depression, anxiety (state conditions).

Usually a number of symptoms (may include both State and Trait measures).

Measure different facets of personality (Traits).

Able to measure change?

Designed to measure change in a symptom; developed for this purpose.

Not designed to measure change.

As personality is thought not to change, these tests are not designed for this purpose.

Can be utilized for outcome?

Yes.

No; possibly.

No.

Pain-state dependent?

Not applicable as designed to change.

May be an issue depending on symptoms measured.

Major issue as personality tests thought to measure unchanging facets of personality.

107

Part 1: General Principles

Table 9.5: Screening Questions and Measurement Approaches for the Psychiatric Comorbidities from Table 9.1 Disorders in Table 9.1

Screening Question

Affective disorders

Has your situation with pain made you feel sad, upset, or both?

Yes

Measurement Approach Psychiatric examination for DSM-IV11 criteria for depression or other form of depression. Beck Depression Inventory.46,47

Suicidal ideation

Have you recently felt like life is not worth living?

Yes

As in #1 above. As in #2 above. Beck Scale for suicide ideation.46,47

Anxiety syndromes

Has your situation with pain made you feel nervous, tense, or anxious? Has your situation with pain made you fearful of certain situations?

Yes

As in #1 above. State-Trait Anxiety Inventory.46,47 As in #1 above. Posttraumatic Chronic Pain Test.51

Yes

Are you the kind of person who is very meticulous, likes to see things in their place and very organized? Psychoactive substance use disorders

Are you a smoker? Has alcohol ever created a problem in your life? Have you ever utilized recreational drugs such as grass, acid, cocaine, downers, uppers, etc.?

Somatoform disorders (pain disorder, conversion disorder, somatization)

No screening questions. Suspicion raised if medically unexplained symptoms, such as paralysis, non-dermatomal sensory abnormalities (62), gait abnormalities, Waddell signs (62), etc. or Suspicion raised for multiple somatic symptoms.

Intermittent explosive disorder

Has your situation with pain made you feel sad, upset, or both? Has your situation with pain made you lose control of your temper?

Secondary gain and malingering

No screening questions. Suspicion raised as under somatoform disorders (above)

Yes

As in #1 above. Padau Inventory for Obsessive Compulsive Disorder.46,47

Yes

As in #1 above. Cage Questionnaire (alcohol abuse).46,47 Michigan Alcohol Screening Test (MAST).46,47 Drug Abuse Screening Test (DAST).45

Yes

As in #1 above. As in #1 above. Pain Patient Profile.48

Yes As in #4 above. State–Trait Anger Expression Inventory.39,40

Yes

Yes

As in #4 above (psychiatric or psychological examinations cannot reliably diagnose secondary gain or malingering). No paper/pencil tests have been shown to reliably diagnose malingering.

Table 9.6: Characteristics of Various Recommended Paper-pencil Tests in Tables 9.5 and 9.7

108

Test

Reliable

Valid

Developed for Pain Patients

Tested on Pain Patients

Significant Pain Literature Supports Use

Predictive Validity Pain Treatment (Outcome)

Type of Test

Beck Depression Inventory

Yes

Yes

No

Yes

Yes

?

Rating scale

Beck Scale for Suicide Ideation

Yes

Yes

No

No

No

?

Rating scale

State–Trait Anxiety Inventory

Yes

Yes

No

No

No

?

Rating scale

Post-traumatic Chronic Pain Test

Yes

Yes

Yes

Yes

No

?

Rating scale

Padau Inventory for Obsessive Compulsive Disorder

Yes

Yes

No

No

No

?

Rating scale

Cage Questionnaire

Yes

Yes

No

Yes

No

?

Rating scale

Michigan Alcohol Screening Test

Yes

Yes

No

Yes

No

?

Rating scale

Drug Abuse Screening Test

Yes

Yes

No

Yes

No

?

Rating scale

Pain Patient Profile

Yes

Yes

Yes

Yes

Yes

?

Multiaxial Inventory

State–Trait Anger Expression Inventory

Yes

Yes

No

No

No

?

Rating Scale

Section 3: General Diagnostic Technique

21.48 However, the BDI does have a significant proportion of items for cognitive symptoms of depression versus other depression rating scales.49 As such, it does not give greater weight to somatic symptoms versus other rating scales. Its use is therefore recommended. The Beck scale for suicide ideation46,47 is designed to measure current suicidal ideation. It is a 21-item scale which has been shown to have significant correlation with the BDI. However, it has been shown not to have predictive validity for suicide completion. It was developed and tested in psychiatric patients and has not had wide use in CPPs. However, it may have some utility in CPPs who voice suicidal ideation, and as it is a rating scale, it can be utilized to measure improvement in suicidal ideation. The State–Trait46,47 anxiety inventory is a 40-item self report rating that differentiates between State anxiety, a temporary condition experienced by some individuals, and Trait anxiety, the general chronic anxiety experienced by some individuals. Thus, it evaluates how likely an individual is to feel anxiety (Trait), and how anxious the individual feels at the moment (State). It has good correlation with other widely used anxiety scales. However, it has not been utilized widely in CPPs. As such, its reliability and validity here have not been determined. Recent reviews have concluded that the prevalence of post-traumatic stress disorder in CPPs has been underestimated.50 Although there are a number of tools available that are developed around the DSM-IV criteria for this diagnosis, none of these is specific to the CPP. The Post-traumatic Chronic Pain Test51 has been specifically developed for use in CPPs and as such is recommended. CPPs may suffer from subclinical obsessive-compulsive disorders. This has now been termed obsessive-compulsive spectrum disorder (OCSD).52 A number of psychiatric disorders, such as body dysmorphic disorder, anorexia nervosa, binge eating, hypochondriasis, sexual compulsions, pyromania, kleptomania, trichotillomania, compulsive buying, pathological gambling, and some self-injurious behaviors appear to demonstrate some obsessive traits and are therefore included in OCSD disorders. The OCSD patients utilize the types of mechanisms and behaviors often noted in obsessive-compulsive disorder (OCD). As such, these mechanisms and behaviors make the index disorder, e.g., gambling, worse and more difficult to treat. At issue, then, is whether these types of mechanism operate in some somatizing disorder such as pain disorder. The features of OCSD and OCD overlap in many respects, including demographics, repetitive intrusive thoughts or behaviors, comorbidity, and etiology. Most importantly, it appears that this group of disorders responds preferentially to antiobsessional drugs, such as clomipramine and the selective serotonin reuptake inhibitors (SSRIs), e.g. fluvoxamine.52,53 There have been no treatment studies utilizing the OCSD concept for pain disorders. However, a number of cases have been published.53 The author has reported15 on the positive response to antiobsessional agents in three cases of chronic atypical facial pain. Recently, there has also been a report of positive response in two patients with schizophrenia and chronic pain to clomipramine.40 This limited evidence indicates that perhaps CPPs with ‘non-specific’ pain and prominent obsessive-compulsive components should be treated with an SSRI at the first opportunity. Thus, it becomes important to identify CPPs who may have prominent OCD traits. As such, the use of the Padau Inventory for OCD is recommended.46,47 However, it is to be noted that this inventory has not been utilized in CPPs. One of the screening questions for psychoactive substance use disorder requires comment. There is currently significant evidence that smokers are at greater risk than nonsmokers for developing psychoactive substance use disorders. This relationship may also hold for CPPs. As such, smoking is including as a screening question.

Multiple somatic symptoms are allegedly found frequently in CPPs. These raise the suspicion of somatization. Historically, somatization has been measured by the MMPI or the SCL-90. However, researchers have argued that these instruments are sensitive to current somatization rather than longstanding somatization traits.54 As such, the Pain Patient Profile55 test is recommended. This inventory measures somatization and has been normed on CPPs.

SCREENING QUESTIONS AND MEASUREMENT APPROACHES FOR THE PSYCHOLOGICAL COMORBIDITIES Screening questions and suggested tests for the psychological comorbidities are presented in Table 9.7. Some of these comorbidities and measurement approaches require comment (below). As noted above, CPPs are subjected to a number of significant stressors. These stressors in some predisposed CPPs lead to the development of severe anger.56,57 Greater levels of anger were shown to be associated with poorer treatment outcome from a pain management program.58 To measure this concept the State–Trait Anger Expression Inventory46,47 is recommended. This inventory is not pain specific, but has been utilized in CPPs. Another anger inventory is the battery for Health Improvement.59 This is an inventory that contains a doctor dissatisfaction scale, which makes it unique. In addition, it has been standardized on patients in rehabilitation, with a significant percentage of those experiencing chronic pain. Its use, especially to measure doctor dissatisfaction, is therefore recommended. Chronic pain rehabilitation programs emphasize return to work. However, recent pain research has demonstrated that pre-injury job stress is predictive for return to work post pain facility treatment.27 As such, the measurement of pre-injury job stress can identify perceptions about work, which can have an impact on rehabilitation and can thus become the target of occupational rehabilitation. For this purpose, the Occupational Stress Inventory60 is recommended. This inventory has satisfactory reliability and validity in CPPs. Another scale that may be useful in such instances is the BH1259 as it has a job dissatisfaction scale. This scale assesses angry feelings directed toward the workplace. These feelings are further broken down into negative attitudes towards the company, supervision, coworkers, and the job itself. This scale has established validity and reliability with patients in physical rehabilitation. Significant others around the CPP can respond in one of three ways to the CPP’s pain behaviors: in a supportive fashion; rejecting fashion; and oversolicitous fashion. Psychological theory holds that oversolicitousness can reinforce pain behavior. On the other hand, the rejecting spouse can lead to stress. The West Haven–Yale Multidimensional Pain Inventory61,62 has a solicitousness scale and also taps the rejecting concept. It has been developed for CPPs. As such, it is recommended to measure these concepts. For a number of years a series of research reports have suggested that there is a greater proportion of victims of sexual abuse in CPP populations than in the general population. A recent review of this literature has, however, concluded that the evidence does not demonstrate a causal relationship between childhood abuse and chronic pain.41 However, the pain clinician may wish to investigate this issue. Two screening questions are suggested for this problem (see Table 9.7) and no questionnaire is recommended. The second screening question, ‘Have you ever, etc.,’ has been shown to have significant reliability as a self-report measure63 and is therefore recommended after the initial open-ended question. If the clinician wishes to investigate this issue further, the BH1259 has a Survivor of Violence scale. This scale assesses a history of physical and sexual abuse, occurring 109

Part 1: General Principles

Table 9.7: Screening Questions and Measurement Approaches for the Psychological Comorbidities from Table 9.2 Problems in Table 9.2

Screening Question

Anger associated with injury circumstances

Do you think that there was some negligence involved in your injury which resulted in your chronic pain.

Anger associated with medical circumstances

Have you been confused about your diagnosis? Will you continue working for a cure even if this treatment fails? Are you disappointed/angry at your physicians for not curing you? Have you felt like your physicians thought that you were faking?

Anger associated with difficulties with the insurance carrier

Have you felt like your insurance carrier has tried to keep you from seeing doctors that you should be seeing? Has the behavior of your insurance carrier made you angry?

Financial issues related to disability status

Has the situation with your pain caused you to experience financial stress?

Yes

As in #1 above.

Litigation issue

Has the litigation over your pain been stressful?

Yes

As in #1 above.

Return to work issues

Did you find your pre-injury job stressful?

Yes

As in #1 above. Occupational Stress Inventory.51 BH12 Job Dissatisfaction scale.50

Disability effect on leisure/sporting activities, etc.

Have you felt less positive about yourself because you could not do your usual activities?

Yes

As in #1 above.

Patient disability effect on others

Has your significant other been helpful to you with things you cannot do because of your pain? Has it seemed to you that your significant other has not believed you about your pain?

Yes

As in #1 above. West Haven–Yale Multidimensional Pain Inventory (MPI).52,53

Childhood/adolescence issues

Is there anything that I need to know about your childhood or adolescence? Have you ever been sexually abused by a relative, acquaintance, or stranger?

Yes

As in #1 above. BH12.50

Coping with pain

Do you have difficulty coping with your pain?

Yes

Coping Strategies Questionnaire Catastrophizing subscale.20

Pain beliefs

Do you lack confidence in dealing with your pain?

Yes

Arthritis Self-efficacy Scale.60

Fear of pain

Are you afraid of your pain? Do you fear moving incorrectly because of your pain.

Yes

Pain Anxiety Symptom Scale.22 Tampa Scale for Kinesophobia.23

both in childhood and adulthood. The scale was also normed on chronic pain patients. Coping can be defined as a purposeful effort to manage or mitigate the negative impact of stress.64 The pain literature has been concerned with problem-focused coping strategies to manage pain where coping has been seen as either active or passive.65 Active coping strategies are attempts by the CPP to obtain some control over the pain by using his/her resources, e.g. using relaxation techniques, etc.65 Passive coping strategies, on the other hand, indicate a reliance on external agents for pain control, e.g. medications, etc.65 The Copies Strategies Questionnaire23 was developed on CPPs and contains the catastrophizing scale. This scale has been shown to predict poor treatment outcome if elevated.66 As such, this scale is recommended to measure this concept. 110

Measurement Approach Yes

Yes

Yes

Psychiatric or psychological examination. State–Trait Anger Expression Inventory.39,40 As in #1 and #2 above. Battery for Health Improvement (Doctor Dissatisfaction Scale).50

As in #1 above.

Pain beliefs is another important concept in the pain literature as it relates to how the pain is viewed. Pain beliefs appear to be important because fear/avoidance beliefs have been shown to predict functional disability.67 Patient confidence (self-efficacy) in handling pain can be assessed via the Arthritis Self-efficacy Scale.68 In addition, CPPs may be anxious about their pain and fear it. These concepts can be evaluated via the Pain Anxiety Symptom Scale25 and the Tampa Scale for Kinesophobia.26 Data obtained through these inventories can identify target behaviors, which can then become the focus of intervention. The final issue relates to the assessment of personality in CPPs. Historically, in CPPs this has been done utilizing the MMPI or the SCL-90. Although there are numerous studies attempting to predict pain facility treatment outcome with these personality assessment tools, the research is equivocal. To date, it is unclear whether these

Section 3: General Diagnostic Technique

tools can serve this purpose, with the majority of researchers claiming that they cannot. In addition, as pointed out above,44 there are major problems with these tools in reference to State–Trait issues. As such, the use of these inventories in CPPs is to be discouraged.

CONCLUSIONS This chapter has attempted to outline an algorithmic approach to the psychiatric and psychological evaluation of the CPP based on the concept of comorbidity. In the future, it is likely that pain clinicians will be better able to define and understand the comorbidities found in CPPs. This approach will allow the identification and further evaluation of comorbidities and their treatment. Such understanding will facilitate the development of more successful treatment approaches for the chronic pain patient.

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23. Rosenstiel AK, Keefe FJ. The use of coping strategies in chronic low back pain patients: relationship to patient characteristics and current adjustment. Pain 1983; 17:33–44. 24. Druley JA, Stephens MA, Mortire LM, et al. Emotional congruence in older couples coping with wives’ osteoarthritis: exacerbating effects of pain behavior. Psychol Aging 2003; 18(3):406–414. 25. Admundson GJG, Norton GR, Allerdings MD. Fear and avoidance in dysfunctional chronic back pain patients. Pain 1997; 69:231–236. 26. Vlaeyen JWS, Kolke-Snijders AMJ, Boeren RGB, et al. Fear of movement/(re)injury in chronic low back pain and its relation to behavioral performance. Pain 1995; 62:363–372. 27. Fishbain DA, Cutler R, Rosomoff HL, et al. The prediction of CPP ‘intent,’ ‘discrepancy with intent’ and ‘discrepancy with non-intent’ for return to work post pain facility treatment. Clin J Pain 1999; 61:165–175. 28. Raphael NG, Spatz Widon C, Lange G. Childhood victimization and pain in adulthood: a prospective investigation. Pain 2001; 92:283–293. 29. Raphael KG, Chandler H, Ciccone DS. Is childhood abuse a risk factor for chronic pain in adulthood? Current Pain and Headache Reports 2004; 8:99–110. 30. Cherkin DC, Deyo RA, Street JH, et al. Predicting poor outcome for back pain seen in primary care using patients’ own criteria. Spine 1996; 21:2900–2907. 31. Fishbain DA, Cutler RB, Cole B, et al. Is pain associated fatigue responsive to multidisciplinary pain facility treatment. Accepted for publication, Pain Med 32. Fishbain DA, Cutler B, Cole B, et al. Is pain fatiguing? A structured evidence-based review. Pain Med 2003; 4(1):51–62. 33. Atkinson JH, Ancoli-Israel S, Slater MA, et al. Subjective sleep disturbance in chronic back pain. Clin J Pain 1988; 4:225–232.

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9. Fishbain DA, Cole B, Cutler RB, et al. A structured evidence-based review on the meaning of non-organic physical signs: Waddell signs (W.S.). Pain Med 2003; 4(1):51–62.

38. Lipowski ZJ. Somatization: the concept and its clinical application. Am J Psychiatry 1988; 145:1358–1366.

10. Fishbain DA, Approaches to treatment decisions for psychiatric co-morbidity in the management of the chronic pain patient. Medl Clin N Am 1999; 33(3):737–760. 11. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th edn. Washington, DC: American Psychiatric Association; 1994. 12. Fishbain DA, Goldberg M, Meagher BR, et al. Male and female CPPs categorized by DSM-III psychiatric diagnostic criteria. Pain 1986; 26:181–197. 13. Fishbain DA, Goldberg M, Steele-Rosomoff R, et al. Case report: completed suicide in chronic pain. Clin J Pain 1991; 7:29–36. 14. Asmudson GJ, Norton GR, Jacobson SJ. Social, blood/injury, and agoraphobic fears in patients with physically unexplained chronic pain: Are they clinically significant? Anxiety 1988; 2:87–95. 15. Fishbain DA, Trescott J, Cutler B, et al. Do some CPPs with atypical facial pain overvalue and obsess about their pain? Psychomatics 1993; 34(4):355–359. 16. Fishbain DA, Cutler RB, Steele-Rosomoff R, et al. The problem-oriented psychiatric examination of the CPP and its application to the litigation consultation. Clin J Pain 1994; 10:28–51. 17. Fishbain DA. Pain and psychopathology. In: Fogel BS, Schiffer RB, Rao SM, eds. Neuropsychiatry. Baltimore: Williams & Wilkins; 1996:443–483. 18. Fishbain DA. Secondary gain concept: definition problems and its abuse in medical practice. Am Pain Soc J 1994; 3:264–273.

39. Turk DC, Matyas TA. Pain-related behaviors: communication of pain. Am Pain Soc J 1992; 1:109–111. 40. Verdugo RJ, Ochoa JL. Reversal of hypesthesia by nerve block, or placebo: a psychologically mediated sign in chronic pseudoneuropathic pain patients. J Neurol Neurosurg Psych 1998; 65(2):196–203. 41. Moriwaki K, Yugae O, Nishioka K, et al. Reduction in the size of tactile hypesthesia and allodynia closely associated with pain relief in patients with chronic pain. Progress Pain Research Management 1994; 2:819–830. 42. Extein I, Bowers M. State and trait in psychiatric practice. Am J Psychiatry 1979; 136(5):690–693. 43. Phillip AE. Psychometric changes associated with response to drug treatment. Brit J Social Clin Psychol 1971; 10:138–143. 44. Fishbain DA, Cole B, Cutler RB, et al. Does the presence of chronic pain as a state phenomenon affect the measurement of personality characteristics (traits)? A structured evidence based review. Pain Med. accepted for publication. 45. Skinner HA. The drug abuse screening test. Addict Behav 1982; 7:363–371. 46. Ishak WW, Burt T, Sederer LI, eds. Outcome measurement in psychiatry, a critical review. Washington DC: American Psychiatric Publishing; 2002. 47. Sajatovic M, Ramirez LF. Rating scales in mental health. Hudson, OH: Lex-Comp; 2001.

19. Fishbain DA, Rosomoff HL, Cutler RB, et al. Secondary gain concept: A review of the scientific evidence. Clin J Pain 1995; 11:6–21.

48. Geisser ME, Roth RS, Robinson ME. Assessing depression among persons with chronic pain using the Center for Epidemiological Studies Depression Scale and the Beck Depression Inventory: a comparative analysis. Clin J Pain 1997; 13:163–170.

20. Fishbain DA, Cutler R, Rosomoff HL, et al. Chronic pain disability exaggeration/ malingering research and submaximal effort research. Clin J Pain 1999; 15(4) 244–274.

49. Marley S, Williams AC, Black S. A confirmatory factor analysis of the Beck Depression Inventory in chronic pain. Pain 2002; 99(1-2):289–298.

21. Glenton C. Chronic back pain suffers, striving for the sick role. Social Sci Med 2003; 57(11):2243–2252. 22. Pawlicki RE. A neglected issue: the family of the CPP. Am Pain Soc Bull 1992; Oct/Nov:5–6.

50. Sharp TJ. The prevalence of posttraumatic stress disorder in chronic pain patients. Current Pain and Headache Reports 2004; 8(2):111–115. 51. Muse M, Frigola G. Development of a quick screening instrument for detecting posttraumatic stress disorder in the CPP: construction of the posttraumatic chronic pain test (PCPT). Clin J Pain 1987; 2:151–153.

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Part 1: General Principles 52. Hollander E. Treatment of obsessive-compulsive spectrum disorders with SSRIs. Brit J Psych 1998; 35(S):7–12.

61. West Haven–Yale Multidimensional Pain (Inventory), Pain Evaluation and Treatment Institute. Pittsburgh, PA: Univ. of Pittsburgh Medical Center; 1995.

53. Kurokawa K, Tanino R. Effectiveness of clomipramine for obsessive-compulsive symptoms and chronic pain in two patients with schizophrenia. J Clin Psychopharm 1997; 17(4):329–330.

62. Bernstein IH, Matthew E, Jaremko, et al. On the utility of the West Haven–Yale multidimensional pain inventory. Spine 1995; 20:956–963.

54. Keller LS, Butcher JN. Assessment of chronic patient patients with MMPF-2 Minneapolis: University of Minnesota Press; 1991. 55. Pain Patient Profile. Minnetonka, MN: NCS Assessments; 1998. 56. Fishbain DA, Cutler RB, Rosomoff HL, et al. Risk for violent behavior in patients with chronic pain: evaluation and management in the pain facility setting. Pain Med 2000; 1(2):140–155. 57. Bruehe S, Burns JW, Chung OY, et al. Anger and pain sensitivity in chronic low back pain patients and pain free controls: the role of endogenous opioids. Pain 2002; 99:223–233. 58. Burns JW, Johnson BJ, Devine J, et at. Anger management style and the prediction of treatment outcome among male and female chronic pain patients. Behav Res Ther 1998; 36:105–162. 59. Bruns D, Disorbio JM. Manual for the Battery for Health Improvement 2. Minnetonka, MN: NCS Assessments; 2003. 60. Occupational Stress Inventory. Odessa, FL: Psychological Assessment Resources; 1989.

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63. Barbe RP, Bridge JA, Brimaher B, et al. Lifetime history of sexual abuse, clinical presentations, and outcome in a clinical trial for adolescent depression. Clin J Psychiatry 2004; 65(1):77–83. 64. Jensen MP, Turner JA, Romano JM, et al. Coping with chronic pain: a critical review of the literature. Pain 1991; 47:249–283. 65. Brown GK, Nicassio PM. Development of a questionnaire for the assessment of active and passive coping strategies in CPPs. Pain 1987; 31:53–64. 66. Coughlan GM, Ridout KL, Williams AC De C, et al. Attrition from a pain management programme. Br J Clin Psychol 1995; 34:471–479. 67. Crombez G, Vlaeyen JW, Heuts PH, et al. Pain-related fear is more disabling than pain itself: evidence on the role of pain-related fear in chronic back pain disability. Pain 1999; 80:329–339. 68. Lorig K, Chastain RI, Ung E, et al. Development and evaluation of a scale to measure perceived self-efficacy in people with arthritis. Arthritis Rheum 1989; 32:37–44.

PART 1

GENERAL PRINCIPLES

Section 4

Practical Pharmacology

CHAPTER

Nonsteroidal Antiinflammatory Drugs

10

Gurkirpal Singh

INTRODUCTION The effective management of acute postoperative pain is important for both humanitarian and psychological reasons. Despite the advances in analgesic agents and delivery systems over recent years, postoperative pain is often undertreated.1,2 The undertreatment of acute postoperative pain has important implications for both patients and the healthcare system. Undertreated postoperative pain prevents sleep, which causes fatigue and delays mobilization.3 It prolongs patient suffering and is associated with a number of undesirable outcomes such as delayed healing, extended hospitalization, and the development of chronic pain conditions and depressive disorders.4–6 Its overall negative effect on patient function increases healthcare utilization and costs.7 Multimodal analgesia is currently recognized as the best postoperative method to reduce pain and analgesia requirements.8 Reduced pain improves recovery, reduces postoperative morbidity, and lowers costs.9–11 The multimodal approach uses a combination of drugs and delivery techniques. For example, the combination of drugs such as opioids, non-specific nonsteroidal antiinflammatory drugs (NSAIDs), cyclooxygenase-2 (COX-2)-specific inhibitors, and local anesthetics may decrease adverse effects and better optimize pain control. Delivery techniques such as patient-controlled analgesia, epidural blocks, and regional blocks are often better at optimizing pain control with fewer adverse effects than single-dose delivery. Although opioids and non-specific NSAIDs are effective analgesic agents, their use is limited by their adverse effect profiles. Opioids can cause respiratory depression, nausea, vomiting, constipation, pruritis, urinary retention, hypotension, tolerance, and dependency.12 Non-specific NSAIDs can cause gastrointestinal toxicity, renal problems, platelet dysfunction, and bleeding complications, the latter of which may be particularly problematic in the surgical setting.13–15 The adverse effects of non-specific NSAIDs arise as a result of their inhibitory effect on COX-1.16,17 COX-2-specific inhibitors were developed to provide the beneficial antiinflammatory and analgesic effects of non-specific NSAIDs while sparing the protective functions mediated by COX-1. This chapter will discuss the epidemiology and pathophysiology of postoperative pain and review the pharmacologic agents available for postoperative pain management, focusing on the non-specific NSAIDs and COX-2-specific inhibitors.

EPIDEMIOLOGY AND UNDERTREATMENT OF POSTOPERATIVE PAIN Postoperative pain is one of the most common types of acute pain. Based on data from the National Hospital Discharge Survey, 42.5 million procedures were performed on hospital inpatients during 2002 in the United States alone.18 The number of outpatient pro-

cedures is difficult to quantify, but probably exceeds this number.7 Up to 88% of patients may report postoperative pain, and of those, 34–62% experience moderate to severe postoperative pain.1,2 Although postoperative pain is treatable, over the last 50 years its undertreatment has been well documented in the literature.19 The reasons for this are not completely understood, but are probably fostered by the notion that pain is an inevitable consequence of surgery.2,20 Other reasons may include a lack of formal education in pain management, physicians’ concerns regarding potential opioid addiction and drug tolerance, and difficulties in assessing pain severity.21 Furthermore, patients themselves may fail to request or use analgesia because of fears about adverse effects or dependency.

PRACTICE GUIDELINES FOR PAIN MANAGEMENT IN THE PERIOPERATIVE SETTING Several organizations have published treatment standards for the management of pain. The World Health Organization has produced guidelines for cancer pain relief,22 and the American Pain Society has developed guidelines for the management of acute and cancer pain (Table 10.1).23 The publication of the Joint Commission on Accreditation of Healthcare Organizations’ pain standards has been instrumental in promoting the increased acceptance of pain as the fifth vital sign.24,25 These guidelines highlight the underlying issues in pain management: (1) pain should be regularly and properly assessed and treated accordingly, and (2) patients in pain should not be ignored and, when possible, should be educated about their treatment options and allowed to participate in decisions on management of their pain. The goal of these and other guidelines is to advocate a comprehensive approach to patient care following surgery that will lead to better patient outcomes through more effective pain management.

PATHOPHYSIOLOGY OF POSTOPERATIVE PAIN Nociception and inflammatory pain Nociceptive input is initiated by tissue damage and prolonged by inflammation. In response to tissue injury, specialized peripheral nociceptors promote the release of inflammatory mediators, neurotransmitters, and growth factors from traumatized tissue and sequestrated intravascular cells.26,27 The resulting sensory input is conveyed by visceral and somatic neurons to the dorsal horns and ascending spinal pathways to the thalamic, limbic, and cortical structures involved in affective and sensory-discriminative responses. Although the sensory 113

Part 1: General Principles

Table 10.1: American Pain Society Quality Improvement Guidelines for the Management of Acute and Cancer Pain23 Recognize and treat pain promptly Chart and display the patient’s self-report of pain Commit to continue improvement of one or several outcome variables Document outcomes based on data and provide prompt feedback Make information about analgesic drugs readily available Promise the patient attentive analgesic care Define explicit policies for the use of advanced analgesic technologies Examine the process and outcomes of pain management with the goal of continuous improvement Reprinted from JAMA, vol. 274, American Pain Society Quality of Care Committee, quality improvement guidelines for the treatment of acute pain and cancer pain, pp. 1874–1888, 1995, with permission from the American Medical Association.

input is extensively modulated both peripherally and centrally, the end result is the subjective awareness of pain.28 This inflammatory pain is characterized by hypersensitivity to stimuli both at the site of injury (primary hyperalgesia) and at sites distant to the site of injury (secondary hyperalgesia).26,29 While primary hyperalgesia is the result of peripheral pain mechanisms, secondary hyperalgesia involves central modulatory systems, including central sensitization.29 Fortunately, the hypersensitivity caused by inflammation usually normalizes if the disease process is controlled.26

Peripheral and central sensitization Peripheral sensitization or heterosensitization is caused by exposure of nociceptor terminals to sensitizing agents. Released by damaged tissue or by inflammatory cells, these sensitizing agents include the inflammatory mediators, prostaglandin E2, bradykinin, and serotonin as well as various nerve growth factors.26,30 By activating intracellular signaling cascades, increased peripheral input into the central nervous system increases neuronal synaptic responses and decreases neuronal inhibition. If this amplification of sensory input is prolonged, both nocuous and innocuous neuroActivation

The synthesis of prostanoids is essential for the generation of inflammatory pain.32 Arachidonic acid is released from phospholipids in the cell membrane by phospholipid A2 enzymes and is converted to prostaglandin G2 and then prostaglandin H2 in a 2-step reaction catalyzed by COX (Fig. 10.2).32 Prostaglandin H2 is converted into the prostaglandin isoforms prostaglandin E2, prostaglandin D2 or prostaglandin F2a, prostacyclin, or thromboxane A2 through the action of tissue-specific isomerases.32,33 Differential expression and induction patterns of these enzymes and prostanoid receptors have important roles in the cellular effects of the prostanoids. COX exists as two isoforms: COX-1, which is responsible for homeostatic prostanoid synthesis, and COX-2, which is responsible

VRI Ca2+

Heat Mechanical

Voltage gated sodium channels

mDEG P2X3

stimuli

Chemical

Generator potentials

Modulation

Sensitizing stimulus PGE2 Bradykinin

PKA PKC3 EP

BK

Modification SNS/PN3 Increased gene expression

Abnormal sensitivity

Action potentials

Peripheral sensitization (heterosensitization)

VRI

External stimulus Heat

114

Prostaglandin production and the expression of COX-1 and COX-2

Pain and auto-sensitization

External

VRI

nal inputs cause activation of spinal cord cells. The result is central sensitization.26,31Prolonged amplification results in anatomic and neurochemical changes leading to neural plasticity in primary sensory neurons and is categorized as activation, modulation, and modification (Fig. 10.1).26

SNS/PN3

Substance P BDNF Epidermis Expression in A fibers of C-fiber markers Phenotype switch

Dermis C-fiber loss Denervation

Fig. 10.1 Categories of neuronal plasticity in primary sensory neurons.26 Reprinted from Science, vol 9, Woolf CJ and Salter MW, Neuronal plasticity: increasing the gain in pain, pp. 1765–1769, 2000, with permission from The American Association for the Advancement of Science.

Section 4: Practical Pharmacology Membrane phospholipids Phospholipase A2 AA Cyclooxygenase activity of COX PGG2

Peroxidase activity of COX

Prostanoid synthase activity PGH2

PGD2

PGF2α

PGE2

PGI2

TXA2

for proinflammatory prostanoid production.34 COX-1 is constitutive within platelets and is associated with the production of thromboxane, which strongly promotes platelet aggregation, and both COX-1 and COX-2 are constitutively expressed in the central nervous system, dorsal root ganglia, and kidney.35–38 In addition, COX-2 expression can be induced by several factors, including neurotransmitters and proinflammatory cytokines,39 and the role of inducible COX-2 in central nervous system responses to inflammation is well established. Its expression is upregulated within the central nervous system in response to interleukin-1β, leading to elevations in central prostanoid production.40 Several animal studies have assessed the relative contributions of COX-1 and COX-2 to prostaglandin release in the spinal cord. The selective COX-1 inhibitor SC560 significantly reduced nociceptive behavior and abolished spinal prostaglandin E2 release in a rat model, while celecoxib had no effect on either parameter.41 These findings indicated that nociception-evoked prostaglandin release was primarily caused by COX-1 and was independent of COX-2, and suggested that the efficacy of celecoxib in early injury-evoked pain may be lower than that of non-specific NSAIDs. In contrast, another study in a rat model suggested that COX-2, but not COX-1, mediated antihyperalgesic activity and release of spinal prostaglandin E2.42 In rats with chronic indwelling catheters, acute thermal hyperalgesia evoked by spinal delivery of substance P or N-methyl-D-aspartate and thermal hyperalgesia induced by carrageenan was suppressed by intrathecal and systemic COX-2 inhibitors, while systemic but not spinal administration of a COX-1 inhibitor reduced carrageenanevoked thermal hyperalgesia, and neither systemic nor spinal COX-1 inhibition had an effect on spinal hyperalgesia evoked by substance P. Intrathecal substance P enhanced prostaglandin E2 release, and this effect was diminished by systemic delivery of non-specific NSAIDs and COX-2-specific inhibitors, but not by a COX-1-specific inhibitor. Therefore, constitutive spinal COX-2, but not COX-1, mediates acute antihyperalgesic effects of both spinal and systemic COX-2 inhibitors. More recently, inhibition of constitutively expressed spinal COX2 immediately following peripheral tissue injury has been found to reduce injury-induced activation of primary afferent neurons and spinal neurons and mechanical and thermal hyperalgesia prior to any measurable upregulation of COX-2 protein.36 This early research has suggested that constitutive spinal COX-2 may play a role in the

Fig. 10.2 Prostanoid biosynthetic pathway.32 Reprinted from Trends in Molecular Medicine, vol 8, Samad TA, Sapirstein A, and Woolf CJ, Prostanoids and pain: unraveling mechanisms and revealing therapeutic targets, pp. 390–396, 2002, with permission from Elsevier.

development of hyperalgesia following peripheral tissue injury, and that blockade of this constitutive expression prior to injury may lessen the peripheral and central sensitization occurring after tissue injury. Considering the intrathecal potency of COX-2 inhibitors, the comparable efficacy of intrathecal and systemic COX-2 inhibitors in hyperalgesic states not associated with inflammation, and the onset of antihyperalgesic activity prior to COX-2 upregulation, it has been hypothesized that modulation of constitutive spinal COX-2 is a principal antihyperalgesic mechanism of COX-2 inhibitors.43

Role of COX-2 in peripheral sensitization Inflammation induces the expression of COX-2, which in turn promotes the release of prostanoids. The resulting sensitization of peripheral nociceptor terminals causes primary hyperalgesia. Secondary hyperalgesia due to increased neuronal excitability in the spinal cord causes central sensitization.26,29

Role of COX-2 in central sensitization Inflammation induces COX-2 expression in spinal cord neurons and other regions of the central nervous system. This widespread induction causes an 80-fold increase in the levels of prostaglandin E2 in the cerebrospinal fluid.40 The major inducer of COX-2 upregulation is interleukin-1β,44,45 and its role in the regulation of central prostanoid production was confirmed by intraspinal administration of an interleukin-converting enzyme or COX-2-specific inhibitor. Intraspinal injection resulted in decreased inflammation-induced central prostaglandin E2 levels and reduced centrally generated inflammatory pain hypersensitivity.40 These experimental findings were confirmed in a study in 30 patients undergoing thoracotomy for lobectomy who were randomized to receive nimesulide 100 mg b.i.d. or ibuprofen 400 mg t.i.d.46 Cerebrospinal fluid samples were analyzed for 6-keto-prostaglandin F1 α, the principle metabolite of prostacyclin. COX-1 and COX-2 activity was determined by measuring serum thromboxane B2 and endotoxin-induced prostaglandin E2 generation in whole blood. Nimesulide was found to be selective for COX-2, while ibuprofen was COX nonselective. Mean levels of 6-keto-prostaglandin F1 α in the cerebrospinal fluid increased following surgery and were significantly suppressed by nimesulide, but not by ibuprofen. Patients receiving nimesulide also had significantly lower pain scores (p<0.001), morphine requirement (p=0.0175), and falls in peak expiratory flow rate (p<0.001). This 115

Part 1: General Principles

study demonstrated that increases in spinal prostaglandin synthesis after thoracotomy were repressed by a COX-2-selective agent.

specific NSAIDs may also be used as adjuncts to opioids for the management of more severe postoperative pain.

PHARMACOLOGIC AGENTS FOR MANAGEMENT OF POSTOPERATIVE PAIN

Monotherapy

Multimodal analgesia using a combination of analgesics, local anesthetics, and delivery techniques is the best method to control postoperative pain. Analgesics that can be used include simple analgesics, opioids, non-specific NSAIDs, and COX-2-specific inhibitors.

Simple analgesics Simple analgesics such as acetaminophen are a common monotherapy for treating mild to moderate pain. While acetaminophen can effectively treat pain of relatively low intensity, it does not provide any therapeutic benefit to an underlying inflammatory process. Acetaminophen is useful for aspirin-sensitive asthmatics and individuals at risk of gastrointestinal complications in whom non-specific NSAIDs are contraindicated.47 Although acetaminophen is routinely used in combination with opioids such as codeine, tramadol, hydrocodone, and oxycodone to reduce opioid use,48 this combination can result in more adverse effects than acetaminophen alone. In adults, acetaminophen is administered to a maximum daily dose of 500 mg, although this should be reduced in patients with a history of heavy alcohol intake. Long-term use in combination with alcohol can be complicated by severe and sometimes fatal liver damage.47

Opioids Opioids are highly effective in the management of severe, acute postoperative pain. The agonist or ‘pure’ morphine-like drugs range in potency from ‘less potent’ agents such as oxycodone, which is suitable for moderate pain, to potent drugs such as fentanyl, which is often used intraoperatively. There are also drugs such as buprenorphine, which possess both agonist and antagonist actions. Although the agonist–antagonist opioids are the least effective opioid type, they have the lowest risk of adverse events and typically show a ceiling effect in both analgesic activity and effect on respiratory depression.6,12 Finally, there are opioid antagonists such a naloxone that are pure antagonists without any analgesic effect.6 Although effective, opioid use is associated with multiple adverse effects, including sedation, hypotension, respiratory depression, emesis, paralytic ileus, urinary retention, pruritis, and dependence.49– 51 These effects can complicate and lengthen the postoperative recovery period, and concerns about poor tolerability and perceived dependency can result in inadequate dosing. Controlling the variability in plasma concentration by the use of patient-assisted devices may reduce these adverse effects. Even though opioids can provide a sustained analgesic effect and improved function in selected, well-monitored patients without the development of tolerance or significant toxicity,12 the use of adjunctive agents in combination with opioids is still often desirable. The synergistic coadministration of other analgesics reduces opioid doses and decreases adverse effects. In addition, opioids are ineffective when used alone for the management of movement-related pain, and supplementation with other types of medication is needed during postoperative mobilization.

Non-specific NSAIDs Non-specific NSAIDs are often effective for mild to moderate pain following outpatient surgery,52 although their analgesic efficacy and adverse effects show marked variation among individuals. Non116

Ketorolac tromethamine is the only parenteral non-specific NSAID approved for use in the United States and is the current standard for comparison. Although ketorolac is useful in the management of postoperative pain, it is a reversible inhibitor of platelet aggregation.53,54 Theoretically, platelet inhibitors should increase the risk of postoperative bleeding. However, a postmarketing surveillance study of patients receiving 10 272 courses of parenteral ketorolac therapy reported only a small increase in operative-site bleeding, which was limited to elderly patients and those receiving high-dose ketorolac or more than 5 days of treatment.55 Other studies, however, have reported an increase in operative and postoperative bleeding,56–59 including cases of severe and near-fatal postoperative bleeding.59 Studies in healthy volunteers have found single-dose ketorolac to prolong bleeding time significantly,60 with one study noting a 50% increase in bleeding time 4 hours after a single intramuscular dose.61 Consequently, ketorolac is not routinely used before surgery in which operative and postoperative bleeding may be problematic. Ketoprofen is a commonly used non-specific NSAID that provides effective analgesia for mild to moderate pain. It is also used concurrently with opioids in the treatment of severe pain, and several studies have investigated its efficacy as a monotherapy for postoperative pain relief. A study in patients with moderate or severe pain following dental surgery reported that ketoprofen provided a superior level of meaningful pain relief at 6 hours compared with liquigel ibuprofen and acetaminophen. Ibuprofen, however, provided faster relief and superior overall efficacy.62 In a further study following dental surgery, ketoprofen demonstrated lower pain intensity from 2 to 6 hours after first drug intake and decreased swelling compared with acetaminophen.63 Following minor pediatric surgery, ketoprofen had an earlier onset and longer duration of analgesia than acetaminophen.64 Although the data were from too small a study to assess the effects of ketoprofen on hemorrhage rate, an anesthetic induction dose of ketoprofen in patients undergoing adenoidectomy did not increase the rate of blood loss.65 A meta-analysis of 7 randomized, double-blind tonsillectomy trials (n=505) showed that postoperative use of non-specific NSAIDs, such as ketorolac, ibuprofen, or ketoprofen, increased both the risk of postoperative bleeding requiring treatment and the risk of reoperation for hemostasis.66 The authors of the meta-analaysis searched PubMed® and the Cochrane Controlled Trials Register for randomized, double-blind studies published between January 1966 and May 2001. Trials were required to meet quality criteria for inclusion and were selected if they reported data on postoperative bleeding in patients treated with non-specific NSAIDs after tonsillectomy with or without adenoidectomy. In the 7 trials combined in the metaanalysis, the incidence of postoperative bleeding treated medically or surgically was 7.3%. The most common consequence of this bleeding was admission to the emergency department.

Adjunctive therapy In the early postoperative period, a combination of opioids and nonspecific NSAIDs can improve analgesic efficacy compared with either agent alone.12 The combined use of ketoprofen and opioids in patients with severe pain lowers opioid doses and reduces the incidence of opioid-related adverse events.67 Other studies have also shown that combination therapy lowers opioid requirements and decreases opioid-induced nausea, constipation, somnolence, and

Section 4: Practical Pharmacology

respiratory depression.52 The resulting increase in gastrointestinal motility may permit an earlier return to oral nutrition.68 Although the use of ketorolac and diclofenac has been reported to reduce morphine consumption by 30–40% following abdominal and orthopedic surgery,69,70 non-specific NSAIDs increase the risk of postoperative bleeding.13 For this reason, non-specific NSAIDs should probably not be used following hip arthroplasty. In addition, the common use of anticoagulation therapy with heparin following total knee surgery to prevent deep vein thrombosis also increases the risk of postoperative bleeding. A study in patients receiving short-term ketorolac infusion following laparoscopic day surgery reported that, although ketorolac had an opioid-sparing effect over 36 hours of postoperative administration, it was not associated with continued benefits after this time.71 Although patients required significantly less fentanyl in the recovery ward and significantly less codeine prior to and following discharge, patients’ description of discomfort on performing common activities did not indicate any beneficial effect of ketorolac.

Adverse effects of non-specific NSAIDs Although non-specific NSAIDs do not share many of the adverse effects associated with opioid use, non-specific COX inhibition can cause gastrointestinal ulceration and bleeding, platelet dysfunction, prolonged bleeding time, elevated blood pressure, renal toxicity, and hepatic dysfunction.13–15,55 These events may range from mild to potentially life-threatening complications. The gastrointestinal adverse effects of non-specific NSAIDs are caused by inhibition of COX-1. In the gastrointestinal tract, COX-1 produces prostaglandin E2, which has a protective effect on the gastrointestinal mucosa by limiting acid damage and promoting mucus secretion, bicarbonate release, and adequate blood flow.16 The resulting gastrointestinal damage caused by COX-1 inhibition increases the incidence of ulceration, perforation, and potentially fatal gastrointestinal bleeding.15 Non-specific NSAIDs also inhibit normal platelet function and aggregation. Inhibition of COX-1 reduces platelet aggregation by blocking the production of thromboxane A2. Because COX-2 normally inhibits prostacyclin, a protein that increases platelet aggregation, normal platelet aggregation is further reduced.60 Although prostaglandins do not play a major role in the maintenance of basal renal function under normal physiologic conditions, prostaglandins produced by constitutive renal COX-1 and COX-2 may be vital to the maintenance of renal perfusion and glomerular filtration rate.72,73 In patients with compromised renal hemodynamics, such as the elderly or those with preexisting renal dysfunction

or congestive heart failure, NSAID-mediated COX-1 inhibition can result in acute renal failure.74

COX-2-specific inhibitors Because of the many adverse effects associated with opioids and non-specific NSAIDs, alternative analgesic agents are needed. The antiinflammatory and analgesic benefits of NSAIDs are due to the inhibition of COX-2 at the site of inflammation.34,39,75 The belief that selective inhibition of COX-2 would produce the beneficial effects of NSAIDs, but avoid disruption of COX-1-mediated protective functions, led to the development of COX-2-specific inhibitors. The indications for the currently available COX-2-specific inhibitors in the United States and Europe are presented in Table 10.2.

Analgesic efficacy of COX-2-specific inhibitors Studies of COX-2-specific inhibitors in the perioperative setting demonstrate that they provide effective analgesia while reducing opioid consumption in the range of 20–70%.7

Parenteral COX-2-specific inhibitors Parenteral administration of analgesia after surgery provides rapid pain relief and facilitates dosing of patients unable to ingest or tolerate oral formulations. Parecoxib sodium (parecoxib) is the only available parenteral COX-2-specific inhibitor. Licensed in Europe, Mexico, and several countries in South America, it is used for the shortterm treatment of postoperative pain at a dose of 40 mg i.v./i.m., with optional repeat dosing of 20 mg daily as needed. Furthermore, parecoxib, as the prodrug of the oral COX-2-specific inhibitor valdecoxib, has the potential to facilitate a parenteral-to-oral switch. Parecoxib and valdecoxib provide analgesic efficacy in a 1:1 ratio, so the preoperative use of parecoxib followed by postoperative oral valdecoxib may provide an effective combination regimen for pain control without the need for further analgesic agents. The analgesic efficacy and opioid-sparing effects of parecoxib have been demonstrated in a number of studies of postoperative pain (Table 10.3). Following total hip arthroplasty, the use of parecoxib 20 mg or 40 mg significantly reduced the total amount of morphine used over 36 hours compared with placebo (p<0.01).76 Patients treated with parecoxib also reported significantly greater maximum pain relief and earlier discontinuation of morphine therapy. Parecoxib 20 mg or 40 mg has also demonstrated opioid-sparing effects and significant analgesic efficacy compared with morphine alone (p<0.05) following total knee replacement surgery.77 Another study compared parecoxib 20 mg and 40 mg, morphine 4 mg, and ketorolac 30 mg following unilateral total knee replacement surgery. Although the onset

Table 10.2: Indications for Currently Available COX-2-Specific Inhibitors in the United States and Europe Indications COX-2-Specific Inhibitor

Formulation

United States

Europe

Celecoxib

Oral

Osteoarthritis Rheumatoid arthritis Acute pain Primary dysmenorrhea Familial adenomatous polyposis

Osteoarthritis Rheumatoid arthritis

Parecoxib

Parenteral

Valdecoxib

Oral

Short-term management of acute postoperative pain Osteoarthritis Rheumatoid arthritis Primary dysmenorrhea

Osteoarthritis Rheumatoid arthritis Dysmenorrhea

117

Part 1: General Principles

Table 10.3: Studies Investigating the Use of Parecoxib in the Management of Preoperative and Postoperative Pain Study

Treatment and Model

Results

Barton et al.81

Parecoxib 20 mg or 40 mg Ketorolac 30 mg Morphine 4 mg Gynecologic laparotomy surgery

Time to onset of analgesia and magnitude and duration of analgesia were similar with parecoxib 20 mg or 40 mg and ketorolac 30 mg

Daniels et al.79

Parecoxib 20 mg and 40 i.m. and i.v. Ketorolac 60 mg Oral surgery

Both parecoxib doses were comparable to ketorolac in time to onset of analgesia, but parecoxib 40 mg had a significantly longer duration of action (p<0.05)

Hubbard et al.77

Parecoxib 20 mg and 40 mg b.i.d. Total knee arthroplasty

Patients receiving parecoxib 20 mg or 40 mg b.i.d. consumed 15.6% and 27.8% less morphine, respectively, than placebo-treated patients (p<0.05 Both doses of parecoxib provided significantly greater pain relief than morphine alone from 6 hours (p<0.05)

Joshi et al.83

Preoperative parecoxib 40 mg followed by oral valdecoxib 40 mg Laparoscopic cholecystectomy

Parecoxib-treated patients used 21% less fentanyl than placebo-treated patients and had a lower pain intensity. Parecoxib/valdecoxib-treated patients also had significantly lower requirement for supplemental analgesics after discharge (p<0.05)

Malan et al.76

Parecoxib 20 mg and 40 mg Total hip arthroplasty

Parecoxib reduced morphine use by 22.1% and 40.5% compared with placebo (p<0.01) Parecoxib was associated with significantly greater maximum pain relief (p<0.05)

Malan et al.82

Parecoxib 40 mg Morphine 12 mg i.m. Gynecologic laparotomy

Parecoxib 40 mg i.m. had comparable analgesic efficacy but a significantly longer duration of analgesic action than morphine 12 mg

Mehlisch et al.80

Parecoxib 1, 2, 5, 10, 20, 50, and 100 mg i.v. Ketorolac 30 mg Oral surgery

Parecoxib 20–100 mg and ketorolac had a similarly rapid onset of analgesia (within 11 min) and similar analgesic efficacy and mean global evaluation scores Parecoxib 50 mg and 100 mg had a significantly longer duration of analgesia than ketorolac

Rasmussen et al.78

Parecoxib 20 mg and 40 mg Morphine 4 mg Ketorolac 30 mg Total knee replacement surgery

Onset of analgesia was similar in all groups, though the level and duration of analgesia with parecoxib 40 mg were similar to ketorolac and significantly superior to morphine

of analgesia in all groups was similar, the level and duration of analgesia with parecoxib 40 mg was significantly superior to morphine 4 mg.78 Single-dose parecoxib 20 mg and 40 mg i.m. and i.v. have been compared with ketorolac 60 mg following oral surgery.79 The analgesic efficacy of both parecoxib dosing regimens was comparable, but time to use of rescue medication was longer following intramuscular administration. Parecoxib 40 mg was found to be comparable to ketorolac in most measures of analgesia, but had a longer duration of action. In another oral surgery study, single-dose parecoxib 20–100 mg and ketorolac 30 mg demonstrated a similarly rapid onset of analgesia (within 11 minutes) and comparable analgesic efficacy.80 Dose-proportional increases in the duration of analgesia were observed with parecoxib 50 mg and 100 mg, showing a significantly longer duration of analgesia than ketorolac. Following gynecologic laparotomy surgery, parecoxib 20 mg or 40 mg demonstrated analgesic efficacy similar to that of intravenous ketorolac 30 mg and a similarly rapid time to onset of analgesia (10–23 min).81 Parecoxib also demonstrated similar analgesic efficacy and a longer duration of action than morphine 12 mg i.m. in this model.82 The use of preoperative single-dose parecoxib 40 mg followed by a single oral dose of valdecoxib 40 mg following laparoscopic cholecystectomy confirmed the opioid-sparing effects and analgesic efficacy of parecoxib compared with placebo.83 118

Parecoxib was well tolerated in all of these trials,77,78,80,82 and the adverse events reported in these studies (such as nausea and dizziness) are typical of those seen after surgery.84 Importantly, parecoxib showed no evidence of treatment-related serious adverse events such as wound bleeding, renal dysfunction, or upper gastrointestinal bleeding.78

Oral COX-2-specific inhibitors The efficacy of the oral COX-2-specific inhibitors celecoxib and valdecoxib for the treatment of preoperative and postoperative pain is summarized in Table 10.4. For treating moderate to severe pain following outpatient orthopedic surgery, multiple dosing with celecoxib 200 mg is significantly more effective and better tolerated than hydrocodone 10 mg/acetaminophen 100 mg.85 The use of celecoxib preoperatively in combination with other analgesics has also been reported to provide improved analgesic efficacy compared with single-agent therapy. Premedication with celecoxib 200 mg and acetaminophen 2000 mg significantly reduced the incidence of severe pain following otolaryngologic surgery compared with either agent alone.86 Patient satisfaction with treatment was also significantly higher with this combination than with acetaminophen alone. A study in 60 patients undergoing spinal stabilization demonstrated significant opioid-sparing effects following preoperative administration

Section 4: Practical Pharmacology

Table 10.4: Studies Investigating the use of Oral COX-2-Specific Inhibitors in the Management of Preoperative and Postoperative Pain Study

Treatment and Model

Results

Gimbel et al.85

Celecoxib 200 mg (single- and multiple-dose) Hydrocodone 10 mg/acetaminophen 100 mg Ambulatory orthopedic surgery

Pain relief at 8 hours was comparable following single-dose treatment. Pain relief over 5 days was superior with celecoxib following multiple-dosing regimen Following multiple dosing, celecoxib-treated patients had a lower requirement for rescue analgesia (12% vs. 20%, p<0.05), lower pain intensity scores (p < 0.001), needed fewer study drug doses (p ≤ 00.01), and a lower incidence of adverse events (43% vs. 89%, p < 0.001)

Issioui et al.86

Celecoxib 200 mg and/or acetaminophen 2000 mg (preoperative) Otolaryngologic surgery

The incidence of severe pain was lower with combination therapy (14%, p < 0.05 versus placebo) than with celecoxib (25%, p < 0.05 versus placebo), acetaminophen (25%) or placebo (50%) Patient satisfaction was also higher with combination therapy (61%, p < 0.05 vs. placebo) than with celecoxib (46%, p < 0.05 vs. placebo), acetaminophen (32%) or placebo (11%)

Reuben & Connelly87

Celecoxib 200 mg Rofecoxib 50 mg Spinal stabilization

Morphine consumption was decreased in celecoxib-treated patients during the first 8 hours after surgery, while rofecoxib-treated patients used less morphine throughout the 24-hour study period Analgesic efficacy was similar in both groups in the first 4 hours, but rofecoxib had an extended analgesic effect that lasted throughout the study

Camu et al.95

Valdecoxib 20 mg or 40 mg b.i.d. (preoperatively and postoperatively in patients receiving morphine) Hip arthroplasty

Patients receiving valdecoxib experienced significant improvements in pain intensity levels (p ≤ 0.05) and satisfaction with treatment (p < 0.001), and required less morphine than those receiving placebo Valdecoxib was well tolerated, and was not associated with an increase in bleeding episodes

Christensen et al.93

Valdecoxib 40 mg Rofecoxib 50 mg Oral surgery

Valdecoxib showed significantly faster onset of action (30 vs. 45 min, p ≤ 0.05) and a similar magnitude of analgesia compared with rofecoxib Valdecoxib was significantly superior to rofecoxib in terms of mean time-specific pain intensity difference and pain relief scores (p < 0.05)

Daniels et al.94

Valdecoxib 20 mg or 40 mg Oxycodone 10 mg/acetaminophen 1000 mg Oral surgery

Valdecoxib had a similar time to onset of analgesia and peak analgesic effect compared with oxycodone/acetaminophen Both valdecoxib doses had a significantly longer duration of analgesia than oxycodone/acetaminophen

Fricke et al.92

Valdecoxib 40 mg Rofecoxib 50 mg Oral surgery

Valdecoxib was associated with a significantly shorter time to perceptible pain relief (p ≤ 0.05), significant improvements in pain intensity and pain relief (p ≤ 0.01), a faster time to onset of analgesia, significantly greater patient satisfaction (p ≤ 0.01) and a significantly lower requirement for rescue medication (p ≤ 0.05) compared with rofecoxib

Reynolds et al.96

Valdecoxib 40 mg or 80 mg daily Total knee arthroplasty

Morphine consumption with valdecoxib 40 mg and 80 mg was 83.7% and 75.8%, respectively) of the amount used by patients receiving morphine alone (p < 0.05) Patients receiving valdecoxib also discontinued morphine sooner that those receiving placebo Valdecoxib was well tolerated and patients experienced significantly lower maximum pain intensity by the end of the study (p < 0.05), and rated their study medication significantly higher than the morphine group (p < 0.01)

Celecoxib

Valdecoxib

of celecoxib 200 mg or rofecoxib 50 mg compared with placebo.87 Although analgesic efficacy was similar in both groups, rofecoxib had an extended analgesic effect. Valdecoxib has demonstrated rapid analgesic efficacy with a long duration of action in various models of surgical pain. In addition, valdecoxib does not affect platelet aggregation and has fewer undesirable effects on the gastrointestinal mucosa compared with nonspecific NSAIDs.88–91 In a comparative study in patients following oral surgery, valdecoxib 40 mg showed a significantly shorter time to

perceptible pain relief and a faster time to onset of analgesia compared with rofecoxib 50 mg.92 Valdecoxib also provided significant pain relief 45 minutes after dosing, lasting up to 24 hours. A separate study also found that single-dose valdecoxib 40 mg had a significantly faster onset of action compared with rofecoxib 50 mg following oral surgery (p=0.05), although the magnitude and duration of analgesia were similar.93 In two other studies following oral surgery, the analgesic efficacy and tolerability of single-dose valdecoxib 20 mg or 40 mg showed a similar time to onset of analgesia and peak 119

Part 1: General Principles

analgesic effect compared with oxycodone 10 mg/acetaminophen 1000 mg.94 However, both valdecoxib doses had a significantly longer duration of analgesia and superior tolerability compared with oxycodone/acetaminophen. Valdecoxib has demonstrated opioid-sparing efficacy as part of multimodal treatment following hip arthroplasty.95 Patients receiving valdecoxib 20 mg or 40 mg b.i.d. preoperatively and postoperatively required less morphine than those receiving placebo, and experienced greater analgesic efficacy compared with morphine alone. Confirming previous findings of its lack of effect on platelet function and bleeding time,90,91 both valdecoxib doses were well tolerated and were not associated with an increase in bleeding episodes. Similar findings were reported in a study following total knee arthroplasty, in which morphine consumption was lower in patients receiving valdecoxib 40 mg or 80 mg daily compared with morphine alone.96 Valdecoxibtreated patients also experienced significantly lower maximum pain intensity and rated their study medication significantly higher than did the morphine group. Although the opioid-sparing efficacy of COX-2-specific inhibitors should reduce the incidence of opioid-related adverse events in postoperative patients, studies of the postoperative use of COX-2-specific inhibitors in addition to standard-of-care opioids have not shown a consistent reduction in opioid-related adverse effects. These trials may have had a low sensitivity for assessing adverse events because they relied on investigator reports. A recent patient-reported health outcome analysis, based on a randomized, controlled, double-blind trial of patients after ambulatory laparoscopic cholecystectomy, allowed patients to self-assess their adverse events using the Symptom Distress Scale (SDS) questionnaire.97 Using the questionnaire, patients assessed 12 opioid-related symptoms by 3 ordinal measures: frequency, severity, and bothersomeness. The outcome analysis showed a significant dose–response relationship between postoperative opioid dose and opioid-related adverse effects.97 Furthermore, once postoperative opioid dose had reached a threshold, approximately every 3–4 mg increase in the morphine equivalent dose resulted in an additional opioid-related clinically meaningful event. These outcome results highlight the potential benefits of reducing postoperative opioid consumption using multimodal treatment with COX-2-specific inhibitors.

Potential drug–drug interactions in the surgical setting Valdecoxib is primarily metabolized by hepatic cytochrome P450 (CYP) 3A4 and to a lesser degree by CYP2C9.98 Therefore, parecoxib (the prodrug of valdecoxib) may interact with other CYP3A4 substrates, so the potential for parecoxib to interact with medications commonly used in surgery has been investigated. Frequently used in the perioperative setting, midazolam is a CYP3A4 substrate whose systemic clearance, magnitude, and duration of effect are highly susceptible to CYP3A4 drug interactions.99 Singlebolus parecoxib has not shown any effects on the plasma concentration, pharmacokinetics, or pharmacodynamics of midazolam when administered at doses expected to be used perioperatively.100 Similarly, bolus parecoxib has not altered the disposition or clinical effects of the opioid analgesics fentanyl or alfentanil, whose systemic clearance is affected by alterations in CYP3A4 activity.101 Parecoxib has also been found to have no effects on the plasma concentration, pharmacokinetics, or pharmacodynamics of propofol, which is the only commonly used anesthetic that undergoes significant metabolism by CYP2C9.102

COX-2-specific inhibitors and platelet function Ketorolac has been associated with an increased risk of gastrointestinal and operative-site bleeding in patients aged 75 years or older 120

and in patients receiving either higher doses of ketorolac or treatment lasting for more than 5 days.55,103 The effects of parecoxib and ketorolac on platelet function and bleeding time have been compared in healthy elderly (aged 65–95 years) and nonelderly subjects (aged 18–55 years).104 Parecoxib had little or no effect on arachidonate-induced platelet aggregation in either study population, while ketorolac demonstrated significant and sustained decreases in platelet aggregation throughout the drug administration period compared with parecoxib and placebo. A high degree of variability was noted in bleeding times in all treatment groups, but significant prolongation was recorded with ketorolac in both study groups. Parecoxib had no effect on serum thromboxane B2 levels in nonelderly subjects, but ketorolac resulted in marked reductions that were significantly greater than parecoxib and placebo at all time points (p<0.001). In elderly subjects, ketorolac significantly reduced serum thromboxane B2 levels (p=0.017 vs. placebo) versus parecoxib. The lack of effects on platelet aggregation and bleeding time recorded with parecoxib in this study suggest that, irrespective of age, parecoxib is less likely to be associated with increased bleeding during surgery than ketorolac and should be a better choice for treating postsurgical pain. Similar findings have been noted with valdecoxib, which has demonstrated a lack of effect on platelet aggregation and bleeding time even when used at supratherapeutic doses.90,91 A study in healthy volunteers also found supratherapeutic doses of celecoxib (600 mg b.i.d.) had no effect on the normal mechanisms of platelet aggregation and hemostasis.105

Gastrointestinal tolerability of COX-2-specific inhibitors Endoscopic studies have reported a 70–75% reduced risk of ulceration at 6 months for COX-2-specific inhibitors compared with non-specific NSAIDs, and an incidence of ulceration similar to placebo.106,107 Two large, randomized, double-blind outcomes studies investigated the risk of clinically important upper gastrointestinal events associated with the COX-2-specific inhibitor celecoxib. The CLASS study (Celecoxib Long-term Arthritis Safety Study) compared the gastrointestinal toxicity of celecoxib, ibuprofen, and diclofenac in patients with osteoarthritis and rheumatoid arthritis.108 The CLASS trial failed to show a statistically significant difference in the primary endpoint, the annualized incidence of upper gastrointestinal ulcers complications, between patients treated with celecoxib 400 mg b.i.d. and those treated with ibuprofen or diclofenac. The failure to show a difference was probably influenced by study design and methodology for evaluating gastrointestinal outcomes, unexpectedly high dropout rates, and concurrent use of low-dose aspirin. The second trial, SUCCESS-1 (SUCcessive Celecoxib Efficacy and Safety Study-1), was the largest, multinational, ‘real-world,’ randomized, controlled clinical trial of a COX-2-specific inhibitor.109 The SUCCESS-1 study showed that patients treated with celecoxib statistically had a significantly lower incidence of upper gastrointestinal complications compared with patients treated with naproxen or diclofenac (p=0.008). Several other observational studies and pooled analyses have also demonstrated the gastrointestinal safety profile of celecoxib.110,111 Studies with the newer COX-2-specific inhibitor valdecoxib have also noted a superior upper gastrointestinal safety profile compared with non-specific NSAIDs in healthy subjects.89 In addition, in patients with osteoarthritis, valdecoxib was associated with a significantly lower incidence of endoscopically detectable gastroduodenal ulcers compared with ibuprofen and diclofenac.112 The development of parecoxib has provided a COX-2-specific inhibitor that combines the analgesic efficacy of NSAIDs with an

Section 4: Practical Pharmacology

improved tolerability profile in a parenteral formulation. The gastrointestinal safety and tolerability of parecoxib, ketorolac, and naproxen over 7 days were compared in a placebo-controlled endoscopic study in 17 healthy elderly subjects who were at increased risk of upper gastrointestinal ulcer complications.113 The rate of ulcers was lower with parecoxib (0/4 subjects) and placebo (2/5 subjects) compared with ketorolac (4/4 subjects) and naproxen (2/4 subjects). Because of the unexpectedly high incidence of gastroduodenal ulceration in patients taking the non-specific NSAIDs, even after short-term treatment, the study was terminated early and the randomization blind broken. A larger study compared the upper gastrointestinal effects of parecoxib, ketorolac, and placebo in healthy elderly subjects aged 65–75 years.114 The use of parecoxib or placebo was not associated with the development of gastric or duodenal lesions, while 22.6% of ketorolac-treated patients developed at least one ulcer within 5 days of administration (16.1% had gastric ulcers and 6.4% had duodenal ulcers; p<0.05 vs. parecoxib). The incidence of an ulcer or at least one erosion in the stomach was 90.3% with ketorolac, 13.8% with parecoxib, and 6.3% with placebo, while the incidence of duodenal ulcers/erosions was 45.2%, 10.3%, and 0%, respectively. This study thus confirms that parecoxib has a significantly reduced incidence of gastroduodenal mucosal injury compared with ketorolac. Lastly, in a multicenter, randomized, double-blind, controlled study of 123 adults with endoscopically confirmed normal upper gastrointestinal mucosae at baseline, treatment for 7 days with parecoxib 40 mg b.i.d. had a gastrointestinal ulceration rate that was comparable to placebo and superior to ketorolac 30 mg 4 times daily for 5 days.115 During the 7-day study, no subjects treated with parecoxib or placebo developed gastroduodenal ulcers or ≥11 erosions/ulcers. Parecoxib was no more likely than placebo to increase the incidence of erosions or ulcers (12% vs. 7%, p=0.419). In contrast, in the ketorolac group, 11 (28%) subjects developed ulcers, 19 (48%) subjects developed ≥11 gastroduodenal erosions/ulcers, and the rate of combined ulcers/ erosions was 85% (p<0.001 vs. placebo and parecoxib).

Renal effects of COX-2-specific inhibitors Inhibition of renal COX-1 and COX-2 by non-specific NSAIDs inhibits prostaglandin-mediated renal function, including renal vascular tone and electrolyte and water excretion.116–118 These effects frequently cause edema and reduced blood pressure control in treated patients with hypertension. Therefore, since COX-2-specific inhibitors also spare inhibition of renal COX-1, it was hoped that they may have decreased rates of renovascular events compared with nonspecific NSAIDs. However, subsequent recognition of the constitutive expression of COX-2 in the human kidney,37 coupled with the profound effects of prostaglandins on renal homoeostasis,72 indicate that COX-2-specific inhibitors are likely to share the nephrotoxic potential of non-specific NSAIDs. In a historical cohort observational analysis of patients with stabilized hypertension, celecoxib was associated with a significantly lower incidence of outpatient blood pressure destabilization (2.27 per 1000 patient-days) compared with non-specific NSAIDs (ibuprofen, diclofenac, naproxen: 2.65 per 1000 patient-days; p<0.001) or rofecoxib (2.66 per 1000 patient-days; p<0.001).119 In two randomized trials, renal adverse events associated with 6 weeks’ treatment with celecoxib 200 mg q.d. or rofecoxib 25 mg q.d. were compared in 1900 elderly osteoarthritis patients taking antihypertensive agents.120,121 Celecoxib treatment was associated with less edema and blood pressure destabilization compared with rofecoxib. In a long-term outcome study, rates of hypertension and edema in 8538 patients taking a non-specific NSAID, rofecoxib, or celecoxib

during the previous 6 months were compared to patients not taking these agents.122 Compared with nonusers, patients treated with rofecoxib had increased rates of edema and hypertension. In contrast, patients taking celecoxib or non-specific NSAIDs had similar rates of edema and hypertension to the nonusers. Taken together, these studies suggest that the renal effects of COX-2-specific inhibitors may be molecule-specific rather than class-specific. Furthermore, in a pooled analysis of 9 arthritis trials of 6–26 weeks duration (including 7 placebo controlled), chronic daily treatment with therapeutic doses of valdecoxib was associated with similar rates of hypertension and edema compared with naproxen, diclofenac, or ibuprofen.123 In terms of their effects of renal function, both non-specific NSAIDs and COX-2-specific inhibitors are generally safe when used in healthy subjects. However, in situations where renal hemodynamics are compromised, such as in the elderly or those with preexisting renal dysfunction or congestive heart failure, it is recommended that non-specific NSAIDs and COX-2-specific inhibitors should be used with caution.124

Potential cardiovascular complications of COX-2-specific inhibitors In September 2004, rofecoxib was withdrawn from the market following an interim analysis of cardiovascular safety data from a prospective, randomized trial that showed an increased relative risk for confirmed cardiovascular events with rofecoxib versus placebo. The Adenomatous Polyp Prevention On Vioxx (APPROVe) trial was designed to evaluate the efficacy of rofecoxib 25 mg in preventing the recurrence of colorectal polyps in patients with a history of the disease.125 Only a minority of these patients had a known history of coronary artery disease. Preliminary data revealed that there was an approximate twofold increase in the rate of cardiovascular events with rofecoxib (46 events per 3059 patient years [1.5 events per 100 patient-years]) compared with placebo (26 events per 3327 patient years [0.78 events per 100 patient-years; p=0.008]). This difference did not become statistically significant until after 18 months of treatment. Earlier studies had also suggested an increased risk of cardiovascular events in patients taking rofecoxib.126–128 The Vioxx Gastrointestinal Outcomes Research (VIGOR) trial showed that patients taking rofecoxib 50 mg had a fourfold increased risk of acute myocardial infarction compared with naproxen 500 mg twice daily.126 This was initially attributed to a potential cardioprotective effect of naproxen rather than a cardiotoxic effect of rofecoxib. However, a meta-analysis of 18 randomized controlled trials and 11 observational studies demonstrated that the cardioprotective effect of naproxen is small and could not have explained the findings of the VIGOR trial.129 The putative cardioprotective effect of naproxen has been further called into question since preliminary data from the Alzheimer Disease Antiinflammatory Prevention Trial (ADAPT; n=2400) demonstrated an increased risk of cardiovascular events in patients taking naproxen versus placebo.130 Because of this finding, the ADAPT study was prematurely halted; however, the events have not been adjudicated, and further evaluation is needed before conclusions about naproxen can be reached. In contrast to the data for rofecoxib, numerous randomized, controlled trials and observational studies have found no elevated risk of cardiovascular events with celecoxib. Data from both the SUCCESS-1 and CLASS trials showed that there was no increased risk of acute myocardial infarction with celecoxib treatment,108,109 and the ADAPT trial described above also failed to find an increased risk for cardiovascular events for celecoxib.130 Furthermore, several 121

Part 1: General Principles

other observational studies have shown a greater risk for cardiovascular events with rofecoxib than celecoxib. For example, Solomon et al. showed a statistically significantly higher rate of myocardial infarction in patients treated with rofecoxib compared with those treated with celecoxib.128 A dose–response relationship was also observed with rofecoxib, such that higher doses of rofecoxib were associated with a greater rate of myocardial infarction; no such relationship was seen with celecoxib.128 Similarly, Ray et al. demonstrated an association of myocardial infarction with high-dose rofecoxib, but not celecoxib treatment; new users of high-dose rofecoxib had a 2.2-fold greater risk of developing serious coronary heart disease compared with patients taking celecoxib.127 Two recent case-control studies have also shown a significantly higher risk of cardiovascular events with rofecoxib than with celecoxib.131,132 The only instance of a potential increase in cardiovascular events with celecoxib was initially reported in December 2004. Following the observations of an increased incidence of cardiovascular events with rofecoxib from the APPROVe trial, the data and safety monitoring board of a similar trial for celecoxib, the Adenoma Prevention with Celecoxib (APC) trial (n=2035), requested a similar assessment of cardiovascular data. This analysis found that celecoxib was associated with a dose-related increase in the risk of serious cardiovascular events, including death from cardiovascular causes, myocardial infarction, stroke, and heart failure.133 However, preliminary analyses from the Prevention of Spontaneous Adenomatous Polyps (PreSAP) trial, conducted in parallel to APC for the same indication, has not shown any increased cardiovascular risk for celecoxib.133 To date, there is no evidence of an increased cardiovascular risk with valdecoxib in patients with osteoarthritis or rheumatoid arthritis. A retrospective pooled analysis of four randomized, placebo-controlled trials of up to 3 months’ duration in patients with rheumatoid arthritis demonstrated that valdecoxib 10–80 mg daily (n=1945) was associated with a similar incidence of serious thrombotic events compared with naproxen 500 mg twice daily (n=744) or placebo (n=529).123 Similarly, a pooled analysis of 10 randomized, placebo-controlled trials in patients with osteoarthritis and rheumatoid arthritis (n=7934) also showed similar incidences of thrombotic events in patients taking valdecoxib, non-specific NSAIDs (e.g. naproxen, diclofenac, and ibuprofen) or placebo.134 In two studies of the investigational use of parecoxib/valdecoxib for postoperative pain relief following coronary artery bypass graft (CABG) surgery, a significantly greater incidence of cardiovascular/thromboembolic events was detected in the parecoxib/ valdecoxib treatment group compared with the placebo treatment group, prompting the recent contraindication of valdecoxib in the treatment of postoperative pain immediately following CABG surgery,135,136 but this risk has not been seen in any other population. Taken together, these data suggest that there may be a true difference in the cardiovascular risk profiles of different COX-2-specific inhibitors, with rofecoxib posing a higher risk than either celecoxib or valdecoxib. Possible mechanisms by which rofecoxib may increase the risk for cardiovascular events are not completely understood, but may include an increase in hypertension, thrombosis, and reduced vascular reactivity.132,137 Clearly, further studies are needed to explain the precise mechanism(s) involved in the cardiovascular safety profiles of COX-2specific inhibitors and to evaluate whether true differences exist.

NON-SPECIFIC NSAIDs AND COX-2-SPECIFIC INHIBITORS: EFFECTS ON BONE HEALING AND SPINAL FUSION An important consideration in the use of non-specific NSAIDs and COX-2-specific inhibitors in the surgical setting is their potential effects on bone healing and spinal fusion. 122

Prostaglandins play an important role in bone healing, which is initiated by an inflammatory phase that involves a number of cytokines, growth factors, and arachidonic acid metabolites.138 Bone repair is mediated by two cell types: osteoblasts that are responsible for bone renewal, and osteoclasts that are involved in bone resorption. Both of these cell types are influenced by a range of mediators, which also influence the production of prostaglandins by bone. Osteoblasts produce prostaglandins that act locally to modulate bone metabolism, while prostaglandins produced by local tissues and inflammatory cells may influence skeletal tissues.139 The production of prostaglandins is also stimulated by weight bearing.140 Because of their effects on prostaglandin formation, non-specific NSAIDs and COX-2-specific inhibitors might be expected to affect bone healing. Although non-specific NSAIDs do not appear to alter normal bone homeostasis, they do affect osteogenesis during bone repair. COX-2 may potentially affect osteoclast and osteoblast function as well as angiogenesis, which may affect the delivery of osteoclasts and osteoblasts.139 There are currently no published prospective studies of the effects on COX-2-specific inhibitors on bone healing in humans, and both non-specific NSAIDs and COX-2-specific inhibitors have been used extensively for the treatment of pain associated with bone fractures and orthopedic surgery without causing any clinical concern.

Effect of non-specific NSAIDs on bone healing Non-specific NSAIDs have been shown to inhibit fracture healing in human and animal models (Table 10.5). A variety of factors have been implicated in this phenomenon, including inhibition of bone-forming cells at endosteal bone surfaces, reductions in immune and inflammatory responses, and inhibition of prostaglandin synthesis.141,142 In a rat model of spinal fusion, a statistically lower level of fusion was achieved with administration of indometacin than with saline (p<0.001).142 The results of this study led the authors to question the widespread use of non-specific NSAIDs in the postoperative period after spinal fusion. A retrospective review of 288 patients who underwent an instrumented spinal fusion found that ketorolac had a significant adverse effect on fusion (p>0.001), with ketorolac-treated patients being five times more likely to experience nonunion.143 Smoking also significantly decreased the fusion rate (p>0.01), with smokers being 2.8 times more likely to develop nonunion. This study reported that non-specific NSAIDs significantly inhibited spinal fusion at doses typically used for postoperative pain control, and recommended that they should be avoided in the early postoperative period. In a similar retrospective study, 83 patients with isthmic spondylolisthesis who underwent decompressive surgery combined with posterolateral spine fusion and who took non-specific NSAIDs for more than 3 months postoperatively experienced a significantly lower spinal fusion rate (44%) compared with overall single-level (82%) and two-level fusion rates (74%).144 A further retrospective study of 32 patients with nonunion of a fracture of the diaphysis of the femur and 67 comparable patients with united fractures found a marked association between nonunion and the use of non-specific NSAIDs after injury (p=0.000001).145 Delayed healing was also noted in those patients who took non-specific NSAIDs and whose fractures had subsequently united. As a result of these effects, non-specific NSAIDs have generally been avoided in the early postoperative period following arthrodesis and fracture fixation.

Effect of COX-2-specific inhibitors on bone healing Several animal studies have also examined the effects of COX-2-specific inhibitors on bone healing (see Table 10.5). In a rat model of

Section 4: Practical Pharmacology

Table 10.5: Studies of Non-Specific NSAIDs and COX-2-Specific Inhibitors on Bone Healing Study

Treatment and Model

Results

Indometacin 3 mg/kg Saline Rat model of 3-level posterior spinal fusion

Spinal fusion was achieved in 10% of indometacin-treated rats and 45% of control rats (27/60 levels) who received saline (p < 0.001)

Deguchi et al.146

Retrospective study of 83 patients with isthmic spondylolisthesis who underwent decompressive surgery combined with posterolateral spine fusion

Patients who received NSAIDs for >3 months postoperatively had a significantly lower spinal fusion rate (44%) compared with overall single-level (82%) and 2-level fusion rates (74%) Smoking also had a negative influence on fusion rate

Giannoudis et al.147

Retrospective study of 32 patients with nonunion of femoral fracture and 67 comparable patients with united fractures

Significant association between nonunion and NSAID use after injury (p < 0.000001), with delayed healing noted in patients with united fractures who took NSAIDs

Glassman et al.145

Retrospective review of 288 patients who underwent an instrumented spinal fusion

Odds ratio demonstrated that nonunion was 5 times more likely with ketorolac administration Cigarette smokers were 2.8 times more likely to develop nonunion

NSAIDs Dimar et al.144

COX-2-Specific Inhibitors Brown et al.154 Indometacin 1 mg/kg/d Celecoxib 3 mg/kg/d No drug Rat model of femoral fracture

At 4 weeks only indometacin-treated animals showed evidence of delayed healing By 12 weeks there were no significant differences among the 3 groups

Gerstenfeld et al.153

Ketorolac 4 mg/kg Parecoxib 0.3 and 1.5 mg/kg Rat model of femoral fracture

Ketorolac-treated animals had a significant reduction in mechanical strength and stiffness compared with controls (p < 0.05)

Goodman et al.149

Naproxen 110 mg/kg/d Rofecoxib 12.5 mg/d Water Harvest chambers implanted in rabbit tibiae

Naproxen (p = 0.031) and rofecoxib (p = 0.035) significantly decreased bone ingrowth compared to drinking water

Leonelli et al.148

Rofecoxib 8 mg/kg Ibuprofen 30 mg/kg Rat model of femoral fracture

Incidence of nonunions was 0% in control group, 65% in the rofecoxib group (p < 0.0001 vs. control) and 18% in the ibuprofen group (p = 0.007 vs. control). Nonunion was significantly more likely with rofecoxib than with ibuprofen (p = 0.007)

Long et al.152

Celecoxib 10 mg/kg Indometacin 10 mg/kg Saline Rabbit spinal fusion model

Fusion rates were 64% in the control group, 45% in the celecoxib group (p < 0.224 vs. control) and 18% in the indometacin group (p < 0.002 vs. control)

Mullis et al.155

Ibuprofen 30 mg/kg Ketorolac 2 mg/kg Celecoxib 10 mg/kg Rofecoxib 1 and 5 mg/kg Indometacin 21 mg/kg Mouse model of tibial fracture

Non-specific NSAIDs and COX-2-specific inhibitors studied had no effect on fracture healing at the end of the study Only ketorolac at week 4 was significantly different from placebo

Reuben et al.156

Rofecoxib 50 mg Celecoxib 200 mg Ketorolac 15–240 mg No NSAIDs Retrospective analysis of 342 patients who underwent spinal fusion

Rates of nonunion were 19% with ketorolac (p<0.01 vs. other groups), 7% with rofecoxib, 6.7% with no NSAID, and 5% with celecoxib. There was no difference in nonunion rates among the rofecoxib, celecoxib, and placebo groups

Simon et al.150

Celecoxib 4 mg/kg Rofecoxib 3 mg/kg Indometacin 1 mg/kg Rat model of femoral fracture

Fracture healing failed in rats treated with celecoxib, rofecoxib, and indometacin, and in COX-2-deficient mice

Zhang et al.151

Investigation of the role of COX-2 in bone formation during skeletal repair in wild-type, COX-1 knockout and COX-2 knockout mouse models of tibial fracture

Healing of stabilized tibial fractures was significantly delayed in COX-2 knockout mice compared with COX-1 knockout mice and wild-type controls

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femoral fracture, a significantly higher incidence of nonunions was observed with rofecoxib 8 mg/kg compared with ibuprofen 30 mg/kg (p<0.007) and controls (p<0.0001).146 Ibuprofen-treated animals also showed reduced healing. A study using a model of osteointegration in rabbits reported that bone formation was significantly suppressed by naproxen 110 mg/kg/d (p=0.031) and rofecoxib 12.5 mg/d (p=0.035) compared with controls.147 A rat model of femoral fracture investigating the effects of celecoxib 4 mg/kg, rofecoxib 3 mg/kg, and indometacin 1 mg/kg for 8 weeks reported similar findings.148 In this study, fracture healing failed in rats treated with celecoxib, rofecoxib, and indometacin, and in COX-2-deficient mice, suggesting that COX-2 function is essential for fracture healing. An analysis of bone healing in wild-type, COX-1 knockout, and COX-2 knockout mouse models of tibial fracture found that fracture healing was significantly delayed in COX-2 knockout mice.149 These investigators concluded that COX-2 may be involved in multiple processes leading to increased bone formation, although it is recognized that there are concerns about the validity of knockout models.139 In contrast, other animal studies have demonstrated that the effects of COX-2-specific inhibitors on bone healing are not significantly deleterious. In a rabbit model of spinal fusion, the rate of fusion was not significantly different in control animals and animals treated with celecoxib 10 mg/kg, but was significantly lower in animals receiving indometacin 10 mg/kg after 8 weeks (p<0.002 vs. placebo).150 These findings suggested that the effects of NSAIDs on bone healing were likely to be mediated by COX-1 inhibition, and indicated that a COX-2-specific inhibitor was the better choice if NSAID treatment was necessary following spinal arthrodesis. PCR analysis of COX expression in a rat model of femoral fracture found that although the relative levels of COX-1 mRNA remained constant over a 21-day period, COX-2 mRNA levels showed peak expression during the first 14 days of healing and returned to basal levels by day 21.151 In this model, animals treated with ketorolac 4 mg/kg had a significant reduction in mechanical strength and stiffness at 21 days compared with controls (p<0.05), while mechanical strength in animals treated with parecoxib 0.3 and 1.5 mg/kg was not significantly different from that in controls. Although the rate of nonunion was higher in ketorolac-treated animals at 21 days, all fractures in the ketorolac and parecoxib groups had reunited at 5 weeks. Ketorolac also had a more deleterious effect on bone healing than parecoxib, which only slightly delayed bone healing, even at doses known to fully inhibit prostaglandin production. Similar findings have been reported in other animal studies of fracture healing. In a 12-week study of indometacin 1 mg/kg/d and celecoxib 3 mg/kg/d versus no drug in a rat model of femoral fracture, only indometacin-treated animals showed evidence of delayed healing at 4 weeks.152 By 12 weeks there were no significant differences among the three groups. A 12-week comparative study of ibuprofen 30 mg/kg, ketorolac 2 mg/kg, celecoxib 10 mg/kg, rofecoxib 1 and 5 mg/kg, and indometacin 21 mg/kg in a mouse fracture model found that only ketorolac-treated animals had a significant difference from placebo in bone healing at 4 weeks, although both NSAIDs and COX2-specific inhibitors showed no effect on fracture healing by the end of the study.153 Few studies have been performed to assess the effects of COX2-specific inhibitors on fracture healing in humans. No prospective analyses have been published and both animal and human data are conflicting. A retrospective analysis of 342 patients who underwent spinal fusion and who received rofecoxib 50 mg, celecoxib 200 mg, ketorolac 15–240 mg, or no NSAIDs in the 5 days following surgery found no statistically significant difference in nonunion rates among celecoxib, rofecoxib, and placebo.154 However, the nonunion rate in the ketorolac group was significantly higher than that in the other 124

three groups (p=0.01) and the effects of ketorolac on nonunion appeared to be dose related.

CONCLUSIONS Despite the availability of effective analgesic drugs and techniques, the treatment of postoperative pain is often suboptimal. The use of multimodal analgesia represents an effective strategy to optimize the management of pain, but many currently available analgesic drugs are associated with adverse event profiles that limit their use in the postoperative setting. COX-2-specific inhibitors are effective in the treatment of postoperative pain following a range of surgical procedures and have been shown to reduce the postsurgical requirement for opioids.155 Clinical studies demonstrate that COX-2 inhibition, administered prior to or soon after the initiation of surgical pain, may prevent peripheral and central sensitization. The findings of preclinical studies on the effects of non-specific NSAIDs and COX-2-specific inhibitors in bone healing are often conflicting or inconclusive, and may not be predictive of the clinical situation in humans.156 Analysis of the results of animal and human fracture studies is also complicated by inconsistencies, including study design and dosages, and by confounding factors such as smoking.143 Some studies also lack sufficient power to detect differences in fusion rates.139 Although a recent comprehensive review of the literature reported that there was no evidence of a clinical effect of NSAIDs on bone healing, there were few large, quality studies investigating this subject. Further studies are needed to characterize the effects of non-specific NSAIDs and COX-2-specific inhibitors on bone healing in humans. Treating postsurgical pain using COX-2-specific inhibitors offers many benefits over existing agents. In contrast to non-specific NSAIDs, COX-2-specific inhibitors do not cause platelet dysfunction or increase bleeding. COX-2-specific inhibitors provide effective pain relief and a reduced requirement for rescue analgesia, and unlike monotherapy using opioids, COX-2-specific inhibitors are effective for treating pain during movement. COX-2-specific inhibitors can be combined with opioids to reduce opioid doses, and to help increase postoperative mobility. Parecoxib has been a particularly valuable addition and can be given intravenously during and after surgery.

NEW DEVELOPMENTS Since this chapter was originally written, the following new developments have occurred in the field of selective cox-2 inhibitors: ●

●

●

●

Valdecoxib was withdrawn voluntarily by its manufacturer because of a potential link with rare but serious cutaneous adverse events such as Stevens–Johnson Syndrome and toxic epidermal necrolysis. An FDA review of NSAIDs concluded that all NSAIDs, both cox-2 selective and non-selective, increase the risk of serious cardiovascular thrombotic adverse events. All NSAIDs marketed in the US are now required to carry a black-box warning to this effect. Etoricoxib was reviewed by an FDA Advisory Committee and not recommended for approval in the United States because of an increased risk of serious cardiovascular adverse events. Lumiracoxib is currently being considered for approval by the FDA, with a decision expected by October, 2007.

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121. Whelton A, White WB, Bello AE, et al. Effects of celecoxib and rofecoxib on blood pressure and edema in patients > or =65 years of age with systemic hypertension and osteoarthritis. Am J Cardiol 2002; 90:959–963. 122. Wolfe F, Zhao S, Pettitt D. Blood pressure destabilization and edema among 8538 users of celecoxib, rofecoxib, and nonselective nonsteroidal antiinflammatory drugs (NSAID) and nonusers of NSAID receiving ordinary clinical care. J Rheumatol 2004; 31(6):1143–1151. 123. Whelton A, White W, Kent J, et al. Hypertension and edema rates in 6,717 patients for the new COX-2 inhibitor, valdecoxib versus the conventional nonselective NSAIDs and placebo [abstract]. Am J Hypertens 2003; 16:P445.

140. Thorsen K, Kristoffersson AO, Lerner UH, et al. In situ microdialysis in bone tissue: stimulation of prostaglandin E2 release by weight-bearing mechanical loading. J Clin Invest 1996; 98:2446–2449. 141. Keller J, Bunger C, Andreassen TT, et al. Bone repair inhibited by indomethacin. Effects on bone metabolism and strength of rabbit osteotomies. Acta Orthop Scand 1987; 58:379–383. 142. Dimar JR 2nd, Ante WA, Zhang YP, et al. The effects of nonsteroidal antiinflammatory drugs on posterior spinal fusions in the rat. Spine 1996; 21: 1870–1876. 143. Glassman SD, Rose SM, Dimar JR, et al. The effect of postoperative nonsteroidal anti-inflammatory drug administration on spinal fusion. Spine 1998; 23:834–838.

124. LeLorier J, Bombardier C, Burgess E, et al. Practical considerations for the use of nonsteroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors in hypertension and kidney disease. Can J Cardiol 2002; 18:1301–1308.

144. Deguchi M, Rapoff AJ, Zdeblick TA. Posterolateral fusion for isthmic spondylolisthesis in adults: analysis of fusion rate and clinical results. J Spinal Disord 1998; 11(6):459–464.

125. Bresalier RS, Sandler RS, Quan H, et al, for the Adenomatous Polyp Prevention on Vioxx (APPROVe) Trial Investigators. Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. Published February 15, 2005 [epub ahead of print. 10.1056/NEJMoa050493]. Available at: http://content. nejm.org/cgi/content/abstract/NEJMoa050493v1. Accessed February 16, 2005.

145. Giannoudis PV, MacDonald DA, Matthews SJ, et al. Non-union of the femoral diaphysis. The influence of reaming and non-steroidal anti-inflammatory drugs. J Bone Joint Surg Br 2000; 82:655–658.

126. Bombardier C, Laine L, Reicin A, et al. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. N Engl J Med 2000; 343:1520–1528.

146. Leonelli S, Goldberg B, Safanda J, et al. The effect of cyclooxygenase 2 (COX-2) inhibitors on bone healing. Presented at: 48th Annual Meeting of the Orthopaedic Research Society; February 9–12, 2002; Dallas, Tex. 147. Goodman S, Ma T, Trindade M. COX-2 selective NSAID decreases bone ingrowth in vivo. J Orthop Res 2002; 20:1164–1169.

127. Ray WA, Stein CM, Daugherty JR, et al. COX-2 selective non-steroidal antiinflammatory drugs and risk of serious coronary heart disease. Lancet 2002; 360:1071–1073.

148. Simon AM, Manigrasso MB, O’Connor JP. Cyclo-oxygenase 2 function is essential for bone fracture healing. J Bone Miner Res 2002; 17:963–976.

128. Solomon DH, Schneeweiss S, Glynn RJ, et al. Relationship between cyclooxygenase-2 inhibitors and acute myocardial infarction in older adults. Circulation 2004; 109:2068–2073.

149. Zhang X, Schwarz EM, Young DA, et al. Cyclooxygenase-2 regulates mesenchymal cell differentiation into the osteoblast lineage and is critically involved in bone repair. J Clin Invest 2002; 109:1405–1415.

129. Juni P, Nartey L, Reichenbach S, et al. Risk of cardiovascular events and rofecoxib: cumulative meta-analysis. Lancet 2004; 364:2021–2029.

150. Long J, Lewis S, Kuklo T, et al. The effect of cyclooxygenase-2 inhibitors on spinal fusion. J Bone Joint Surg Am 2002; 84-A:1763–1768.

130. US Food and Drug Administration. FDA statement on naproxen. Available at: http://www.fda.gov/bbs/topics/news/2004/NEW01148.html. Accessed February 16, 2005.

151. Gerstenfeld LC, Thiede M, Seibert K, et al. Differential inhibition of fracture healing by non-selective and cyclooxygenase-2 selective non-steroidal antiinflammatory drugs. J Orthop Res 2003; 21:670–675.

131. Graham DJ, Campen D, Hui R, et al. Risk of acute myocardial infarction and sudden cardiac death in patients treated with cyclo-oxygenase 2 selective and non-

152. Brown KM, Saunders MM, Kirsch T, et al. Effect of COX-2-specific inhibition on fracture-healing in the rat femur. J Bone Joint Surg Am 2004; 86-A:116–123.

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Part 1: General Principles 153. Mullis B, Copeland S, Weinhold P, et al. Effect of COX-2 inhibitors and NSAIDs on fracture healing in a mouse model. Presented at: 48th Annual Meeting of the Orthopaedic Research Society; February 9–12, 2002; Dallas, Tex. 154. Reuben S, Rizvi A, Steinberg R, et al. The effects of NSAIDs on spinal fusion. Presented at: American Society of Regional Anesthesia and Pain Medicine 27th Annual Spring Meeting & Workshops; April 25–28, 2002; Chicago, Ill. ASRA PD-16.

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155. Katz WA. Cyclooxygenase-2-selective inhibitors in the management of acute and perioperative pain. Cleve Clin J Med 2002; 69(Suppl 1):S165–S175. 156. Arnoczky SP, Wilson JW. Experimental surgery of the skeletal system. In: Gay WI, Heavner JE, eds. Methods of animal experimentation. Vol. II: Research surgery and care of the research animal. London: Academic Press; 1996:67–108.

PART 1

GENERAL PRINCIPLES

Section 4

Practical Pharmacology

CHAPTER

Adjuvant Analgesics for Radicular Pain

11

Sang-Ho Ahn

PATHOPHYSIOLOGIC BACKGROUND OF RADICULAR PAIN The pathophysiology of radicular pain remains incompletely understood. It is known that radicular pain is caused by disorders of the nerve root proximal to the dorsal root ganglion (DRG) or at the DRG itself. Proposed mechanisms of radicular pain include: (1) local neuropathic pain originating from lesions of nociceptive sprouts within the degenerated disc, (2) mechanical neuropathic root pain originating from mechanical compression of the nerve root, or (3) inflammatory neuropathic root pain derived from the action of inflammatory mediators originating from the degenerative disc.1 Traditionally, it has been thought that radicular pain arises from mechanical nerve root compression by herniated discs or osteophytes. However, increasing evidence suggests that radicular pain may involve chemical irritation or damage mediated by various agents released from the degenerated nucleus pulposus of herniated discs. These agents may include phospholipase A2,2 TNF-α,3 interleukin (IL)-8,4 IL-6, IL-1β,5 and nitric oxide.6 Chemical damage may lead to a state of hyperexcitability in the injured DRG or nerve root, a phenomenon called peripheral sensitization. The net result is ectopic neuronal firing7 transmitted via sensory neuron-specific, voltage-gated sodium channels. Ectopic neuronal firing also activates N-type voltage-gated calcium channels, permitting calcium influx and the promotion of excitation. As a result, dorsal horn neurons or central neurons innervated by the injured DRG or nerve root undergo dramatic functional changes, including a state of hyperexcitability termed central sensitization.8 Normally, these sensitization events spontaneously resolve as tissue healing occurs and inflammation subsides. Yet, when the primary afferent function is persistently altered by chemical or mechanical injury to the nerve roots, these processes may be highly resistant to treatment.9 Early antiinflammatory intervention (e.g. steroid injection) may reduce nerve root damage, thereby lessening the chance of developing chronic radicular pain. Indeed, this outcome may be the result of treating the peripheral disease, which in turn may eliminate the triggering of central sensitization.10

USE OF ANTIEPILEPTIC DRUGS IN CHRONIC RADICULAR PAIN Current first-line analgesic therapies for chronic radicular pain rely mostly on nonsteroidal antiinflammatory drugs (NSAIDs) known to relieve nociceptive pain only. Since the pathophysiology of neuropathic pain and epilepsy are similar, the use of antiepileptic drugs (AEDs) in the treatment of neuropathic pain is also an attractive option.11 Mechanisms of central sensitization and ectopic neuronal firing are common to both epilepsy12 and neuropathic pain.13 Given the similarities between these two disorders, it is reasonable to speculate that the mechanisms of action that may be responsible for the

therapeutic efficacy of the newer AEDs in the treatment of epilepsy may also prove beneficial in the treatment of neuropathic pain.14 Several mechanisms of action shared by the newer AEDs relate directly to the pathophysiology of neuropathic pain. Any or all of these actions may account for the effectiveness of these medications: (1) sodium channel blockade,15 (2) calcium channel blockade,15 (3) enhancement of GABAergic transmission,16 (4) inhibition of glutamatergic transmission,16 and (5) inhibition of carbonic anhydrase17 (Table 11.1). The mechanisms of chronic radicular pain may differ somewhat from those of peripheral neuropathic pain, resulting in varying of response to medication.18 Interestingly, a recent survey in the US19 indicated that AEDs are the third most commonly used class of medications for treating radiculopathy, after NSAIDs and opioids. Clinical trials demonstrating the efficacy of AEDs in this indication would be highly valuable, since therapeutic modalities such as AEDs could be a useful alternative for patients who do not respond to NSAIDs.1

NEWER ANTIEPILEPTIC DRUGS Recommendations for first-line AEDs are based on the positive results from multiple randomized, controlled trials. First-line medications for neuropathic pain include gabapentin, tricyclic antidepressants (TCAs), and tramadol hydrochloride (Fig. 11.1).9

Gabapentin: first-line antiepileptic drugs for chronic radicular pain Gabapentin is an AED with an unknown mechanism of action apparently dissimilar to that of other antiepileptic agents. This agent also possesses desirable pharmacokinetics: gabapentin is not protein bound and is not metabolized, and does not induce liver enzymes, diminishing the likelihood of interactions with other antiepileptic agents and with other drugs such as oral contraceptives. Although gabapentin is a structural analog of the neurotransmitter gammaaminobutyric acid (GABA), which does not cross the blood–brain barrier, gabapentin does penetrate into the CNS.20 Evidence suggests that its mechanism of action most likely involves complex synergy between increased GABA synthesis, non-NMDA receptor anatagonism, and binding to the α2δ subunit of voltage-dependent calcium channels. The latter action inhibits the release of excitatory neurotransmitters.21 The most important action of gabapentin appears to be its binding to the α2δ subunit of voltage-dependent calcium channels (see Table 11.1).22 These binding sites are located in the spinal cord, with particularly high density in the superficial laminae of the dorsal horn. The action of gabapentin at these sites may inhibit the release of excitatory neurotransmitters and reduce glutamate availability at NMDA and non-NMDA receptors.23 129

Part 1: General Principles

Table 11.1: Proposed Mechanisms of Action of Antiepileptic Drugs11,15–17,22,35,37,43 Mechanism of Action Na+ Channel Blockade

Drug

Gabapentin

Ca2+ Channel Blockade

Enhancement of GABAergic Transmission

Inhibition of Glutamatergic Transmission

Inhibition of Carbonic Anhydrase

x

Lamotrigine

x

x

Oxcarbazepine

x

x

Topiramate

x

x

Zonisamide

x

x

Levetiracetam

x

Pregabalin

x

Carbamazepine

x

x

x

x x

x

In chronic radiculopathy, mechanical and chemical nociceptive stimuli lead to the production of ectopic impulses. These ectopic discharges are seen along the length of the nerve root fiber. Ectopic discharges can provide sustained afferent input to the spinal cord from a damaged root or DRG. Gabapentin may inhibit these discharges at the level of the nerve root, DRG,24 spinal cord,21,23 or brain.20

Dosing and titration Titration and dosing schedules (Table 11.2 ) may potentially be efficacious in treating radicular pain and promoting tolerability, particularly in elderly patients, who make up a large proportion of radicular pain patients.25

Initiation Based on the schedule of treatment initiation used in study protocols, it is reasonable to start gabapentin at 300 mg once daily on day 1, 300 mg twice daily on day 2, and 300 mg thrice daily on day 3 (see Table 11.2). This stepwise escalation was well tolerated in clinical studies and has the advantages of simplicity and rapidity in reaching the goal dosage of 900 mg/day. These factors may contribute to patient compliance. Although infrequent, in cases of intolerance gabapentin should be initiated at lower dosages, such as 100 mg in a single dose at bed time, then titrated daily by 100 mg three times.25

Titration and maintenance In the reviewed trials, clinically relevant improvements were noted at week 2, during which patients received gabapentin 1800 mg/day. Thereafter, dosages were increased from 1800 to 3600 mg/day as tolerated to achieve better efficacy. In many patients, further dose escalations up to 3600 mg/day may be necessary to reach individ-

ualized maximally effective doses that can be maintained without compromising tolerability. Table 11.2 provides a possible schema for stepwise escalations in gabapentin dosing. Dosage increases can be simplified by the availability of 600 and 800 mg gabapentin tablets. Although drowsiness may occur during the initial titration period, the overall low rate of serious side effects associated with gabapentin treatment in clinical trials indicate that rapid dose escalations are probably safe.20,26,27 In most cases, drowsiness generally resolves within 7–14 days from the initiation of treatment. Contrary to previously published reports, however, some patients may continue to complain of drowsiness of moderate severity even at a daily dose of 900 mg. Based on study findings and the author’s clinical experience, some adverse events may be due to the dose titration process itself. Therefore, patient education about the transient nature of such adverse events may allow early achievement of effective doses and improve patient satisfaction.25 To minimize the problem of persistent drowsiness or other side effects, one can increase the intervals between dosage escalations, based on each patient’s tolerance.

1st line

Gabapentin or Pregabalin

2nd line

Lamotrigine

3rd line

Oxcarbazepine, Zonisamide, or others

Fig 11.1 Proposed antiepileptic drug treatment strategy for chronic radicular pain.

Table 11.2: Proposed Dosing Schedule for Maximally Effective Dose of Gabapentin in Treating Neuropathic Pain Initial Dose (mg) TID Schedule

Day 1

Day 2

PM

300

Maintenance Dose (mg)

Days 4–6

Days 7–10

Days 11–14

Day 15~

300

300

300

600

600–1200

300

300

300

600

600

600–1200

300

300

600

600

600

600–1200

AM Noon

Titration Dose (mg)

Day 3

Reprinted by permission of the publisher from Backonja M, Glanzman RL. Gabentin Dosing for Neuropathic Pain: Evidence from Randomized, Placebo-Controlled Clinical Trials. Clin Ther 2003; 25:2506–2538. Copyright, Excerpta Medica, Inc.

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Maximal effective dose On the basis of reviewed trials, doses of up to 3600 mg/day may be used when required and tolerated, and can be achieved by week 4 of treatment. In an animal model, gabapentin was shown to be more efficacious at lower doses in treating radicular pain than peripheral neuropathic pain.18 However, these findings need to be investigated further in future studies.

Combination treatment with tricyclic antidepressants, and tramadol Gabapentin, tricyclic antidepressants (TCAs), and tramadol hydrochloride have been used as first-line medications for neuropathic pain. It is common for patients to have a partial response to these medications, and in these cases combination treatment should be considered. No studies have systematically examined the efficacy of various combinations of these three medications, as compared with monotherapy. Despite the lack of controlled data, combinations of two or more of these first-line medications can be recommended when patients have a partial response to monotherapy or at the beginning of treatment. The disadvantage of combination therapy is the difficulty in identifying which medication is responsible for any adverse effects.9

Clinical reports on chronic radiculopathy Although several published, double-blind, placebo-controlled, randomized clinical trials of gabapentin in the treatment of chronic neuropathic pain have been published,27–30 there are only a few clinical reports designed to study the effect of gabapentin on pathological processes involving the dorsal root ganglion and proximal nerve root. These processes include chronic radiculopathy, arachnoiditis, and epidural fibrosis.

Chronic radiculopathy A unique randomized, placebo-controlled study evaluated the efficacy of gabapentin monotherapy in patients with chronic radiculopathy over 8 weeks. The results showed significant improvement in the

following: pain at rest, straight-leg raise test (SLR), and limitation of spinal flexion. The gabapentin group was treated with doses ranging from a total of 900 mg/day to 3600 mg/day divided into three doses.31

Arachnoiditis In one open-label study, three patients with arachnoiditis were treated with gabapentin at a maximum of 2700 mg/day. One patient discontinued the study because of adverse effects, and the other two had moderate improvement in their pain.32

Epidural fibrosis There was one case report in which two patients were treated for radicular pain resulting from epidural fibrosis caused by failed back surgery syndrome. It was reported that functional status improved markedly and pain was significantly diminished with gabapentin regimens of 1500 mg and 2100 mg/day.33

Drug interactions The paucity of interactions between gabapentin and other drugs distinguishes it from most other oral medications used for the treatment of chronic neuropathic pain. However, one notable interaction exists: antacids reduce the bioavailability of gabapentin by up to 24%; therefore, these drugs should not be taken concurrently.

Adverse effects The adverse effects of gabapentin include somnolence, fatigue, dizziness, and, less commonly, mild peripheral edema and gastrointestinal symptoms (Table 11.3). The incidence of mild adverse events has been reported in up to 35–75% of gabapentin recipients, seemingly in a dose-dependent manner.20,26,27 All of these effects require monitoring and dosage adjustment, but usually not discontinuation of the drug. In elderly patients in particular, gabapentin may cause gait and balance problems, as well as cognitive impairment. In addition, dosage adjustment is necessary in patients with renal insufficiency. However, generally excellent tolerability and safety of gabapentin

Table 11.3: Adverse Effects of Newer Antiepileptic Drugs11,34,36,37,40,42,46,48,51,52 Adverse Event

Gabapentin

Lamotrigine

Oxcarbazepine

Topiramate

Zonisamide

Levetiracetam

Pregabalin

Dizziness/ataxia

3

3

3

2

2

2

2

Somnolence

3

1

3

3

3

2

2

Fatigue

2

1

2

1

1

1

0

Peripheral edema

2

0

0

0

0

0

2

Cognitive dysfunction

1

1

1

3

1

1

0

Diplopia

1

3

3

1

1

0

1

Nausea/vomiting

1

3

3

1

1

0

0

Anorexia/weight loss

0

0

0

3

3

2

0

Kidney stone

0

0

0

1

1

0

0

Rash

0

3

0

0

1

0

0

+

++

The grading system used in the table was as follows: 0 = same as placebo; 1 = 2–5% more than placebo; 2 = 6–10% more than placebo or >2 times placebo; 3 = >10% or >3 times placebo. Adapted from Pappagallo M. Clin Ther 2003; 25:2506–2538. + <1% Incidence of serious rash. ++ <0.1% Incidence of serious rash. 131

Part 1: General Principles

distinguish it from most other oral medications used for the treatment of chronic neuropathic pain. In effect, it is often the first choice for treating many types of neuropathic pain.34 Gabapentin is absorbed orally without interference by food, and it reaches peak serum concentrations after 2–3 hours. No blood monitoring is required with gabapentin therapy because of the absence of toxic effects.20

Lamotrigine Lamotrigine is a novel AED with at least two antinociceptive properties: it stabilizes the neural membrane through blocking the activation of voltagesensitive sodium channels, and it inhibits the presynaptic release of glutamate.15 Abnormal neural firing is a principle cause of nerve injury-induced pain,7 and glutamate plays a key role in dorsal horn spinal hyperexcitability by acting at the NMDA receptor (see Table 11.1),35 providing a strong rationale for the use of lamotrigine in the treatment of radicular pain.

Dosing and titration Titration (Table 11.4) is initiated at a dose of 25 mg daily for 2 weeks, increasing to 50 mg/day for 2 weeks. Further increases are by 50 mg b.i.d. for 2 weeks, then by 100 mg/day b.i.d. every week,11,36 until the desired daily dose is achieved. The regimen of gradual dose increments is chosen to avoid the occurrence of adverse drug reactions.20 The analgesic effects of lamotrigine become more profound after prolonged treatment with a steady dose.36

Clinical reports on chronic radiculopathy Lamotrigine in doses higher than 200–400 mg daily has demonstrated efficacy in relieving pain in patients with trigeminal neuralgia, complex regional pain syndrome type I, chronic neuropathic pain syndrome, painful HIV neuropathy, central post-stroke pain, and incomplete spinal cord lesions.9 A unique open-label study investigated the effect of lamotrigine on chronic radicular pain, and showed that spontaneous pain, pain associated with the straight-leg-raising test), and pain associated with bending the affected side reached a statistically significant level of improvement only at a 400 mg dose. These results suggest that lamotrigine is a potentially effective treatment for painful lumbar radiculopathy, and that it is likely to act in a dose- and plasma concentration-dependent fashion.36Because of the slow and careful titration required and risk of both severe rash and Stevens-Johnson syndrome associated with its use, lamotrigine should, however, only be considered in cases of chronic radicular pain refractory to gabapentin.

Drug interactions Lamotrigine is absorbed rapidly and completely from the gastrointestinal tract, and it is approximately 55% bound to plasma protein. The drug is extensively metabolized by conjugation with glucuronic acid. The elimination half-life is 25–30 hours. Because of the wide variability in kinetics caused by interaction with concomitant medications, monitoring serum lamotrigine concentrations could be theoretically useful in clinical practice.34 Plasma lamotrigine levels are reduced by barbiturates, carbamazepine, phenytoin, oxcarbazepine, and steroid oral contraceptives, and they are increased by valproate.37

Adverse effects Common adverse effects (see Table 11.3) include dizziness, ataxia, somnolence, diplopia, nausea, vomiting, and constipation. A more serious side effect is rash, which, in rare instances, can progress to Stevens-Johnson syndrome. However, the chance of this event is drastically decreased when the drug is titrated slowly. Adverse effects are more pronounced in patients concurrently taking valproate.34

Oxcarbazepine Oxcarbazepine has been shown to inhibit high-frequency nerve firing without impairing normal impulse conduction. The agent exerts a dual mode of action involving the modulation of both voltage-sensitive sodium channels and high-voltage activated N-type calcium channels (see Table 11.1). As a result, there is a possibility that oxycarbazepine can target certain underlying mechanisms known to be important in the genesis of both peripheral and central sensitization.15,38

Dosing and titration Since oxcarbazepine does not autoinduce its metabolism, dosage titration and adjustments (see Table 11.4) are relatively simple, and steady-state levels of the drug can be achieved. The recommended adult starting dosage is 150–300 mg/day. The dosage is slowly titrated at weekly intervals, based on clinical response, to a usual maintenance dosage of 600– 1800 mg/day. Doses are given twice daily. Some patients with refractory neuropathic pain may require doses as high as 2400 mg/day.11,38

Clinical reports on chronic radiculopathy An open-label study of adjunctive oxcarbazepine involved 36 consecutive patients with various neuropathic pain disorders that did not respond to treatment with gabapentin. In this study, the addition of

Table 11.4: Dosing and Titration of Antiepileptic Drugs11,16,36,38,39,40,42,43,44,46,51,52 Drug

Initial Daily Dose

Titration Schedule

Target Daily Dose

Lamotrigine

25 mg q.d.

Increase to 25 mg b.i.d. for 2 weeks, then 50 mg b.i.d. for 2 weeks, then by 100 mg increments each week

200–500 mg/day b.i.d.

Oxcarbazepine

150–300 q.h.s.

Increase by 150–300 mg every week

600–1800 mg/day b.i.d.

Topiramate

25–50 mg q.d.

Increase by 25–50 mg every 1–2 weeks

200–400 mg/day b.i.d.

Zonisamide

100 mg q.h.s.

Increase to 200 mg/day after 2 weeks, then to 300 mg/day for 2 weeks, then by 100 mg increments every week

200–500 mg/day b.i.d.

Levetiracetam

500 mg q.d.

Increase by 500 mg every 2 weeks

1000–3000 mg/day b.i.d.

Pregabalin

50 mg t.i.d.

Increase by 150 mg every 3 days

300–600 mg/day t.i.d.

Carbamazepine

100 mg b.i.d.

Increase by 200 mg every 3 days

600–1200 mg/day t.i.d.

From Pappagallo M. Newer antiepileptic drugs: possible uses in the treatment of neuropathic pain and migraine. Clin Ther 2003; 25:2506–2538. Copyright, Excerpta Medica, Inc.

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oxcarbazepine at dosages of 600–1200 mg/day was helpful in almost two-thirds of patients. Excellent results (>70% improvement in neuropathic symptoms) were reported in 22.2% of patients, good results (51–70% improvement) in 41.7%, and fair or poor results (<50% improvement) in 38.9%. In a subset of patients who presented with radiculopathy (n=18), the proportion of those with excellent or good results was greater than in the entire sample (84% vs. 64%, respectively). Significant improvement was seen in patients with symptoms described as ‘burning’ and allodynia.39 There is growing clinical evidence that oxcarbazepine may be equal to or better than carbamazepine for the treatment of both painful diabetic neuropathy and trigeminal neuralgia. Oxcarbazepine is reported to have a better side effect profile than carbamazepine, and it is now the drug of choice for trigeminal neuralgia in several Western countries.40,41 However, oxcarbazepine still requires further well-designed research and clinical experience. In the interim, it is recommended that this agent be used to treat neuropathic pain only when gabapentin or lamotrigine cannot be used, or when the response to these agents is suboptimal.42

Drug interactions Oxcarbazepine has predictable, linear pharmacokinetics and minimal drug interactions which facilitate its use in combination therapy. In contrast to carbamazepine, oxcarbazepine does not generally induce hepatic enzymes. However, the agent selectively enhances the metabolism of felodipine. In addition, it induces the CYP3A4 system, affording more rapid metabolism of estrogen and progesterone. Thus, it is recommended that oxcarbazepine recipients not use oral contraceptives.11,42

Adverse effects The most common side effects of oxcarbazepine (see Table 11.3) include sedation, dizziness, diplopia, nausea, vomiting, vertigo, ataxia, and headache. These effects appear to be dose-dependent. The side effect profile of oxcarbazepine is favorable relative to carbamazepine. Oxcarbazepine is not associated with serious idiosyncratic hematologic or hepatic effects. For this reason, there is no need for routine monitoring of hematologic and hepatic profiles during treatment with the drug. The frequency of hyponatremia with oxycarbazepine has been reported to range from 22% to 73%. Most cases are asymptomatic, but severe cases have been seen occasionally.40,42

Topiramate Topiramate is a newer AED with several mechanisms of action. It has been shown to modulate voltage-gated sodium and calcium channels, potentiate GABAergic inhibition, block excitatory glutamate activity via the AMPA and kinase receptors, and inhibit carbonic anhydrase (see Table 11.1).43 Based on these mechanisms of action, topiramate should be well suited to inhibit several of the mechanisms putatively involved in neuropathic pain.

Dosing and titration The recommended starting dosage of topiramate (see Table 11.4) in adults is 25–50 mg/day, followed by titration in 25–50 mg/day increments every 1–2 weeks based on clinical response, to a usual maintenance dosage of 200–400 mg/day (maximum of 600 mg/day). Doses are given twice daily.11,42,43

Clinical reports on chronic radiculopathy Some small clinical trials showed pain reduction with topiramate therapy at doses up to 400 mg/day in painful diabetic neuropathy,

trigeminal neuralgia, intercostal neuralgia, and neuropathic pain after spinal cord injury. Effectiveness in neuropathic pain remains unclear.11,41 Presently, there are no published reports of topiramate’s effect on chronic radicular pain.

Drug interactions Topiramate induces the CYP3A4 system, inducing more rapid metabolism of most of the steroid hormones in oral contraceptives, and can thus lead to failure of birth control. For that reason, it is recommended that patients taking topiramate not use oral contraceptives. In addition, topiramate enhances the hypoglycemic effect of metformin, although the mechanism by which this occurs is unknown.42

Adverse effects The most common adverse effects of topiramate (see Table 11.3) are anorexia, nausea, diarrhea, and CNS-related symptoms (including somnolence, dizziness, ataxia, fatigue, impaired cognitive function and concentration, speech disturbance, and digital and perioral paresthesia). The frequency and severity of these effects are increased at higher doses, with more rapid dose escalation, and as part of combination therapy, as opposed to monotherapy. Behavioral events are rarely seen. Nephrolithiasis, particularly calcium phosphate stones, are seen in ≈1.5% of topiramate recipients, yet most stones are very small and are passed spontaneously. In addition, two non-CNS adverse effects are of particular interest. First, the drug may cause acute myopia and secondary angle-closure glaucoma, presumably mediated by carbonic anhydrase inhibition. Symptoms include severe bilateral ocular pain and hyperemia, which usually remit within 24 hours of drug withdrawal. Second, most topiramate recipients experience weight loss, which becomes apparent within the first 3 months of therapy.42

Zonisamide A newer AED, zonisamide, is believed to exert its effects by inhibiting voltage-dependent sodium and T-type calcium channels, both of which have a pivotal role in membrane excitability. The agent binds but does not modulate GABA receptors and inhibits a carbonic anhydrase (see Table 11.1).17 Thus, the activity profile of zonisamide appears favorable for the treatment of neuropathic pain.

Dosing and titration The recommended starting dose of zonisamide (see Table 11.4) is 100 mg/day at bedtime, followed by dose titrations every 2 weeks up to 300 mg/day. Dose increases of 100 mg are then made weekly based on response, to a usual maintenance dosage of 200–500 mg/ day. Doses are given twice daily.42

Clinical reports on chronic radiculopathy Although zonisamide has not been evaluated in randomized, controlled trials in patients with neuropathic pain, a number of openlabel case series and anecdotal reports have been published. In the largest open-label study,44 zonisamide was added to existing therapy in 40 patients with treatment-refractory neuropathic pain that was primarily associated with cervical or lumbar radiculopathy. At a mean daily dosage of 260 mg/d, daily pain scores were decreased by >60% in 10 patients (25%) and by 30–60% in 8 patients (20%). Only 2 of 40 patients (5%) chose to discontinue the drug because of drowsiness. As a result of starting zonisamide therapy, 18 of 40 patients (45%) were able to discontinue the AED they had originally been taking at the time of entry (gabapentin in 12 of 18 patients, and topiramate in 3 patients). There is also a retrospective study45 that 133

Part 1: General Principles

included 142 patients with neuropathic pain who received a prescription for zonisamide. Eighty-six of these patients had a diagnosis of cervical or lumbar radiculopathy, 30 had painful diabetic neuropathy, 19 had fibromyalgia, and 7 had pelvic pain. Only 10 patients (7%) discontinued zonisamide because of adverse effects. At a mean daily dose of 252 mg, 100 of 142 patients (70%) reported at least moderate reduction of pain, and only 9 (6%) felt they received no benefit. One other clinical trial with a smaller study population showed pain reduction with zonisamide therapy at dosages up to 400 mg/day in the setting of various neuropathic pain syndromes.42

Pregabalin

Concurrent use of hepatic enzyme inducers such as phenobarbital, carbamazepine, and phenytoin are known to reduce plasma zonisamide levels.37

Pregabalin is an α2δ ligand that has analgesic, anxiolytic, and anticonvulsant activity. The auxiliary protein α2d is associated with voltagegated calcium channels (see Table 11.1). Pregabalin binds potently to the α2δ subunit,22 which, in turn, reduces calcium influx at nerve terminals. As a result, there is a decrease in the release of several neurotransmitters, including glutamate, noradrenaline, and substance P.49,50 This activity produces the analgesic, anxiolytic, and anticonvulsant activity exhibited by pregabalin. The dual benefits of relieving both pain and anxiety (independent of pain relief) may prove to be highly beneficial clinically.51

Adverse effects

Dosing and titration

The most common adverse effects of zonisamide (see Table 11.3) are somnolence, ataxia, anorexia, impaired cognitive function, nervousness, fatigue, and dizziness. Clinically significant weight loss may also occur, but is less problematic than with topiramate. In one epilepsy trial, kidney stones were suspected in 4% of patients receiving zonisamide.46 As a member of the sulfonamides, zonisamide poses a risk for serious dermatologic and hematologic reactions. However, the incidence of such adverse effects has been extremely small, and the background rate of rash is reported as very low. Both zonisamide and topiramate are weak carbonic anhydrase inhibitors, and their concomitant use may increase the risk for kidney stones.11,42

The recommended starting dose of pregabalin (see Table 11.4) is 150 mg/day (50 mg three times daily), followed by dose titration every 3 days based on response, to a usual maintenance dosage of 300–600 mg/day. The drug is given three times daily.51,52

Drug interactions

Clinical reports on chronic radiculopathy

Levetiracetam inhibits calcium channels and delayed-rectifier potassium currents, and antagonizies negative allosteric modulators of the GABA and glycine responses at nonbenzodiazepine sites (see Table 11.1).37

Two randomized, placebo-controlled trials focused on the treatment of postherpetic neuralgia with pregabalin at dosages of 150–600 mg/ day. Results showed that pregabalin is safe, efficacious in relieving pain and sleep interference, and associated with greater global improvement than placebo. Pregabalin treatment groups demonstrated significant improvement in pain compared to placebo as early as week 1.51,52 Although no clinical trials have compared pregabalin with gabapentin, it appears that pregabalin has a more rapid onset of action than does gabapentin.51 While this agent shows promise, there has not yet been a report on the effect of pregabalin on chronic radicular pain.

Dosing and titration

Drug interactions

The recommended starting dose of levetiracetam (see Table 11.4) is 500 mg/day, followed by dose titration every 2 weeks based on response, to a usual maintenance dosage of 1000–3000 mg/day. The drug is given twice daily.42

Pregabalin has a predictable pharmacokinetic profile, few drug interactions, and a rapid onset of action.52

Levetiracetam

Clinical reports on chronic radiculopathy A few clinical trials have demonstrated pain reduction in various neuropathic pain syndromes and neoplastic plexopathies with levetiracetam therapy at dosages of 1000–3000 mg/day.42 However, the effectiveness of levetiracetam in neuropathic pain requires further detailed study.

Drug interactions No clinically significant drug interactions with levetiracetam have been identified to date due to low protein-binding (<10%) and lack of hepatic metabolism.47

Adverse effects Levetiracetam has a favorable side effect profile (see Table 11.3). The most common adverse effects of levetiracetam occur only occasionally, and include dizziness, headache, fatigue, somnolence, and asthenia. Behavioral effects are rare. Levetiracetam appears to be one of the easiest AEDs to use, since there is no need for dose adjustments in cases of organ dysfunction, and laboratory monitoring is 134

not required. It is one of the best-tolerated agents, and has not been associated with the toxicities seen with oxcarbazepine, topiramate, and zonisamide.42,48

Adverse effects The most frequent adverse events (see Table 11.3) are dizziness, somnolence, peripheral edema, headache, and dry mouth, all of which are mild to moderate in intensity. These adverse effects are dose dependent. In one study, more patients in the pregabalin treatment groups completed therapy than in the placebo group. This result suggests that the adverse effects associated with pregabalin may be of no clinical significance.51 The frequency of adverse events occurring in patients taking pregabalin seems to be less than in patients taking gabapentin.20,26,27,52

OLDER ANTIEPILEPTIC DRUGS Carbamazepine Carbamazepine emerged as a treatment for trigeminal neuralgia before the discovery of much of what is now known about the pathophysiology of nociception and neuropathic pain. Since that time, little progress has been made in the development of medications for neuropathic pain. Carbamazepine is an iminostilbene derivative chemically related to the TCAs. The analgesic effect of carbamazepine is thought possibly to result from its peripheral or central activity.

Section 4: Practical Pharmacology

The drug’s ability to block calcium and sodium channels appears to suppress A-delta and C-fiber activity (see Table 11.1) implicated in the genesis of pain.34

Dosing and titration The recommended starting dose of carbamazepine (see Table 11.4) is 200 mg/day (100 mg twice daily), increased every 3 days based on response to a usual maintenance dosage of 600–1200 mg/day. The drug is given three times daily.16

Clinical reports on chronic radiculopathy Carbamazepine has a well-established beneficial effect on trigeminal neuralgia,53 and has been approved by the FDA for this indication. Some evidence suggests that carbamazepine is beneficial in the treatment of patients with painful diabetic neuropathy.54 On the basis of clinical trials with AEDs used for chronic neuropathic pain, carbamazepine can be recommended for patients for whom AED treatment is desired, yet who have not responded to an adequate trial of gabapentin. The effect of carbamazepine on chronic radicular pain, however, remains speculative and is supported only by a few case reports and anecdotal experience.

Drug interactions Carbamazepine is a potent enzyme inducer which causes many drug interactions. This agent reduces plasma levels of lamotrigine, oxcarbazepine, topiramate, and zonisamide.37

Adverse effects Common adverse effects of carbamazepine (see Table 11.3) include somnolence, dizziness, diplopia, blurred vision, gait disturbance, nausea, and vomiting. In elderly patients, several issues may complicate treatment with carbamazepine, including cardiac disease, water retention, decreased osmolality, and hyponatremia. Hematologic problems, such as agranulocytosis, were of concern during early experiences with carbamazepine, and it is still advisable to monitor patients for this possible complication. Induction of the microsomal enzyme system by carbamazepine may influence drug metabolism.41

Clonazepam Clonazepam is a GABA agonist that has analgesic properties in the spinal cord and brainstem of animal models.55 In the absence of definitive data, clinical experience suggests clonazepam may relieve trigeminal neuralgia and various neuropathic pain syndromes.56 As of yet, there is no report on the effect of this drug on chronic radicular pain. Clonazepam should probably not be considered a first-line choice even for the above indications, since potential benefits must be weighed against the potential for developing cognitive impairment, physical and psychological dependence, worsening depression, overdose, and other side effects.57 The recommended starting dose of clonazepam is 0.5–1 mg/day, which is increased to a usual maintenance dosage of 4–6 mg/day. The drug is given three times daily.16

Phenytoin Phenytoin exerts its membrane-stabilizing effect by blocking sodium channels, and it is generally held that it reduces neuronal excitability of pain fibers by this mechanism. Phenytoin was the first drug to be used for trigeminal neuralgia, but there is no randomized, controlled

trial on the use of the agent for this condition. Today, phenytoin has limited use for the treatment of chronic neuropathic pain due to its side effects and complicated pharmacokinetic profile. Instead, it has been replaced by drugs such as gabapentin, lamotrigine, oxcarbazepine, and carbamazepine.41

Valproic acid Valproic acid inhibits sustained neuronal firing in murine cortical and spinal neurons. This effect is mediated by prolonging repolarization of voltage-activated sodium channels. Moreover, the drug increases the amount of GABA in the brain, enhancing the activity of glutamic acid decarboxylase, and inhibiting GABA degradation enzymes.16 In the absence of definitive data, anecdotal experience suggests that valproic acid relieves trigeminal neuralgia and various neuropathic pain syndromes.16 Recently, a randomized, double-blind, placebo-controlled study showed that valproic acid is well tolerated and provides significant subjective improvement in painful diabetic neuropathy.58 However, there was no difference between valproic acid and placebo in regards to the treatment of neuropathic pain after spinal cord injury.59 There are not yet any reports on the effect of valproic acid on chronic radicular pain.

OTHER ANTIEPILEPTIC DRUGS Because of the similarities in the mechanisms underlying neuropathic pain and epilepsy, AEDs other than those previously discussed may prove useful in treating neuropathic pain syndromes. Due to serious toxicity risks, felbamate and vigabatrin should be prescribed only in patients refractory to other drugs. Antiepileptic agents currently under clinical investigation for use in neuropathic pain include tiagabine and lorazepam, although there are not yet any reports regarding these drugs for treating chronic radicular pain.

CONCLUSION Interest in the mechanism and treatment of chronic radicular pain has increased during the past several years, coupled with continued research in the pathophysiology of chronic radicular pain. We will see significant treatment advances in the future. Already, the newer AEDs have safer side effect profiles than the older AEDs, and even though clinical data are lacking, preliminary study results highlight the potential of these newer AEDs to be an important treatment option for chronic radicular pain. Gabapentin, in particular, has emerged as a first-line AED for treating chronic radicular pain. In addition, pregabalin may be expected to have potential promise as a therapy for chronic radicular pain (see Fig. 11.1). Finally, in addition to the adjunctive analgesic drugs discussed, continued research will also lead to better early antiinflammatory interventions for patients susceptible to chronic radicular pain.

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12. Engelborghs S, D’Hooge R, De Deyn PP. Pathophysiology of epilepsy. Acta Neurol Belg 2000; 100:201–213.

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13. Chaplan SR, Guo HQ, Lee DH, et al. Neuronal hyperpolarization-activated pacemaker channels drive neuropathic pain. J Neurosci 2003; 23:1169–1178.

40. Beydoun A, Kutluay E. Oxcarbazepine. Expert Opin Pharmacother 2002; 3:59–71.

14. Backonja MM. Anticonvulsants (antineuropathics) for neuropathic pain syndromes. Clin J Pain 2000; 16(Suppl 2):S67–S72. 15. Wallace MS. Calcium and sodium channel antagonists for the treatment of pain. Clin J Pain 2000; 16(Suppl 2):S80–S85. 16. Tremont-Lukats IW, Megeff C, Backonja MM. Anticonvulsants for neuropathic pain syndromes: mechanisms of action and place in therapy. Drugs 2000; 60:1029–1052. 17. Leppik IE. Zonisamide. Epilepsia 1999; 40(Suppl 5):S23–S29. 18. Abe M, Kurihara T, Han W, et al. Changes in expression of voltage-dependent ion channel subunits in dorsal root ganglia of rats with radicular injury and pain. Spine 2002; 27:1517–1524. 19. Cluff R, Mehio AK, Cohen SP, et al. The technical aspects of epidural steroid injections: a national survey. Anesth Analg 2002; 95:403–408. 20. Goa KL, Sorkin EM. Gabapentin. A review of its pharmacological properties and clinical potential in epilepsy. Drugs 1993; 46:409–427. 21. Bennett MI, Simpson KH. Gabapentin in the treatment of neuropathic pain. Palliat Med 2004; 18:5–11. 22. Gee NS, Brown JP, Dissanayake VU, et al. The novel anticonvulsant drug, gabapentin (Neurontin), binds to the α2d subunit of a calcium channel. J Biol Chem 1996; 271:5768–5776.

41. Jensen TS. Anticonvulsants in neuropathic pain: rationale and clinical evidence. Eur J Pain 2002; 6(Suppl A):61–68. 42. Guay DRP. Oxcarbazepine, topiramate, zonisamide, and levetiracetam: Potential use in neuropathic pain. Am J Geriatr Pharmacother 2003; 1:18–37. 43. Chong MS, Libretto SE. The rationale and use of topiramate for treating neuropathic pain. Clin J Pain 2003; 19:59–68. 44. Krusz JC. Zonisamide in the treatment of pain and headache disorders. J Neurol Sci 2001; 187(Suppl 1):S107. abstract. 45. Kaplan M. Zonisamide – benefits in chronic pain patients. Arch Phys Med Rehabil 2002; 83:1671(a). 46. Leppik IE. Three new drugs for epilepsy: levetiracetam, oxcarbazepine, and zonisamide. J Child Neurol 2002; 17(Suppl 1):S53–S57. 47. Hachad H, Ragueneau-Majlessi I, Levy RH. New antiepileptic drugs: review on drug interactions. Ther Drug Monit 2002; 24:91–103. 48. Glauser TA, Pellock JM, Bebin EM, et al. Efficacy and safety of levetiracetam in children with partial seizures: an open-label trial. Epilepsia. 2002; 43(5):518–524. 49. Fink K, Dooley DJ, Meder WP, et al. Inhibition of neuronal Ca(2+) influx by gabapentin and pregabalin in the human neocortex. Neuropharmacology 2002; 42:229–236.

23. Shimoyama M, Shimoyama N, Hori Y. Gabapentin affects glutamatergic excitatory neurotransmission in the rat dorsal horn. Pain 2000; 85:405–414.

50. Maneuf YP, Hughes J, McKnight AT. Gabapentin inhibits the substance P-facilitated K(+)-evoked release of [(3)H]glutamate from rat caudal trigeminal nucleus slices. Pain 2001; 93:191–196.

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25. Backonja M, Glanzman RL. Gabapentin dosing for neuropathic pain: evidence from randomized, placebo-controlled clinical trials. Clin Ther 2003; 25:81–104.

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26. Ahn SH, Park HW, Lee BS, et al. Gabapentin effect on neuropathic pain compared among patients with spinal cord injury and different durations of symptoms. Spine 2003; 28:341–346.

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27. Levendoglu F, Ogun CO, Ozerbil O, et al. Gabapentin is a first-line drug for the treatment of neuropathic pain in spinal cord injury. Spine 2004; 29:743–751.

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28. Backonja M, Beydoun A, Edwards KR, et al. Gabapentin for the symptomatic treatment of painful neuropathy in patients with diabetes mellitus: a randomized controlled trial. JAMA 1998; 280:1831–1836.

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29. Pandey CK, Bose N, Garg G, et al. Gabapentin for the treatment of pain in Guillain-Barré syndrome: a double-blinded, placebo-controlled, crossover study. Anesth Analg 2002; 95:1719–1723. 30. Rowbotham M, Harden N, Stacey B, et al. Gabapentin for the treatment of postherpetic neuralgia: a randomized controlled trial. JAMA 1998; 280:1837–1842. 31. Yildirim K, Sisecioglu M, Karatay S, et al. The effectiveness of gabapentin in patients with chronic radiculopathy. Pain Clin 2003; 15:213–218. 32. Merren MD. Gabapentin for treatment of pain and tremor: a large case series. South Med J 1998; 91:739–744.

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56. Bouckoms AJ, Litman RE. Clonazepam in the treatment of neuralgic pain syndrome. Psychosomatics 1985; 26(12):933–936. 57. Reddy S, Patt RB. The benzodiazepines as adjuvant analgesics. J Pain Symptom Manage 1994; 9(8):510–514. 58. Kochar DK, Rawat N, Agrawal RP, et al. Sodium valproate for painful diabetic neuropathy: a randomized double-blind placebo-controlled study. QJM 2004; 97(1):33–38. 59. Drewes AM, Andreasen A, Poulsen LH. Valproate for treatment of chronic central pain after spinal cord injury. A double-blind cross-over study. Paraplegia 1994; 32(8):565–569.

PART 1

GENERAL PRINCIPLES

Section 4

Practical Pharmacology

CHAPTER

Pharmacology of Local Anesthetic Agents

12

Tom Edrich, Kamen Vlassakov and Peter Gerner

INTRODUCTION The development of general and, in particular, local anesthetics (LAs), required both socioeconomic and cultural changes, as well as certain landmark scientific discoveries. Pain had long been linked to the concept of the original sin, and the ability to endure pain was regarded as a sign of character and, in men, was even associated with virility. Nevertheless, throughout human history, healers, magicians, medicine men, and learned physicians had passionately sought cures not only for disease, but also for pain and suffering. However, it was not until the 1840s that industrialization, progressive humanization and democratization, which altered the cultural, political, and religious climate, as well as some revolutionary achievements in basic and applied science, including physics, chemistry and physiology, provided the basis for a revolutionary breakthrough. This new era officially began on October 16, 1846, with the first successful public demonstration of ether anesthesia. Horace Wells and William Thomas Green Morton, two American dentists, introduced to the world the anesthetic properties of nitrous oxide and ether, respectively. Local and regional anesthesia had to wait several more decades until the recognition of the first true local anesthetic, cocaine. Medical doctors, led by those with surgical interests and the training to realize this new great opportunity, embraced and developed it further. The coca plant had been cultivated and its leaves chewed since ancient times in South America. In 1858 Karl von Scherzer brought a sizable amount of coca leaves to Europe and sent a sample for analysis, which allowed the isolation of the active component, an alkaloid named erythroxyline, and its purification in 1860 by Albert Niemann to obtain cocaine. Over this period, the introduction of the syringe and hypodermic needle had led to many attempts to produce local anesthesia for surgery, using such agents as morphine, chloroform, water, and hypertonic salt solutions. The reinvention of older empirical methods such as cold surface anesthesia and the introduction of newer ideas based on the increasing knowledge of human anatomy and physiology such as neural compression conduction anesthesia had been important advances, but were providing insufficient pain relief. A major early influence on the development of cocaine as a local anesthetic was a paper published in 1880 by Vassiliy von Anrep, in which he described the pharmacology of cocaine and suggested its use for surgery. Anrep systematically investigated its effects on different tissues in frogs and various mammals. He described the stimulating effect when cocaine was administered systemically and the depressant effect at high doses, with death apparently from respiratory arrest. Although Moréno and Bennett had previously investigated the effects of cocaine in animals, and Moréno had described the blocking action of cocaine when injected near the sciatic nerve in frogs and suggested its use as a local anesthetic, Anrep’s study was much more detailed and comprehensive, going through all

the body’s systems methodically in different species. He was the first to inject cocaine subcutaneously into humans (himself), and the first to report the anesthetic effect produced by the injection. (He described the feeling of warmth and numbness which persisted for 25–30 minutes.) He also confirmed the numbing effect when cocaine was placed on the tongue. Anrep suggested that these properties could have very important applications in surgery and the treatment of painful conditions, concluding that thus far he had been too busy to explore them.1 Anrep’s paper came at a perfect time, and would surely have led to wider use of cocaine had he been a surgeon and published it in a mainstream surgical journal. In fact, it took another scientist, Sigmund Freud, to recognize the potential of cocaine and act upon Anrep’s suggestion. He obtained cocaine and gave it for independent testing to two young ophthalmologists, Carl Koller and J. Königstein. Koller’s now famous paper was presented to the German Ophthalmological Society in Heidelberg on September 15, 1884; he noted in his report that he was familiar with Anrep’s experiments and started by confirming Anrep’s results in animals before applying cocaine to the human eye. The news spread quickly and only 2 weeks later, Jellinek reported similar anesthetic and analgesic effects when cocaine solution was applied to the mucous membrane of the pharynx and larynx. Over the next 2 months many other investigators from all over the world published reports of the use of topical cocaine for anesthetizing the ears, nose, mouth, trachea, rectum, and genital tract. On November 15, Hepburn published his observations on the numbing effect of cocaine after hypodermic injection. Other reports followed throughout November, 1884. On December 6, 1884, Hall announced his and Halsted’s experiences in producing nerve blockade with cocaine (ulnar nerve, musculocutaneous nerve of the leg, anterosuperior dental nerve, inferior dental nerve, and lingual nerve) in a letter dated November 26. Many reports of cocaine’s use followed, mostly involving topical application and/or infiltration.1 Local and regional anesthesia were born! The introduction of cocaine into medical practice by Koller revolutionized surgery, starting with ophthalmology and spreading rapidly to urology, gynecology, otolaryngology, and general surgery, as well as to dentistry. The use of local and regional anesthesia remained uncommon for a few more years until the synthesis of pure cocaine in 1891 by the techniques of modern organic chemistry.2 Soon, however, the toxic effects of cocaine, resulting in the deaths of many patients as well as addictions among the medical staff, were also identified. The need for better and safer local anesthetics became apparent. Procaine, an alternative to cocaine, belonging to the class of structures called amino esters, appeared in 1905. Other amino esters synthesized between 1891 and 1930 included tropocaine, eucaine, holocaine, orthoform, benzocaine, and tetracaine. Marketed under 137

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138

traumatic approach to plexus anesthesia and peripheral nerve blocks as well as the quest for the ‘ideal’ local anesthetic continues to this day.

MECHANISM OF ACTION Pharmacokinetics and pharmacodynamics Local anesthetics are frequently applied directly on or near their target via techniques of regional anesthesia. Thus, plasma levels rarely bear a relationship to their desired effects; however, these plasma levels are critical for systemic toxicity. The pharmacokinetics describing the blood concentration after administration of a drug are illustrated in Figure 12.1. Clearance of amide-type local anesthetics depends on liver function and may be limited in any disease state that reduces hepatic blood flow. An increase of α-1-acid glycoprotein and other plasma proteins (e.g. due to cancer) can lead to more rapid delivery of the drug to the liver and therefore lead to faster clearance. Ester-type drugs are hydrolyzed by plasma pseudocholinesterase. Thus, patients with genetically abnormal pseudocholinesterase are at increased risk for toxic side effects, since metabolism is slower. However, to a limited degree, the liver also extracts and metabolizes ester-type compounds. An increase of apparent volume of distribution may occur in older and more adipose patients. The lung has also been implicated as a site of local anesthetic metabolism, providing a dose-dependent first-pass uptake effect. Renal disease has little effect on these pharmacokinetics. Pharmacodynamics, or the relative potency and efficacy of the medication, depends on the mode of application, e.g. peripheral nerve blockade, spinal, or epidural injection. Table 12.1 summarizes some pharmacokinetic and -dynamic parameters for amide- and ester-type local anesthetics.

Transport to the ion channel Most local anesthetics are weak bases that are converted to their uncharged lipid-soluble form to pass through the phospholipid membrane into the cell as shown in Figure 12.2. However, once inside they are converted to the charged form to block the sodium channel. The Henderson-Hasselbalch equation relates the pH to the pKa and the relative concentrations of uncharged base (B) and charged base (BH+). Given the reaction:

Toxic plasma level Intravascular

Free plasma concentration

the name Novocaine™, procaine, which demonstrated predictable effects and low systemic toxicity, remained the most important local anesthetic until the 1940s.. However, the relatively frequent allergic reactions to Novocaine™, due to the metabolite p-aminobenzoic acid (PABA), prompted the search for newer, less allergenic substances. In 1908, intravenous regional anesthesia was first described by August Bier. This technique is still in use and is remarkably safe when drugs of relatively low systemic toxicity such as lidocaine and prilocaine are used. Spinal anesthesia was first described in 1885 but not introduced into clinical practice until 1899, when August Bier subjected his assistant and himself to a clinical experiment in which they observed the anesthetic effect, but also the typical side effect, of postpunctural headache. Within a few years, spinal anesthesia became widely used for surgical anesthesia and was accepted as a safe and effective technique. Although atraumatic (non-cutting-tip) needles and modern drugs are used today, the technique has otherwise changed very little over many decades.3 Within only two decades of Koller’s breakthrough, most of the currently used regional anesthesia blocks were developed in one form or another, including brachial plexus block, celiac plexus block, caudal and epidural anesthesia, hyperbaric and hypobaric spinal anesthesia, and most of the minor nerve blocks. Since then, many modifications of approach and technique, including the use of nerve stimulators and ultrasound for nerve localization, have been introduced, in order to improve patient safety and comfort. A new substance, lidocaine, was first developed in 1943 and marketed in 1947 under the name Xylocaine™. It was the first amino amide local anesthetic, and it carried a significantly reduced risk of allergic reactions. Other amide local anesthetics including nirvaquine, cinchocaine, mepivacaine, prilocaine, efocaine, bupivacaine, etidocaine, and articaine were ostensibly less toxic than cocaine, but they had differing amounts of central nervous system (CNS) and cardiovascular (CV) toxicity. Bupivacaine is of special interest because of its high potency, long duration of action, and history of clinical application. It was synthesized in 1957 and first marketed in 1965. However, increasing reports of CNS and CV toxicity, and especially the identification of special therapy-resistant cardiotoxicity, led to restriction of its use. The numerous experimental studies that followed to identify the cellular mechanism of this toxicity increased our understanding of the action of local anesthetics greatly.2 Thereafter, further impetus to the synthesis and clinical introduction of other amide-type local anesthetics came from the continuing development of regional anesthesia and pain medicine. The identification of optically active isomers of the mepivacaine family and technological advances led to the ability to selectively produce the pure S-(-) enantiomer of ropivacaine, whose toxicology was extensively studied before its introduction on the market in 1996. During extensive clinical use unwanted side effects have been limited.2 Ropivacaine is structurally related to bupivacaine and mepivacaine. However, it possesses a different pharmacodynamic profile, specifically on cardiac electrophysiology (less arrhythmogenic than bupivacaine). Studies on the anesthetic activities and toxicity of the individual enantiomers of bupivacaine and mepivacaine generally indicate that the S-enantiomers are less toxic than the R-enantiomers.4 Today, lidocaine, prilocaine, mepivacaine, bupivacaine, ropivacaine, and levobupivacaine are the local anesthetic drugs used most often, in many cases mixed with opiates or other adjuvant drugs. In recent decades, continuous regional anesthesia using catheters and automatic pumps has evolved. The search for the most effective and least

Interpleural Intercostal Epidural Plexus blockade Subcutaneous

Time

Fig. 12.1 Plasma levels, and therefore the likelihood of systemic toxicity, depend on the location of injection. It should also be noted that significant individual variations are observed both in the pharmacokinetics and the pharmacodynamics, including the ‘toxic plasma level’.

Section 4: Practical Pharmacology

Table 12.1: Pharmacokinetic and -dynamic properties of several amide- and ester-type local anesthetics

pKa 9.0 8.9

2-chloroprocaine

8.6 8.5

Tetracaine Locaine, Benzicaine

8.1

Bupivacaine

VD (L/kg)

CL (L/kg/h)

T½ (h)

Relative potencya

1.3

0.85

1.6

1

Prilocaine

2.73

2.03

1.6

1

Mepivacaine

1.2

0.67

1.9

1

8.09

Chirocaine, levobupivacaine

Etidocaine

1.9

1.05

2.6

2

8.07

Ropivacaine

Ropivacaine

0.84

0.63

1.9

4

7.9

Prilocaine

Bupivacaine

1.02

0.41

3.5

4(5)

7.7 7.6

Elidocaine, Lidocaine Mepivacaine

Chloroprocaine

0.5

2.96

0.11

0.5

7.4

Normal arterial pH

Procaine

0.93

5.62

0.14

b

Tetracaine

b

b

b

b

Amides Lidocaine

Esters

Fig. 12.3 Commonly used local anesthetics and their pKa values.

7.0

a

Measured after epidural administration. Data not available. VD, volume of distribution at steady state; CL, total plasma clearance; T½, terminal half-life time. b

B + H+ → BH+ The pH determines the ratio of B and BH+: pH = pKa + ln [B]/[BH+] By definition, the pKa is the pH at which 50% of the local anesthetic is uncharged ([B]=[ BH+]). As shown in Figure 12.3, the pKa range for commonly used local anesthetics lies in a narrow band. For amide local anesthetics, the pKa generally correlates with the speed of onset. In general, it is thought that the closer the pKa is to the pH in the tissue surrounding the nerve, the faster the onset, as there are more local anesthetic molecules available in the neutral (uncharged) form. The neutral form is largely responsible for traversing the membrane. However, lipid solubility also plays an important factor. Unlocked open channel

B

Na+

Cytoplasm

+ HI

Modulation of pH by carbonation The addition of bicarbonate has also been used to increase the pH of local anesthetic solutions, thus increasing the concentration of nonionized lipophilic free base. This will theoretically increase the rate of diffusion of the drug and its speed of onset. Figure 12.4 illustrates this concept using lidocaine. Clinically, the addition of 1 mEq of sodium bicarbonate to each 10 mL of commercially prepared 1.5% lidocaine solution produces a significantly faster onset of anesthesia and more rapid spread of sensory block.5 Most local anesthetics are bases that are poorly soluble in water, but that can be dissolved in hydrophobic organic solvents. Therefore, most local anesthetics are marketed in the form of hydrochloride salts. Table 12.2 lists several common local anesthetics with their pKa values and their usual pH in storage.

Percent in lipophilic form (B) 95%

When pH = pKa + log B/BH+ pH = 7.7 – log 95/5 = 10.64

75%

pH = 7.7 – log 3/1 = 8.17

50%

pH = 7.7 + log 1/1 = 7.7

25%

pH = 7.7 – log 1/3 = 6.60

5%

pH = 7.7 + log 5/95 = 4.76

BHI

B

BH+

B

+ HI

BH+

Phosphobilipid chains

Fig. 12.2 Local anesthetics are weak bases that preferentially travel into the cell in their uncharged, lipid-soluble form. Once inside, they enter the pore of the channel in the pharmacologically active protonated form.

Fig. 12.4 The pH of a solution containing local anesthetics (e.g., lidocaine) can be manipulated by adding bicarbonate. This changes the proportion of uncharged, lipid-soluble drug and can have a pronounced effect on the speed of onset of the block.

139

Part 1: General Principles

Table 12.2: pKa and pH of commonly used local anesthetics Drug

pKa

pH of solution in vial

2-chloroprocaine

9.1

2.5–4

Procaine

8.9

5.5–6

Tetracaine

8.4

4.5–6.5

Cocaine

8.5

variable

Lidocaine

7.9

5.6 (without epi)

Electrode for voltage clamping and current passing Glass pipette

3.5–5.5 (with epi) Levobupivacaine

8.1

Bupivacaine

8.1

Local anesthetic molecules in solution

4.0–6.5 (without epi) 4.5–5.5 (without epi) 3.5–5.5 (with epi)

Mepivacaine

7.7

5.5

epi, epinephrine.

Molecular mechanism of sodium channel blockade Although LAs may also interfere with other channels, their interaction with sodium channels is clinically most relevant. The generation and propagation of impulses in nerve axons to carry afferent (sensory) and efferent (motor, sympathetic) information requires the flow of specific ionic currents through channels in the plasma membrane. These channels open and close depending on the electrical potential of the cell membrane. The major determinant of the depolarization of nerve fibers is the specific influx of Na+ ions through sodium channels located in nerve axons. Local anesthetic agents reversibly bind to and block sodium channels, thereby preventing the initiation or propagation of the electrical impulses required for nerve conduction. It now appears that although the uncharged form of a local anesthetic is more likely to cross into the cell membrane as mentioned above, either form may bind to the Na+ channel. The local anesthetic blocks the channel by binding to the receptor from inside the cell. A well-established technique in electrophysiology, the patchclamp technique (Figure 12.5, illustrating the ‘whole-cell’ mode of this technique), was instrumental in explaining the basic molecular mechanism of Na+ channel blockade caused by LAs. Most LA enter the channel from cell cytoplasm when the channel has been activated to the ‘open’ state. Upon blocking the flow of sodium ions, the channel enters the ‘inactivated’ state. LA bind tightly to and stabilize the inactivated state.

Use-dependent block (additional block when stimulating at a high frequency) Local anesthetics such as lidocaine and bupivacaine exhibit a phenomenon called use dependency.6,7 This means that if a neuronal cell is stimulated at a low frequency of 0.03 Hz (e.g., once every 30 sec) at a given concentration, a certain amount of inhibition of Na+ current will ensue and establish a steady state block. This block is called a tonic block and is thought to be equivalent to the regional/local block performed in the operating room when there is no high-frequency stimulation by pain fibers (before surgery). If, however, under the same conditions (same concentration of drug) the frequency is increased (e.g., 5 Hz, or once every 200 msec), an additional block will occur, and a new steady state will result. This interesting feature is called use-dependent block. It is seen with all local anesthetics, and is particularly prominent with amitriptyline, which also has local anesthetic properties, and has been commonly used orally for neuropathic pain. 140

Whole-cell mode Fig. 12.5 Whole-cell patch-clamp technique. With this method, the tip of the patch electrode (glass pipette) is brought into contact with the cell surface. The cell membrane is then ruptured by applying brief suction. This allows free exchange between the solution inside the glass pipette and the cytoplasm. The electrode that is inside the glass pipette is connected to the patch clamp device, which measures the current flow through the cell membrane during depolarization.

However, due to a very narrow therapeutic ratio, amitriptyline has no clinical use as a local anesthetic. It is thought that bupivacaine and amitriptyline have a higher affinity to the LA binding site than, for example, lidocaine, and therefore at higher stimulation frequencies there is not enough time for the drug to dissociate from the binding site and leave the channel.8 The concept of use-dependent block is illustrated in Figure 12.6, depicting amitriptyline versus bupivacaine, as the former also has significant local anesthetic properties.

Clinical relevance of use-dependent block With the currently available, and also some of the experimental local anesthetics, relatively little tonic block can be found at low concentrations.9 This suggests that discharge at a high rate from stimulated sensory/ pain fibers could be blocked, while leaving other nerve fibers (motor) undisturbed. Therefore, this property may make it possible to selectively block the ‘firing’ of high-frequency action potentials produced by pain fibers while leaving the ‘normal’ action potential transmission intact. For the same reason, drugs inducing a high degree of use-dependent block, when given at higher concentrations, should prolong the duration of a complete block. In other words, a drug with a high degree of use-dependent blockade could give a differential block, i.e. a selective block of specific (pain-transmitting) nerve fiber groups10 at lower concentrations, and a prolonged complete block at higher concentrations (similar to bupivacaine, but to a much greater extent). Preclinical in vivo11 and clinical studies12 appear to confirm the role of use-dependent block in anesthesia/analgesia.

EFFECTS OF LOCAL ANESTHETICS OTHER THAN NA+ CHANNEL BLOCKADE Local anesthetics also have been shown to inhibit K+ channels, Ca2+channels, nicotinic acetylcholine-activated conductance, the

Section 4: Practical Pharmacology Fig. 12.6 Use-dependent block of bupivacaine versus amitriptyline. Initially, a steady-state tonic block is achieved with amitriptyline and bupivacaine at a concentration of 3 μM; this inhibition of Na+ current is considered to be the baseline. With stimulation at a frequency of 5 Hz, an additional ≈10% Na+ current block is achieved with bupivacaine, compared to ≈ 40% with amitriptyline.

Baseline block at low frequency stimulation – so-called ‘tonic block’ New baseline after highfrequency stimulation (with the same concentration of drug)

Bupivacaine 3 μM

Amitriptyline 3 μM

substance P receptor, and even the G protein modulation of certain channels. These alternative actions may contribute to local anesthesia and to some aspects of toxicity.

Inhibition of current flow through other ion channels Voltage-gated and voltage-independent K+ channels were found to be blocked by relatively low concentrations of local anesthetics. The respective affinity varies among the different subtypes. Similarly, Ca2+channels are also blocked by local anesthetics. The exact role and contribution to the desired effect and upon the potential side effects of local anesthetics is not known.

Inhibition of signaling through G proteincoupled receptors Local anesthetics have may have significant effects in several settings other than local and regional anesthesia or antiarrhythmia. Some of these effects occur at concentrations that are much lower than those required for Na+ channel blockade. For example, the half-maximal inhibitory concentration (IC50) of lidocaine at the neuronal Na+ channel is approximately 50–100 mM (depending on the specific channel subtype and study preparation), whereas the compound inhibits signaling through M1 muscarinic receptors (expressed recombinantly in Xenopus laevis oocytes) with an IC50 of 20 nM, that is, 1000- to 5000- fold lower. This greatly increased sensitivity of other targets implies that at relatively low LA concentrations (such as attained in blood during epidural anesthesia or analgesia or during intravenous LA infusion) other significant pharmacologic effects may be present.13

Interactions of LAs with neutrophil signaling Polymorphonucleocytes (PMNs) do not express Na+channels, and LA effects on these cells therefore are not caused by Na+channel blockade. LA effects on these cells are also not affected by experimental Na+ channel blockers such as tetrodotoxin or veratridine. Overactive inflammatory responses that destroy rather than protect are critical in the development of a number of perioperative disease states, such as postoperative pain, adult respiratory distress syndrome (ARDS), systemic inflammatory response syndrome, and multiorgan failure. Perioperative modulation of such responses is therefore relevant to the practice of anesthesiology and interventional spine medicine, and LAs may play significant roles in this regard.13 Leukotriene B4, formed in inflammatory cells such as PMNs and monocytes, is a potent stimulator of PMN activity and therefore has an important role in inflammation.14 It induces margination at endothelial cells, degranulation, diapedesis, and superoxide generation and acts synergistically with prostaglandin E2 to enhance vascular permeability. Therefore, renewed interest has been created following the discovery that LAs block leukotriene release.15

Similarly, interleukin (IL)-1α is another inflammatory mediator, which acts on its receptor on PMNs, stimulating phagocytosis, respiratory burst, chemotaxis, and degranulation. Lidocaine and bupivacaine dose-dependently inhibit IL-1α release in lipopolysaccharide-stimulated human peripheral blood mononuclear cells.15

Effects of local anesthetics on polymorphonucleocyte adhesion Excessive adhesion of PMNs to endothelium may induce endothelial injury, which is mediated by several adhesion molecules. One of the most important for firm adhesion of PMN to endothelium and subsequent transmigration (diapedesis) is CD11b–CD18, a member of the integrin family. This receptor is expressed constitutively on the surface of nonactivated PMN, but expression increases markedly after inflammatory stimulation. Binding of activated PMN to endothelial cells by CD11b–CD18 increases intracellular peroxide levels in the endothelial cells, in which reactive oxygen species can have detrimental effects. Monoclonal antibodies against CD11b–CD18 protect in vitro against endothelial cell injury. In vitro studies have shown a reduction of TNFα-induced upregulation of CD11b–CD18 surface expression on PMN after ropivacaine or lidocaine treatment. This may contribute to the beneficial in vivo effects of ropivacaine on ulcerative colitis at tissue concentrations (100–300 mM) obtained after rectal LA administration.13

Effects of local anesthetics on PMN priming The priming process can be described as a potentiated response of PMNs after previous exposure to priming agents, such as TNF-α, platelet-activating factor, IL-8, lipopolysaccharide, or granulocytemacrophage colony stimulating factor. Priming is a key regulatory mechanism of PMN function and seems to play a pivotal role in the ‘overstimulation’ of inflammatory pathways, which then induces tissue damage rather than protection of the host. It is possible that inhibition of priming contributes to the antiinflammatory actions of LAs, and in particular suppresses the deleterious effects of the uncontrolled, overactive response of inflammatory cells to a stimulating agent. This might explain how LAs can decrease tissue damage without significantly inhibiting PMN functions required for host defense. In summary, LAs do not scavenge the reactive oxygen species generated, but rather inhibit the ability of PMNs to produce them.13

SUMMARY OF LOCAL ANESTHETIC AGENTS General considerations Clinically used local anesthetics may be classified as amino esters (procaine, chloroprocaine, tetracaine, and cocaine) or amino amides 141

Part 1: General Principles O CO OH + HO

CH2

C

O

CH2

Onsetb

Maximum dose for plain solution

Maximum dose with epinephrinec

Lidocaine

Rapid

5 mg/kg

7 mg/kg

Mepivacaine

Rapid

5 mg/kg

7 mg/kg

Chloroprocaine

Rapid

10 mg/kg

15 mg/kg

Prilocaine

Rapid

7 mg/kg

8 mg/kgd

Ropivacaine

Slow

3 mg/kg

3 mg/kg

Bupivacaine

Slow

2.0 mg/kg

2.5 mg/kg

Levobupivacaine

Slow

2.5 mg/kg

3 mg/kg

Procaine

Slow

8 mg/kg

10 mg/kg

Tetracaine

Slow

1.5 mg/kg

2.0 mg/kg

Drug

Ester linkage

Aromatic acid + amino alcohol

Table 12.3: Maximum recommended doses of local anestheticsa

O NH H + HO OC

CH2

NH

Aromatic amine + amino acid

C

CH2

Amide linkage

Fig. 12.7 Biochemical synthesis of ester and amide bonds.

(lidocaine, mepivacaine, prilocaine, bupivacaine, ropivacaine, levobupivacaine) as shown in Table 12.1 (Fig. 12.7). Ester and amide local anesthetics differ in their chemical stability, metabolism, and allergic potential. Amides are extremely stable, whereas esters are relatively unstable in solution. Esters are hydrolyzed in plasma by the cholinesterase enzymes, whereas the amide compounds undergo enzymatic degradation in the liver. Cocaine is an exception to this as it is metabolized predominantly by the liver. The metabolites of esters include p-aminobenzoic acid (PABA), which can rarely induce allergic-type reactions. Allergies to amides are extremely rare. Tables 12.3–12.8 list usual doses of local anesthetics based on the type of block. A brief synopsis of commonly used local anesthetics follows below.

Amide-type local anesthetics Lidocaine This agent was the first amino amide type widely used, and is available for infiltration, as well as peripheral, plexus, spinal, and epidural blocks. Its use in spinals has declined due to concerns about possible

d

a

The maximal recommended dose of local anesthetics is influenced by various factors (see text) and should be adjusted for each injection site. b Onset times vary significantly with the injection site. For example, all of the commonly used local anesthetics have fast onset when used for infiltration anesthesia, but most of them are very slow topical anesthetics. c Caution: Maximal adult recommended dose of epinephrine –250 mcg per dose; for children –3 mcg/kg per dose. d Maximal recommended adult dose of prilocaine is 600 mg, due to clinically significant methemoglobinemia.

neurotoxicity and transient neurological symptoms (TNS). Lidocaine causes vasodilation at most concentrations. Thus, addition of epinephrine can reduce the absorption of lidocaine by nearby vasculature significantly, prolonging the duration of action by approximately 50%. It can be applied topically as an ointment or jelly, or nebulized as an aerosol to anesthetize the upper airway. Intravenous injection

Table 12.4: Tissue infiltration Drug

Volume for 70 kg person (mL)

Usual duration (min)

Chloroprocaine 1–2% plain

70–35

15–30

Chloroprocaine 1–2% with epinephrine (1:200 000–1:400 000)

105–53

30–60

Prilocaine 0.5–1% plain

100–50

30–90

Prilocaine 0.5–1% with epinephrinea (1:200 000–1:400 000)

112–56

60–120

Lidocaine 0.5–1% plain

70–35

30–60

Lidocaine 0.5–1% with epinephrinea (1:200 000–1:400 000)

100–50

60–120

Mepivacaine 0.5–1% plain

70–35

45–90

Mepivacaine 0.5–1% with epinephrine (1:200 000–1:400 000)

100–50

60–120

Bupivacaine 0.25–0.5% plain

56–28

120–180

Bupivacaine 0.25–0.5% with epinephrine (1:200 000–1:400 000)

70–35

150–240

Levobupivacaine 0.25–0.5%

70–35

120–180

Levobupivacaine 0.25–0.5% with epinephrine (1:200 000–1:400 000)

84–42

150–240

Ropivacaine 0.2–0.5%

105–42

90–150

a

a

a

a

Note: do not exceed maximum dosage listed in Table 12.3. a Caution: Maximal adult recommended dose of epinephrine –250 mcg per dose; for children –3 mcg/kg per dose.

142

Section 4: Practical Pharmacology

Table 12.5A: Minor nerve blocks (single nerve such as ulnar or radial, blocks below the knee) Drug

Volume (mL)

Lidocaine 1–2% plain

5–10

60–120

Lidocaine 1–2% with epinephrine (1:200 000–1:400 000)

5–10

120–180

Chloroprocaine 2–3% plain

5–10

15–30

Chloroprocaine 2–3% with epinephrinea (1:200 000–1:400 000)

5–10

30–60

Prilocaine 1–2% plain

5–10

60–120

Prilocaine 1–2% with epinephrinea (1:200 000–1:400 000)

5–10

120–180

Mepivacaine 1–1.5% plain

5–10

60–120

Mepivacaine 1–1.5% with epinephrine (1:200 000–1:400 000)

5–10

120–360

Bupivacaine 0.25–0.5% plain

5–10

180–480

Bupivacaine 0.25–0.5% with epinephrine (1:200 000–1:400 000)

5–10

240–960

Levobupivacaine 0.25–0.5% plain

5–10

180–480

Levobupivacaine 0.25–0.5% with epinephrinea (1:200 000–1:400 000)

5–10

240–960

Ropivacaine 0.2–0.5%

5–10

120–480

a

a

a

Usual duration (min)

Note: most minor nerve blocks are performed without the addition of epinephrine. Epinephrine is contraindicated in blocks of the digits or penis because tissue ischemia may result. Also, do not exceed maximum dosage listed when blocking several nerves. a Caution: Maximal adult recommended dose of epinephrine – 250 mcg per dose; for children – 3 mcg/kg per dose.

Table 12.5B: Major nerve blocks (several nerves or a plexus) Drug

Volume (mL)

Usual duration (min)

Lidocaine 1–2% plain

50–30

60–180

Lidocaine 1–2% with epinephrinea (1:200 000–1:400 000)

50–30

120–240

Prilocaine 1–2% plain

50–30

60–180

Prilocaine 1–2% with epinephrinea (1:200 000–1:400 000)

50–30

120–300

Mepivacaine 1–1.5% plain

50–30

60–180

Mepivacaine 1–1.5% with epinephrine (1:200 000–1:400 000)

50–30

180–300

Bupivacaine 0.25–0.5% plain

40–20

180–720

Bupivacaine 0.25–0.5% with epinephrine (1:200 000–1:400 000)

50–30

360–1440

Levobupivacaine 0.25–0.5% plain

50–30

Same numbers as for bupivacaine

Levobupivacaine 0.25–0.5% with epinephrinea (1:200 000–1:400 000)

50–30

Ropivacaine 0.5–0.75% plain or with epinephrinea (1:200 000–1:400 000)

50–30

a

a

360–720

Note: do not exceed maximum dosage listed in Table 12.3. a Caution: Maximal adult recommended dose of epinephrine – 250 mcg per dose; for children – 3 mcg/kg per dose.

of lidocaine results in systemic analgesia possibly not only due to an action in the CNS, but also by effecting peripheral nerves or cutaneous nerve endings. Experimentally, intravenous lidocaine profoundly suppresses injury-induced spinal nociception and secondary sensitization (‘windup’) of wide dynamic range neurons in the spinal cord’s dorsal horn. Clinically, lidocaine has been administered as an infusion to treat chronic neuropathic pain and can predict efficacy with oral sodium channel blocking drugs, such as mexiletine.16

Prilocaine With a similar clinical profile as lidocaine, prilocaine is used for infiltration, peripheral nerve blocks, spinal and epidural anesthesia. Since significantly less vasodilation is caused, addition of epinephrine is not necessary to prolong the duration of action; this may be an advantage when epinephrine is contraindicated. Prilocaine shows the least toxicity of the amide local anesthetics and is therefore useful for intravenous regional anesthesia.17 However, it causes methemoglobinemia, and has therefore been abandoned for obstetric use. 143

Part 1: General Principles

Table 12.6: Epidural anesthesia Drug

Volume (mL)

Usual duration (min)

Chloroprocaine 2–3% plain or with epinephrine (1:200 000)

30–15

30–60

Lidocaine 1–2% plain

25–15

45–60

Lidocaine 1–2% with epinephrine (1:200 000)

25–15

60–75

Prilocaine 1–3% plain

20–10

45–60

Prilocaine 1–3% with epinephrine (1:200 000)

20–10

60–180

Mepivacaine 1–2% plain

25–15

45–75

Mepivacaine 1–2% with epinephrine (1:200 000)

25–15

60–180

Bupivacaine 0.25–0.75% plain

20–10

90–240

Bupivacaine 0.25–0.75% with epinephrine (1:200 000)

25–10

120–300

Levobupivacaine 0.25–0.75% plain

25–10

Same numbers as for bupivacaine

Levobupivacaine 0.25–0.75% with epinephrine (1:200 000)

30–10

Ropivacaine 0.2–1.0% plain or with epinephrine (1:200 000)

20–10

90–300

Note: do not exceed the maximum recommended dose listed in Table 12.3. Administration in fractionated doses of 3–5 mL is recommended.

Table 12.7: Spinal anesthesia – commonly used agents/ dosesa Drug

Dose (mg)b

Usual durationc (min)

Procaine 5–10%

80–160

30–75

Lidocaine 1–2%

20–100

30–90

Mepivacaine 1.5–4%

20–80

30–90

Bupivacaine 0.5–0.75%

5–18

75–300

8–18

75–300

Levobupivacaine: same as bupivacaine Ropivacaine 0.5–1% a

While the injected volume of local anesthetic solution (with sufficiently high concentration) is critical in providing successful epidural, plexus, and peripheral nerve blockade, it is the actual local anesthetic dose (mg) that defines effective spinal anesthesia. b The choice of appropriate local anesthetic dose for spinal anesthesia is influenced by the desired block level (segmental spread) and duration. c Duration (and spread) is also dependent on baricity of spinally injected local anesthetic solution.

Mepivacaine The anesthetic profile of mepivacaine is similar to lidocaine. It is not as effective when applied topically. Although its toxicity appears to be close to that of lidocaine, the metabolism of mepivacaine is prolonged in the fetus and newborn; it is therefore not used for obstetric anesthesia. Vasodilation is mild, but significant prolongation of action can be attained by adding epinephrine.

Bupivacaine Bupivacaine provides prolonged and intense analgesia outlasting the motor block. In interventional pain management, 0.25% is the preferred concentration as it ensures more than adequate analgesia

144

with minor to moderate motor block. The 0.5% solution is used when profound muscle relaxation is needed, such as in joint manipulation. Other clinical uses include tissue infiltration with 0.25% concentration with the duration of action of 2–4 hours, or greater, useful in trigger point injections in myofascial pain. Epidural analgesia and anesthesia are performed (0.25–0.5% bupivacaine) with 2–5 hour duration of action. Peripheral nerve blocks are performed with concentrations of 0.25–0.50%, depending on the amount of motor block sought. The block may last for 12–24 hours. Intrathecal use provides approximately 2–3 hours of anesthesia and 4–6 hours of analgesia. For chronic intrathecal infusions it is combined with opioids and is given in doses of 3 mg or more over 24 hours. The dose is increased by 0.5–1 mg per week until pain relief is obtained. Epinephrine is often added as a marker for intravascular injection and to prolong the duration of action due to decreased vascular absorption. Considerable controversy surrounds the use of bupivacaine (see toxicity below). Early reports of sudden cardiac arrest with bupivacaine injection are associated with considerable morbidity and mortality. The high protein binding and lipid solubility of the agent may be the main cause. By consensus, the 0.75% concentration of bupivacaine is not used in obstetrics because of the associated mortality/ toxicity with this use. Currently, labor analgesia is usually provided using 0.125% bupivacaine combined with fentanyl 2 mcg/mL. It is clear that the toxicity associated with bupivacaine is in fact magnified by respiratory acidosis, hypoxia, and in the parturient, probably because of the associated effects of progesterone.

Levobupivacaine Levobupivacaine is the S-enantiomer of bupivacaine. In comparison to bupivacaine, the CNS and cardiovascular toxicity is considerably reduced. In sheep the convulsive dose was reduced by approximately 30%. In human volunteers the dose required to elicit early signs of toxicity was reduced by 15%. The clinical profile and potency of levobupivacaine appears to be similar to bupivacaine for epidural anesthesia. Levobupivacaine is particularly useful when large doses are required, e.g. for peripheral nerve blocks.

Section 4: Practical Pharmacology

Table 12.8: Miscellaneous blocks Block

Drug

Volume/dose

Epidural roots

Bupivacaine 0.25%

1–1.5 mL

Facet joint blockade

Bupivacaine 0.25%

2–2.5 mL

Intra-articular facet joint injection

Bupivacaine 0.25%

Less than 1 mL as the joint capacity is limited

Epidural lidocaine and steroid injection

Prednisolone and lidocaine

3 mL of lidocaine 0.5% with 3 mL of methylprednisolone (40 mg/mL)

Peripheral nerve, e.g. occipital nerve

Bupivacaine 0.25–0.5%

2–5 mL

Trigger point

Bupivacaine 0.25–0.5%

1–2 mL

Intravenous regional anesthesia

0.5% lidocaine

30–40 mL

Intravenous lidocaine infusion

5 mg/kg over 45 min

Intrathecal therapy

Lidocaine 2% without preservatives

Start 3 mg/day, increase by 20% per week till analgesia

Intra-articular facet joint injection

Bupivacaine 0.25% Bupivacaine 0.5–0.75%

0.5–1 mL

Medial branch blockade

Bupivacaine 0.25%

2–2.5 mL

The duration is dependent on patient factors and confounded by admixture of steroid; the analgesic phase lasts beyond the usual duration of action of the selected local anesthetic (approximately 2–8 hours).

Ropivacaine Concerns about the cardiotoxicity of bupivacaine led also to the development of ropivacaine. In humans, ropivacaine can be administered in larger doses than bupivacaine before early signs of toxicity develop.18 However, it is still not clear how to directly compare ropivacaine and bupivacaine, as their equipotential drug concentrations are still a matter of controversy. The clinical profile is similar to bupivacaine. Epidural application may allow for even greater sensory block without significant motor block.19 An intrinsic vasoconstricting effect may augment the duration of action.

Ester-type local anesthetics Procaine A low potency, slow onset, and short duration of action limit the use of procaine. Allergic reactions are possible due to the production of the metabolite PABA (Fig. 12.8). Procaine is used mainly for infiltration and differential spinal blocks in chronic pain patients.

Chloroprocaine Chloroprocaine has a rapid onset of action despite a high pKa. (In most local anesthetics a pKa close to physiologic pH is associated with a rapid onset.) Due to its extremely low toxicity relatively high concentrations are used. It also has an extremely short plasma halflife because it is metabolized by cholinesterase. Reports of CNS toxicity are extremely unusual. It is thought to be the least CNS and cardiovascular toxic of all agents in current use. Chloroprocaine is used commonly for epidural anesthesia. It is also used in peripheral blocks with short duration, as well as combined with other long-acting, slow-onset local anesthetics for the combined effect of rapid onset with prolonged duration. Examples of these agents are bupivacaine and tetracaine. In obstetrics, epidural chloroprocaine,

O H2N

C

C2H5 OCH2CH2

N

Procaine

C2H5

Hydrolysis C2H5 H2N

COOH

PABA

+

HOCH2CH2

N

C2H5 Diethylaminoethanol

Fig. 12.8 The metabolic pathway of procaine by hydrolysis, producing the allergenic metabolite p-aminobenzoic acid (PABA).

with or without bicarbonate, is used to rapidly attain surgical levels of anesthesia in preparation for cesarean section. Another advantage in obstetrics is that there is limited or no transmission of chloroprocaine to the fetus. Controversy exists regarding the use of chloroprocaine. It is related to reports of persistent, serious neurological deficits associated with accidental massive subarachnoid injection of chloroprocaine. This can also occur if an epidural catheter erodes through the dura and arachnoid membrane. Initially, the agent itself was felt to be implicated. Subsequent evaluation suggests that the preservative antioxidant, bisulfite, may, by itself, produce the phenomenon. However, after elimination of bisulfite, a number of reports of back pain have appeared. Factors implicated have been the EDTA preservative, use of large volumes of the agent, low pH of the solution, and irritation of the perispinous tissues by infiltrating with the numbing local anesthetic (in preparation for epidural placement). An increased incidence of back pain was demonstrated when volumes greater than 145

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40 mL were injected. Injecting 25 mL or less did not increase the incidence of back pain.20 Recently, a renewed interest has actually suggested that bisulfite may be neuroprotective in an animal model (see direct neuronal toxicity below).

Tetracaine Tetracaine has been used commonly for spinal anesthesia. In adults, it provides a relatively rapid onset (3–5 min), a profound depth of anesthesia, and a duration of 2–3 hours (4–6 h with epinephrine). Its duration is relatively unpredictable and could reach 8–10 hours of motor block, which renders this drug impractical. In children, the duration of action is significantly shorter when used spinally. Systemic toxicity is reported to be considerably higher than with procaine and chloroprocaine. Therefore, other forms of regional anesthesia that require larger volumes (nerve blocks, epidural anesthesia) are rarely performed with tetracaine. It is also used by ophthalmologists for topical anesthesia of the eye and has been found useful for topical anesthesia of the airway.

Cocaine This original local anesthetic is also the only local anesthetic that causes intense vasoconstriction. Thus, it is used as a topical anesthetic, e.g. when anesthetizing the nasal airway before intubation. Impaired neuronal reuptake of catecholamines can cause hypertension, tachycardia, arrhythmia, and other serious cardiac effects.

Benzocaine Benzocaine has a slow onset, short duration, and moderate toxicity. Clinical use is limited to topical anesthesia to anesthetize mucous membranes. Excessive use of benzocaine in pediatric cases is associated with methemoglobinemia.

Mixture of local anesthetic agents The rationale for mixtures of local anesthetics is the attempt to benefit from the quick onset of the short-lasting drug while maintaining the long duration of the long-acting drug. At present, there do not appear to be any clinically significant advantages to the use of mixtures of local anesthetic agents. For example, bupivacaine provides clinically acceptable onset of action as well as prolonged duration of anesthesia. In addition, the use of catheter techniques for many forms of regional anesthesia makes it possible to extend indefinitely the duration of action of rapidly acting agents such as chloroprocaine or lidocaine. Most importantly, one should be cautioned not to use maximum doses of two local anesthetics in combination in the mistaken belief that toxicities of these agents are independent; the toxicities should be presumed to be additive.21

TOPICAL LOCAL ANESTHETIC AGENTS EMLA EMLA cream is a eutectic mixture of the local anesthetics lidocaine and prilocaine, each at a concentration of 2.5%. It is a eutectic mixture because the mixture has a melting point below room temperature and therefore exists as a liquid oil, rather than a powder. EMLA should be applied to intact skin surfaces because application to locations where a breach of the skin has occurred may lead to unpredictable absorption. It provides dermal analgesia by the release of the lidocaine and prilocaine from the cream into the skin, which leads to blockade of pain transmission originating from the free nerve endings. The onset, qual146

ity, and particular duration of dermal analgesia is primarily dependent on the duration of skin application. Although there is considerable interpatient variation, the EMLA cream should be applied under an occlusive dressing for about 1 hour to provide adequate analgesia for insertion of an intravenous catheter. The maximum recommended duration of exposure is 4 hours, although exposures of up to 24 hours did not lead to toxic levels of local anesthetics. For i.v. catheter placement or blood draws, roughly 2.5 grams of the cream should be applied over a 25 cm2 area of skin about 1 hour before the procedure. Caution must be taken in children or very small adults as plasma levels of lidocaine and prilocaine are dependent on patient size and the rate of systemic drug elimination. Large treatment area, long duration of application, and impaired elimination may result in high blood values. Plasma concentrations to be expected are reported in Figure 12.1. The above data were obtained from a study of 18 healthy volunteers. The dressing and cream were removed after 3 hours and after 24 hours, respectively. Sixty grams of EMLA cream was applied to the lateral thigh (n=8 per group). The peak levels of lidocaine after 10 hours were about 5% of toxic levels, whereas the peak levels of prilocaine were about 2.5% of toxic levels.

Lidoderm 5% patch The Lidoderm patch was approved by the FDA in 1999 for the treatment of pain associated with postherpetic neuralgia, a chronic neuropathic pain condition. The Lidoderm patch is a topical delivery system intended to deliver low doses of lidocaine to superficial damaged or dysfunctional nociceptors in an amount sufficient to produce analgesia but not sensory block. This can be an advantage in patients who may already have sensory loss as a result of their underlying neuropathy. Its recommended dosing is an application of up to 3 patches to intact painful skin areas for 12 hours per day. Pharmacokinetic studies have demonstrated that clinically insignificant levels are achieved with this formulation. They are 1⁄10 of those required to produce cardiac activity and 1⁄32 of those required to produce toxicity.22,23 Patients often report relief even during the 12 hours per day without the patch. Practitioners have also administered the patch continuously for 24 hours/day with sustained pain relief for up to 8 weeks.

LOCAL ANESTHETIC TOXICITY In general, the toxicity is dependent on the plasma level, which is influenced by dose and mode of application as shown in Figure 12.1.

Cardiovascular toxicity Recent studies show that the incidence of cardiovascular collapse from local anesthetic injection is very low (1:40 000 in epidural blocks,24 and zero in 25 000 in brachial blocks/caudal/lumbar epidural blocks25). In animal experiments (rats and dogs), the rank order for cardiac toxicity is bupivacaine > levobupivacaine > ropivacaine > lidocaine.26 Several mechanisms may be involved.

Myocardial contractility Local anesthetics produce a dose-dependent decrease in myocardial contractile force. Recent investigations have shown that receptors other than voltage-gated Na+ channels may be significant. Local anesthetic blockade of cardiac Ca2+ channels causes decreased inward Ca2+ influx, a shortened action potential, and therefore weakened contraction of the myocardium.27 Potent effects on the potassium channel

Section 4: Practical Pharmacology

may contribute as well. Disruption of cellular energy metabolism can occur. Especially, the inhibition of cyclic adenosine monophosphate (cAMP) production (most potently by bupivacaine) may contribute to the negative inotropy and interfere with resuscitation with epinephrine.28 Bupivacaine depresses contractility more than lidocaine at equipotent doses, as demonstrated by injecting the local anesthetic directly into the coronaries while avoiding other systemic effects such as vasomotor changes. This may be due to a fivefold greater potency of bupivacaine over lidocaine as a Ca2+ channel blocker.27

Vasomotor changes Both vasodilation and vasoconstriction may occur, depending on the dose.29,30 Toxic bupivacaine levels raised systemic vascular resistance in intact animals, perhaps due to elevated sympathetic tone produced by CNS stimulation. Vasodilation did not occur in these studies until serum concentrations were several orders of magnitude higher.31 Clinically, major overdoses of bupivacaine have resulted in cardiovascular collapse with systemic vasodilation and extreme hypotension, perhaps resulting from increasing hypoxia, hypercarbia, acidosis, and hyperkalemia rather than due to a direct vasomotor effect of bupivacaine.32,33

Altered electrophysiology Conduction alterations produce the most troublesome clinical complications. Cardiac impulse conduction is slowed because inward Na+ current is impaired. The resulting prolongation of the PR interval may lead to atrioventricular blockade. Widening of the QRS, unidirectional block, and reentry leads to ventricular tachycardia and fibrillation. Intracoronary doses necessary to produce these dysrhythmias are 16 times as great for lidocaine as for bupivacaine.34 The CNS may have an independent role in cardiac toxicity as demonstrated in animals where intracranial or intraventricular bupivacaine injections causes ventricular dysrhythmias, possibly due to sympathetic nervous system activation.35–37 Cardiovascular collapse after bupivacaine occurs at a dose only 3.7 times the dose that causes seizures. In contrast, the ratio for etidocaine and lidocaine is 4.4 and 7.1, respectively.38 Bupivacaine is twice as toxic as ropivacaine in animal studies.38 The S isomer of bupivacaine (levobupivacaine) has less arrhythmogenic potential.39 Automaticity is somewhat depressed by local anesthetics in most studies due to the inhibition of the slow diastolic depolarization of the pacemaker cells (Ca2+ block). Pacemaker rates are slowed more by bupivacaine than by lidocaine in isolated adult guinea pig hearts; this effect is amplified by hypoxia and acidosis and is greater in neonatal guinea pig hearts.40 Bupivacaine also displays unique features due its slow dissociation from the inactivated cardiac Na+ channel. Its rate of dissociation is 10 times slower than that of lidocaine (1.5 vs. 0.15 seconds). Thus, usedependent blockade occurs even in the nontachycardic heart because there is insufficient time for dissociation during diastole.

Treatment of cardiovascular toxicity Mortality from massive intravascular bupivacaine injection can be reduced by aggressive and repeated large doses of epinephrine.41 Surprisingly, in the setting of bupivacaine cardiotoxicity, epinephrine is less dysrhythmogenic than would be expected.42 Bretylium has also been used with epinephrine to reduce dysrhythmias. However, it is ineffective in the presence of hypoxia and hypercarbia.43 Lidocaine is ineffective and worsens dysrhythmias,44 isoproterenol counteracts the electrophysiologic effects of bupivacaine,45 and clonidine reverses EKG changes but worsens bradycardia and hypotension; yet, if com-

bined with administration with dobutamine, it has been used successfully in dogs. Hemodynamic resuscitation has been assisted with amrinone which augments intracellular Ca2+ levels.46 Magnesium sulfate suppresses dysrhythmias but does not counteract CNS effects.47 In comparison to bupivacaine and etidocaine, other local anesthetics are less likely to impair myocardial performance.48 In summary, no magic formula for circulatory resuscitation has been identified. Prolonged aggressive standard Advanced Cardiac Life Support measures should be taken, as bupivacaine will dissociate from cardiac Na+ channels slowly. No permanent injury results if circulation can be supported adequately during this time period. Cardiopulmonary bypass may be necessary to maintain adequate perfusion. Experimental studies in rats receiving intravenous bupivacaine suggest that resuscitation with a lipid infusion may be beneficial because bupivacaine is partitioned into the new lipid phase. Thirty percent Intralipid® (Baxter HealthCare) was infused as a bolus of 7.5 mL/kg over 30 seconds followed by an infusion at 3 mL/kg/min for 2 minutes. In the rats, the lethal dose of bupivacaine increased by 48% when resuscitated with Intralipid.49

Central nervous system toxicity Local anesthetics may produce CNS toxicity either through direct overdose, unintentional administration of drug into an epidural vein, or indirectly by inadvertent intrathecal injection of the dose.

Toxicity after inadvertent intravenous injection Central nervous system effects after systemic injection occur at lower blood levels than cardiovascular side effects (see above). Initially, net stimulation of the CNS results due to inhibition of inhibitory neurons in the cerebral cortex, thus allowing facilitatory neurons to discharge in an unopposed fashion.50 At higher blood levels, both inhibitory and facilitatory pathways are inhibited, leading to CNS depression. Symptoms may commence with feelings of lightheadedness, dizziness, sense of doom, disorientation, and drowsiness followed frequently by visual and auditory disturbances such as difficulty focusing and tinnitus. Objective signs include shivering, muscle twitching, and tremors initially involving muscles of the face and extremities. Ultimately, generalized tonic–clonic seizures occur followed by a state of generalized CNS depression. Seizure activity ceases and respiratory arrest may occur.

Treatment of inadvertent intravenous injection Symptomatic treatment of signs of CNS toxicity aims to prevent development of hypoxemia, hypercarbia, and acidosis. Occurrence of seizures may mandate tracheal intubation and administration of anticonvulsants such as sodium thiopental or midazolam. The use of neuromuscular blockade during persistent seizures is controversial. In rats with status epilepticus due to toxic lidocaine doses, neuromuscular blockade with succinylcholine prevents systemic acidosis but does not prevent cerebral lactic acidosis. The lidocaine uptake of the brain was actually higher in the paralyzed rats, presumably because the pH gradient between brain and blood affected the partitioning of the weak base lidocaine (pKa 7.86).51

Toxicity after inadvertent intrathecal injection When an epidural is performed and a higher-than-expected block develops after a short delay (several minutes), intrathecal placement of local anesthetic must be suspected. Symptoms depend on the spinal segments involved as the medication spreads cephalad through the cerebrospinal fluid (CSF). Hypotension with reflex tachycardia 147

Part 1: General Principles

results from blockade of the sympathetic nervous system and loss of vascular muscle tone. Local anesthetics spreading up to the thoracic level T1–T4 may block the sympathetic fibers innervating the heart and cause hypotension with bradycardia. Further spread up to the brainstem may cause reversible dilation of the pupils.

Treatment of inadvertent intrathecal injection As in any neuraxial block that reaches high levels, blood pressure and heart rate should be supported with intravenous fluid boli, ephedrine and phenylephrine. Atropine and potent catecholamines may also be required. If the block has been established, the Trendelenburg position can be used to maximize venous return. However, in the case of an overdose with a hyperbaric solution, care must be taken so that further cephalad spread of local anesthetic does not occur with the Trendelenburg position. Tracheal intubation and mechanical ventilation may be needed until the ability to maintain adequate spontaneous ventilation returns. In an recent case report, CSF lavage was employed to reverse a high spinal block.52

Prevention and recognition of inadvertent intravenous or intrathecal injection When administering local anesthetic with a catheter, an attempt to aspirate blood with the syringe should be performed first to detect an inadvertent intravenous placement. Then, a small test dose of local anesthetic which includes epinephrine (1:200 000) should be administered.38 If a sudden increase in heart rate (20 beats per minute) occurs within minutes after administering the test dose, an intravenous injection should be suspected and the catheter should be removed and not be used to administer the full dose. Development of a dense sensory and motor block within minutes after administration of the test dose may indicate an inadvertent intrathecal injection. The catheter should be removed. Alternatively, some practitioners used the spinal catheter at appropriate spinal dosages.

Direct neuronal toxicity Perioperative and/or regional anesthesia and/or local anestheticrelated nerve injuries have long been recognized as a complication of surgery and/or regional anesthesia. Fortunately, severe or disabling neurologic complications rarely occur. Factors contributing to neurologic deficit after regional anesthesia include neural ischemia (direct action of LAs,53 or related to the use of vasoconstrictors, or severe and prolonged hypotension), infection, and traumatic injury to the nerves during needle or catheter placement. In addition, postoperative neurologic injury due to pressure from improper patient positioning or from tightly applied casts or surgical dressings, as well as surgical trauma are often attributed to the regional anesthetic. Patient factors such as body habitus and preexisting neurologic dysfunction may also contribute. For example, the incidence of peroneal nerve palsy following total knee replacement is increased in patients with significant valgus or a preoperative neuropathy.54 However, the focus below is on the neural toxicity caused directly by the (widely unknown) direct actions of LAs.

Mechanism of toxicity High concentrations of local anesthetics are neurotoxic, but the mechanism for this neurotoxicity is unclear. An increased level of glutamate seems to be at least a contributing factor. For example, increased concentrations of glutamate in the CSF after intrathecal injections of high concentrations of tetracaine were found in animals. In the group receiving tetracaine 4%, the peak concentrations 148

of glutamate was 10-fold higher than baseline value, and no animal was able to hop, and vacuolation of the white matter and/or central chromatolysis of the motor neurons was observed.55 Mitochondrial uptake of Ca2+ has recently been found to play an important role in glutamate-induced neurotoxicity as well as in the activation of Ca2+-dependent molecules, such as calmodulin and neuronal nitric oxide synthase (nNOS), in the cytoplasm. Prolonged exposure to glutamate injures motor neurons predominantly through the activation of Ca2+/calmodulin–nNOS. An NMDA receptor antagonist eliminated the increase of mitochondrial Ca2+. These data indicate that acute excitotoxicity in spinal neurons is mediated by mitochondrial Ca2+ overload with subsequent accumulation of reactive oxygen species through the activation of NMDA receptors.56 However, other mechanisms might be contributory. A study exposing rat cerebellar granule cell cultures to neurotoxins that specifically enhances the open state probability of voltage-dependent Na+ channels, indicates that prolonged opening of Na+ channels induced neuronal death of cerebellar granule cells which is not mediated by glutamate, nor by voltage-sensitive calcium channel antagonists such as omega-Conotoxin-GVIA (N-type channels), omega-Agatoxin-IVA (P-type channels), nimodipine and nitrendipine (L-type channels) and reveals an additional neurotoxic mechanism in addition to the wellestablished excitatory amino acid receptor (glutamate) pathway.55

Transient neurologic symptoms (TNS) and cauda equina syndrome In the early 1990s, case reports about neurologic deficits after intrathecal LA (mostly lidocaine) application appeared. If complete recovery occurred, the term TNS was applied. More extensive lesions were summarized as cauda equina syndrome. Most cauda equina syndromes occurred after introduction of subarachnoidal microcatheters, most likely due to a pooling effect of higher concentrations of lidocaine. Although the controversy is far from over, there are several reasons to consider a reduction in the maximal dose of lidocaine for spinal anesthesia. The potency ratio of lidocaine to bupivacaine is roughly 1:4, yet the maximum doses recommended for spinal anesthesia are 100 mg and 20 mg, respectively. This discrepancy assumes even greater significance when one considers that lidocaine is inherently more toxic than bupivacaine. Further, virtually all of the reported cases of suspected neurotoxicity have been associated with administration of 75 mg or higher. Finally, 100 mg exceeds the dose of lidocaine needed for reliable spinal anesthesia. Although the data are inadequate to know the impact of reduction in dose on neurotoxic risk, a dosage not to exceed 60 mg and a concentration of 2.5% has been suggested.57 Vasoconstrictors might contribute to toxicity by promoting ischemia, decreasing anesthetic uptake, or by directly affecting neural elements. Recent data obtained in rats suggest that epinephrine potentiates injury induced by intrathecal lidocaine.58 These data, combined with the narrow therapeutic index for spinal lidocaine and the report of a clinical deficit following 100 mg with epinephrine, argue against using a vasoconstrictor with lidocaine for spinal anesthesia. Furthermore, the principal reason for using epinephrine is to provide longer-duration anesthesia, which can easily be achieved with bupivacaine without the addition of epinephrine. In addition to having a better therapeutic index than lidocaine (even without epinephrine’s potentiation of toxicity), bupivacaine is rarely associated with TNS. In summary, in animal models, intrathecal and peripheral nerve application of epinephrine can worsen nerve injury induced by local anesthetics. Nevertheless, the observations gleaned from clinical practice do not concur. Since the clinical relevance is unknown, a reduction

Section 4: Practical Pharmacology

of epinephrine or avoidance in selected patients is recommended.59 Similarly, the presence of glucose in rat models60 and humans61 does not appear to impact the incidence of TNS.

Sodium bisulfite The development of severe back pain and neurologic deficits after apparent intrathecal injection of 3% Nesacaine-CE, intended for epidural administration, created concern about the potential toxicity of chloroprocaine and the preservative sodium bisulfite. A study in rabbits investigated whether pure 2-chloroprocaine or sodium bisulfite, two components of Nesacaine-CE, caused these complications when injected separately into the lumbar subarachnoid space. Repeated 2–4-mg spinal anesthetic doses of pure 2-chloroprocaine in lactated Ringer’s solution did not produce chronic hindlimb paralysis even though accumulated doses reached 50 mg. However, 1.2–2.4 mg of sodium bisulfite, the antioxidant in Nesacaine-CE added to prolong shelf-life, resulted in irreversible hindlimb paralysis in 12 out of 14 animals. This amount of bisulfite was contained in 12–24 mg of 2% Nesacaine-CE. The demonstration that persistent paralysis resulted from low dosages of sodium bisulfite contained in commercially available 2-chloroprocaine led to a change of this antioxidant.62 Although bisulfite-free formulations of chloroprocaine were subsequently introduced into clinical practice, the relative toxicities of this anesthetic and preservative were recently questioned. In a recent study, rats implanted with intrathecal catheters were given one of two commercially available solutions of chloroprocaine, one of which contained sodium bisulfite; control animals received saline or sodium bisulfite alone.63 Animals were assessed for sensory impairment 7 days after administration using the tail-flick test and were killed to obtain histologic specimens to quantify nerve injury. Interestingly, nerve injury scores after administration of plain chloroprocaine were significantly greater than those of chloroprocaine containing bisulfite. Injury scores for animals receiving chloroprocaine with bisulfite were elevated compared with those for animals given saline. Nerve injury scores with chloroprocaine containing bisulfite were greater than with saline or bisulfite alone. Tail-flick latencies and nerve injury scores with bisulfite alone were similar to those with saline. It was concluded that clinical deficits associated with unintentional intrathecal injection of chloroprocaine likely resulted from a direct effect of the anesthetic, not the preservative. The data also suggest that bisulfite can reduce neurotoxic damage induced by intrathecal local anesthetic.63

Myotoxicity All local anesthetics produce skeletal muscle damage in clinical concentrations, with the most profound alterations resulting from bupivacaine. It has been suggested that such muscle injury may be caused by an increased intracellular level of Ca2+. In a mouse study investigating direct intracellular effects of bupivacaine on Ca2+ release from the sarcoplasmic reticulum on Ca2+ uptake into the SR, and on Ca2+ sensitivity of the contractile proteins, it was found that bupivacaine does not only induce Ca2+ release from the SR, but also inhibits Ca2+ uptake by the sarcoplasmic reticulum. This latter function is primarily regulated by sarcoplasmic reticulum Ca2+ adenosine triphosphatase activity. Bupivacaine also has a Ca2+-sensitizing effect on the contractile proteins. These mechanisms result in increased intracellular Ca2+ concentrations and may thus contribute to its pronounced skeletal muscle toxicity.64 Interestingly the tissue matrix and the essential neurovascular elements remain undamaged and structural regeneration is usually rapid and complete. Bupivacaine 0.25% is widely used for muscle trigger point injections and the reported incidence of clinical myotoxicity is low.

CURRENT DRUG DEVELOPMENT Single enantiomers (ropivacaine and levobupivacaine), rather than racemic mixtures have been introduced, based on the finding of some degree of stereoselectivity in cardiotoxicity and degrees of sensory versus motor blockade for these agents in preclinical and clinical studies. These agents produce a controversial improvement in either sensory selectivity or therapeutic indices (ratio of effective to toxic doses) compared to the racemic mixtures.65 The degree of improvement in sensory selectivity has appeared variable in previous studies, particular when comparison of an equipotent concentration was attempted. Clinicians have long sought an LA to selectively inhibit sensory nerve fibers. As LAs block smaller diameter nerve fibers only of the same type of nerve fiber at lower concentrations than that are required to block larger fibers, a true sensory anesthesia sufficient for surgery/ skin incision usually cannot be obtained without significant motor blockade.66 The ideal LA would provide a high level of use-dependent block and selectively block sensory neuron-specific Na+ channels. An ideal LA will preferentially block firing of high-frequency action potentials in sensory/pain fibers/nociceptors and leave the normal action potential transmission intact, and will have limited ability to cross the blood–brain barrier, therefore exerting no unwanted effect on the CNS. Also of major importance is that by sparing cardiac Na+ channels, the most feared complication of regional anesthesia, cardiac arrest, can be avoided.

Advantages of long-acting and pain-selective local anesthetics Local anesthetics are an integral component of intraoperative, postoperative, and interventional spine management. Unfortunately, all too often, the benefits of regional nerve blockade are diminished by unwanted side effects. For example, in obstetric anesthesia, nonselective blockade of motor fibers leads to decreased patient mobility and reduced/compromised participation during labor and delivery. In almost all types of neuraxial anesthesia, sympathetic blockade can cause a dangerous decrease in blood pressure. Also, as currently available local anesthetics have a similar affinity for cardiac and brain Na+ channels, systemic absorption or accidental intravascular injection can cause seizures, coma, and cardiovascular collapse. Thus, successful development of a pain-selective local anesthetic would not only improve their safety, but also extend their clinical utility beyond their current indications. As well, the ability to provide an extended duration of analgesia for several days following a single injection without the need of catheters, pumps, and infusion systems would be a great benefit in interventional spine care. Of note, there is some difficulty in defining precisely what ‘pain selective’ actually means. To some extent the term sensory-selective or nociceptor-selective may be used interchangeably. Similarly, the term ‘differential block’ is often used, which should more accurately be labeled a ‘selective block of specific nerve fiber groups.’ The ideal pain/nociceptor/sensory-selective local anesthetic would provide minimal motor blockade, minimal cardiac toxicity, and minimal sympathetic blockade. However, there is also an indication for short-acting local anesthetics that produce a sympathetic block. Currently, there are many efforts to increase the duration and pain selectivity of LAs. Innumerable new compounds have been synthesized, but only a few drugs have become clinically useful. Ropivacaine and levobupivacaine are relatively new long-acting local anesthetics with a variable degree of motor blockade. To date, most new compounds that produce ultra-long nerve block as a single agent (such 149

Part 1: General Principles

as tetraethylammonium derivatives and cyclizing compounds) have been found to be unsatisfactory.

ing the impact of up/downregulation of various Na+ channels will be critical in determining which sensory neuron-specific Na+ channels should be targeted.

Liposomes and microspheres Promising progress is being made with technology that combines local anesthetics with biological delivery systems such as liposomes.67 These interesting formulations in animal models have allowed up to 4 days of analgesia. Their use clinically will be a great advance, which could possibly occur in the near future. In an animal model (sheep), a single administration of bupivacaine-dexamethasone microspheres to the intercostal nerves produced an effective chest wall analgesia of several days’ duration. Commercial development has begun, but is currently stalled in phase II trials.65

Catheter techniques Recently, catheter techniques have been gaining popularity. The ability to provide safe, continuous peripheral nerve blockade to patients on an outpatient basis has been a major advance in ambulatory surgery over the past several years.68

Future drugs specific for sensory neuron-specific Na+ channels These voltage-gated ion channels are a main target for pain-selective local anesthetics. Sensory neuron-specific Na+ channels have been identified predominantly in DRG neurons, which function as key elements in the transmission of sensory stimuli to the CNS. Small myelinated Aδ fibers and unmyelinated C fibers, which transmit nociceptive sensation, are believed to arise from small DRG neurons, whereas large myelinated Aδ and Aβ fibers arise from large DRG neurons. Previous studies have revealed that small DRG neurons tend to express a Na+ current that is resistant to tetrodotoxin (TTX, a toxin produced by puffer fish), whereas large DRG neurons tend to express a Na+ current that is sensitive to tetrodotoxin. For example, it was shown that the TTX-resistant Na+ channel Nav1.8 / SNS/PN3 (Scn10a) has a specialized function in pain pathways.69 SNS-null mutant mice were bred so that they only expressed TTX-sensitive Na+ currents, suggesting that all slow TTX-resistant currents are encoded by the SNS gene. These null-mutant mice were healthy, fertile, and apparently normal, but behavioral studies demonstrated a markedly reduced response to noxious mechanical stimuli. SNS/PN3 appears to be predominantly located within the DRG neuron and has not been found in other types of peripheral tissue (e.g. heart) or in the CNS;70 the distribution of these channels in humans is similar. Each of the aforementioned channels was originally cloned from rat DRG, but SNS/PN3 (termed hPN3) and PN1 (termed hNE-Na) have also been cloned from humans.71 Since rSNS/PN3 and rPN1 have been implicated in nociceptive transmission and the amino acid sequence of the human clone is very close to the rat, these channels may prove to be a valuable testing target for therapeutic agents. Of course, this supposition requires that novel drug molecules are identified that selectively interact at these sites. Major advances have been made recently in the cloning of sensory neuron-specific Na+ channels. The results of ongoing research will provide information as to which of the above mentioned sensory-selective Na+ channels will have the most clinical significance. Therefore, heterologous expression of sensory neuron-specific Na+ channels in mammalian cells will serve as an excellent tool for testing the potency/selectivity of drugs developed for pain management. As this new area of research unfolds, the knowledge garnered regard-

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Adjuvants Many adjuvant drugs such as clonidine and epinephrine may prolong blockade or decrease the toxicity of LAs. Toxins are being investigated as well. Unlike traditional LAs, which bind to a variety of other channels, TTX and saxitoxin (STX) bind specifically to sodium channels. They exhibit this property even when used at concentrations several orders of magnitudes higher than necessary for conduction block. Severe systemic toxicity (diaphragmatic paralysis and severe hypotension due to vasodilation) at doses sufficient to produce reliable conduction blockade of peripheral nerves preclude these toxins from use as the sole agent for nerve conduction blockade. Recent investigations using combinations of these toxins with conventional local anesthetics and/or slow-release microspheres suggest that these combinations may greatly improve their therapeutic ratio, thereby enabling their use for long-acting local anesthesia/analgesia.72,73

Ketamine Ketamine interacts with sodium channels in a fashion similar to local anesthetics and shares a binding site with commonly used clinical local anesthetics.74 Currently, it is unclear if the combined usage of ketamine and an LA confers clinically relevant improvements in safety, duration, or sensory selectivity.

Butamben Butamben is a lipophilic local anesthetic of the ester class, produces a differential nerve block of long duration, and has been used to provide prolonged analgesia for patients with terminal malignancy. Its mechanism of action is unclear. Like most LAs, butamben blocks sodium as well as potassium channels, and also appears to act as a neurolytic agent in higher concentrations. It is formulated as a 5–10% suspension and results in prolonged analgesia without significant motor blockade. When the effect of butamben on sciatic nerve block was evaluated on antinociception using the rat paw formalin test, butamben injection decreased the formalin-induced flinches up to 28 days. Histologic changes were minimal. This study demonstrated that a prolonged antinociceptive effect from butamben nerve block to formalin-induced nociception is possible without an effect on gross motor function or histologic morphology (including electron microscopic examination).75

TACHYPHYLAXIS Repeated administration can sometimes fail due to rapidly developing tolerance (tachyphylaxis). It is believed that the pharmacodynamic mechanism is more important. However, the pharmacokinetic mechanism may also play a significant role. Tachyphylaxis occurs more commonly in the setting of hyperalgesia and unrelieved pain. Coadministration of systemic or neuraxial opioids with local anesthetics in epidural infusions may slow the development of tachyphylaxis.65

CONCLUSION Local anesthetics were among the first drugs used for effective pain relief. Their application spread rapidly to all surgical specialties. The ability to provide surgical anesthesia without rendering the patient unconscious has led to widespread acceptance among patients as well.

Section 4: Practical Pharmacology

The success of local anesthesia depends on the precise delivery to the appropriate segment of the nervous system via epidural or spinal injection, tissue infiltration, or deposition of local anesthetic in tissue planes close to peripheral nerves. Imprecise administration can increase the risk of absorption into the intravascular system, resulting in serious cardiovascular or nervous system complications. The choice of local anesthetic involves a balance between the desired qualities (duration, intensity of the block) and the risk of adverse effects. In some applications such as intrathecal injection, the dose of local anesthetic is so small that adverse systemic reactions are unlikely regardless of the local anesthetic chosen. The block of a peripheral nerve, however, may require a much larger volume and dose. This carries a significant risk if inadvertent intravascular uptake results. Further development of less toxic local anesthetics is ongoing and will certainly increase the spectrum of applications. In addition, the antiinflammatory properties of local anesthetics most likely will extend future indications beyond their traditional role in regional anesthesia and pain medicine.

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22. Gammaitoni AR, Alvarez NA, Galer BS. Pharmacokinetics and safety of continuously applied lidocaine patches 5%. Am J Health Syst Pharm 2002; 59:2215–2220. 23. Gammaitoni AR, Davis MW. Pharmacokinetics and tolerability of lidocaine patch 5% with extended dosing. Ann Pharmacother 2002; 36:236–240. 24. Tanaka K, Watanabe R, Harada T, et al. Extensive application of epidural anesthesia and analgesia in a university hospital: incidence of complications related to technique. Reg Anesth 1993; 18:34–38. 25. Brown DL, Ransom DM, Hall JA, et al. Regional anesthesia and local anestheticinduced systemic toxicity: seizure frequency and accompanying cardiovascular changes. Anesth Analg 1995; 81:321–328. 26. Groban L, Deal DD, Vernon JC, et al. Cardiac resuscitation after incremental overdosage with lidocaine, bupivacaine, levobupivacaine, and ropivacaine in anesthetized dogs. Anesth Analg 2001; 92:37–43. 27. Coyle DE, Sperelakis N. Bupivacaine and lidocaine blockade of calcium-mediated slow action potentials in guinea pig ventricular muscle. J Pharmacol Exp Ther 1987; 242:1001–1005. 28. Butterworth JF, Brownlow RC, Leith JP, et al. Bupivacaine inhibits cyclic-3′,5′adenosine monophosphate production. A possible contributing factor to cardiovascular toxicity. Anesthesiology 1993; 79:88–95. 29. Stadnicka A, Stekiel TA, Hogan QH, et al. Hypoxic contraction of isolated rabbit mesenteric veins. Contribution of endothelium and attenuation by volatile anesthetics. Anesthesiology 1995; 82:550–558. 30. Johns RA, Difazio CA, Longnecker DE. Lidocaine constricts or dilates rat arterioles in a dose-dependent manner. Anesthesiology 1985; 62:141–144. 31. Johns RA, Seyde WC, Difazio CA, et al. Dose-dependent effects of bupivacaine on rat muscle arterioles. Anesthesiology 1986; 65:186–191. 32. Avery P, Redon D, Schaenzer G, et al. The influence of serum potassium on the cerebral and cardiac toxicity of bupivacaine and lidocaine. Anesthesiology 1984; 61:134–138.

5. Difazio CA, Carron H, Grosslight KR, et al. Comparison of pH-adjusted lidocaine solutions for epidural anesthesia. Anesth Analg 1986; 65:760–764.

33. Sage DJ, Feldman HS, Arthur GR, et al. Influence of lidocaine and bupivacaine on isolated guinea pig atria in the presence of acidosis and hypoxia. Anesth Analg 1984; 63:1–7.

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34. Nath S, Haggmark S, Johansson G, et al. Differential depressant and electrophysiologic cardiotoxicity of local anesthetics: an experimental study with special reference to lidocaine and bupivacaine. Anesth Analg 1986; 65:1263–1270.

7. Strichartz GR. The inhibition of sodium currents in myelinated nerve by quaternary derivatives of lidocaine. J Gen Physiol 1973; 62:37–57.

35. Thomas RD, Behbehani MM, Coyle DE, et al. Cardiovascular toxicity of local anesthetics: an alternative hypothesis. Anesth Analg 1986; 65:444–450.

8. Courtney KR, Strichartz GR. Structural elements which determine local anesthetic activity. Handb Exp Pharmacol 1987:53–94.

36. Heavner JE. Cardiac dysrhythmias induced by infusion of local anesthetics into the lateral cerebral ventricle of cats. Anesth Analg 1986; 65:133–138.

9. Gerner P, Haderer AE, Mujtaba M, et al. Assessment of differential blockade by amitriptyline and its N-methyl derivative in different species by different routes. Anesthesiology 2003; 98:1484–1490.

37. Bernards CM, Artu AA. Hexamethonium and midazolam terminate dysrhythmias and hypertension caused by intracerebroventricular bupivacaine in rabbits. Anesthesiology 1991; 74:89–963.

10. Raymond SA, Gissen AJ. Mechanism of differential nerve block, local anesthetics. In: Strichartz GR, ed. Local Anesthetics. Berlin, Heidelberg: Springer-Verlag; 1987: 95–164. 11. Gokin AP, Philip B, Strichartz GR. Preferential block of small myelinated sensory and motor fibers by lidocaine: in vivo electrophysiology in the rat sciatic nerve. Anesthesiology 2001; 95:1441–1454. 12. Stevens MF, Klement W, Lipfert P. [Conduction block in man is stimulation frequency dependent]. Anaesthesist 1996; 45:533–537. 13. Hollmann MW, Durieux ME. Local anesthetics and the inflammatory response: a new therapeutic indication? Anesthesiology 2000; 93:858–875. 14. Samuelsson B, Dahlen SE, Lindgren JA, et al. Leukotrienes and lipoxins: structures, biosynthesis, and biological effects. Science 1987; 237:1171–1176. 15. Sinclair R, Eriksson AS, Gretzer C, et al. Inhibitory effects of amide local anaesthetics on stimulus-induced human leukocyte metabolic activation, LTB4 release and IL-1 secretion in vitro. Acta Anaesthesiol Scand 1993; 37:159–165. 16. Tanelian DL, Brose WG. Neuropathic pain can be relieved by drugs that are usedependent sodium channel blockers: lidocaine, carbamazepine, and mexiletine. Anesthesiology 1991; 74:949–951. 17. Cousins MJ. Neural blockade in clinical anesthesia and management of pain. 2nd edn. Philadelphia: JB Lippincott; 1988. 18. Scott DB, Lee A, Fagan D, et al. Acute toxicity of ropivacaine compared with that of bupivacaine. Anesth Analg 1989; 69:563–569. 19. McClure JH. Ropivacaine. Br J Anaesth 1996; 76:300–307. 20. Stevens RA, Urmey WF, Urquhart BL, et al. Back pain after epidural anesthesia with chloroprocaine. Anesthesiology 1993; 78:492–497. 21. Miller RD. Anesthesia. 5th edn. Pennsylvania: Churchill Livingstone; 2000.

38. Hogan Q. Local anesthetic toxicity: an update. Reg Anesth 1996; 21:43–50. 39. Huang YF, Pryor ME, Mather LE, et al. Cardiovascular and central nervous system effects of intravenous levobupivacaine and bupivacaine in sheep. Anesth Analg 1998; 86:797–804. 40. Bosnjak ZJ, Stowe DF, Kampine JP. Comparison of lidocaine and bupivacaine depression of sinoatrial nodal activity during hypoxia and acidosis in adult and neonatal guinea pigs. Anesth Analg 1986; 65:911–917. 41. Feldman HS, Arthur GR, Pitkanen M, et al. Treatment of acute systemic toxicity after the rapid intravenous injection of ropivacaine and bupivacaine in the conscious dog. Anesth Analg 1991; 73:373–384. 42. Kulier AH, Woehlck HJ, Hogan QH, et al. Epinephrine dysrhythmogenicity is not enhanced by subtoxic bupivacaine in dogs. Anesth Analg 1996; 83:62–67. 43. Haasio J, Pitkanen MT, Kytta J, et al. Treatment of bupivacaine-induced cardiac arrhythmias in hypoxic and hypercarbic pigs with amiodarone or bretylium. Reg Anesth 1990; 15:174–179. 44. Kasten GW, Martin ST. Bupivacaine cardiovascular toxicity: comparison of treatment with bretylium and lidocaine. Anesth Analg 1985; 64:911–916. 45. Lacombe P, Blaise G, Hollmann C, et al. Isoproterenol corrects the effects of bupivacaine on the electrophysiologic properties of the isolated rabbit heart. Anesth Analg 1991; 72:70–74. 46. Saitoh K, Hirabayashi Y, Shimizu R, et al. Amrinone is superior to epinephrine in reversing bupivacaine-induced cardiovascular depression in sevoflurane-anesthetized dogs. Anesthesiology 1995; 83:127–133. 47. Solomon D, Bunegin L, Albin M. The effect of magnesium sulfate administration on cerebral and cardiac toxicity of bupivacaine in dogs. Anesthesiology 1990; 72: 341–346.

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Part 1: General Principles 48. Kasten GW, Martin ST. Resuscitation from bupivacaine-induced cardiovascular toxicity during partial inferior vena cava occlusion. Anesth Analg 1986; 65:341–344. 49. Weinberg GL, VadeBoncouer T, Ramaraju GA, et al. Pretreatment or resuscitation with a lipid infusion shifts the dose–response to bupivacaine-induced asystole in rats. Anesthesiology 1998; 88:1071–1075. 50. Tanaka K, Yamasaki M. Blocking of cortical inhibitory synapses by intravenous lidocaine. Nature 1966; 209:207–208. 51. Simon RP, Benowitz NL, Culala S. Motor paralysis increases brain uptake of lidocaine during status epilepticus. Neurology 1984; 34:384–387. 52. Tsui BC, Malherbe S, Koller J, et al. Reversal of an unintentional spinal anesthetic by cerebrospinal lavage. Anesth Analg 2004; 98:434–436. 53. Kalichman MW, Powell HC, Myers RR. Quantitative histologic analysis of local anesthetic-induced injury to rat sciatic nerve. J Pharmacol Exp Ther 1989; 250:406– 413. 54. Horlocker TT, Cabanela ME, Wedel DJ. Does postoperative epidural analgesia increase the risk of peroneal nerve palsy after total knee arthroplasty? Anesth Analg 1994; 79:495–500. 55. Ohtake K, Matsumoto M, Wakamatsu H, et al. Glutamate release and neuronal injury after intrathecal injection of local anesthetics. Neuroreport 2000; 11:1105– 1109. 56. Urushitani M, Nakamizo T, Inoue R, et al. N-methyl-D-aspartate receptor-mediated mitochondrial Ca(2+) overload in acute excitotoxic motor neuron death: a mechanism distinct from chronic neurotoxicity after Ca(2+) influx. J Neurosci Res 2001; 63:377–387. 57. Drasner K. Is lidocaine safe for spinal and epidural anesthesia? 54th Annual Refresher Course Lectures, Clinical Updates and Basic Science Reviews, 243 page 1–243 page 7. 10-11-2003. San Francisco, CA, American Society of Anesthesiologists. 10-11-0003. Ref Type: Conference Proceeding 58. Hashimoto K, Hampl KF, Nakamura Y, et al. Epinephrine increases the neurotoxic potential of intrathecally administered lidocaine in the rat. Anesthesiology 2001; 94:876–881.

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62. Wang BC, Hillman DE, Spielholz NI, et al. Chronic neurological deficits and Nesacaine-CE – an effect of the anesthetic, 2-chloroprocaine, or the antioxidant, sodium bisulfite? Anesth Analg 1984; 63:445–447. 63. Taniguchi M, Bollen AW, Drasner K. Sodium bisulfite: scapegoat for chloroprocaine neurotoxicity? Anesthesiology 2004; 100:85–91. 64. Zink W, Graf BM, Sinner B, et al. Differential effects of bupivacaine on intracellular Ca2+ regulation: potential mechanisms of its myotoxicity. Anesthesiology 2002; 97:710–716. 65. Berde CB. Local anesthetics: basic mechanisms and clinical implications. 54th Annual Refresher Course Lectures, Clinical Updates and Basic Science Reviews, 616 page 1–616 page 7. 10-11-0003. San Francisco, CA, American Society of Anesthesiologists. 10-11-0003. Ref Type: Conference Proceeding. 66. Butterworth J. Local anesthetic: agents, actions and misconceptions. 54th Annual Refresher Course Lectures, Clinical Updates and Basic Science Reviews, 134 page 1–134 page 6. 10-11-2003. San Francisco, CA, American Society of Anesthesiologists. 10-11-0003. Ref Type: Conference Proceeding. 67. Grant GJ, Bansinath M. Liposomal delivery systems for local anesthetics. Reg Anesth Pain Med 2001; 26:61–63. 68. Enneking FK, Ilfeld BM. Major surgery in the ambulatory environment: continuous catheters and home infusions. Best Pract Res Clin Anaesthesiol 2002; 16:285–294. 69. Akopian AN, Souslova V, England S, et al. The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways. Nat Neurosci 1999; 2:541– 548. 70. Novakovic SD, Tzoumaka E, McGivern JG, et al. Distribution of the tetrodotoxinresistant sodium channel PN3 in rat sensory neurons in normal and neuropathic conditions. J Neurosci 1998; 18:2174–2187. 71. Rabert DK, Koch BD, Ilnicka M, et al. A tetrodotoxin-resistant voltage-gated sodium channel from human dorsal root ganglia, hPN3/SCN10A. Pain 1998; 78:107–114. 72. Kohane DS, Yieh J, Lu NT, et al. A re-examination of tetrodotoxin for prolonged duration local anesthesia. Anesthesiology 1998; 89:119–131.

59. Neal JM. Effects of epinephrine in local anesthetics on the central and peripheral nervous systems: neurotoxicity and neural blood flow. Reg Anesth Pain Med 2003; 28:124–134.

73. Kohane DS, Lu NT, Gokgol-Kline AC, et al. The local anesthetic properties and toxicity of saxitonin homologues for rat sciatic nerve block in vivo. Reg Anesth Pain Med 2000; 25:52–59.

60. Hashimoto K, Sakura S, Bollen AW, et al. Comparative toxicity of glucose and lidocaine administered intrathecally in the rat. Reg Anesth Pain Med 1998; 23:444– 450.

74. Wagner LE, Gingrich KJ, Kulli JC, et al. Ketamine blockade of voltage-gated sodium channels: evidence for a shared receptor site with local anesthetics. Anesthesiology 2001; 95:1406–1413.

61. Liu S, Pollock JE, Mulroy MF, et al. Comparison of 5% with dextrose, 1.5% with dextrose, and 1.5% dextrose-free lidocaine solutions for spinal anesthesia in human volunteers. Anesth Analg 1995; 81:697–702.

75. McCarthy RJ, Kerns JM, Nath HA, et al. The antinociceptive and histologic effect of sciatic nerve blocks with 5% butamben suspension in rats. Anesth Analg 2002; 94:711–716.

PART 1

GENERAL PRINCIPLES

Section 4

Practical Pharmacology

CHAPTER

Steroids in Spine Interventions

13

Omar El Abd

Corticosteroids currently constitute the cornerstone of spinal injections for management of painful inflammatory conditions unresponsive to oral treatment. Steroids are potent antiinflammatory medications. Originally introduced for treatment of adrenal insufficiency, they have evolved into an integral treatment of inflammatory conditions such as rheumatoid arthritis since their introduction in 1949.1 Robechhi and Capra,2 in 1952, in Italy followed by Lievre et al.3 in France provided the initial reports of the use of glucocorticoids as a therapeutic component in an epidural injection. Goebert and Gardner,4,5 in 1961 reported the first use of epidural steroid injections in the USA. Since 1961, the use of locally acting injectable steroids in the treatment of painful spine conditions has expanded steadily. Steroids are currently used in a variety of spine injection procedures. They are used in caudal, interlaminar, and transforaminal epidural injections, intrathecal injections,6 intra-articular facet joint injections, and in intra-articular sacroiliac joint injections. Although other therapeutic agents are used for spine injections, the frequency of steroid use surpasses the use of all other agents by far. Although steroids are the leading therapeutic agent in spinal injections, many studies have advocated and debated the use of steroids for spinal injections. The focus of this chapter is to provide the spine specialist with an overview of the physiology and pharmacology and to highlight the evidence-based medicine supporting the use of steroids in painful spinal conditions, as well as to discuss potential side effects and complications.

STEROID PHYSIOLOGY The adrenal gland is comprised of two distinct anatomical and histologic parts, the cortex being on the periphery while the medulla is located centrally (Fig. 13.1). The cortex is considered a component of the endocrine system normally producing steroids, hence their name corticosteroids. The medulla is considered a modified ganglion and a component of the sympathetic nervous system, producing epinephrine, norepinephrine, and dopamine. The adrenal cortex produces multiple, yet structurally similar steroids. The only steroids produced in physiologic amounts are of three types: mineralocorticoids, glucocorticoids, and androgens. The adrenal cortex is divided into three distinct zones: the zona glomerulosa, the zona fasciculata, and the zona reticularis. Notably, all three zones produce the glucocorticoid, corticosterone. The zona glomerulosa comprises 15% of the glandular mass and is the only zone that produces the mineralocorticoid, aldosterone. Aldosterone regulates electrolyte homeostasis and intravascular volume. It increases the reabsorption of sodium from the kidneys, the gastrointestinal tract, saliva, and sweat causing sodium retention in the extracellular fluid, thus expanding its volume. It also increases

potassium and decreases sodium ions in muscle and brain cells. It increases potassium diuresis and urine acidity. The zona glomerulosa lacks the 17α-hydroxylase enzyme; therefore, this zone fails to produce 17-hydroxysteroids or sex hormones. This zone is under the influence of the pituitary gland and is coregulated by the renin–angiotensin system. The zona glomerulosa has the ability to produce new cortical cells and regenerating cells of the zona fasciculata and the zona reticularis. The zona fasciculata predominantly produces the glucocorticosteroids, cortisol and corticosterone, due to an abundance of 3β-hydroxysteroid dehydrogenase enzyme activity. The main endogenous glucocorticosteroid produced is cortisol. It is produced at a daily rate of 10 mg/day.7 The production of the cortisol is regulated by the hypothalamus and the pituitary gland using a negative feedback mechanism. The hypothalamus produces corticotropin releasing hormone (CRH) which releases adrenocorticotrophic (ACTH) hormone from the anterior pituitary gland. ACTH in turn stimulates the zona fasciculata to produce cortisol. The zona reticularis predominantly produces androgens due to the presence of relatively increased amounts of the cofactors required for the expression of the 17,20-hydroxylase activity of the 17αhydroxylase. The equivalent of adrenal androgens is only about 20% of testosterone produced in the testicles. The activation of this zone is under the influence of the pituitary gland through ACTH and possibly by a pituitary adrenal–androgen stimulating hormone and not by gonadotropins. The adrenal androgen, androstenedione, is converted to testosterone and estrogen in the circulation. All of the hormones produced by the adrenal cortex are derivatives of cholesterol, which contains the cyclopentanoperhydrophenanthrene nucleus. The adrenal cortex primarily secretes C21 (two carbon side chain at position 17) and C19 steroids (keto or hydroxyl group at position 17). Most of the C19 steroids have a keto group at position 17 and are therefore called 17-ketosteroids. The C19 steroids have androgenic activity. The C21 steroids have a hydroxyl group at the 17 position and are therefore called 17-hydroxycorticosteroids. The C21 steroids are further subdivided into mineralocorticoids and glucocorticoids. Hydrocortisone and similar compounds are readily absorbed on oral intake. When water-soluble hydrocortisone and similar compounds are used intravenously, they achieve rapid and high concentration in the body fluids. More prolonged effects are obtained by intramuscular injections. Glucocorticoids can also be administered selectively in joint spaces, respiratory tract, epidural space, conjunctival sac, and skin with minimal systemic absorption. Ninety percent of cortisol is reversibly bound in the circulation to an α-globulin called transcortin or corticosteroid-binding globulin (CBG) with a small amount of binding to albumin. CBG has a high affinity to cortisol leaving corticosterone relatively less bound. The half-life of cortisol in the circulation is about 1 hour. Cortisol 153

Part 1: General Principles Right adrenal gland

Cortex Medulla

and β-adrenergic receptor agonists in inducing lipolysis in adipocytes, which results in an increase in free fatty acids.

Cardiovascular effects

Right kidney Cross section

Fig. 13.1 Location and cross section of the adrenal gland.

Glucocorticoids have a mild mineralocorticoid action enhancing the absorption of sodium ions from the distal tubules and the collecting ducts of the kidneys. This results in hypertension which can be partially reversed by a sodium-restricted diet. Even synthetic glucocorticoids which are designed to lack a significant mineralocorticoid effect enhance vascular reactivity. Glucocorticoids have permissive actions on different metabolic reactions without participating in the reaction themselves. Their presence is required for catecholamines to produce pressor and bronchodilatation responses. As well, glucocorticoids enhance vascular reactivity to norepinephrine.

Central nervous system effects Glucocorticoids have various neurological and psychological effects that can alter personality, mood, behavior, concentration, and brain excitability to olfactory and gustatory stimuli. Glucocorticoids inhibit adrenocoticotrophic hormone secretion and, therefore, suppress the production of vasopressin.

Immunologic effects is metabolized mostly in the liver and to a lesser extent in the kidneys. Steroid metabolism involves sequential additions of oxygen and hydrogen atoms followed by conjugation with sulfates or glucoronides to form water-soluble and inactive products. These products are predominantly excreted in urine.

ACTION OF STEROIDS There are two well-studied mechanisms of action for glucocorticoids. The first, which occurs over several hours and explains the delayed onset of action, is through its interaction with specific receptor proteins in target tissues to regulate the expression of corticosteroid responsive genes. This gene regulation changes the levels of an array of proteins synthesized by target tissues. Glucocorticoids predominantly increase expression of target genes. The second mechanism is an immediate one and it is mediated through membrane-bound receptors. It is important to note that the maximum steroid pharmacologic activity lags behind the peak blood levels. This suggests that most of the steroid effect results from enzymatic activity modification rather than from direct action of steroids. Glucocorticoids exert a variety of effects on most of the body’s systems. They regulate various physiologic organs functions. Disturbance of physiologic glucocorticoids levels causes multiple organ and system irregularities. Relevant glucocorticoid effects are discussed below.

Glucocorticoids have a potent antiinflammatory and immunosuppressive action, which is accomplished mainly through their action on lymphocytes. By inhibiting lymphocyte mitotic activity and reducing interleukin (IL)-2 release through the inhibition of the movement of NFκB, they decrease the blood lymphocytic count and profoundly alter the immune responses of lymphocytes. They reduce local inflammation through the upregulation of lipocortin, which inhibits the action of phospholipase A2. Ultimately the release of arachidonic acid from tissue phospholipids is impeded and the formation of leukotrienes, thromboxanes, prostaglandins, and prostacyclines is necessarily reduced. Glucocorticoids increase the number of neutrophils by increasing demargination from blood vessel walls, increasing their release from bone marrow, diminishing their removal from the circulation. They reduce the number of eosinophils by increasing their sequestration into the spleen and lungs. Glucocorticoids reduce the number of basophils as well.

Antiinflammatory effects The antiinflammatory action of epidural steroids is suggested to be secondary to:8 ● ● ●

154

Inhibition of phospholipase A2 activity. Prevention of degranulation of granulocytes, mast cells and macrophages. Suppression of macrophage migration inhibitory factor. Stabilization of lysosomal and other membranes.

Metabolic effects

●

Glucocorticoids are historically described as regulating carbohydrate metabolism. They increase protein catabolism and increase hepatic glycogenesis and gluconeogenesis by increasing glucose-6-phosphatase activity. They exert an anti-insulin action in peripheral tissues and raise the plasma glucose levels. The brain and the heart are spared from the anti-insulin effect and are protected from starvation by glucocorticoids. In diabetics, glucocorticoids raise plasma lipid levels and increase ketone formation. Glucocorticoids redistribute body fat with increasing fat deposition in the posterior neck and upper back, face, supraclavicular area along with loss of fat in the extremities. They also facilitate the action of agents such as growth hormone

In addition to the antiinflammatory effects, epidural steroids cause prolonged suppression of ongoing neuronal discharge and suppression of the sensitivity of dorsal horn neurons. Synthetic steroids are more potent than endogenous cortisol and possess variable glucocorticoid and mineralocorticoid activity. Chemically engineered modifications have generated a variety of steroid compounds with different glucocorticoid and mineralocorticoid activity, enhanced potency, and longer duration of action. Since glucocorticoids act at the same receptors, it is not yet possible to separate the antiinflammatory effects from the action on carbohydrate, protein, and fat metabolism, much less its effect on the hypothala-

Section 4: Practical Pharmacology

mus–pituitary axis. To achieve an effective therapeutic level of serum glucocorticoid, the administration of high oral or parenteral doses may be necessary. The administration of such doses produces the deleterious systemic side effects and simultaneously inhibits ACTH secretion that can lead to adrenal insufficiency.

SYSTEMIC ABSORPTION It has been proposed and widely accepted that the selective administration of steroids, such as in epidural, perineural, or intra-articular injections produces high local concentration of the steroids without significant systemic absorption. The consensus is that systemic absorption after spine procedures is insufficient to cause serious systemic side effects. We observe through our clinical experience that the most commonly reported systemic side effect of steroids after spine injections is temporary hyperglycemia in diabetics. A few patients experience temporary hypertension, insomnia, nervousness, and rash in the anterior chest and face. The issue of systemic absorption of epidural injections and the systemic side effects are the subject of many studies. There are several reports suggesting that following epidural steroid injections hypothalamic–pituitary–adrenal axis suppression occurs for a period of 4 days to 6 weeks.9,10 Tuel et al. also reported the development of cushingoid syndrome after the epidural use of methylprednisolone.64 Janicki et al.12 analyzed the pharmacokinetics of methylprednisolone after epidural administration in rabbits of different doses of 1.25, 2.5 and 5 mg/kg. At 6 and 12 hours after administration, plasma levels of methylprednisolone was detectable only after administration of the highest dose (5mg/kg) and was undetectable at 24 and 72 hours. Plasma methylprednisolone levels were not detectable for doses 1.25 mg and 2.5 mg/kg at all sampling times. Jacobs et al.13 evaluated systemic steroid absorption after a single epidural steroid injection of methylprednisolone acetate 80 mg, and found no significant systemic absorption. While the extreme systemic complications that can ensue following the local deposition of glucocorticoids in the spinal canal are rare, this does not in any way suggest that the effects are all local. Indeed, a recent study, by Bhat et al.14 unequivocally demonstrated that transforaminal epidural steroid instillation results in a transient insignificant, but nevertheless, systemic side effect of dysphonia or hoarseness. Ward et al.15 studied systemic side effects following the use of epidural steroids. Ten patients with sciatica underwent a short insulin tolerance test, when fasting glucose, insulin, and cortisol concentrations were measured before and twice following (at 24 h and 1 week) a caudal epidural of 80 mg triamcinolone. Serum glucose after insulin administration declined from 3.6% μ min before the epidural to 1.9% μ min 24 h afterward and returned to pretreatment values by 1 week. Significantly elevated fasting insulin and glucose levels also reflected impaired insulin sensitivity immediately after the epidural injection. Furthermore, morning cortisol levels were suppressed after the epidural injection (49 nmolul at 24 h and 95 nmolul at 1 week vs. 352 nmolul at baseline). Hsu et al.16 evaluated the plasma cortisol and ACTH profiles after a single epidural injection of 40 mg and 80 mg of triamcinolone. Plasma cortisol was markedly reduced for only 24 hours, whereas the group receiving 80 mg of triamcinolone showed reduction for up to 14 days, with hypothalmic–pituitary axis (HPA) returning to normal at 35 days in both groups.

STEROID COMPLICATIONS AND SIDE EFFECTS Local side effects after spinal injections Steroid side effects occurring after spine injections have been reported; however, they are considered to be clinically uncommon

compared to the number of procedures performed. The reported side effects are either due to the steroid itself or components of the steroid preparation. A number of complications are due to technical errors in performing the procedures, and this is discussed in detail elsewhere in this book. One report suggested that steroid injections can have a detrimental effect on the function of the inflammatory process, which in its turn suppresses the resorption of disc herniations.16a Intradiscal injection of methylprednisolone acetate and its vehicle polyethylene glycol in rabbits caused degeneration and primary calcification of the discs.17 Polyethylene glycol and other glycols present in steroid preparations have been reported to cause degenerative changes in the nervous tissues and even arachnoiditis when injected into the subarachnoid space.18–21 In contrast, many reports dispute this notion.6,22,24 Abram and O’Connor reviewed 65 studies of epidural and subarachnoid injections from 1960 to 1994; they reported no incidence of adhesive arachnoiditis in patients after receiving epidural steroid injections.24 There are studies that demonstrate a beneficial effect of injected steroids in the treatment of arachnoiditis.6,23 Although anaphylactic reactions were reported in patients using parentral corticosteroids, allergic reactions rarely occur after spinal steroid injections. Allergic reactions may be secondary to the paraben preservative present in some injectable preparations. Some injectables such as betamethasone and hydrocortisone contain sulfites, which may cause allergic reactions including anaphylaxis and asthma.25 Facial flushing and generalized erythema, a warm sensation or fever less than 100°F after epidural and intra-articular steroid injections have also been reported26,27,28 with an incidence between 1.4%26 and 9.3%.29 Antihistamines, when used, improve facial flushing.26 Facial flushing after epidural steroid injections is reported to last from 12 hours29 to 72 hours.26 Insomnia, nonpositional headache, and temporary increase in pain were also reported.28 Spinal cord injury has been reported after lumbosacral nerve root block with steroid injections.30 This is postulated to be secondary to an injury or an injection of particulate steroids involving an aberrant artery of Adamkiewicz. Spinal epidural lipomatosis is another rare spinal complication reported after multiple epidural steroid injections. Roy-Camille31 reported the development of epidural lipomatosis in a patient after 103 epidural steroid injections and in another after oral steroid intake.

Side effects of systemic glucocorticoids Side effects of the therapeutic use of steroids can be divided into two categories.

Side effects of withdrawal of therapy Withdrawal of systemic corticosteroids can cause a rebound effect of the underlying pathology for which the steroids were originally prescribed. The most severe complication of withdrawal is acute adrenal insufficiency from abrupt discontinuation of steroids. This occurs because of the suppression of the hypothalamus–pituitary–adrenal axis by exogenous circulating steroids. The duration of suppression can vary from several weeks to more than a year. To diminish the risks of iatrogenic acute adrenal insufficiency, tapering steroid doses are recommended for patients receiving long-term treatment.32 Fever, myalgia, malaise, arthralgia, and rarely pseudotumor cerebrii can also be precipitated by withdrawal of systemic steroids.

Side effects of prolonged therapy Prolonged systemic therapy results in many side effects. It is these potential side effects that created the stigma of steroid use. Patients almost invariably inquire about these side effects when steroid spine 155

Part 1: General Principles

injections are suggested as a treatment option. These side effects encompass all the body systems, with occasionally severe and disabling manifestations. Below are the most prominent side effects concerning the spine interventionist.

Increased susceptibility to infections Due to their function suppressing the immune system and the inflammatory response, corticosteroids can increase the risk of infections.

Osteoporosis This is a common and serious complication of chronic systemic therapy. Systemic steroid intake is the most common cause of drug-induced osteoporosis.33 Glucocorticoids cause osteoporosis through various mechanisms. They reduce the total body calcium stores through the reduction of the gastrointestinal absorption by an unknown mechanism and increase calcium excretion at the kidney. This increases the parathyroid hormone level which increases bone resorption. In addition, glucocorticoids suppress gonadal hormone production and inhibit bone formation because of osteoblast suppression.34 Osteoporosis usually occurs in the first 6 months of glucocorticoids therapy. It predominantly affects trabecular bones; thus, the ribs and the vertebral bodies are commonly involved. For the prevention of glucocorticoid-induced osteoporosis calcium and vitamin D intake is recommended. Gonadal hormone replacement is indicated in certain populations, such as in postmenopausal women, unless contraindicated. Bisphosphonates are also reported to be effective.33 Dubois et al.35 found no relationship between cumulative epidural injections of methylprednisolone of a total minimum dose of 3 g and bone mineral density in 28 subjects.

Osteonecrosis Systemic glucocorticoids are the second common cause of osteonecrosis with prevalence varying between 3% and 38%,36 only surpassed by trauma. Osteonecrosis usually starts between 6 months and 3 years of the initiation of oral treatment. Earlier onset of this condition after systemic steroid use was reported.37 The head of the femur is most commonly involved, but the head of the humerus and the distal femur may be involved as well, though less frequently. The risk increases with chronic use of high doses, especially if given for a short duration. Osteonecrosis is more common in patients with systemic illnesses that negatively impact bone mineralization, such as renal failure, or in systemic immune complex deposition. The mechanism appears to be multifactorial. At the cellular level, glucocorticoids reduce the number of osteoclasts and increase osteoblast and osteocyte apoptosis. Altered fat metabolism and fat embolism, intravascular coagulation, and vascular occlusion have been suggested as possible etiologies as well. Treatment of osteonecrosis is usually surgical, and frequently requires joint replacement after failure of conservative management.

Fluid and electrolyte disturbance Hypertension is a common side effect of glucocorticoids as all glucocorticoids have some minimal mineralocorticoid activity. Edema and hyperglycemia with glycosuria are also frequently observed. These manifestations are usually treated symptomatically.

Muscle weakness Glucocorticoids are required for normal muscle function. With steroid deficiency, such as in Addison’s disease, patients often report weakness and fatigue. On the other hand, patients taking systemic steroids have a tendency to develop muscle weakness as well. Excess 156

glucocorticoids over prolonged periods of time either iatrogenic or secondary to hypercorticism causes a muscle-wasting syndrome known as steroid myopathy through an unknown mechanism. The weakness is usually present in the proximal lower and upper extremities muscles. There is a relative sparing of distal muscles, facial muscles, and sphincters. The incidence of weakness is not clearly identified. It is estimated that 50–80% of patients with Cushing’s disease have some degree of weakness, and women are more prone than men with a 2:1 ratio for a given dose of steroid. Fluorinated steroids have a greater tendency to cause weakness than nonfluorinated compounds (triamcinolone > betamethasone > dexamethasone). Muscle biopsy will reveal a preferential loss of type II muscle fibers, especially type II B fast twitch glycolytic fibers, with lack or only a minimal loss of type I muscle fibers. The exact cause of this condition is not clear. It is suggested that it could be related to protein, carbohydrate, electrolyte metabolism, mitochondrial changes, and reduced sarcolemmal excitability. Because of the lack of involvement of type I fibers, electrodiagnostic examination for assessment of this condition is usually unremarkable, unless the condition becomes very severe.

Behavioral Patients taking glucocorticoids commonly experience psychological symptoms such as nervousness, insomnia, mood changes, psychosis, and even suicide.

Opthalmologic Developing cataracts, especially the subcapsular type, is a known complication of chronic systemic use of glucocorticoids, occurring in up to 60% of patients.38 There is a higher risk of cataracts in children. In adults it is common in patients with diabetes, those with a history of smoking or alcohol abuse, and in those with a family history of cataracts. Cataracts have also been reported with the use of epidural steroids.39 Glaucoma with optic nerve complications can occurs.

Peptic ulcers Glucocorticoid intake is a possible cause of peptic ulcer disease including bleeding and perforation. This is of particular concern when there is the concomitant use of nonsteroidal antiinflammatory drugs.

Growth retardation Even small doses of glucocorticoids result in growth retardation in children.40 There are reports that linear growth can be restored with growth hormone treatment. Glucocorticoids cause growth retardation through a direct effect on glucocorticoid receptors in the epiphyseal growth plates by inhibiting the release of growth hormose (GH) from the pituitary gland. They also modify GH, insulin like growth factor-1 (IGF-1) and IGF-1 receptors mRNA in growth plates and inhibit basal and IGF-1 DNA synthesis. Glucocorticoids also modulate T3 levels within the growth plate.41 A recent animal study demonstrated that glucocorticoids compete with T4 receptors, causing growth retardation.42

Coagulation Steroids rarely increase blood coagulability or precipitate intravascular thrombosis. Steroids should be used with caution in patients with thromboembolic disorders.

Cushingoid features Chronic use of steroids results in the characteristic cushingoid habitus including fat redistribution, striae, hirsutism, ecchymoses, and acne.

Section 4: Practical Pharmacology

THERAPEUTIC USE OF GLUCOCORTICOIDS IN THE SPINE Glucocorticoids are used both systemically and locally in the treatment of various painful spine conditions. Systemic use is mostly oral, typically using a tapering dose of prednisone. The use of the Medrol Dosepack® is becoming common, especially among primary-care physicians for treatment of acute spinal and radicular pain. Oral steroids are also commonly used for treatment of malignant metastatic spine lesions. Locally injected glucocorticoids are gaining widespread acceptance. Spinal injection requires technical expertise and is currently performed by trained interventional physicians from a variety of medical specialties such as physiatry, anesthesiology, radiology, neurology, orthopedics, and neurosurgery. The advantage of using this route is the benefit of administering potent steroids into and around the affected area. Consequently a lower dose is needed and ultimately this minimizes the potential systemic side effects while enhancing the therapeutic benefit. Local spine steroid injections include interlaminar and caudal epidural,43,44 transforaminal epidural and selective nerve root,45–48 intra-articular zygapophysial and sacroiliac joint,49,50 intrathecal,6 and intradiscal injections.51

Capsule Zona glomerulosa Zona fasciculata Zona reticularis Medulla

Fig. 13.2 Cross section of the adrenal gland.

SYSTEMIC STEROIDS The use of systemic steroids for the treatment of painful spine conditions is mostly through oral intake. Intravenous use of steroids is virtually never used in the management of painful nonmalignant spine conditions. Methylprednisolone is currently popular especially among primarycare physicians for treatment of acute painful spine conditions. It is used in a tapering dose to maintain an adequate clinical response. The Medrol Dosepack® and the Meprolone Unipack® are available in a form convenient to both the patients and the physicians. Twenty-four milligrams are used as an initial dose (6 tablets of 4 mg), tapered daily with 4 mg decrements until 21 tablets are given. Prednisone is administered orally in tablet or suspension form. Obviously, the use of oral steroids carries the risks of developing a variety of systemic side effects. In addition, the effectiveness of oral administration is presumed to be proportional to the dose of medicine delivered to the site of pathology,28 which can be impaired by compressive lesions in radiculopathy.52

Locally injectable steroids The commonly used glucocorticoids preparations used in spine injections are discussed below. The Food and Drug Administration has not formally approved epidural use of these steroid preparations. These preparations are used by spine interventionists throughout the United States and are considered an ‘off-label’ route of administration.53 Indeed, their use in this manner has evolved into the standard of practice. Studies to evaluate efficacy of spine injections, side effects, and complications were performed using these preparations, with generally good results and a good safety profile. As there are different steroid preparations, different laboratories have established equivalent doses of these steroids (Fig. 13.2) (Table 13.1).25 Celestone consists of a suspension containing betamethasone sodium phosphate and betamethasone acetate (Fig. 13.3). Absorption of betamethasone sodium phosphate is rapid, while the absorption of acetate is much slower. This makes the action of Celestone® Soluspan® a rapid onset of 1–3 hours and of a longer duration persisting 7 days after administration. It should not be mixed with diluents or local anesthetics containing preservatives such as phenol or parabens because of flocculation and clogging of the suspension. It is avail-

Table 13.1: Antiinflammatory Equivalent Doses of Steroids Drug

Equivalent Dose

Cortisone

25 mg

Hydrocortisone

20 mg

Prednisolone

5 mg

Prednisone

5 mg

Methylprednisolone

4 mg

Triamcinolone

4 mg

Dexamethasone

0.750 mg

Betamethasone

0.6 mg

able in multidose 5 mL vial of 6 mg/mL. The suspension is the most soluble when mixed with local anesthetics. The suspension should be protected from light and stored at 2–25°C. There is currently a shortage of this preparation in the US. In the author’s institution, the allotted quantity is used for newborns with respiratory distress to accelerate the maturation of lung surfactant. Methylprednisolone (Depo Medrol®) is an antiinflammatory with minimal mineralocorticoid effects (Fig. 13.4). Intrathecal injection of steroids54 especially methylpredinsolone55 have been reported to cause arachnoiditis. The manufacturer’s label warns against intrathecal use

CH2OH C

O

H3C HO H3C

OH

CH3

F O

Fig. 13.3 Celeston® Soluspan®.

157

Part 1: General Principles CH2OCOCH3

CH2OH

CO CH3

H HO

C HO H3C

OH

H

CH3

H

H

O

H3C OH

OH

F

O

Fig. 13.5 Triamcinolone.

O H

CH3

Fig. 13.4 Depo Medrol®.

based on reports of adverse neurologic reactions including arachnoiditis. Its absorption is very slow. It is reported that intra-articular injection takes up to 7 days. It is available in 3 strengths: 20 mg/mL, 40 mg/mL, and 80 mg/mL. The preparations also contain: polyethylene glycol 3350, polysorbate, monobasic sodium phosphate, dibasic sodium phosphate USP, and benzoyl alcohol as a preservative. Sodium chloride (NaCl) is added to adjust tonicity. The pH is adjusted by adding NaOH or HCl, to be maintained between 3.5 and 7.0 (Table 13.2). Methylprednisolone acetate was used extensively in the early 1980s. This steroid mixture contains polyethylene glycol, which is considered neurotoxic and linked to complications that included aseptic meningitis and arachnoiditis from intrathecal injections.18,20,56–58 As a precaution, if spinal fluid is encountered during an epidural injection, it is recommended to withdraw the needle and reintroduce it at an adjacent level to prevent accidental intrathecal injection.24,59 Abram and O’Connor’s literature review60 concluded that epidural injection of steroid preparations containing

polyethylene glycol is safe. The preparation is currently widely used in spine injections. Triamcinolone is a potent antiinflammatory with virtually no mineralocorticoid activity (Fig. 13.5). All the injectable forms of triamcinolone contain benzoyl alcohol as a preservative. The available injectable triamcinolones are (Table 13.3): ●

●

●

Table 13.2: Contents of 1 mL of Depo Medrol® Methylprednisolone

20 mg

40 mg

80 mg

Polyethylene glycol

29.5 μg

29.1 μg

28.2 μg

Polysorbate

801.97 μg

1.94 μg

1.88 μg

Monobasic sodium phosphate

6.9 μg

6.8 μg

6.59 μg

Dibasic sodium phosphate USP

1.44 μg

1.42 μg

1.37 μg

Benzoyl alcohol (preservative)

9.3 μg

9.16 μg

8.88 μg

Aristocort® (triamcinolone diacetate): It is slowly absorbed. It should not be mixed with diluents or local anesthetics containing preservatives such as phenol or parabens because of flocculation and clogging of the suspension. Kenalog® (triamcinolone acetonide): It is slowly absorbed with effects persisting for several weeks. Kenalog® is difficult to dissolve, in comparison to Celestone®, but reported to have a longer duration of action and a higher efficacy.53 The difference is secondary to a difference in their structure. Kenalog® is frequently used in spine injections despite the increased risk of a deleterious reaction. The author does not use it regularly as the author performs a large number of cervical transforaminal injections, and prefers the more soluble preparations Celestone® Soluspan® and Depo Medrol®. Aristopan® (triamcinolone hexacetonide): It can be administered intra-articularly, intrasynovially, and intralesionally. It has the longest duration of all the injectable triamcinolones and is also believed to have the maximum suppression of the hypothalamic–pituitary axis.30 It should not be mixed with diluents or local anesthetics containing preservatives such as phenol or parabens because of flocculation and clogging of the suspension.

Injectable forms are either dexamethasone sodium phosphate or dexamethasone acetate (Fig. 13.6). Dexamethasone acetate has a slow absorption rate and peak plasma concentration is reached in about 8 hours. It is not recommended when immediate action is desirable.

Table 13.3: Common Steroids Used in Spinal Interventions Compared to Hydrocortisone

158

Hydrocortisone

Methylprednisolone (Depo Medrol®)

Triamcinolone Acetonide (Kenalog®)

Betamethasone Sodium Phosphate and Acetate (Celestone® Soluspan®)

Relative antiinflammatory potency

1

5

5

25

pH

5.0–7.0

7–8

4.5–6.5

6.8–7.2

Onset

Fast

Slow

Moderate

Fast

Duration of action

Short

Intermediate

Intermediate

Long

Concentration mg/mL

50

40-80

20

6

Relative mineralocorticoid activity

2+

0

0

0

Section 4: Practical Pharmacology

using locally acting steroids when administered under fluoroscopy in expert hands is low. The use of steroid injections should be considered for pain nonresponsive to oral antiinflammatory medicines prior to surgical interventions.

CH2OH C

O

H3C HO H3C

OH

References

CH3

1. Hench PS, Slocum CH, Polley HF, et al. Effect of cortisone and pituitary adrenocorticotropic hormone (ACTH) on rheumatic diseases. JAMA 1950; 144:1327–1335.

F Fig. 13.6 Dexamethasone.

O

Dexamethasone sodium phosphate is rapidly absorbed. The suspensions should be protected from light and freezing. It is stored at room temperature below 40°C. Dexamethasone preparations are not widely used in spine injection procedures. There is a lack of consensus on the amount of steroid used and the frequency of therapeutic steroid injections. Buchner et al.61 described three epidural injections in 2-week duration of methylpredinisolone 100 mg. Riew et al.62 used one injection of 1 cc of betamethasone (6 mg/mL). For treatment of cervical radicular pain, Slipman et al.63 used 1.0–1.5 cc of Celestone® Soluspan® (6 mg/mL) performing two injections 2 weeks apart and canceled the second injection if there was more than 90% relief after the first injection. There may be an additive effect of repeat steroid injections.64 In the author’s institution, based on clinical experience and using Slipman’s method, spinal steroid injections are performed 2 weeks apart with a maximum of four injections within a 6-month period. Repeat injections are cancelled if there is an improvement of more than 90%, allowing patients to start physical therapy promptly. At the time of writing this chapter, single-dose Depo Medrol® (40 mg/mL vials) or Celestone® Soluspan® (6 mg/mL 5 cc vials) are used when available. The author believes that the listed amounts of steroids outlined in Table 13.4 are safe and provide patients with the best outcomes.

2. Robechhi A, Capra R. L’idrocortisone (composto F). Prime esperienze cliniche in campo reumatologico. Minerva Med 1952; 98:1259–1263. 3. Lievre JA, Bloch-Michel H, Pean G, et al. L’hydrocortisone en injection locale. Rev Rhum 1953; 20:310–311. 4. Gardner WJ, Goebert HW Jr, Sehgal AD. Intraspinal corticosteroids in the treatment of sciatica. Trans Am Neurol Assoc 1965; 86:214–215. 5. Goebert HW, Jallo SJ, Gardner WJ, et al. Painful radiculopathy treated with epidural injections of procaine and hydrocortisone acetate results in 113 patients. Anesth Analg 1961; 140:130–134. 6. Wilkinson HA. Intrathecal Depo-Medrol: A literature review. Clin J Pain 1992; 8:49–56. 7. Esteban N, Loughlin T, Yergey A, et al. Daily cortisol production in man determined by stable isotope dilution/mass spectrometry. J Clin Endocrinol Metab 1991; 72:39–45. 8. Hayashi N, Weinstein J, Meller S, et al. The effect of epidural injection of betamethasone or bupivacaine in a rat model of lumbar radiculopathy. Spine 1998; 23(8):877–885. 9. Mikhail GR, Sweet LC, Mellinger RC. Parenteral long-acting corticosteroid effect on hypothalamic pituitary adrenal function. Ann Allergy 1973; 31:337–343. 10. McEvoy GK, Litvak K, Welsh OH, et al. AHFS 99 drug information. Bethesda: American Society of Health-System Pharmacists; 1999:2636–2662. 11. Tuel SM, Meythaler JM, Cross LL. Cushing’s syndrome from epidural methylprednisolone. Pain 1990; 40:81–84. 12. Janicki PK, Johnson B, Parris WC. Pharmacokinetic analysis of plasma methylprednisolone after administration in rabbits. ASRA Annual meeting, 7, 1995. 13. Jacobs A, Pullan PT, Potter JM, et al. Adrenal suppression following extradural steroids. Anaesthesia 1983; 38:953–956. 14. Bhat AL, Chow D, DePalma MJ, et al. Incidence of vocal cord dysfunction following fluoroscopically guided steroid injections in the axial skeleton. Arch Phys Med Rehab (in press).

CONCLUSION

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The use of steroid injections in spine procedures is an important intervention by which control of inflammation and pain can be achieved. This will not only accelerate the rehabilitation phase of treatment, but it makes it more effective as patients participate in their exercise programs with less pain. When properly administered in the specific area of pathology, steroids followed by a specific rehabilitation program can prevent the prolongation of spine pain. This improves quality of life, reducing the need for surgery and its potential complications. Early return to work has a positive impact on the financial burden to individuals, to the healthcare industry, and to society. The risk when

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Table 13.4: Suggested Steroid Doses

21. Johnson A, Ryan MD, Roche J. Depo-Medrol and myelographic arachnoiditis. Med J Aust 1991; 155:18–20.

Depo Medrol® (40 mg/mL)

Celestone® Soluspan® (6 mg/mL)

22. Rivera VM. Intraspinal steroid therapy. Neurology 1981; 31:1060–1061.

Cervical, thoracic and lumbar transforaminal

2.4 cc

3.0 cc

Cervical nerve root block

1.4–1.6 cc

2 cc

24. Latham JR, Fraser RD, Moore RJ, et al. The pathologic effects of intrathecal betamethasone. Spine 1997; 22: 1558–1562.

Lumbar nerve root block

1.6 cc

2 cc

25. American Society of Health-System Pharmacists. Corticosteroids general statement; 68:04:2874. AHFS Drug Information.Corticosteroids general statement. 2003.

Cervical and lumbar intra-articular facet joint

0.8 cc

0.8 cc

26. DeSio JM, Kahn CH, Warfield CA. Facial flushing and/or generalized erythema after epidural steroid injection. Anesth Analg 1995; 80:617–619.

SacroIliac intra-articular

1.6 cc

2.0 cc

Type of Injection

23. Tkaczuk H. Intrathecal prednisolone therapy in postoperative arachnoiditis following operation of herniated disk. Acta Orthop Scand 1976; 47:388–390.

27. Pattrick M, Doherty M. Facial flushing after intra-articular injection of steroid. Br Med J (Clin Res Ed) 1987; 295(6610):1380.

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48. Botwin KP, Gruber RD. Lumbar epidural steroid injections in the patient with lumbar spinal stenosis. Phys Med Rehabil Clin N Am 2003; 14(1):121–141. 49. Mooney V, Robertson J. Facet joint syndrome. Clin Orthop 1976; 115:149–156.

31. Roy-Camille R, Mazel CH, Husson JL, et al. Symptomatic spinal epidural lipomatosis induced by a long-term steroid treatment. Spine 1991; 16:1365–1371.

50. Murtagh FR. Computed tomography and fluoroscopy guided anaesthesia and steroid injection in facet syndrome. Spine 1988; 13:686–689.

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37. Sakamoto M, Shimizu K, Iida S, et al. Osteonecrosis of the femoral head: a prospective study with MRI. J Bone Joint Surg Br 1997; 79(2):213–219.

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38. Skalka HW, Prchal JT. Effect of corticosteroids on cataract formation. Arch Ophthalmol 1980; 98:1773–1777.

56. Roche J. Depo-Medrol and myelographic arachnoiditis. Med J Aust 1991; 155:574– 575.

39. Chen YCJ, Gajraj NM, Clavo A, et al. Posterior subcapsular cataract formation associated with multiple lumbar epidural corticosteroid injections. Anesth Analg 1998; 86:1054–1055.

57. Dullerud R, Morland TJ. Adhesive arachnoiditis after lumbar radiculopathy with Dimer-X and Depo-Medrol. Radiology 1978; 119:153–155.

40. Halliday HL. Use of steroids in the perinatal period 1. Paediatr Respir Rev 2004;5(Suppl 1):S321–S327. 41. Van der Eerden BC, Karperien M, Wit JM. Systemic and local regulation of the growth plate. Endocr Rev 2003; 24(6):782–801. 42. Rooman RP, Kuijpers G, Gresnigt R, et al. Dexamethasone differentially inhibits thyroxine- or growth hormone-induced body and organ growth of Snell dwarf mice. Endocrinology 2003; 144(6):2553–2558. 43. Lieberman R, Dreyfuss P, Baker R. Fluoroscopically guided interlaminar cervical epidural injections. Arch Phys Med Rehabil 2003; 84(10):1568–1569. 44. Hession WG, Stanczak JD, Davis KW, et al. Epidural steroid injections. Semin Roentgenol 2004; 39(1):7–23. 45. Lutz GE, Vad VB, Wisneski RJ. Fluoroscopic transforaminal lumbar epidural steroids: an outcome study. Arch Phys Med Rehabil 1998; 79:1362–1366. 46. Vad VB, Bhat AL, Lutz GE, et al. Transforaminal epidural steroid injections in lumbosacral radiculopathy: a prospective randomized study. Spine 2002; 27(1): 11–16.

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47. Botwin KP, Gruber RD, Bouchlas CG, et al. Fluoroscopically guided lumbar transforaminal epidural steroid injections in degenerative lumbar stenosis: an outcome study. Am J Phys Med Rehabil 2002; 81(12):898–905.

58. Strong WE, Wesley R, Winnie AP. Epidural steroids are safe and effective when given appropriately. Arch Neurol 1991; 48:1012. 59. Abram. SE. Perceived dangers from intraspinal steroid injections. Arch Neurol 1989; 46:719–720. 60. Abram SE, O’Connor TC. Complications of epidural steroid injections. Reg Aneth 1996; 2:149–162. 61. Buchner M, Zeifang F, Brocai DRC, et al. Epidural corticosteroid injection in the conservative management of sciatica. Clin Orth 2000; 375:149–156. 62. Riew KD, Yin Y, Gilula L, et al. The effect of nerve-root injections on the need for operative treatment of lumbar radicular pain. A prospective, randomized, controlled, double-blind study. J Bone Joint Surg Am 2000; 82-A(11):1589–1593. 63. Slipman CW, Lipetz JS, Jackson HB, et al. Therapeutic selective nerve root block in the nonsurgical treatment of atraumatic cervical spondylotic radicular pain: a retrospective analysis with independent clinical review. Arch Phys Med Rehabil 2000; 81(6):741–746. 64. Manchikanti L. Neuroaxial steroids. In: Low back pain diagnosis and treatment. Kentucky: ASIPP; 2002:132–145.

PART 1

GENERAL PRINCIPLES

Section 4

Practical Pharmacology

CHAPTER

Opioid Analgesics

14

Jerome Schofferman and S. Ali Mostoufi

The use of opioid analgesics is an important part of the practice of pain medicine. Most physicians who treat chronic low back pain (CLBP) will prescribe opioid analgesics for well-selected patients at some time. Opioids are usually prescribed for CLBP when pain has proven refractory to rehabilitation, therapeutic injections, and less potent primary and adjunctive analgesics. Pharmacological treatment should be just one part of a comprehensive plan to improve pain and function (Fig. 14.1).

OPIOID ANALGESICS The efficacy and safety of long-term opioid analgesics specifically for CLBP has been reviewed recently, and much of the following discussion regarding efficacy appears from that paper.1 There are now multiple randomized, controlled trials that consistently demonstrate efficacy and safety of opioid therapy for patients with CLBP.2–11 The strongest evidence comes from numerous prospective randomized, placebo-controlled trials (PRPCT) that compared a particular opioid to placebo.12 Katz et al. performed a 12-week enriched enrollment PRPCT to compare pain relief of oxymorphone-ER to placebo in 325 opioid-naive patients with CLBP.2 During titration, 120 patients discontinued treatment for reasons that included lack of efficacy and adverse events. In the 205 remaining patients who obtained adequate analgesia and tolerable side effects during titration, pain intensity measured by visual analogue scale (VAS) decreased from 69 mm to 23 mm. These patients were subsequently randomized to continue oxymorphone-ER or placebo. After 12 weeks, the opioid group had statistically better pain numerical rating scores and patient satisfaction scales. There were 34 patients in the oxymorphone group who discontinued treatment for reasons that included lack of efficacy (12 patients) and adverse events (9 patients). In the placebo group, 53 discontinued treatment for similar reasons, lack of efficacy (35 patients) and adverse events. The authors concluded that oxymorphone-ER was safe and effective for opioid-naive patients with CLBP. Hale et al. performed a 12-week enriched enrollment PRPCT to compare pain relief of oxymorphone-ER to placebo in 250 opioid-experienced patients with CLBP.3 Function was not addressed. During the titration period, 108 patients discontinued treatment due to adverse events (47), lack of efficacy (7), among other reasons. In 143 remaining patients who obtained adequate analgesia and tolerable side effects during titration, there were significant decreases in pain. These patients were subsequently randomized to continue oxymorphone-ER or placebo. After 12 weeks, there were clinically better outcomes in the oxymorphone-ER group for both numerical rating and patient satisfaction scales. There were 20 patients in the oxymorphone group who discontinued treatment due to lack of efficacy (8),

adverse events (7), or other reasons. In the placebo group there were 55 who discontinued treatment due to lack of efficacy (39), adverse events (8) including opioid withdrawal (5), or other reasons. These authors also concluded that oxymorphone-ER was safe and effective for opioid-experienced patients with CLBP. Hale et al. reported an 18-day multicenter randomized, doubleblind, active and placebo-controlled comparison of oxymorphoneER, oxycodone-CR, and placebo in 213 patients with CLBP.4 The mean change in pain intensity was significantly greater in both opioid-treated groups compared to placebo, and there were no clinically meaningful differences between opioids. Categorical pain ratings were most impressive. About 35% of the opioid-treated groups described their pain as absent or mild versus 12% in the placebo group. Sixtyone percent of the opioid groups reported moderate to complete pain relief versus 28% of the placebo group. Conversely, 45% of the placebo group described their pain as severe versus 14% in the opioid groups. There were statistically significant improvements in general activity, mood, normal work, and enjoyment of life, but not walking ability. During the titration phase about 15% of opioid-treated patients withdrew due to side effects and 4% due to lack of efficacy. In the treatment phase, 25–33% of the opioid groups withdrew due to adverse effects. There were no instances of addictive behavior. Side effects were common, but only sedation and constipation were more frequent in the opioid groups compared to controls. Peloso and associates performed a 91-day randomized doubleblind, placebo-controlled study comparing the efficacy and safety of flexible dose tramadol 37.5 mg plus acetaminophen (APAP) 325 mg to placebo in 338 patients with CLBP.5 The active treatment group had statistically and significantly better improvements in pain (VAS) and function (Roland Disability Questionnaire) compared to placebo patients. About 49% of the active treatment patients had ≥30% reduction in pain and 49% had ≥50% relief. The number needed to treat was 4 for ≥30% relief and 5 for ≥50% relief. Schnitzer et al. reported a prospective randomized, controlled 4-week trial that compared tramadol to placebo in 254 patients with CLBP who had had been shown to be tramadol responders in the open-label phase of the study.6 The tramadol group had significantly greater improvements in pain (VAS) and function (Roland) compared to the control group. Ruoff and associates reported a 91-day PRCT that compared tramadol plus acetaminophen to placebo in patients with CLBP.7 The active treatment group had significantly better pain (VAS) and function compared to placebo. There are also numerous prospective, randomized active-control trials (PRACT) that compared opioids to one another.8–11,13,14 Rauck et al. performed an 8-week open-label PRACT to compare effectiveness and safety of a once-a-day morphine sulfate-SR (Avinza®) with twice daily oxycodone-CR (Oxycontin®) in 392 patients with moderate to

161

Part 1: General Principles A. Nociceptive pain Noxious peripheral stimuli Pain Autonomic response Withdrawal reflex

Heat Cold Intense mechanical force

Nociceptor sensory neuron Brain

Chemical irritants Spinal cord B. Inflammatory pain Inflammation

Spontaneous pain Pain hypersensitivity Reduced threshold: Allodynia Increased response: Hyperalgesia

Macrophage Mast cell Neutrophil Granulocyte Tissue damage

Nociceptor sensory neuron Brain

Spinal cord

C. Neuropathic pain

Spontaneous pain Pain hypersensitivity

Peripheral nerve damage Brain Stroke Spinal cord injury

D. Functional pain Spontaneous pain Pain hypersensitivity Normal peripheral tissue and nerves

Brain

Abnormal central processing

severe CLBP.8 Both groups had statistically and clinically significant reductions in pain. Although there were slightly better outcomes in the morphine group, the authors recognize that the study protocol mandated 12-hour dosing of the oxycodone-CR rather than 8-hour dosing that is more often necessary. This may have biased the results slightly in favor of the morphine group. Numerical rating scale (NRS) decreased from a mean of about 6.5 to a mean of 3.4–3.7. The morphine-SR group had somewhat smoother pain control. Function was not addressed. About 32–43% of patients withdrew, most often due to side effects, but also due to inadequate pain relief. There were four instances of abuse or diversion in the oxycodone-CR group. Allan et al. performed a 13-month unblended, randomized parallel group study to compare titrated doses of transdermal fentanyl (TDF) to morphine-SR in 680 patients with CLBP.9 Doses of drugs were titrated according to individual patient response. The TDF and morphine-SR 162

Fig. 14.1 The four primary types of pain. (Adapted from Woolf CJ. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med 2004; 140(6): 441–451).

produced similar results. Depending on level of activity, 50–65% of patients described themselves as improved, and 37–53% of patients had at least 50% reduction in pain. There were significant improvements in mean SF-36 scores for physical functioning, bodily pain, role-physical, vitality, social function and role-emotional. About 31–37% of patients withdrew the due to adverse events. Over the 13 months of the study, opioid doses increased only slightly, usually early in treatment, and were attributed to titration to optimal dose rather than tolerance. There were no instances of addiction or abuse behavior. Hale et al. performed a 10-day randomized, double-blind trial to compare the efficacy and safety of titrated doses of oxycodone-CR and to oxycodone-IR in 47 CLBP patients.10 There were equal and significant improvements with both formulations. Pain intensity decreased from moderate to severe at baseline to slight at the end of

Section 4: Practical Pharmacology

titration with both oxycodone formulations. Eleven patients (23%) withdrew due to side effects. Jamison et al. performed a 16-week randomized, prospective study to compare naproxen, fixed dose oxycodone, and a titrated dose of oxycodone plus morphine-ER in 36 patients.11 All three groups had improvement in pain, activity level, and emotional distress. The titrated dose opioid group did best with less pain and less emotional distress than the other two groups. Both opioid groups were better than the naproxen group. There were 86% who found opioids beneficial. Three patients in the opioid groups withdrew due to side effects and one patient had an abuse problem. In addition, there are multiple prospective observational studies that have shown consistent findings of efficacy and safety for opioids in patients with CLBP. Simpson et al. found statistically significant improvement in pain in 50 patients changed to TDF compared to their prior regimens of pain-contingent oral opioids for chronic LBP.13 Gammaitoni et al. prospectively studied 33 patients with CLBP treated with titrated doses of oxycodone-IR plus APAP three times daily for 4 weeks.14 Three patients were not able to tolerate the oxycodone and two others withdrew for other reasons. The mean NRS was reduced from 6.4 to 4.4 and worst pain from 7.7 to 5.6. There were significant improvements in general activities, mood, walking tolerance, and sleep. Side effects were common, but there were no serious adverse effects. There were no instances of addictive behavior or other abuse. Recently, Martell and associates published a systematic review of opioid treatment for CLBP.15 Despite the fact that the authors did not include several PRPCTs that showed both efficacy and safety of opioids for CLBP, they still concluded that opioids ‘may be efficacious for short-term pain relief.’2,6,7,9 They also state that ‘long-term efficacy is unclear.’ However, they did not include the study with the longest duration of 13 months9 and gave less weight to other longterm studies that are of lower quality but provide the best available evidence.16,17 While it is clear that the evidence regarding long-term efficacy and safety of opioid use is not strong, there are several prospective observational and retrospective studies that are consistent in showing long-term efficacy and safety and no studies that demonstrate loss of effectiveness over time unless there is disease progression.16,17 Schofferman reported a prospective case series of 33 patients with refractory CLBP treated with opioids for 1 year.16 There were no control or comparison groups. The specific opioid was selected by response during the trial titration phase. Five (15%) patients withdrew because of side effects. In the remaining 28, there were statistically and clinically significant improvements in pain and function at one year. The mean NRS improved from 8.6 to 5.9 and mean Oswestry Low Back Disability Index (OSI) from 64 to 54. There was a biphasic response. In 21 patients there was an improvement of NRS from 8.45 to 4.9, while 7 others had no change. Overall, of the 33 patients who started the study, opioids were beneficial in 21 (64%). Mahowald et al. reviewed their experience with opioid use over a period of 3 years in an orthopedic spine clinic.17 Opioids were prescribed for 152 patients, 58 of whom received opioids long term. There was adequate follow-up in 117. Pain was reduced from a mean of 8.3 to 4.5. It is noteworthy that there was no significant dose increase over time and the authors stated that they did not see tolerance in their patients. Side effects were common but well tolerated by most patients. There was a low prevalence of abuse. The authors concluded that there was clinical evidence to support treating CLBP patients with opioids. There are multiple studies and systematic reviews that examined the efficacy and safety of opioid analgesics for the treatment

of chronic musculoskeletal pain, all of which included but were not limited to patients with CLBP. Furlan’s meta-analysis of opioids for chronic pain concluded that opioids were more effective than placebo for pain and functional outcomes in patients with nociceptive pain, including CLBP.18 With respect to side effects, only nausea and constipation were clinically and statistically significantly greater in the opioid than placebo patients. Study withdrawal rates averaged 33% in the opioid groups and 38% in placebo groups. The MONTAS study group performed a 2-week prospective, randomized double-blind, placebo-controlled trial of MS-ER in 48 patients, 12 of whom had refractory CLBP.19 In 17 (35%) patients, pain was reduced from a mean of 7.4 to 2.9 (excellent responders). In 17 others, pain was reduced from 7.8 to 5.6 (partial responders). In 14 (29%) (non-responders) there was either no meaningful relief or intolerable side effects. Markenson et al. performed a 90-day RCT comparing oxycodone-CR to placebo in 107 patients with moderate to severe osteoarthritis, 40–50% of whom had CLBP.20 There were statistically significant differences favoring the oxycodone-CR group versus controls in pain intensity, pain-induced interference with general activity, walking, work, mood, sleep, and enjoyment in life. The improvements in pain were only modest. The discontinuation rate was similar between groups, either due to inadequate pain control or side effects. In summary, there is sufficient evidence to make a Grade A recommendation that opioid analgesics are safe and effective for the treatment of patients with CLBP, at least in the short term. In all high-quality studies there is clinically and statistically significant improvements in pain and the results are uniformly better for opioid than placebo. There is sufficient but less robust evidence to state that opioids retain their effectiveness over the longer term and no reports of loss of efficacy over time. About 10–20% of patients do not tolerate opioids due to side effects. Of those patients who tolerate opioids, about one-third are excellent responders, one-third fair responders, and one-third non-responders. The evidence for improvement of function with opioids is also good, but not as strong as for improvement in pain. There is no evidence to show any opioid to be best. Each opioid that has been studied has been shown to be more effective than placebo and clinically effective for change in LBP. However, because there is individual patient variability in opioid responsiveness, it is not uncommon to have to rotate opioids to find the best one for an individual patient. Opioids are generally safe. Toxicity is rare. The incidence of diversion, addictive behavior, or other social problems is low. Side effects are common, but are usually manageable.

OPIOIDS: CELLULAR MECHANISM OF ACTION Opioids bind with delta, kappa and mu receptors in the central nervous system (CNS) and peripheral tissues to provide analgesic effects. Mu receptors are located in the CNS and provide central analgesia, but also play a role in the development of respiratory depression, physical dependence, and withdrawal symptoms. Most commonly used opioids such as morphine, codeine and fentanyl are mu-agonists. The majority of kappa receptors are located in the cerebral cortex and substantia gelatinosa of the dorsal horn. Kappa receptors are responsible for analgesia at the level of the spinal cord, the brain, and also kappa-mediated dysphoria. Kappa receptors have less of a role in physical dependence and withdrawal. Delta receptors are concentrated in the substantia gelatinosa of the dorsal horn and have a primary effect upon spinal and supraspinal analgesia. There is evidence that points to the involvement of N-methylD-aspartate (NMDA) receptors in the development and maintenance 163

Part 1: General Principles

Added

20 Increased

8

40

6 60 4 2

80

Chronic pain is undertreated. There are many complex reasons for this, most of which are based on anecdotes and social pressures. Some of the circumstances that contribute to the prevalence of undertreated pain include:

0

100

■

■ ■

Lack of knowledge of medical standards, current research and clinical guidelines for appropriate pain treatment; The perception that prescribing adequate amounts of controlled substances will result in unnecessary scrutiny by regulatory authorities; Misunderstanding of addiction and dependence; Lack of understanding of regulatory policies and processes.

Some physicians continue to have a bias against the use of long-term opioid analgesics for chronic pain. The most prevalent concerns are organ toxicity, tolerance, dependency, addiction and fear of legal consequences, and at least in theory the development of opioid-induced hyperalgesia. In addition, there is a concern that the side effects may outweigh benefits.

Organ toxicity Opioids are less toxic than nonsteroidal antiinflammatory medications and probably have less overall risk than spinal injections or spine surgery. Organ toxicity is rare. Opioids are not toxic to the liver, kidneys, brain, or other organs. Respiratory depression is highly unusual with appropriate doses of oral opioids except in persons with significant pulmonary disease, sleep-apnea syndrome or other serious medical conditions.

Tolerance Tolerance is the need for progressively higher doses of an analgesic to produce the same degree of pain relief, which would translate into partial loss of opioid efficacy over time. True tolerance is a biological process at the cellular level based on downregulation of opioid receptors, desensitization of receptors or both.22 True tolerance is not common in the clinical setting. Once the proper balance of pain control, function, and side effects has been reached; there is rarely dose escalation unless there is disease progression. Early in treatment it is common to note ‘pseudotolerance,’ the need for increased dosage due to an increase in function, which in turn is due to better pain control. The development of pseudotolerance requires rebalancing the opioid dose for maximal pain control and function with minimal adverse effects. When tolerance appears to occur well after stable doses have been reached, it is most likely due to diseases progression. However, the other factors that must be considered include lack of compliance, change in other medications with unexpected drug interaction and diversion of medications (Fig. 14.2).23

Opioid-induced hyperalgesia There are recent suggestions that a small number of patients who are taking long-term opioids become desensitized to their analgesic effects,

(NRS)

Time

Function

10

CLINICAL CONCERNS REGARDING LONG-TERM OPIOID THERAPY

■

164

Opioid

Pain

of neuropathic pain.21 It follows that NMDA receptor antagonists may be helpful in the treatment of neuropathic pain. However, in order to obtain complete analgesia, a combination of an NMDA receptor antagonist and an opioid receptor agonist may be needed. In vitro data have demonstrated some medications (such as methadone), in addition to being opioid receptor agonists, are also weak noncompetitive NMDA receptor antagonists.21

(OSI)

Fig. 14.2 Pseudotolerance. NRS is a numerical rating score for pain. A lower score indicates less pain. OSI is Oswestry Disability Index for function. A lower score indicates better function.

and in fact develop more rather than less pain. This is referred to as opioid-induced pain hyperalgesia (OIH). The prevalence of OIH is not known. Some studies imply that repeated opioid administration or continuous infusion could lead to a progressive, long-lasting, dose and time-dependent reduction of baseline antinociceptive thresholds, hence an increase in pain sensitivity. There are anecdotal reports of patients who are not obtaining good relief with opioids whose pain actually improves after opioids are withdrawn. EXPERIMENTAL EVIDENCE: More of the recently published data show decrease in the dose–response effects of opioids on nociception during acute administrations in animals. This decline in antinociceptive efficacy is much more rapidly observed with short-acting opioids than with long-acting opioids.24 Mao et al. and Kissin et al. both demonstrated progressive reduction of baseline nociceptive thresholds (allodynia) in rats receiving repeated morphine and alfentanil.25,26 Laulin et al. reported an obvious relationship between acute tolerance and hyperalgesia in rats receiving a repeated once-daily dose of heroin.27 A progressive decrease in heroin analgesic effects was combined with a gradual lowering of the nociceptive threshold. This same group reported that opioid-induced hyperalgesia is dose-dependent.28 The larger the dose of subcutaneous fentanyl bolus, the more noticeable was the reduction of baseline nociceptive thresholds. In this study, decreased baseline nociceptive thresholds lasted as long as 5 days after the cessation of four fentanyl bolus injections. Opioid-induced hyperalgesia is also time-dependent. In a 2002 study, allodynia following an opioid infusion was increased with longer opioid infusions in comparison to shorter ones.29 CLINICAL EVIDENCE: In volunteers, tolerance to analgesia during remifentanil infusion at a constant rate for 4 hours was profound and developed very rapidly within 60–90 minutes after the start of infusion.30 Some authors report delayed hyperalgesia from shortacting opioid exposure.31–33 Some other data show the larger the intraoperative opioid dose, the greater was postoperative opioid consumption and the higher were the pain scores.34–36

Dependence and addiction DEPENDENCE: Dependence is a state of physiological adaptation induced by the chronic use of a psychoactive substance, which would include alcohol and opioids. There is an abstinence syndrome when the drug is suddenly stopped or the dose is reduced rapidly.37 Dependence is very common in patients treated with opioids, but it is rarely a clinical problem. Physical dependence and tolerance are

Section 4: Practical Pharmacology

Table 14.1: Comparison between dependence and addiction Dependence

Addiction

Definition

It is characterized by a strong psychological dependence and an overpowering compulsion to continually take opioids

Compulsive physiological and psychological need for a habit-forming substance

Mechanism

Psychological

Neurobiological with environmental, genetic and psychosocial influences

Characteristics

Abstinence syndrome associated with discontinued use or decreased intake

Abnormal behavior including impaired control, compulsivity, continuation of use despite harm

Considered normal physiological end-result of chronic opioid use

Considered abnormal outcome of use of opioids

normal physiological consequences of extended opioid therapy for pain and are not the same as addiction (Table 14.1). ADDICTION: Addiction is a primary, chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing its development and manifestations. It is characterized by behaviors that include the following: impaired control over drug use, craving, compulsive use, and continued use despite harm.

Fear of disciplinary action The fear of disciplinary action by medical boards, medical societies or government agencies is cited as yet another concern. However, most agencies, including the Department of Justice, have reiterated official positions that the treatment of pain is a very high medical priority and those physicians who use opioid analgesics appropriately are practicing good medicine and will not be subject to disciplinary action. In 1997, the Federation of State Medical Boards of the USA undertook an initiative to develop model guidelines and to encourage state medical boards and other healthcare regulatory agencies to adopt policy encouraging adequate treatment, including use of opioids when appropriate for patients with pain. Since it was adopted in April 1998 (and updated in May 2004 as the Model Policy), the Model Guidelines for the Use of Controlled Substances for the Treatment of Pain have been widely distributed to state medical boards, medical professional organizations, other healthcare regulatory boards, patient advocacy groups, pharmaceutical companies, state and federal regulatory agencies, and practicing physicians and other healthcare providers. The Model Policy is designed to communicate certain messages to licensees: that the state medical board views pain management to be important and integral to the practice of medicine; that opioid analgesics may be necessary for the relief of pain; that the use of opioids for other than legitimate medical purposes poses a threat to the individual and society; that physicians have a responsibility to minimize the potential for the abuse and diversion of controlled substances; and that physicians will not be sanctioned solely for prescribing opioid analgesics for legitimate medical purposes. In addition, this policy is not meant to constrain or dictate medical decision-making. The Model Guidelines have been endorsed by the American Academy of Pain Medicine, the Drug Enforcement Administration, the American Pain Society, and the National Association of State Controlled Substances Authorities. As of January 2004, twenty-two state medical boards have policy, rules, regulations, or statutes reflecting the Federation’s Model Guidelines for the Use of Controlled Substances for the Treatment of Pain.

GUIDELINES The California Medical Board has adopted the following criteria when evaluating the physician’s treatment of pain, including the use of controlled substances.38

Evaluation of the patient A medical history and physical examination must be obtained and documented in the medical record. The history should document the nature and intensity of the pain, current and past treatments for pain, underlying or coexisting diseases or conditions, the effect of the pain on physical and psychological function, and any current or past history of substance abuse. There should be a documented medical condition that supports the use of opioid analgesics.

Treatment plan The written treatment plan should state objectives that will be used to determine treatment success, such as pain relief and improved physical and psychosocial function, and should indicate if any further diagnostic evaluations or other treatments are planned. After treatment begins, the physician should adjust drug therapy to the individual response of the each patient. Other treatment modalities or a rehabilitation program may be necessary depending on the etiology of the pain and the extent to which the pain is associated with physical and psychosocial impairment.

Informed consent and agreement for treatment The physician should discuss the risks and benefits of the use of opioid analgesics with the patient. The patient should receive prescriptions from one physician only and fill them at only one pharmacy whenever possible. If the patient is at high risk for medication abuse or has a history of substance abuse, the physician should strongly consider collaboration with a specialist in addiction medicine as well as the use of a written agreement between physician and patient outlining patient responsibilities, including random urine/serum medication levels and reasons for which drug therapy may be discontinued (e.g. violation of agreement).

Periodic review The physician should periodically review the course of treatment and any new information about the etiology of the pain or satisfactory response to treatment may be indicated by the patient’s decreased pain, increased level of function, or improved quality of life. If the patient’s progress is unsatisfactory, the physician should consider a different opioid. If treatment continues to be unsatisfactory, opioids

165

Part 1: General Principles

may need to be discontinued. There will be the need for frequent visits during initiation of opioid therapy and early dose and drug titration, perhaps as frequently as weekly. Once patients are stable, they should be seen at least quarterly in most instances.

Table 14.2: Guidelines for chronic opioid treatment PATIENT EVALUATION Detailed medical and pain history

Consultation

Physical examination

The physician should be willing to refer the patient as necessary for additional evaluation and treatment in order to achieve treatment objectives. Special attention should be given to those patients with pain who are at risk for medication misuse, abuse, or diversion. The management of pain in patients with a history of substance abuse or with a comorbid psychiatric disorder may require extra care, monitoring, documentation, and consultation with or referral to an expert in the management of such patients.

Review of imaging Review of medical records A treatment plan that states the goals of therapy Informed consent and agreement for treatment Potential risks, probable and possible side effects

Medical records The physician should keep accurate and complete records that include the medical history and physical examination; diagnostic, therapeutic and laboratory results; discussion of risks and benefits; informed consent; prior treatments; all medications (including date, type, dosage, and quantity prescribed); instructions and agreements; and periodic reviews. Records should remain current and be maintained in an accessible manner and readily available for review. All HIPPA regulations should be observed in this regard.

Compliance with controlled substances laws and regulations To prescribe, dispense, or administer controlled substances, the physician must be licensed in the state and comply with applicable federal and state regulations. Physicians are referred to The Practitioner’s Manual of the US Drug Enforcement Administration (and any relevant documents issued by the state medical board) for specific rules governing controlled substances as well as applicable state regulations (Table 14.2).

RECOMMENDATIONS FOR SAFE AND EFFECTIVE USE OF OPIOIDS IN SPINE CARE In the patient with severe chronic spinal pain that has proven refractory to rehabilitation and interventional techniques, longterm treatment with opioid analgesics may be appropriate for well-chosen patients. The decision to treat with opioids may mean committing to a lifelong treatment plan for this chronic and incurable illness. In these cases, there must be a well-defined structural or neuropathic disorder that either cannot be treated definitively or the patient is too ill for surgical correction. The level of pain and impairment should be consistent with the structural pathology. There should be no significant psychological illness. A history of prior alcohol or other substance abuse does not preclude patients from receiving opioid treatment as long as there is sufficient medical justification. However, these patients should most often be treated in collaboration with an addiction specialist. Some centers choose to obtain an opioid treatment agreement between the physicians and the patient that outlines the respective responsibilities of both patient and physician. The terms of the contract must be clear and should outline the circumstances that may result in discharge of the patient from the clinic should the contract not be honored. This may include receiving narcotics from different sources, evidence of substance abuse, noncompliance with medication, and failed random urine or blood test for narcotics and illicit substances. 166

Consequences of abuse, diversion, or illicit use of opioids Periodic review EFFICACY Side effects Signs of abuse or diversion Consultation when necessary with specialists in psychology/psychiatry Chemical dependence The maintenance of good medical records Compliance with controlled substances laws and regulations

PRACTICAL ASPECTS OF OPIOID USE Opioid dosing: time-contingent versus pain-contingent There are two ways to prescribe analgesics: pain-contingent or timecontingent dosing. Pain-contingent dosing means that the analgesic is taken when pain occurs. Usually, short-acting analgesics that have a rapid onset are used for pain-contingent treatment. Time-contingent dosing means the analgesic is taken on a regular schedule based on the expected duration of analgesia of the particular drug and formulation. With time-contingent dosing, there is usually better analgesia and fewer side effects, and therefore it is usually preferred for chronic pain. Most often, long-acting or continuous-release formulations are used for time-contingent treatment. However, pain-contingent rescue doses should be made available for breakthrough pain.

Short-acting versus long-acting opioids For chronic use, it is best to use a continuous release (CR) or longacting (LA) opioid. A short-acting (SA) opioid should be available for breakthrough pain. The SA opioids are not usually used alone for long-term therapy because there will be wide swings in the blood levels, which leads to poor pain control and potentially more side effects. LA opioids (e.g. methadone) or CR formulations are preferred for chronic pain.

Routes of administration and doses For the treatment of chronic pain, CR or LA opioids are administered orally or transdermally. The dose and dosing interval is adjusted based on the degree and duration of pain relief experienced by the

Section 4: Practical Pharmacology

Table 14.3: Samples of equianalgesia with opioids Drug

Dose frequency

Oral dose

Half-life

Morphine sulfate

4 hr

15

3.2 hr

Oxycodone

4 hr

7.5–10

4 hr

Hydromorphone

4 hr

4

2.5 hr

Hydrocodone

4 hr

15

3 hr

Codeine

4 hr

100

2.9 hr

Methadone

8–12 hr

5–10

15–30 hr

Fentanyl (transdermal)

72 hr

50 mcg/h patch

1.5–6 hr

Oxycodone CR

12 hr

10

4.5 hr

There is no universal agreement on equivalent doses.

patient versus side effects until there is good control of baseline pain with tolerable side effects. There is no best or correct drug nor is there a best or correct dose. There are many drug choices available, some of which are listed in Table 14.3. In addition, the patient should be provided with a prescription for ‘rescue doses’ of an immediaterelease (rapid-onset, short-acting) opioid available for breakthrough pain or flares.

Efficacy Efficacy should be the treating physician’s main concern. Does the long-term use of opioid analgesics help well-selected patients or does it harm them? Is the risk to benefit ratio favorable? The answers should be based on published medical literature, not anecdotes and untested anachronistic beliefs. The evidence for efficacy has been reviewed at the beginning of this chapter.

Side effects As mentioned earlier in this chapter, the side effect profile also affects prescribing pattern and frequency of opioid use. The mechanisms and treatment of opioid side effects have been studied extensively in the literature.39 Most side effects are not serious and can be managed by the use of adjuvant medications. The decision whether to continue opioid analgesic therapy depends on the balance of improved pain, improved function, and side effects. CONSTIPATION: Constipation occurs in most patients on opioids and tolerance does not develop to this side effect. The main goal is to prevent this side effect, so early prophylactic intervention is recommended. Patients must be reminded to drink adequate fluid. The role of fiber is not at all clear. Virtually all patients require laxatives. Most often, patients are started prophylactically on stimulant laxatives such as senna. If these are not successful, patients may need osmotic laxatives such as polyethylene glycol powder. Opioid analgesics bind to the opioid receptors in the gastrointestinal (GI) tract, and thereby cause constipation and perhaps some degree of abdominal pain. Alvimopan is a small molecule, peripherally acting mu opioid receptor antagonist designed to block the adverse side effects of opioid analgesics on the GI tract without blocking their beneficial analgesic effects. It is the first of a new class of drugs known as peripherally acting mu opioid receptor antagonists to be accepted by the FDA for review. NAUSEA AND VOMITING: Nausea or vomiting occurs frequently in patients on opioids. They are more common in opioid-naive patients, and often subside after days to weeks despite continued

use.39 There are several potential causes including stimulation of the chemoreceptor trigger zone (CTZ), gastric stasis and stimulation of vestibular centers. Stimulation of the CTZ usually responds to oral medications such as prochlorperazine or haloperidol (suppositories may be needed initially). Gastric stasis usually responds to metoclopramide. Patients with nausea due to vestibular stimulation feel ill with head rotation. They may respond to antihistamines such as meclizine. SEDATION: Sedation is common, especially at the onset of opioid treatment or when the dose is raised. It usually improves in days or weeks of continued treatment. If the opioid is effective, but there is excess sedation, modafinil or methylphenidate can be of value.40 COGNITIVE CHANGES: Cognitive changes are potential side effects that concern treating physicians. It is important to note that severe chronic pain has been shown to cause decreased cognitive abilities, and if opioids improve pain, cognitive abilities may actually improve.41,42 Many patients feel just a bit ‘off,’ but state the minor side effect is worth the realized pain reduction. Delirium can potentially occur in the elderly or patients with significant medical illnesses. The combination of opioids and long-acting benzodiazepines may be particularly prone to cause sedation or other neuropsychological side effects.43 PRURITUS: Several mechanisms have been proposed including the direct stimulation of ‘itch receptors’ and the release of histamine from mast cells.39 It is important to note pruritus is not an allergic reaction. Treatment with antihistamines is occasionally helpful. MYOCLONUS: Myoclonus, although rare, can occur with all opioids, but the degree of myoclonus is variable. Some patients have mild twitching, especially when trying to fall asleep. Others have jerking of one or more extremities. Treatment with clonazepam at night is often effective. OPIOID-INDUCED HORMONAL CHANGES AND SYMPTOMS: The two hormonal systems mainly affected by opioids are hypothalamicpituitary-adrenal axis and the hypothalamic-pituitary-gonadal axis. In both animal studies44,45 and human studies,46 morphine has been reported to cause a progressive decline in the plasma cortisol level. The effects of opioids on the hypothalamic-pituitary-gonadal axis are changes in hormonal release, including an increase in prolactin and a decrease in LH, FSH, testosterone, and estrogen levels.47 In methadone maintenance patients, heroin addicts, and patients on intrathecal morphine, a drop in testosterone is seen and is associated with decreased libido, aggression, and drive; amenorrhea or irregular menses; and galactorrhea.48–51 These patients may benefit from testosterone replacement therapy.52

SPECIFIC OPIOIDS No one opioid has been shown to be superior for chronic use. The eventual choice of opioid is based on finding the best balance point between efficacy and side effects. It is now clear that there are individual variations among patients with respect to which opioid will work best for a particular patient.53 This phenomenon may be genetic and there is an emerging field of ‘pharmacological genomics’ that eventually hopes to make these laboratory observations clinically useful. At the initiation of opioid therapy it may be necessary to try several before the optimal opioid is identified for a particular patient based on pain control and side effects. If a patient does not respond to the initial opioid, even after appropriate dose escalation, it makes sense to try a second or a third before considering the pain unresponsive to opioids. It also may make sense to rotate to another opioid if there are significant side effects with the initial drug. In fact, in a retrospective review, about 36% of patients responded well to the first opioid tried, 40% to the second and 56% to the third.54 167

Part 1: General Principles

Table 14.4: Some historical dates regarding opioids c3400 BC

The opium poppy is cultivated in lower Mesopotamia. The Sumerians refer to it as Hul Gil, the ‘joy plant’.

460 BC

Hippocrates, the father of medicine, acknowledges usefulness of opium as a narcotic and styptic in treating internal diseases, diseases of women and epidemics.

1300s

Opium had become a taboo subject for those in circles of learning during the Holy Inquisition.

1527

Opium is reintroduced into European medical literature by Paracelsus as laudanum. These black pills or ‘Stones of Immortality’ were made of opium the baicum, citrus juice and quintessence of gold, and prescribed as painkillers.

1729

Chinese emperor, Yung Cheng, issues an edict prohibiting the smoking of opium and its domestic sale, except under license for use as medicine.

1803

Friedrich Sertürner of Paderborn, Germany discovers the active ingredient of opium by dissolving it in acid then neutralizing it with ammonia. The result: alkaloids – Principium somniferum or morphine.

1827

E. Merck & Company of Darmstadt, Germany, begins commercial manufacturing of morphine.

1843

Dr Alexander Wood of Edinburgh discovers a new technique of administering morphine, injection with a syringe. He finds the effects of morphine on his patients instantaneous and three times more potent.

1874

English researcher, C.R. Wright first synthesizes heroin, or diacetylmorphine, by boiling morphine over a stove.

1902

In various medical journals, physicians discuss the side effects of using heroin as a morphine step-down cure. Several physicians would argue that their patients suffered from heroin withdrawal symptoms equal to morphine addiction.

JANUARY 2004

Consumer groups file a lawsuit against Oxycontin maker Purdue Pharma. The company is alleged to have used fraudulent patents and deceptive trade practices to block the prescription of cheap generic medications for patients in pain.

DECEMBER 2004

McLean pain-treatment specialist Dr William E. Hurwitz is sent to prison for allegedly ‘excessive’ prescription of opioid painkillers to chronic pain patients. Testifying in court, Dr Hurwitz describes the abrupt stoppage of prescriptions as ‘tantamount to torture’.

It is noteworthy that the most expensive component of treatment for chronic LBP may be medications. In view of the current crisis in healthcare finance, it is reasonable to consider cost as one of the many factors used to determine the choice of opioid. However, evidencebased medicine is directed toward obtaining the best outcomes for the most patients under most circumstances. Cost is a societal problem that must be considered, but best patient care is paramount. There are six opioids that most pain specialists find to be most suitable for long-term use: continuous or sustained release drugs such as morphine (MS-Contin™, Avinza™, Kadian™, etc.), transdermal fentanyl (Duragesic™), oxycodone (Oxycontin™), oxymorphone (OpanaER), methadone, and levorphanol. There are other opioids such as buprenorphine that might be used in specialized circumstances or in refractory cases. There is no correct initial dose of opioid. Patients who have no prior opioid exposure and are considered ‘opioid naive’ should be started on lower doses than those being changed from a short- to long-acting drug or rotated between long-acting opioids.

Morphine Morphine has remained the gold standard against which all other analgesics are compared. There are numerous short-acting or sustainedrelease preparations available that could provide analgesia for 8–24 hours, depending on the particular formulation. Morphine is the most commonly used narcotic in terminally ill patients. The starting dose of oral morphine is usually in the order of 60–90 mg per day in divided doses. The drug is administered in a time-contingent manner according to the expected duration of analgesia of the particular formulation. The dose and dosing intervals are increased or decreased according to the degree and duration of analgesia and side effects. Common dose increases are usually 15–25% of the prior dose.

Oxycodone (Oxycontin™) Controlled-release oxycodone (Oxycontin™) is an effective analgesic. It usually provides 12 hours of analgesia, but many patients may 168

experience relief for only 8 hours. Unfortunately, there are drawbacks to this otherwise good analgesic. In the United States in the past 1 or 2 years, many cases of abuse and pharmacy burglaries have been reported to be linked to this medication. Since then, both prescribing physicians and patients have been apprehensive of its use. Some pharmacies do not keep it in stock for fear of theft.

Methadone Methadone is gaining in popularity as an analgesic among pain specialists because it is effective, has high biologic availability, has no known active metabolites, and has no known neurotoxicity.55 Further, it has a theoretical advantage of having fewer opioid-induced hyperalgesic side effects. It is also far less expensive than other opioids. Methadone is somewhat more difficult to initiate and titrate given its particular lipid storage and elimination pattern. It takes about 5–7 days to reach a steady state; therefore the dose should only be adjusted about once per week. After steady state is reached, analgesia usually is sustained for 8–12 hours. Once the proper dose is established, the drug is no more difficult to use than other opioids. Some patients may initially hesitate to try methadone because of its social stigma (use in heroin detoxification programs) but will accept it after the differences in uses are explained. Because of its long halflife, high potency, and less predictable pharmacokinetics, methadone should be started at low doses and titrated upwards carefully with provision of adequate breakthrough pain medications during the titration period.

Transdermal fentanyl Transdermal fentanyl (TDF) is an effective analgesic for long-term use. The transdermal route is particularly useful for patients who have difficulty with oral absorption and for those with severe opioidinduced constipation. The patch is commonly changed every 3 days but in some patients there is the need to change the patch every 48 hours. One disadvantage to TDF is the loss of ability to vary doses at

Section 4: Practical Pharmacology

different times of day for those patients with predictable daily activity cycles. It is important to have an immediate-release opioid available for breakthrough pain until the final effective dose of fentanyl is established.

Oxymorphone (Opana-ER) Oxymorphone is the newest opioid and perhaps it is the best studied specifically for the treatment of CLBP.3,4 It is administered twice daily with oxymorphone-IR available for breakthrough pain. The average final dose of oxymorphone-ER in study patients was 39–79 mg per day.

Tramadol Tramadol is a semisynthetic opioid that is available alone or combined with acetaminophen, and is also available in an extendedrelease formulation. It has been shown to be effective in patients with CLBP.5–7 The mean final dose in several studies was about 158 mg per day. The maximum safe daily dose is 400 mg daily. The drug is both an opioid agonist and an inhibitor of serotonin and norepinephrine reuptake. As a result of the latter mechanism, concomitant administration with antidepressants of the selective serotonin reuptake inhibitor class (SSRIs) risks development of a ‘serotonin syndrome.’

Meperidine (Demerol™) This opioid is often used in emergency rooms due to rapid onset of action. It has a slightly shorter duration of action compared to morphine. It is poorly absorbed orally so an injectable route is preferred when used. Meperidine (Demerol™) should not be used as a long-term oral opioid analgesic. Its primary metabolite, normeperidine, is neurotoxic. Normeperidine can accumulate over days to weeks and cause generalized hyperexcitablity and even seizures. Since there are better alternatives to this medication, we do not recommend this medication for pain of spine origin (see Table 14.2).

DRUG–DRUG INTERACTION AND OPIOIDS Most drug interactions stem from a drug’s effects on the liver enzymes which are largely responsible for the elimination of drugs from the body. These interactions can either slow down or speed up that elimination and can be most noticeable among the opioid drugs. An example of an interaction that speeds up a drug’s elimination from the body is the withdrawal symptoms reported in patients maintained on methadone when they are given phenytoin or rifampicin. Potential interactions with antibiotics include those with erythromycin and rifampicin. Erythromycin increases and rifampicin decreases the effects of opioids. Some of the anticonvulsants used to treat neuropathic pain, particularly carbamazepine and phenytoin, can speed up the metabolism of opioids in the liver. The tricyclic antidepressants, clomipramine and amitriptyline, have been shown to increase the plasma availability of morphine when given to cancer patients taking oral morphine solution.

HOW TO TAPER PATIENTS OFF OPIOIDS When the decision has been made to stop opioids in a patient, slow taper is recommended. This is especially true for patients who have been on this medication for a longer period of time (over 2 weeks). Most practitioners will taper the dose by 15–20% every other day. In case the patient develops signs and symptoms of withdrawal (flu-like

symptoms, abdominal cramping, diarrhea), the dose may need to be decreased in smaller amounts over a longer period of time. Clonidine in oral or transdermal route could be used to decrease the withdrawal symptoms (close monitoring of blood pressures on this medication is recommended). In rare cases when patients are on multiple narcotics at the same time, converting all of them to a single long-acting agent first and then slow tapering off that agent over a period of time is recommended. Alternatively, opioids could be tapered off one by one; the short-acting agent should be the last to be discontinued for a safe taper and avoidance of withdrawal symptoms.

CONCLUSION Pharmacological therapy of chronic refractory spinal pain can reduce suffering and improve function in many patients. Medication therapy should not be used alone, but can be a very useful part of a comprehensive pain management program that also includes rehabilitation, interventional pain therapies, psychotherapy, and occasionally surgery. Long-term opioid analgesic therapy is now considered an important treatment option among spine specialists. The key to a successful treatment with opioids is patient selection. In well-selected patients with pain, these drugs are safe and associated with little abuse or diversion. Although monotherapy with opioids may be effective, most often opioids are part of a multidrug regimen. In the hands of experienced physicians, the results of opioid analgesic therapy are favorable and will provide a better quality of life to their patients.

References 1. Schofferman J, Mazenak D. Opioid analgesic therapy. Spine J (in press). 2. Katz N, Rauck R, Ahdieh H, et al. A 12 week, randomized, placebo-controlled trial assessing the safety and efficacy of oxymorphone extended release for opioid-naïve patients with chronic low back pain. Curr Med Res Opin 2007; 23:117–128. 3. Hale M, Ahdieh H, Ma T, et al. Efficacy and safety of OPANA-ER (oxymorphone extended release) for relief of moderate to severe chronic low back pain in opioid-experienced patients: a 12-week, randomized, double-blind, placebo-controlled study. J Pain 2007; 8:175–184. 4. Hale M, Dvergsten C, Gimbel J. Efficacy and safety of oxymorphone extended release in chronic low back pain: results of a randomized, double-blind, placebo and active-controlled phase III study. J Pain 2005; 6:21–28. 5. Peloso P, Fortin L, Beaulieu A, et al. Analgesic efficacy and safety of tramadol/ acetaminophen combination Tablets (Ultracet®) in treatment of chronic low back pain: a multicenter, outpatient, randomized, double blind, placebo controlled trial. J Rheumatol 2004; 31:2454–2463. 6. Schnitzer T, Gray W, Paster R, et al. Efficacy of tramadol in treatment of chronic low back pain. J Rheumatol 2000; 27:772–778. 7. Ruoff G, Rosenthal N, Jordan D, et al. Tramadol/acetaminophen combination tablets for the treatment of chronic lower back pain: a multicenter, randomized, doubleblind, placebo-controlled outpatient study. Clin Ther 2003; 25:1123–1141. 8. Rauck R, Bookbinder S, Bunker T, et al. The ACTION study: a randomized, openlabel, multicenter trial comparing once-a-day extended-release morphine sulfate capsules (Avinza®) to twice-a-day controlled-release oxycodone hydrochloride tablest (OxyContin®) for the treatment of chronic, moderate to severe low back pain. J Opioid Manag 2006; 2:155–166. 9. Allan L, Richarz U, Simpson K, et al. Transdermal fentanyl versus sustained release oral morphine in strong-opioid naïve patients with chronic low back pain. Spine 2005; 30:2484–2490. 10. Hale ME, Fleisschmann R, Salzman R, et al. Efficacy and safety of controlledrelease versus immediate-release oxycodone: randomized, double-blind evaluation in patients with chronic back pain. Clin J Pain 1999; 15:179–183. 11. Jamison RN, Raymond SA, Slawsby EA, et al. Opioid therapy for chronic noncancer back pain. A randomized prospective study. Spine 1998; 23:2591–2600. 12. Katz N. Methodological issues in clinical trials of opioids for chronic pain. Neurology 2005; 65(S4):833–849.

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Part 1: General Principles 13. Simpson RK, Edmondson EA, Constant CF, et al. Transdermal fentanyl as treatment for chronic low back pain. J Pain Symptom Manage 1997; 14:218–224. 14. Gammaitoni AR, Gaier BS, Lacouture P, et al. Effectiveness and safety of new oxycodone/acetaminophen formulations with reduced acetaminophen for the treatment of low back pain. Pain Med 2003; 4:21–30.

42. Jamison RN, Schein JR, Vallow S, et al. Neuropsychological effects of long-term opioid use in chronic pain patients. J Pain Symptom Manage 2003; 26:913–921.

15. Martell B, O’Connor P, Kerns R, et al. Systematic review: opioid treatment for chronic back pain: prevalence, efficacy, and association with addiction. Ann Intern Med 2007; 146:116–127.

43. Ciccone D, Just N, Bandilla E, et al. Psychological correlates of opioid use in patients with chronic nonmalignant pain. A preliminary test of the downhill spiral hypothesis. J Pain Symptom Manage 2000; 20:180–192.

16. Schofferman J. Long-term opioid analgesic therapy for severe refractory lumbar spine pain. Clin J Pain 1999; 15:136–140.

44. Collu R, Clermont MJ, Ducharme JR. Effects of thyrotropin-releasing hormone on prolactin, growth hormone and corticosterone secretions in adult male rats treated with pentobarbital or morphine. Eur J Pharmacol 1976; 37:133–140.

17. Mahowald M, Singh J, Majeski P. Opioid use by patients in an orthopedic spine clinic. Arthrit Rheumat 2005; 52:312–321. 18. Furlan A, Sandoval J, Mailis-Gagnon A, et al. Opioids for chronic noncancer pain: a meta-analysis of effectiveness and side effects. CMAJ 2006; 174:1589–1594. 19. Maier C, Hildebrandt J, Klinger R, et al. Morphine responsiveness, efficacy and tolerability in patients with chronic non-tumor associated pain – results of a doubleblind placebo-controlled trial. Pain 2002; 97:223–233. 20. Markenson J, Croft J, Zhang P, et al. Treatment of persistent pain associated with osteoarthritis with controlled-release oxycodone tablets in a randomized controlled clinical trial. Clin J Pain 2005; 21:524–534. 21. Ebert B, Thorkildsen C, Andersen S, et al. Opioid analgesics as noncompetitive N-methyl-D-aspartate (NMDA) antagonists. Biochem Pharmacol 1998; 56(5): 553–559.

45. Bartolome MB, Kuhn CM. Endocrine effects of methadone in rats: acute effects in adults. Eur J Pharmacol 1983; 95:231–246. 46. Rolandi E, Marabini A, Franceschini R, et al. Changes in pituitary secretion induced by an agonist–antagonist opioid drug, buprenorphine. Acta Endocrinol (Copenh) 1983; 104:257–260. 47. Malaivijitnond S, Varavudhi P. Evidence for morphine-induced galactorrhea in male cynomolgus monkeys. J Med Primatol 1998; 27:1–9. 48. Mendelson JH, Mendelson JE, Patch VD. Plasma testosterone levels in heroin addiction and during methadone maintenance. J Pharmacol Exp Ther 1975; 192:211–217. 49. Mendelson JH, Meyer RE, Ellingboe J, et al. Effects of heroin and methadone on plasma cortisol and testosterone. J Pharmacol Exp Ther 1975; 195:296–302.

22. Ballantyne J, Mao J. Opioid therapy for chronic pain. N Engl J Med 2003; 349:1943– 1953.

50. Rasheed A, Tareen IA. Effects of heroin on thyroid function, cortisol and testosterone level in addicts. Pol J Pharmacol 1995; 47:441–444.

23. Pappagallo M. The concept of pseudotolerance to opioids. J Pharm Care Pain Symptom Control 1998; 6:95–98.

51. Malik SA, Khan C, Jabbar A, et al. Heroin addiction and sex hormones in males. J Pak Med Assoc 1992; 42:210–212.

24. Kissin I, Brown PT, Bradley EL Jr. Magnitude of acute tolerance to opioids is not related to their potency. Anesthesiology 1991; 75:813–816.

52. Abs R, Verhelst J, Maeyaert J, et al. Endocrine consequences of long-term intrathecal administration of opioids. J Clin Endocrinol Metab 2000; 85:2215–2222.

25. Mao J, Price DD, Mayer DJ. Thermal hyperalgesia in association with the development of morphine tolerance in rats: roles of excitatory amino acid receptors and protein kinase C. J Neurosci 1994; 14:2301–2312.

53. Galer BS, Coyle N, Pasternak G, et al. Individual variability in the response to different opioids: report of five cases. Pain 1992; 49:87–91.

26. Kissin I, Bright CA, Bradley EL Jr. The effect of ketamine on opioid-induced acute tolerance: can it explain reduction of opioid consumption with ketamine-opioid analgesic combinations? Anesth Analg 2000; 91:1483–1488. 27. Laulin JP, Célèrier E, Larcher A, et al. Opiate tolerance to daily heroin administration: an apparent phenomenon associated with enhanced pain sensitivity. Neuroscience 1999; 89:631–636. 28. Célèrier E, Rivat C, Jun Y, et al. Long-lasting hyperalgesia induced by fentanyl in rats: preventive effect of ketamine. Anesthesiology 2000; 92:465–472. 29. Ho ST, Wang JJ, Huang JC, et al. The magnitude of acute tolerance to morphine analgesia: concentration-dependent or time-dependent? Anesth Analg 2002; 95(4):948–951. 30. Vinik HR, Kissin I. Rapid development of tolerance to analgesia during remifentanil infusion in humans. Anesth Analg 1998; 86:1307–1311. 31. Koppert W, Dern S, Sittl R, et al. A new model of electrically evoked pain and hyperalgesia in human skin: the effects of intravenous alfentanil, S(+)-ketamine, and lidocaine. Anesthesiology 2001; 95(2):395–402.

54. Quang-Cantagrel N, Wallace M, Magnuson S. Opioid substitution to improve the effectiveness of chronic non-cancer pain control: a chart review. Anesth Analg 2000; 90:933–937. 55. Fishman SM, Wilsey B, Mahajan G, et al. Methadone reincarnated: novel clinical applications with related concerns. Pain Med 2002; 3:339–348.

Further Reading Banki CM, Arato M. Multiple hormonal responses to morphine: relationship to diagnosis and dexamethasone suppression. Psychoneuroendocrinology 1987; 12:3–11. Brodner R, Taub A. Chronic pain exacerbated by long-term narcotic use in patients with non-malignant disease: clinical syndrome and treatment. Mt Sinai J Med 1978; 45:233–237. Collin E, Poulain P, Gauvain-Piquard A, et al. Is disease progression the major factor in morphine ‘tolerance’ in cancer pain treatment? Pain 1993; 55:319–326. Compton P, Athanasos P, Eloashoff D. Withdrawal hyperalgesia after acute opioid physical dependence in nonaddicted humans: a preliminary study. J Pain 2003; 4:511–519.

32. Koppert W, Alsheimer M, Sittl R, et al. Remifentanil-induced hyperalgesia in new human pain model. Anesthesiology 2001; 95:A861.

Craig D. Is the word ‘narcotic’ appropriate in patient care? J Pain Palliative Care Pharmacother 2006; 20:33–34.

33. Petersen KL, Jones B, Segredo V, et al. Effect of remifentanil on pain and secondary hyperalgesia associated with the heat-capsaicin sensitization model in healthy volunteers. Anesthesiology 2001; 94(1):15–20.

Dalman FC, O’Malley KL, Opioid tolerance and dependence in cultures of dopaminergic midbrain neurons. J Neurosci 1999; 19(14):5750–5757.

34. McQuay HJ, Bullingham RE, Moore RA. Acute opiate tolerance in man. Life Sci 1981; 28(22):2513–2517.

Daniell H. Hypogonadism in men consuming sustained-action oral opioids. Pain Med 2002; 3:377–384.

35. Chia YT, Liu K, Wang JJ, et al. Intraoperative high dose fentanyl induces postoperative fentanyl tolerance. Can J Anaesth 1999; 46:872–877.

Fanciullo G, Ball P, Giralut G, et al. An observational study of the prevalence and pattern of opioid use in 25,479 patients with spine and radicular pain. Spine 2002; 27:201–205.

36. Guignard B, Bossard AE, Coste C, et al. Acute opioid tolerance: intraoperative remifentanil increases postoperative pain and morphine requirement. Anesthesiology 2000; 93:409–417.

Federation of State Medical Boards of the United States, Inc. Model policy for the use of controlled substances for the treatment of pain. 2004. Online Available: http://www.fsmb.org/pdf/2004_grpol_Controlled_Substances.pdf

37. Liaison Committee on Pain and Addiction. Definitions related to the use of opioids for the treatment of pain. 2001: www.ampainsoc.org/advocacy/opioids2.htm

Finch PM, Roberts LJ, Price L, et al. Hypogonadism in patients treated with intrathecal morphine. Clin J Pain 2000; 16:251–254.

38. Medical Board of California. Guidelines for prescribing controlled substances for pain (revised). Action Report: Medical Board of California 2003; 87:1–4.

Gallagher R, Welz-Bosna M, Gammaitoni A. Assessment of dosing frequency of sustained release opioid preparations in patients with chronic nonmalignant pain. Pain Med 2007; 8:71–74.

39. McNicol E, Horowicz-Mehler N, Fisk RA, et al. Management of opioid side effects in cancer-related and chronic noncancer pain: a systematic review. J Pain 2003; 4:231–256. 40. Webster L, Andrews M, Stoddard G. Modafinil treatment of opioid-induced sedation. Pain Med 2003; 4:135–140.

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41. Tassain V, Attal N, Fletcher D, et al. Long term effects of oral sustained release morphine on neuropsychological performance in patients with chronic non-cancer pain. Pain 2003; 104:389–400.

Haddox J, Jordanson D, Angarola R, et al. The use of opioids for the treatment of chronic pain. A consensus statement from the American Academy of Pain Medicine and the American Pain Society. Glenview IL: 1997.

Section 4: Practical Pharmacology Hale ME, Fleisschmann R, Salzman R, et al. Efficacy and safety of controlledrelease versus immediate-release oxycodone: randomized, double-blind evaluation in patients with chronic back pain. Clin J Pain 1999; 15:179–183. Jamison RN, Raymond SA, Slawsby EA, et al. Opioid therapy for chronic noncancer back pain. A randomized prospective study. Spine 1998; 23:2591–2600. Lotsch J, Geisslinger G. Current evidence for a genetic modulation of the response to analgesics. Pain 2006; 121:1–5. MacLaren J, Gross R, Sperry J, et al. Opioid use and functional restoration. Clin J Pain 2006; 22:392–398. Maier C, Hildebrandt J, Klinger R, et al. Morphine responsiveness, efficacy and tolerability in patients with chronic non-tumor associated pain – results of a double-blind placebo-controlled trial. Pain 2002; 97:223–233.

Novak S, Nemeth W, Lawson K. Trends in medical use and abuse of sustainedrelease opioid analgesics: a revisit. Pain Med 2004; 5:59–65. Portenoy RK. In: Fields HL, Liebeskind JC,eds. Pharmacological approaches to the treatment of chronic pain. Seattle, WA: IASP Press; 1994. Portenoy R, Foley K. Chronic use of opioid analgesics in non-malignant pain: report of 38 cases. Pain 1986; 25:171–186. Rashiq S, Koller M, Haykowsky M, et al. The effect of opioid analgesia on exercise test performance in chronic low back pain. Pain 2003; 106:119–125. Rowbotham M, Twilling L, Davies P, et al. Oral opioid therapy for chronic peripheral and central neuropath pain. N Engl J Med 2003; 348:1223–1232. Schofferman J. Long-term opioid analgesic therapy for severe refractory lumbar spine pain. Clin J Pain 1999; 15:136–140.

Marcus D, Glick R. Sustained-release oxycodone dosing survey of chronic pain patients. Clin J Pain 2004; 30:363–366.

Vogt M, Kwoh K, Dope D, et al. Analgesic usage for low back pain: impact on health care costs and service use. Spine 2005; 30:1075–1081.

Miyoshi H, Leckband S. Systemic opioid analgesics. In: Loeser J, Butler S, Chapman C, et al., eds. Bonica’s management of pain. New York: Lippincott Williams & Wilkins; 2001:1682–1709.

Woolf CJ. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med 2004; 140(6):441–451.

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PART 1

GENERAL PRINCIPLES

Section 4

Practical Pharmacology

CHAPTER

The Diagnosis and Treatment of Anxiety Disorders in Chronic Spinal Pain

15

Carlos F. Tirado and Rollin M. Gallagher INTRODUCTION Patients with chronic painful spine conditions are anxious, and for good reason. Uncertain about the cause and eventual outcome of their spine disease or spinal injury, they may worry about the consequences to their own and their families’ well being. Can they work and maintain their financial solvency? Will the stress of pain and disability interfere with their recreational activities and their important relationships such as families, coworkers, friends, and particularly spouses, including their ability to be sexually active and emotionally intimate? Will they become more depressed? Which of the many treatment options should they pursue and will they have access to the best treatment for their condition? This situational anxiety often worsens pain or contributes to morbidity and poor treatment outcomes. Uncertainty in the healthcare system also contributes to patient anxiety, both directly and indirectly. Despite advances in diagnostic and therapeutic spine medicine, which creates hope and relief for many with spine pain, healthcare systems are notoriously unable to adequately manage chronic spine pain, for several reasons. ●

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High rates of spinal injury. These high rates and their high costs to society persist in our culture because for every preventive innovation, such as ergonomics in the workplace and seatbelts in cars, mankind inevitably finds new ways to injure the spine at war, at work, and at play. Unavailable chronic disease management. Unless offending spine pathology is clearly identified and its treatment straightforward and successful initially, in at least 20% of cases spine pain becomes chronic or recurrent, causing secondary mechanical, emotional, and psychosocial effects that complicate the clinical picture and require a chronic disease management approach. Chronic pain management, which to be successful requires attention to all the biopsychosocial factors affecting pain and its consequences, is beyond the scope of practice of most physicians, most spine treatment centers, and the organizational and financial capacities of many healthcare organizations. The emergence of chronic pain as a disease. When pain and its emotional effects are not controlled, a new neuropathological process, independent of the initial cause of nociception, may lead to the development of pain as a disease of the central nervous system, or ‘maldynia’ (as distinct from ‘eudynia,’ or normal pain), associated with phenomena such as central sensitization, mood disorder and kindling. These cases require sophisticated and intensive management by a comprehensive pain medicine center, generally not available to the public. Dysfunction in the present healthcare delivery system. As suggested, a final factor perpetuating the uncertainty in the management of spine pain relates to the structure and function of

today’s healthcare system. The present system is not governed by principles of optimal clinical care demonstrated by longitudinal evidence of functional recovery, but rather by business principles such as income generation and short-term expenditure reduction. Adhering to these principles has several effects: (1) over-use of well-reimbursed procedures that may have minimal if any scientific support of efficacy; (2) restricted access to comprehensive rehabilitative care; (3) cost shifting from the private sector to the public through underfunding disability recovery programs; and, (4) the subsequent high use of emergency room care by uninsured patients. To maintain economic viability, pain treatment centers must emphasize well-reimbursed procedures while de-emphasizing time-consuming chronic disease management approaches that are poorly reimbursed, and thus not available, even for Americans with excellent insurance. The calculus is clear – even when an intervention temporarily remediates pain in 40–60% of cases, if additional perpetuating causes are not remediated, outcomes will be suboptimal. Most patients require chronic disease management of varying intensity, ranging from simple ergonomic instructions and life-style changes, such as exercise and weight management, to sophisticated, integrated multimodality care that includes psychological, pharmacological, and physical therapies. Formulas for the economically viable management of this entire disease continuum are not yet established in our current healthcare system. A central feature of any dysfunctional system is the uncertainty and anxiety of its constituents; just ask the investment business. As mentioned earlier, persons with spinal pain with or without its complications is uncertain about their own and their family’s future. The physician treating pain is uncertain as to how to proceed with treatment once initial treatment has failed and how to maintain a financially viable practice in the face of nonreimbursement of timeconsuming office visits and phone calls from patients with chronic pain. The policy-makers and operatives of the governmental agencies and third parties funding the healthcare system, beset with competing interests and responsible for the economic viability of their portion of the healthcare system, are uncertain about the most effective strategies and policies. Their reflex is to discourage innovation in hopes of reducing expenditures. This chapter will review principles of managing the problem of fear and anxiety in patients with spinal pain in the context of this insecure and anxiety-provoking healthcare environment.

ORIGIN AND DEFINITION OF THE MODERN CONCEPT OF ANXIETY The concept of anxiety as an emotional experience distinct from fear is a relatively modern notion with its origins in the works of

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Sigmund Freud. It is interesting historical trivia that the German word for fear, ‘angst’ was inappropriately translated in some of Freud’s work to the subtly different word, ‘anxiety.’1 Although Freud made no distinction between fear and anxiety in his writings, this linguistic accident helped create a distinction between the concepts of fear and anxiety.1 This distinction, especially in relation to chronic anxiety disorders, has held up to scientific scrutiny. Fear, broadly defined, is a complex emotional and physical response to an actual threat (i.e. response to a physical attack.) Anxiety, by contrast, is a complex emotional and physical response to a perceived threat (i.e. believing an attack is imminent). Both fear and its analog, anxiety, are responses to stress that, when functioning properly, are adaptive and necessary for survival. It is when the physical and emotional sequelae of fear and anxiety are excessive in relation to their context, or when they lead to a state of chronic incapacity and loss of function, that they become a cause for clinical concern. As outlined above, chronic pain creates many situations that may provoke fear or anxiety. Acute fear in a perceived dangerous situation has the effect of modulating pain sensation to enable successful fight-or-flight reactions. In the patient with chronic pain, the role that fear and chronic anxiety has in the maintenance and exacerbation of their symptoms cannot be underestimated. The common physical symptoms of anxiety, such as muscular tension, hyperarousal, insomnia, palpitations, and poorly localized pain, often confound a patient’s primary medical or surgical pain complaint. Anxiety, through activation of the noradrenergic system in the locus coeruleus, has both peripheral and central effects on pain perception in persons with nociceptive, neuropathic and visceral pain conditions, as listed in Table 15.1. Add to this the psychological symptoms associated with anxiety (worry, apprehension, irritability, poor concentration, overinterpretation of symptoms) along with the effects of anxiety on illness behavior, including presentation of pain complaints and compliance with treatment regimens, and the complexity of treating a patient with chronic pain with acute or chronic anxiety becomes obvious. Before moving to a discussion of the treatments for acute and chronic anxiety, it is necessary to briefly describe in more detail the neuroanatomical and biological correlates of fear, anxiety, and pain so we may better understand how they are interrelated.

THE BIOLOGICAL BASIS OF FEAR AND ANXIETY The biological and anatomical substrates of fear as a trigger for a fightor-flight response are ancient. Countless behavioral experiments have established that nearly every species, from snails to humans, can develop a conditioned fear response to noxious stimulus. By contrast, chronic anxiety, because of its anticipatory nature, requires a greater degree of biological processing capacity. Humans, with a near infinite capacity to perceive and anticipate threat, are exquisitely equipped to experience anxiety. Figure 15.1 is a conceptual rendition of the basic neuroanatomical components of fear. The connections between these structures are much more complex than the pathways depicted in this illustration, but they provide a general idea of how these anatomical structures communicate and synthesize environmental, emotional, and learned stimuli. The spatial relationship of the brain regions depicted in this illustration is generally analogous to their location in the human brain. Figure 15.1 highlights the crucial role the amygdala plays in the fear response. It is essentially the central processor of fear. The amygdala receives and transmits information from the external world (via the thalamus, ventral tegmental area, and reticular formation). It merges this information with our memory, senses, executive functions, endocrine and musculoskeletal systems (via the hippocampus, sensory/motor cortex, association cortex, hypothalamus and brainstem) to elicit a complex emotional and behavioral response. In humans, the amygdala is thought to be essential for the recognition of threatening environmental cues and modulation of the emotional response to them. Neuroimaging experiments of normal human brains show that the amygdala is important in our ability to recognize and respond to threatening stimuli in the form of disturbing faces, gestures, and scenes that evoke fear.2,3 This basic finding corresponds to the deficits observed in persons with surgical destruction of the amygdala and children with autism. In both cases, there is an enormous deficit in the individual’s ability to accurately identify and respond to fear-evoking stimuli.4,5 Other experiments have suggested the amygdala also plays an important role in the development of chronic anxiety and pain.

Table 15.1: Effects of Anxiety on Pain Conditions and Disorders Condition

Physiologic Effect of Anxiety

Consequences for Pain

Nociceptive pain

Sympathetic nervous system activation (1) lowering threshold for nociceptor activation (2) activation of efferent motor neurons

Higher pain levels Increased sensitivity to pain stimuli Muscle spasm

Neuropathic pain

Sympathetic nervous system activation

Acute activation of pain in response to stressful circumstances Increase in spontaneous neuronal firing with worsening pain

(1) Activation of sodium channels in primary pain neurons and polymodal sensory neurons recruited to pain. (2) Recruitment of inflammatory cells to injured neurons Visceral pain

Sympathetic nervous system activation

Stimulation of visceral plexuses with secondary pain effects such as activation of bowel in irritable bowel and bladder irritation in interstitial cystitis

Central pain

Activation of noradrenergic projections to brain centers of pain suffering and mood dyscontrol

Reduced descending modulatory control of ascending pain signal. Conditioned activation of pain suffering Reduced distraction-based modulation of pain

Interference with task-oriented concentration

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Increase in spontaneous neuronal firing with worsening pain

Section 4: Practical Pharmacology Input Emotional stimulus

Nociceptive stimulus

Associative stimulus

Structures and function: CNA = Central nucleus of the amygdala. [controls ouput from the amygdala to all other structures in the circuit]

Hippocampus

Hypo = Hypothalamus [sympathetic and parasympathetic activation involved in physical fight/flight response]

Thalamus

Association cortex CNA

VTA Brainstem

Amygdala

Sensory cortex

VTA = Ventral tegmental area. [Dopamine ñ reward system important for reinforcement of learned behavior. Role in addiction] RF = Reticular formation [norepinephrine and serotonin ouput to amygdala. Important role in modulation of amygdala activity]

RF

Hypo

Thalamus: Principle conduit of information to amygdala from the environment. Hippocampus: Provides input of stored memory to moderate response to fear. Output

Emotional • Fear/anxiety • Sense of pleasure

Physical • Para/sympathetic activation • Motor activation (fight/flight) • Pleasure seeking/avoidance

Cortex: Sends sensory and abstract associative information to amygdala and helps consolidate memory in hippocampus.

Fig. 15.1 The circuitry of fear.

One study has found that activation of the basolateral nucleus of the amygdala causes the emotional experience of anxiety without a corresponding increase in heart rate (which is controlled by the hypothalamus via a separate pathway).6 There is growing evidence that the amygdala plays a crucial role in the up- or downregulation of the emotional response to pain and that this ‘nociceptive amygdala’ can be influenced by a wide range of environmental and internal stimuli to modulate the subjective experience of pain.7 The hippocampus, a structure with robust connections to the amygdala, is a center for memory formation, storage, and retrieval. It provides information from detailed memories that are processed by the amygdala and given a particular emotional value. The emotional value the amygdala places on a particular memory is then fed back to the hippocampus, where it integrates this information and either strengthens or weakens the memory. This is why it is believed that events associated with high emotional content (a car accident, being wounded in battle, one’s first kiss) tend to be remembered in greater detail than those with little emotional significance (the drive to work every morning). In persons with bilateral destruction of the hippocampus secondary to herpes encephalitis, there is a preservation of memory related to processes (such as tying shoes, using a fork), but a deficit in memory related to particular events, persons, and experiences along with mood problems.8,9 In persons with post-traumatic stress disorder (PTSD), changes are seen in the amygdala, hippocampus, and other areas of the limbic system (the neural circuits of complex emotional experience). Neuroimaging studies have found consistent reductions in either total hippocampal volume or blood flow in men and women with PTSD.10–13 The primary function of the hypothalamus is to regulate the body’s homeostatic and endocrine systems. In relation to the fear response, the hypothalamus sends projections to the medulla which controls

autonomic (fight-or-flight) functions such as heart rate, muscle tone, digestion, sweating, etc.14 With input from the amygdala, the hypothalamus contributes the hormonal and autonomic component of the fear response. The ventral tegmental area (VTA) and reticular formation (RF) are brainstem structures with projections throughout the brain. These structures are rich in dopaminergic (VTA), noradrenergic (locus coeruleus), and serotinergic (raphe nuclei) neurons. The role of neurotransmitters will be discussed in greater detail later in this chapter. Research on other structures within this fear circuit has expanded our understanding of how the cortical structures influence the amygdala. Human brain imaging studies have found that the fusiform gyrus, prefrontal, and anterior cingulate gyrus are preferentially activated in response to fearful stimuli.3,15 The orbitofrontal cortex (OFC), which is involved in the evaluation of risk and reward and social norms, may also have a direct role in regulation of anxiety via its connection to the amygdala (Fig. 15.2).16 The cortex, then, plays an essential role in the categorization, appraisal, and attenuation of our reactions to fearful stimuli. The higher cortical connections to the more primitive fight, flight, and reward circuitry is what allows humans to have a degree of conscious recognition and control over these processes. These connections and their conditioning form the biological basis for the effects of behavioral training used widely in the treatment of pain, such as relaxation and biofeedback. More recent functional brain chemistry research has provided neuroanatomical evidence for the overlap between the processing and perception of pain and anxiety. In an experiment comparing patients with chronic low back pain (CLBP) to normal controls, significant differences were found in two regions of the association cortex (orbitofrontal [OFC] and dorsolateral prefrontal cortex [DLPFC]), 175

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Lateral ventricle

the amygdala and hippocampus are the areas in which the reward circuit influences the emotional and memory-forming structures in the brain. The VTA is also regulated by the amino acid neurotransmitter GABA (γ-aminobutyric acid) and opioid peptide neurotransmitters (enkephalins, endorphins). This convergence of GABAergic and opioid peptide receptors with the dopaminergic neurons of the VTA may be an important pathway in the development of benzodiazepine and opiate addiction.

Corpus callosum

Serotonin and norepinephrine

The central nervous system processes pain information and modulates pain responses through descending pain pathways

Cortex Inferior horn of lateral ventricle

Thalamus Amygdala Hypothalamus

Medulla

− NE 5-HT

Serotonin (5-HT) and norepinephrine (NE) are key modulatory transmitters in the descending inhibitory pathways and are part of the body’s endogenous analgesic system

Nociceptors Fig. 15.2 Serotonin (5-HT) and norepinephrine inhibit painful physical symptoms.

cingulate gyrus (part of the limbic system), and thalamus.17 The study showed that persons with CLBP have differences in regional brain chemistry in the OFC and DLPFC when comparing their perception of pain. Additionally, persons with CLBP and anxiety had changes in brain chemistry suggesting increased interaction between all four brain regions, whereas anxious controls only had changes observed in the OFC. Anxiety and pain, therefore, share common neurochemical pathways and can interact in a way that leads to the reorganization of normal perceptual pathways in the brain.

Role of neurotransmitters Well over 300 different chemicals have been identified as ‘neurotransmitters.’ Endogenous neurotransmitters are broadly defined as chemicals synthesized in neurons, released in response to electrical impulses and acting on other neurons to cause changes in their electrochemical properties.17 There are three major classes of neurotransmitters: biogenic amines, amino acids and peptides. All three classes are relevant to our discussion, but we will limit our discussion to the biogenic amine and amino acid neurotransmitters because they are most relevant to the topic of anxiety. The major biogenic amines acting within the fear circuit are dopamine (DA), serotonin (5-HT) and norepinephrine (NE).

Biogenic amines Dopamine The VTA sends dopaminergic projections throughout the brain. The VTA is primarily associated with reward and its connections with the nucleus accumbens are believed to be at the heart of the reinforcing effects of drugs of abuse.18 The VTA’s dopaminergic projections to 176

The cell bodies of 5-HT and NE neurons are located in the dorsal raphe nuclei and locus ceruleus, respectively. Like the DA neurons of the VTA, the 5-HT and NE neurons have diffuse projections throughout the brain. Drugs such as tricyclic antidepressants (TCAs), and selective serotonin reuptake inhibitors (SSRIs) have been used to treat mood disorders for the last several decades. Although the exact mechanism of how these drugs act to produce therapeutic efficacy is unknown, the central role of 5-HT and NE in chronic mood disorders (especially major depression and anxiety disorders) is strongly supported by the weight of controlled trials supporting the efficacy of drugs that act directly on these neurotransmitter systems. There is a growing body of research that supports the role of 5HT in modulating the amygdala and other limbic structures in persons with chronic anxiety disorders. Specifically, the SSRI drug paroxetine (Paxil) has been associated with a reduction of amygdala volume in persons with obsessive compulsive disorder (OCD), an anxiety disorder believed to be associated with a hyperactive amygdala.19 Conversely, in persons with PTSD, increases in hippocampal volume are positively associated with paroxetine treatment.20 A study examining the effects of tryptophan (the dietary amino acid precursor of 5-HT) depletion found decreases in the ability to recognize fear-related cues.21 Allelic variations in amygdalar 5-HT transporter proteins have also been found to correlate with individual responses to fear-related cues.22 Severe acute pain activates stressrelated noradrenergic systems in the brain. Descending projections to the sympathetic nervous system may cause increased firing of pain neurons through several mechanisms as well as nociceptor activation and muscle tension and spasm. Ascending noradrenergic projections to the forebrain cause cognitive–emotional reactions, such as fear and anxiety, which to some degree are contextually determined. For example, pain in childbirth often does not evoke fear or anxiety, whereas pain in traumatic spinal and/or limb injury, with uncertain outcome, often does. The association of pain, anxiety, and depression may have a common neurochemical substrate in the serotonergic systems.

Amino acids Glycine and GABA are amino acid neurotransmitters. Glycine is known as the primary excitatory neurotransmitter in the brain. GABA is the primary inhibitory neurotransmitter in the brain. Together, glycine and GABA are the most common endogenous neurotransmitters and 75–90% of all neurons in the CNS have glycine and GABA receptors.17 A thorough discussion of the biology of glycine and GABA is beyond the scope of this chapter. However, it is important to discuss the basic biology of GABA in the context of this chapter because of its central role in the action of benzodiazepines.

GABA As mentioned previously, GABA is the primary inhibitory neurotransmitter in the CNS. It is estimated that 30% of all CNS synapses use GABA as a neurotransmitter and it is found in very high concentra-

Section 4: Practical Pharmacology GABA site Agonist: muscimol Antagonist: bicuculine

α

Benzodiazepine site Agonists: diazepam, many others Inverse agonist: β-carboline Antagonist: flumazenil

γ

β

Cl–

α

β Channel site(s) Inhibits channel activity: picrotoxin Facilitates channel activity: barbiturates Fig. 15.3 Subunit structure and pharmacology of the GABAA receptor.

tions in CNS tissues (1000 to 1 000 000 times greater than concentrations of biogenic amines).23 The synaptic receptor for GABA is composed of two major receptor subtypes known as the GABAA and GABAB receptors. All benzodiazepines work at the GABAA receptor. Rather than occupying the entire GABA receptor as a competitive agonist (like morphine’s action at the opioid receptor), benzodiazepines bind to the GABAA subunit and actually facilitate endogenous GABA binding at the GABAA receptor. GABAA receptor activation opens chloride ion channels which hyperpolarizes neuronal membranes and inhibits firing (Fig. 15.3).23 This elegant mechanism is believed to be the primary pathway for the anxiolytic effects of benzodiazepines. Psychoactive compounds such as barbiturates and ethanol also act at the GABA receptor to produce similar anxiolytic and CNS depressant effects. In an interesting study of the effects of benzodiazepines in acute pain, Di Piero and colleagues studied cerebral blood flow (CBF) by single photon emission computed tomography (SPECT), with and without diazepam.24 Diazepam, a benzodiazepine, binds to the benzodiazepine receptor on the GABAA receptor site and enhances GABA’s opening of the chloride channel, activating the GABA system and its anxiolytic actions. Diazepam, when given to healthy volunteers, following induction of pain by the cold pressor test (CPT), inhibited activation of the temporal regions, which was interpreted as part of the affective–emotional component of pain response. Diazepam-treated subjects tolerated the pain better and on SPECT this was associated with lack of temporal lobe activation of sensory–discriminative painrelated brain regions (contralateral hand region in the sensory motor cortex, pre-motor cortex and thalamus, and left anterior cingulate gyrus). This activity suggests that diazepam, which is useful in managing acute anxiety, interferes with affective–emotional components of pain perception and modifies temporal lobe activation patterns. The role of benzodiazepines in the treatment of acute and chronic anxiety will be discussed later in this chapter as will issues related to tolerance, dependence, and addiction to these medications.

DIAGNOSIS OF ANXIETY DISORDERS Introduction There are two major national surveys that estimated the prevalence of anxiety disorders in the United States. The Epidemiologic Catchment Area study estimated that 7% of people in the United

States have a clinically significant anxiety disorder.25 The National Comorbidity Study (NCS) reported even higher prevalence rates for anxiety disorders. NCS estimated 12 month prevalence rates of 17.7% for at least one anxiety disorder and lifetime prevalence rates near 25%.1 The majority of persons with anxiety disorders suffer from simple phobias (i.e. needles, insects, heights). The NCS estimated the lifetime prevalence of generalized anxiety disorder (4.1–6.6%), PTSD (1.0–9.3%), panic disorder (2.3–2.7%), and social phobia (2.6– 13.3%). The prevalence of any current psychiatric disorder in one survey of a large city spine clinic was estimated to be 59% and as high as 77% for lifetime prevalence.25 Of those with chronic anxiety disorders, 95% had evidence of a disorder before the onset of back pain.26 This strongly supports the need to carefully screen for anxiety disorders at the time of first intake to a spine clinic and to integrate treatment for anxiety disorders into the comprehensive treatment plan.

Clinical vignette 1: A case of untreated obsessive compulsive disorder Pain medicine is asked to consult on a 38-year-old married disabled healthcare worker hospitalized for recurrent gastric bleeding. She has undergone two surgeries for gastric bleeds and suffers from dumping syndrome. On this admission she requires ice lavages for homeostasis, but avoids a third surgery. She also complains of neck and upper extremity pain which has been persistent since a discectomy for a herniated cervical disc 11 years before, when she suffered terrible pain postoperatively in hospital. Since then she has subsequently engaged in daily compulsive postprandial use of NSAIDs to control pain, starting 1 year prior to cervical spine surgery. She never discussed this behavioral pattern with her physicians. Further evaluation reveals a 15-year history of repetitive ritualized hand washing and housecleaning for hours daily, aggravating radicular and myofascial pain. The diagnoses of obsessive–compulsive disorder (OCD) and secondary major depression are made. OCD requires intensive treatment with SSRIs, cognitive behavioral therapy, and couples therapy over 1 year, with follow-up supportive psychotherapy. The patient stops NSAID abuse and her chronic gastric ulcers gradually heal. She also reduces daily hours of ritualized cleaning, and radiculopathy is now controlled with routine use of gabapentin, long-acting oxycodone, and occasional trigger point injections for myofascial pain. She functions well at home although is unable to return to work. Two years later when she gradually develops progressive symptoms and signs of cervical myelopathy, an MRI is recommended. The patient is frightened that an MRI will lead to surgery, and avoids this for 6 months. Finally, she agrees to premedication with clonazepam for 3 days, and accompanied by the pain management nurse, whom she likes and trusts, successfully completes the MRI which reveals cord compression. Surgical decompression and fusion is recommended; however, terrified of the prospect of another surgery, which recalls the terrible postoperative pain of her first surgery, she refuses to consider surgery as an option. This case illustrates post-traumatic phobic anxiety complicating poorly managed acute postoperative pain as well as, the activation of a premorbid anxiety disorder, in this case OCD, with almost fatal consequences. Furthermore, her long history of undiagnosed and untreated ritualized hand washing and housecleaning caused by OCD certainly worsened cervical radiculopathy. Now, her residual phobic anxiety, resulting from poorly managed postoperative pain years ago,

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causes her to refuse consideration of needed spine surgery. This is a case in which appropriate postoperative pain pharmacotherapy and early screening and diagnosis for a chronic anxiety disorder might have prevented such an outcome.

Evaluation of clinical anxiety The DSM IV-TR lists the following anxiety disorders: panic disorder with or without agoraphobia, agoraphobia without history of panic disorder, specific and social phobias, obsessive–compulsive disorder, post-traumatic stress disorder, acute stress disorder, generalized anxiety disorder, anxiety disorder due to general medical condition, substance-induced anxiety disorders, and anxiety disorders not otherwise classified. Going through this list of anxiety disorders, it is easy to imagine how these disorders can complicate a pain disorder and vice versa. Table 15.2 lists major anxiety disorders recognized in DSM IVTR along with questions that can help a clinician screen for anxiety disorders. An affirmative answer to these questions should prompt a clinician to obtain further history, treat, or prompt a referral to a mental health professional. The assessment of anxiety should include a detailed medical, and selective physical and laboratory examination, and a history to

exclude other medical conditions which can present with anxiety. Medical conditions that can present with symptoms of anxiety include neurological disorders (cerebral neoplasm, CVA), systemic conditions (hypoxia, hypoglycemia, cardiac arrhythmias, anemia) endocrine disturbances (thyroid, pituitary, parathyroid) and deficiency states (B12, pellagra). In addition, it is also important to rule out anxiety secondary to medication effects or withdrawal, toxins, and psychoactive substance abuse. A common phenomenon is rebound pain and anxiety, which occurs when a patient with pain disorder takes shortacting analgesics frequently during the day, in the case of headache, often called ‘transform’ headache. In patients with pain disorders, the physician must be alert to several situations that commonly precipitate anxiety: increases in pain; threat of withdrawal of workers’ compensation benefits; threat of job loss; threat of marital discord or even spousal desertion caused by the stress of pain and disability; fear of surgery; fear of worsening disease, particularly when increasing or new pain may indicate cancer recurrence or spread; withdrawal from medications that are abruptly stopped, including opioids, antidepressants, anticonvulsants, sedatives and benzodiazepines; withdrawal from alcohol; stimulant intoxication; side effects of certain medications, such as SSRIs, tricyclics, and theophylline derivatives used for asthma; and drug–drug interactions, such as serotonin syndrome.27

Table 15.2: Screening Questions for Common Anxiety Disorders Panic disorder with and without agoraphobia ‘Do you ever have panic attacks?’ ‘Do you ever get attacks where you suddenly feel terrified or like you are about to die?” ’ ‘Do you ever suddenly feel overwhelmed to the point where you become physically ill?’ ‘Do you ever feel afraid to go out of the house because you are worried about becoming overwhelmed or having an attack in front of people?’ Generalized anxiety disorder ‘Are you a chronic worrier?’ ‘Do you worry about things you really can’t control?’ ‘When you worry, do you get physically ill or uncomfortable?’ Obsessive–compulsive disorder ‘Do you worry excessively about: being dirty or contaminated with germs? doing certain things exactly the same way?’ ‘Do you feel like you have to do certain things over and over again, such as: wash your hands, shower? count or check things? say certain words?’ ‘Is it hard to stop thinking about (obsessive thought)?’ ‘Is it hard to keep yourself from (compulsive behavior)?’ Post-traumatic stress disorder ‘Have you ever been in a situation where you, or someone close to you, was almost killed, injured, or threatened in a way that caused you to feel terrified or extremely emotional?’ Some experiences to ask about: sexual trauma combat experience witnessing death and destruction physical assault ‘Do you feel like you’ve never quite gotten over (traumatic event)?’ ‘Did you ever feel back to normal after you experienced (traumatic event)?’ ‘Do you have dreams or disturbing thoughts about (traumatic event)?’ Specific phobia ‘Are there any specific things such as animals, insects, needles, and heights that make you very nervous?’ ‘Do you think your fear is more than normal?’ ‘If were faced with it right now, do you think you could handle it?’

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INTRODUCTION AND GENERAL PRINCIPLES OF THE TREATMENT OF ANXIETY DISORDERS General principles of biobehavioral medication use in chronic pain The successful use of medications in chronic spine pain depends upon careful clinical reasoning, founded upon a working knowledge of the phenomenology and physiology of pain syndromes and anxiety disorders and the ability to assess how anxiety and pain interact in any one patient, to cause and perpetuate pain and functional disability. In any patient with spine disease, anxiety can: ● ● ●

Activate neuropathic pain and muscle pain; Interfere with concentration and effective coping strategies; Precipitate maladaptive coping such as poor decision-making, task avoidance, misuse of medications, or drug abuse.

To minimize the effects of anxiety on patients with chronic pain, physicians should routinely give patients behavioral tools for selfcare and symptom management.28 Simple behavioral interventions, such as asking a patient to keep a diary and handing them a relaxation tape with instructions for daily use, take little time and may pay large benefits. Diaries give the physician important information about the pattern of pain and anxiety over each 24 hour period – factors such as activities that increase the pain or anxiety, or factors such as medication or activity avoidance that prevent escalations of anxiety and pain. The effects of new medications against baseline anxiety and pain scores can document effectiveness more robustly than questions such as, ‘How effective is the medication?,’ which may lead to information subject to recall bias, and does not provide the detail needed for effective treatment decisions. Relaxation tapes help patients restore control over emotions in response to pain or to stress that activates neuropathic pain and also helps them relax muscle groups. When patients become disabled by chronic pain, to counter the impact of emotional factors, such as anxiety, and negative conditioning, comprehensive integrated, biobehavioral pain rehabilitation programs are more effective than both conventional medical treatment or ‘alternative’ therapies,29 for example, returning low back pain patients to work at a rate that is about 40% higher than conventional treatment.30 The ability to orchestrate constructively the complex network of supportive relationships necessary to rehabilitate these patients is essential. Skills in pain and stress management, such as pharmacology and behavioral pharmacology, group therapy and psychotherapy, greatly complement the skills of the rest of the team. Pain management training, usually taking place in behavioral educational groups, complemented as needed by individual psychotherapies, is effective in chronic pain patients and can reduce medical visits and costs.31 The sequence of tasks in such a group work in conjunction with physical rehabilitation and pharmacotherapy to enable helpless-feeling, functionally impaired patients to develop a sense of control over their pain, their fear of activity and their anxiety.28,32

Psychotherapy for anxiety disorders Empathic listening and reassurance are the cornerstones of therapy for acute and chronic anxiety disorders. In addition to, or instead of, medication, talk therapies such as cognitive behavioral therapy (CBT) have proven efficacy in the treatment of panic disorder, PTSD, and social anxiety disorder. Behavioral therapies such as progressive relaxation, meditation, proper sleep hygiene, and exercise

also have been shown to improve depression and anxiety. Specific phobias (i.e. needle or other medical procedure phobias) respond very well to CBT that emphasizes graduated exposure to the fearful stimulus in a controlled environment. It is important to consider that severe forms of OCD, PTSD, panic disorder, and specific phobias may be so incapacitating that psychological and behavioral therapies, applied over a significant period of time, may be required in addition to medication. The principles of CBT for anxiety and pain are similar, in that the practitioner focuses on helping the patient learn specific cognitive and behavioral coping skills to prevent, abort, or ameliorate symptoms – in this case, anxiety. In panic disorder, cognitive therapy challenges false beliefs and information about panic attacks and is used in conjunction with respiratory training, applied relaxation, and in vivo exposure and response prevention. In OCD, behavior therapy may be as effective as pharmacotherapy, with some suggestion that the beneficial effects are longer lasting, and together they are more effective than either alone. The principle behavioral approaches in OCD are exposure and response prevention. Desensitization, thought stopping, flooding, and aversive conditioning have also been used.

Clinical vignette 2: A man with chronic low back pain Pain medicine is asked to evaluate a 36-year-old man for opioid pharmacotherapy after he continues to report back pain unresponsive to NSAIDs and a brief trial of gabapentin. The patient’s symptoms worsened dramatically after he received the results of his MRI report. At the time of his initial pain clinic assessment, the patient, obviously anxious and sullen, reported little hope for a return to his previous level of functioning saying, ‘I’m going to wind up in a wheelchair by the time I’m fifty.’ When asked to say how he came to this conclusion, the patient reported, ‘The MRI, it says I have “degenerative changes” and my doctor told me it’s worse than what I had 3 years ago.’ After the patient was allowed to discuss his thoughts and fears about this, he was asked if he’d like to just go over the results of his MRI report again, this time with the opportunity to ask questions about the report. The patient was clearly preoccupied with the terms ‘degenerative’ and ‘arthropathy’ and took them to mean that he suffered from a severe, incurable skeletal disease that would leave him permanently disabled, well before his time. After a simple explanation of the medical jargon on the report and what the spine of a person his age looks like, the patient was able to realize that, in fact, the results of his MRI were within the normal limits for his age and amount of physical activity. Further questioning revealed that he was in a major depressive episode, was having occasional panic attacks, and was coping with the stress of his wife, who was going through chemotherapy for ovarian cancer. The patient was started on an SSRI and a 1-week trial of clonazepam 1 mg b.i.d. with excellent results, and no initiation of opioids. The patient also self-initiated an at home exercise program and reported 75% improvement in his pain after 2 weeks. This case clearly indicates how easily a communication gap between a patient and treating physician can quickly turn into a therapeutic chasm. The only ‘interventions’ in this case were 30 minutes of empathic listening, reassurance, and demystification of medical jargon, which led to three things: (1) richer understanding of the social and psychological irritants of the patient’s low back pain, (2) diagnosis and treatment of a mood and anxiety disorder, and (3) empowering the patient to take control of his rehabilitation. 179

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Pharmacologic treatment of anxiety disorders Anxiolytics for acute anxiety Table 15.3 provides a list of medications that are commonly used to relieve acute anxiety. When trying to find a medication that is well suited for the purpose of relieving acute anxiety, the time of onset of peak anxiolytic effect is most important, and sometimes not at all related to the elimination half-life of the drug. For example, diazepam has a very long elimination half-life, but a peak anxiolytic effect on par with, or even superior to, alprazolam.

Benzodiazepines The basic biology of benzodiazepines described previously in this chapter makes them excellent anxiolytic medications. By increasing the activity of CNS GABA, benzodiazepines can exert powerful tonic inhibition of the entire CNS and therefore control hyperexcitable states such as seizure, acute psychosis, mania, anxiety, and panic. Their action as a hypnotic–amnestic compound also makes them very

useful for uncomfortable or confining procedures such as spinal injections, MRI scans, etc. Since most benzodiazepines go through extensive hepatic metabolism and have many pharmacologically active metabolites, repetitive use of long-acting benzodiazepines in the elderly or in persons with hepatic disease should be avoided. Alprazolam, lorazepam and oxazepam undergo less hepatic metabolism and therefore are preferred in these patients. Overall, benzodiazepines have an excellent side effect profile compared to other anxiolytic medications. Sedation, ataxia, and cognitive changes are the principal adverse effects associated with benzodiazepine use. Sedation can occur with variable intensity in persons on the same dose of a benzodiazepine, so it is important to vary dosage according to individual tolerability. In the elderly, ataxia associated with benzodiazepine intoxication is a major clinical concern because of the risk of falls and fractures. Persons should also be warned about using benzodiazepines when driving or operating heavy machinery. The cognitive side effects of benzodiazepines include anterograde amnesia, cognitive slowing, and mental confusion. Again, elderly patients and patients early in the course of treatment are most

Table 15.3: Oral Medications for Acute Anxiety CLASS

Generic Name

Brand Name

Usual Adult Dosage (mg)

Peak Anxiolytic Effect*

Elimination Half-life (h)**

Comments:

Alprazolam

Xanax

1–6

Rapid

6–20

Good rapid anxiolytic. High abuse potential with chronic use.

Triazolam

Halcion

0.125–0.25

Intermediate

1.5–5

Mostly limited to brief treatment for insomnia. Associated with anterograde amnesia.

Temazepam

Restoril

7.5–30

Intermediate

8–20

Less hepatic metabolism. Commonly used as a hypnotic.

Benzodiazepine

Clorazepate

Tranxene

15–60

Rapid

30–200

Lorazepam

Ativan

1–6

Intermediate

10–20

Less hepatic metabolism. Widely used in hospital setting.

Oxazepam

Serax

30–120

Intermediate

8–12

Less hepatic metabolism. Good choice for detox in persons with hepatic DZ.

Clonazepam

Klonipin

1–6

Intermediate

18–50

High-potency, long-acting alternative to Alprazolam. Not as good for acute anxiety.

Diazepam

Valium

4–40

Very rapid

30–100

Excellent as rapid anxiolytic. Many active metabolites.

Chlordiazepoxide

Librium

10–150

Intermediate

30–100

Many active metabolites.

Hydroxyzine HCl

Atarax

25–100

Rapid

7–20

Favored by some for treatment of acute anxiety in known substance abusers.

Hydroxyzine pamoate

Vistaril

25–100

Rapid

7–20

Favored by some for treatment of acute anxiety in known substance abusers.

β blocker

Propranolol

Inderal

10–40

Rapid

3–6

Of some use for anticipatory and performance anxiety.

α blocker

Clonidine

Catapres

0.1–0.2

Rapid

9

Use as anxiolytic is limited. Orthostasis is a common problem. Used in opioid withdrawal.

Antihistamine

Adrenergic

180

Section 4: Practical Pharmacology

at risk. Mental confusion is seen usually as the result of an overdose (either intentional or accidental) or from the build-up of long-acting metabolites (i.e. from chronic administration of diazepam or chlordiazepoxide). In the context of spine rehabilitation, chronic use of benzodiazepines may inhibit the learning of new coping skills.

Antihistamines Atarax and Vistaril are two formulations of hydroxyzine that are effective as acute anxiolytics. They are H1 antagonists and their use as anxiolytics comes primarily as a byproduct of their sedative side effects. In clinical practice, hydroxyzine is commonly given as a prn anxiolytic to patients as an alternative to benzodiazepines. Atarax is also indicated for the symptomatic treatment of alcohol withdrawal with or without benzodiazepines. Unfortunately, tolerance to the sedating and anxiolytic effects is common, so their use for chronic anxiety is limited. Like all H1 antagonists, they are also associated with occasional hypotension, dizziness, and anticholinergic side effects (dry mouth, urinary retention, constipation) that are usually mild, but can be severe or fatal in overdose. Because of their sedating and anticholinergic properties, they should be used with caution in elderly patients.

Adrenergic drugs The β blocker propranolol and the α2 agonist clonidine are the most commonly used adrenergic medications for acute anxiety. Both medications have effects on sympathetic and vascular tone and therefore can be used to control states of autonomic arousal modulated by norepinephrine. Propranolol has nearly equal affinity for the β1 and β2 receptors and most of the therapeutic benefit for anxiety is related to β1 blockade at the myocardium. Often, the increase in heart rate and sympathetic tone associated with acute situational stressors (i.e. public speaking), is uncomfortable and can lead to increasing states of sympathetic arousal and even panic in some people. The effect of β1 blockade is to decrease sympathetic stimulation of the heart during periods of acute stress, such as situational or performance anxiety. Propranolol, taken about 20–30 minutes before an anticipated anxiety-provoking event, can be very useful in preventing this sympathetic, anxiousness cascade. It is important to always encourage the patient to try a test dose of propranolol well in advance of their expected anxiety-provoking event, in case there are any unwanted side effects. Because it blocks both β receptors, propranolol can have a variety of cardiac, vascular, metabolic, and pulmonary side effects. The most common side effects associated with propranolol are bradycardia and hypotension. It is generally contraindicated in persons with congestive heart failure, AV node conduction abnormalities, angina, asthma, diabetes, and hyperthyroidism. It has rarely been reported to be associated with depression. Clonidine is an α2 receptor agonist principally used to treat hypertension, but also has some effect controlling sympathetic activation associated with acute opioid, nicotine, alcohol, and benzodiazepine withdrawal. Clonidine has also been used to control agitation and aggression in children and also the acute arousal associated with PTSD. Clonidine acts at the presynaptic α2 receptor to downregulate norepinephrine (NE) activity and thereby decrease sympathetic tone. It has strong effects on peripheral vasculature and therefore is an effective antihypertensive. Acute administration of clonidine can cause severe hypotension, and is therefore not recommended in persons with a blood pressure below 90/60 mmHg. Other side effects associated with clonidine are sedation, dry mucous membranes, constipation, bradycardia, and dizziness. Abrupt discontinuation of clonidine is also associated with a withdrawal syndrome characterized by rebound hypertension, anxiety, tremor, headache, diaphoresis, and

abdominal pain. The risks associated with clonidine withdrawal justify a gradual reduction in dose and counseling patients to avoid skipping doses.

Medications for chronic anxiety disorders Antidepressants Selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs) have important roles in the treatment of chronic anxiety disorders. Only venlafaxine (Effexor) extended-release (XR) has been shown to possess unequivocal efficacy in generalized anxiety disorder (GAD).33,34 Pharmacotherapy of post-traumatic stress disorder includes several antidepressants.35–37 SSRIs protect against PTSD’s overwhelming intensity by modulating affect, memories, and impulses while loosening excessive inhibitions. Fluoxetine, fluvoxamine, sertraline, and paroxetine have all been FDA approved for the treatment of OCD. Higher doses may be necessary, such as fluoxetine 80 mg a day. The best outcomes are obtained when pharmacotherapy and behavior therapy are combined.38 Social phobia responds well to SSRIs and propanalol, a β blocker, can be used preemptively to quell anxiety prior to a performance. For panic disorder, generally, start with an SSRI, such as citalopram, sertraline, or fluoxetine.39 If a rapid control of anxiety symptoms is needed, a short acting benzodiazepine such as lorazepam should be used until the effects of SSRI are felt, keeping in mind the abuse potential and other potential negative effects of prolonged use of benzodiazepines. Once the SSRIs begin working, a benzodiazepine should be tapered and regular use avoided. Medications approved for use in the treatment of chronic anxiety disorders are listed in Table 15.4, starting and maintenance doses of selected anxiolytics are listed in Table 15.5, and side effects of SSRIs are listed in Table 15.6.

Buspirone Buspirone (Buspar) is a unique anxiolytic medication indicated for the treatment of GAD and anxiety related to major depression. It has a mechanism of action different from traditional antidepressants and benzodiazepines. Buspirone works as a partial agonist at two serotonin receptor subtypes (5-HT1A and 5-HT2) and as a combined agonist/antagonist at the dopamine D2 receptor.39 Buspirone is effective for the treatment of GAD in doses of 30 mg per day. Because of its short half-life, it is usually given three times a day, although some trials have found twice-daily dosing to be efficacious. Compared to benzodiazepines, it has the advantage of being nonsedating, and non-habit forming. It also is not associated with a withdrawal syndrome from abrupt discontinuation (a problem with benzodiazepines and some antidepressants). The major side effects associated with buspirone are dizziness, headache, nausea, and occasional insomnia. Because it has few cognitive side effects and no significant sedation, it is relatively safe to use in elderly patients. Although buspirone has chemical and side effect profiles that should make it an ideal choice, its efficacy as an anxiolytic has been less dramatic in clinical studies. In particular, patients with a history of prior benzodiazepine use for anxiety, tend to have poor response to buspirone. The onset of clinical efficacy can be as long as 3 weeks, which some patients find unacceptable.

Benzodiazepines This chapter advocates for the use of benzodiazepines to be limited to the treatment of anxiety associated with acute and/or anticipated stressors. Certain benzodiazepines have clinical trial data supporting their efficacy for the treatment of GAD and panic disorder. 181

Part 1: General Principles

Table 15.4: Effective Medications for Chronic Anxiety Disordersa Panic Disorder

Generalized Anxiety Disorder

Post-Traumatic Stress Disorder

Social Anxiety Disorder

Obsessive–Compulsive Disorder

Sertraline (Zoloft)

Paroxetine (Paxil)

Sertraline (Zoloft)

Sertraline (Zoloft)

Fluoxetine (Prozac)

Paroxetine (Paxil)

Escitalopram (Lexapro)

Paroxetine (Paxil)

Paroxetine (Paxil)

Sertraline (Zoloft)

Fluoxetine (Prozac)

Venlafaxine (Effexor XR)

Fluoxetine (Prozac)

Venlafaxine (Effexor XR)

Paroxetine (Paxil)

Imipramine (Tofranil)

Imipramine (Tofranil)

Clomipramine (Anafranil)

Alprazolamb (Xanax)

Buspirone (Buspar)

Citalopram (Celexa)

Clonazepam (Klonipin)

Alprazolam (Xanax)

Fluxoxamine (Luvox)

b

b

a

Efficacy of these medications supported by randomized controlled trials (RCT). b Must balance efficacy with risk of physical and psychological dependence.

Table 15.5: Starting and Maintenance Doses for Selected Anxiolytics Medication

Starting Dose (mg/day)

Maintenance Dose (mg/day)

Maximum Dose (mg/day)

Medication

Starting Dose (mg/day)

Maintenance Dose (mg/day)

Maximum Dose (mg/day)

Sertraline (Zoloft)

25

50–100

200

Escitalopram (Lexapro)

5–10

10

10

Paroxetine (Paxil)

10–20

20

50

Venlafaxine (Effexor XR)

37.5–75

150–225

375

Fluoxetine (Prozac)

5–20

20

80

Imipramine (Tofranil)

75

150–300

300

Citalopram (Celexa)

10–20

20

40

Clomipramine (Anafranil)

50

150–250

250

Fluxoxamine (Luvox)

50

50–300

300

Buspirone (Buspar)

15

15–60

60

Nevertheless, it is important to weigh the risks of using benzodiazepines with the potential benefits, especially when using the medication for more than 4 weeks. It is important to identify at-risk patients, such as an elderly person, a person with a history of substance abuse, a person on multiple medications, and significantly limit or totally eliminate the use of benzodiazepines for anything other than acute or brief, time-limited treatment. There are invariably cases in which one inherits a patient who has been taking a benzodiazepine for years and absolutely refuses to discontinue the medication. In this instance, a common-sense approach is appropriate and it may be the better part of valor to avoid a direct confrontation in favor of watchful waiting and gathering clinical data to assess whether or not the patient is using benzodiazepines compulsively or having negative side effects (memory loss, falls, withdrawal, rebound anxiety). The use of a benzodiazepine as a hypnotic should almost never extend beyond 14 days.

Tolerance, withdrawal, and addiction Perhaps the greatest clinical concern regarding the use of benzodiazepines for chronic anxiety or as a hypnotic is the potential for abuse and dependence. Although the vast majority of persons who are prescribed benzodiazepines do not go on to develop a clinically significant substance use disorder, regular use of benzodiazepines invariably causes physiologic tolerance (requiring larger amounts of a drug to achieve the same therapeutic effect) and 182

withdrawal (a sign of physical dependence) if the medication is abruptly discontinued.40,41 It is important to distinguish between the physiological states of tolerance and dependence and the complex physical, behavioral, and psychological syndrome of addiction. Addiction is a pattern of compulsive use that causes significant impairment in functioning and this use persists despite evidence of harm to the individual (which includes familial, occupational, and societal relationships) and/or a persistent desire to stop the drug. The following case provides a good example of how problems with benzodiazepines can develop over time and how an undertreated anxiety disorder can lead to the development of an addiction to benzodiazepines.

Clinical vignette 3: A patient with benzodiazepine dependence Pain medicine requests the assistance of an addiction psychiatrist to assess a 48-year-old man whose urine drug screens occasionally come up positive for cocaine. The patient also tests positive for benzodiazepines, but this is not discussed in the clinic because he gets them from his regular doctors. The pain service is reluctant to discharge this patient because of cocaine use as he has been in the clinic for a long time and has severe chronic pain from steroidinduced avascular necrosis (AVN), bilateral hip fractures, and arm fractures with multiple repairs. The addiction specialist does a thorough psychiatric evaluation and the patient reports that he uses cocaine recreationally about 2–4

Section 4: Practical Pharmacology

Table 15.6: Side Effects of SSRIs, Venlafaxine, and Duloxetine Sexual inhibition Diminished libido Inhibited orgasm

Dose related. 50–80% incidence.

Gastrointestinal Nausea/vomiting Diarrhea Anorexia Dyspepsia

Most frequent with sertraline, fluvoxamine and citalopram. Usually transient symptoms that resolve within 4 weeks.

Weight gain Up to 30% of patients

Most common with paroxetine.

Headache Fluoxetine most common

Usually subsides in 2–4 weeks.

Anxiety Fluoxetine most common

Insomnia greatest with fluoxetine.

Insomnia/sedation Helped by taking medication qam or qhs

Somnolence greatest with citalopram and paroxetine.

Dreams/nightmares Seizures

Low incidence (0.1–0.2%). Increased risk with high doses.

Extrapyramidal symptoms

Mainly limited to fine tremor. Rarely causes dystonia or pseudoparkinsonism.

Anticholinergic Dry mouth Constipation Sedation Hypertension

Dose related. Most often with paroxetine. Much lower than with tricyclics.

Mild increases with higher doses (>150 mg) venlafaxine.

Withdrawal/discontinuation syndrome Flu-like illness, dizziness, anxiety, paresthesias, migraine, insomnia

Abrupt withdrawal of short acting medication. Most common with paroxetine and fluvoxemine.

Serotonin syndrome Diarrhea, restlessness, agitation, hyperreflexia, autonomic instability, myoclonus, seizure, delerium, coma

Potentially fatal. Maximum risk with MAO + SSRI combined. In patients with migraine headaches, caution when prescribing SSRIs and SNRIs with serotonin (5-HT 1b/1d) agonists, the so-called tryptans (e.g., sumatriptan and its successors).

times a year and has never met criteria for cocaine dependence. The patient also has a significant history of GAD. The patient, however, has been on three benzodiazepines for the last 4 years, ‘for my anxiety and to help me sleep.’ The patient, who saw his regular psychiatrist about 3 times a year, was getting clonazepam (Klonipin) for GAD and lorazepam (Ativan) for ‘breakthrough’ anxiety. The patient was getting temazepam (Restoril) from his PCP when he complained of trouble sleeping. The patient reported that he frequently ran out of benzodiazepines, traded them with his wife who was also prescribed benzodiazepines, experienced intense rebound anxiety, and became tremulous and diaphoretic when he went more than a day without them. Furthermore, he reported that on at least two occasions in the last 3 months he fell a short distance off his front porch and at the shopping mall. He also reported buying alprazolam (Xanax) from friends when he ‘just couldn’t handle it anymore.’ Review of his medical record also showed that he was admitted for a seizure 2 years earlier. After some discussion about his chronic, compulsive use of benzodiazepines and the risks associated with them, the patient agreed

that his use of benzodiazepines was problematic. The patient reported previous unpleasant physical and cognitive side effects to both sertraline (Zoloft) and paroxetine (Paxil) and therefore did not want to consider another SSRI for GAD. The patient was persuaded to begin a trial of venlafaxine (Effexor XR), which he discontinued after 2 weeks, reporting similar problems he had with the SSRIs. The patient remained extremely reluctant to discontinue his use of benzodiazepines because he believed they were the only things that relieved his anxiety. This case provides ample evidence that the patient suffers from an addiction, not to cocaine, but to benzodiazepines. He certainly meets criteria for cocaine abuse by virtue of the fact that he used it despite the recurrent problems this caused with the pain clinic. However, the clinical history indicates that he has a severe benzodiazepine addiction. Not only does he manifest features of tolerance and withdrawal (his seizure 2 years ago was probably secondary to benzodiazepine withdrawal), but he also has engaged in compulsive use, drug-seeking behavior, and suffered physical injuries while intoxicated. 183

Part 1: General Principles

A patient who has reached this level of compulsive use clearly needs the help of professionals trained in the management of addiction. However, ‘treatment’ for a benzodiazepine addiction can start when a clinician first recognizes it. Simple, nonjudgmental recognition of a compulsive pattern of drug use is the first step, followed by education about the risks associated with benzodiazepine abuse. Very often, such a brief intervention can accurately assess a patient’s motivation to come off benzodiazepines and lead to a plan of action for discontinuation or dose reduction of the medication. Although there is no strict consensus on the best way to successfully taper and discontinue benzodiazepines, Table 15.7 provides some general principles to apply with both inpatient and outpatient populations.40,41 Before initiating a benzodiazepine taper it is important to consider the following factors, which are associated with greater severity of withdrawal symptoms: ● ● ● ● ●

High daily doses of benzodiazepines; Use of high-potency, short half-life benzodiazepines (i.e. alprazolam [Xanax]); Daily use for longer than 4 weeks; Female gender; High initial psychopathology.

In these risk groups, the rate and duration of a benzodiazepine taper may be longer and associated with more physical and psychological complications. It may take some patients several months before they are able to successfully taper off a benzodiazepine. Table 15.8 provides a list of equivalent dose ranges for commonly prescribed benzodiazepines that is useful for conversion to a long- or short-acting medication when tapering or optimizing a benzodiazepine regimen.

SUMMARY Anxiety is common and carries with it the potential for significant morbidity in patients suffering from spine pain. Patients may have a specific premorbid anxiety disorder with an exacerbation of symptoms as a result of reacting to the stress and pain of their spinal condition, or may develop distressing, even disabling, anxiety following

Table 15.8: Equivalent Benzodiazepine Dosing Chart (Based on Lorazepam Equivalents) Benzodiazepine

Dosage

Half-Lifea

Lorazepam

1.0 mg

Short

Alprazolam

0.25 mg

Short

Triazolam

0.125 mg

Short

Temazepam

15.0 mg

Short

Oxazepam

30 mg

Short

Clonazepam

0.25 mg

Long

Clorazepate

3.75 mg

Long

Diazepam

5.0 mg

Long

Chlordiazepoxide

25.0 mg

Long

Half-life is defined as ‘short’ if ≤24 hours and ‘long’ of ≥24 hours. This is meant to be a general guide to pick equivalent doses for crosstapering benzodiazepines. a

spinal injury and prolonged pain with no evidence of a premorbid condition. Acute anxiety in reaction to pain, stress, and fear may be effectively treated by providing information about the condition and its treatment and by reassuring the patient that they will not be abandoned to agonizing pain. Anxiety is contagious, and insecure physicians can transmit uncertainty to their patients. The opposite happens as well; insecure patients and their resulting behavioral strategies, over which they may have little control, such as becoming demanding or refusal to participate in necessary aspects of care (e.g., further procedures), can exasperate physicians. A kindly, explanatory bedside manner calms the patient and, when necessary, benzodiazepines are situationally very effective, with the caveat that their use for more than 4 weeks carries an added risk of addiction. If anxiety persists, or if screening questions suggest a specific chronic anxiety disorder, patients should be treated by a clinician who can manage the psychopharmacology of each disorder. Patients with specific anxiety

Table 15.7: General Recommendations for Tapering Benzodiazepines32,33 Try to switch the patient to an equivalent cross-tolerant dose of longer-acting benzodiazepine (i.e. 4 mg of lorazepam to 100 mg of chlordiazepoxide). Usually favor a benzodiazepine that is longer acting and of lower potency than the current benzodiazepine with the following exceptions: Elderly patients; Persons with hepatic disease; Persons with medical problems in which long-acting sedatives are undesirable or contraindicated; Persons severely addicted to alprazolam; The risk of withdrawal seizures is greatest with short-acting, high-potency benzodiazepines. For patients addicted to alprazolam, first try to stabilize the patient on a cross-tolerant dose of clonazepam before trying to use a low potency benzodiazepine. Inpatient taper1 Reduce dose by 50% every 5 days; Peak psychological withdrawal symptoms usually occur at one-fourth of the baseline dose; Peak physical withdrawal symptoms usually occur at one-fourth to one-eighth of the starting dose. Outpatient taper2 Reduce baseline dose by 50% within 2–4 weeks; Continue reduced dose for 8 weeks without a reduction; After 8 weeks, decrease dose by one-eighth every 4–7 days until complete. 1. Brenner P, Wolf B, Rechlin T. Benzodiazepine dependence: detoxification under standardized conditions. Drug Alcoh Depend 1991; 29:195–204. 2. Rickels K, DeMartinins N, Rynn M. Pharmacologic strategies for discontinuing benzodiazepine treatment. J Clin Psychopharmacol 1999; 19(6 Suppl 2):12S–16S.

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Section 4: Practical Pharmacology

disorders respond well to antianxiety medication regimens that are specific for that particular disorder, as well as to the short-term use of benzodiazepines. Selectively and skillfully integrating anxiolytic treatment with psychotherapeutic treatments, such as coping skills training, including cognitive behavioral therapy and relaxation, usually confers the greatest benefit. Creating attitudes of self-help through knowledge (www.painconnection.org) and behavioral pain management training are complementary to the selective use of anxiolytics. A prevailing challenge to spine medicine is the mobilization of the needed resources to coordinate effective treatment for anxiety, with the treatment of spinal pain. The advent of evidence-based medicine, with reimbursement increasingly determined by outcomes, rather than procedural credentialing, encourages physicians to address more effectively the anxiety associated with spinal pain.

19. Szeszko PR, et al. Amygdala volume reductions in pediatric patients with obsessive–compulsive disorder treated with paroxetine: preliminary findings. Neuropsychopharmacology 2004; 826–832.

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PART 2 1

SPECIFIC DISORDERS INTERVENTIONAL SPINE TECHNIQUES

Section 1 3

Cervical Spine Principles and Concepts ■ iii: Other Underpinning disorders of the Spinal cervical Injection spineProcedures

CHAPTER

Principles of Diagnostic Blocks

14 16

Nikolai Bogduk

A critical property of any diagnostic test is that it must be valid. If a test is not valid, the information that it provides will not be correct; the diagnosis will be wrong, and any treatment that ensues will not be appropriate and will probably fail. Along with all other diagnostic tests, diagnostic blocks are subject to this requirement for validity.

the same thing. A procedure will lack validity if a practitioner fails to observe all the details contained in the definition. Under those conditions, the procedure executed may fail to achieve correctly what it is supposed to achieve or what others achieve when the procedure is correctly performed according to its strict definition.

VALIDITY

Face validity

Various subtypes of validity have been described in the scientific literature. However, there is no established consensus as to the definitions of each subtype. Certain definitions can be found in the sociology literature, but those definitions do not readily translate into concepts recognized in medical practice. The following discussion addresses validity in the context of diagnostic blocks. The terms used are those that have been used, to date, in the literature on blocks. Definitions are provided, but may not necessarily be shared by all who use the terms. In recognition of that potential dissent, the definitions are provided not so much to argue for a dissonant lexicon, but rather to describe concepts that are pertinent to responsible medical practice. Others may choose to name these concepts differently, but they are not likely to dispute their fundamental importance.

Concept validity is the weakest form of validity. It amounts to no more than the procedure in question sounds like a good idea. In formal terms it is that the procedure appears in theory to have a reasonable anatomical or physiological basis. Diagnostic blocks have concept validity on the grounds that it sounds reasonable that if a structure is a source of pain, anesthetizing it will relieve that pain. Whether or not the block actually anesthetizes that structure, and whether or not the pain is genuinely relieved are not at issue in this context. Those properties of the test are covered by more senior subtypes of validity. Concept validity is limited to the abstract, i.e. theoretical, basis of the test.

For a diagnostic block to have face validity it must be shown that the block actually does what it is supposed to do in an anatomical or physiological sense. If a particular structure is said to be the target, it must be shown that the structure is anesthetized. Too often, some diagnostic blocks are assumed to have face validity simply because their name implies that they have. Face validity can be tested and established in either of two ways. A study might be conducted to show, as a general rule, that the block always reaches its target. If other studies replicate those results, practitioners can be assured that if they perform the block correctly they, too, can expect that it will retain face validity. The alternative is to test for face validity in each in every case. This might be done anatomically or physiologically. Fluoroscopy and a test dose of contrast medium, prior to a block, can be used to show that the injectate goes correctly to the intended target. This establishes face validity anatomically. A physiological approach might be used if the target has some detectable and testable function other than pain. Thus, a sympathetic block can be tested by change in temperature or change in blood flow. Face validity, however, is not limited to showing that the intended target is accurately reached. It also requires showing that other, potentially confounding, targets are not also affected. The objective of face validity is to show that the intended target is selectively, or discretely, anesthetized. Flooding everything in the vicinity of the target with local anesthetic does not secure face validity, for under those conditions, the operator cannot tell if the effects of the block are due specifically to the intended target having been anesthetized or to some other, unintended structure having been blocked.

Content validity

Construct validity

Content validity amounts to no more than the test being accurately defined. It ensures that one person’s version of the test is the same as another person’s. If this is not the case, what one practitioner performs as a particular diagnostic block may not be what another practitioner performs when they report using the procedure by the same name. Spelling out the definition of a procedure in detail secures content validity. An example might be that fluoroscopic guidance should be used. A fluoroscopically guided block will not necessarily be the same as a ‘blind’ procedure. Content validity does not render the procedure itself valid, but it ensures that the name of the procedure is used consistently to mean

Construct validity is perhaps the most critical of the subtypes of validity. It establishes if the test actually achieves what it is supposed to achieve. It measures the extent to which a test correctly distinguishes the presence but also the absence of the condition that the test is supposed to detect. In colloquial terms, construct validity measures if the test actually works or not, and how well it works. In the past, it was the habit of medicine to believe that all test results were correct and true; that if a test result was positive, the condition truly was present; and that if the test result was negative, the condition was definitely not present. This tradition was been refuted and supplanted.

Concept validity

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There is a science that involves testing tests. It involves comparing, in the same sample of patients, the results of a test with unknown validity with the results of some other test whose validity is beyond question. That latter test is known as the criterion standard, formerly known as the ‘gold’ standard. In reality, no test is perfect; and no criterion standard is absolute. The working definition of a criterion standard is that it is a test about whose results there is substantially less dispute than the test undergoing scrutiny. Examples of a criterion standard might include imaging findings, operative findings, or what a pathologist finds at postmortem. In practice, the criterion standard is usually a test that allows a more direct detection of the condition in question than the test under scrutiny, and which is less subject to errors of observation. When a test is compared with a criterion standard, the results can be expressed as a contingency table (Table 16.1). Such a table shows the number of patients who have the condition according to the criterion standard, and how many do not; and in how many of each category the test in question was positive or negative. Four cells emerge. The ‘a’ cell is the number of patients in whom the condition is present and in whom the results of the test are positive. These are patients with true-positive responses. The ‘b’ cell contains those patients who do not have the condition but in whom the test was nevertheless positive. These responses are false-positive. The ‘c’ cell represents those patients who have the condition but the test is negative. These responses are false-negative, for the test failed to detect the condition when it should have done so. The ‘d’ cell represents those patients who do not have the condition and in whom the test is negative. The test correctly identified these patients as not having the condition, and their responses are true -negative. From such a table, several descriptive statistics can be derived, which can be used to quantify the virtues of a diagnostic test, or the lack thereof. Paramount amongst these are the sensitivity and the specificity of the test. Sensitivity is the extent to which the test correctly detects the condition that the test is supposed to detect. Conceptually, this is read down the first column of the figure. Numerically, sensitivity is the ratio between ‘a’ and ‘a+c’, for ‘a’ is the number of patients known to have the condition in whom the test was positive, while ‘a+c’ is the total number of patients who had the condition. Sensitivity is also known as the true-positive rate, for it describes the proportion of cases who should have been positive that the test actually did find, correctly, as positive. Specificity is the extent to which the test correctly detects the absence of the condition. Conceptually it is read up the second column of the figure. Numerically, specificity is the ratio between ‘d’

False-positive rate = (1− specificity) Failure to recognize both the occurrence and the prevalence of false-positive responses has been one of the major transgressions of medicine in the past. It is both false and illusory to assume that every test result that is positive is correctly positive. A test can be positive for reasons other than the sought-for condition being present. Unless the prevalence of false-positive results is known, the validity of the test remains in question, for an investigator cannot otherwise tell if a positive result is true-positive or false-positive. The significance of false-positive responses can be realized by analyzing the contingency table. The total number of positive responses to the test is the number of true-positive cases (‘a’) and the number of false-positive cases (‘b’). The confidence that an investigator can have, that a given positive response is true-positive, is determined by the ratio of ‘a’ to ‘b’, or the ratio of ‘a’ to ‘a+b’. The greater the value of ‘b’, the less confidence an investigator can have that a given positive response is true-positive. In other words, false-positive responses compromise diagnostic confidence. The ratio, a:(a+b), is known as the positive predictive value of the test. It should be contrasted with the false-positive rate, which is b:(b+d). Although both ratios contain ‘b’, and are both compromised by high values of ‘b’, they reflect different properties of the test. In the false-positive rate, ‘b’ indicates how often the test is positive in patients who should not be positive. In the positive predictive value, ‘b’ indicates how often the test is wrong when the result is positive. Notwithstanding these differences, the relationship between false-positive rate and positive predictive value means that once the false-positive rate is known, the value of ‘b’ can be derived and used to calculate the positive predictive value. In that latter form it indicates how often a positive test is likely to be wrong. For that reason it is imperative that false-positive rates of diagnostic tests be known.

Predictive validity

Table 16.1: A contingency table from which to determine the construct validity of a diagnostic test

A final form of validity lies in the ability of a diagnostic block to lead to better treatment and to predict successful outcome from treatment. Optimally, there should be a treatment that can be implemented if a diagnostic block is positive. This constitutes the therapeutic utility of the block. If a positive response consistently predicts successful relief of pain following treatment, the block has predictive validity.

Results of test in question

DIAGNOSTIC BLOCKS

Results of criterion standard Positive

Totals

Negative

Positive

a

b

a+b

Negative

c

d

c+d

Totals

a+c

b+d

N = a+b+c+d

Sensitivity is calculated down the first column and equals a/(a+c). Specificity is calculated up the second column and equals d/(b+d).

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and ‘b+d’, for ‘d’ is the number of patients known not to have the condition in whom the test was negative, while ‘b+d’ is the total number of patients who did not have the condition. Specificity is also known as the true-negative rate, for it describes the proportion of cases who should has been negative that the test actually did find, correctly, as negative. A companion statistic is the false-positive rate. This is the proportion of cases who did not have the condition but in whom the test was, incorrectly, positive. Numerically it is the ration of ‘b’ to ‘b+d’. It is also the complement of the specificity, i.e.:

There is no contention about the concept validity of diagnostic blocks. It makes perfect sense that anesthetizing a structure, or its nerve supply, should be a means of determining if that structure is a source of pain or not. There should not be a problem with content validity. All that is required is that the component details of a diagnostic be carefully defined, and that all practitioners of the same block in name correctly execute those details. For this reason, some organizations, such as

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

the International Spine Intervention Society, have formulated definitions and detailed descriptions of certain diagnostic blocks, in order to provide a reference standard.1 It is with respect to face validity and construct validity that many diagnostic blocks used in practice fail. Either they have not been shown to have face validity, or they have been shown to lack face validity. Meanwhile, few blocks have been shown to have construct validity. Instead, the practice has been to assume that blocks are valid. The results of research show otherwise.

Face validity Practitioners are not entitled to assume, or to believe, that just because they aim an injection of local anesthetic at a particular structure that either the structure will be anesthetized or that only that structure will be anesthetized. For many blocks used in pain medicine this assumption nevertheless prevails. Yet in those few instances where the assumption has been tested, the assumption has been proved false. In the case of ‘blind’ epidural injections, several limitations have been described. Caudal epidural injections can fail to reach the epidural space in up to 30% or more of injections.2–4 Instead, the injections were behind the sacrum or intravascular. Lumbar epidural injections may fail to reach the epidural space.5 Even when the injectate does reach the epidural space, it does not necessarily flow across the entire space; it can remain in the dorsal epidural space and fail to reach the ventral space.6 For these reasons several investigators have urged that epidural injections should be performed under fluoroscopic control,3,4,7 so that operators can determine whether or not their injectate reached the desired target. Similarly, it has been shown that the flow of injectate during lumbar medial branch blocks depends on the technique used.8 If needles are placed too far anteriorly on the transverse process, or if the needle is aimed cephalad, injectate can spread to the intervertebral foramen, where it might compromise the specificity of the block. In order to avoid these problems, needles need to be directed slightly caudally, and placed opposite the middle of the neck of the superior articular process. For procedures such as sympathetic blocks, their face validity remains contentious. For lumbar sympathetic blocks, some operators believe that they can achieve accurate placement of needles simply using surface markings.9 Other operators contend that in order to secure face validity, lumbar sympathetic blocks should be performed under fluoroscopic guidance.10 Only under those conditions can target specificity be secured, in each and every case. Even classic blocks of the shoulder lack face validity. A study has shown that expert rheumatologists fail to gain access to the glenohumeral joint or the subacromial space in up to 70% of ‘blind’ injections.11 Fluoroscopic guidance is the only means available at present by which the face validity of diagnostic blocks can be confidently demonstrated. Blocks of superficial, palpable, or easily accessible nerves might be exempt; but fluoroscopy is all but mandatory for diagnostic blocks of any deep structures.

Construct validity For diagnostic blocks in pain medicine, there is no conventional criterion standard, for there is no more senior means of determining if a patient has pain from a particular source, Consequently, diagnostic blocks cannot be tested in the conventional manner, by comparing the results of blocks against a criterion standard. However, the construct validity of diagnostic blocks can be estimated piecemeal by other means.

Features such as the false-positive rate can be estimated by determining how often a diagnostic block is positive in patients who should not, or demonstrably do not, have the condition in question. Once the false-positive rate is known, the specificity of the test can be derived, as the complement of the false-positive rate.

Control blocks If a patient genuinely has pain from a particular target structure, complete relief of that pain should be obtained consistently whenever that structure is anesthetized. Furthermore, there should not be relief if some other structure is anesthetized, or if an inactive agent is used to block the target structure. If a patient fails to respond according to these precepts, doubts can be raised about the target structure being the source of the pain. This becomes the theoretical basis of controlled blocks. Controlled blocks involve repeating the diagnostic block either or both to test for consistency of response and for the effect of different agents. If a patient responds to a first block but fails to respond appropriately to subsequent, control blocks, their initial response can be deemed to have been false-positive. To this end, three types of control can be used. Anatomical controls involve deliberately anaesthetizing some adjacent structure that is not the suspected source of pain. Construct validity is achieved if the patient obtains relief whenever the suspected source is anesthetized but not when the adjacent structure is anesthetized. Any other pattern of response constitutes a false-positive response. Anatomical controls, however, are suitable only if the targets are small and imperceptibly displaced, for otherwise blinding cannot be secured. If the block is performed at an obviously different location, the patient will know that they are undergoing the control procedure. The most rigorous from of control involves using a placebo agent. The protocol requires a sequence of three blocks. The first block must involve an active agent, in order to establish, prima facie, that the target structure does appear to be the source of pain. There is no point wasting time and resources testing with placebo a structure that is patently not the source of pain. The second block cannot be the inactive control, for under those conditions patients would know that the second block is the control. In order to maintain chance, the second block must be a randomized choice of either normal saline or an active agent, administered on a double-blind basis. The third block will use the agent not used for the second block. The code is broken once all three blocks have been completed. Under these conditions, a true-positive response would be one in which the patient obtained relief on each occasion that an active agent was used but no relief when the inactive agent was used. Any other pattern constitutes a false-positive response. Failure to respond on each occasion that an active local anesthetic was used provides evidence of inconsistency of response. Relief of pain when the inactive agent was used indicates a placebo response, and refutes the target structure being the source of pain. A less rigorous, but more pragmatic, approach is to use comparative blocks. The blocks are performed on separate occasions using local anesthetic agents with different durations of action.9,12–17 Two phenomena are tested: the consistency of response and the duration of response. In the first instance, the patient should obtain relief on each occasion that the block is performed. Secondly, they should obtain long-lasting relief when a long-acting agent is used, but shortlasting relief when a short-acting agent is used. Failure to respond to the second block constitutes inconsistency, and indicates that the first response was false-positive. A response concordant with the expected duration of action of the agent used strongly suggests a 189

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genuine, physiologic response. However, lack of concordance does not invalidate the response. Comparative blocks are confounded by a peculiar property of local anesthetics, particularly lidocaine. Some patients can obtain prolonged effects from lidocaine,16 the basis of which is discussed elsewhere.17 Such prolonged responses do not invalidate the block or the response, provided that the relief is complete. When tested against placebo, comparative blocks prove valid, but to different extents according to the duration of response.18 If the patient reports a concordant response, the chances of the response being false-positive are only 14%. If the responses are complete but prolonged in duration, the chances of a false-positive response are 35%, but in 65% of patients the response is likely to be genuine. Comparative blocks do not prove that the response is true-positive. They are designed to test specificity by detecting false-positive responses. The objective is to identify patients whose responses to repeated blocks is not consistent. If the response is patently false, no further arguments are required. On the other hand, consistent responses to blocks do not necessarily prove that the responses are true-positive. They only imply a true-positive response by reducing the likelihood that the response is false-positive. There is always the possibility that all of the patient’s responses were due to placebo effects. That possibility persists even if blocks are repeated endlessly. However, if the number of repetitions is increased, but the responses remain consistent, the probability that the responses are false becomes dwindling small. Practitioners can judge how many blocks are required to reduce the probability of false-positive response to an acceptable level for practical purposes. Sometimes, the practitioner might care to perform three or four blocks, just to be certain that the response is consistent. The minimum number, however, would be two, because single diagnostic blocks are associated with unacceptably high false-positive rates. For other types of diagnostic blocks, controls have not been routine, or even recommended practice. Instead, these blocks have simply been assumed to have construct validity and, therefore, are excused the need for controls. Research studies have refuted this assumption. Price et al.19 performed stellate ganglion block on patients with complex regional pain syndromes of the upper limb, using either a local anesthetic or normal saline. They found that normal saline was virtually as effective as local anesthetic in relieving pain and other features. Indeed, there was no significant difference in the incidence of positive responses, or the degree of pain-relief, when the two agents were compared. Similarly, another study showed that the motor features of some patients with presumed complex regional pain syndrome are relieved by placebo infusions.20 Such results seriously call into question the validity of uncontrolled sympathetic blocks or infusions. Consequently, practitioners are not entitled to assume that a positive response to a conventional sympathetic block is true-positive. That fact is that false-positive responses can and do occur. The only way that these responses can be detected is to perform controls in each and every case.

DISCUSSION It is intriguing that there is an imbalance in attitude and demands concerning the validity of diagnostic blocks. Traditional blocks constitute accepted practice, but innovative procedures are subject to criticism and scrutiny. Traditional blocks are excused the requirement for controls, but validation studies are demanded for innovative procedures. Yet ironically, innovative procedures are the most validated procedures in pain medicine, while traditional procedures have not been validated.18 190

For example, medial branch blocks have been maligned in the literature,21,22 but they have been thoroughly tested for face validity, construct validity, and therapeutic utility. For no other block has this been paralleled. When performed using the correct technique, lumbar medial branch blocks accurately reach the target nerve, and do not affect any other structure that might confound the response.8 Therefore, lumbar medial branch blocks have face validity. Lumbar medial branch blocks protect normal volunteers from experimentallyinduced zygapophyseal joint pain.23 This reinforces their face validity as a test for zygapophyseal joint pain. Single blocks have an unacceptably high false-positive rate of 25–41%.24–26 Given the low prevalence of lumbar zygapophyseal joint pain, this rate means that for every three blocks that appear to be positive, two will be false-positive.24 To be valid, lumbar medial branch blocks have to be performed under controlled conditions. If positive under controlled conditions, lumbar medial branch blocks predict successful outcome following medial branch neurotomy.27 False-negative responses to lumbar medial branch blocks can occur, but are due to inadvertent intravascular injection. This can be detected and avoided if a test dose of contrast medium is injected once the needle is placed. Accordingly, false-negatives are all but eliminated by using contrast medium. As a result, the sensitivity of controlled, lumbar medial branch blocks is virtually 100%. Cervical medial branch blocks also have proven face validity. Material injected onto the waist of the articular pillar pools in that location, where it infiltrates the target nerve.28 Otherwise, cervical medial branch blocks do not spread to adjacent levels, they do not spread to the spinal nerve, and they do not anesthetize the posterior neck muscles indiscriminately. Single blocks have a false-positive rate of 27%.29 Therefore, to be valid, cervical medial branch blocks must be performed under controlled conditions in each and every case. The construct validity of cervical medial branch blocks has been established, both by statistical methods and by comparing their effects with those of placebo blocks.16,18 Cervical medial branch blocks predict successful outcome from radiofrequency neurotomy. The outcomes are comparable irrespective if placebo-controlled blocks are used or if comparative blocks are used.30,31 For no other diagnostic blocks have comparable data been produced. Face validity, construct validity, and predictive validity have not been comprehensively established for lumbar or cervical sympathetic blocks, spinal nerve blocks, greater occipital nerve blocks, blocks of the temporomandibular apparatus, or intra-articular blocks. Proponents and exponents of these procedures have a long way to come in order to catch up with the necessary data on the validity of their procedures. But unless these data emerge, pain medicine will remain a discipline based on convenient, if not self-serving, assumption.

References 1. Bogduk N, ed. Practice guidelines for spinal diagnostic and treatment procedures. San Francisco: International Spine Intervention Society; 2004. 2. White AH, Derby R, Wynne G. Epidural injections for diagnosis and treatment of low-back pain. Spine 1980; 5:78–86. 3. Stitz MY, Sommer HM. Accuracy of blind versus fluoroscopically guided caudal epidural injection. Spine 1999; 24:1371–1376. 4. Renfrew DL, Moore TW, Kathol MH, et al. Correct placement of epidural steroid injections: fluoroscopic guidance and contrast administration. AJNR 1991; 12:1003–1007. 5. Mehta M, Salmon N. Extradural block. Confirmation of the injection site by X-ray monitoring. Anaesthesia 1985; 40:1009–1012. 6. Botwin KP, Natalicchio J, Hanna A. Fluoroscopic guided lumbar interlaminar epidural injections: a prospective evaluation of epidurography contrast patterns and anatomical review of the epidural space. Pain Phys 2004; 7:77–80.

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures 7. El-Khoury G, Ehara S, Weinstein JW, et al. Epidural steroid injection: a procedure ideally performed with fluoroscopic control. Radiology 1988; 168:554–557. 8. Dreyfuss P, Schwarzer AC, Lau P, et al. Specificity of lumbar medial branch and L5 dorsal ramus blocks: a computed tomographic study. Spine 1997; 22:895–902.

19. Price DD, Long S, Wilsey B, et al. Analysis of peak magnitude and duration of analgesia produced by local anesthetics injected into sympathetic ganglion of complex regional pain syndrome patients. Clin J Pain 1998; 14:216–226. 20. Verdugo RJ, Ochoa JL. Abnormal movements in complex regional pain syndrome: assessment of their nature. Muscle Nerve 2000; 23:198–205.

9. Buckley FP. Regional anesthesia with local anesthetics. In: Loeser JD, ed. Bonica’s management of pain. 3rd edn. Philadelphia: Lippincott Williams & Wilkins; 2001:1893–1952.

21. Hogan QH, Abram SE. Diagnostic and prognostic neural blockade. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. 3rd edn. Philadelphia: Lippincott-Raven; 1998:837–977.

10. Hanningto-Kiff JG. Sympathetic nerve blocks in painful limb disorders. In: Wall PD, Melzack R, eds. Textbook of pain. 3rd edn. Edinburgh: Churchill Livingstone; 1994:1035–1052.

22. Hogan QH, Abrams SE. Neural blockade for diagnosis and prognosis: a review. Anesthesiology 1997; 86:216–241.

11. Eustace JA, Brophy DP, Gibney RP, et al. Comparison of the accuracy of steroid placement with clinical outcome in patients with shoulder symptoms. Ann Rheum Dis 1997; 56:59–63.

23. Kaplan M, Dreyfuss P, Halbrook B, et al. The ability of lumbar medial branch blocks to anesthetize the zygapophysial joint. Spine 1998; 23:1847–1852. 24. Schwarzer AC, Aprill CN, Derby R, et al. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophysial joints. Pain 1994; 58:195–200.

12. Bonica JJ. Local anesthesia and regional blocks. In: Wall PD, Melzack R, eds. Textbook of pain. 2nd edn. Edinburgh: Churchill Livingstone; 1989:724–743.

25. Manchikanti L, Pampati V, Fellows B, et al. Prevalence of lumbar facet joint pain in chronic low back pain. Pain Phys 1999; 2:59–64.

13. Bonica JJ, Buckley FP. Regional analgesia with local anesthetics. In: Bonica, ed. The management of pain. Vol. II. Philadelphia: Lea and Febiger; 1990:1883–1966.

26. Manchikanti L, Pampati V, Fellows B, et al. The diagnostic validity and therapeutic value of lumbar facet joint nerve blocks with or without adjuvant agents. Curr Rev Pain 2000; 4:337–344.

14. Boas RA. Nerve blocks in the diagnosis of low back pain. Neurosurg Clin North Am 1991; 2:807–816. 15. Bonica JJ, Butler SH. Local anaesthesia and regional blocks. In: Wall PD, Melzack R, eds. Textbook of pain. 3rd edn. Edinburgh: Churchill Livingstone; 1994:997–1023. 16. Barnsley L, Lord S, Bogduk N. Comparative local anaesthetic blocks in the diagnosis of cervical zygapophysial joints pain. Pain 1993; 55:99–106. 17. Bogduk N. Diagnostic nerve blocks in chronic pain. Best Pract Res Clin Anaesthesiol 2002: 16:565–578. 18. Lord SM, Barnsley L, Bogduk N. The utility of comparative local anaesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophysial joint pain. Clin J Pain 1995; 11:208–213.

27. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophyseal joint pain. Spine 2000; 25:1270–1277 28. Barnsley L, Bogduk N. Medial branch blocks are specific for the diagnosis of cervical zygapophyseal joint pain. Reg Anesth 1993; 18:343–350. 29. Barnsley L, Lord S, Wallis B, et al. False-positive rates of cervical zygapophyseal joint blocks. Clin J Pain 1993; 9:124–130. 30. Lord SM, Barnsley L, Wallis BJ, et al. Percutaneous radiofrequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med 1996; 335:1721–1726. 31. McDonald G, Lord SM, Bogduk N. Long-term follow-up of cervical radiofrequency neurotomy for chronic neck pain. Neurosurgery 1999; 45:61–68.

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INTERVENTIONAL SPINE TECHNIQUES

Section 1

Principles and Concepts Underpinning Spinal Injection Procedures

CHAPTER

Neurophysiology of Diagnostic Injections

17

Christopher W. Huston and Curtis W. Slipman

INTRODUCTION In the patient presenting with symptoms in a classic dermatomal pattern and a corroborative imaging study, the diagnosis may not be in question. However, cervical radicular pain may not radiate in a classic dermatomal distribution, creating doubt in diagnosis.1 Furthermore, patients often do not present with classic symptoms. A patient presenting with posterior arm pain radiating into the radial aspect of the forearm to the wrist in the presence of multilevel cervical foraminal stenosis may have involvement of either the C6 or C7 nerve root. The ability to selectively anesthetize a specific nerve root would be helpful to determine the involved nerve root and confirm the diagnosis. A variety of structures are potential pain generators for those patients presenting with axial pain. Potential pain generators include bone, muscle, tendon, ligament, intervertebral disc, zygapophyseal joint, and sacroiliac joint. Bone pathology can typically be diagnosed by imaging studies. Magnetic resonance imaging (MRI) has been disappointing for diagnosing discogenic pain as disc pathology can be seen in asymptomatic individuals.2–5 Furthermore, annular fissures seen on discography has been reported after normal MRI.6 Discography has been utilized to diagnose a painful disc and is discussed in greater detail in Chapter 25. History and physical examination has not been reliable to diagnose pain of Z-joint or sacroiliac joint etiology.7–9 Imaging studies have not been helpful in diagnosing pain from the Z-joint or sacroiliac joint.10–14 Diagnosis has been based upon anesthetizing the joint.15–19 The diagnosis of mechanical low back pain has been reported to be elusive.20 However, with the advent of diagnostic injections, the etiology of mechanical low back pain can frequently be determined. With a more specific diagnosis, more specific treatment may be rendered.

PREMISE OF DIAGNOSTIC INJECTIONS Diagnostic injections are performed to confirm or exclude a pain generator. Diagnostic injections may be utilized prior to surgery or therapeutic interventional spine management. A diagnostic injection is indicated when the diagnosis is in question despite less invasive testing and further invasive treatment is indicated.21 More specifically, when history, physical examination, imaging studies, and electrodiagnostic testing have failed to elucidate the etiology of the patient’s symptoms, a diagnostic injection may be indicated. Additionally, the patient should be a candidate for more invasive treatment such as interventional or surgical procedures. If the diagnostic injection is not going to affect treatment, the injection should not be performed. The underlying premise of a diagnostic injection is that an anesthetic can block pain emanating from a specific spinal structure. The resulting pain relief identifies the anesthetized structure as the pain generator. More specifically, the injection needs to block conduction of pain fibers – A delta or C fibers. To achieve this goal, the

structure has to be readily accessible for delivery of the anesthetic agent. The anesthetic needs to block the pain fibers or receptors of the targeted structure without spreading to adjacent pain generators, which may themselves be included in the differential diagnosis. The general notion is that only one structure is anesthetized; therefore, inadvertent block of nearby structure must be avoided. Ideally, the test would have both high sensitivity and specificity.

NEUROANATOMY The cell bodies of sensory fibers reside in the dorsal root ganglion. The cell bodies for motor neurons reside in lamina IX of the anterior horn of the spinal cord. The motor neuron axons traverse through the ventral root and the sensory axons through the dorsal root. The roots leave the thecal sac and are covered by an extension of the dura termed the root sleeve. The ventral and dorsal root combine to form the spinal nerve just distal to the dorsal root ganglion. The motor and sensory axons of the spinal nerve roots are covered by endoneurial tissue. The axon is accompanied by collagen, fibroblasts, and blood vessels. The amount of collagen tissue around the spinal nerve root axons is one-fifth of a peripheral nerve. Within the endoneurial tissue there is a thin layer of connective tissue consistent with pia mater. More distally, the outer layer of cells resembles arachnoid tissue. The inner layer of the nerve root sheath is similar to perineurium. Perineurium serves as a diffusion barrier between endoneurium, axon, and cerebrospinal fluid (CSF). The diffusion barrier is weak, but may block diffusion of macromolecules such as local anesthetics. The spinal dura encloses the nerve root and is similar to the epineurium of peripheral nerves. The dura mater ends just proximal to the dorsal root ganglion. The dorsal root ganglion is covered by perineurium and epineurium. The epineurium at the dorsal root ganglion consists of collagen fibrils and fibroblasts heavier than peripheral nerve as it nears transition with the thicker dura mater.22 The perineurium has multiple layers with basement membrane separating epi- and endoneurium. The endoneurium has finer collagen fibrils in the dorsal root ganglion compared to peripheral nerve.22,23 The subarachnoid angle marks the lateral border of the subarachnoid space. The dorsal root proximal to the spinal ganglion continues with epi-, peri- and endoneurium until 170 microns from the subarachnoid angle in the rat model.22 In the subarachnoid region, cells bordering the subarachnoid space may either reflect back onto itself or attach to the root sheath with punctate junctions at the subarachnoid angle. The epineurium in the subarachnoid space becomes the dura mater. The outer layers of the perineurium continue between the dura mater and arachnoid membrane. The inner layers of the perineurium becomes highly irregular. For the ventral root, highly hydrated cells, lacking basement membrane, replace the 193

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inner layers of the perineurium. In the dorsal root, the perineurium at the subarachnoid angle loses continuity with irregular tissues. In the subarachnoid space, loosely arranged cells overly the root sheath, which has endoneurial tissue similar to peripheral nerve. The basement membrane of perineurium serves as a diffusion barrier to substances such as anesthetic agents. The discontinuity of perineurium at the subarachnoid angle for the dorsal root, and lack of basement membrane for ventral root, allow easier penetration of substances to the nerve sheath.22 In the subarachnoid region, the nerve root arachnoid tissue is not as effective a barrier as perineurium to anesthetic substances. Hence, lower dosages will result in block compared to the epidural space.23 However, the subarachnoid angle may also allow quicker diffusion of anesthetics because of the discontinuity of the perineurium. Peripheral nerve consists of three sheaths – epineurium, perineurium, and endoneurium. These layers do continue from peripheral nerve to the spinal nerve and nerve roots. Within the spinal nerve and nerve roots are individual motor and sensory axons. The individual axons are surrounded by Schwann cells. These Schwann cells may form layers of myelin that wrap around the axon or an axon may simply be just enveloped by a Schwann cell. The axolemma and basal cell membrane serve as a barrier to axonal cytoplasm. In myelinated nerves, the myelin is present in 0.25–0.3 mm segments with bare axon between these segments. These bare gaps of axon are the nodes of Ranvier and involved in salutatory conduction of impulses discussed later. In myelinated nerves, each segment of myelin is accompanied by one Schwann cell. In unmyelinated nerve, one Schwann cell may accompany multiple unmyelinated axons. Surrounding each axon and Schwann cell is a connective tissue tube of endoneurium. Capillaries, fibrocytes, and collagen fibrils are within the endoneurium. Bundles of axons are surrounded by another tube of connective tissue – the perineurium. The perineurium, which has a basement membrane, serves as a barrier to macromolecules such as local anesthetics. Epineurium is the outer layer of nerves and covers one or more perineural bundles. Nutrient arteries form a vascular lattice of arterioles and capillaries within the epineurium that penetrate the perineurium. The axolemma is formed by a mosaic bilayer of primarily phospholipids with lesser amounts of glycolipids and cholesterol. The outer layers of the membrane contain the hydrophobic portion of the lipid molecule while the inner layers consist of the hydrophilic portion. Interspersed within the membrane are proteins, many of which are glycosylated. The protein moieties are fixed within the membrane and compose the ion pores or channels. Various ions such as Na+, K+, Ca+, and Cl– pass through these pores that traverse the width of the membrane. In myelinated nerve, the Na+ channels are located at the nodes of Ranvier with the K+ channels interspersed between the nodes.24 In unmyelinated nerves, the Na+ and K+ channels are not selectively located.25 The flow of ions through these channels is dependent upon various factors such as ion concentration gradient, voltage gradient, and configuration of the channel. The channels may exist in an open state, closed resting state, or closed inactivated state. The channels are ion specific, primarily only allowing the passage of a specific ion. For example, voltage-gated Na+ channels allow predominately only Na+ to pass through the channel. The voltage-gated Na+ channel is typically closed at the resting membrane potential of –60 mV, but with chemical or electrical depolarization, the transmembrane potential may reach threshold of –45 mV, resulting in opening of these voltage-gated Na+ channels. With opening, extracellular Na+ flows rapidly into the axon, resulting in an action potential with subsequent depolarization of adjacent membrane. The wave of depolarization is then propagated down the axon. In a closed state, the Na+ cannot traverse this channel.

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NEUROPHYSIOLOGY The peripheral nervous system is involved in the transmission of information from one location to another. The messages propagate electrically from the cell body to the axon terminal as an action potential. The propagation of an action potential is dependent upon the existence of a resting membrane potential across the neural membrane. Positively and negatively charged ions are present in the intracellular and extracellular neuronal environment. Intracellularly, there is an overall negative charge and extracellularly an overall positive charge. This separation of charges results in a resting potential across the membrane. The major ions responsible for the charge are Na+, Cl–, K+, and organic anions. The organic anions, such as amino acids, remain intracellular and are not permeable to the axolemma. The concentrations of Na+ and Cl– are higher extracellularly and K+ concentrations higher intracellularly. Typically, ions will diffuse from a higher concentration to a lower concentration. Electrically, positively charged ions will tend to diffuse to the more negative side. These forces interact until equilibrium develops between the electropotential and concentration gradient. This has been termed the equilibrium potential and for each ion is dependent upon concentration gradients, electropotential gradients, ion charge, and permeability. The neural membrane affects these factors.26 Ions flow across the membrane through channels. These channels are ion specific. The permeability of an ion is dependent upon the number of channels present per area of membrane for that specific ion. The concentration of Na+ is high extracellularly and a negative charge is present intracellularly. While this would favor an influx of Na+ into the cell, the passive Na+ permeability is low. In contradistinction, the permeability for K+ is high. The flow of K+ is extracellular, because the low concentration overrides the repulsion from the positive charge extracellularly. Chloride ion is very permeable and is free to passive distribution. Chloride equilibrates based upon the concentration gradients and the electropotential difference. However, Na+ and K+ do not equilibrate based upon these two forces alone. A Na+–K+ pump regulates the flow of these ions with three Na+ ions pumped extracellularly to every two K+ ions pumped intracellularly. The energy-dependent pump is driven by the hydrolysis of ATP. The pump accounts for maintenance of the ion gradient across the membrane and maintains the resting potential. Without the pump, Na+ accumulates intracellularly and K+ extracellularly until the electropotential gradients for both become zero. The pump maintains the potential difference at a metabolic cost – hydrolysis of ATP. The Na+–K+ pump, high permeability of K+, and low permeability of Na+ results in a zero net influx:efflux of ions, maintaining the resting potential.26 Membrane phospholipids have an insulating property separating the negatively charged axoplasma from the positively charged extracellular fluid. The charge is separated and maintained with a negative charge on the inner membrane and positive charge on the outer membrane with a potential difference. The membrane phospholipids bilayer serves as a capacitor.27 Current flow across the membrane is dependent upon resistance to current through the ion channels and capacitance current. As the membrane holds a charge, current across the membrane will have to alter the charge on the capacitor for current to flow. The change in resting potential to an electric stimulus will be time dependent upon the charge of the capacitor and the resistance of the membrane. The product of membrane resistance and capacitance is the membrane time constant. With a longer time constant, subthreshold stimuli may accumulate until threshold is met. This is termed temporal summation.

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

Another factor that will affect electrical conduction longitudinally down the axon is axon diameter. With a larger axoplasmic core, more ions are available for transmission of the current, resulting in a lower resistance. Smaller axons have higher resistance. For a given voltage potential across the membrane, a higher resistance will result in lower conductance (I=V/R). Another factor is the length constant. The length constant is the length of axon that a voltage potential can spread passively. The decay of voltage down the length of axon is exponential and related to the loss of current through the membrane and resistance to current in the axoplasmic core. The higher the membrane resistance the longer the length constant will be as there is less decay in the potential. Conversely, the lower the axoplasmic resistance the longer the length constant will be. A longer length constant allows spatial summation of impulses.27 The length constant is important in allowing the propagation of a depolarizing current to adjacent sections of axon without decay. The velocity of depolarization is dependent upon membrane capacitance and axon resistance. A lower resistance allows a larger conductance. A larger capacitance will require a larger ion flow to alter the charge to change the transmembrane potential. The velocity of depolarization down an axon is dependent upon the product of axon resistance and membrane capacitance. With increasing axon diameter, the resistance is exponentially decreased with only linear increase in capacitance. This leads to higher velocity. Another way to affect velocity favorably is to increase the thickness of the capacitor, which results in decreased capacitance. Myelination achieves this goal. Myelin will also decrease the amount of ion flow across the membrane with less decay. However, the depolarization would dissipate without the node of Ranvier to allow Na+ channel conductance. This results in saltatory conduction as the action potential jumps from node to node. Sodium channels are located at the nodes. Potassium channels are primarily located along the axon between the nodes of Ranvier with few if any potassium channels at the nodes.24 The axonal membrane between nodes functions as a passive cable unless demyelination occurs. With demyelination, the bare axon becomes excitable.25 However, demyelination can result in conduction block due to decay of the propagating action potential. The generation of synaptic potentials changes the transmembrane potential with opening of voltage-gated Na+ channels followed by a rapid influx of sodium. If this reaches threshold for a given segment of nerve, depolarization occurs. Multiple voltage-gated Na+ channels open with generation of an action potential. The action potential alters the transmembrane potential of the adjacent nerve segment. Depolarization occurs with additional Na+ channels opening with propagation of the action potential. As depolarization progresses, the voltage-sensitive Na+ channel closes with a decline in Na+ influx and decrease in the action potential. With depolarization there is a lag in opening of active K+ channels with efflux of K+. This results in repolarization of the membrane. The increased K+ conductance leads to a hyperpolarization after-potential. Additionally, the increased K+ conductance along with sodium inactivation causes an absolute and relative refractory period to depolarization. Subthreshold changes in the transmembrane potential can result in intermediate opening of only a few voltage-sensitive Na+ channels which flip between open and closed states. Additionally, these subthreshold spikes may increase K+ conductance extracellularly. This can lead to some resistance to depolarization creating a higher threshold, termed accommodation.28 Once a threshold stimulus occurs, then depolarization occurs with opening of all sodium channels with development of an action potential. The action potential is then propagated down the axon. This process allows transmission along long neural pathways in the body.

Neurophysiologic effects of local anesthetics Local anesthetics block nerve impulses by inhibiting depolarization. Local anesthetic exists in both a neutral and cation form. The cation moiety has been determined to be the active form.29–31 The cation form binds to a receptor located on the alpha subunit of the ionconducting pore. The receptor consists of an amino acid chain within the pore.32 The cation-receptor complex alters the configuration of the sodium channel. The influx of sodium is blocked. Depolarization does not occur and the propagating impulse is blocked. The blocked segment of nerve maintains the resting potential with resultant membrane stabilization.33 Local anesthetic then dissociates from the receptor, allowing sodium conductance to resume. The cation binds and dissociates from the receptor through open channels.34 Complexed channels open and close normally but do not conduct sodium.34 Depolarizing impulses open the channels. In the presence of local anesthetic, further binding occurs leading to greater inhibition.34 Increased inhibition with depolarization has been termed phasic inhibition. With increasing discharges, more channels are opened and subject to greater blockade.35,36 The amplitude of the conditioning impulse – larger impulse with more channels open – will affect the number of channels opened and subsequent inhibition.35 Recovery from this frequency-dependent block is dependent on the concentration of anesthetic.36 Another factor that affects whether the propagating wave of the depolarizing is aborted is the length of nerve inhibited. Previously, the inhibition of depolarization at three consecutive nodes was considered the critical length for conduction block.37,38 Local anesthetic was found to result in graded reduction in nodal action potential current. Graded reduction of the sequential nodes occurred until propagation ceased.39 Complete conduction block at three consecutive nodes was found not to be necessary. However, the concept of graded reduction across sequential nodes and complete block at three consecutive nodes are not mutually exclusive.38 The graded response is dose dependent. With higher dosages complete block of sequential nodes can occur. Various factors affect the rapidity, density, and duration of neural blockade. The onset of blockade is affected by anesthetic permeability. The anesthetic agent needs to penetrate epineurium, perineurium, endoneurium, and axolemma. In myelinated nerves, penetration would occur through the myelin sheath or at the nodes of Ranvier. Diffusion across these structures is dependent upon the ion state of the local anesthetic. The neutral form of local anesthetic is more lipophilic and can diffuse across the phospholipid bilayer of the axonal membrane.31 Alkaline pH favors the neutral form and more readily penetrates mammalian A, B, and C fiber than the cation form.30 However, the neutral form is not the active form. The neutral form needs to be converted to the cation form for blockade to occur. Conversely, the active charged cation has greater difficulty penetrating and diffusing across the axonal membrane.29,30,40 The environmental pH determines the ratio of neutral and cation form present. An alkaline pH favors the neutral form and allows more rapid penetration of the axolemma. A more acidic pH favors the cation form. The molecular structure of the local anesthetic determines the ratio of neutral to cation form at a given pH by the following formula: Log [cation]/[base] = pKa – pH The pKa is the pH at which an anesthetic is present equally in neutral and cation form. Intracellularly, the pH is 7.4 and will favor anesthetics with a pKa lower than this – a greater concentration of the

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active cation form. The onset of anesthesia is faster for agents with a lower pKa.41,42 Other factors affect the ability of local anesthetics to diffuse across nerve membrane. Besides lipid solubility, permeability is additionally affected by molecular volumes, specific chemical groups, and position of chemical groups on the molecule.42 Once the neutral form of anesthetic diffuses into the phospholipid bilayer, the anesthetic agent has to desorb from the membrane into the axolemma. The benzene ring of the local anesthetic may be strongly associated to the membrane.42 The NH-C4H9 group of tetracaine is more hydrophobic than the NH2 group of procaine, with resultant slower desorption.42 The desorption of the neutral forms is inverse to the partition coefficients. The desorption rate may be the rate-limiting factor to the onset of blockade.42 Once the neutral form desorbs from the phospholipid bilayer, the cation form is then able to bind to the protein receptor in the sodium channel. The anesthetic agent-receptor complex changes the configuration of the sodium channel, blocking entrance of sodium into the axolemma. The duration of sodium channel blockade is partly dependent upon the protein affinity of the anesthetic molecule. Greater affinity results in longer blockade. Other factors may affect the degree and duration of blockade. Anesthetics with a longer alkoxyl chain have greater hydrophobia which enhances voltage-dependent block.35 The potency between anesthetic compounds is probably secondary to different kinetics within the sodium channels during the step-depolarizing pulses.35 The differences in lipid solubility among anesthetic agents relative to impulse frequency conduction block has been evaluated in frogs.36 Low and high lipid-soluble anesthetics required large number of impulses to reach maximum block in vitro.36 Intermediate lipid-soluble agents required 4–8 impulses at 40 Hz to reach maximum effect. The recovery from blockade was quicker with the intermediate lipid-soluble agents.36 Low lipid-soluble agents were the quartenary compounds. Intermediate lipid-soluble agents were procaine, lidocaine, prilocaine, and mepivacaine. High lipid-soluble agents were bupivacaine, tetracaine, etiodocaine.36 The potency of an anesthetic is increased with more lipophilia, stronger protein binding, and rapid onset. Not all nerves have the same degree of susceptibility to anesthetic agents. Differential block refers to preferential blocking of small fibers over large fibers. The smaller fibers are blocked more easily as there is less tissue for local anesthetic to diffuse across. The unmyelinated C-fibers and smaller-diameter myelinated A-delta fiber are more easily blocked than A-alpha and beta fibers. Hence, pain is preferential blocked over light touch, pressure, and motor. A higher concentration of anesthetic is needed to block these larger fibers. However, fiber size is not the only factor that leads to differential block. Another factor that may be related to differential block is frequency-dependent block. An extremely phasic sensory nerve with short, widely spaced bursts may be resistant to block.36 Nerve firing at 10–50 Hz with burst durations greater than 0.5 seconds are more apt to be blocked.36 In a painful spine condition, the C-fibers and A-delta fibers are actively firing and may be preferentially blocked. The minimum concentration of anesthetic agent to block a nerve in vitro is the Cm. The Cm between spinal nerve and peripheral nerve is the same.41 However, the Cm is lower for subarachnoid versus epidural blockade. Various factors account for this difference. The nerve roots within the thecal sac have less tissue and barrier to anesthetic agent. Lymphatics and the venous plexus in the epidural space can carry local anesthetic away from the site. Local tissue within the epidural space can bind local anesthetic, rendering it unavailable to the spinal nerve and nerve root. Fluid within the space can dilute anesthetic agent. Any fibrous tissue between the anesthetic agent and targeted nerve serves as a barrier that anesthetic agent has to cross. 196

Another factor that can affect the onset of blockade is the presence of a rapid transport route between the epidural space and endoneurial space.43 This rapid transport is postulated to occur through epidural venous system with retrograde flow into intraneural capillaries of the nerve roots – bypassing diffusion across the dura. Local anesthetic in the epidural space may have direct transport to the axons of the nerve roots.43 In the performance of spinal injections, the goal is to place the anesthetic agent as close as possible to the dorsal root ganglion to help minimize these other factors. Posterior epidural injections compared to selective nerve root injections would be more prone to venous absorption, lymphatic uptake, and tissue binding. Other factors that effect Cm are the pKa, metabolism, elimination, and distribution of the anesthetic. Local anesthetics are divided into ester and amide anesthetics. Local anesthetics consist of an aromatic and amine group connected by an intermediate chain. For ester local anesthetics, the intermediate chain is an ester group. The ester anesthetics are metabolized by cholinesterase into para-aminobenzoic acid (PABA), which can result in allergic reactions. The amide anesthetics have an amide link as the intermediate chain. The amide group is metabolized in the liver but not into PABA. The molecular structure of the local anesthetic agents affects their properties. For example, exchanging the butyl group of mepivacaine for methane on the amine branch increases the protein binding affinity. This substitution creates bupivacaine which has a longer duration of neural blockade than mepivacaine secondary to improved binding to the protein receptor in the sodium channel. Changes on the aromatic head affect lipid solubility. As lipid solubility is a primary determinant of onset latency, any alteration of the aromatic head will affect the onset of neural blockade.44

Other physiologic actions of local anesthetics Local anesthetics are primarily utilized in painful spine disorders as a diagnostic tool to determine pain generators. Local anesthetic may potentially have therapeutic benefits besides just neural blockade effects. In 1930, Evans proposed that infusing large volumes of fluid could disrupt perineural adhesions.45 However, this is unlikely, as fluids tend to flow in paths of least resistance as demonstrated by radiographic contrast flow patterns.46 Local anesthetic may have an antiinflammatory effect. Local anesthetics have been shown to inhibit peritonitis in a rat model.47 Greater inhibition occurred with lidocaine than bupivacaine. The authors of the study postulate local anesthetic antagonizes prostaglandin release, leukocyte migration, and neutrophil lysosomal release. In burn injuries, topical lidocaine resulted in local vasoconstriction, reducing albumin extravasation. However, at high dosage, lidocaine results in vasodilation.48 Lidocaine has been found to affect neutrophil function. Exposure to local anesthetic (lidocaine, tetracaine) resulted in reduced superoxide release, lysosomal release, phagocytosis, exocytosis, reduced adherence, granulocyte colony stimulating factor, and bactericidal activity.49–53 Peck et al.49 postulated the mechanism of inhibition was probably stabilization of the neutrophil membrane through sodium channel blockade. Goldstein et al.50 stated tetracaine acts on the neutrophil membrane modifying stimulus–membrane interactions and retarding membrane fusion similar to corticosteroid. Local anesthetic inhibits neutrophil NADPH oxidase activity in a dose-dependent manner, resulting in decreased superoxide release.53 Local anesthetic has been found to decrease macrophage superoxide anion release.54 Lymphocyte adherence and mobility was reduced by local anesthetic.55 Local anesthetic has been postulated to effect the cell membrane, calmodulin-dependent pathways affect calcium dependent function and inhibiting protein synthesis.55

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

In vitro, local anesthetic has be shown to inhibit human fibroblast, endothelial cell, and keratinocyte proliferation,56 which may potentially reduce scar formation. Another potential benefit of local anesthetics is sympathetic blockade.57,58 Central processing theories may provide an explanation for the observed therapeutic effect. One theory is the benefit occurs from a placebo response, which has been reported in one-third of all interventions.59,60 Another theory is that a neural engram of pain in the brain forms from repetitively firing of wide dynamic range neurons in the substantia gelatinosa. Each of these areas incites afferent information, thereby triggering activity. Peripheral blockade can disrupt or shut off these central processing zones, resulting in pain relief or mitigation.

DIAGNOSTIC SELECTIVE NERVE ROOT INJECTIONS The purpose of a diagnostic selective nerve root injection is to identify the nerve root causing extremity pain. A positive selective nerve root injection identifies that specific nerve root as the cause of pain. A negative selective nerve root injection rules out that nerve root as the cause of pain. To achieve this, the nerve fibers transmitting pain must be blocked without blocking fibers from an adjacent level. For example, with L5 radicular pains the L5 and not the L4 or S1 nerve needs to be blocked. Blockade of unmyelinated C and small, myelinated A-delta fibers is the objective as these fibers transmit acute, sharp pain and delayed-onset dull aching or burning pain in radicular pain.61 The goal of a diagnostic injection is to anesthetize these fibers at the spinal nerve, dorsal root ganglion, and/or dorsal nerve root. Motor blockade does not need to be achieved and these larger myelinated fibers are more resistant to blockade than the smaller fibers conducting pain. Additionally, with a radicular pain the pain fibers may be easier to block secondary to phasic inhibition. The main diffusion barrier to the anesthetic agents reaching myelinated and unmyelinated fibers within the spinal nerve, dorsal root ganglion, and nerve root is the basement membrane of the perineurium. Once crossed, the anesthetic agent may need to diffuse across the myelin sheath or enter through open sodium channels to reach the anesthetic receptor within the ion pore. Additionally, some anesthetic agent will be absorbed by non-neural tissues in the epidural space. The venous plexus and lymphatics can absorb anesthetic molecules, carrying them away from the target site. The interventionist spine specialist needs to deliver the anesthetic as close to the target as possible without causing neural injury. The chapter on spinal injection techniques addresses this issue (Ch. 23). Additionally, consideration must be given to the volume and concentration of anesthetic required to optimally block the targeted nerve root without spread to adjacent spinal levels. The block also needs to be rapid enough to allow assessment of pain relief within a reasonable time after injection, typically within the first 20 minutes. North et al. utilizing 3 ml of 0.5% bupivacaine found selective nerve root injections to be non-specific.62 However, Van Akkerveeken utilizing only 1.0 cc of lidocaine found a sensitivity of 90% and positive predictive value of 95%.63 In this study, subjects with known radiculopathy secondary to either tumor or herniated nucleus pulposus underwent selective nerve root injection at multiple levels with the subject blinded to the levels injected. Van Akkerveeken was also able to determine the sensitivity of selective nerve root injections, which was 100%. The study of North et al.62 suggests that utilizing a volume of 3.0 cc is unacceptable as specificity is lost as medication travels to adjacent levels. Blockage of multiple levels is undesirable as it may not only incorrectly identify the nerve root level in an individual suffering from radiculitis but could also incorrectly miss a peripheral nerve

lesion. Peripheral nerve lesions are typically composed of nerve fibers from multiple adjacent nerve root levels. Blockage of these multiple levels could potentially relieve peripheral nerve pain, as in North’s study. Blockage of a single nerve root level is theoretically less apt to result in 80% decrement in pain with pain emanating from multiple levels. For a diagnostic selective nerve root injection to be positive, an 80% decrement in pain from preinjection to postinjection must be achieved.21 The study of Van Akkerveeken suggests 1 cc of lidocaine is adequate for both sensitivity and specificity. Besides temporary spinal nerve root blockade of pain transmission, local anesthetic may have other affects. Local anesthetics may improve blood flow. Yabuki and Kikuchi64 demonstrated increased radicular blood flow both proximal and distal to nerve root compression in dogs with nerve root infiltration of lidocaine. This effect was not seen with injection of saline. Localized ischemia has been postulated to cause symptoms in spinal stenosis.65 Additionally, in an animal model, exposure to autologous nucleus pulposus was found to impair blood flow along with intraneural edema, demyelination, and axon loss.66 Improvement in radicular blood flow by anesthetic agent may impart a therapeutic benefit. Whether increased radicular blood flow in an animal model translates to a therapeutic effect in humans has been questioned.44 One concern is whether the increased radicular blood flow is transient. Another concern is whether the increased blood flow produces a clinical effect. Hayashi et al.67 had no lasting effect from bupivacaine with chemical radiculitis in an animal model. However, Yabuki et al.,68 utilizing a different animal simulating inflammatory radicular pain from nucleus pulposus, found less inflammation and nerve injury in the animals that received lidocaine. In earlier work, Yabuki and Kikuchi64 postulated the improved radicular blood flow from lidocaine may improve intraneural tissue metabolism or simply wash away chemical inflammogens. In 1998, Yabuki et al.68 postulated the therapeutic benefit of lidocaine may be the antiinflammatory effect as opposed to improved blood flow. Local anesthetic may have an antiinflammatory or antiimmune affect, as previously discussed. Whether this imposes any therapeutic effect would be dependent upon the pathophysiology of the radicular pain. The intervertebral disc may result in radicular pain via involvement of the dorsal root ganglion (DRG) or nerve root. Compression of the DRG does result in repetitive electrical discharge, which could result in continued radicular pain with foraminal stenosis or a foraminal disc protrusion. Frequently, however, disc herniations are posterolateral in location and compress the nerve root, not the dorsal root ganglion. With compression of the nerve root, only a single burst of electrical discharge occurs.69 This would not explain continuous radicular pain. Howe et al.69 noted repetitive nerve root firing when a combination of inflammation with compression occurred. Kawakami et al.70 also noted severe hyperalgesia in rats with nerve root compression from chromic suture as opposed to silk suture or clip. The chromic suture resulted in inflammation whereas silk suture or clip did not. Kawakami et al.70 postulated inflammation, not compression, was the important factor in producing radicular pain. Various animal studies have been performed to understand the effect of nucleus pulposus or disc protrusions in the pathophysiology of radicular pain. Leukocytes, macrophages, and lymphocytes were found at surgically created porcine disc protrusions.71 Introduction of nucleus pulposus into the epidural space of canines resulted in edema, fibrin deposition, and marked neutrophil infiltrate at 5 and 7 days postexposure. At 14 and 21 days postexposure regional fibrosis, vascular infiltration, and marked histiocytic–lympocyte infiltration was noted. Granulation tissue was present.72 Nucleus pulposus has been demonstrated to induce leukotaxis.73 197

Part 2: Interventional Spine Techniques

Olmarker et al.74 evaluated the effect of methylprednisolone upon porcine cauda equina exposed to nucleus pulposus. The cauda equina was found to be red and swollen in the untreated group and pale and not swollen in the methylprednisolone group. Histologic analysis demonstrated inflammatory cells in both groups. Nerve conduction velocity was slowed in the untreated group. Olmarker et al. hypothesized subcellular processes resulted in the slowed conduction since there was no difference histologically between groups.74 In another study, nerve conduction slowing was noted following exposure of the cauda equina to autologous porcine nucleus pulposus.75 Kayama et al.75 postulated the effect to structures in the membrane of the nucleus pulposus cells. Human studies have also been performed. Inflammatory cells with a predominance of macrophages were noted in disc material obtained at surgery in subjects with disc herniation.76 Disc material in subjects suffering from radiculopathy due to disc herniation was found to have elevated levels of phospholipase A2.77 Phospholipase A2 has been shown to be neurotoxic.78 Phospholipase A2 is the rate-limiting step in the liberation of arachidonic acid and the generation of leukotrienes and prostaglandins in inflammation. Prostaglandin E2 and E1 have been found in surgical disc specimens.79 Prostaglandin E2 is involved in sensitizing nociceptors to bradykinins. Takahashi et al.80 studied human disc material from surgical specimens in subjects with either a disc protrusion, extrusion, or sequestration. While there was no difference in the cytokines produced, there was difference in the cells that produced the cytokines. The disc protrusion group had elevated levels of chondrocytes. The disc extrusion and sequestration groups had elevated levels of histiocytes, fibroblasts, and endothelial cells with few chondrocytes. Betamethasone added to the cultures inhibited cytokine production and prostaglandin E2 levels.80 Granulation tissue with mononuclear infiltrates were found in two-thirds of samples from disc extrusions or sequestration.81 The mononuclear cells expressed interleukin-1. Interleukin-1 stimulates inflammatory mediators and proteolytic enzymes such as collaganese, stromelysis, and plasminogen activators.81 Disc material obtained from herniated disc subjects compared to scoliosis subjects demonstrated elevated levels of matrix metalloproteinase activity, nitric oxide, prostaglandin E2, and interleukin-6.82 Interleukin-1, tumor necrosing factor, interleukin-1 receptor antagonist protein (IRAP), and substance P were not found at appreciable levels in either group. Matrix metalloproteinase is involved in disc degeneration and nitric oxide in inflammation and immune regulation. Increased levels of matrix metalloproteinase-3 and tissue inhibitor of metalloproteinase-1 have been found in disc extrusions and sequestrations compared to protrusions. These substances are involved in disc degeneration, and whether there is any role in discogenic low back pain is unclear. Various neuropeptides are also involved in disc pathology. Substance P and calcitonin gene-related peptide (CGRP) have been found in the outer anulus fibrosus and posterior longitudinal ligament.83,84 Anulus was found to have nerve fibers immunoreactive to vasoactive intestinal peptide (VIP) and C-flanking peptide.83 VIP is involved in vasodilation and possibly sensory transmission. C-flanking peptide is a vasoconstrictor. CGRP and substance P are involved in nociception. Substance P additionally increases prostaglandins, interleukin-1, collagenase, and tumor necrosing factor. Measurement of neuropeptides in the dorsal root ganglion of compressed porcine nerve root found increased substance P but not VIP, while in canines undergoing discography both substance P and VIP were elevated.85,86 Disc compression has been postulated to pump fluid into vertebral body, anulus, and posterior longitudinal ligament with stimulation of nociceptive fibers.86 Mechanical stimulation of rat DRG resulted in elevated 198

substance P in DRG, Lissauer’s tract, and substantia gelatinosa laminae I–III.87 Chronic inflammation secondary to immune response to nucleus pulposus has been postulated.88 Elevated lymphocyte transformation test, indicating a cellular immune response, was found in disc sequestrations as opposed to contained disc protrusions.88 The sequestered nucleus pulposus is exposed to the vascular space with postulated immune response and subsequent antibody formation.88 In subjects suffering from discogenic back pain or sciatica, six of nine subjects had elevated titers of IgM. Alteration of vascular flow has been postulated as a potential etiology of chronic low back pain.89 Cadaveric intervertebral foramen specimens in chronic low back pain sufferers demonstrated perineural fibrosis, epidural vein compression, and dilation of noncompressed veins. Direct nerve root compression by osteophyte or disc was rarely found. Venous obstruction and dilatation with anoxia, fibrosis, and neuronal atrophy is hypothesized to result from mechanical damage.89 Tissue injury can result in fibrin deposition. Tissue plasminogen activator activates plasminogen in the fibrinolytic system to cleave fibrin for clearance. Tissue plasminogen activator inhibitor balances this response. Increased levels of tissue plasminogen activator antigen and inhibitor were reported and may be involved in pain production, though further research is required.89 The pathophysiology of neurogenic claudication secondary to spinal stenosis is incompletely understood. Porter90 postulates neurogenic claudication occurs from venous pooling with subsequent impaired blood flow. This results in metabolite buildup and decreased nutrients with nerve dysfunction. Walking impairs venous flow by increased spinal canal pressure with arteriole dilation, upright position increases epidural pressures, increasing venous return from the lower extremities. Increased venous flow from the lower extremities through the pelvic veins results in engorgement of Batson’s plexus with impairment of spinal venous flow. Nerve root compression, various vascular pathology, demyelination, and loss of neurons was found in symptomatic spinal stenosis subjects postmortem.91 Watanabe and Parke91 postulate neurogenic claudication arises from avascular atrophy of nerve fibers with constriction of nerve root pia-arachnoid mater. The pia-arachnoiditis results in adherence of the nerve root with susceptibility to mechanical spinal excursions. The thickened pia-arachnoid mater impairs CSF nutrients from diffusing across to the nerve root. Nutrient delivery to the nerve root is dependent upon both vascular system and CSF. A porcine model of compression demonstrated significant impairment of CSF flow with even low compression. CSF flow is also subject to postural changes in spinal stenosis subjects. Takahashi et al.80 evaluated epidural pressure in lumbar spinal stenosis and normal control subjects. Lumbar spinal stenosis subjects in upright position had significantly increased pressure (82 mmHg) compared to flexed position (37 mmHg) and normal upright controls (34 mmHg). There was no statistical difference between the stenosis subjects in a flexed position versus normal upright controls. Increased epidural pressure in the upright posture of spinal stenosis subjects was postulated to impair nutrition to the nerve root or cauda equina. For impaired venous flow, either two adjacent levels or levels above and below a spinal segment needs to be involved.92 The above studies suggest a role of vascular or CSF flow impairment in the pathology of spinal stenosis. However, these morphologic models do not account for radiologic findings of spinal stenosis in asymptomatic subjects.2 The successful treatment of neurogenic claudication secondary to spinal stenosis by injection of corticosteroids is not explained by the anatomic model.93–95 Biochemical studies of the role of inflammatory mediators, cytokines, and neuropeptides in neurogenic claudication are needed.

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

The use of local anesthetics in the performance of both diagnostic injections and therapeutic injections when mixed with corticosteroid may hypothetically provide a therapeutic benefit. Local anesthetics have been shown to have antiinflammatory activity. The affect on leukocytes could alter not only the inflammatory reaction but also the release of various neuropeptides and cytokines. The affect on local blood flow by local anesthetics may also serve a role in both herniated disc and spinal stenosis subjects. However, whether these effects are clinically relevant requires further study.

ZYGAPOPHYSEAL JOINT PAIN In vivo studies have been performed provoking Z-joint pain referral patterns.96–98 Intra-articular Z-joint instillation of local anesthetic has provided relief of low back pain.99 These studies suggest the Z-joint as a potential source of low back pain. To be a cause of pain, the structure should have nociceptive fibers. Afferent impulses are propagated from the zygapophyseal joints through medial branch of the posterior primary ramus. Complex unencapsulated nerve fibers probably involved in nociception have been found in the joint capsule.100 However, speculation existed as to whether these small fibers were just accompanying blood vessels or involved in Z-joint nociception. Plica synovial tissue obtained from surgical specimens demonstrated staining of substance P, CGRP, and PGP 9.5 but perivascularly.101 Plica tissue was felt not to be painful and the nerve fibers identified were postulated to be involved in vascular regulation.101 However, nerve fibers have been found in the Z-joint synovial folds not associated with vascular structures.102 Small unmyelinated and myelinated fibers were found corresponding to C and A-delta fibers, respectively.102 Other afferents have been found and studied in the Z-joint. The facet joint contains group III and IV mechanosensitive units which respond to joint movement.103,104 Group II units are involved in proprioception and correspond to A-beta fibers found in adjacent musculotendinous units. The Group III units are involved in nociception. Mechanical strain may activate these group III receptors, causing pain. In vitro evaluation of neuronal discharge from mechanosensitive afferents were evaluated in rabbits subjected to mechanical forces.103 Various types of mechanoreceptors were found in the capsule of Z-joints. High-threshold type III and IV mechanoreceptors were found with neuronal discharges responding to load postulated to be noxious.103 Group III fibers were found to correspond to A-delta fibers. Human surgical specimens have been evaluated to elucidate the pathophysiology of Z-joint pain. Z-joints specimens obtained in human subjects undergoing fusion demonstrated cartilage fibrillation, cartilage loss, exposed subchondral bone, fissuring, chondrocyte clustering, subchondral cysts, and erosion channels from subchondral bone through the tidemark region to the articular cartilage. These erosion channels contained small blood vessels and granulation tissue.105 The presence of granulation tissue suggests an inflammatory process. Surgical specimens of Z-joints were obtained from subjects undergoing surgery for spinal stenosis and herniated disc.106 The specimens were evaluated for B and T lymphocytes involved in inflammation or immune reactions. The specimens revealed primarily monocytes and collagen-producing fibroblasts. Inflammatory cells were not verified in this study. The authors concluded mechanical irritation leads to fibroblastic collagen production and not inflammation. However, this study has a serious flaw. The Z-joints studied were not in subjects suffering from Z-joint pain but from spinal stenosis and disc pathology. Since the specimens were not from symptomatic Z-joints the pathophysiology of Z-joint from these specimens is suspect. The authors did state inflammation could not be excluded.

Various neuropeptides have been isolated from Z-joint specimens.102,105,107 C-flanking peptide of neuropeptide Y (CPON) is a potent vasoconstrictor. Substance P, VIP, and CGRP have been found and suggest a potential for pain production.102,105,107 Increased levels of prostaglandin E2 and F1-alpha have been demonstrated in Z-joints obtained from human subjects undergoing lumbar fusion.83 The affect of phospholipase A2 on Z-joint nerve fibers obtained in rabbits has been studied.78 Histologic and electrophysiologic analysis demonstrated phospholipase A2 induced an inflammatory reaction with subsequent neurotoxicity.78 As with other synovial joints, the Z-joint may be subject to rheumatologic disorders such as rheumatoid arthritis and gout. Degenerative osteoarthritis may develop from trauma, repetitive microtrauma, and altered biomechanics of the spine. However, this has not been adequately evaluated. While the pathophysiology of Z-joint pain is incompletely understood, the above studies suggest both biomechanical and biochemical irritation of the Z-joint can occur. Additionally, the studies suggest the Z-joint as a possible source of pain. Pain emanating from the Z-joint can be determined by use of local anesthetics. If the joint can be anesthetized, then pain emanating from the joint should be eliminated. Diagnostic injections utilizing local anesthetics have been performed to diagnose Z-joint pain. These injections have demonstrated specificity and validity for pain emanating from the Z-joint.14–19,108 The Z-joint can be anesthetized through neural blockade of the medial branch of the posterior primary ramus.16–18 Alternatively, the joint can be anesthetized through intraarticular instillation of local anesthetic.15,108–113 Blockade of the joint would require anesthetizing A-delta and C fibers along with A-alpha and A-gamma fibers.114 In joint injections, the amount of anesthetic should be small enough to avoid leakage to adjacent structures and sufficient enough for neural blockade. The chapter on spinal injection techniques addresses concentration and amounts of local anesthetics to achieve this, along with placement at the targeted structure. Local anesthetics may additionally have a therapeutic effect in Z-joint pain. Local anesthetics have been shown to have an antiinflammatory effect and alter leukocyte function which may reduce neuropeptide and cytokine concentrations in the joint.47,49–55 Whether this effect is clinically relevant has not been demonstrated. However, there are individuals who present with lasting relief following a diagnostic injection. While this can potentially be a placebo effect, one can not discount the possibility of a therapeutic effect of the local anesthetic.

SACROILIAC JOINT The sacroiliac joint (SIJ) is an auricular-shaped diarthrodial joint with joint capsule, synovial fluid, hyaline cartilage on the sacral side, and fibrocartilage on the iliac side.115 The sacroiliac joint is partially innervated by the posterior rami of the lumbosacral roots.116 The anterior joint receives innervation from L3–S2 and the superior gluteal nerve.117 The posterior joint innervation has been reported from S1–2117 and L4–S3.118 The S1 level may be the major contributor to the joint.119 Possible autonomic contribution adds to the complexity of innervation of the sacroiliac joint.120,121 The lumbosacral trunk is just anterior to the joint in the lower third.122,123 The L4 and L5 nerve roots are 1 cm medial to sacroiliac joint at the level of the pelvic brim.124 The L4 and L5 nerve roots are 23 and 26 mm medial to sacroiliac joint, respectively, and 4.0 cm above the pelvic brim.124 The innervation of the joint is not completely understood at this time. As the innervation is unknown, utilization of nerve blockade as in medial branch blockade for Z-joint pain cannot be recommended for diagnosing SIJ pain. 199

Part 2: Interventional Spine Techniques

Injection of contrast into the SIJ was found to result in pain, suggesting the joint as a potential source of pain.125 Additionally, infection and rheumatologic condition affecting the joint have been found to be painful.126–131 The pathophysiology of sacroiliac joint pain is not known at this time. With normal aging the joint capsule thickens, plaques develop along the cartilage surface, erosions develop, fibrous interconnections develop, the joint surface becomes irregular, and eventual ankylosis can occur.115,132–134 Infectious and rheumatologic conditions have affected the joint, resulting in pain. Fluoroscopic injection of corticosteroid into the joint of seronegative spondyloarthropathy sufferers has been reported to result in greater than 70% pain relief in 79.2% of subjects.131 At a mean follow-up of 22.9 months a 50% decrement in VAS score occurred in those with positive diagnostic SIJ injection treated with SIJ corticosteroid injection and physical therapy. This may suggest an inflammatory component to SIJ syndrome. However, this is an uncontrolled study. The pathophysiology of SIJ syndrome is unknown. Anesthetic agent has been shown to relieve SIJ pain.9,135,136 The specificity and sensitivity for diagnostic SIJ injection is unknown. The double-block paradigm has been performed, suggesting a falsepositive rate of 47%.136 To maintain specificity, a volume of no more than 2.0 cc is recommended as joint capsule leakage through rents in the joint capsule may occur with larger volumes.135 Leakage of anesthetic can anesthetize the lumbosacral plexus resulting in false positives. False-negative diagnostic injections can occur even with correct placement due to loculations within the joint preventing anesthetic agents from reaching the target.137 To avoid inadvertent extravasation through rents in the joint capsule, injection under live fluoroscopy of combined nonionic contrast agent and local anesthetic has been proposed.138 If leakage outside the joint begins to occur the injection is stopped.

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98. Bogduk N. Lumbar dorsal ramus syndrome. Med J Aust 1980; 2:537–541.

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Part 2: Interventional Spine Techniques 101. Gronblad M, Korkala O, Konttinen YT, et al. Silver impregnation and immunohistochemical study of nerves in lumbar facet joint plical tissue. Spine 1991; 16: 34–38. 102. Giles LGF, Harvey AR. Immunohistochemical demonstration of nociceptors in the capsule and synovial folds of human zygapophyseal joints. Brit J Rheum 1987; 26:362–364. 103. Avramov A, Cavanaugh JM, Ozaktay CA, et al. The effects of controlled mechanical loading on group II, III, and IV afferent units from the lumbar facet joint and surrounding tissue. J Bone Joint Surg [Am] 1992: 74A:1464–1471. 104. Yamashita T, Cavanaugh JM, El-Bhoy AA, et al. Mechanosensitive afferent units in the lumbar facet joint. J Bone Joint Surg [Am] 1990; 72A:865–870.

121. Pitkin HC, Pheasant HC. Sacroarthrogenetic telalgia. 1: a study of referred pain. J Bone Joint Surg [Am] 1988; 70A:31–40. 122. Albee FH. A study of the anatomy and the clinical importance of the sacroiliac joint. JAMA 1909; LIII:1273–1276. 123. Hershey CD. The sacro-iliac joint and pain of sciatic radiation. JAMA 1943; 122:983–986. 124. Ebraheim NA, Padanilam TG, Waldrop JT, et al. Anatomic consideration in the anterior approach to the sacro-iliac joint. Spine 1994; 19:721–725.

105. Beaman DN, Graziano GP, Glover RA, et al. Substance P innervation of lumbar spine facet joints. Spine 1993; 18:1044–1049.

125. Fortin JD, Dwyer AP, West S, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique. Part I: Asymptomatic volunteers. Spine 1994; 19:1475–1482.

106. Knottinen YT, Gronblad M, Korkala O, et al. Immunohistochemical demonstration of subclasses of inflammatory cells and active, collagen-producing fibroblasts in the synovial plicae of lumbar facet joints. Spine 1990; 15:387–390.

126. Engelsbel S, Swartjes JM, Schutte MF. Case report. Pyogenic sacro-iliitis, a rare cause of peripartum pelvic pain. Eur J Obstetrics Gyn Reproductive Bio 1995; 62:125–126.

107. Ashton IK, Ashton BA, Gibson SJ, et al. Morphological basis for back pain: the demonstration of nerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum. J Orthop Res 1992; 10:72–78.

127. Brand C, Warren R, Luxton M, et al. Cryptococcal sacroiliitis. Case report. Annals Rheum Dis 1985; 44:126–127.

108. Dreyfuss P, Tibiletti C, Dreyer S, et al. Thoracic zygapophyseal joint pain: A review and description of an intra-articular block technique. Pain Digest 1994; 4:46–54.

128. Reginato AJ, Ferreiro-Seoane JL, Falasca G. Unilateral sacroiliitis in secondary syphilis. J Rheum 1988; 15:717–719.

109. Bogduk N, Marsland A. The cervical zygapophyseal joints as a source of neck pain. Spine 1988; 13:610–617.

129. Pouchot J, Vinceneux P, Barge J, et al. Tuberculosis of the sacroiliac joint: Clinical features, outcome, and evaluation of closed needle biopsy in 11 consecutive cases. Am J Med 1988; 84:622–628.

110. Carrera GF. Lumbar facet joint injection in low back pain and sciatica. Description of technique. Radiology 1980; 137;661–664.

130. Dunn EJ, Bryan DM, Nugent JT, et al. Pyogenic infections of the sacro-iliac joint. Clin Ortho Rel Res 1976; 118:113–117.

111. Carrera GF. Lumbar facet joint injection in low back pain and sciatica. Preliminary results. Radiology 1980; 137:665–667.

131. Maugars Y, Mathis C, Vilon P, et al. Corticosteroid injection of the sacroiliac joint in patients with seronegative spondylarthropathy. Arthritis Rheum 1992; 35: 564–568.

112. Fairbanks JCT, Park WM, McCall IW, et al. Apophyseal injection of local anesthetic as a diagnostic aid in primary low-back pain syndromes. Spine 1981; 6:598–605. 113. Fortin JD, Mckee MJ. Thoracic facet blocks: bent needle technique. Pain Phys 2003; 6:513–516. 114. LaMotte RH, Campbell JN. Comparison of responses of warm and nociceptive C-fiber afferents in monkey with human judgements of thermal pain. J Neurophysiol 1978; 41:509–528.

132. Stewart TD. Pathologic changes in aging sacroiliac joints. A study of dissectingroom skeletons. Clin Orthop Rel Res 1984; 183:188–196. 133. Sashin D. A critical analysis of the anatomy and the pathologic changes of the sacro-iliac joints. J Bone Joint Surg [Am] 1930; 12A:891–910. 134. MacDonald GR, Hunt TE. Sacro-iliac joints. Observations on the gross and histological changes in the various age groups. Canad M A J 1952; 66:157–163.

115. Bowen V, Cassidy JD. Macroscopic and microscopic anatomy of the sacroiliac joint from embryonic life until the eighth decade. Spine 1981; 6:620–628.

135. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37.

116. Steindler A, Luck JV. Differential diagnosis of pain low in the back. Allocation of the source of pain by the procaine hydrochloride method. J Am Med Assoc 1938; 110:106–113.

136. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation test in 54 patients with low back pain. Spine 1996; 21:1889–1892.

117. Solonen KA. The sacroiliac joint in the light of anatomical, roentgenological and clinical studies. ACTA Orthop Scand (Suppl) 1957; 27:1–127.

137. Miskew DB, Block RA, Witt PF. Aspiration of infected sacro-iliac joints. J Bone Joint Surg [Am] 1979; 61A:1071–1072.

118. Bertrand TN Jr, Cassidy JD. The sacroiliac joint syndrome. Pathophysiology, diagnosis, and management. In: Frymoyer JW, Ducker TB, Hadler NM, et al., eds. The adult spine. Principles and Practice. New York, NY: Raven Press; 1991:2107–2130.

138. Slipman CW, Huston CW. Diagnostic sacroiliac joint injections. In: Interventional pain management. Low back pain: Diagnosis and treatment. Manchikanti L, Slipman CW, Fellows B, eds. Paducah, KY: ASIPP; 2002:269–274.

119. Greenman PE. Clinical aspects of sacroiliac joint function in walking. J Man Med 1990; 5:25–130.

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120. Norman GF, May A. Sacroiliac conditions simulating intervertebral disc syndrome. West J Surg 1956; 64:461–462.

PART 2

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Section 1

Principles and Concepts Underpinning Spinal Injection Procedures

CHAPTER

Placebo

18

Nikolai Bogduk

When used as a noun, placebo means a treatment that lacks any specific therapeutic effect. In the case of a drug, a placebo would be an agent that lacks any pharmacological effect. In the case of a procedure, a placebo would be one that lacks any specific anatomical or physiological effect. Nevertheless, in other respects a placebo has all of the features of an intervention that should work. When used as an adjective, placebo occurs in two forms: the placebo effect, and the placebo response. Placebo effect is the presumed or perceived effect that a placebo has on an individual. Placebo response is what the individual reports after having been administered a placebo, and is ostensibly due to the placebo effect. Essentially, a placebo is not supposed to work. Any effect or response that it evokes is, therefore, paradoxical. The resultant paradox is difficult to handle in clinical practice. Consequently, placebo is a commonly misunderstood concept that is subject to abuse, misinterpretation, and myths.

PLACEBO RESPONDER When patients exhibit a placebo response, practitioners and authors sometimes, if not often, refer to them as ‘placebo-responders.’ This term implies that the patient has an inherent trait that means that they will consistently respond to placebos. This is wrong. There is no personality trait or psychological trait that causes individuals to respond consistently to placebos.1 Experimental studies have shown that any individual at any time is liable to express a placebo response, depending on the circumstances; but also that such responses are not consistent.1–3 Indeed, one authority has ventured to conclude that proneness to placebo is universal.4 The placebo response is a variable phenomenon, and does not reflect anything about the individual who reports it. The term placebo responder, therefore, can have only a pejorative connotation, to dismiss or relegate patients for having exhibited a paradoxical phenomenon. When used, it expresses more about the prejudices of the practitioner than anything about the patient. Consequently, the term should be expunged from clinical vocabulary, and never used.

PLACEBO RESPONSES ARE FAKE Some practitioners handle the paradox of placebo responses by dismissing them on the grounds that the patient has a psychological problem, is malingering, or is frankly lying. This is both a misinterpretation and misrepresentation of the placebo response. The distinction is that a placebo response occurs after the intervention, ostensibly because of it. In contrast, malingering and lying require premeditation. To accuse a patient of malingering or lying, because they have a placebo response, is therefore tantamount to accusing them of premeditation. The placebo response provides no

evidence of this. Such an interpretation, therefore, reflects the prejudices of the practitioner. Nor is the placebo response a sign of psychological distress. Placebo responses occur under experimental conditions in individuals with no evidence of psychological disturbance.5,6 Among patients with chronic pain, profiles of psychological distress do not differ between patients who have true-positive responses to placebo-controlled diagnostic blocks and those who have placebo responses,7 or between patients who have successful outcomes after treatment and those who do not.8

NOT IN CLINICAL PRACTICE A common belief, though rarely enunciated, is that placebo responses occur only in research studies and, reciprocally, that they do not occur in ‘real’ practice. Implicitly, placebo responses are somehow precipitated only if and when patients enroll in controlled trials. This is a self-serving belief, designed to excuse practitioners in the ‘real’ world of any responsibility to be alert to placebo responses, or to have their practices accountable to placebo effects. The belief conveniently ignores the realization that controlled trials are simply the means by which placebo responses can be demonstrated and quantified. That having been done, practitioners are warned to expect the same phenomenon, with the same prevalence, in conventional practice. Practitioners choose to ignore this warning. They prefer, instead, to believe that all positive therapeutic effects of their practice must be due to the specific effects of their ministrations, and that their successes could not be due to something as ephemeral as a placebo effect. Under these conditions, ignoring the prevalence of placebo effects serves to protect the ego of a practitioner, while offending scientific accountability to the truth.

CONSTANT RATE A widespread urban myth is that about one-third of patients in any cohort will express a placebo response, implying some sort of endemic influence. This myth has been traced to an early study of placebo responses.1,3 In reviewing the literature, Beecher9 encountered a wide variety of placebo response rates, ranging from 15% to 58%. A figure of 35.2% arose as a numerical average of these rates, unweighted for sample sizes. Subsequent studies have encountered placebo response rates from as low as 0% to as high as 100%.1 There is nothing constant about 35%. Placebo response rates differ considerably according to the circumstances of the study.

MECHANISM In the context of pain medicine, a placebo would be an agent or a procedure that should have no effect on pain by pharmacological,

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anatomical, or conventional physiological means. A placebo response would be relief of pain despite this lack of a conventional means by which the pain could be relieved. The occurrence of a placebo response implies a placebo effect. The mechanism or mechanisms of that placebo effect remain largely elusive. Theories have been proposed; but, of late, experimental studies have pursued its physiological basis. The fact that pain is relieved implies that whatever the mechanism is of placebo effects, it must involve the nociceptive system. The prevailing theories about placebo invoke some sort of suppression at one level or another of the nociceptive system.

Conditioning Conditioning is a prominent theory amongst psychologists who seek to explain the placebo effect.2,3 The theory is based largely on data from experimental studies, in which subjects previously exposed to an intervention have continued to express positive responses when that intervention was surreptitiously or progressively replaced with a sham intervention. However, it is hard to reconcile this theory with the nature of interventional spine medicine. If anything, patients are likely to encounter repeated failures of treatment and, therefore, would be conditioned not to respond. Indeed, the conditioning theory has been adapted to fit this phenomenon by becoming an explanation for nocebo responses or ‘placebo sag.’2 In contrast, if the contention is that patients expect relief when they consult a doctor, instead of conditioning theory, expectation is a more appealing explanation.

Expectation One of the prominent explanations for the placebo effect is that patients who undergo a treatment for pain expect the treatment to work.2,3 This expectation can be reinforced if the practitioner engenders or fosters the expectation. It is reinforced if the treatment is undertaken in an impressive manner in an impressive setting, such as a high-tech facility. Indeed, factors found to enhance the placebo effect are: the credibility of the therapist, the credibility of the therapeutic setting, the credibility of the treatment, the credibility of the administrative setting, and the nature of the interaction between the patient and the therapist.2 The expectation model implies an interruption of the pain experience at a cortical level. One could say that the patient imagines receiving relief, because that is what is expected to occur. More graciously, one could infer that a subliminal, cortical effect occurs, in which the patient is distracted from the pain by the promise of expected relief. Since they involve cerebral mechanisms, these conjectures are difficult to test. The pathways and processes are not amenable to experimental manipulation. Another interpretation, however, is that cerebral processes may invoke spinal mechanisms.

Spinal mechanisms Diffuse noxious inhibitory control (DNIC) operates as a normal physiological process within the nociceptive system. Under normal conditions, its function is to discriminate incoming nociceptive information by center-surround inhibition. Under artificial conditions, however, DNIC can suppress nociception. Suppression occurs when brainstem nuclei are stimulated globally, which sends inhibitory influences through descending pathways to all segmental levels of the spinal cord. This is one of the purported mechanisms of acupuncture, and the possible mechanism by which deep brain stimulation relieves pain. Conversely, systemic opioids

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work by globally inhibiting descending pathways. The resultant loss of inhibition causes any nociceptive information to be obscured by uninhibited background noise at the spinal level of the nociceptive system. Placebos might work if subliminal cerebral processes activate the descending nociceptive systems. Under those conditions, placebo responses are not psychological in nature, but involve physiological processes in the central nervous system. Indeed, those processes are similar to or the same as those by which drugs and neuroaugmentative surgery achieve relief of pain. The distinction is only that the mind, rather than an exogenous agent, switches on the descending inhibition. Circumstantial evidence to this effect arises in experiments in which placebo responses have been reversed by the administration of opioid antagonists such as naloxone.1,3,5,10 Conversely, antagonists to cholecystokinin enhance placebo analgesia.6 The fact that drugs, known to block analgesic pathways in the brainstem and spinal cord, also block placebo effects implies that the same physiological systems are involved.

Meaning model The meaning model invokes quite a different process.3 It suggests that, in order to maximize the placebo response, the patient must feel listened to, must receive what they perceive to be a valid explanation for their illness, feels care and compassion from their treatment environment, and feels empowered. This model does not invoke antinociception, nor does it invite it. Instead, it predicts that patients who exhibit a placebo response are ones who have amplified their symptoms, at the time of treatment, because of fear, ignorance, and forlornness. When these are addressed, the amplification is removed; the report of pain is less; and the treatment appears to have relieved pain. Psychic amplification can be reduced by directly addressing the patients’ fears and ignorance, and having them feel understood and cared for. Alternatively, the same effects might occur circumstantially when a practitioner delivers an otherwise inactive treatment but with confidence and conviction, which implicitly relieves the patient’s psychic concerns.

MAGNITUDE Many studies have demonstrated that placebo effects and placebo responses are ubiquitous. Essentially, every intervention for pain will have a placebo component. Either an individual will have a response that is partially due to the active treatment and partially due to a placebo effect or, within a cohort of patients, some may have an effect that is entirely due to placebo. Controlled trials reveal how often this effect occurs and its magnitude. Placebo-controlled trials of analgesics have shown fairly consistently that the placebo effect amounts to at least 50% or up to 80% of the effect of the active agent. Whereas an analgesic might reduce pain, on the average, from 6 to 3 on a 10-point scale, placebo drugs will reduce pain from 6 to between 4 and 5. This implies that more than half the efficacy of analgesics must be attributed to placebo effects. In other instances, the efficacy of analgesics is not significantly different from that of placebos. That implies that the apparent efficacy of these analgesics, in the ‘real’ world, is entirely due to placebo effects.11 Similar proportions apply to those surgical interventions for pain that have been subjected to placebo controls. On average, shamtreated patients experience 50% as much relief of pain as do patients treated with antiradical intradiscal electrothermal therapy.12 But

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

these average figures belie the actual situation. While some patients have no response to sham treatment, others can obtain complete relief of pain. This combination results in an average of about 50%, but that average is not shared by all patients. The same applies to less-invasive procedures. The efficacy of lumbar intraparticular injection of corticosteroids is no greater than that of intraparticular injection of saline,13 intramuscular injection of either steroids or saline,14 or of simple medial branch blocks.15 Even diagnostic procedures are subject to placebo effects. Patients who believe that they are undergoing zygapophyseal joint blocks report complete relief of pain following subcutaneous injection of normal saline.16 Stellate ganglion blocks with normal saline relieve the symptoms of complex regional pain syndrome.17 Intravenous infusions of normal saline relieve the motor features of complex regional pain syndrome.18 Such data warn that practitioners in conventional practice have no right to believe that the success that they achieve is due to the purported mechanism of their treatment. That is not to say that the successes are not real. The issue is one of attribution. In principle, the outcome might be due to a placebo effect. Unless and until that is excluded, claims that the outcome is wholly due to the purported active component of the treatment cannot be sustained. Practitioners face a professional, if not ethical and moral, dilemma. It is convenient to believe that placebo effects do not occur in conventional practice. It serves the ego to believe that all interventions work because of the practitioner’s ability to perform the treatment, and their knowledge of how the intervention is said to work. It is anathema to accept that it could all be a sham: that the treatments work because of non-specific factors that the practitioner does not acknowledge, and which ostensibly lessen the expertise and skill of the practitioner. Yet, to ignore placebo amounts to creating an illusion that is perpetrated on the patient, and perpetuated in the interests of sustaining the standing of the practitioner. Therein lies the dilemma: whether to be loyal to the facts or to the reputation. If interventional spine medicine is to be accountable to science, the role of placebo must be acknowledged, measured, and accommodated. To ignore it, relegates interventional spine medicine to the status of a medieval guild, whose purpose is only to exploit the suffering of patients for its own gain.

References 1. Wall PD. The placebo effect: an unpopular topic. Pain 1992; 51:1–3. 2. Peck C, Coleman G. Implications of placebo theory from clinical research and practice in pain management. Theoret Med 1991; 12:247–270. 3. Brody H. The placebo response: recent research and implications for family medicine. J Fam Pract 2000; 49:649–654. 4. Shapiro AK. Semantics of the placebo. Psychiatr Q 1968; 42:635–695. 5. Amanzio M, Benedetti F. Neuropharmacological dissection of placebo analgesia: expectation-activated opioid systems versus conditioning-activated specific subsystems. J Neurosci 1999; 19:484–494. 6. Benedetti F, Amanzio M. The neurobiology of placebo analgesia; from endogenous opioids to cholecystokinin. Prog Neurobiol 1997; 51:109–125. 7. Lord S, Barnsley L, Wallis BJ, et al. Chronic cervical zygapophyseal joint pain after whiplash: a placebo-controlled prevalence study. Spine 1996; 21:1737–1745. 8. Wallis BJ, Lord SM, Bogduk N. Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomised, doubleblind, placebo-controlled trial. Pain 1997; 73:15–22. 9. Beecher HK. The powerful placebo. JAMA 1955; 159:1602–1606. 10. Ter Riet G, de Craen AJM, de Boaer A, et al. Is placebo analgesia mediated by endogenous opioids? A systematic review. Pain 1998; 76:273–275. 11. Van Tulder MW, Scholten RJPM, Koes BW, et al. Nonsteroidal anti-inflammatory drugs for low back pain. A systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2000; 25:2501–2513. 12. Pauza KJ, Howell S, Dreyfuss P, et al. A randomised, placebo-controlled trial of intradiscal electrothermal therapy for the treatment of discogenic low back pain. Spine J 2004; 4:27–35. 13. Carette S, Marcoux S, Truchon R, et al. A controlled trial of corticosteroid injections into facet joints for chronic low back pain. New Engl J Med 1991; 325:1002– 1007. 14. Lilius G, Laasonen EM, Myllynen P, et al. Lumbar facet joint syndrome: a randomised clinical trial. J Bone Joint Surg 1989; 71B:681–684. 15. Marks RC, Houston T, Thulbourne T. Facet joint injection and facet nerve block: a randomised comparison in 86 patients with chronic low back pain. Pain 1992; 49:325–328. 16. Schwarzer AC, Wang S, Bogduk N, et al. Prevalence and clinical features of lumbar zygapophyseal joint pain: a study in an Australian population with chronic low back pain. Ann Rheum Dis 1995; 54:100–106. 17. Price DD, Long S, Wilsey B, et al. Analysis of peak magnitude and duration of analgesia produced by local anesthetics injected into sympathetic ganglion of complex regional pain syndrome patients. Clin J Pain 1998; 14:216–226. 18. Verdugo RJ, Ochoa JL. Abnormal movements in complex regional pain syndrome: assessment of their nature. Muscle Nerve 2000; 23:198–205.

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Section 1

Principles and Concepts Underpinning Spinal Injection Procedures

CHAPTER

Patient Education and Support

19

Andrea Tarquinio, Colleen McLaughlin, Faisel M. Zaman and Curtis W. Slipman

This chapter was designed with the purpose of providing insight into the role of the medical staff in patient education and assessment, both prior to and after spinal injection procedures. This chapter will also discuss the importance of appropriate and effective communication in carrying out the algorithmic approach to patient care that was initially formulated. Education and assessment are a continuous process that begins with the initial consultation and continues throughout the patient’s course of care.

Penn Spine Center Spinal injection procedure education confirmation form

NEW PATIENT VISIT At the initial consultation and evaluation, a thorough, detailed history and physical examination is conducted. This information, in addition to the findings of other pertinent diagnostic studies such as radiographic and neurophysiologic data (i.e. magnetic resonance imaging and electrodiagnostic studies) is incorporated into formulating a comprehensive plan of care. Once spinal injections are integrated into the course of care, there are several ways in which education is provided. First, the physician explains the algorithmic approach to spinal injections which may include selective nerve root, facet joint, piriformis, hip, and sacroiliac joint injections of a diagnostic or therapeutic nature. The physician obtains informed consent, and discusses in detail the nature and purpose of the procedure, as well as the potential side effects, risks, and complications of the specific spinal injections being considered.1–4 Certain medications, such as anticoagulants (e.g. warfarin, clopidogrel) or certain oral antidiabetic agents such as metformin, are to be withheld prior to any spinal injection procedure. If warfarin is in the medication list, the medication should be withheld for 72 hours prior to the procedure. Warfarin usage may restart the evening of the day after the procedure. If there is any concern as to whether or not it is safe to perform a spinal injection procedure, it is prudent to check a coagulation profile. Clopidogrel is to be withheld for 5 days, and usage may be resumed the next day. Metformin is to be withheld the day of the procedure and for 48 hours afterwards. In order to provide a better understanding of what may be expected the day of the procedure, a spinal injection guide is handed out at the initial visit. Information found inside this guide includes definitions of relevant terms, medications administered, and expectations prior and subsequent to the procedure, as well as an explanation of possible complications. Since oftentimes one may forget that these important details surrounding the injection procedure were discussed, the authors ask that a patient information form be signed (Fig. 19.1). The form simply states that they have received an information booklet, and that the logistics of the procedure have been discussed.

Patient information booklet received

Logistics of injection procedure explained by

Possible side effects and complications of procedure

Explained by

, M.D.

Print name

Signature

Date

Fig. 19.1 Spinal injection procedure education confirmation form.

PREPROCEDURE At the time of the actual spinal injection procedure, in addition to performing a re-assessment, the authors reinforce and provide further education, ease anxiety, and make the experience a more comfortable one in any way possible. Prior to any procedure, informed consent must be obtained. The importance of properly obtaining informed consent cannot be overemphasized. The components of informed consent include discussion of the nature, purpose, and potential benefits of a procedure, as well as potential side effects, risks and complications.1–4 These issues are discussed in fine detail at the initial consultation, and at many other times during the course of care. In addition to obtaining written informed consent prior to the injection procedure, a pain assessment drawing must be completed. (Fig. 19.2)

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UPHS – PHM – Low back pain PENN SPINE CENTER – PAIN ASSESSMENT FORM

Name

Example

Date Draw the location of your pain on the body outlines and mark how severe it is on the pain line at the bottom of the page

Aching Burning Numbness Pins and Stabbing Other needles ooooo / / / / / / xxxx ^^^^^ ooooo / / / / / / xxxx ^^^^^

^ ^ x x x x x x x

PAIN DRAWING

PAIN LINE

Draw a perpendicular line or arrow to indicate your usual level of pain

Example No pain 0%

Worst pain 100%

0%

50%

100%

Fig. 19.2 Pain assessment form.

According to the National Institutes for Health (NIH), patient self-reporting is the ‘most reliable indicator of the existence and intensity of pain.’5 The pain drawing is completed according to the patient’s discomfort pattern at the specific moment in time just prior to the procedure, as opposed to where the discomfort was at the initial visit, or where it is on average. A pain drawing is to be completed at every encounter, including injection procedures. The location and character of the pain complaint (e.g. numbness, stabbing, burning) as well as the intensity of pain on the 11-point visual analog scale (VAS) is to be documented. By illustrating the discomfort present at the specific encounter, a visually recorded diary of symptom progression is created. If the case is one of successful pain mitigation, or failure to progress, it will be illustrated upon review of the pain drawings. Studies have shown that there is an ‘amnestic property of pain.’ This means that one may not remember the level of pain which was previously experienced. This is true especially if the current pain is severe.6 The VAS was introduced in the early part of the last century as a psychologic assessment tool for the measurement of pain and mood. The popularity of the VAS stems from its simple construction and ease of use.7 It is best used in the sequential evaluation of pain; the broad range of scores allows for subsequent statistical analysis. The VAS ranges from 0 to 10 (or 100), and is most often measured on a 10 cm horizontal line.8,9 The VAS is a unidimensional assessment 208

tool based on self-report and is the most commonly used and validated scale to assess pain.10–12 The ideal tool in the assessment of pain should include the identification of the presence of pain, as well as the progress of pain with time or treatment.10,13 Studies have shown that outside observers are often inaccurate in their assessment of a patient’s pain on an individual basis; thus, pain drawings and VAS ratings are of utmost importance.14,15 Incidentally, a study by Todd and Funk correlated a change of 1.8 cm on a scale of 10 cm in the physician’s assessment of the patient as the patient’s feeling ‘a little bit better.’16 In another recent study, Farrar et al. showed that widely different patient populations interpret changes in VAS similarly.17 In some instances, even after a thorough explanation of the algorithmic approach at the initial consultation, some questions may still remain regarding the ‘next step’ in the process. For example, if a patient had a positive diagnostic selective nerve root block, usually a therapeutic selective nerve root injection is scheduled to follow. In this case, it would be explained that steroids are to be administered along with either 2% or 1% lidocaine. In addition, it is important to present an estimated duration for the procedure. If, on the other hand, a diagnostic injection were to be performed, in order to ensure that the usual symptoms were present, ‘yes’ or ‘no’ would need to be checked on a form that states ‘Are you experiencing your usual pain right now?’ (Fig. 19.3).

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

DIAGNOSTIC INJECTIONS ARE YOU EXPERIENCING YOUR USUAL PAIN RIGHT NOW?

YES

NO

Fig. 19.3 Diagnostic injection pain verification form.

The words ‘right now’ are the key words in this particular situation. In order to receive the necessary information that a diagnostic injection may provide, the usual symptoms must be present preprocedure. This is because the diagnostic test injection determines the plan of care based upon symptom presence right before the diagnostic injection and symptom attenuation or persistence approximately 20–30 minutes afterwards. It is important to note that diagnostic injections are not performed for numbness alone, and that there must be a significant ‘pain’ component. While these concepts may seem intuitive to the reader they are not so obvious to the patient. The authors have encountered numerous instances in which highly educated individuals, who had received a detailed explanation of the purpose and method of interpretation of diagnostic injections, presented for a diagnostic injection despite the complete absence of pain. Everyone undergoing a diagnostic test injection must be properly informed and educated prior to the procedure. Many hold the incorrect belief that all injections are expected to provide long-lasting improvement. Again, this is when the communication between staff and patient is critical; providing re-education of what a diagnostic test injection is and that any symptom relief is expected to be temporary. If a patient comes in and is not experiencing their usual pain, they are instructed either to perform a provocative maneuver they are familiar with or to reschedule the diagnostic injection when the pain is present.

THE INJECTION PROCEDURE Anxiety regarding the scheduled procedure may be a significant concern for some. If present, instruction is provided regarding various coping strategies utilizing one or a combination of well-known relaxation techniques. The techniques include slow, deep breathing in the

nose and out of the mouth, along with staying focused with concentration on the procedure at hand. This combination explained both prior to and during the procedure helps to reduce or ease anxiety levels. In certain instances a member of the medical staff may provide tactile stimulation to comfort the patient, such as holding the patient’s hand. At the time of the injection, the medical staff assists the physician by setting up a sterile injection tray with the appropriate supplies to perform the injection and also assist in drawing up medications. The most commonly used medications are 2% or 4% lidocaine for diagnostic injections or betamethasone (most recently and hopefully temporarily, methylprednisolone acetate) combined with 1% or 2% lidocaine for therapeutic injections. During the procedure the nursing staff is responsible for monitoring the appropriate vital signs for each patient. During the injections, the medical support staff (nurse, physician assistant, or radiology technologist) has several responsibilities which include verifying the correct patient, correct injection (whether diagnostic or therapeutic), and the correct side and level. The authors invariably double check the side of injection by conferring with the patient just prior to needle insertion. Other responsibilities include verifying allergies to materials such as contrast agents, latex, or shellfish. If there is an allergy to iodine-based contrast material or shellfish the authors will corroborate the type of reaction that previously occurred, and inquire about a gadolinium (MRI dye) allergy. The authors prefer to use gadolinium when there is an allergy to iodinated contrast, and do this in lieu of an allergy preparation. This agent can be use for any spinal injection procedure.18–21 In addition to assisting with the above issues, the medical staff also must query whether or not necessary medications such as warfarin, clopidogrel, or metformin were withheld and, if so, for what duration. This information is then documented in the chart, and further instruction is later given as to when resumption of these medications may occur. In the majority of cases, the primary-care physician or prescribing specialist, such as the cardiologist or endocrinologist, are consulted prior to recommending temporary modification of the patient’s medication profile.

POST-INJECTION ASSESSMENT At completion of the procedure the post-injection assessment period begins. The focus of this period is resuming the usual plan of care and ensuring a safe discharge to home. Following the conclusion of each procedure it is essential to check for dizziness or lightheadedness (most commonly resulting from a vasovagal reaction) when rising from a prone or supine position. These symptoms are important warning signs that one may have a syncopal episode. In order to prevent such from occurring, the patient should be assisted onto a stretcher in the reverse Trendelenburg position until they have recovered and are ready to be safely discharged. Weakness or numbness may also ensue after injection procedures, especially if 4% lidocaine is used, as this may produce a motor blockade. Any injection recipient, regardless of the injection type, must be able to stand safely and walk independently before being discharged (provided such was possible prior to the injection, of course). A continuous re-assessment process takes place to ensure that discharge occurs safely and smoothly. The post-injection assessment communication is particularly critical after a diagnostic injection is completed because the response to the injection will dictate the next step in the algorithm. It is important that the location and severity of the symptoms just prior to the injection are not forgotten, in order that an accurate post-injection

209

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determination regarding the persistence or attenuation of those specific symptoms is made in comparison. The following are examples of post-injection assessment scenarios which may arise. If pain is only present while walking; the patient must walk before and after the diagnostic injection, in order to provide a reliable response to direct future treatments. Another, more complex situation is one in which there may be more than one pain generator. For example, if a patient has axial low back pain attributable to lumbar internal disc disruption and sitting as provocative influence, this individual may also experience buttock, posterior thigh, and posterior calf pain with standing and ambulating that is likely due to an S1 radiculopathy. An S1 selective nerve root block may be performed to address the buttock and leg pain only. In this situation, it is important that both parties understand that if the diagnostic S1 selective nerve root block alleviates the leg pain and not the back pain, that this would be considered a positive response. Thereafter, therapeutic S1 selective nerve root blocks may be performed to address these S1 nerve root-generated symptoms. If symptoms improve but are not completely alleviated, the percentage of improvement is estimated and recorded. This estimation is derived by comparing the pre- and post-VAS ratings. The authors typically use an 80% VAS reduction to define a positive response. Of course, the situation is more complicated when there are multiple pain generators. In that circumstance, a process must be derived that allows the interventionist to determine if a single pain generator has been identified. The details of this process will depend upon the mechanism of injury and the location of symptoms. In general, any pain that is acute or subacute, that begins spontaneously, should be considered to emanate from a single cause, while traumatic insults can create painful symptoms that emanate from more than one source. Most commonly, traumatic etiologies are associated with a single injured structure. After all provocative maneuvers have been performed, and the appropriate questions asked, a positive or negative response determination is made after each diagnostic injection. Such questions would include ‘Are you experiencing your usual discomfort that was present prior to the injection?’ If the answer is ‘no,’ there is an ensuing assessment to determine if alleviation is complete or not, and again by what estimated percentage. If the pain is persistent, the response is recorded as negative. These questions are always raised after the pain diagram is completed. Any discrepancy between the verbal responses and the information gleaned from the pain drawing/VAS scale must be rectified. This requires patience and expert verbal communication. As previously mentioned, in order to progress from diagnostic to therapeutic injections, at least 80% symptom attenuation must be obtained. If this degree of pain relief is not realized a determination of the next step is made by utilizing the algorithm set up at the time of the initial consultation. Formal discharge instructions, which include information on checking for signs and symptoms of infection, such as excessive redness, swelling, or pain at the site of injection and watching for any drainage from the site of the injection, are provided. In addition, injection recipients are advised to monitor for an increase in body temperature, and are instructed to apply ice to the injection site to minimize any local irritation due to the needle track. Limitation in physical activities is advised for 24 hours. Ice helps to reduce blood flow and pain, and minimizes inflammation. In many instances, the usual occupation may resume following the injection, depending, of course, on the specific job requirements. If any complications or concerns were to arise, patients may contact the physician on call via an emergency beeper number that is provided upon discharge. 210

DISCOGRAPHY One particular procedure in which communication is of the utmost importance is provocative discography. A discogram is performed when the most likely pain generator is the intervertebral disc itself. Prior to scheduling discography, a thorough consultation is conducted to ensure that the nature, purpose, risks, alternatives, and potential benefits of the procedure are fully understood. The patient should be aware that the purpose of provocative discography is to reproduce their usual and familiar pain; thus, it is meant to be a painful procedure. At the time of the procedure, the role of the medical support staff is to counsel and provide re-education regarding the entire discography procedure. Once a patient is admitted for the procedure, he or she is positioned appropriately on the fluoroscopy table (usually a left anterior oblique position), and prepped and draped using strict aseptic technique. The needles are then placed in the appropriate discs to assess the disc levels in question. Once all needles are placed, the assessment process begins. Upon disc stimulation, the patient must communicate if their usual, familiar pain is recreated or not. In addition to pain familiarity, further details such as pain intensity, location, and character are sought. If symptoms are partially concordant, further details are again sought as to which components of their pain symptoms are reproduced and which components are not. These details are recorded diligently on the discography form (Fig. 19.4), which is subsequently placed in the chart in the appropriate location. When the procedure has been completed, the patient is assisted off the fluoroscopy table and transported to the radiology department for CT scanning for further evaluation of each disc level in question. Subsequently, another follow-up visit is conducted in

PENN SPINE CENTER DISCOGRAM FORM Patient Name:

MRN:

Level assessed: Amount of contrast injected: Normal Resistance:

Date: cc Decreased

Pain response: P0 P1 P2 P3 Pain line

None

Location:

(no pain provocation) (partial concordant) (discordant response) (concordant response)

Local anesthetic cc Pain response: P0 (no pain provocation) P1 (partial concordant) P2 (discordant response) P3 (concordant response) Post anesthetic pain line

type

level injected Location:

DISCOGRAM TYPE 1. Cottonball

STAGE OF DEGENERATION No degeneration. Soft white amorphous nucleus.

2. Lobular

Mature disc with nucleus starting to coalesce into fibrous lumps.

3. Irregular

Degenerated disc with fissures and rents in the nucleus and inner annulus.

4. Fissured

Degenerated disc with radial fissures leading to the outer edge of the annulus.

5. Ruptured

Disc has a complete radial fissure that allows injected fluid to escape. Can be any stage of degeneration. Disruption of end plate.

6. End plate fracture

Curtis W. Slipman, M.D. Director, Penn Spine Center

Fig. 19.4 Discogram form.

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

approximately 2 weeks, to discuss the discogram and the postdiscography CT scan findings, and to determine the next step in the patient’s plan of care.

9. Jensen MP, Karoly P, Braver S. The measurement of clinical pain intensity: A comparison of methods. Pain 1986; 27:117–126. 10. Ho K, Spence J, Murphy MF. Review of pain-measurement tools. Ann Emerg Med 1996; 27:427–432.

CONCLUSION

11. McCormack HM, Horne DJ, Sheather S. Clinical applications of visual analogue scales: A critical review. Psychological Med 1988; 18 1007–1019.

Appropriate patient education and assessment by the medical staff is an exceedingly critical process in the ongoing direction of the plan of care. The importance of efficient and effective communication in the physician–patient relationship cannot be emphasized enough.22,23 In managing a chronic illness, the physician–patient partnership is crucial, and the same goes for any acute situation.24 The treatment goal is to safely provide quality care for each and every patient in order to maximize quality of life and hopefully provide a pain-free environment in which to do so.

12. Zealley AK, Aitken RCB. Measurement of mood. Proc R Soc Med 1969; 62:993–996.

References

17. Farrar JT, Young JP, LaMoreaux L, et al. Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale. Pain 2001; 94:149–158.

1. Meisel A, Kuczewski M. Legal and ethical myths about informed consent. Arch Internat Med 1996;1 56(22):2521–2526. 2. Faden RR, Beauchamp TL, King N. A history and theory of informed consent. New York: Oxford University Press; 1986. 3. Brody H. Transparency: informed consent in primary care. Hastings Center Report 1989; 19(5):5–9. 4. Applebaum PS, Lidz CW, Meisel A. Informed consent: legal theory and clinical practice. New York: Oxford University Press; 1987. 5. Acute Pain Management Guideline Panel. Acute pain management: operative or medical procedures and trauma: clinical practice guideline. Washington DC: US Department of Health and Human Services; 1992. 6. Menegazzi J. Measuring pain at baseline and over time. Ann Emerg Med 1996; 27:433–435. 7. Torrance GW, Feeny D, Furlong W. Visual analog scales: do they have a role in the measurement of preferences for health states? Med Decis Making 2001; 21:329–334.

13. Fordyce WE. The validity of pain behaviour measurement. In: Melzack R, ed. Pain measurement and assessment. New York: Raven Press; 1983:145–153. 14. Grossman SA, Sheidler VR, Swedeen K, et al. Correlation of patient and caregiver ratings of cancer pain. J Pain Sympt Manage 1991; 6:53–57. 15. Farrar JT, Portenoy RK, Berlin JA, et al. Defining the clinically important difference in pain outcome measures. Pain 2000; 88:287–294. 16. Todd KH, Funk JP. The minimum clinically important difference in physicianassigned visual analog pain scores. Acad Emerg Med 1996; 3:142–146.

18. Slipman CW, Rogers DP, Isaac Z, et al MR Lumbar discography with intradiscal gadolinium in patients with severe anaphylactoid reaction to iodinated contrast material. Pain Med 2002; 3:23–29. 19. Falco FJ, Moran JG. Lumbar discography using gadolinium in patients with iodine contrast allergy followed by postdiscography computed tomography scan. Spine 2003; 28:E1–E4. 20. Wagner AL. Gadolinium diskography. Am J Neuroradiol 2004; 25:1824–1827. 21. Falco FJ, Rubbani M. Visualization of spinal injection procedures using gadolinium contrast. Spine 2003; 28:E496–E498. 22. Emanuel EJ, Emmanuel LC. Four models of the physician–patient relationship. JAMA 1992; 267:323–329. 23. Rees AM. Communication in the physician–patient relationship. Bull Med Library Assoc 1993; 81:1–10. 24. Clark NM, Nothwehr F, Gong M, et al. Physician–patient partnership in managing chronic illness. Academic Med 1995; 70:957–959.

8. Huskisson EC. Visual analogue scales. In: Melzack R, ed. Pain management and assessment. New York: Raven Press; 1983:33–37.

211

PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 1

Principles and Concepts Underpinning Spinal Injection Procedures

CHAPTER

Side Effects and Complications of Injection Procedures: Anticipation and Management

20

Kenneth P. Botwin, Lee Ann Brown, Durgadas Sakalkale and Robert Savarese INTRODUCTION This chapter will focus on reviewing the known complications of spinal injections. Preventive strategies to avoid these complications are discussed. Topics discussed include: injectates (local anesthetics, corticosteroids, contrast media), cardiologic, infectious, hematologic, neurological, respiratory, and urological complications. Anticipation and management of procedure-specific complications in the cervical, thoracic, and lumbosacral spine are also included.

Preprocedural and postprocedural management and care Preprocedural intake should include patient education regarding the procedure including its benefits/risks, informed consent, NPO status, and intravenous access if indicated. This includes ascertaining stable hemodynamic status, noting cardiorespiratory/systemic comorbidities, allergies, and ruling out any procedural contraindications. A physical examination may need to be performed in order to rule out any significant change since the last office visit. Preprocedural preparation includes patient positioning, attachment of cardiorespiratory monitoring equipment, sterile preparation and draping, supplemental i.v. fluids/antibiotics and oxygen if needed. Postprocedural patient care includes vital sign monitoring and brief neurological examination to rule out any significant change. Clinical observation following a spinal injection should take place for at least 30–40 minutes prior to discharge, depending on the procedure and whether conscious sedation was used. Procedure-specific discharge instructions should be explained, and a written copy should be given to all patients. Routine use of these steps in all patients may help to minimize potential complications.

GENERAL COMPLICATIONS Medication complications Commonly utilized medications in injection procedures include local anesthetics, corticosteroids, and contrast media. Reactions to such medications are extremely rare. The spinal interventionist needs to be aware, however, of the possible side effects, allergic reactions, and proper dosage of these medications. In order to prevent possible reactions to these medications, the spinal interventionist needs to perform strict cardiovascular and neurological monitoring in order to assure optimum safety for the patient.

Anaphylactic and allergic reactions Anaphylactic and allergic reactions are exceedingly rare in interventional spinal procedures. These systemic reactions can occur with anesthetics, corticosteroids, or contrast media. Anaphylactic reac-

tions occur most often within 2 hours after an epidural is performed.1 This can result in sudden cardiovascular and respiratory collapse, which can possibly be followed by death. Abnormal rates of absorption and bi-transformation of the local anesthetic can also lead to such a reaction. Systemic reactions may be mild, moderate, or severe. In a mild reaction the patient may experience light-headedness, headache, vertigo, tinnitus, metallic taste, hypertension, tachycardia, nausea, and slight muscle cramps. A moderate reaction can result in loss of consciousness, convulsions, or both. Severe toxic reactions caused by massive overdosage can result in coma, respiratory depression, and death. The lowest concentration and volume of local anesthetic drug should be used to prevent such adverse reactions. Care should be taken to avoid intravascular injection by using contrast dye and fluoroscopic guidance. Blood pressure, pulse oximetry, and ECG monitoring must be performed if anesthesia is used. All necessary resuscitation equipment should be available. Clinical management of anaphylactic reaction is seen in algorithmic form in Figure 20.1.

Anesthetics Local anesthetics are used in diagnostic and therapeutic spinal injections. The volume of the anesthetic is variable depending on the type of procedure performed. A typical interlaminar lumbar epidural injection may consist of 3–10 mL of anesthetic while a transforaminal epidural injection may consist of 1–3 mL. Allergic reactions to local anesthetic, although rare, may occur either from the local anesthetic agent, or if present, the methylparaben used as a preservative. There is a higher likelihood of reaction to procaine than amide-based local anesthetics. In a prospective review of 10 440 patients who received lidocaine for spinal anesthesia, the incidence of adverse reactions was reported to be about 3% for positional headaches, hypotension, and backache, 2% from shivering, and less than 1% each for peripheral nerve symptoms, nausea, respiratory inadequacy, and diploplia. Many of these observations may be related to injection techniques, with or without a contribution from the local anesthetic used.2 Inadvertent puncture of the thecal sac while injecting local anesthetic for an epidural can result in prolonged paresthesia, pains in the legs, and even transient paralysis.3 Bupivacaine can cause degeneration of muscle fibers after a single injection into a skeletal muscle.4 There have been reports of anesthetic injections outside of the neurofascicle which can lead to alterations in the blood–nerve barrier and consequent edema and swelling of the nerve.5 This can lead to a progressive decrease in nerve blood flow as the concentration increases.6 If a local anesthetic is injected intrafascicularly there can be devastating consequences from cytotoxicity and edema.7,8 These possible complications can be avoided using appropriate techniques, 213

Part 2: Interventional Spine Techniques Oxygen, IV access, airway intubation if needed

Stridor, wheeze, respiratory distress or clinical signs of shock1

Adrenaline (epinephrine)2,3 1:1000 solution 0.5 ml (500 μg) intramuscularly

Repeat in 5 minutes if no clinical improvement

Antihistamine (chlorpheniramine) 10 – 20 mg intramuscularly or slowly intravenously

In addition

For all severe or recurrent reactions and patients with asthma give hydrocortisone 100 – 500 mg intramuscularly or slowly intravenously.

If clinical manifestations of shock do not respond to drug treatment give 1 – 2 L of fluid intravenously4 Rapid infusion or one repeat dose may be necessary.

1. Inhaled O2 against such as salbutamol may be used if bronchospasm severe and does not respond rapidly to treatment. 2. If profound shock immediately life threatening give cardiopulmonary resuscitation or advanced life support if necessary. Consider giving adrenaline 1:10,000 solution slowly intravenously. Hazardous and recommended only for experienced physician. Note different strengths used for intramuscular and intravenous routes. 3. If treated with Epipen, 300 μg will usually be sufficient. A second dose may be required. Half doses of epinephrine may be safer for patients taking tricycle and antidepressants or beta-blockers. 4. Crystalloid may be safer than a colloid. Fig. 20.1 Management of anaphylactic reaction.

and utilizing contrast media prior to introduction of anesthetic near a nerve. Attention must be given to the amount of anesthetic administered in order to avoid the possibility of central nervous system toxicity. The total dosage of lidocaine should remain below 400–500 mg or 40 mL of 1% lidocaine. Bupivacaine is about 4 times more toxic than 1% lidocaine with a toxic bolus of 175 mg (or 17.5 cc) in a 70 kg patient.9 The signs of central nervous toxicity are disorientation, light-headedness, nystagmus, tinnitus, and muscle twitching in the face or distal extremities. Peak plasma concentrations occur 10–20 minutes after injection. Therefore, ongoing monitoring of the patient for the postoperative period for over 30 minutes is suggested strongly to avoid any possible potential nervous system toxicity from anesthetics. Other complications which can arise from local anesthetics for epidural analgesia include motor block, hypotension, urinary retention, and pressure necrosis.10 Higher doses of local anesthetics appear to increase the risk of motor block and hypotension.11,12 214

Cardiovascular complications If high systemic levels of local anesthetics are injected intravascularly and/or intrathecally during a spinal interventional procedure cardiovascular complications can arise. Usually, such reactions are preceded by central nervous system toxicity prior to cardiovascular complications arising. The cardiovascular toxicity is a direct result of anesthetics acting upon the myocardium and peripheral vasculature. In vitro studies using isolated myocardial tissue have shown anesthetics to have a dose-dependent negative inotropic action.13,14 The effects of local anesthetics on the cardiovascular system when at low levels can slightly increase blood pressure due to an increase in cardiac output and heart rate, which can enhance sympathetic activity and cause direct vasoconstrictor action. At higher concentrations, which produce CNS toxicity, they can cause a marked increase in heart rate, cardiac output, peripheral resistance, and blood pressure. With further increase in dosage there can be severe hypotension and cardiovascular collapse due to decreased cardiac output and peripheral

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

vascular dilation. Prevention of such complications certainly depends on avoiding intravascular injection. Thus, appropriate needle localization with fluoroscopy and contrast media is essential. Once CNS toxicity symptoms are present, the interventionist needs to prepare for possible cardiovascular complications. Institution of appropriate cardiopulmonary resuscitation is imperative for the management of such complications. Management of the patient using advanced cardiac life support (ACLS) would be implemented any time there is such a need. Appropriate management through emergency cardiac care algorithms is recommended and the reader is referred to more detailed sources for further information with regard to these algorithms and management.15–17

Corticosteroids Several injectable corticosteroid preparations have been utilized in interventional spinal procedures. These include, most commonly, triamcinolone, methylprednisolone, and betamethasone. Each of these corticosteroids has a different chemical composition. There have been several reports in the literature that have stated arachnoiditis may be related to the use of intrathecal steroids.18–22 A study by Latham23 has been done to assess intrathecally injected betamethasone in sheep, which did not reveal any evidence of arachnoiditis until high doses were utilized, and thus the study concluded intrathecal injection of betamethasone in low doses, such as those given in humans, is unlikely to cause arachnoiditis.23 Several studies have examined the effects of epidural and subarachnoid-deposited injections into the meninges and spinal cord. Cicala et al.24 looked for evidence of acute neurotoxicity (within 30 days) after injection of epidural corticosteroids. They examined the effects of a mixture of 1% lidocaine and methylprednisolone on the meningeal membranes and nerve roots 4 or 10 days after epidural injection. Microscopic examination revealed a complete lack of inflammatory changes in neural tissue and meningeal thickening. Abram et al.25 examined histological sections of spinal cords of rats that received 4 subarachnoid injections of triamcinolone at 5-day intervals and compared them with sections from animals that received subarachnoid saline solution during the same time periods. They found a few large, common dark-stained neurons in several preparations, but these were invariably in areas adjacent to spinal catheters, where mechanical compression of the cord was evident. There was no difference in the incidence of such occurrences between steroidtreated and saline-treated animals. A study by Delaney and colleagues26 evaluated possible long-term histological effects of a mixture of 2% lidocaine and triamcinolone following epidural injection and catheterizations. They found that the nerve root and the root entry zone in the meninges when examined by light microscopy 30 and 100 days after injection showed only a minor inflammatory response at the 30 day period. The reaction was completely resolved at 100 days. It has been proposed that polyethylene glycol (PEG), a preservative agent in methylprednisolone, has been implicated in cases of sterile meningitis and arachnoiditis when injected intrathecally.20 A study performed on the toxicity of PEG was performed by Benzon et al.27 They showed a concentration of 20% PEG or greater resulted in a swelling and a reduction in compound muscle potential in isolated nerve preparations. However, this concentration is clearly higher than that found in commercial corticosteroids preparations, which is 3–9%. These preparations are subsequently diluted with saline and local anesthetics, which would indicate an even lower predisposition for any neurotoxicity. Epidural administration of corticosteroids has several known side effects. These include fluid retention, which can lead to congestive heart failure.28–30 Case reports of steroid myopathy have been

reported.13 There have also been reports of irregular menses.31 Epidural lipomatosis has been associated with prolonged corticosteroid therapy.32–34 Minor digestive disturbances and occasional minor changes in serum glucose have been documented.35 Less-common side effects are elevated temperature, euphoria, depression, mood swings, local fat atrophy, deep pigmentation of the skin, and pain flare. Other rare but reported side effects include weight gain,28 deep vein thrombosis,36 and hypertension,37 and allergic reactions to triamcinolone.1 An uncommon but serious complication is development of Cushing’s syndrome from excess glucocorticoid administration.38 This syndrome usually occurs when exceptionally high dosages of corticosteroid are given over a short period of time. One such case occurred when a patient received two 80 mg injections of methylprednisolone 1 week apart.39 Serum cortisol levels have been shown to be depressed for 1–2 weeks after epidural injections but may return to normal after 3 weeks.40,41 The recommended dose to avoid systemic side effects from epidural steroids has been stated by Knight and Burrell42 to be no more than 3 mL/kg of methylprednisolone. Despite adhering to this, there have been reports of cumulative effects from long durations of steroid preparations. Kay43 and coworkers have shown both acute and chronic suppression of the hypothalamic– pituitary–adrenal axis in a clinically relevant study of 14 patients who received a total of three epidural steroid injections once weekly with 80 mg of triamcinolone in 7 mL of 1% lidocaine. Within 15 minutes of injection, there was evidence of the suppression of endogenous corticosteroids, manifested by a significant decrease in both ACTH and cortisol. The median duration of such effect was 1 month, but 5 of 14 patients showed suppression for up to 3 months. Adrenal function returned to a normal status after 3 months. In a study by Manchikanti44 it was concluded that low-dose administration of neuroaxial steroids are not deleterious and did not result in any significant deterioration in bone mineral density, causing neither osteopenia or osteoporosis.

Contrast media Because fluoroscopic procedures are combined with introduction of radiographic contrast media, it is important to know the potential adverse effects of contrast media. The largest study to compare the effects of intrathecal nonionic (iopmanidol) to ionic (metrizamide) contrast found substantially fewer adverse reactions in the nonionic group.45 The contrast currently used in myelography and fluoroscopic injections is nonionic, either iso-osmolar or of a low osmolality. The risk of anaphylactic reaction using iso-osmolar contrast is extremely low (0.04%) In 337 647 cases in which iso-osmolar contrast was used, only 1 death occurred.46 Patients with a known sensitivity to iodine, prior reaction to contrast media, food allergies, asthma, and hay fever have a higher incidence of anaphylactic or cardiovascular reactions. Premedication with histamine H1 and histamine H2 blockers and corticosteroids may reduce the incidence and severity of life-threatening reactions in patients with a known allergy. Controlled studies on nonionic contrast agents used intrathecally in myelography have shown adverse reactions including headache (18%), nausea (7.3%), muscular pain (3.7%), and hypotension (1.1%).47 These studies were performed using 10–15 mL of contrast injectate, which is a larger dose than the 1–3 mL used during fluoroscopic injections. The fluoroscopic technique in combination with extradural myelography can avoid intrathecal injections. Intravascular injection can occur in 9.2% of cases despite a negative aspiration for blood in lumbar epidural injections, without fluoroscopic guidance.48 When utilizing fluoroscopy and contrast media, Sullivan et al.49 found a 215

Part 2: Interventional Spine Techniques If cannot avoid use of contrast with known allergy

Administer Prednisone 20 – 50 mg, PO, 12 hours prior to procedure and 2 hours prior.

Administer Diphenhydramine (Benadryl) 50 mg, PO, 1 hour prior to procedure. Administer Tagamet (Cimetidine) 300 mg PO 12 hours, 8 hours and 1 hour prior to procedure. Fig. 20.2 AP/PA fluoroscopic image showing intravascular contrast during a caudal injection.

Fig. 20.3 Fluoroscopic image of sacroiliac joint showing intervascular contrast pattern.

similar overall incidence of 8.5% intravascular uptake in lumbar spinal injections. The caudal and transforaminal routes were intravascular 10.9% (Fig. 20.2) and 10.8% of the time, respectively, sacroiliac joint injections 6.3% (Fig. 20.3), zygapophyseal joint injections 6.1%, and interlaminar injections 1.9%. The intravascular pattern in lumbar transforaminal epidural injections was also described by Furman to be 11.2%50 and in cervical transforaminal injections, and intravascular uptake is 19.4%.51 These studies unequivocally demonstrate the importance of introducing contrast media prior to the infusion of anesthetics or corticosteroids in spinal interventional injections. Prophylaxis may be utilized in patients with known allergy to contrast media (Fig. 20.4). An alternative in patients allergic to iodinated contrast is to utilize gadolinium contrast.52

Infectious complications Infectious complications can arise from spinal injections. These complications can include epidural abscess,53–55 meningitis56–58 and osteomyelits/discitis.59

Epidural abscess These have been reported after epidural injections in the cervical, thoracic, and lumbar spine. There have been cases of epidural abscess following thoracic epidural injections of steroids and bupivacaine to treat postherpetic neuralgia.57,60 A thoracic epidural abscess has 216

Prepare for bronchospasm/seizures or hypotension with appropriate resuscitative equipment on hand.

Fig. 20.4 Prophylaxis for patients with known allergy to contrast media.

also been reported after four epidural injections in a patient with metastatic disease.53 Five other cases of abscesses were reported, three after lumbar, one after cervical, and one after caudal epidural injections.54,55,61–63 The bacteria identified in these cases was Staphylococcus aureus. Of these patients, three patients had diabetes mellitus, one had a surgical infection with S. aureus 2 weeks prior to the epidural injection, and one had carcinoma with spinal metastasis. All of these patients presented with fever, spinal pain, radicular pain, and/or progressive neurologic deficit 3 days to 3 weeks following their injections. It is presumed that the most common bacterial etiology for spinal infection from a spinal injection is S. aureus. The likely mechanism of infection is introduction by the needle, carrying an inoculum from the skin to deeper structures. In order to diagnose an epidural abscess resulting from a spinal procedure, there must be careful and close clinical observation. There should be a high suspicion for this potential complication in any patient with a history of an immunocompromised condition or diabetes mellitus. Clinically, the patient with epidural abscess presents with pain in the local area, neck or back stiffness, soreness, fever, and/or malaise. Prompt diagnosis of infection is necessary in order for a patient to recover with intact neurologic function. Laboratory evaluation with erythrocyte sedimentation rate (ESR), C-reactive protein, and complete blood count (CBC) needs to be obtained. Magnetic resonance imaging (MRI) with contrast is the radiological procedure of choice for the diagnosis of epidural abscess.55,64 Once diagnosed, appropriate antibiotic therapy can be administered and surgical debridement performed if necessary.

Meningitis This is a rare phenomenon, which can occur following spinal injections. It can occur when the dura is accidentally punctured during epidural procedures or other spinal interventional procedures. There are two types of meningitis that have been reported following spinal injections: bacterial and aseptic. Several cases of bacterial meningitis have been reported following lumbar epidural injections.57 Of the two cases reported by Dougherty, one patient had a documented dural puncture and the other patient had an inadvertent unrecognized dural puncture. Cases of aseptic meningitis have been reported by Nelson et al.19 following subarachnoid injection with methylprednisolone. The manifestations included headache, fever, nausea, leg pain, and convulsions.

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

Cerebrospinal fluid (CSF) analysis revealed elevated protein, leukocytes, and red blood cells, while CSF culture was negative. Spontaneous recovery ensued over a 3-week period. Several other cases of aseptic meningitis have been reported after a subarachnoid injection.25,64,65 In each instance the symptoms resolved within several days. A case report by Morris66 of aseptic meningitis began 48 hours after an epidural injection of methylprednisolone without any anesthetic. The symptoms included fever, headaches, lethargy, and meningismus. CSF evaluation in this case revealed pleocytosis, elevated protein values, and diminished glucose levels. CSF culture was negative. Thus, in a patient with presumptive meningitis, appropriate evaluation of CSF fluid is needed in order to appropriately treat this potential complication. A history needs to be obtained from the patient regarding headache, lethargy, and photophobia, followed by evaluation for signs of meningeal irritation. Prevention of meningitis can be enhanced by utilizing a strict sterile technique, but even the best precautions do not entirely mitigate this possible complication.

Obtain clinical history from patient: 1. fever/chills 2. increase pain 3. headache/meningeal signs Physical exam

for neurologic deficit

If patient has a positive history and/or physical exam suspicious for infectious process following a spinal interventional procedure obtain: 1. ESR, CBC, C-reactive protein, blood cultures 2. Magnetic resonance imaging with contrast of presumed symptomatic region

Osteomylitis/discitis Cases of osteomyelitis and discitis have been reported following cervical, thoracic, and lumbar discography. This is a potential lifethreatening complication if it develops in the cervical or thoracic spine. As previously mentioned, these infectious complications can be minimized by adhering to sterile technique along with the use of intravenous and intradiscal antibiotics. The use of antibiotics are further discussed in the section on discography. Patients who have undergone a discographic procedure should be observed clinically for symptoms of osteomyelitis or discitis. The typical signs of infection include fever, malaise, lethargy, pain, and/or neurological symptoms. These typically present 1–4 weeks after injection although neurological symptoms are uncommon. Laboratory studies can reveal leukocytosis, elevated sedimentation rate, and/or an increase in C-reactive protein. MRI with contrast has been shown to be superior to bone scan for the early diagnosis of discitis and osteomyelitis.67 In summary, early detection of infectious complications from injection procedures is necessary in order to avoid morbidity and mortality. In patients who have a history of prior infection, consideration should be given to prophylactic antibiotic treatment in these patients, prior to their procedure. An algorithmic approach to managing these infectious complications is seen in Figure 20.5.

Hematologic complications Many factors are involved in evaluating the bleeding risk in patients who are undergoing spinal interventional procedures. Patients who suffer from coagulation disorders are at increased risk of bleeding.68 These include patients with hemophilia and von Willebrand’s disease. Spinal blocks have been performed in hemophiliacs utilizing recombinant factor VIIa.69 Von Willebrand’s disease can lead to spontaneous bleeding following epidural procedures.70 However, there are cases of epidural catheterization which have been performed in patients with von Willebrand’s disease without complications.71–73 Patients with thrombocytopenia and idiopathic thrombocytopenic purpura can be at risk for complications from spinal injections. Epidural catheterization is believed to be safe in patients with platelet counts of greater then 100 000.74 There are, however, case reports of patients safely receiving epidural injections with platelet counts below 100, 000.75,76 Obtaining a baseline CBC prior to a spinal injection can identify a patient with thrombocytopenia. Patients who have liver and renal disease may have altered coagulation, which could lead to a complication with hepatic dysfunction accompanied with portal hypertension, resulting in increased epidural

Examples and signs of meningitis

MRI finding consistent with abscess

MRI finding consistent with osteomyelitis discitis

Neurology/infectious disease consult

Surgical consult

Antibiotic Rx possible surgical consult

Fig. 20.5 Possible spinal abscess, meningitis, or osteomyelitis/discitis.

venous congestion, which can lead to increased likelihood of bleeding.77 Epidural hematomas following lumbar puncture78 and epidural catheter placement79,80 have been reported in patients with known liver disease. They have also been reported in patients with renal disease.81,82

Epidural hematoma Epidural hematomas can develop spontaneously and in patients with no evidence of any bleeding tendency, anticoagulation, or traumatic needle insertion.83,84 In a review of epidural steroid injections in 65 published series with a total of 69 047 patients receiving one or more epidural injections, there was only one case of an epidural hematoma.85 Hematomas can be localized in the cervical, thoracic, or lumbosacral spine. Symptoms will vary depending on the location and size f the hematoma. The presentation can be immediate or delayed up to several days.86,87 In order to diagnose patients with such a complication, prompt spinal imaging is recommended. MRI is the most sensitive modality in order to diagnose a hematoma, define the extent of its spread, and distinguish it from other space-occupying lesions.88–90 Once identified, treatment of the hematoma can involve high-dose corticosteroid therapy and/or emergency decompressive surgery in order to prevent further compromise of neurologic function. If an epidural catheter is present with a hematoma, infusion should be stopped and the catheter removed in order to avoid increasing compression.84 In order to minimize the risks to the patient when performing spinal interventional procedures, the interventionist can do several things that can minimize the potential possibility of causing an epidural hematoma. These include minimizing the passes of the needle (needle trauma) utilizing fluoroscopic guidance, use of smaller-caliber needles,91 and aspiration can be performed in order to determine if the needle is intravascular. See Figure 20.6 for an algorithmic approach to the evaluation of a patient with a presumptive epidural hematoma. 217

Part 2: Interventional Spine Techniques

History: • Pain, weakness, numbness, bowel/bladder dysfunction • Presence of coagulopathy or anticogulants Physical examination: • Sensory/motor deficits

Obtain MRI of suspected involved area

+

Referral for surgical management, possible decompression

−

Continue pain management

Fig. 20.6 Evaluation of patient with suspected epidural hematoma.

Management of anticoagulant medications in interventional spinal procedures Clinically apparent epidural hematomas are rare, with an incidence between 1:40 000 and 1:150 000.84,.85,92,93 Aspirin and nonsteroidal antiinflammatory drugs may effect platelet function and subsequently increase the risk of an epidural hematoma. These medications have Patient on Warfarin

Stop Warfarin 4 – 5 days prior to procedure with consent of cardiologist/internist.

Obtain PT/INR INR < 1.0 ideal (literature supports an INR < 1.5)

been reported to increase the occurrence of epidural hematoma from both spinal anesthesia and epidural injection.94–97 It should be noted, however, that there are other studies, which report no increased incidence of epidural hematomas in patients who are receiving aspirin and nonsteroidal antiinflammatory medications.98–101 Patients using thienopyridine derivatives and glycoprotein receptor antagonists have developed hematomas from interventional spinal injections.86,102 Since the risk associated with these medications is unknown, the American Society of Regional Anesthesia recommends withholding ticlopidine 14 days, clopidogrel 7 days, and Gp antagonists for 4 weeks prior to procedure.87 Oral anticoagulation with warfarin is a contraindication to spinal anesthesia.87 The American Association of Regional Anesthesia suggests that warfarin should ideally be stopped 4–5 days prior to spinal injection. The prothrombin time (PT) and international normalized ratio (INR) should be checked prior to a spinal injection. There is no consensus regarding the delineation of a safe PT/INR prior to performing a spinal injection. There is some literature that supports an INR of 1.5 as safe for major surgical procedures including spinal injections while an INR greater than 1.5 is unsafe.103,104 It should be noted that identification of risk factors for bleeding disorders does not eliminate the risk of a spinal hematoma. This has been shown in the study by Vandermeulen94 in which 87% of patients who had spinal hematomas had a hemostatic abnormality but, 13% had no identifiable risks. See Figure 20.7 for an algorithmic approach to the management of patients on warfarin, aspirin, or NSAIDs.

Neurological complications Neurological injuries are an uncommon complication which can occur when performing spinal injections.

Patient on aspirin NSAIDs Thienopyridine derivatives (ticlopidine/clopidogrel) GP IIb/IIIa receptor antagonists (abciximab, eptifibatide, tirofiban Optional to stop ASA 7 days prior and NSAIDs 5 days prior. Stop GP II/IIIa antagonists 8 – 48 hours prior Stop ticlopidine 14 days prior Stop clopidogrel 7 day prior

Can obtain bleeding time to assure normal coagulation for procedure, however is not wholly accepted and clinical history of easy bruising/bleeding and age needs to be considered.

* Note: these are guidelines derived from: Regional Anesthesia in the Anticoagulated patient: Defining the risks (The second ASRA Consensus Conference on Neuroaxial Anesthesia and Anticoagulation) by Horlocker TT, Wedel DJ, Benzon H et al. Regional Anesthesia and Pain Medicine; 28(32) (May – June) 2001: 172 – 197. ** For a detailed description on the management of the patient on low molecular weight heparain, unfractionated IV and subcutaneous heparin see above manuscript. *** Herbal medications (garlic, ginko and ginseng) have potential to affect hemostasis’ however, there is no evidence to support mandatory discontinuation prior to a neuroaxial procedure. 218

Fig. 20.7 Anticoagulated patterns,

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

Several studies have shown prospectively that the incidence of neurological injuries is approximately 0.002–0.7% and that they are usually self-limiting.105–107 Placement of thoracic epidural catheters has been shown to have an incidence of neurological injury of 0.7%.107 There have been case reports of upper limb weakness and nerve root injury and even intrinsic spinal cord damage from spinal injections.54,108–110 Neurological compromise can also occur from spinal infection such as epidural abscess or epidural hematoma. There have been case reports of transiently increased sciatic pain and paresthesia following spinal injections.111–119 Spinal injections carry a higher risk when performed in the cervical spine. In particular, this is due to the closer proximity of important structures to the target site, such as the vertebral or carotid artery. Inadvertent injection into these arteries could result in stroke, hematoma formation, or even an occlusion of the involved vessel. In order to avoid these potential complications, constant and careful fluoroscopic guidance with administration of contrast media prior to injection of anesthetics and corticosteroid medications is essential. CNS toxicity can occur in patients who received local anesthetic as a component of a spinal injection. Signs of this toxicity can be lightheadedness, tinnitus, perioral numbness, numbness of the tongue, and blurred vision. As the symptoms become more advanced, patients may show signs of nervous system excitation, which can present as shivering, muscle twitches, confusion, and tremors of the facial muscles followed by those of the extremities. As the central nervous system toxicity progresses, CNS activity is slowed and can become depressed and manifest as respiratory depression or arrest. Seizures can also result from spinal injections. These seizures may be a result of anesthetic or cardiac-induced hypotension secondary to neural blockade. Prolonged seizures can result in brain injury if they last longer than 30 minutes.120–122 In order to possibly prevent such consequences the interventional physician should carry out a comprehensive neurologic and physical examination and immediately treat the seizure activity. See Figure 20.8 for an algorithmic approach in the management of a seizure.

Dural puncture and post-dural puncture headache The potential complication of entering the subarachnoid space due to penetration of the dura exists with any spinal injection. Cardiac/respiratory monitoring (B/P, pulse, oxygen saturation, EKG)

Oxygen via mask 6 – 10 L/min

If insulin dependent diabetic – 500cc 5% Dextrose

If seizure persists > 2 minutes • Administer Diazepam 5 mg IV or Midazolam 2.5 mg IV

ACLS protocol if needed Fig. 20.8 Management of seizures.

This can occur in any region of the spine (cervical, thoracic, or lumbosacral). The incidence of an inadvertent dural puncture in lumbar epidural injections has been reported to be as low as 0.5% and as high as 5%.109,123 Incidence of dural puncture in the cervical spine can be as high as 20%.108 The incidence of headache following dural puncture in the lumbar spine has been reported to be 7.5–75% depending on technique, experience, and size of needle used.124,125 These headaches may emanate from an unrecognized dural puncture causing a leakage of cerebrospinal fluid (CSF) or they may result from inadvertent injection of air into the subarachnoid space.126,127 When small-gauge needles are used in spinal anesthesia there is a lower incidence of postdural puncture headache. The incidence is approximately 40% with a 22-gauge (ga) needle, 25% with a 25-ga needle,128,129 2–12% with a 26-ga Quincke needle,130 and less than 2% with a 29-ga needle.131 If a postdural puncture headache occurs, the headache will usually occur within 3 days of the procedure. Up to 66% start within the first 48 hours.132,133 The headache can also present immediately following a dural puncture.134 The pain associated with the headache is described as being a shearing and severe spreading pain. Distribution of the pain appears to be in the frontal and occipital areas, which can radiate into the neck and shoulders. There tends to be stiffness in the neck and the pain is exacerbated with head movements and relieved by lying down.134,135 Symptoms that can also appear in dural puncture headaches include nausea, vomiting, hearing loss, tinnitus, vertigo, dizziness, paresthesias of the scalp, and upper/lower limb pains. There have also been reports of visual disturbances such as diplopia or cortical blindness.3,136,137 There are also reports of intracranial subdural hematomas, cerebral herniation, and death.138 A review of the literature has revealed that the spontaneous rate of recovery from postdural puncture headache is typical with 85% recovering within 6 weeks.3,139,140 Even though this side effect can spontaneously resolve, there are frequent circumstances during which the severity of the headaches necessitates treatment. A variety of strategies can be undertaken including rehydration, acetaminophen, nonsteroidal antiinflammatory drugs, opioids, and antiemetics.141 Caffeine has been utilized in the treatment of postdural headache at a dose of 300–500 mg of oral or i.v. caffeine once or twice daily.142,143 The most definitive method of treatment, however, is an epidural blood patch.144–146 The first report of epidural blood patch for treatment of postdural puncture headache was described by Gormley in 1960.147 This technique has a success rate of 70–98%.148 The exact mechanism by which the epidural blood patch eliminates the headache is unknown. However, it has been postulated that the headache is believed to be due to a reduction of CSF volume or pressure, which leads to traction and tension across the pain-sensitive dural sinuses that occurs in the upright position.149 It should be noted that lumbar extradural blood patch has been shown to be effective even in the treatment of a cervical postdural puncture headache, supporting this theory.149 Slipman et al.150 have reported the successful use of a cervical transforaminal epidural blood patch in a patient with a postdural puncture headache from an interlaminar cervical epidural injection in which cervical interlaminar epidural blood patch failed to relieve symptoms. Another theory for how the blood patch works is that the blood clot adheres to the dura matter which may perhaps seal the hole in the dura and prevent CSF leak.151 Another possible mechanism of action is that the mixing of blood with the CSF lends to rapid coagulation response, sealing the dural tear even if it is far from the blood patch site.151 219

Part 2: Interventional Spine Techniques Utilize precision fluoroscopic technique to avoid needle stray

If dural puncture occurs during procedure, DO NOT inject anesthetics/corticosteroid solution.

infection such as an epidural abscess or epidural hematoma, which can compromise the spinal cord and/or cauda equina.

SPECIFIC COMPLICATIONS OF CERVICAL SPINAL INJECTIONS Cervical spinal injections Cervical epidural steroid injections

Recommend supportive therapies if patient develops post-dural headache. • Acetaminophen or NSAIDs • Rehydration • Caffeine

If headache symptoms persist Perform epidural blood patch 5 – 30cc Can repeat if needed Fig. 20.9 Dural puncture prevention and management of postdural puncture headache.

Complications can arise as well from the epidural blood patch. These can include exacerbation of symptoms and radicular pain.152 Pneumocephalus has also been described following epidural blood patch.153 An inadvertent subdural blood patch has been described, resulting in a nonpositional persistent headache with resulting lower extremity discomfort.132 An algorithmic approach to avoiding dural puncture, and the treatment of dural puncture can be seen in Figure 20.9.

Respiratory complications Respiratory complications can arise following interventional spinal procedures. These complications are very rare and may be the result of sedation, central nervous system trauma due to needle puncture of the spinal cord (SC), or lung (pneumothorax). Pneumothorax can occur in a lower cervical or any thoracic spinal interventional procedure. A pneumothorax tends to be self-limiting and the treatment of this potential complication would require supportive care, observation, and follow-up serial chest radiographs. If a pneumothorax becomes significant, with greater than 25% collapse of the lung, then a chest tube may need to be placed to maintain respiration.154 Cervical spinal injections can injure the recurrent laryngeal nerve. A patient with such an injury may present with a reduction in the ability to protect the airway and may also have hoarseness. This condition is usually self-limiting and resolves. Vocal cord dysfunction has been reported transiently with a 12% incidence in patients receiving steroid injections in the axial skeleton.155 Respiratory depression can arise from all neuraxial opioids. The incidence of clinical respiratory depression with a bolus of morphine is 0.2%.156,157

Urological complications The incidence of urological complications are very few, if any, from interventional spinal procedures. The most common problem is urinary retention, which may follow injections of spinal local anesthetic.158 The other possible cause of urological problems can be an 220

The complications of cervical epidural steroid injections include dural puncture headache, pneumothorax, pneumocephalus,159 bloating, nausea,108,160 vomiting, fever, spinal nerve injury, epidural hematoma, 93 subdural hematoma,161 hypotension, transient paresis, and respiratory insuffiency.162 Facial flushing has a 9.3% incidence and a stiff neck has a 13.2% incidence.108,163 Cervical epidural abscess61,164,165 and complex regional pain syndrome166 have also been reported. Subdural or subarachnoid injections of large doses of anesthetic may cause loss of consciousness,163 hypotension, spinal anesthesia, cardiovascular arrest, apnea, or death. An infrequent although serious complication of cervical interlaminar epidural steroid injection is spinal cord injury from direct needle trauma.53,54,110,164 Spinal cord injuries from direct trauma have occurred when patients were sedated to such a degree that they did not report pain.110 Therefore, heavy sedation is contraindicated for cervical interlaminar epidurals. Botwin et al.167 found an incidence of minor complications in fluoroscopically guided interlaminar cervical epidural injections of 16.8%. The most common complications were neck pain 6.7%, nonpositional headache 4.6%, insomnia 1.7%, vasovagal reactions 1.7%, facial flushing 1.5%, and dural puncture 0.3%. Spinal cord infarction has been reported in cervical transforaminal epidurals, possibly through intravascular injection into a radicular artery.166,168,169 Brouwers et al. described a cervical anterior spinal artery syndrome after a diagnostic block of the right C6 nerve.170 Similarly, Ludwig169 described spinal cord infarction following a left C6 transforaminal epidural steroid injection. A case of quadriparesis and brainstem herniation after a selective cervical transforaminal injection on the right at C5–6 has been reported by Tiso et al.171 Brady et al.163 found two complications following 357 transforaminal epidural steroid injections. Both complications were transient loss of consciousness followed by nausea and vomiting. A study by Slipman et al.172 reported no complications in 20 patients with cervical spondylitic radicular pain who underwent cervical transforaminal injection. Slipman et al.,173 in a prospective study of 89 cervical selective nerve root injections found immediately following the procedure, found that 22.7% of injections resulted in increased pain at the injection site, 18.2% had increased radicular pain, 13% had light-headedness, 9.1% had increased spine pain, 4.5% had non-specific headache, and 3.4% had nausea. Ninety-one percent experienced no complications or side effects during the procedure. The incidence of dural puncture using the cervical interlaminar technique is 0.25–2.0%.108,164 Slipman173 reported an incidence of dural puncture in cervical selective nerve root injections of 0.33%. Dural headaches may be from unrecognized dural punctures causing leakage of cerebral spinal fluid or they may result from inadvertent injection of air into the subarachnoid space.126,127 A study injecting 10 mL of intrathecal normal saline prophylactically showed a favorable response in reducing the severity of postdural puncture headaches.173 Many headaches resolve with conservative management including bed rest and fluids. Persistent postural headache may require an epidural blood patch using 5–30 mL of autologous blood under aseptic conditions and using fluoroscopy. The cervical epidural space is densely vascularized.174 The incidence of intravascular penetration in cervical transforaminal injections is

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

19.4%.50 The incidence of intravascular injection using interlaminar technique is considered to be much lower but has not been studied. Unrecognized inadvertent intravascular needle placement delivers the medication systemically instead of locally and the treatment effect may not be obtained. Misplacement of the anesthetic intravascularly may result in local anesthetic toxicity, requiring immediate supportive measures.174 Neuropathic pain has been reported after cervical epidurals and may result from spinal nerve irritation caused by the injectate or by compression of neural elements.175–177 Absolute contraindications to cervical epidural injections include anticoagulation and coagulopathy because of a risk of epidural hematoma. Batson’s plexus may potentiate the hematogenous spread of an existing infection; thus, epidural injections should be avoided in patients with local infection and sepsis. Laminectomy and significant central canal stenosis resulting from congenital shortening of the pedicles, central disc herniation, or bone spurring are absolute contraindications to an interlaminar epidural injection at the affected level. Pregnancy is a contraindication for cervical transforaminal injections because of the necessity for fluoroscopic guidance. Relative contraindications to injection are a known anaphylactic reaction to the contrast, an immunocompromised state, hypertension, hypotension, and/or an inability to remain still for the procedure. Introduction of contrast under fluoroscopic guidance is required for all cervical epidurals. In the patient allergic to contrast one may consider gadolinium or use prophylactic treatment.

Cervical zygapophyseal intra-articular injections While performing the cervical zygapophyseal joint injection (z-joint) there is a risk of entry into the intervertebral foramen, spinal canal, and vertebral artery, which can result in direct trauma to a vessel or motor and sensory blockade. Further, local pain, postinjection, and light-headedness are possible transient complications from local anesthetics. Puncture of the vertebral artery may result in air embolus, stroke, hematoma, or occlusion of a vessel. Seizure and/or cardiac-induced hypotension may occur if local anesthetic is injected into a vessel. Spinal anesthesia may occur with cervical z-joint injection if the thecal sac is entered through abnormal communication with the z-joint capsule. Further leakage into the epidural space may occur with over distension of the z-joints. Absolute contraindications include localized infection, bleeding diathesis, an unsigned consent form, a patient unable to remain still, and inability to assess patient response to procedure.

Cervical median branch block/radiofrequency ablation Potential complications from cervical radiofrequency ablation (RFA) include needle entry into the vertebral artery, intervertebral foramen, and spinal canal. Another potential complication is lidocaine extravasation when anesthetizing the medial branch prior to neurotomy. Local pain at the procedure site may occur but is usually transient. According to the literature, complications from third occipital nerve (TON) lesioning include ataxia, numbness, dysesthesias and hypersensitivity in the area of the treated nerves.178,179 Numbness is a predictable side effect which is usually well tolerated by patients.178–180 In fact, absence of numbness indicates a technical failure.178 The dysesthesia is temporary and not usually distressing to the patient.178 Tricyclic antidepressants and anticonvulsants can be used to manage these symptoms. Ataxia can be expected due to the interruption of the tonic neck reflexes and proprioception when the semispinalis is denervated in TON neurotomy.181 The ataxia causes unsteadiness

when looking down and, according to Govind, was not disabling to the patient.178

Cervical discography Discitis is the most widely recognized complication associated with discography and can be difficult to eradicate due to the limited blood supply of the disc. The most common infectious etiologic agent is S. aureus followed by other staphylococcus species and anaerobic organisms.170,177 Inadvertently piercing the esophagus during the procedure may seed the disc with Gram-negative and anaerobic organisms. The patient usually presents 1–4 weeks after the procedure with increased neck pain. Initially, there is usually no change at neurologic examination. Epidural abscess may follow cervical discography and generally presents within 24–48 hours. The signs and symptoms are high fever, spine pain, and progressive neurologic deficit. White blood cell count (WBC), ESR, and C-reactive protein should be obtained if either discitis or epidural abscess is suspected. WBC is an unreliable marker. ESR and the C-reactive protein are the most sensitive laboratory markers.181 MRI with contrast is the radiographic imaging modality of choice in diagnosing postprocedural discitis and epidural abscess. MRI has a reported sensitivity of 93% and specificity of 97% in suspected cases of discitis.182 Blood cultures have a 55.6% positive rate in the setting of a culture-positive discitis.183 When the organism is determined, antibiotics should be instituted. Surgical intervention is required with large lesions or lack of improvement with antibiotics and immobilization. Another potential complication from cervical discography is injury to the recurrent laryngeal nerve, which can cause vocal cord paralysis, hoarseness, and decreased ability to protect the airway. The injury is usually self-limited and resolves without intervention. The patient’s respiratory status should be monitored during recovery from sedation. Patients with preexisting oropharyngeal dysfunction are at greater risk of aspiration. Pneumothorax is another rare complication of cervical discography. It usually is self-limited and causes only minor lung collapses (10%).184 Treatment includes supportive care in a hospital setting with serial chest X-rays and possibly placement of a chest tube. Direct trauma to the spinal cord and the spinal nerves can occur if the needle is placed too far lateral or allowed to traverse the entire disc. Cervical cord trauma can result in syrinx formation and progressive neurologic deficits including tetraplegia. These complications should rarely occur if fluoroscopic guidance and appropriate technique are used. Absolute contraindications to cervical discography include the patient unable or unwilling to sign consent, localizing infection, known bleeding diathesis, inability to assess patient response to the procedure, and the patient being unable to remain still during procedure.

Thoracic spinal injections Potential complications of thoracic spinal injections include dural puncture, infection, vascular and neurological injury.107,184 Thoracic spinal procedures have greater propensity for occurrence of complications secondary to unique inherent anatomical properties of the thoracic region. These include a narrow epidural space, which leads to a closer proximity to the spinal cord. The proximity of the lung poses a significant risk of developing a pneumothorax. Injection of local anesthetic in the mid-thoracic epidural space may cause inhibition of the cardiac accelerator leading to bradycardia and/or hypotension.185 Thoracic motor blockade can impair ventilation with up to 50% reduction in tidal volume.185 Slipman et al.186 have reported persistent hiccups associated with thoracic epidural injection. Arterial 221

Part 2: Interventional Spine Techniques

supply by means of the artery of Adamkiewicz and its anatomical variations make it vulnerable to injury during lower thoracic or upper lumbar transforaminal epidural injections.187–189

Lumbar spinal injections Lumbar epidural steroid injections Interlaminar lumbar epidural injections Complications following interlaminar lumbar epidural injections can be broadly divided into septic, vascular, neurological, and idiopathic. Vascular complications include vascular damage and development of epidural hematoma. Vascular infiltration can lead to subsequent cardiorespiratory and/or neurologic complications (i.e. seizures), which have been discussed in depth in the beginning of this chapter. Since the lumbar epidural space is highly vascularized, inadvertent intravenous placement of the epidural needle can occur in 0.5–1% of patients undergoing lumbar epidural injection.123 When fluoroscopy is used, the injection of contrast can rule out any significant intravascular injection. Development of an epidural hematoma is a potentially dangerous complication of vascular injury. Any rapidly progressive neurological deficit or cauda equina syndrome should elevate the suspicion of the development of an epidural hematoma and CT/MRI scan should be done to rule this out.190,191 The presence of an epidural hematoma should be dealt with by prompt surgical decompression. Neurologic complications include dural puncture and injury to the cauda equina or nerve roots. The former has been discussed in detail earlier in this chapter. Direct nerve injury usually elicits painful symptoms. Therefore, increased pain during insertion of the spinal needle should alarm the interventionist to reconfirm needle placement to avoid possible nerve injury.123 McLain et al.192 reported transient, profound paralysis after an epidural steroid injection, which was carried out without fluoroscopic control and was complicated by a puncture of the thecal sac. Radiographic studies suggested three possible explanations for the paralysis: (1) inadvertent thecal penetration during injection may have produced an atypical anesthetic block; (2) location of the injected fluid may have caused a transient compressive lesion; or (3) intrathecal injection may have produced an iatrogenic arachnoid cyst. Conscious sedation or general anesthesia prior to epidural injection can reduce the patient’s ability to provide optimal feedback to painful stimuli; thus, greater caution should be exercised while using them.193,194 Idiopathic complications of lumbar epidural steroid injections include acute retinal necrosis and retinal hemorrhage. The retinal adverse effects are related to rapid increase in intracranial pressure. Browning195 reported acute retinal necrosis following epidural steroid injections. Young196 published a case report and literature review of transient blindness after lumbar epidural steroid injection and suggested strategies for prevention of this complication. This included avoidance of rapid injection into the epidural space and limiting of the amount of fluid injected during the procedure. Although these complications were noted with volumes of injectate as high as 20 mL, the literature fails to advocate ideal volume of injectate to avoid such complications.

Caudal epidural injections Specific complications of caudal epidural steroid injections include dural puncture, infection, and effects of local anesthesia. Failure of correct needle placement has been reported to be as high as 25– 40%197–200 using a blind technique. This can lead to the injection of air or fluid into subcutaneous tissues, periosteum, sacrococcygeal ligament, sacral marrow cavity, and pelvic cavity with the likelihood of penetrating the rectum or vagina. Renfrew et al.48

222

reported 9.2% of vascular infiltration with caudal epidural injections. Figure 20.2 shows a case of vascular infiltration during a caudal epidural injection. Fluoroscopy can help recognize these potential pitfalls. El Khoury et al.201 supported this, as they found the incidence of incorrect placement of needle during caudal injections was reduced to 2.5% when fluoroscopy was utilized. Dural puncture following caudal epidural injection is very rare. Although the thecal sac usually ends at the S2 bony level, in rare variants it may end as low as S4. Hence, the needle should not be placed superior than absolutely necessary to assure epidural injection.188 The use of anesthesia in caudal injections can anesthetize the sacral nerve roots. This can lead to an increased incidence of urinary retention. The use of smaller doses of local anesthetic can minimize this complication without adversely affecting the efficacy of caudal epidural steroid injections when treating painful conditions.188 Earlier literature mentions use of higher volumes of injectate for caudal epidural injections.202,203 Surprisingly, the adverse effects noted with higher volumes of injectate during the interlaminar epidural approach do not necessarily translate to the caudal epidural approach. Cyriax203 reported on the use of 50 mL of procaine following 50 000 caudal injections and had only five adverse effects; one case of hypersensitivity, two cases of transient paraplegia, and two cases of chemical meningitis. All these recovered without any residual damage. Bogduk204 suggested volumes of 10 mL and 15 mL of epidural injectate are adequate to reach L5 and L4 levels, respectively, during a caudal approach. Bryan et al.205 found that contrast reaches the L4–5 intervertebral level in 85% of patients with a volume of <8 mL during caudal approach. Botwin et al.206 reported a 15.6% incidence of minor complications in fluoroscopically guided caudal epidural injections. The most common minor complications observed was 4.7% insomnia the night of injection, 3.5% nonpositional headache, 3.1% increased back pain at injection site, and 0.4% increased leg pain.

Lumbar transforaminal epidural steroid injections Complications related to the lumbar transforaminal technique are relatively fewer as compared to the interlaminar technique. Lutz and Wisneski207 as well as Kraemer et al.208 reported no dural punctures or any other major complications related to this technique. The placement of the needle in the safe triangle described by Derby et al.209 reduces the chances of dural puncture or nerve injury. Botwin et al.,210 in their study of 322 lumbar transforaminal injections, reported a 9.6% incidence of minor complications, which were entirely transient and resolved without morbidity. Complications included postprocedural back pain at the injection site, increased leg pain, and transient leg weakness. Slipman et al.,173 in a prospective study of 217 lumbosacral nerve root injections, found no major complications but did report an immediate postprocedure incidence of 17.1% increased pain at injection site, 8.8% increased radicular pain, 6.5% light-headedness, 5.1% increased spine pain, 3.7% nausea, 1.4% non-specific headache, and 0.5% vomiting per injection. The potential complications of lumbar transforaminal epidural injections include infection, dural puncture, nerve injury, and vascular infiltration. Furman et al.50 reported an 11.2% incidence of intravascular injections in 761 transforaminal epidural injections with a significantly higher rate of intravascular injections (21.3%) at S1 level. They also concluded that contrast enhancement is mandatory to rule out vascular infiltration, as negative flash or aspiration was found to be unreliable. There have been reports of acute paraplegia following left-sided high lumbar transforaminal injections, possibly secondary

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

to disruption of the artery of Adamkiewicz leading to anterior spinal artery ischemia and cord infarction.189,211 The artery of Adamkiewicz is the principal blood supply to the lower spinal cord and like other radicular arteries typically enters the spinal canal along the anterior, superior aspect of the spinal nerve.212 The usual technique of placing a needle tip for a left transforaminal epidural injection at the midthoracic to upper lumbar region can place the artery of Adamkiewicz at risk. A modified technique has been suggested to keep the needle tip in the posterior, inferior location within the foramen in order to reduce disruption of the radicular artery.185 More research is needed to reduce the risk of entering the artery of Adamkiewicz. Extreme caution should also be exercised in rare conditions such as far lateral/ foraminal disc herniations where there can be likelihood of injecting the disc itself if the needle tip is too far medial in the intervertebral foramen.

Lumbar intradiscal electrothermal annuloplasty/ nucleoplasty Potential complications of intradiscal annuloplasty would include those incurred with discography. Reported complications of intradiscal electrothermal annulopasty (IDEA) include cauda equina syndrome240 and disc herniation.241 There have been no reports of infection, bleeding, or other equipment- or technique-related complications so far mentioned in the literature.242,243 Cohen et al.,244 in their study of 78 patients treated with IDEA, reported a 10% incidence of transient complications ranging from paresthesia radicular pain to weakness. No complications have been reported in two prospective outcome studies evaluating percutaneous disc decompression using nucleoplasty.245,246

Lumbar sympathetic blocks Lumbar zygapophyseal joint injections Potential complications include infections and inadvertent entry into intervertebral foramen or spinal canal causing dural puncture and/ or nerve injury. Infectious complications range from delayed septic arthritis of facet joints to development of an epidural abscess.213–215 The most often noted complication (2%) is transient exacerbation of pain.216 Spinal anesthesia can occur if there is an abnormal communication between facet joint capsule and the thecal sac. Authors have reported chemical meningitis following facet joint blocks.217,218

Lumbar medial branch block/radiofrequency ablation Potential complications of radiofrequency zygapophyseal denervation or medial branch block include infection, nerve root injury, and dural puncture. The reported complication rate for radiofrequency zygapophyseal denervation is quite low.219–223 Superficial infections and reactions to the local anesthetic are the most common complications incurred.224 In a recent study of 92 patients who received 616 radiofrequency lesions, six complications arose for a 1% complication rate per lesion site. Among these complications were three cases of localized pain at lesion site lasting more than 2 weeks and three cases of neuropathic pain lasting less than 2 weeks.225

Potential complications of lumbar sympathetic blocks consist of accidental spread of anesthetic to the neuraxis causing a blockade of somatic nerves (lumbar plexus). Vascular injury/infiltration, lymphatic infiltration, or nerve root injury can occur as well.247– 252 If the transverse process is mistakenly identified as the vertebral body, and a large volume of drug is injected into the intervertebral foramen, an ipsilateral lumbar plexus block and/or epidural spread of solution may occur. Therefore, authors advocate diluting the concentration of anesthetic so as not to produce motor blockade.248 Anterior advancement of needle has the potential danger of penetrating either the aorta or the inferior vena cava where injection of local anesthetic could produce systemic toxicity.252 Fluoroscopic guidance can help minimize these potential complications.

SUMMARY Any spinal injection carries an inherent risk of complication; however, strict adherence to proper technique may aid in avoidance of some complications. Proper reasoning and evaluation can also serve to minimize the potential for complications to evolve into more serious life-threatening consequences. The above algorithmic approach to complications seeks to alert the spinal interventionist to potential complications and institute appropriate preventative and diagnostic measures to minimize their occurrence.

References Lumbar discography Potential complications of discography include nerve root injury, dural puncture, intradural injection, meningitis, arachnoiditis, intrathecal hemorrhage, and discitis. Discitis is the single most significant complication of discography with the incidence ranging from 0% to 4.9%.2,,224,,226–229 Osti et al.227 performed a prospective clinical study of 127 patients treated with intradiscal cefazolin 1 mg/mL mixed with diatrozoate contrast. None of these patients developed discitis. Klessig et al.230 indicated that intradiscal antibiotics mixed with iohexol provided adequate antibacterial prophylaxis against discitis. Use of intradiscal antibiotics has been recommended as an integral part of practice guidelines issued by the International Spinal Injection Society.231 Other rare complications of discography include vascular injury, retroperitoneal hemorrhage,232 disc herniation,233 and pulmonary embolism.234 DeSeze235 and Bernard228 have raised the possibility of discography causing degenerative changes; however, various other studies have disputed these claims.235–238 There has been a case of seizure and death from an inadvertent injection of 12.5 mg/mL of cefazolin intrathecally during a discogram at L5/S1.239

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140. MacArthur C, Lewis M, Knox EG. Accidental dural puncture in obstetric patients and long-term symptoms. Br Med J 1992; 304:1279–1282. 141. Ostheimer GW, Palahniuk RJ, Shnider SM. Epidural blood patch for postlumbar puncture headache. Anesthesiology 1974; 41:307–308. 142. Camann WR, Murray RS, Mushlin PS, et al. Effects of oral caffeine on post-dural puncture headache. A double blind placebo controlled trial. Anesth Analg 1990; 70:181–184. 143. Jarvis AP, Greenawalt JW, Fagraeus L. Intravenous caffeine for post-dural puncture headache. Anesth Analg 1986; 65:316–317. 144. Brownridge P. The management of headache following accidental dural puncture in obstetric patients. Anesth Intensive Care 1983; 11:4–15. 145. Deisenhammer EL. Clinical and experimental studies on headache after myelography. Neuroradiology 1985; 74:615–618. 146. Digiovanni A. Epidural injection of autologous blood for post-lumbar puncture headache. Anesth Analg 1979; 49:268–271. 147. Gormly JB. Treatment of post-spinal headache. Anesthesiology 1960; 39:613–617. 148. Abouleish E, Vega S, Blendinger I, et al. Long-term follow-up of epidural blood patch. Anesth Analg 1975; 54:459–463. 149. Colonna-Romano P, Linton P. Cervical dural puncture and lumbar extradural blood patch. Can J Anesth 1995; 42:1143–1144. 150. Slipman CW, Ed Abd OH, Bhargava A, et al. Transforaminal cervical blood patch for the treatment of postdural puncture headache. Am J Phys Med Rehabil 2005; 84:76–80. 151. Cook M, Watkins-Pitchford J. Epidural blood patch: A rapid coagulation response. Anesth Analg 1990; 70:567–568. 152. Woodward WM, Levy DM, Dixon AM. Exacerbation of postdural puncture headache after epidural blood patch. Can J Anaesth 1994; 41:628–631. 153. Kawamata T, Omote K, Matsumoto M, et al. Pneumocephalus following an epidural blood patch. Acta Anaesthesiologica Scandinavica 2003; 4:907–909. 154. Idrees M, Ingleby A, Wali S. Evaluation and management of pneumothorax. Saudi Med J 2003; 24:447–452. 155. Slipman CW, Bhat AL, Chow DW, et al. Incidence of vocal cord dysfunction following fluoroscopically guided steroid injection in the axial skeleton. Arch Phys Med Rehabil 2005; 86:1330–1332. 156. Chaney MA. Side effects of intrathecal and epidural opioids. Anaesth 1995; 42:891–903. 157. Ready LB, Loper KA, Nessly M. Postoperative epidural is safe on surgical wards. Anesthesiology 1991; 75:452–456. 158. Armitage EN. Lumbar and thoracic epidural. In: Wildsmith JAW, Armitage EN, eds. Principles and practice of regional anesthesia. New York: Churchill Livingstone; 1987:109. 159. Simopoulos T, Peeters-Asdourian C. Pneumocephalus after cervical epidural steroid injection. Anesth Analg 2001; 92:1576–1577.

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160. Shulman M. Treatment of neck pain with cervical epidural steroid injections. Reg Anesth 1986; 11:92–94.

171. Tiso RI, Cutler T, Catania JA, et al. Adverse central nervous system sequelae after selective transforaminal block: the role of corticosteroids. Spine 2004; 4:468–474. 172. Slipman CW, Lipetz, JS, Jackson HB, et al. Therapeutic selective nerve root block in the nonsurgical treatment of atraumatic cervical spondylitic radicular pain: A retrospective analysis with independent clinical review. Arch Phys Med Rehabil 2000; 81:741–746. 173. Huston CW, Slipman CW, Garvin C. Complications and side effects of cervical and lumbosacral selective nerve root injections. Arch Phys Med Rehabil 2005; 86:277–283. 174. Carpenter M. Core text of neuroanatomy. 4th edn. In: Satterfield T, ed. Baltimore: Williams & Wilkins; 1991:434–438. 175. Stav A, Ovadia L, Sternberg A, et al. Cervical epidural steroid injection for cervicobrachialgia. Acta Anaesthesiol Scand 1993; 37:562–566. 176. Field J, Rathmell JP, Stephenson JH, et al. Neuropathic pain following cervical epidural steroid injection. Anesthesiology 2000; 93:885–888. 177. Baker R, Dreyfuss P, Mercer S, et al. Cervical transforaminal injection of corticosteroids into a radicular artery: a possible mechanism for spinal cord injury Pain 2003; 103:211–215. 178. Govind J, King W, Bailey B, et al. Radiofrequency neurotomy for the treatment of third occipital headache. J Neuro Neurosgy Psychiatry 2003; 74:88–93. 179. Lord SM, Barnsley L, Wallis B, et al. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med 1996; 335:1721–1726. 180. McDonald GJ, Lord SM, Bogduk N. Long-term follow-up of patients treated with cervical radiofrequency neurotomy of chronic neck pain. Neurosurgery 1999; 45:61–67. 181. Lord S, Barnsley L, Bogduk N. Percutaneous radiofrequency neurotomy in the treatment of cervical zygapophyseal joint pain: A caution. Neurosurgy 1995; 36:732–739. 182. Guyer RD, Colleir RC, Smith WJ. Discitis after discography. Spine 1988; 13:1352–1354. 183. Silber, JS, Anderson DG. Management of postprocedural discitis. Spine J 2002; 3:279–287. 184. Zaugg M, Stoehr S, Weder W. Accidental plural puncture by a thoracic epidural catheter. Anesthesia 1998; 53:69–78 185. Giebler RN, Scherer RU, Peters J. Incidence of neurologic complications related to thoracic epidural catheterization related to thoracic epidural catheterization. Anesthesiology 1997; 86:55–56. 186. Slipman CW, Shin CH, Patel RK, et al. Persistent hiccup associated with thoracic epidural injection. Am J Phy Med Rehab 2001; 80:618–621. 187. Lo D, Vallee J, Spelle L. Unusual origin of the artery of Adamkiewicz from the fourth lumbar artery. Neurorodiology 2002; 44:153–157. 188. Windsor RE, Storm S, Sugar R. Prevention and management of complications resulting from common spinal injections. Pain Physician 2003; 6:473–483. 189. Houten JK, Errico TJ. Paraplegia after lumbosacral nerve root block: report of three cases. Spine J 2002; 2:70–75.

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures 190. Cousins M. Hematoma following epidural block. Anesthesiology 1972; 37:263. 191. Lerner S, Gutterman P, Jenkins F. Epidural hematoma and paraplegia after numerous lumbar punctures. Anesthesia 1973; 39:550–553. 192. McLain RF, Fry M, Hecht ST. Transient paralysis associated with epidural steroid injection. J Spinal Disord 1997; 10:441–444.

222. Burton CV. Percutaneous radiofrequency facet denervation. Appl Neurophysiol 1976; 39:80–86. 223. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophyseal joint pain. Spine 2000; 25:1270–1277. 224. Guyer RD, Ohnmeiss DD. Lumbar discography. Spine J 2003; 3:11S–27S.

193. Braid D, Scott D. Dosage of lignocaine in epidural block in relation to toxicity. Br J Anaesth 1966; 38:596–602.

225. Kormick C, Klromarich S, Lamer TJ, et al. Complications of lumbar facet radiofrequency denervation. Spine 2004; 29:1352–1354.

194. Cousins M. Epidural neural blockade. In: Cousins MJ, Bridenbaugh MJ, Phillip O, eds. Neural blockade in clinical anesthesia and management of pain. Philadelphia: Lippincott; 1988:340–341.

226. Jackson RP, Cain JE, Jacobs RR. The neuroradiographic diagnosis of lumbar herniated nucleus pulposus. A comparison of computed tomography (CT), myelography, CT-myelography, discography and CT-discography. Spine 1989; 14:1356–1361.

195. Browning DJ. Acute retinal necrosis following epidural steroid injections. Am J Ophthalmol 2003; 136:192–194.

227. Osti OL, Fraser RD, Vernon-Roberts B. Discitis after discography. J Bone Joint Surg [Br] 1990; 72-B:271–274.

196. Young WF. Transient blindness after lumbar epidural steroid injection: a case report and literature review. Spine 2002; 27:E476–E477.

228. Bernard TN. Lumbar discography and post-discography computerized tomography: refining the diagnosis of low back pain. Spine 1990; 15:690–707.

197. Singh V, Manchikanti L. Role of caudal epidural injections in the management of chronic low back pain. Pain Physician 2002; 5:133–148.

229. Fraser RD, Osti OL, Veron-Roberts B. Discitis after discography. J Bone Joint Surg [Br] 1987; 69:31–35.

198. Bogduk N. Epidural steroids for low back pain and sciatica. Pain Digest 1999; 9:226–227.

230. Klessig HT, Showsh SA, Sekorski A. The use of intradiscal antibiotics for discography: an in vitro study of gentamicin, cefazolin, and clindamycin. Spine 2003; 28:1735–1738.

199. White A. Injection techniques for the diagnosis and treatment of low back pain. Orthop Clin North Am 1983; 14:553–567. 200. Manchikanti L, Staats P, Singh V, et al. Evidence-based practice guidelines for interventional techniques in the management of chronic spinal pain. Pain Physician 2003; 6:3–80. 201. el-Khoury GY, Ehara S, Weinstein JN, et al. Epidural steroid injection: a procedure ideally performed with fluoroscopic control. Radiology 1988; 168:554–547. 202. Evans W. Intrasacral epidural injection in treatment of sciatica. Lancet 1930; 2:1225–1229. 203. Cyriax JH. Epidural anesthesia and bed rest in sciatica. Br Med J 1961; 1:20–24. 204. Bogduk N, Christophifid N, Cherry D. Epidural use of steroids in the management of back pain. Commonhealth of Australia: National Health and Medical Research Council. Canberra; 1994:1–76.

231. Endres SM, Bogduk N. International Spinal Injection Society Practice Guidelines and Protocols: Lumbar Disc Stimulation. ISIS 9th Annual Scientific Meeting. Boston, MA: Syllabus; 2001:56–75. 232. McCulloch JA, Waddell G. Lateral lumbar discography. Br J Radiol 1978; 51: 498–502. 233. Grubb SA, Lipscomb HJ, Guilford WB. The relative value of lumbar roentgenograms, metrizamide myelography, and discography in the assessment of patients with chronic low-back pain syndrome; Spine 1987; 12:282–286. 234. Schreck RI, Manion WL, Kambin P, et al. Nucleus pulposus pulmonary embolism: a case report: Spine 1997; 22:2191–2193 235. DeSeze S, Levernieux J. Les accidents de la discographie. Rev Rheum Mal Osteoartic 1952; 19:1027–1033.

205. Bryan BM, Lutz C, Lutz GE: Fluoroscopic assessment of epidural contrast spread after caudal injection. J Orthoped Med 2000; 22:38–41.

236. Johnson RG. Does discography injure normal discs? An analysis of repeat discograms. Spine 1989; 14:424–426.

206. Botwin KP, Gruber RD, Bouchlas CG, et al. Complications of fluoroscopically guided caudal epidural injections. Am J Phys Med Rehab 2001; 80:416–424.

237. Kahanovitz N, Arnoczky SP, Sissons HA. The effect of discography on canine intervertebral disc. Spine 1986; 11:26–27.

207. Lutz GE, Vad VB, Wisneski RJ. Fluoroscopic transforaminal lumbar epidural steroids: an outcome study. Arch Phys Med Rehabil 1998; 79:1362–1366.

238. Saifuddin A, Renton P, Taylor BA. Effects on the vertebral end plate of uncomplicated lumbar discography: an MRI study. Eur Spine J 1998; 7:36–39

208. Kraemer J, Ludwig J, Bickert U, et al. Lumbar epidural perineural injection: a new technique. Eur Spine J 1997; 6:357–361.

239. Boswell MV, Wolfe JR. Intrathecal cefazolin induced seizures following attempted discography. Pain Physician 2004; 7:103–106.

209. Derby R, Bogduk N, Kine G. Precision percutaneous blocking procedures for localizing spinal pain: Part 2. The lumbar neuroaxial compartment. Pain Digest 1993; 3:175–188.

240. Hsia AW, Isaac K, Katz JS. Cauda equina syndrome from intradiscal electrothermal therapy. Neurology 2000; 55:320–326.

210. Botwin KP, Gruber RD, Bouchlas CG, et al. Complications of fluoroscopically guided transforaminal lumbar epidural injections. Arch Phys Med Rehabil 2003; 81:1045–1050.

241. Cohen SP. A giant herniated disc following intradiscal electrothermal therapy. J Spinal Disord 2002; 15:537–541. 242. Biyani A, Anderson GB, Chaudhary H, et al. Intradiscal electrothermal therapy: a treatment option in patients with internal disc disruption. Spine 2003; 28:S8–S14.

211. Windsor RE, Falco FJ. Paraplegia following selective nerve root blocks. Int Spine Injection Soc; Scientific Newsletter 2001; 4:53–54.

243. Heary RF. Intradiscal electrothermal annuloplasty: the IDET procedure. J Spinal Disord 2001; 14:353–360.

212. Alleyne C, Cawley C, Shengelaia. Microsurgical anatomy of the artery of Adamkiewicz and its segmental artery. J Neurosurgery 1998; 89:791–795.

244. Cohen SP, Larkin T, Abdi S, et al. Risk factors for failure and complications of intradiscal electrothermal therapy: a pilot study. Spine 2003; 28(11):1142–1147.

213. Cook NJ, Hanrahan P, Song S. Paraspinal abscess following facet joint injection. Clin Rheumatol 1999; 18:52–53.

245. Sharps LS, Isaac Z. Percutaneous disc decompression using nucleoplasty. Pain Physician 2002; 5:121–126.

214. Magee M, Kannangara S, Dennien B. Paraspinal abscess complicating facet joint injection. Clin Nucl Med 2000; 25:71–77.

246. Singh V, Piryani C, Ligo K, et al. Percutaneous disc decompression using coblation (nucleoplasty) in the treatment of chronic discogenic pain. Pain Physician 2002; 5:250–259.

215. Alcock E, Regaard A, Browne J. Facet joint injection: a rare form of epidural abscess formation. Pain 2003; 103:209–210. 216. Bous R. Facet joint injections. In: Stanton-Hicks M, Bous R, eds. Chronic low back pain. New York: Raven Press; 1982:199–211. 217. Thomson SJ, Lomax DM, Collett BJ. Chemical meningism after lumbar facet joint nerve block with local anesthetic and steroids. Anesthesia 1991; 46:563–564.

247. Schmidt S, Gibbons J. Postdural puncture headache after fluoroscopically guided lumbar paravertebral sympathetic block. Anesthesiology 1993; 78:78–98. 248. Murphy TM. Chronic pain. In: Miller RD, ed. Anesthesia, 4th edn. New York: Churchill Livingstone; 1994:2345.

218. Berrigan T. Chemical meningism after lumbar facet joint block. Anesthesia 1992; 47:905–906.

249. Hogan QH. Neural blockade for diagnosis and treatment of painful conditions. In: Ashburn MA, Rice LJ, eds. The management of pain. New York: Churchill Livingstone; 1998:275.

219. North RB, Han M, Zahurak M. Radiofrequency lumbar facet denervation: Analysis of prognostic factors. Pain 1994; 57:77–83.

250. Bonica JJ, Buckley FP. Regional analgesia with local anesthetics. In: Bonica JJ, ed. The management of pain, 2nd edn. Philadelphia: Lea & Febiger; 1990:1883.

220. Shealy CN. Percutaneous radiofrequency denervation of spinal facets. J Neurosurg 1979; 43:448–451.

251. Rowlingson JC. Lumbar ganglion. In: Hahn MB, McQuillan PM, Sheplock GJ, eds. Regional anesthesia: an atlas of anatomy and techniques. St. Louis: CV Mosby; 1996:183.

221. Lora J, Long D. So-called facet denervation in the management of intractable back pain. Spine 1976; 1:121–126.

252. Miller RD. The treatment of chronic pain. Anesthesia, 5th edn. New York: Churchill Livingstone; 2000: 2363–2367.

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PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 1

Principles and Concepts Underpinning Spinal Injection Procedures

CHAPTER

Radiation Safety – Theory and Practical Concerns

21

Robert E. Windsor and Mathew Michaels

INTRODUCTION Interventional pain management and spinal diagnostic procedures may require substantial amounts of ionizing radiation and thus attention is required to the management of radiation and the equipment that produces it. Fluoroscopy and computed tomography are routinely used in spinal medicine and pain management procedures. A wide variety of procedures require the use of real-time imaging and, thereby, ionizing radiation for needle localization during procedures as well as for evaluation and documentation of the results. Such procedures may include discography, myelography, spinal cord stimulation, sympathetic blockade, radiofrequency procedures, epidural and intrathecal injections, and catheter placements to name a few. This chapter reviews radiation theory, basic concepts of X-ray circuitry, and radiation safety for the physician and patient.

BASIC TERMINOLOGY The X-ray generator produces X-rays when an electrical current is applied to it. The X-ray generator is a device that acts as the primary control mechanism for the entire fluoroscope. It is through the X-ray generator that current is allowed to flow into the X-ray tube. The basic function of adjusting the voltage differential and current of the X-ray tube are controlled automatically to maintain optimal contrast and brightness. Generator types used in fluoroscopy include single phase, three phase, constant potential, and high frequency. High-frequency generators provide superior exposure reproducibility along with the most compact size, lowest purchase price, and lowest repair costs. As a result, high-frequency generators are commonly used in new radiographic equipment.1 X-rays may be generated in either a continuous or a pulsed mode. Automatic brightness control is a standard feature of the majority of modern fluoroscopes. Through this system mA and kVp are constantly monitored and adjusted to optimize the image.2 The X-ray source is generally referred to as either the ‘anode’ or the ‘cathode.’ Both of these terms are in fact inaccurate. The source of X-rays is the cathode ray tube. As ‘cathode ray’ is an outdated term and the tube contains both a cathode and an anode the correct term would appear to be simply X-ray tube, or X-ray source.1 The cathode (negatively charged electrode) is a cup-shaped holder with a coiled wire filament. The wire is made of tungsten. When the wire is heated, it emits electrons. The cup shape of the cathode serves to focus the electrons so they will strike a specific point on the anode target.2 The anode (positively charged electrode) attracts the electrons emitted by the cathode. The anode is usually made of copper. The target is an area of tungsten on the face of the anode. The specific point at which the electrons are focused is called the focal spot. The focal spot is where X-rays are generated. Due to the amount of heat

generated by this reaction many X-ray tubes use a ‘rotating anode.’ The rotating anode dissipates heat more effectively, thereby prolonging the life of the X-ray tube.1 The collimator is an iris and/or set of sliding plates of radiopaque material that defines the shape of and limits the size of the X-ray beam. Use of collimation has another important effect. By reducing the area of the X-ray beam, the amount of scattered radiation that reaches the image receptor is also decreased. The resulting images have better contrast. It sits in line immediately after the X-ray tube but before the filtration.1 Filtration X-rays of differing energy levels are generated by the X-ray tube. Only the high-energy beams are useful for producing an image of the patient, yet the low-energy beams will contribute to dose. Therefore, it is essential in overall dose management and image refinement to filter out all nonessential beams. This is done with either copper or aluminum filters. It is important to note the presence of ‘inherent filtration’ in all X-ray systems. Inherent filtration consists of the glass casing of the X-ray tube and the surrounding coolant oil. Inherent filtration is usually expressed in millimeters of aluminum equivalent (typically 0.5–1.0 mm).1 Beam equalization filters are partially radiolucent wedgeshaped (tapered) blades and are constructed of lead-rubber or lead-acrylic sheets. They sit at the margins of field and are used to compensate for variations in the radiodensity at the edge of the patient, particularly when moving from a larger to a smaller section of the body. They provide for an image of relatively even consistency. They improve operation of the automatic brightness control system.1 The grid is a radiotransparent plate composed of a radiopaque material aligned perpendicular to the beam such that only those X-rays traveling in the intended direction can reach the image intensifier, thus minimizing ‘Compton-scatter fog’ by only allowing those X-rays with the intended angle of incidence or very close to the intended beam angle of incidence to strike the image intensifier. However, it also prevents some useful photons from contributing to the image. For this reason, while a grid reduces Compton scatter it also necessitates a higher mA setting, thereby increasing the exposure to the subject.1 The image intensifier is designed to convert the X-ray image into a visible real-time image. Rather than use the focused beam of X-ray energy to produce an image on film, the fluoroscope converts this energy into light photons by accelerating and focusing them, through a series of electrodes, onto an ‘output phosphor.’ The characteristics of this output phosphor impregnated upon the viewing screen of the image intensifier play a role in determining the amount of energy required to produce an image. Most modern image intensifiers use cesium iodide for the input phosphor due to its high absorption efficiency. This decreases patient dose.3 229

Part 2: Interventional Spine Techniques

Optical coupling, video camera and monitor: When one looks at the screen of a modern fluoroscope, the image directly viewed is not produced by the image intensifier. Modern imaging technology has allowed for a series of refinements in imaging. An optical coupling device interfaces with the image intensifier, assuring proper transference of the image to a video camera. Most modern fluoroscopes use digital imaging technology in order to produce images that are more easily manipulated in cyberspace. This is where technology is introduced into the fluoroscope. Additionally, the video monitor provides a superior image to the image intensifier (Fig. 21.1).4

RADIATION SAFETY TERMINOLOGY X-rays are any of the rays produced when cathode rays strike upon the surface of a solid (such as the wall of the vacuum tube). An X-ray is a form of electromagnetic energy of very short wavelength (0.05–0.06 angstrom), which allows it to readily penetrate matter.5 X-rays are also noted for their action on photographic plates, their ability to ionize gases, and their fluorescent effects, as well as the fact that they cannot be reflected, polarized, or deflected by a magnetic field.2 They were called X-rays by their discoverer, W. K. Roentgen. X-rays and gamma rays are identical in their physical properties and biologic effects except that gamma rays are natural products of radioactive atoms and X-rays are produced in man-made machines.3 X-rays are produced by the acceleration of electrons (negatively charged particles) via the heating of a cathode. These electrons are then accelerated towards a positively charged anode based on the kilovolt potential across the terminals. Two separate processes produce radiation at the anode. First, as the electrons approach the anode, they produce radiation via a process referred to as bremsstrahlung, a German word for ‘brake radiation.’ In this process the high-speed electrons themselves give off radiation as they decelerate or come to a complete stop in passing near the positively charged nuclei of the anode material. In a second process, the electrons of the anode atoms emit radiation when incoming electrons from the cathode knock electrons near the nuclei out of orbit. These electrons must be replaced. The replacement electrons come from higher-energy outer orbits. As these outer orbit electrons

Monitor Video camera Optical coupling Image intensifier Grid Patient Table Filtration Collimator X-ray tube X-ray generator

230

Fig. 21.1 The major components of a fluoroscope.

drop down to a lower energy state, they lose energy. This energy is given off in the form of X-ray radiation. This process is referred to the K-shell process. The anode material used in a given X-ray tube determines the spectrum of frequencies given off by that X-ray tube.6 Bremsstrahlung is a German word for brake radiation. In this process the high-speed electrons themselves give off radiation as they decelerate or come to a complete stop in passing near the positively charged nuclei of the anode material. In the United States, Conventional Nomenclature is used for radiation exposure, dose, dose equivalent, and activity while the International System that was defined by the General Conference of Weights and Measurements in 1960 is primarily used in other parts of the world. kVp (kilovoltage peak) is the voltage differential between the cathode and anode in the X-ray tube. kVp is generally set at 50–120 kV. kVp influences the force of attraction experienced by an electron drawn from the cathode to the anode. This is an accelerating force. If kVp is increased, the kinetic energy of the electron will be increased. An increase of the maximum energy photons in the beam will occur. This acceleration controls the quality of the X-ray beam. The higher the voltage, the greater the speed of the electrons and therefore the penetrating power of the X-ray beam.1 mA (milliamperage) is the current setting for fluoroscopy, and typically ranges 0.5–5 mA. Increasing the current in the radiograph tube increases the number of X-ray photons emitted per second. If the current (mA) through the X-ray tube is doubled, the number of electrons flowing across the tube is doubled.1 The Roentgen unit (0.25 mC.kg) measures the ion pair production in a standard volume of air, or radiation exposure, and is a Conventional unit while the coulomb per kilogram (C/kg or 3876 R) is an International unit. The gray (Gy) is the International unit used to measure the radiation absorbed dose and is equal to 1 J/kg or 100 rads. It is named for Louis Harold Gray, 1905–1965, British physician who was an authority on the use of radiation in the treatment of cancer. The rad is the Conventional unit used to measure the quantity of radiation and is equal to 0.01 Gy. The sievert (Sv): Particles of ionizing radiations other than X- and gamma rays, such as particles or neutrons, may induce a greater biologic effect per gray. The Sv is an International unit used to measure the dose equivalent and is equal to the number of grays multiplied by a quality factor ranging from 1 to 20 that expresses the degree of biologic insult for equal doses of different types of ionizing radiation. The quality factor for X- and gamma radiation is equal to 1. The quality factor of 1 is simply a number assigned to the most commonly used and manipulated form of ionizing radiation in order to allow all forms of ionizing radiation to be ordered according to their potential to produce biological insult (Table 21.1). Kerma: To characterize an X-ray field, the quantity of exposure is being replaced by the quantity of air or kerma. Kerma (an acronym for kinetic energy released per unit mass) is defined for air as well as for other interacting media such as tissue. Kerma takes into account the bremsstrahlung interactions in air and tissue. The unit of kerma is the gray (formerly, rad; 1 Gy = 100 rad). Exposure excludes any further energy loss by the charged particles that are subsequently given up as photons or to other charged particles (i.e. exposure discounts the bremsstrahlung interactions).10 The absorbed dose refers to the energy that is deposited locally in an absorbing medium from ionizing radiation. For the energies typically used in diagnostic X-ray procedures, absorbed dose and kerma are equivalent. Scatter radiation is the primary source of radiation exposure to radiology personnel, particularly the interventionist. Scatter is the

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

Table 21.1: Radiation quantities and units Quantity

Conventional unit

SI unit

Conversion

Radiation exposure

Roentgen (R)

Coulomb/kg of air (C/kg)

1 C/kg = 3876 R 1R = 258 uC/kg 1R = 2.58 × 10−4 C/kg

Absorbed dose

Rad (100 ergs/g)

Gray (Gy) ( joule/kg)

1 Gy = 100 rad 0.01 Gy = 1 cGy = 1 rad 0.001 Gy = 1 mGy = 100 mrad

Dose equivalent

Rem (rad × Q)

Sievert (Sv) (Gy × Q)

1 Sv = 100 rem 0.01 Sv = 1 cSv = 1 rem 0.001 Sv = 1 mSv =11 00 mrem

The rem is a Conventional unit used in patient dosimetry and is equal to 0.01 Sv. This unit is most often used in health physics and radiation monitoring measures for personnel.

result of X-ray beams failing to penetrate the patient or any surface they are aimed at and therefore being ‘reflected’ away in another direction. Scatter radiation comes in two forms: primary and secondary. Primary scatter is the radiation scatter coming directly off of the patient's skin surface. Secondary scatter results from the X-rays that fully penetrated the patient and had incidence upon the grid. Some of these will be scattered as well.10 Compton scattering is the scattering of photons from charged particles. It was named after Arthur Compton who was the first to measure photon-electron scattering in 1922. This is the process by which X-rays are generated (Fig. 21.2). Leakage of radiation from the anode of the fluoroscopic unit is the result of poor maintenance of the X-ray tube. This should be mitigated by routine preventive maintenance. Radiation dosimetry is the measurement of the dose of radiation deposited in a given target material which is known as the ‘radiation dose’ and is expressed in grays. This is performed through the use slow film exposure badges worn in specific places. ‘Half-value layer’ (HVL) quantifies the beam quality, representing the penetrability (or energy) of the X-ray beam. As a characteristic of individual beams, and therefore individual X-ray machines, the HVL is a means of describing the quality of the beam produced by a given X-ray machine. An important factor to note is that as the beam of an X-ray passes through X-ray filters, its HVL increases. This is a function of the lower energy portion of the beam being removed. The remaining beam is proportionally more penetrative. This is normally expressed in aluminum or copper thickness and is measured at specific kVps. A beam is more penetrative/of higher quality if it has a higher halfvalue layer. The more penetrating the beam the harder the radiation.5

Compton scattering – Target electron at rest – λi Incident proton

Recoil electron Ø θ

Scattered proton

λf

Fig. 21.2 Compton scattering.

Linear attenuation coefficient is the fraction of a beam of X-rays or gamma rays that is absorbed or scattered per unit thickness of the absorber. Quite simply, this is the shielding factor of a substance.

FUNDAMENTALS OF X-RAY GENERATION Electrical current that is open and flowing is always surrounded by a magnetic field.8 The process of electromagnetic induction can produce current from a second wire. Since both coils are not electrically connected, placing a second coil of wire adjacent to the first coil induces an electrical current in the second coil by mutual induction. The force in the second wire loop is directly proportional to the number of turns in the first wire loop. When the wire of a conductor is coiled, a helix is formed. A helix with current flowing through it is called a solenoid. The solenoid, an electromagnet, has a strong magnetic field in its center when current is flowing through the coiled wire. Rheostats are controls used to add resistance to the circuit to adjust incoming voltage and amperage values. A break in the circuit can be achieved with switches that are used to control the length of time that the current may flow. Fuses or circuit breakers are protective devices that open at pre-set levels of current and thus prevent circuit overloading and damage. The X-ray circuit is divided into a low voltage or primary subsection and a high voltage or secondary circuit.10 The primary circuit consists of the following: 1. The main switch: Power from an electrical source is turned off and on at this point. 2. A line voltage compensator: This is used to compensate for variations in power supply. It is important to monitor the incoming line voltage. Line voltage compensation is automatic in some units. 3. Fuses or circuit breakers: These are used to prevent equipment overload or tube damage. 4. An autotransformer: This is used to control voltage supplied to the primary of the step-up transformer, to allow for minimal variations in kilovoltage selection. 5. A pre-reading voltmeter: This indicates the voltage being sent to the primary of the step-up transformer. Kilovoltage is determined by the voltage supplied to the step-up transformer and is present only when the exposure is being made. 231

Part 2: Interventional Spine Techniques

6. Timer and exposure switches: Timers are used for manual or automatic exposure control. The timer is situated between the autotransformer and the primary of the step-up transformer. 7. A filament circuit: Thermal energy is created from this circuit to heat the filament of the X-ray tube. High amperage is used to heat the filament for production of thermionic emission. The heating of the filament is then controlled by the rheostats or resistors, which regulate the milliamperage delivered to the filament circuit and resultant heating. 8. A filament ammeter: This is used to measure the filament current. 9. The primary coil of the step-up transformer. The secondary or high-voltage circuit consists of: 1. The secondary coil of the step-up transformer: This is ‘centertapped’ to allow a milliampere meter to be installed at ground potential. 2. The milliampere meter: This is used to measure tube current. 3. A milliampere-second (mAs) meter: This is used to measure mAs values at short time intervals. Once the electrical signal is sent through the circuitry, the filament is energized to ‘boil off ’ electrons as a thermionic emission. As the increase of kilovolt (peak) passes through the filament, the creation of a higher potential difference results in the emission of electrons beyond the ‘cloud’ of electrons that are found in the vicinity of the filament. The attraction of the electrons into the metal anode (+) surface and the following abrupt stopping of the electrons produce X-radiation and heat. Unfortunately, 99% of this energy is converted into undesired heat and less than 1% is converted into X-radiation. The variation of the kilovoltage affects the speed of the electrons directed at the anode and generates different wavelengths of the X-rays. For example, a shorter wavelength makes the beam more penetrating. A longer wavelength X-ray is less energetic and less penetrating. In clinical practice the control panel is the most common interface of the fluoroscope and the radiographer. From this panel, variations in power delivered through the X-ray tube can be controlled for improved images. The milliamperage determines the number of electrons flowing in the system that will produce the X-ray beam. Kilovoltage determines the speed of the electrons and quality of the X-ray beam. The length of exposure to the target is often measured in seconds and is the most obvious factor in measuring X-ray exposure. Voltage (kVp) is adjustable over a range of approximately 50–120 kV; the current (mA) setting for fluoroscopy typically ranges 0.5–5 mA. Increasing the current in the radiographic tube increases the number of X-ray photons emitted per second and increases the image contrast; increasing the voltage of the tube increases the energy of each individual photon and primarily effects brightness. Decreasing the voltage (kVp) and thus the energy of the particles by too large of an amount allows fewer particles to pass through the patient's tissue and strike the image intensifier. Contrast and brightness are controlled by the automatic brightness control.1 It is generally considered good technique to use a high voltage (kVp) to attain a useful contrast and a low current (mA) to achieve the desired brightness. If the quality of the picture were improved by increasing the kVp by 15%, the mA would need to be doubled to obtain a similar level of improvement with only a current increase. The most effective guidelines for the optimal initial tube settings on a fluoroscopy machine call for the current (mA) to be set at the lowest possible level and the energy (kVp) at the highest possible setting that will produce a useful image; nominal initial values may be 1 mA at 75 kVp.11 The current starts at 1 mA and is ramped up from there 232

to minimize the amperage used to achieve optimal brightness. If one examines the logic of this carefully, it is perfectly reasonable. Adding current to the system simply uses more electrons to provide more radiation. Increasing the kVp derives more radiation from the same number of electrons by accelerating those electrons. The software in digital fluoroscopy essentially monitors the intensity of the radiation striking the image intensifier surface and within milliseconds adjusts the X-ray tube output and exposure time to optimize the image quality and minimize the radiation dose. Frame grabbing (storing images to disc) avoids the need for many spot films. This makes it essential that the fluoro device have two monitors: one for maintaining stored images for reference and one for viewing in real time. The most important dose-reduction feature available with digital equipment is variable pulsed fluoroscopy.12 Rather than delivering a constant X-ray beam to maintain the image on the screen, the pulsed mode delivers X-rays intermittently, with the most recent image being displayed until the next one becomes available (last image hold).

Absorbed dose quantities and units for quantifying biologic risks Absorbed dose refers to the energy that is deposited locally in an absorbing medium from ionizing radiation. For the energies typically used in diagnostic X-ray procedures, absorbed dose and kerma are equivalent. By contrast, for high-energy photon interactions, the more highly charged particles may deposit energy at sites distant from the initial interaction site, with a corresponding loss of electronic equilibrium. In this case, absorbed dose and kerma are not equivalent. The unit of absorbed dose is the gray, which is the same unit as for kerma, and 1 Gy of absorbed dose is equivalent to 1 J of energy absorbed by the medium per kilogram of absorbing medium. One gray of absorbed dose is equivalent to 100 rad, the traditional unit of absorbed dose. Doses, including skin dose, include the contributions from scattered radiation in addition to the primary radiation. Organ doses consist of the total energy absorbed by an organ per unit mass of the organ.1 Practitioners are often concerned about the absorbed dose to the eye, inducing cataracts.13,17,18 This biologic effect appears to have a threshold in that about 6 Gy of diagnostic X-irradiation over several weeks is necessary to produce cataracts in humans. It may be that absorbed doses of about 15 Gy are necessary to induce cataracts in the diagnostic fluoroscopy setting (Tables 21.2–21.4; Fig. 21.3) Organ doses consist of the total energy absorbed by an organ per unit mass of the organ.

Radiation safety philosophy The interventional physician must be recognized as ‘the captain of the ship’ in the procedure room. Therefore, this individual is not only responsible for the outcome of the procedure at hand, but also for minimizing the dose of radiation to every individual in the procedure room. This responsibility does not fall on any other individual. The

Table 21.2: Maximum permissible dose equivalents (mSv) Area

13 weeks

Yearly

Cumulative

Total effective dose equivalent

12.5

50

Age × 10

Lens of eye

37.5

150

125

500

Other organs (individually) 8

From Raj et al. 2003 with permission of Churchill Livingstone.

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures Annual dose limits for radiation worker (10 CFR 20.1201)

Table 21.3: Minimum half-value layers X-ray tube voltage (kilovolt peak)

Minimum HVL (mm of Al)

50

1.5

60

1.8

70

2.1

80

2.3

90

2.5

100

2.7

110

3.0

120

3.2

130

3.5

140

3.8

150

4.1

>150

See note 2

Skin 0.50 Sv (50 rems)

Eyes 0.15 Sv (15 rems)

Elbows to hands 0.50 Sv (50 rems)

1. Half-value layers (HLV) for intermediate selected voltages are to be obtained by linear interpolation. 2. Linear extrapolation is to be used. Reference: http://www.doh.gov.za/ department/radiation/licensing/ electronicproducts/protocols/new/general.pdf

Knees to feet 0.50 Sv (50 rems)

Table 21.4: Radiation dose limits Annual

50 mSv

5 rem

Cumulative

10 mSv

1 rem × age

Annual dose limits for tissues and organs Lens of the eye

150 mSv

15 rem

Skin, hands, and feet

500 mSv

50 rem

Total dose equivalent

5 mSv

0.5 rem

Monthly dose equivalent

0.5 mSv

0.05 rem

Total effective dose equivalent TEDE (whole body) 0.05 Sv (5 rems)

Fig. 21.3 The total annual allowable radiation exposure for various portions of the body.

Fetus

9

From Gruber et al. 2000 with permission of Hanley & Belfus.

interventionist is solely responsible. Therefore, any questions, right down to the issue of fluoroscope maintenance, must be asked sooner rather than later. Radiation exposure to the patient is also a very important consideration and most of the issues discussed which limit exposure to the medical personnel also limit exposure to the patient. The major factors impacting radiation dose are field size, subject density (body part, etc,), c-arm position, proximity of the body part to the X-ray source, shielding and time of exposure, and clinical efficiency.

Basic safety procedures of dose management for radiology staff Distance: Increasing the distance between the source of radiation and the object being radiated is the most effective means of reducing exposure to a given source of ionizing radiation. The physician's exposure is 1/1000th the patient's exposure at a distance of 1 meter from the X-ray tube. As a result of this observation and logic, it is

strongly suggested that the technician and physician remain as far away from the fluoroscopic table as practical during fluoroscopic procedures. This is due to the fact that radiation follows the inverse square law. As X-ray beams travel through space they diverge. Therefore, radiation intensity decreases as the inverse square of the distance from the source of radiation (I2/I1 = d12/d22).2 This can also be thought of in terms of radiation density. At a distance of 1 standard unit from the point source of radiation, the radiation density will be 1/12 or 1, meaning that unit is the reference and all radiation is equal in that sphere. Any initial unit can be taken as one.2 At a distance of 2 units, one sees the effects of the inverse square law where the distance is great enough to have allowed the radiation beams to diverge, decreasing radiation density at the target distance so the density drops to 1/22 or 1/4. At a distance of 3 units, the effect grows ever greater at 1/32 or 1/9, followed by 1/16 and 1/25, etc. The physician's exposure is 1/1000th the patient's exposure at a distance of 1 meter from the X-ray tube (Fig. 21.4). Strictly speaking, this postulate is for a point source of radiation and may not be precisely applicable to the clinical use of radiation in the context discussed in this chapter; however, the general principle may be applied effectively. Additionally, good technique dictates that the X-ray source be kept as far from the patient as possible. By default, this will place the image intensifier as close to the patient as is reasonable, allowing 233

Part 2: Interventional Spine Techniques Sphere area 4πr2 Source strength

Intensity at surface of sphere S 4πr2 = I

S

I 9 I 4

I

r 2r The energy twice as far from the source is spread over four times the area, hence one-fourth the intensity.

3r

Fig. 21.4 Radiation deteriorates at the inverse square of the distance from the source.

room to work between the skin surface and the image intensifier (Figs 21.5, 21.6). Control: Who will control the on/off function of the fluoroscope, the proceduralist or the technician? This may seem to be a trivial question, yet it can make a large difference in exposure. Operating the fluoroscope via foot pedal allows the proceduralist to be sure the beam will not be activated inadvertently while one's hand is in the path of the beam, and allows for the foot pedal to be placed a safe distance away from the cathode. This requires the operator to take one step away from the fluoroscope before activating the beam whenever practical. For many, this choice is simply a matter of style. Nonetheless, whether one works consistently in the same procedure suite, or move consistently, the decision as to who will operate the fluoroscope should be crystal clear before anyone presses any buttons. If practical during the procedure, the physician should step away from the patient before acquiring each image and also use extension tubing during contrast injection to maximize the physician's distance from the beam.16 This once again argues for the logic of having the interventionist use the foot pedal for activation of the beam. Placing the foot pedal 1 meter away from the table thereby requires the interventionist to take one step away from the table before activating the beam. This may seem cumbersome, but the reduction in radiation dose over time can be enormous. It should be clear that distance between the source of radiation and the object being radiated is the most effective means of reducing exposure to a given source of ionizing radiation. As a result of this

X-ray tube positioning

ESER (mGy/min): 22 DAP rate (Gy-cm2/min): 4.8 Scatter rate (mGy/hr): 6.3

18

18

4.8

4.3

6.1

5.2

Fig. 21.5 The energy scatter rate is least with the energy source furthest from the patient and the image intensifier distance controlled. 234

observation and logic, it is strongly suggested that the technician and physician remain as far away from the examining table as practical during fluoroscopic procedures. If practical during the procedure, the physician should step away from the patient before acquiring each image and also use extension tubing during contrast injection to maximize the physician's distance from the beam.17 Shielding has a major impact on radiation dose. The radiation intensity of an X-ray beam decreases exponentially as the beam passes through a material. The relevant equation is (I=I0e−ux). In this equation, I = the ‘initial’ and I0 = ‘resultant’ radiation intensity’ respectively; whereas u is the attenuation coefficient of the material and x is the thickness of the attenuating material. In keeping with these postulates, the principles of time, dose, and shielding must be considered when evaluating safety. Given the above information, it becomes clear that each factor must be considered in very different ways in limiting radiation exposure in clinical practice. Shielding produces the most utilitarian results in the reduction of staff dose, as there are times when the proceduralist simply must function in close proximity, even directly in cinefluoroscopy. In these circumstances there simply is no substitute for the best modern flexible lead gloves, lead glasses, lightweight lead aprons, and lead-lined thyroid shields available. Appropriate shielding is mandatory for the safe use of ionizing radiation for medical imaging.17 Other methods of shielding include beam collimation, protective drapes, and panels. Protective apparel such as aprons should be lined with 0.5 mm thick lead or greater to reduce 90% of the radiation exposure of the physician or other medical personnel. Half-a-millimeter thick lead reduces 90% of the radiation exposure at 80 kVp while 0.58 mm thick lead reduces 90% of the radiation exposure at 120 kVp.18 Leadlined glasses and thyroid shields likewise reduce 90% of the exposure to the eyes and thyroid, respectively. Lead-lined gloves reduce radiation exposure to the hands; however, they are no substitute for strict observation of appropriate fluoroscopic hygiene.18 Gloves should be considered as an effective means of reducing scatter radiation only. If the interventionist places his or her gloved hands in the fluoroscopic field, he or she will note that initially their phalanges are barely visible; however, as exposure time increases, the phalanges become progressively more visible. This is because the automatic adjustment features of the fluoroscopy unit automatically increase the intensity of radiation, thus penetrating the gloves with stronger radiation. Also note that for the interventionist to see their phalanges on the fluoroscopic monitor the radiation is penetrating both the dorsal and ventral surfaces of the glove and those radioactive particles that only penetrate the ventral surface of the glove and not the dorsal surface of the glove may cause additional damage to the phalanges as they reverberate in the interventionist's digits. The major factors in radiation dosimetry are collimation, time, distance, and shielding. Clinical planning and the use of contrast will also be discussed. Time: Radiation dose is directly proportional to time; thus, by doubling the radiation time the dose is doubled and by halving the radiation time the dose is halved.1 Many factors impact the ‘on time’ of a fluoroscopic procedure. Modern fluoroscopes provide a variety of technique-based systems that assist in the reduction of fluoro time per procedure. These include pulse mode, last image hold, and minimization of the use of magnification. Exposure time: As discussed in this chapter, exposure time should be kept to an absolute minimum. Methods of reducing exposure time include meticulous advanced planning of the procedure, judicious use of contrast enhancement, appropriate positioning of the patient, orientation of the fluoroscopic unit prior to beginning the procedure, utilization of the pulsed mode of fluoroscopy, appropriate training of

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

0.25

1.0

5

0.5

0.2

5

0.2

1.0

8.0 4.0

0.5

4.0

0.25

2.0

0.2

5

2.0

1.0

1.0

0.5

0.5

A

B

0.5

0.25

0.2

5

0.5

0.5

4.0

2.0 2.0

0.5

1.0

1.0

0.25

5

0.2

0.5 C

0.5

D

Fig. 21.6 Stray radiation fields measured in a cardiac catheterization suite for a 90° left anterior oblique projection, with the X-ray beam approximately 1 m above the floor. Scale bar is 0.5 m. Curves represent the kerma rates at 1.5 m above the floor (approximating eye level) (A) and 1.0 m above the floor (approximating waist level) (B). (From Balter 199815 with permission of Radiological Society of North America) Stray radiation fields measured in a cardiac catheterization suite for a 60° left anterior oblique projection, with the X-ray beam approximately 1 m above the floor. Scale bar is 0.5 m. Curves represent the kerma rates at 1.5 m above the floor (approximating eye level) (C) and 1.0 m above the floor (approximating waist level) (D). 235

Part 2: Interventional Spine Techniques

the interventionist and/or technician to only radiate the patient when the interventionist is looking at the monitor, using the last image hold functions, and saving images to review during the case to minimize retracing steps during the procedure with active fluoroscopy.

RADIATION DOSE MONITORING Radiation badges must be worn if it is at all likely that a person could receive 25% of the maximum permissible dose in the discharge of his or her duties.19 At minimum, a radiation badge should be worn on the trunk under the lead apron and under the thyroid shield.20 Other places where it may be important to wear a radiation badge is on the outside of the thyroid shield to measure the radiation exposure to the face and eyes, on the finger in the form of a ring badge if the interventionist may have his or her hands in the field, and on the posterior torso under the wrap-around lead jacket if the staff member may have his or her back turned to the field during fluoroscopy.

STAFF RADIATION MANAGEMENT DURING FLUOROSCOPY The radiation exposure to the interventionist is largely dependent on positioning of the radiation source. There is a tremendous increase in operator exposure when the X-ray tube is not positioned properly, or is not directly below the patient (Fig. 21.7). This increase occurs for two reasons: the overall intensity of the scattered radiation beam is approximately 1000 times greater at the radiation entrance site on the skin compared to the exit site, and there is less attenuating material (e.g. image intensifier) between the patient and the operator. As a rule of thumb, the maximum operator exposure at a given distance occurs when there is an unobstructed path between the operator and the location at which the X-ray beam enters the patient.19

STAFF RADIATION MANAGEMENT IN COMPUTED TOMOGRAPHY Radiation exposure to the interventionist during a procedure guided by computed tomography may be quite high unless appropriate precautions are taken. Absorbed doses range from 3–9 mGy for a procedure involving 10–20 images. However, if the interventionist

X-ray tube

A

B

X-ray tube

Fig. 21.7 The radiation exposure effects to the interventionist when improper radiation source positioning is used. 236

stands to the side of the gantry instead of directly in front of it, the radiation dose is greatly reduced. Collimation: Radiation field size effects radiation dose directly.1 Clearly, the larger the field to irradiate, the more radiation is required. For this reason, collimation is the first factor to consider in attempting to minimize radiation dose to the patient, the staff, and the interventionist. The only time the collimator should be wide open is when the interventionist is performing the initial scout films for localization of anatomic structures. Once the interventionist has become oriented to the anatomy, the following images should be collimated as tightly as possible to minimize dosing.1 C-arm position: C-arm positioning effects radiation scatter in two major modes. For the vast majority of projections the X-ray source should be under the table. Placing the X-ray source above the table dramatically increases scatter (see Fig. 21.5). Scatter is likewise increased ipsilateral to the tube by oblique views (see Fig. 21.5). Good technique demands that the X-ray source be placed as far from the patient as possible while concomitantly placing the image intensifier as close to the patient as possible in order to minimize scatter and even out the distribution of incident X-rays. When it is absolutely necessary to work on an oblique view or a cross-table lateral, the operator and other staff must be places on the side of the table away from the X-ray source, and follow the same directions as above for proximity of the tube and intensifier. Turning the room around like this can be a cumbersome process, yet it is critical in managing staff dosing. Technique factors: Collimation reduces exposure simply by reducing beam size, as well as by reduction of beam source area minimizing scatter. Magnification control allows the field size to be adjusted. The smaller the field size, the more magnified the image appears on the television monitor. The entrance dose rate increases if the image is magnified. The most appropriate rule is that the smallest magnification mode consistent with the type of procedure being performed should be used with tight collimation. Using a minimal magnification setting is preferred from a risk management standpoint because it allows for a lower mA setting to be employed and decreased scatter. Pulsed mode fluoroscopy ensures an adequate exposure with minimal ‘on time’ of the beam. When using pulsed fluoroscopy in the 7.5 pulses-per-second mode, radiation exposure can be reduced by as much as 75% of that from conventional fluoroscopy.21 Contrast enhancement: In the process of the pursuit of a minimal dose of radiation during interventional procedures in which fluoroscopy is utilized, always consider the use of a contrast agent in advance. The contrast, being radiodense, will produce a focal increase in cathode output. However, in skilled hands, judicious placement of contrast can dramatically shorten procedure time by outlining anatomic structures that would otherwise be obscure. Likewise, injudicious placement of contrast will obscure the operating field, resulting in the nearly insurmountable obstacle of dense clouding. In the hands of the novice interventionist this generally leads to the ongoing process of additional volumes of contrast media being placed in non-helpful locations, serving only to further obscure the field and increase the radiodensity of the field. In this circumstance there is the double jeopardy of a field obscured by contrast causing the interventionist to have great difficulty visualizing anatomic structures, causing a lengthening of the time of radiation exposure. Still worse, the high density of the dye will cause the automatic output of the fluoroscope to increase via automatic increases in kVp and mA. This significantly increases radiation exposure per unit time. If the target is obscured by contrast injection, the interventionist should abort the procedure, attempt to ‘wash it out’ with normal saline, or approach the target via a different trajectory.

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

In order to minimize the occurrence of the above situation, remember to ‘plan the procedure, and proceed along the plan,’ acknowledging that even the best-laid plan in medicine must be open to modification in the face of evolving circumstance. Few things can be more clinically dangerous than a poorly planned procedure. Contrast dye: In this modern era of medicine there is little debate that nonionic contrast is the medium of choice for interventional pain procedures for a wide variety of reasons. Ionic contrast has the potential to produce significant complications. Specifically when inadvertently introduced into the intrathecal space, ionic contrast has the significant possibility of producing a stereotypical syndrome of ascending myoclonic spasms, resulting in rhabdomyolysis and possibly death.22–24 For this reason nonionic contrast, such as iohexol or iopamidol, has become the medium of choice when there is any risk of penetrating the thecal sac. These agents are relatively safe for intrathecal injection and are in fact routinely used for myelography.25–27

PATIENT PROTECTION DURING RADIATION EXPOSURE Patient skin doses are 8–10 times higher during interventional procedures than during angiography, which are about 10 times higher than from conventional diagnostic procedures utilizing fluoroscopy or computed tomography. Skin entrance doses have been reported in the range of 6–18 Gy for certain interventional procedures.9,28 On the basis of reports of a small number of severely injured patients, in 1994 the FDA issued a warning to all users of fluoroscopy equipment to be alert for doses that may lead to severe skin damage. Acute doses in excess of 2 Gy may lead to erythema and localized, transient alopecia; 6 Gy may cause permanent alopecia; 10 Gy may lead to dry desquamation, dermal atrophy, and telangiectasia; and 15 Gy or more may lead to moist desquamation and necrosis. Injury to other organs may also be possible at these higher dose levels.28,29 Reducing radiation doses to the patient also generally reduces doses to the medical personnel. Methods of limiting radiation exposure include: making certain that the fluoroscopy unit is functioning properly through routine maintenance, limiting fluoroscopic exposure time, reducing field of exposure through collimation, keeping the X-ray source under the table by avoiding cross-table lateral visualization when possible, utilizing pulsed fluoroscopic visualization when possible, and bringing the image intensifier down close to the patient are all methods of reducing radiation exposure to the patient and medical personnel. The latter method causes the automatic brightness system of the X-ray generator to drop the radiation output. Regulatory authority for radiation safety: X-ray use is not completely regulated at the federal level. There is not a single regulatory body that oversees the use of X-rays in medicine. Regulations concerning equipment are devised by the Center for Devices and Fluoroscopic Health within the US Food and Drug Administration (FDA);8 the Occupational Safety and Health Administration (OSHA) places limits on the radiation doses of employees in the workplace, and individual state departments of services place additional regulations on users of X-ray equipment. Most states patterned their regulations after the recommendations of the National Council on Radiation Protection and Measurements (NCRP). This body has developed an extensive set of regulatory guidelines that have become de facto standards for the safe and proper use of ionizing radiation. Other sources give further details of the general philosophy of radiation protection, as well as specific recommendations for particular situations. The International Commission on Radiation Protection (ICRP) and the International Commission on Radiological Units and Measurements (ICRU) publish recommendations for radiation protection.11–14,19,30–32

The Occupational Safety and Health Administration (OSHA) allow only one-third the maximum quarterly dose to the eyes permitted by other regulatory organizations. Doses should always be kept ‘as low as reasonably achievable’ (ALARA). These quarterly allowances set I and Io as the initial and transmitted radiation intensity, respectively; K is the attenuation coefficient of the material (which depends on the atomic number and density of the material and on the energy of the photons); and x is the thickness of the attenuating material. Small amounts of attenuating (shielding) material can greatly reduce the intensity of an X-ray beam. For example, more than 90% reduction of a diagnostic X-ray beam is obtained by using material equivalent to 0.5 mm of lead (the nominal equivalent of a typical lead apron). Lead aprons should always be worn by anyone in a fluoroscopy suite. Because fluoroscopy is used extensively during some interventional procedures, the continual observation of these fundamental principles is of far greater importance than in other areas of diagnostic fluoroscopy.

Fluoroscopic systems – basic set-up This is a selected listing of basic factors essential for the set-up of a fluoro suite. Derived from the State of Tennessee Deptartment of Environment and Conservation.24 For a full list of regulations see applicable state or national regulations. 1. A dead-man switch must control X-ray production. A dead man switch is a device (switch) constructed so that a circuit closing contact can only be maintained by continuous pressure on the switch by the operator. Therefore, when the machine is turned on by any means, whether by the push button at the control panel, or by the foot pedal, this switch must be held in for the machine to remain ‘on.’ 2. The ‘on-time’ of the fluoroscopic tube must be controlled by a timing device, and must end or alarm when the exposure exceeds 5 minutes. An audible signal must alert the user to the completion of the preset on time. This signal will remain on until the timing device is reset. 3. The X-ray tube used for fluoroscopy must not produce X-rays unless a barrier is in position to intercept the entire cross-section of the useful beam. The fluoroscopic imaging assembly must be provided with shielding sufficient that the scatter radiation from the useful beam is minimized. 4. Protective barriers of at least 0.25 mm lead equivalency must be used to attenuate scatter radiation above the tabletop (e.g. drapes, bucky-slot covers). This shielding does not replace the lead garments worn by personnel. Scattered radiation under the table must be attenuated by at least 0.25 mm lead equivalency shielding. Additionally, most c-arm fluoroscopes have a warning beeper or a light that activate when the beam is ON, some have both. NEVER inactivate any warning devices, and keep one's foot OFF the foot pedal whenever possible. Planning: No single issue is more significant in the reduction of flouro time than advanced planning. Prior to entering the procedure room review all materials, particularly all radiologic films in detail. With the understanding that even the best laid plans must be subject to modification in the face of the unexpected, plan your procedure in detail, based on the unique clinical situation involved with each individual patient. This simple process will produce a striking decrease in your fluoro time. Contrast media can be an invaluable boon in localizing anatomic structures for the interventionist. However, when used injudiciously or haphazardly contrast will obscure the operating field making it nearly impossible to visualize the target structure, while increasing the radiodensity of the operating field, thereby causing a compensatory increase in the radiation output of the fluoroscope. 237

Part 2: Interventional Spine Techniques

When thinking in terms of the reduction of radiation time exposure remember, ‘Plan your procedure, and proceed along your plan.’

Considerations for pregnant workers – regulations Consistent with the Supreme Court decision in the case of UAW vs. Johnson Controls, a woman has the right to choose whether or not to declare her pregnancy, including the right to revoke her declaration. It is the woman's right to choose the declaration of pregnancy regardless of any evidence pregnancy. The key issue is the pregnant worker's right to privacy. Until such time as the pregnant worker makes it known that she is pregnant, i.e. officially declares her pregnancy in writing including the estimated date of conception, no specific rules apply to the conceptus. After declaration of the pregnancy the following rules apply. (1) The licensee shall ensure that the dose equivalent to the embryo/ fetus during the entire pregnancy, due to the occupational exposure of a declared pregnant woman, does not exceed 0.5 rem (5 mSv). (For recordkeeping requirements, see Section 20.2106.) (2) The licensee shall make efforts to avoid substantial variation above a uniform monthly exposure rate to a declared pregnant woman so as to satisfy the limit in paragraph (a) of this section. (3) The dose equivalent to the embryo/fetus is the sum of: (A) The deep-dose equivalent to the declared pregnant woman; and (B) The dose equivalent to the embryo/fetus resulting from radionuclides in the embryo/fetus and radionuclides in the declared pregnant woman. (4) If the dose equivalent to the embryo/fetus is found to have exceeded 0.5 rem (5 mSv), or is within 0.05 rem (0.5 mSv) of this dose, by the time the woman declares the pregnancy to the licensee, the licensee shall be deemed to be in compliance with paragraph (a) of this section if the additional dose equivalent to the embryo/fetus does not exceed 0.05 rem (0.5 mSv) during the remainder of the pregnancy. [56 FR 23396, May 21, 1991, as amended at 63 FR 39482, July 23, 1998] Maternity aprons are available and are constructed with a double thickness of lead in the sensible area. The declared pregnant worker should be aware that the back of the apron still leaves her unprotected.

CONCLUSION In conclusion, radiation exposure is critical to the well-being of both healthcare staff and patients. The physics and biological impact of radiation as well as methods of reducing exposure to radiation during interventional procedures have been discussed. Radiation safety should be a mutual goal for all healthcare workers, not only for their own health, but also for the health of their patients. The reader is encouraged to pursue further investigation utilizing the references cited.

References

6. Parry RA, Glaze SA, Archer R. The AAPM/rsna physics tutorial for residents typical patient radiation doses in diagnostic radiology. Radiographics 1999; 19:1289–1302. 7. Wycoff HO The international system of units. Radiology 1978; 128:833–835. 8. Raj PP, Lou L, Erdine S, et al. Equipment used for radiographic imaging. In: Raj PP, Lou L, Erdine S, et al., eds. Radiographic imaging for regional anesthesia and pain management. New York: Churchill Livingstone; 2003:5–8. 9. Gruber RD, Botwin KP, Shah CP. Radiation safety for the physician. In: Lennard T, ed. Pain procedures in clinical practice. Philadelphia: Hanley & Belfus; 2000:31. 10. Brateman L. The AAPM/RSNA physics tutorial for residents radiation safety considerations for diagnostic radiology personnel. Radiographics Volume 19. Number 4 11. Broadman LM, Navalgund YA, Hawkinberry DW. Radiation risk management during fluoroscopy for interventional pain medicine physicians. Current pain and headache reports. 2004; 8:49–55. 12. Performance standards for ionizing radiation emitting products. 21 CFR part 1020.30(k): leakage radiation from the diagnostic source assembly. 1998; April 1; 562. 13. National Council on Radiation Protection and Measurements: Medical X-ray, Electron Beam, and Gamma Ray Protection for Energies Tip to 50 Mev. NCRP Report No. 102. Washington, DC; 1989. 14. International Commission on Radiological Protection (ICRP): Radiation Protection. ICRP Publication No. 26. Oxford, Pergamon Press; 1977. 15. Balter S. Stray radiation in the cardiac catheterization laboratory. In: Nickoloff EL, Strauss KJ, eds. Categorical course in diagnostic radiology physics: cardiac catheterization imaging. Oak Brook, Ill: Radiological Society of North America; 1998:223–230. 16. Marshall NW, Faulkner K. The dependence of the scattered radiation dose to personnel on technique factors in diagnostic radiology. Med Phys 1996; 23:1271–1276. 17. Payne JT, Shope TB. Proceedings of the ACR/FDA Workshop on Fluoroscopy: Strategies for Improvement in Performance. In: Payne JT, Shope TB, eds. Radiation Safety and Control. American College of Radiology. 1993. 18. Boone JM, Levin DC. Radiation exposure to angiographers under different fluoroscopic imaging conditions. Radiology 1991; 180:861–865. 19. National Council on Radiation Protection and Measurements: Limitation of Exposure to Ionizing Radiation. NCRP Report No. 116. Washington, DC; 1993. 20. Code of Federal Regulations, Title 29, Part 16, Chapter 17, Section 1910.96. Washington, DC, US Government Printing Office; 1971. 21. Hernandez RJ, Goodsitt MM. Reduction of radiation dose in pediatric patients using pulsed fluoroscopy. Am J Roentgenol 1996; 167:1247–1253. 22. Killeffer JA, Kaufman HH. Inadvertent intraoperative myelography with Hypaque: case report and discussion. Surg Neurol 1997; 48(1):70–73. PMID: 9199689 23. Sahjpaul RL, Lee D, Munoz DG. Fatal reaction from inadvertent intrathecal entry of ionic contrast medium during a nephrogram. Acta Neuropathol (Berl) 1997; 93(1):101–103. PMID: 9006664 24. Rosati G, Leto di Priolo S, Tirone P. Serious or fatal complications after inadvertent administration of ionic water-soluble contrast media in myelography. Eur J Radiol 1992; 15(2):95–100. PMID: 1425760 25. Latchaw RE, Hirsch WL Jr, Horton JA, et al. Iohexol vs. metrizamide: study of efficacy and morbidity in cervical myelography. Am J Neuroradiol 1985; 6(6):931–933. PMID: 3934932 26. Haughton VM. Intrathecal toxicity of iohexol vs. metrizamide. Survey and current state. Invest Radiol 1985; 20(1 Suppl):S14–S17. PMID: 3918951 27. Wang YS, Jiang YH, Hou ZY. Intrathecal injection of Iohexol for routine myelography and CT myelography in 1,000 cases. Chin Med J (Engl) 1990; 103(6):497–502. PMID: 2209203 28. Houda W, Peters KR. Radiation-induced temporary epilation after a neuroradiologically guided embolization procedure. Radiology 1994; 193:642–644. 29. Wagner LK, Eifel PJ, Geise RA. Potential biological effects following high X-ray dose interventional procedures. J Vasc Intervent Radiol 1994; 5:71–84.

1. Schueler BA. The AAPM/RSNA physics tutorial for residents general overview of fluoroscopic imaging. Radiographics 2000; 20:1115–1126.

30. Code of Federal Regulations, Title 21, Parts 1000–1050. US Government 1985. Revision of the Radiation Control for Health and Safety Act of 1968.

2. Carlton RR, Adler AM. Principles of radiographic imaging. Stamford: Delmar; 2001:111–114.

31. National Council of Radiation Protection and Measurements: Recommendations on Limits for Exposure to Ionizing Radiation. NCRP Report No. 91. Washington, DC; 1987.

3. Wang J, Blackburn, TJ. The AAPM/RSNA physics tutorial for residents x-ray image intensifiers for fluoroscopy. Radiographics 2000; 20:1471–1477. 4. Statkiewicz MA, Ritenour ER. Radiation protection for student radiographers. St. Louis: Mosby; 1983.

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5. Gruber RD, Botwin KP, Shah CP. Radiation safety for the physician. In: Lennard T, ed. Pain procedures in clinical practice. Philadelphia: Hanley & Belfus; 2000:25,26.

32. National Council on Radiation Protection and Measurements: Structural Shielding Design and Evaluation for Medical Use of Xrays and Gamma Rays of Energies up to 10 Mev. NCRP Publication No. 49. Washington, DC; 1976.

PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 1

Principles and Concepts Underpinning Spinal Injection Procedures

CHAPTER

Sedation for Percutaneous Procedures

22

Mohammad Uddin and Salahadin Abdi

INTRODUCTION ‘Sedation and analgesia’ describe a state in which patients can tolerate unpleasant procedures while maintaining cardiac and respiratory function and still maintain the ability to respond purposefully to both verbal commands and tactile stimulation. The Task Force on sedation and analgesia decided that the term ‘sedation and analgesia’ (sedation/analgesia) more accurately defines this therapeutic goal than does the commonly used but imprecise term ‘conscious sedation.’ This level of sedation does not include a level in which the only intact reflex is withdrawal from a painful stimulus.1 Although sedation has been described as ‘light sleep’2 and textbooks note that ‘the terms sleep, hypnosis, and unconsciousness are used interchangeably in anesthesia literature to refer to the state of drug-induced sleep,’3 pharmacological sedation is not the same as physiological sleep. During interventional procedures the goal is to provide enough sedation to keep the patient comfortable, relaxed, and communicative. Even though this preferred light sedation is relatively safe, rescue medications and equipment to support respiration and circulation should be readily available.

LEVELS OF SEDATION See Table 22.1. Minimal sedation (anxiolysis) is a drug-induced state during which patients respond normally to verbal commands. Although cognitive function and coordination may be impaired, ventilatory and cardiovascular functions are unaffected. Moderate sedation/analgesia (i.e. ‘conscious sedation’) is a druginduced depression of consciousness during which patients respond

purposefully* to verbal commands, either alone or accompanied by light tactile stimulation. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained. Deep sedation/analgesia is a drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully* following repeated verbal or painful stimulation. The ability to independently maintain ventilatory function may be impaired, necessitating assisted airway support. Cardiovascular function is usually maintained. General anesthesia is a drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. The ability to independently maintain ventilatory function is often impaired. Patients often require assistance in maintaining a patent airway, and positive-pressure ventilation may be required because of depressed respiration or drug-induced neuromuscular depression. Cardiovascular function may be impaired. Because sedation is a continuum, it is not always possible to predict how an individual patient will respond. Hence, practitioners intending to produce a given level of sedation should be able to rescue patients whose level of sedation becomes deeper than initially intended. Individuals administering moderate sedation/analgesia (i.e. ‘conscious sedation’) should be able to rescue patients who enter a state of deep sedation/analgesia, while those administering deep sedation/analgesia should be able to rescue patients who enter a state of general anesthesia. Deep sedation and general anesthesia are not usually recommended for most of pain management procedures, as an awake, cooperative patient is needed to prevent complications related to nerve injury, allergic reactions, or medication toxicity (Table 22.2).

Table 22.1: Definition of General Anesthesia and Levels of Sedation/Analgesia1 Minimal Sedation (Anxiolysis)

Moderate Sedation/Analgesia (Conscious Sedation)

Deep Sedation/ Analgesia

General Anesthesia

Responsiveness

Normal response to verbal stimulation

Purposeful response to verbal or tactile stimulation

Purposefula response following repeated or painful stimulation

Unarousable even with painful stimulus

Airway

Unaffected

No intervention required

Intervention may be required

Intervention often required

Spontaneous ventilation

Unaffected

Adequate

May be inadequate

Frequently inadequate

Cardiovascular function

Unaffected

Usually maintained

Usually maintained

May be impaired

a Monitored Anesthesia Care does not describe the continuum of depth of sedation; rather it describes ‘a specific anesthesia service in which an anesthesiologist has been requested to participate in the care of a patient undergoing a diagnostic or therapeutic procedure.’

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Table 22.2: Ramsay Level of Sedation Scale2 Clinical Score

Level of Sedation Achieved

6

Asleep, no response

5

Asleep, sluggish response to light glabellar tap or loud auditory stimulus

4

Asleep, but with brisk response to light glabellar tap or loud auditory stimulus

3

Table 22.4: Summary of American Society of Anesthesiologists Preprocedure Fasting Guidelines for Healthy Patients Who Are Undergoing Elective Procedures Ingested Material

Minimum Fasting Period

Clear liquids

2h

Nonhuman milk

6h

Sleepy, but responds to commands

Light meal

6h

2

Patient cooperative, oriented and tranquil

1

Patient anxious, agitated or restless

The fasting periods noted in Table 22.4 apply to all ages. Examples of clear liquids include water, fruit juices without pulp, carbonated beverages, clear tea, and black coffee. Since nonhuman milk is similar to solids in gastric emptying time, the amount ingested must be considered when determining an appropriate fasting period. A light meal typically consists of toast and clear liquids. Meals that include fried or fatty foods or meat may prolong gastric emptying time. Both the amount and types of foods ingested must be considered when determining an appropriate fasting period.

GENERAL PREPARATION The risks, benefits, and alternatives of sedation should be explained to the patient in lay terms. The main goals in administering sedatives and analgesic medications are to facilitate the completion of a potentially difficult procedure and to provide a safe and comfortable environment for the patient. The most feared risk of sedation is respiratory depression, which can result in catastrophic consequences if not recognized and treated promptly. The patient may also decline sedation, at which point alternatives can be considered including local anesthesia, relaxation techniques and, for pediatric patients, general anesthesia. After thorough explanation is provided and all questions are answered, informed consent is obtained before any sedation is administered.

Preprocedural assessment All patients who are scheduled to receive sedation should be thoroughly evaluated prior to the procedure. Relevant issues that should be addressed include past medical history, past surgical history to include any anesthetic complications, drug allergies, and current medications to include anticoagulants, smoking, alcohol use and recreational drug history, and NPO status. The risk stratification classification of the American Society of Anesthesiologists (ASA) provides an excellent preprocedure assessment tool for this purpose (Table 22.3). Table 22.4 provides a summary of the American Society of Anesthesiologists preprocedure fasting guidelines. The recommendations apply to healthy patients who are undergoing elective procedures. They are not intended for women in labor. Following the guidelines does not guarantee complete gastric emptying has occurred.

bronchospasm, and laryngospasm requiring tracheal intubation and ventilatory support. Intubation may be especially difficult in patients with atypical airway anatomy. Airway abnormalities may also increase the likelihood of airway obstruction following the administration of sedatives and analgesics. Warning signs of a difficult airway are listed in Table 22.5. Recommendations for frequency of monitoring and documentation during sedation/analgesia are listed in Table 22.6.

Table 22.5: Warning Signs of a Difficult Airway Previous problems with sedation Stridor, snoring, or sleep apnea Advanced rheumatoid arthritis Chromosomal abnormality (e.g. trisomy 21) Significant obesity (especially involving the neck and facial structures) Short neck and limited neck extension Decreased hyoid-mental distance (<3 cm in an adult) Neck or anterior mediastinal mass Cervical spine disease or trauma Tracheal deviation

Airway assessment procedures for sedation and analgesia

Dysmorphic facial features (e.g. Pierre–Robin syndrome)

The airway should be evaluated prior to giving sedative medications. Oversedation will cause respiratory depression and may require respiratory support. Oversedation can also cause aspiration, obstruction,

Edentulous

Small opening (< 3 cm in an adult) Protruding incisors Loose or capped teeth Dental appliances

240

Table 22.3: American Society of Anesthesiologist Physical Class Risk Stratification

High, arched palate

Class I

Normal healthy patient

Tonsillar hypertrophy

Class II

Mild systemic disease

Nonvisible uvula

Class III

Severe systemic disease

Micrognathia

Class IV

Life-threatening illness

Retrognathia

Class V

Moribund patient

Trismus and significant malocclusion

Macroglossia

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

Table 22.6: Recommendations for Frequency of Monitoring and Documentation During Sedation/Analgesia1

Table 22.8: Emergency Medications

Monitoring

Conscious Sedation

Deep Sedation

Atropine

Heart rate

Continuous

Continuous

Diazepam

Oxygen saturation

Continuous

Continuous

Diphenhydramine

Respiratory rate

Minimum of every 15 min

Minimum of every 5 min

Ephedrine

Noninvasive blood pressure

Minimum of every 15 min

Minimum of every 5 min

Glucose (50%) (10% or 25% glucose)

Level of consciousness

Minimum of every 5 min

Minimum of every 5 min

Amiodarone

Epinephrine Hydrocortisone, methylprednisolone, or dexamethasone Lidocaine Midazolam

EMERGENCY EQUIPMENT FOR SEDATION AND ANALGESIA Appropriate emergency equipment should be available whenever sedative or analgesic drugs capable of causing cardiorespiratory depression are administered. Items in brackets are recommended when infants or children are sedated (Tables 22.7, 22.8).

DRUG PRINCIPLES FOR SEDATION AND ANALGESIA 1. Always titrate to effect rather than using predetermined dosing guidelines. 2. Use the safest intravenous drug with the shortest duration of effect appropriate for the procedure. 3. Avoid using drugs that require infusion pumps for administration. 4. Benzodiazepines alone rarely cause apnea. 5. Benzodiazepines produce anxiolysis and amnesia, not analgesia. 6. The shortest-acting benzodiazepines have durations of action considerably longer than the shortest-acting opioids.

Table 22.7: Emergency Equipment

Vasopressin

7. Opioid-induced apnea frequently responds to tactile stimulation. 8. Opioids produce analgesia, not amnesia. They may produce apnea prior to sedation. 9. Benzodiazepines markedly potentiate opioid-induced respiratory depression. 10. Flumazenil antagonizes benzodiazepines; naloxone antagonizes opioids. 11. Propofol is an intravenous general anesthetic with a narrow therapeutic index that is sometimes used for sedation. Its use should be restricted to individuals with the expertise and privileges to use such agents. 12. Ketamine is an intravenous induction agent with profound analgesic effects that is frequently used for painful procedures in ICUs and burn units. Advantages over opioids include better preservation of ventilation and airway reflexes, and stimulation of the cardiovascular system. Psychomimetic effects are common with ketamine, but may be prevented by coadministration of a benzodiazepine.

Common drugs for sedation

BASIC AIRWAY MANAGEMENT EQUIPMENT Compressed oxygen (tank with regulator or pipeline supply with flow meter) Ambu-bag Suction Suction catheters (pediatric suction catheters) Yankauer-type suction Face masks (various sizes) Oral and nasal airways (various sizes) Lubricant ADVANCED AIRWAY MANAGEMENT EQUIPMENT

Nitroglycerin (tablets or sprays)

(in addition to the above listed equipment) For practitioners with intubation skills, laryngeal mask airways Rescue airways such as Combitube and esophageal obturatory airway Laryngoscope handles (tested) and laryngoscope blades Endotracheal tubes Cuffed # 6.0, 7.0, 7.5, 8.0 Uncuffed # 2.5, 3.0, 3.5, 4.0, 4.5, 5.0, 5.5, 6.0 Stylets

There is a variety of pharmacological agents commonly used for sedation/analgesia during interventional procedures. The most common reasons for using these agents are to promote anxiolysis, amnesia, analgesia, and sedation. Each of these agents have the potential to cause sedation and all can effect respiratory and cardiovascular function. The choice of the drug depends on whether the primary goal is anxiolysis, analgesia, or both. Generally, short-acting drugs are recommended for early recovery. In cases when polypharmacy is required, physicians must be aware of the synergistic and/or additive effects of these drugs. Sedating drugs should be administered slowly, with enough time for absorption. Only one drug should be administered at a time and the doses should be conservative. If necessary, a moderate dose of an additional drug may be added, but always infused slowly (Tables 22.9, 22.10). As previously mentioned, pharmacological antagonists or ‘reversal agents,’ such naloxone and flumazenil, must be readily available. Because these reversal drugs have their own side effects and complications, their routine use is discouraged. When used, the patients must remain for an extended duration to allow for monitoring of cardiovascular and respiratory depression, until the effects of the reversal agents dissipate (Table 22.11). Because propofol, ketamine, pentothal, methohexial, and etomidate can easily and quickly result in general anesthesia for which no 241

Part 2: Interventional Spine Techniques

Table 22.9: The Most Commonly Used Opioid Analgesics Drug

Pediatric Dosing

Adult Dosing

Onset/Duration

Comments

Morphine sulfate

i.v.: 0.05–0.1 mg/kg Max 0.3 mg/kg IM: 0.1–0.2 mg/kg Max 15 mg PO: 0.2–0.5 mg/kg Max 30 mg

i.v.: 1–2 mg increments Max 15–20 mg

Onset: 1–3 min Duration: 8 hr

Assess for respiratory depression Assess for hypotension, more so if hypovolemic May cause delirium and dysphoria Assess for nausea and vomiting and pruritus

Meperidine

i.v.: 0.5–1 mg/kg Max 100 mg IM: 1–2 mg/kg Max 100 mg PO: 1–2 mg/kg Max 100 mg

i.v.: 10 mg increments Max 50–150 mg

Onset: 1–3 min Duration: 5 hr

Assess for respiratory depression. Assess for hypotension, especially if hypovolemic Reduce dose in renal failure patients, toxicity includes seizures Assess for nausea and vomiting. May cause more than morphine May cause dysphoria and delirium Do not use with tricyclic antidepressants and phenothiazides

Fentanyl

i.v.: 0.25–0.5 μg/kg Max 100 ug Transmucosal: 5–15 μg/kg if >2 y and >10 kg

i.v.: 0.05 μg/kg increments Max: 2 μg/kg

Onset: 1–3 min Duration: 30 min to over an hour

Rapid IV infusion can cause maseter and chest wall rigidity Assess for respiratory depression and bradycardia May cause pruritus and urinary retention Assess for hypotension, especially if hypovolemic Assess for nausea & vomiting

All doses should be titrated to effect. Decrease doses to 25% when used in conjunction with benzodiazepines.

Table 22.10: Sedatives Drug

Pediatric Dosing

Adult Dosing

Onset/Duration

Comments

Diazepam

i.v.: 0.05–0.25 mg/kg Max 10 mg p.o.: 0.1–0.25 mg/kg

i.v.: 1–5 mg titrate p.o.: 1–5 mg titrate i.m.: 1–5 mg titrate Max 20 mg healthy Max 5 mg for elderly and debilitated

Onset: 0.5–2 min Duration: 2–8 h

Respiratory depression synergistic with narcotics… reduce dose by 1/3 Irritates veins…can cause phlebitis, thrombosis, swelling, local inflammation…use large veins Precipitates when mixed Contraindicated in acute narrow glaucoma

i.v.: 0.02–0.08 mg/kg Max 0.15 mg/kg i.m.: 0.02–0.1 mg/kg Max 2.5–5 mg p.o.: 0.25–0.75 mg/kg Max 20 mg p.r.: 0.5–0.75 mg/kg

i.v.: 0.5–1 mg until desired effect is achieved. i.m.: 0.02-0.1 mg/kg Max 1–7.5 mg p.o.: 0.5–0.8 mg/kg Max 50 mg

Onset: 3–5 min Duration: max. 5 min declined 30–40 min Gross recovery 6 h

Synergistic action with narcotics Retrograde and antegrade amnesia Reduce dose in elderly, debilitated and patients With compromised renal function May result in patient agitation and myoclonic activity Does not irritate veins Dilution to 1 mg/ml is suggested for accurate dosing

reversal agent is available, the authors recommend that these drugs should only be used by an anesthesia team.

Complications The main complication of the sedation is oversedation. Since oversedation can cause respiratory and cardiovascular depression, the person responsible for monitoring the patient must be capable of rescuing the patient. Other side effects include irritation of the injection site, cognitive impairment and, rarely, allergic reactions.

POSTOPERATIVE CARE It is important for the recovery room personnel to monitor vital signs and neurological condition of the patient. The duration in recovery 242

room is determined by the both the condition of the patient and institution protocols. When necessary, a wheelchair can be used fortransporting patients until full motor strength and recovery from the sedation is achieved. Then patients should be discharged from the recovery room with an escort.

Recovery and discharge criteria following sedation and analgesia1 Patient care facilities administering sedation/analgesia must each develop recovery and discharge criteria based on the type of patients seen and the type of procedures performed. Some of the basic principles are detailed below.

Section 1: Principles and Concepts Underpinning Spinal Injection Procedures

Table 22.11: Reversal Agents Drug

Pediatric Dosing

Adult Dosing

Onset/Duration

Comments

Naloxone

i.v.: 0.5–1 μg/kg titrate Max 1 mg i.v.: 0.1 mg/kg in respiratory arrest Max 2 mg

i.v.: 0.1–0.2 mg slow and titrate to response

Onset: 1–2 min Duration: 30 min when given i.v.

‘Reverses’ narcotics only Rapid administration can produce nausea, sweating, hypertension and dysrhythmias. May cause pulmonary edema, MI and seizures Contraindicated in drug abusers or chronic pain patients who regularly take narcotics Reversal effect may not outlast narcotic effect … consider giving an i.m. dose

Nalmefene (Revex)

i.v.: 10 μg/kg May repeat at 2 and 5 min Max 1 mg

i.v.: 0.25 ug/kg May repeat at 2 and 5 min Max: 1 μg/kg

Duration: half life is 9 times longer than Narcan

‘Reverses’ narcotics only

Flumazenil

i.v.: 10 μg/kg slow Max 0.2 mg/kg or 2 mg i.m./s.c.: 0.005– 0.001 mg/kg Max 1 mg

i.v.: 0.2 mg slow Onset: 1–2 min May repeat peak in 10 min q60 sec Duration: 30–60 min Max 1 mg Max/hr: 3 mg i.m./s.c.: 0.1–0.2 mg Max 1 mg

General principles 1. Medical supervision of recovery and discharge following moderate or deep sedation is the responsibility of the operating practitioner or a licensed physician. 2. The recovery area should be equipped with or have direct access to appropriate monitoring and resuscitation equipment. 3. Patients receiving moderate or deep sedation should be monitored until appropriate discharge criteria are satisfied. The duration and frequency of monitoring should be individualized depending upon the level of sedation achieved, the overall condition of the patient, and the nature of the intervention for which sedation/ analgesia was administered. Oxygenation should be monitored until patients are no longer at risk for respiratory depression. 4. Level of consciousness, vital signs and oxygenation (when indicated) should be recorded at regular intervals. 5. A nurse or other individual trained to monitor patients and recognize complications should be in attendance until discharge criteria are fulfilled. 6. An individual capable of managing complications (e.g., establishing a patent airway and providing positive-pressure ventilation) should be immediately available until discharge criteria are fulfilled.

Guidelines for discharge 1. Patients should be alert and oriented; infants and patients whose mental status was initially abnormal should have returned to their baseline. Practitioners and parents must be aware that pediatric patients are at risk for airway obstruction should the head fall forward while the child is secured in a car seat. 2. Vital signs should be stable and within acceptable limits. 3. Use of scoring systems may assist in documentation of fitness for discharge. 4. Sufficient time (up to 2 hours) should have elapsed following the last administration of reversal agents (naloxone, flumazenil) to ensure that patients do not deteriorate after reversal effects have worn off.

‘Reverses’ benzodiazepines, not narcotics May cause seizures, cardiac arrhythmias and death Causes anxiety, dizziness, sweating and emotional liability Reversal effect may not outlast sedative … monitor for one hour after reversal. Resedation may occur requiring additional doses. Question administration to patients who take benzodiazepines regularly…may cause seizures in these patients.

5. Outpatients should be discharged in the presence of a responsible adult who will accompany them home and be able to report any postprocedure complications. 6. Outpatients and their escorts should be provided with written instructions regarding postprocedure diet, medications, and activities, and a phone number to be called in case of emergency.

Continuing quality improvement indicators8 If any of the following occur and are caused by the sedatives and/ or analgesics administered, and not the preexisting and underlying disease or its treatment, a review of the chart must be performed and appropriate action taken immediately. 1. Oxygen saturation 90% and a drop of 5% from baseline for longer than 1 min. 2. Use of opioid or benzodiazepine reversal agents. 3. A decrease in blood pressure or heart rate requiring pharmacologic intervention or rapid fluid administration. 4. Failure to respond to physical stimulation. 5. Assisted ventilation and/or unanticipated endotracheal intubation. 6. Unplanned admission. 7. Cardiac or respiratory arrest.

SUMMARY The choice of sedating drugs is based on patient health, type of procedure, and the level of cooperation needed. Each of the sedative agents has advantages and disadvantages. There are no perfect agents. Physicians administering sedation should follow national and institutional guidelines throughout the sedation period. Sedated patient require vigilant monitoring by trained professionals during the entire period of sedation. Monitoring is required during the procedure, during transport, and during recovery. Finally, using strict discharge criteria and warning the patient about possible delayed side effects will further decrease sedation-related complications. 243

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References 1. Gross JB, Bailey PL, Caplan RA, et al. Practice guidelines for Sedation and Analgesia by Non-Anesthesiologist. A report developed by the Task Force on Sedation and Analgesia by Non-Anesthesiologists. Anesthesiology 1996; 84:459–71. 2. Lydic R, Baghdoyan HA, eds. Handbook of behavioral state control: cellular and molecular mechanisms. Boca Raton, FL: CRC Press; 1999. 3. Lydic R, Biebuyck JF. Sleep neurobiology; relevance for mechanistic studies of anesthesia. Br J Anesth. 1994; 72:506–508.

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4. Warner MA, Robert A. Caplan RA, Burton S, Epstein BS, et al. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: Application to healthy patients undergoing elective procedures. A report by the American Society of Anesthesiologists. Developed by the Task Force on Preoperative Fasting and the Use of Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration.

PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

Spinal Injections

23

Christopher W. Huston, Curtis W. Slipman, Michael B. Furman, Syed Hasan and Richard Derby

INTRODUCTION A variety of spinal injections are currently utilized in the diagnosis and treatment of axial and radicular pain. The various diagnostic and therapeutic injections include epidural injections, selective nerve root/ spinal nerve injections, zygapophyseal intra-articular joint injections, synovial cyst aspiration, medial branch and dorsal ramus nerve blocks, atlanto-occipital joint injection, lateral atlantoaxial joint injection, sacroiliac joint injection, and sacrococcygeal disc injection. The epidural space can be entered by different anatomic approaches: epidural injections are further divided into transforaminal, interlaminar, and caudal. Though there are subtle differences, terminology for the transforaminal approach differs depending on whether it is used for therapeutic or diagnostic purposes. The term ‘selective nerve root block’ is often used synonymously with selective nerve root injection. This procedure has been used for both diagnostic and therapeutic purposes. Selective nerve root injections may be performed both diagnostically and therapeutically. At the Penn Spine Center we differentiate a transforaminal injection from selective nerve root injection by the explicit purpose of the procedure. Transforaminal injections are meant to address axial pain, presumably arising from a lumbar disc. This necessitates that the needle is placed in a location that assures spread of the therapeutic agent ventrally. In contrast, a therapeutic selective nerve root injection requires more posterior needle placement so that the nerve root, dorsal root ganglia (DRG), and some of the epidural space are bathed with the therapeutic solution. Finally, a diagnostic selective nerve block is one that only anesthetizes the existing (target) nerve root. It should be pointed out that the term selective nerve root injection has been challenged. Some interventionalists would classify the injection as a selective spinal nerve injection. While the spinal nerve is targeted, for diagnostic purposes the DRG needs to be anesthetized. Many spinal disorders such as foraminal stenosis or disc herniation involve the DRG. Blocking only the spinal nerve distal to the DRG could result in a false-negative injection. The injection incorporates the spinal nerve, ventral ramus, and dorsal root ganglion. Zygapophyseal intra-articular injections may be performed for diagnostic or therapeutic purposes. Frequently, medial branch blocks are performed instead of intraarticular zygapophyseal joint injections to diagnose pain emanating from the zygapophyseal joints. Each of these spinal injections may be performed in the cervical, thoracic, and lumbosacral spine. The thought process underpinning the use of these injections for specific diagnosis is discussed in other chapters. It should be emphasized that a general principle invoked is that injections are performed for specific diagnoses and that proper testing is performed prior to an injection procedure. This insures that the minimum number of invasive procedures is performed. This chapter focuses on technique and not rationale. Contraindications to the performance of spinal injections include systemic infection, local infection at the injection site, bleeding dyscrasia, and anticoagulation. A detailed analysis of the variety

of complications that can result from each of the described spinal injections is covered in Chapter 20 by Botwin. Spinal injections are performed under fluoroscopic guidance to improve accuracy, efficacy, and safety. The interventionalist must be cognizant to limit radiation exposure to the patient, staff, and interventionalist to a minimum. The reader is directed to the radiation safety chapter by Windsor. Local anesthesia is recommended prior to performing the spinal injection procedures discussed in this chapter. Unless there are known ‘caine’ allergies, local anesthesia is done with 1% Xylocaine injecting through a 25-gauge needle creating a skin wheal. The skin wheal can be quite small as it needs to only be greater than the diameter of the needle. Larger skin wheals provide more flexibility for selection of needle placement. The disadvantage of a larger skin wheal is that the skin wheal can be painful to the patient. The acidity of Xylocaine injection can cause a painful burning sensation. Because of this, the Xylocaine can be mixed with sodium bicarbonate to neutralize the acidity and make the injection more comfortable. A 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate is used. The decision to use 1% Xylocaine or the Xylocaine–bicarbonate mixture is under the discretion of the interventionalist. For very experienced spine interventionalists local anesthesia may not be required. Some patients may prefer moderate sedation to better tolerate the procedure. This includes those patients who are anxious, needle-phobic, have lower pain thresholds or are at increased risk of a vasovagal reaction. Additionally, some patients in severe pain may have difficulty getting into the proper position on the fluoroscopy table and may benefit from moderate sedation. In particular, those with severe radicular pain, particularly in the presence of a foraminal disc protrusion or foraminal stenosis may experience severe pain with injection of medication around the involved spinal nerve. However, the level of moderate sedation should be limited. The patient still needs to be awake to appropriately respond to painful stimuli, and should have the ability to communicate with the interventionalist. If nerve is contacted, the patient requires the ability to verbalize that extremity pain is perceived to avoid nerve injury. If the patient is too sedated, the nerve or spinal cord could be penetrated with the patient and interventionalist unaware, resulting in neurologic injury. It is preferable to avoid moderate sedation for diagnostic injections, but this is not always feasible. The intravenous anxiolytic or opiate medication may influence the results, increasing the risk of a false-positive diagnostic injection. One way to mitigate that scenario is to ask the patient to complete the pain drawing and VAS scale after sedation is provided.

NEEDLE TECHNIQUES The standard spinal needle has an angled opening of the needle referred to as the bevel. The hub of the needle has a ‘notch.’ The notch and bevel are on the same side in a standard spinal needle. As a needle is advanced through tissue it tends to move towards the 245

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sharper side and away from the bevel and notch. The interventionalist, however, does not see the needle tip and bevel, which are already in the patient’s soft tissues. Instead, one typically sees the part of the needle protruding from the skin, the hub portion and notch. Therefore, the interventionalist must be cognizant of the orientation of the notch as the needle is advanced, since the needle tip will tend to move 180 degrees away from the notched side as it is advanced. Novice interventionalists ignore this tendency and often end up trying to fight the needle’s trajectory, while advanced interventionalists learn to use this ‘bevel control’ to their advantage and, instead, drive the needle. Bevel control can be even more accentuated by placing a 10–20 degree bend on the needle tip away from the notched and bevel side as close to the needle tip as possible. We recommend using a sterile gauze when placing the bend to prevent inadvertent contamination of the needle tip. Another technique to enhance control of the needle is to use a concave arc on the needle for even more precision and steerability. The arc is created by holding the needle between the thumb and index fingers while using one of the other digits closer to the skin surface to create the concavity on the same side the needle is being directed toward (Fig. 23.1). This concavity tends to further slide the needle into position. The combination co of bevel control and a concave arc directing the needle are effectively like having ‘power steering’ to direct the needle tip wherever it is needed. However, like power steering, the needle will be much more sensitive and less forgiving if these techniques are not understood. Thinner needles (i.e. 25 or 27 gauge) are much more responsive to these techniques than the thicker (18 gauge) needles which tend to respond more to ‘brute force.’ Twenty-two-gauge needles tend to be intermediate in response to these techniques and brute force.

FLUOROSCOPIC VIEWS All physicians practicing fluoroscopically guided procedures understand that at least two views are needed to confirm needle tip position. Biplanar imaging, such as anteroposterior (AP) and lateral, are typically utilized. Additionally, other views may be utilized to increase precision, safety, and efficiency in interventional spine care. Therefore, throughout this section, we will describe additional terminology regarding fluoroscopic imaging for each spinal procedure: Trajectory

Fig. 23.1 Bent needle technique of medication delivery. Same technique for bending needle may be utilized to advance needle without syringe attached. 246

view, Safety view, and the two final-position views. These views are obtained by appropriately positioning the fluoroscope and/or patient. Each procedure is done by using a trajectory view for original needle entry, the Safety View during needle advancement to avoid relevant structure, and two final views to confirm needle position prior to contrast and subsequent medication injection. Trajectory view (aka hubogram, needle view) is the initial one which visualizes the path or route the needle will travel to get to the ultimate target. The image is obtained on the fluoroscope, and this determines the initial skin entry position. When utilizing an unencumbered trajectory view during needle advancement, the target can be efficiently approached without encountering obstructions. As well, radiation and procedure time can be minimized by making sure the needle is positioned parallel to the fluoroscopic beam prior to taking additional fluoroscopic pictures. This is accomplished by advancing the needle along the trajectory established by the fluoroscope’s image intensifier relative to the patient. As the needle is advanced down the fluoroscope’s beam a ‘dot’ rather than a ‘line’ is noted on the image (Fig. 23.2). As the needle tip is advanced close to the desired target, biplanar imaging is utilized. However, to safely advance the needle and avoid penetrating ‘dangerous’ structures, we recommend using the ‘Safety (aka danger)’ view during needle advancement. The ‘Safety’ view is used to ensure that the needle does go where it is supposed to and, more importantly, does not go where it should not be. Careful interventionalists are cognizant of the structures to avoid such as thecal sac, spinal cord, major vessels, lung, and kidney. The safety view is that which best visualizes where these structures are known to lie. Unfortunately, fluoroscopy does not enable visualization of the soft tissue structures to be avoided. However, understanding the correlation of fluoroscopic with three-dimensional anatomy enables safe advancement of the needle using identifiable landmarks. Once the needle tip is believed to be at the desired target, we recommend confirming location with biplanar imaging, or two views prior to confirming with contrast injection. For the experienced interventionalist, biplanar imaging at this stage may not be required. Subsequent to this confirmation, contrast is injected. Once the ideal position and contrast flow is confirmed, the injectate is administered. When advancing spinal needles, the needle should be advanced parallel to the X-ray beam towards the target using the trajectory view. The needle tip and hub of the needle will be superimposed, resembling a target when viewed on the monitor (see Fig. 23.2). When advancing

Fig. 23.2 Spinal needle parallel to X-ray beam resembles a target with hub of needle the outer target and needle shaft the bull’s eye.

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the needle, the hand holding the needle should be braced against the patient. This keeps the needle from advancing with inadvertent patient movement. In the cervical spine or with other delicate procedures, a two-handed technique is often utilized. The ulnar palm of the hand is placed against the patient with thumb and index finger on the sides of the hub to maintain correct orientation of the needle. Such positioning guards against advancing the needle too deep, especially if the patient moves. The second hand advances the needle in small increments in the desired direction (Fig. 23.3). The needle is advanced under intermittent fluoroscopic guidance, checking the direction and advancement of the needle. A metal surgical sponge stick can be used in some injections under continuous fluoroscopic guidance. This is an advanced technique and not recommended in the cervical spine or for novice interventionalists. Total fluoroscopy time with continuous fluoroscopy should not exceed that for the same procedure utilizing intermittent fluoroscopy. If it does, the interventionalist should do the procedure with intermittent fluoroscopy. Additionally, the interventionalist must be careful not to expose his/her hand to the X-ray beam. When viewing the monitor, the interventionalist’s hand should not be present on the images. Partitions on the c-arm can be adjusted to cone down the view and decrease radiation exposure to both the patient and interventionalist. Extension tubing between the needle and syringe limits radiation exposure to the interventionalist’s hands. As well, the using of tubing prevents inadvertent movement of the needle tip during the exchange of syringes and while any agent is being injected. As of 2003, the standard of care for injections that involve the epidural space and/or nerve root dictates that extension tubing be utilized.1 Usually, when performing spinal injection procedures, the needle is advanced to abut upon bone or periosteum next to the target for injection. While some advocate that ‘bone is the interventionalist’s friend,’ others argue that teaching a novice to advance until contact with periosteum may lead to false security while advancing the needle too far. Most of the techniques utilize an approach that traverses skin, subcutaneous tissue, muscle, and then bone. The various approaches try to provide the safest path to the desired target. Bone is often utilized to gauge needle depth and avoid dangerous advancement into deeper structures such as subarachnoid space, spinal cord, spinal nerve, vertebral artery, and/or peritoneum. Once periosteum is reached, the needle is usually carefully redirected only a few millimeters in the desired

location utilizing biplanar imaging. A thorough understanding of three-dimensional anatomy and the associated structures is required. The needle is advanced in the ‘Safety’ view which demonstrates structures that must be avoided. Non-ionic contrast is utilized to confirm proper spinal needle placement. Contrast may also demonstrate inadvertent intravascular placement, thereby minimizing potential complications due to vascular injection of medications and will increase the probability of an effective injection. The non-ionic contrast agents typically utilized for spinal procedures are Omnipaque or Isovue, both approved for intrathecal usage. When injecting contrast or medication, it is important not to move the needle tip. As previously mentioned, extension tubing is frequently used for this purpose and is required for epidural space and or nerve root injections. With longer spinal needles in the thoracic and lumbar spine, the needle may be bent while injecting. This keeps the force of depressing the plunger from inadvertently advancing the needle (Fig. 23.4). Of course, since extension tubing is used this potential problem should not be an issue. It should be understood that for intra-articular injection, the therapeutic agent must be injected by connecting the syringe to the hub or the joint space will be rapidly and unnecessarily filled with extra contrast (the contrast that filled the extension tubing). Real-time imaging must be employed regardless of whether extension tubing is used or not. When real-time imaging is used to confirm accurate placement, it inherently means the needle has come to a stop. Then contrast is injected. Simultaneous advancement of the needle and contrast injecting while using continuous fluoroscopy is not appropriate. Unless real-time imaging is performed, vascular uptake may be missed. This means that relying on static fluoroscopy performed after the injection of contrast is insufficient. Aspiration looking for vascular flash-back has a sensitivity of only 46% in the cervical spine2 and 45% in the lumbosacral spine.3 In caudal injections, negative vascular flash-back occurred in only 9.2% of venously placed injections.4 For transforaminal lumbosacral epidural injections, the overall rate of vascular placement was 11.2%.3 At the level of S1, the rate was as high as 21% and in the lumbar level 8.1%. Not only do misplaced needle tips result in suboptimal treatment, but inadvertent intravascular injections can lead to serious complications to include cardiovascular collapse requiring resuscitation,1 spinal cord infarction and cerebral vascular thrombosis.19,20 For these reasons, we reiterate our recommendation that real-time injection of a non-iodinated contrast agent such

Fig. 23.3 Two-handed technique. The lower hand controls needle orientation and prevents uncontrolled needle advancement. The hand on top gently advances the needle.

Fig. 23.4 Bent needle technique to inject non-ionic contrast. The hand is kept out of the X-ray beam. The needle is bent to avoid advancement of needle by depressing the plunger. 247

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as Isovue or Omnipaque (and in rare cases gadolinium) be utilized. Some advocate using digital subtraction to even further confirm a nonvascular injection.

DIAGNOSTIC PROCEDURES When correct needle placement is confirmed by the injection of contrast, medication can then be instilled. Injections may be of two types: diagnostic or therapeutic. With diagnostic injections, local anesthetics without preservatives are used. The agents most frequently used are 1–2% Xylocaine and 0.25–0.5% bupivacaine. A double-block paradigm has been described to reduce false-positive injections.5–7 With the comparative block paradigm, anesthetics of two different half-lifes are utilized. Typically, Xylocaine or bupivacaine is used. The patient is blinded to the medication utilized. Another method to reduce false positives is the use of placebo–control blocks. For that type of double-block paradigm local anesthetic is injected on one occasion and normal saline during another. Ideally, the patient and the interventionalist are blinded to the agent used. With either a comparative or placebo–control injection, the patient is instructed post injection to perform maneuvers that would typically aggravate pain. At The Penn Spine Center we usually require at least an 80% decrement in pain from pre- to post-injection for the diagnostic injection to be considered positive. Others use 50% as the target decrement. Following the injection, the patient is instructed to keep a prospective pain dairy. Since we have found that many patients forget their pain diaries on follow-up, we recommend recording pain response every 15 minutes for 2 hours post procedure, keeping the patient for at least 1 hour and copying their pain diary before they leave. After the first 2 hours, the patient records on an hourly basis the maximum percentage of relief and severity of pain on visual numeric scale until pain returns to less than 50% relief. The patient then returns on a separate day for repeat injection with the other anesthetic. Prior to injection, the patient’s pain dairy is reviewed and the duration of relief and maximum percentage of relief is recorded. If the patient once again has at least 80% relief with the other anesthetic, the patient is instructed in keeping a pain dairy. At follow-up, the patient’s pain dairy is reviewed. The appropriate response is longer relief with bupivacaine over Xylocaine. If this occurs, the patient passes the double-block paradigm and pain is attributed to the structure injected. The patient is then a candidate for various therapeutic interventions related to the structure, as clinically indicated. If the patient has longer relief with the shorter-acting agent or less than the targeted percentage of relief for the procedure to be deemed positive with the second injection, the initial injection was a false positive. In that case, the patient is not a candidate for therapeutic intervention. Most studies utilizing the double-block paradigm have not used a strict criteria regarding the degree of pain relief to be determined a positive block. Studies of the zygapophyseal joint utilized definite relief as positive for the initial injection and 50% relief with the second injection.5,7 Use of 80% relief with the second injection probably increases the specificity by eliminating patients with 50–79% relief. However, sensitivity is lowered and potential positive responders are lost.

THERAPEUTIC PROCEDURES Corticosteroids For therapeutic injections, a mixture of local anesthetic and corticosteroid or just corticosteroid is used. The corticosteroids most frequently used are betamethasone, dexamethasone, triamcinolone, and methylprednisolone. In the discussion of the specific injections, the preferred agents and dosages of the authors is presented. These recommendations are guidelines and interventionalists may have other reasonable preferences. 248

Additional recommendations We recommend that procedures are done in a fluoroscopy suite with personnel trained in advanced cardiac life support nearby. As a minimum, continuous monitoring of blood pressure heart rate should be done every 1–5 minutes. If moderate sedation is administered, oxygen saturation, pulse, blood pressure, and level of sedation should be monitored.8–10 In those with hypertension or cardiac pathology, continuous electrocardiogram monitoring should be included.8 Airway and ventilator support should be available in case of respiratory depression. After the procedure, the patient should be taken to recovery and monitored for at least 20–30 minutes for any adverse reaction. Prior to discharge, patients should be alert and able to ambulate independently. We recommend a pain assessment be done prior to discharge. A driver should be present to take the patient home.

Considerations for specific procedures Anatomic considerations in epidural injections The epidural space is a triangular space extending from the foramen magnum to the sacral hiatus. The inner border of the epidural space is the thecal sac with the outer meningeal layer of the thecal sac, the dura mater. The dura extends from the foramen magnum to the level of S2. The outer border of the epidural space is the bony spinal canal with its covering periosteum. The anterior border is the posterior longitudinal ligament. The posterior border is composed of the lamina and ligamentum flavum. The lateral border is the pedicle and intervertebral foramina. The epidural space contains loose areolar tissue, a venous plexus, spinal nerve roots, radicular arteries, superficial and deep cervical arteries, arachnoid granules, and lymphatics. A cryomicrotome study of the epidural space found the epidural space to be widest at the midlumbar level with progressive narrowing at more cephalad levels.11 Above C7–T1 no posterior epidural space was evident.11 The width of the epidural space is 1–1.5 mm at C5, 2.5–3 mm at T6, and 5–6 mm at L2.12 In the cervical and thoracic region, the ligamentum flavum in about half of specimens did not fuse in the midline.11 In the cervical spine, the interspinous ligament was absent.11 Absence of the interspinous ligament and midline fusion of the ligamentum flavum have clinical significance when utilizing the loss of resistance technique with a midline interlaminar epidural injection. The lack of resistance from these ligaments could lead to inadvertent entry into the epidural space or dura unbeknownst to the interventionalist. In the lumbar and lower thoracic region exists the dorsomedian dural fold (plica mediana dorsalis).13 The dorsomedian dural fold divides the epidural space into three compartments: ventral and two dorsolateral compartments. The dorsomedian fold also affects the width of the space dorsally, which may be as little as 2 mm or less.13 The presence of the dorsomedian fold can affect epidural injections. The smaller width may predispose to dural puncture with a midline interlaminar approach.13 Additionally, the separate compartments can lead to incomplete flow of medication. Within the thecal sac the spinal cord is present until approximately L2. Rootlets arise from the cord to form the ventral and dorsal nerve roots and pass inferiorly. These roots exit the thecal sac with the dura forming the root sleeve. The dura ends at the proximal margin of the DRG. The dorsal and ventral roots then coalesce to form the spinal nerve as it exits the neural foramen. The dura extends as the epineurium of the spinal nerve. Fibrous tissue of the anterior and posterior epidural space extends as the epiradicular sheath. The epiradicular sheath encloses the dorsal root ganglion and spinal nerve. The epiradicular sheath is the target for a diagnostic selective spinal nerve root injection as it exits the foramen. The foramen is formed superiorly and inferiorly by the pedicle of the superior and inferior vertebrae, respectively. The superior articular process of the zygapophyseal joint forms

Section 2: Interventional Spine Techniques

the posterior wall. The inferior vertebral endplate and disc form the anterior wall. The foramen consists of entrance, mid, and exit zones. The mid-zone of the foramen contains the DRG, ventral root, sinuvertebral nerve, and vascular interconnections. Approaching the exit zone, the ventral root and DRG coalesce to form the spinal nerve. In general, the relation of the DRG to the pedicle is immediately inferior in 90%, medial 2%, and inferolateral in 8%.14 However, in the lumbar spine the location of the DRG may vary dependent upon the level of the lumbar spine.15 Hamanaishi and Tanaka,15 studying the location of 442 DRGs in 104 MRI scans reported: (1) extraforaminal location in 100% at L2, 48% L3, 27% L4, and 12% L5; (2) intraforaminal location in 52% L3, 72% L4, and 75% L5; and (3) intraspinal location 13% L5 and 65% S1. In the cervical spine, the spinal nerve exits in the inferior aspect of the foramen with vascular structures in the superior aspect of the foramen. The spinal nerve is posterior to the vertebral artery.16 In the lumbar spine, the spinal nerve and vessels are in the superior aspect of the foramen. The spinal nerve upon exiting the foramen travels inferior, lateral, and anterior. The spinal cord receives blood supply to the posterior third via the two posterior spinal arteries. The posterior spinal arteries arise from the posterior inferior cerebellar arteries. The posterior spinal arteries consist of plexiform channels and run along the line of attachment of the dorsal roots of the spinal nerves.17 The arteries also receive supply from the posterior radicular arteries. The anterior spinal artery arises from the vertebral artery and is only sufficient for the upper cervical region.17 The vertebral artery arises from the subclavian and enters the costotransverse foramen at C6 and exits at C1 and crosses posteriorly behind the arch of C1 before entering the skull through the foramen magnum. Branches from the vertebral artery descend and form a single artery, the anterior spinal artery. The anterior spinal artery receives added supply at different intervals throughout the spine. The anterior spinal artery is divided into cervical, thoracic, and lumbar segments.18 Spinal arteries arising from the vertebral, subclavian, intercostals, aortic, and iliac arteries enter through the intervertebral foramen and divide into the anterior and posterior radicular arteries.17 The majority of the radicular arteries supply primarily the nerve root. A variable number of anterior radicular arteries help supply the anterior spinal artery. These feeder arteries are larger arteries and have been termed radiculomedullary arteries.19 These arteries may ascend and descend within the thecal sac to supply the anterior spinal artery. A variable number of these feeder arteries are present in the cervical region but at least one or two are typically present, usually entering at the level of C5–6.20 Below T8 the major supply of the anterior spinal artery is through the artery of Adamkiewicz.19 Interruption of this artery can result in cord infarction of the anterior two-thirds, the anterior spinal artery syndrome. The artery of Adamkiewicz arises as a branch from the aorta and enters from the left side at T9–L2 in 85% but can enter as low as S1.21,22 A right-sided radiculomedullary artery in the lumbar region can contribute to the anterior spinal artery. Injury to a radiculomedullary artery compromises circulation to the cord with the risk of ischemia or infarction. Drainage of blood from the cord occurs through the anterior and posterior spinal veins. These veins drain into radicular veins which in turn drain into the epidural venous plexus. The plexus exits the intervertebral foramen and enters into the external venous plexus. Blood then drains into the vertebral, intercostals and lumbar veins.17

Clinical considerations regarding pathoanatomy The typical therapeutic goal of placing glucocorticoids into the epidural space and/or around a nerve root is to treat the nerve(s) affected by the herniated disc(s) or stenotic levels. Since we are advocating treating specific levels using these precision techniques, a clear understanding of ‘which nerve’ to treat is paramount to improving

clinical outcomes. In the cervical level (above C8), a central or far lateral disc will involve the more inferiorly numbered level. For example a central or far lateral C5–6 herniation will involve the C6 (more inferior) nerve. Likewise, a stenotic C5–6 foramen will involve the more inferiorly numbered nerve (C6). To access the nerve, one directs treatment between the same numbered levels, in this example, between C5 and C6. In the thoracic and lumbar levels, however, this can be more challenging for the novice injectionist. Central herniations involve the more inferiorly numbered nerve and far lateral herniations involve the more superiorly numbered nerve. For example, a central L4–5 herniation will involve the L5 (more inferiorly numbered) nerve and a far lateral L4–5 disc herniation will involve the L4 (more superiorly numbered) nerve. A stenotic L4–5 foramen will involve the more superiorly numbered L4 nerve since the pathology is also far lateral. Choosing injection levels is ‘easier’ for the stenotic foramen and far lateral herniations since the involved nerve and injected level is the same as the pathologic level. For example, for a far lateral or stenotic L4–5 level, the L4 nerve is involved and the treatment is directed at the L4–5 level to treat the L4 nerve. Central herniations, however, are far more frequent than far lateral herniations. Choosing the level to inject for these central herniations can be a bit more challenging. For example, an L4–5 central herniation involves the L5 nerve. To treat the L5 nerve, one needs to place the needle between the L5 and S1 levels. In contrast, novices often incorrectly surmise that to treat an L4–5 central herniation, they should access the ‘L4–5 foramen’ which would instead place the needle, incorrectly, at the L4 level. With the above in mind, it is more prudent to think about the nerve that needs to be treated (i.e. L5) rather than the disc to be treated (i.e. L4–5).

TYPES OF EPIDURAL INJECTIONS Injections into the epidural space are of three general types: caudal, interlaminar, and transforaminal. Although interlaminar and caudal injections may be performed with or without fluoroscopic guidance (we advocate the former as routine), transforaminal injections require fluoroscopic guidance. Interlaminar or caudal epidural injections done without fluoroscopic guidance are also termed blind epidural injections. Techniques of hanging drop and loss of resistance are utilized to identify entry into the epidural space. The accuracy of blind epidurals has been tested. The loss of resistance technique in the cervical spine for blinded interlaminar injections has a miss rate of 53%.23 In the lumbar spine the miss rate ranges from 17% to 30%.24,25 Caudal epidural injections have a miss rate of 25–52%.4,25 However, if the sacral cornu are easily palpated and there is no palpation of subcutaneous air, loss of resistance blinded injection with an experienced interventionalist may be successfully performed in 91.3%.26 If the landmarks are not easily the palpated, the success rate in the same study was 54.5%. Landmarks were readily palpable in only 59.3% of subjects.27 Under fluoroscopic guidance, El-Khoury27 had a failure rate of 2.5% for caudal injections. Of two failures, one was secondary to dural puncture and the other was from inability to place the needle in a subject who had suffered a sacral fracture. Anatomic variance of the sacral hiatus in 15% may prevent successful caudal injection.28 Variations included a hiatus of less than 8 mm in length, severe partial agenesis, complete agenesis, absent hiatus, bony septum in canal, and angulation of the sacrum.29 The rate of misplacement of blind epidural injections is unacceptable, especially considering the routine availability of fluoroscopy. For additional safety, digital subtraction should be considered, if available, when performing transforaminal injections with precarious vascular anatomy such as in the cervical spine or high lumbar locations (L1–3, artery of Adamkiewicz watershed zone). Other safety measures include using a local anesthetic test dose and 249

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routine remixing of the glucocorticoid if it is of the type that tends to accrete. Transforaminal injections have theoretic advantages over interlaminar injections. Interlaminar injections place medication in the posterior epidural space. Stojonavic et al.23 demonstrated that cervical interlaminar injections contrast entered the ventral epidural space in only 28% and remained unilateral in 51% of injections. In the thoracic spine, contrast entered the ventral epidural space in only 24% injections.29 Kraemer et al.30 demonstrated medication flowed dorsally with interlaminar epidural injections. In a randomized, controlled trial, perineural injection was found to be superior to interlaminar epidural injection in radiculitis from herniated lumbar disc,30 supporting the benefits of target-specific injection. With therapeutic selective nerve injections, medication is delivered directly to the targeted spinal nerve, dorsal root ganglion, and nerve root. This is particularly important where resistance to fluid flow occurs such as in spinal stenosis, foraminal disc protrusions, and epidural fibrosis. In cases of axial pain felt to be discogenic in origin, transforaminal injections place the medication ventrally in the epidural space adjacent to the posterior anulus, posterior longitudinal ligament, and sinuvertebral nerve. Diagnostic selective spinal nerve root injections target the spinal nerve, nerve root, and DRG only. A small aliquot of local anesthetic is injected to anesthetize the spinal nerve to determine if pain is emanating from the specific spinal nerve and nerve root. Diagnostic selective spinal nerve root injections are indicated when the etiology of pain radiating into an extremity is in question. A pre- and postinjection pain drawing and visual analogue scale is obtained. Post procedure, the patient should perform activities which usually provoke the pain. If the patient has an 80% decrement in pain, the diagnostic injection is considered positive.31

General techniques Non-ionic contrast is utilized to confirm proper needle placement. Contrast should outline the epidural space and/or the spinal nerve depending on the type of injection performed. The contrast will display either a negative or positive outline of the epidural space or the nerve (Fig. 23.5). Injection into the epiradicular sheath usually is of low resistance and not painful. However, the injections may be painful when there is severe nerve irritation and/or compression, such as with a foraminal disc herniation. In these situations, inject

A

medication slowly, approximately 1 second per 0.25 cc per second, to minimize pain. Also, slower injection may reduce the incidence of postinjection headache. If pain develops during the injection, stop injecting until the discomfort dissipates. Then resume injecting, but slowly to avoid pain. If significant resistance is encountered, do not force the medication. Recheck the needle placement with real-time fluoroscopy to insure proper placement and that the needle tip has not been advanced intraneurally. With intraneural needle placement and injection of contrast, the patient typically experiences severe radicular pain. When severe radicular pain is described by the patient the injection should be stopped immediately. The contrast will usually demonstrate a sharp line within the substance of the nerve. The needle should be withdrawn back into the epiradicular sheath and rechecked with real-time fluoroscopy. The other contrast pattern that is important to recognize is a subarachnoid pattern. This pattern will give a myelographic outline. If this occurs, the procedure is abandoned as subarachnoid instillation of medication can be catastrophic. There is the risk of respiratory depression, hypotension, syncope, and arachnoiditis.32–36 Transforaminal injections can be performed by CT scan with advantages of less radiation to the interventionalist along with visualization of nerve and soft tissue structures.37 However, CT has disadvantages of greater expense, being less rapid to perform, and there being no ability to perform real-time injection of contrast.37 The latter is a major disadvantage as inadvertent radiculomedullary injection can result in paralysis.19,20 Fluoroscopic guidance with real-time injection of contrast is recommended.

Caudal epidural injection The caudal epidural space extends between the sacral hiatus and the caudal end of dura which terminates anywhere between S1 and S3, but usually at the inferior border of S2 segment. The contents of the canal include sacral nerves, fatty tissue, and sacral venous plexus, the latter usually terminating at S4 segment but may continue inferiorly in some patients. The canal size is variable, with documented volumes from 15 to 60 ml. Variations in sacral anatomy have been mentioned by several authors. These variations include, but are not limited to absence of sacral hiatus (prevalence in general population is reported to be about 8%), location of the sacral hiatus, curvature and location of sacral foramina, bifid sacrum and sacral canal stenosis secondary to previous sacral fracture. The radiologi-

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Fig. 23.5 Epiradicular sheath injection with (A) negative outline of spinal nerve and (B) positive outline of spinal nerve. 250

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cal landmark of the sacral canal is a translucent layer posterior to the sacral segments in lateral views with the sacral hiatus visible as a translucent opening at the base of the caudal canal. After consenting, the patient is placed prone on the fluoroscopic table with a pillow under the abdomen and legs abducted. For the right-handed interventionalist, it is usually recommended to stand on the left side of the patient. In nonobese patients, the sacral cornua can actually be palpated, which provide landmark to locate the hiatus. The skin of the region is then prepped with povidone-iodine and draped with a fenestrated sterile drape. A 3 inch, 22-gauge needle is usually selected for the procedure. The entry point of the skin is approximately 2 cm distal to the sacral hiatus. The needle is advanced at about 45 degrees until it reaches the sacrococcygeal ligament. The needle is then slightly withdrawn, and the hub made to lie parallel to the skin surface, before advancing the needle through the sacral hiatus into the sacral canal. The needle is advanced to the interval between the sacral foramina of S2 and S3. Any further advancement of the needle could result in advertent dural puncture. The position of the needle is verified on lateral fluoroscopic views to avoid the incorrect placement because of anatomical variations. The use of contrast material is highly recommended to confirm the absence of venous run off, as the needle might be in the sacral venous plexus without actually causing a flash back. The most common contrast spread pattern is a ‘Christmas tree’ shape. Typically, 1.0–3.0 mL of contrast material will demonstrate appropriate position. After aspiration for blood and CSF is negative and venous run-off ruled out by contrast fluoroscopy, 2–3 mL of methylprednisolone along with 10 mL of lidocaine is instilled. This provides enough volume for the injectate to reach the level of L3 vertebral body.

Interlaminar epidural injection Cervical With progressive cephalad narrowing of the epidural space, the width at C5 has been shown to be 1–1.5 mm12 with no evident posterior epidural space above C7–T1. It has also been shown11 that in 50% of the specimens ligamentum flavum did not fuse in the midline, and the interspinous ligament was absent. With these anatomic considerations, the most common injection site for cervical interlaminar injection is the C7–T1 or C6–7 interspace. Because of the relatively small size of the cervical epidural space, a catheter technique is recommended, particularly in an elderly population. Feeding a catheter from the upper thoracic, preferably T1–2, epidural space to the desired segmental level in the cervical spine significantly reduces the chance of cervical cord damage. The recommended positions for the cervical interlaminar injections include sitting, lateral, and prone. The sitting position is easiest for the patient and enhances operator’s ability to flex the cervical spine and identify the midline. However, its use is limited practically in patients prone to vasovagal syncope and those who are unable to assume a sitting position because of underlying vertebral compression fractures. In these situations, a lateral position is recommended, particularly when tunneled epidural catheters or implantable devices are considered. This position may, however, pose technical difficulty because of spine rotation. The most commonly used position is the prone position. One must, however, ensure flexion of the cervical spine to widen the epidural space. After optimal position and skin prep with povidone-iodine, the appropriate landmarks are identified. A midline approach is selected. The midline of the desirable interspace is identified by palpating the spinous processes above and below the space, with a lateral rocking motion of these processes. Usually 3 inch or 1½ inch, 22-gauge needle is selected, and advanced in the midline. Cervical epidural injections have been performed blind

without fluoroscopic guidance. However, anatomic studies have found high rates of discontinuity in the ligamentum flavum in the cervical region and a smaller epidural space than lumbar levels. This variability can potentially result in higher rate of dural puncture and unsuspected spinal cord injections during blinded injections. Fluoroscopy and contrast administration are, therefore, highly recommended to obviate these complications. If a blind technique is used, the epidural space is identified by the loss of resistance technique without ballottement. The hanging drop method is not used because of the associated 2.0% failure rate, compared with less than 0.5% failure rate for the loss of resistance technique. After satisfactory needle position is confirmed and gentle aspiration negative for both blood and the CSF, medications are injected. Because of the relatively small size of the cervical epidural space, a catheter technique is recommended, particularly in an elderly population. Feeding a catheter from the upper thoracic, preferably T1–2, epidural space to the desired segmental level in the cervical spine significantly reduces the chance of cervical cord damage.

Thoracic The thoracic vertebral column has a kyphotic apex at T6 with the inclination different at each level: T1–4 and T9–12 incline very little while T5–8 inclines downward significantly. With steep inclination of the spinous processes at T5–8, often covering the entire interlaminar space below, a paraspinous, paramedian approach is recommended at this level in contrast to upper thoracic level where a median approach is possible. The thoracic ligamentum flavum is thinner than in the lumbar area. Thus, when inserting the needle within the epidural space, resistance will not be encountered. It is recommended to advance the needle during inspiration to allow for the maximum pressure gradient between the epidural space and outside of the body. When considering the paraspinous approach for lower thoracic spine, the entry point of the needle is next to the caudal edge of the superior spinous process of the required interspinous space. The needle is advanced with an upward angulation of 55 degrees to the long axis of spine and inward angulation of 10–15 degrees. The choice of needles is between Crawford and Tuohy needles, with the bevel of former oriented cephalad and that of the latter directed caudally. Similar to cervical epidural injection, a catheter technique may be used.

Lumbar The lumbar interlaminar epidural injection is performed at the interspace most closely located to the level of suspected source of pain, with the needle placed just below the target level. The sitting and lateral positions are recommended, with the latter favoring the spread of injectate to the dependent side. Either the midline or paraspinous approach can be used in the lumbar spine. As with the cervical and thoracic spine, fluoroscopy and real-time injection of contrast is essential. With the midline position, the entry point is closer to the superior spinous process of the required space with an upward angulation of 10 degrees. When using the paraspinous approach, the entry point is close to the cauded edge of the inferior spinous process with 45 degrees angulation to the long axis of spine below.

Transforaminal epidural injection Cervical Anterior, lateral, posterior and oblique approaches have been utilized for cervical transforaminal epidural injections. The anterior approach has been described by many practitioners.16,38–40 The main disadvantage 251

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of this technique is the vertebral artery is at risk of puncture since it is located anterior to the spinal nerve. When placing the needle into the foramen, the posterior wall of the foramen is targeted to avoid vertebral artery puncture.37 Also, the interventionalist has to use their fingers to push the trachea and esophagus to one side and the carotid artery to the other. These structures are also at risk for puncture. With a left-sided approach, the thoracic duct could also be inadvertently punctured. These problems led Vallee et al.41 to propose a sitting, lateral approach. With the lateral technique, the patient is placed in a sitting position to help lower the shoulder.41 The lateral approach targeted the superior articular process to gauge depth and to avoid the more anteriorly located vertebral artery. The c-arm is then aligned obliquely to advance the needle medially and ventrally into the foramen under fluoroscopy. Position is then checked in the anterior plane. The main disadvantage of placing the patient in a sitting position would be in the event a vasovagal reaction or in a patient requiring moderate sedation. A posterior approach has been described.16 The patient is placed in the lateral decubitus position. The needle is entered 5–7 cm from midline and directed at 45–60 degree angle until it touches the transverse process.16 The needle is then advanced to touch the nerve root extraforaminally. An oblique approach with the patient lying supine has the advantages of the lateral technique without its disadvantages. With this technique the needle can be placed into any portion of the foramen instead of being relegated to an extraforaminal location. The oblique approach also keeps the spinal nerve posterior to the vertebral artery, decreasing the risk of puncture compared to an anterior approach. The oblique approach is the recommended technique. Patient and fluoroscopy positioning are critical to allow the procedure to be done safely and easily. The patient is placed in a supine or supineoblique position. A towel or blanket is placed under the head to place the spine parallel to the fluoroscopy table. A common mistake is to allow the patient to shrug the shoulder (Fig. 23.6A). The shoulder

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should be depressed to keep it from interfering with viewing the spine under fluoroscopy (Fig. 23.6B). The patient or c-arm is then rotated to place the foramen perpendicular to the radiographic imager. In this position, the superior articular process is well visualized (Fig. 23.6C). Avoid placing the spine too obliquely, which can rotate the vertebral artery into the area of injection (Fig. 23.7). Remember, the vertebral artery runs through the costotransverse foramen from C1 to C6. Once positioned, the patient is prepped and draped in a sterile manner. A skin wheal is raised with a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, though some interventionalists do not perform this step. The bicarbonate is used to neutralize the acidic Xylocaine and diminish the burning sensation the patient may feel with the skin wheal. A 22or 25-gauge 1.5–2.5 inch spinal needle is then inserted perpendicular to the midportion of the superior articular process and advanced until bone is reached. As touching periosteum is painful, one must only gently touch bone. As described above, it is not necessary to contact periosteum. During needle insertion, the ulnar aspect of the hand that is holding the needle should be against the patient. If the patient moves, the hand against the patient keeps the needle from inadvertently being advanced. By utilizing bone to gauge depth, dural puncture and spinal cord puncture can be averted. As well, biplanar imaging and utilizing a ‘safety’ view will also assist in avoiding inadvertent injection into undesired structures. Additionally, by targeting the superior articular process in the oblique position, the vertebral artery, which is anterior, is kept away from the needle. For a therapeutic injection, the needle is directed only slightly caudal and ventral a couple of millimeters into the foramen. Transforaminal injections are completed by passing the needle tip to the anterior half of the foramen. This is accomplished with minimal pain when the needle tip is advanced along a line that bisects the cephalad and caudal portions of the foramen. In this fashion, the existing root is typically missed and unnecessary pain is avoided. A diagnostic selective nerve root injection requires the needle

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Fig. 23.6 Cervical spine patient positioning. (A) Incorrect patient positioning with shoulder shrugged. (B) Correct patient positioning with shoulder depressed. Fluoroscopy images with shoulder shrugged (C) and depressed (D).

Section 2: Interventional Spine Techniques

be directed caudally and slightly ventral to touch the spinal nerve just as it exits or where it resides outside of the foramen. Care must be taken not to pierce the spinal nerve and every effort is made to minimize the production of radicular pain during needle placement. If radicular pain is experienced, the needle should be slightly withdrawn. Position is then checked in the oblique and AP planes. In the oblique plane, the needle should just be slightly anterior to the superior articular process but still in the posterior aspect of the foramen. In the AP plane the needle should not be beyond the six o’clock position of the pedicle or there may be risk of dural puncture (Fig. 23.8). The stylus is then removed. A syringe filled with contrast agent is connected to tubing and flushed with contrast. The tubing is then connected to the spinal needle. Under real-time fluoroscopy, contrast is injected to confirm needle placement (Fig. 23.9). Contrast flow should clearly be along the targeted spinal nerve and if desired into the epidural space (medial to the ipsilateral lateral mass) (Fig. 23.10). One must carefully watch for any vascular pattern. If available, digital subtraction is used to confirm a nonvascular injection. If a vascular pattern is noted, the needle needs to be repositioned in the foramen. If there is an arterial pattern, we recommend aborting the injection at that level. When repositioning the needle away from a venous injection, the needle is withdrawn out of the foramen. The tubing is removed and the stylus replaced into the spinal needle. The needle is then repositioned on the

Fig. 23.7 Cervical spine transforaminal injection: too oblique with vertebral artery rotated near path of injection.

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Fig. 23.8 (A) Oblique position with neuroforamen perpendicular to imager and spinal needle within inferior–posterior foramen. (B) AP view of spinal needle at six o’clock position. (C) Contrast outline spinal nerve in oblique orientation. (D) AP view with negative outline of cervical spinal nerve.

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there is no adverse reaction. At 90 seconds post-injection, the patient must be queried regarding experiencing periorbital numbness, a metallic taste, auditory changes, agitation, and difficulty breathing and observed for seizure activity. If no complaints are articulated that would suggest intravascular or subarachnoid placement of the local anesthetic, a quick motor screen must be conducted. The patient is asked to move the fingers and toes. If no paresis is observed, a glucocorticoid with or without local anesthetic may then be injected. We typically utilize 1–2.0 cc of dexamethasone Soluspan and 0.25 cc of 1% Xylocaine. Some interventionalists are now injecting the therapeutic agent under continuous fluoroscopy to ensure there is no intravascular flow. It is believed that this will help prevent radiculomedullary injection with risk of anterior spinal artery syndrome or vertebral artery injection with subsequent cerebral or spinal cord ischemic event. This latter step is unnecessary provided the other safety measures described have been properly performed. For a diagnostic selective spinal nerve root injection, the needle bevel is rotated inferiorly and 0.5 cc of contrast injected. Contrast should outline the spinal nerve root and DRG but should not extend beyond this (Fig. 23.11). Then 0.5 cc of 1% Xylocaine is instilled. Again, continuous fluoroscopy with injection is recommended.

Additional safety concerns in cervical transforaminal epidural steroid injections Fig. 23.9 Tubing connection to spinal needle for contrast instillation. Tubing allows continuous fluoroscopic imaging with injection: recommended method.

There have been many recent reports regarding serious adverse outcomes directly related to cervical transforaminal ESIs. Although they are not published, the authors are aware of at least 10 litigation cases involving post-procedural infarction of structures supplied by either the cervical, cerebellar, or cerebral vasculature. These procedures have resulted in long-term cognitive or physical dysfunction and

Fig. 23.10 Cervical transforaminal injection. Contrast outlines spinal nerve and demonstrates epidural flow.

superior articular process. The needle is then advanced in a different angle, typically more caudally as radicular vein and artery are in the cranial aspect of the foramen. The position is once again checked in the oblique and AP planes. With correct placement, the tubing with contrast is then reattached and contrast injected to check placement. Contrast should outline the spinal nerve and demonstrate epidural flow without evidence of subarachnoid flow. It is absolutely necessary to use a test dose of about 0.8–1.0 cc of 1–2% lidocaine to confirm that 254

Fig. 23.11 Diagnostic cervical selective nerve root injection. Contrast outlines spinal nerve with no epidural flow.

Section 2: Interventional Spine Techniques

even death. The current consensus theory for the etiology of these catastrophic events is that particulate from the steroid suspension is injected into the cervical arterial vasculature, resulting in subsequent infarction. In an effort to lower the risk:benefit ratio, we reiterate our recommendations. We need to clarify, however, that these recommendations have not been proven to decrease the procedural risk but are based on informal consensus discussions. Nevertheless, the following steps, exclusive of the use of digital subtraction, represent the minimum standard that must be followed to be safe: 1. Confirm that the patient’s clinical scenario warrants the procedure and that conservative treatments have been attempted. Verify that the patient is on no medications which can increase bleeding (i.e. aspirin, Coumadin, nonselective NSAIDs, Plavix, etc.). 2. Informed consent should include the potential for nerve damage, paralysis, stroke, and/or death. 3. Fluoroscopic and patient oblique positioning should demonstrate the best possible view of the foramen to be injected. The needle tip needs to clearly be in the posterior aspect of the foramen in oblique view and not beyond the six o’clock position of the lateral mass in AP view. Document these two pre-contrast pictures. 4. Prior to injecting contrast, drip a small amount of the contrast into the needle hub. This will decrease the chance of injecting air. 5. Use a small extension tube during all injections. As described above, always have physical contact with the patient while handling the extension tube or needle. This will minimize the chance of unintended needle movement during the injection. 6. Real-time fluoroscopy should demonstrate that there is no arterial flow. Digital subtraction should be utilized, if available, to enhance sensitivity. Arterial flow will be either horizontal or cephalad. Document biplanar contrast flow images as well as one from digital subtraction, if available. Should an arterial injection be observed, abort the procedure at that level. Flow should clearly be along the targeted spinal nerve and, if desired, into the epidural space (medial to the ipsilateral lateral mass). 7. Once satisfactory placement is obtained, utilize a test dose of 1% lidocaine without epinephrine (0.5–1 cc). Ninety seconds postinjection, confirm there are no neurologic sequelae or other adverse events before injecting the final steroid or steroid/anesthetic. 8. Use a steroid solution which minimizes particulate size in the suspension. 9. Should an adverse event occur, insure you have access to appropriate imaging (i.e. CT/MRI) and neurosurgical consultation.

keeping the needle posterior to avoid a pneumothorax. The position of the needle should be checked frequently in the AP and lateral planes to ensure the needle is neither too ventral nor dorsal. In the AP plane the needle is advanced just short of the six o’clock position of the pedicle. Position is then checked in the lateral plane to ensure the needle is in the foramen. Contrast is then injected to confirm needle placement and should outline the spinal nerve around the pedicle and demonstrate no vascular or subarachnoid pattern (Fig. 23.12). In the case of a diagnostic injection, there should be no contrast flow to adjacent levels or epidural spread. To help avoid epidural spread, the bevel of the spinal needle should be directed inferiorly. With a therapeutic injection, 2.0 cc of Celestone Soluspan and 1.0 cc of 1% Xylocaine may be instilled. Of course, the therapeutic agent is only injected once the a test dose of local anesthetic is injected through extension tubing. Each of the steps previously enumerated for the cervical region regarding assessing for neurologic sequelae must be followed. With a diagnostic injection, 0.5–1.0 cc of 1% or 2% Xylocaine is instilled, dependent upon the amount of contrast injected that did not result in extension beyond the nerve root.

Lumbar In 1971, MacNab42 discussed the use of selective spinal nerve root injections to identify radicular pain that allowed for successful surgical explorations in the setting of a negative imaging work-up. Various causes were found to include foraminal stenosis, subarticular stenosis, foraminal disc herniation, lateral disc herniation, and pedicular kinking. The method of nerve root injection was a posterolateral approach. The patient was placed in a lateral position. The needle was directed under fluoroscopic guidance until nerve pain was experienced. The illustration in the study demonstrated a cranial to caudal and posterolateral approach which abuts the spinal nerve extraforaminally. Several authors have utilized a similar approach in the prone or lateral position.41–47 In each study, the spinal nerve was targeted extraforaminally, with the needle striking the nerve perpendicularly, resulting in radicular pain. A spinal needle was inserted 4–10 cm lateral to the spinous process and directed to the inferior edge of the transverse process. Once touched, the needle was redirected caudally and medially until the patient experienced lacinating radicular pain. Contrast was

Thoracic The patient is placed in the prone position on the fluoroscopy table and the back is prepped and draped in the usual sterile fashion. The level to be injected is located by counting the ribs to the appropriate level. One must be cognizant of whether a cervical rib exists to ensure proper level identification. A metal pointer is utilized to mark the proper level. The c-arm is then rotated obliquely and the pedicle, rib, and transverse process are identified. A metal pointer is used to place a skin wheal with a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, although not all interventionalists perform this step. A 22or 25-gauge 3.5 inch needle is then grasped by the sponge stick and advanced under continuous fluoroscopy to touch the inferior edge of the costotransverse joint. During advancement, the hand grasping the sponge stick should have the fingertips braced against the patient. This helps prevent any inadvertent needle advancement if the patient moves. Alternatively, the needle may be advanced by hand under intermittent fluoroscopy to the inferior edge of the costotransverse joint. Then under intermittent fluoroscopy the needle is advanced toward the inferior aspect of the pedicle along the margin of the ribs,

Fig. 23.12 Thoracic transforaminal injection. Contrast outlines spinal nerve and demonstrates transforaminal epidural flow. 255

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Fig. 23.13 Lumbar transforaminal injection. Advancement of needle under continuous fluoroscopy utilizing sponge stick.

then injected and outlined the spinal nerve with both proximal and distal flow. This approach has the risk for neural injury. The needle is perpendicular to the nerve and not parallel, increasing the chance for intraneural injection. When attempting to anesthetize higher roots, one would be concerned about injuring renal structures. Castro and van Akkerveeken48 described a posterolateral approach in which the needle is directed just inferior to the pedicle to the midline of the pedicle, the six o’clock position.48,49 Van Akkerveeken49 also notes referral of pain into the extremity is not reliable for nerve root pain as periosteum, joint capsule, and anulus may result in referred pain. Van Akkerveeken49 utilized 0.2–0.5 mL of 0.5% Marcaine for diagnostic selective spinal nerve root injections. The specificity was 90% and sensitivity of 100%. North et al.50 concluded diagnostic selective nerve root injections were non-specific. However, North utilized 3 cc of bupivacaine.50 This large volume would not be selective and would result in adjacent levels being anesthetized along with the sinuvertebral nerve. The study emphasized the importance of utilizing a small aliquot of anesthetic (0.2–1.0 mL) to target the spinal nerve and dorsal root ganglion only. We currently utilize a technique similar to van Akkerveeken.49 The advantage of this technique is to place the needle in the epiradicular sheath more parallel to the nerve than perpendicular to avoid intraneural injection. We do not attempt to induce radicular pain. The following technique can be utilized for both transforaminal epidural injection and diagnostic selective spinal nerve injections with slight modifications. The patient is placed in a prone position on the fluoroscopy table and the back is prepped and draped in the usual sterile manner. The level to be injected is established by locating the lowest lumbar segment. For those with a transitional segment, such as a lumbarized S1 or sacralized L5, the level should be adjusted accordingly. The c-arm is rotated obliquely to create the trajectory view visualizing the pedicle and superior articular process. The pedicle will appear oblong. The superior articular process will point up at the pedicle. The target is just inferior to the pedicle and just lateral to the point of the superior articular process. A metal pointer is then utilized to locate the skin wheal of a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, though not all interventionalists perform this step. Care must be taken to avoid too lateral an approach which could result in peritoneal or renal puncture. Typically, 12 cm from 256

the midline is the furthest recommended lateral distance for needle insertion. A 22- or 25-gauge, 3.5 inch spinal needle is grasped with the sponge stick and under continuous fluoroscopy is then advanced just anterior to the uppermost aspect of superior articular process and just inferior to the pedicle (Fig. 23.14). Once the needle finds purchase in adjacent paraspinal muscle, the c-arm is rotated to the AP position. With intermittent fluoroscopy and utilizing the two-hands technique, the needle is advanced just inferior to the pedicle and to the six o’clock position. The needle should be in the safe triangle formed by the pedicle, the outer line of the foramen, and the spinal nerve.51 Position is then checked in the lateral plane to ensure the needle is within the foramen. One milliliter of contrast agent is then injected though extension tubing and under continuous fluoroscopy. The spinal nerve should be outlined without any demonstration of a vascular pattern or subarachnoid flow. With a therapeutic injection contrast should flow around the spinal nerve, the DRG, and into the epidural space (Fig. 23.15). When a transforaminal injection is done, flow should be demonstrated ventrally such that it encompasses the most ventral aspect of the epidural space. A diagnostic injection should not demonstrate contrast spread beyond the dorsal root ganglion. To minimize excess spread during a diagnostic injection, the bevel of the spinal needle should be rotated inferiorly. With a therapeutic injection for radicular pain, a mixture of 1.0–2.0 cc of Celestone Soluspan mixed with 1.0–2.0 cc of 1% Xylocaine may be injected. Transforaminal injections typically involve 3 cc of Celestone and 5 cc of 1% Xylocaine. With a diagnostic injection, 0.5–1.0 cc of 2% Xylocaine may be utilized. In the past, CT-guided transforaminal technique utilizing CT was believed to be superior to utilizing c-arm fluoroscopy.52 However, there was no statistical significance in the outcomes between the two techniques. Additionally, while contrast was utilized to confirm placement with the CT method, no contrast was utilized with the c-arm method. As previously discussed, real-time contrast is required not only to exclude intravascular placement but also to ensure the correct structures are infused with the injected agents.

Fig. 23.14 Lumbar transforaminal injection. (A) Proper needle position at the six o’clock position. (B) Contrast outline spinal nerve with contrast around medial aspect of pedicle.

Section 2: Interventional Spine Techniques

Fig. 23.15 Sacral transforaminal injection: Sponge stick superior and lateral to S1 pedicle is point for raising skin wheal.

Fig. 23.16 Sacral transforaminal injection: Needle at one o’clock position adjacent to foramen to gauge depth.

Sacral The sacral foramen posteriorly is directed lateral to medial. Early techniques utilized a 10–15 degree prone oblique approach with reproduction of radicular pain.44,45 We utilize a similar approach, but avoid spearing the nerve. The patient is placed in a prone position on the fluoroscopy table and the back is prepped and draped in the usual sterile manner. The sacral foramen is located under fluoroscopic guidance and a metal pointer is placed on the patient’s back superior and lateral to the foramen (Fig 23.16). The c-arm may be obliqued slightly to allow better visualization of the sacral foramen. At the marked point, a skin wheal is raised with a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, although not all interventionalists complete this step. A 22- or 25-gauge, 3.5 inch needle is grasped by a sponge stick and under continuous fluoroscopy is advanced to abut upon the periosteum adjacent to the sacral foramen at the eleven o’clock or one o’clock position for left and right sides, respectively (Fig. 23.17). The needle is advanced in a cranial to caudal direction and lateral to medial direction to conform to the direction of the sacral foramen. Once periosteum is reached, redirect the needle 2–3 mm medially and inferiorly by hand into the foramen. Often, a slight loss of resistance will be felt upon entering the foramen. Onehalf to 1 mL of contrast agent is injected. For a S1 transforaminal injection, contrast should outline the S1 nerve and flow around the S1 pedicle (Fig. 23.18). Position is checked in the AP and lateral planes. There should be no vascular or subarachnoid pattern. With a diagnostic spinal nerve injection, there should be no epidural spread to adjacent levels. Once proper placement is confirmed, medication can then be instilled. For therapeutic injection, a mixture of 2.0 cc of Celestone Soluspan and 2.0 cc of 1% Xylocaine is used. For a diagnostic injection, 1.0 cc of 2% Xylocaine may be used.

Special situations A patient’s anatomy may prevent a straight-line approach to the intervertebral foramen. The L5–S1 foramen may be blocked by the iliac crest

Fig. 23.17 S1 transforaminal injection. Contrast around S1 nerve spinal nerve and flows medial to S1 pedicle demonstrating proper placement.

or a broad L5 transverse process. In skilled hands, a single-needle technique utilizing the bevel to curve the needle around bony structures can be used (Fig. 23.19). The needle will tend to curve away from the bevel. Another approach is to start the needle more ventrally than usual toward the iliac crest, then bounce the needle off the crest, directing the needle medially towards the foramen. One should note this technique can be painful when the needle touches the iliac crest, so be gentle with this technique or instill local anesthetic at the target site of the iliac crest. These latter two techniques are advanced and great care needs to be taken to avoid placing the needle too ventrally with possible peritoneal or vascular penetration of the common iliac vessels. Another method is a two-needle technique. An 18–20-gauge, 3.5 inch needle can be directed toward the inferior aspect of the transverse process of L5. Once bone is touched to gauge depth, the needle is directed inferiorly and ventrally 257

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Fig. 23.18 L5 transforminal injection entry blocked by iliac crest. Use of curved, single-needle technique to direct needle past iliac crest and around superior articular process to enter foramen.

underneath the transverse process. The bevel is rotated towards the foramen with the needle tip dorsal and lateral to the foramen. A 22–25gauge, 6 inch needle is then curved. Hold the needle at the hub with one hand. With the opposite hand, fold sterile gauze around the needle with the index finger and thumb grasping the needle. Then slide the gauze down the needle and curve the needle away from the bevel (Fig. 23.20).

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The amount of curve is based upon a three-dimensional visualization of the path the curved needle will need to travel to reach the foramen. Insert the pre-curved needle through the 3.5 inch, 20-gauge needle and direct it toward the foramen. This may require frequent checks in both the AP and lateral planes to avoid too ventral placement with subsequent viscus perforation. As the curved needle extends beyond the shorter needle, the shorter needle may be withdrawn slightly. This allows more of the curve to develop without having to advance the needle too ventrally. Once the needle reaches the foramen, check proper placement in the AP and lateral planes. One-half to 1 mL of contrast is then infused to ensure proper placement and is checked in two planes under fluoroscopy. Contrast should outline the L5 nerve and spread around the medial aspect of the L5 pedicle. There should be no vascular or subarachnoid pattern. Once proper placement is confirmed medication can be instilled. Patients who have undergone a posterolateral fusion may present similar problems. A single technique with curving the needle around the fusion can be done in some cases. Otherwise, a two-needle technique is utilized. The method is similar as that described above except for placement of the 20-gauge, 3.5 inch needle. With a posterolateral fusion the transverse process cannot be directly targeted. The c-arm is slightly obliqued and the 3.5 inch, 20-gauge needle is directed to the fusion mass just inferior to the transverse process. The needle should abut the fusion mass on the lateral edge. The needle is then directed ventrally just beyond the fusion. The needle bevel is rotated toward the foramen. The pre-curved 25-gauge, 6 inch needle is then inserted. With frequent checks in AP and lateral planes, the needle is directed towards the foramen. Once reached, confirmation is obtained with instillation of contrast and checking in two planes. Contrast should outline the spinal nerve and flow around the medial aspect of the pedicle. The pedicle may not be directly visualized secondary to pedicle screws, but since the screw is in the pedicle, one may visualize contrast around the medial aspect of the screw (Fig. 23.21). Sometimes the posterolateral approach may be unsuccessful. If a posterolateral fusion is present with concomitant laminectomy, a medial approach may be tried. A 22- or 25-gauge, 3.5 inch needle in the AP plane is inserted 1 cm medial to the pedicle at the inferior edge.51 The needle is advanced to the five o’clock or seven o’clock position for left and right sides, respectively. The needle is advanced until bone is reached.51 This method is similar to the technique for perineural injection described by Kraemer and co-investigators.30 In their technique, a medial to lateral approach with the needle parallel to the plane of the lamina, is utilized. The needle is advanced until bone is reached.30 Both techniques risks spearing the nerve root, intravascular

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Fig. 23.19 Technique for bending needle. (A) Holding needle with gauze and curving needle away from bevel. (B) Curved needle. 258

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Fig. 23.20 Lumbar transforaminal injection in patient’s instrumented posterolateral fusion. Note bend in needle near foramen. A bent needle technique was utilized to go around the fusion.

penetration (epidural plexus is lateral, and radicular vessels accompany the nerve roots), and dural puncture. To obviate spearing of the nerve, the needle can be directed to the superior articular process to gauge depth. With laminectomy, a medial facetectomy may be done, but the lateral facet (superior articular process) is still present. Once the needle touches the superior articular process the needle may be advanced slowly a few millimeters ventrally. Non-ionic contrast can then be injected to confirm placement. If a soft tissue pattern occurs, the needle may be slightly advanced and contrast agent re-injected. Once a spinal nerve

A

B

pattern with flow around the pedicle occurs, injection of medication can then be done. If during advancement the patient experiences radicular pain, the needle should be slightly withdrawn. Contrast can then be injected to confirm proper placement. If a dural puncture occurs, the procedure is discontinued. Transitional segments can pose technical challenges. First, the correct level needs to be identified. This should have been determined as part of the presurgical evaluation process. An MRI with scout view or AP view plain films of the cervical, thoracic, and lumbosacral spine is utilized. The vertebrae are counted from C2 caudally to determine if the transitional segment is a sacralized L5 or lumbarized S1 segment. In partial sacralization of L5, a PA or slightly obliqued view of the foramen is obtained.51 A 22-gauge, 3.5 inch spinal needle is inserted obliquely until there is gentle contact with the medial edge of the iliac crest. Two-tenths to 1.0 cc of 1% Xylocaine can be infused to anesthetize the periosteum of the iliac crest. The needle is then deflected off the crest medially and ventrally to the foramen.53 Alternatively, the spinal needle may not need deflection off the iliac crest and can be curved by utilizing the bevel of the needle. When the needle is near the depth of the iliac crest, the needle is curved medially and ventrally toward to the foramen. The foramen is typically larger with the transitional segment.53 As the needle is advanced, a loss of resistance occurs before reaching the pedicle as it enters this potentially larger space.53 Care must be taken to gently advance the needle, as the L5 nerve root is a risk of being contacted. The patient should be instructed to inform the interventionalist of any lower extremity pain. If this occurs the needle may need to be readjusted more cranially. The needle is then slowly advanced to the six o’clock position of the L5 pedicle. However, if a diagnostic injection is being performed, this extraforaminal location may be acceptable. One cubic centimeter of contrast may then be injected. If the contrast outlines the L5 spinal nerve and extends to the dorsal root ganglion, 1.0 cc of 2% Xylocaine may then be infused. For therapeutic selective nerve injection, combined nerve root, DRG, and epidural flow is desirable. For a transforaminal injection, placement of the medication should be along the ventral epidural space. In the presence of partial lumbarization of S1, a skin wheal is raised with 1% Xylocaine just lateral and parallel to the foramen rather than superior and lateral to the foramen.53 A 22–25-gauge, 3.5 inch spinal needle is then advanced to abut upon periosteum adjacent to the lateral aspect of the foramen to gauge depth. The needle is then redirected medially into the foramen. Contrast is then infused. Contrast should outline the S1 nerve root. In the presence of a lateral disc herniation, the involved spinal nerve and DRG is targeted. The goal is to place medication between the lateral disc herniation and the epiradicular sheath of the spinal nerve and not the nerve root.54 The spinal nerve is targeted more infe-

C

Fig. 23.21 Lateral C1–2 joint injection. (A) Lateral view with arthrogram. (B) AP view. (C) Slightly oblique view to visualize joint better. 259

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rior and at the five o’clock or seven o’clock position of the pedicle for right and left sides, respectively. On lateral view, the needle will be more ventral and inferior. With injection of contrast, distal spread should be along the ventral ramus at the level of the disc and proximally around the spinal nerve and DRG.

CERVICAL SYNOVIAL JOINTS Anatomy The C1 vertebra consists of an anterior and posterior arch that are connected by paired lateral masses. The lateral masses are concave and articulate with the occipital condyles superiorly. The atlantooccipital joint is a synovial joint with an average joint space of 1 mm on CT scan.54 The vertebral artery exits the costotransverse foramen and passes posteriorly around the lateral masses. The vertebral arteries then run along a smooth groove in the posterior arch before piercing the atlanto-occipital membrane. The C1 spinal nerve gives off the dorsal and ventral rami as it crosses inferior to the third part of the vertebral artery and just superior to the posterior arch of C1.55 The atlanto-occipital joint receives innervation from the C1 ventral ramus and not the dorsal ramus.56 The C1 dorsal ramus and vertebral artery are adjacent to the medial, posterior aspect of the atlanto-occipital joint. The superior and lateral aspect of the atlanto-occipital joint is farthest away from the vertebral artery.57 The inferior articular process of C1 articulates with the superior articular process of C2. The C1 inferior articular process is concave and points medially. The C2 superior articular process is convex and slopes laterally. The lateral C1–2 joint is also known as the lateral atlantoaxial joint and is a synovial joint. The median atlantoaxial joint is the synovial joint between the median-located facet of the anterior arch of C1 and the dens. The anterior or posterior joint gap for the lateral atlantoaxial joint is 3.5 mm but the main part of the joint is 1 mm wide.55 The lateral atlantoaxial joint is innervated by the C2 ventral ramus and not the dorsal ramus.56 The C2 spinal nerve exits the dura medial to the lateral atlantoaxial joint. The dura covers the medial half of the joint. The C2 spinal nerve quickly divides into ventral and dorsal rami. The C2 ganglion lies across the posterior medial half of the joint. The ventral ramus travels laterally across the lateral mass and vertebral artery to join the cervical plexus. The dorsal ramus passes inferior and posterior to the joint. The spinal cord is medial to the joint. Dreyfuss evaluated the location of the internal carotid artery to the atlanto-dental space.58 Fifty lateral internal carotid artery angiograms were reviewed with variation in the anteroposterior position.58 In the majority, the ICA was anterior to the atlanto-dental interval. Occasionally, arterial loops or curves in the ICA juxtaposed the artery to the lateral anterior atlantoaxial joint and posterior to the atlanto-dental interval. There were no cases with the ICA at the mid or posterior part of the atlantoaxial joint.58 Dreyfuss also reports the occipital artery frequently passes anterior to the midlateral lateral atlantoaxial joint space and rarely the external carotid artery anterior to the joint.58 Posterior to the lateral atlantoaxial joint are the C2 ganglion, anterior posterior ramus, dural sac, venous plexus, and posterior musculature, subcutaneous tissue, and skin. As the dorsal rami of C1 and C2 do not supply the atlanto-occipital or atlantoaxial joints, blockade of these nerves is not discussed. Additionally, the proximity of the vertebral artery to the C1 dorsal ramus makes this unsuitable for blockade.56

Technique Atlanto-occipital joint The technique as described by Dreyfuss et al. is utilized.57 The patient is placed in a lateral decubitus position. The head is rotated 30 degrees down to the table and the neck flexed. The mastoid pro260

cess and occipital prominens are palpated. An indelible skin marking pen is used to mark the location of these two structures. Between these two structures one then palpates a cleft. The skin is once again marked. The neck is prepped and draped in the usual sterile fashion. A metal pointer is placed over the cleft. The head is then rotated up or down from the table and the neck flexed and extended until the cleft overlies the most superior, lateral, and posterior aspect of the atlantooccipital joint.57 The occipital brim must also be superior to this target location. In some cases, the occipital brim may overlie the target location. Moving the neck into flexion and extension should be tried to avoid this. If unavoidable, the skin wheal is located slightly below the target location and occiput. At the target position – superior, lateral, and posterior aspect of the joint – the vertebral artery is furthest away from the joint.57 A skin wheal is raised with 1% Xylocaine. A 22–25gauge, 3.5 inch spinal needle is guided toward the target point under intermittent fluoroscopic guidance with the needle parallel to the Xray beam. The needle is advanced until bone is reached or there is 3–5 cm of needle advancement.57 The c-arm is then rotated to provide an AP open-mouth view. The needle should be just lateral and inferior to the superior-lateral aspect of the joint. If the needle is too far medial or lateral the needle will need to be withdrawn somewhat and redirected to the target position by alternating frequently between AP and oblique views. If the needle is placed too medial and inferior, there is risk of vertebral artery or dural puncture.57 Further advancement could result in cord puncture. If the needle is advanced too lateral and anterior there is risk of penetrating the internal jugular vein and vagus nerve.57 Once the needle abuts bone at the target location, the needle is walked off the joint edge into the most superior-lateral joint space. After negative aspiration, tubing containing contrast agent is attached to the needle. Position of the needle is rechecked to ensure the needle was not moved when attaching the tubing. Then 0.2 cc of contrast is injected and should demonstrate an arthrographic pattern with no vascular or soft tissue flow. If soft tissue or vascular flow occurs, stop injecting contrast immediately. Remove the tubing and replace the needle stylus. The needle is withdrawn back to the edge of the joint/ target location. The needle is then walked off the joint edge into the joint. After negative aspiration, the tubing is reconnected and contrast is once again instilled. Once an arthrogram is obtained without vascular flow or soft tissue pattern, medication is instilled. For diagnostic injection, 0.5 cc of 1% Xylocaine or 0.5% bupivacaine is instilled. For therapeutic injections, 0.8 cc of Dexamethasone or Celestone Soluspan mixed with 0.2 cc of 1% Xylocaine is infused. Injection is done until resistance is reached or 1.0 cc is instilled. The joint volume is 1–1.2 mL.59

Lateral atlantoaxial synovial joint The patient is placed in the prone position on the fluoroscopy table. A pillow is placed under the chest and a cushion under the forehead. The height of the pillow and cushion can be adjusted to place the spine in neutral and allow the patient to breathe comfortably. In the AP view, bilateral C1–2 joints should be visualized. The joints should appear symmetric bilaterally to ensure the joint is in the AP position with no rotation. The c-arm is rotated in a cranial or caudal direction to optimally visualize edges of both the inferior articular process of C1 and the superior articular process of C2. Sometimes the mandible, teeth, or dental work may obscure visualization of the joint. Movement of the c-arm, the patient’s head in flexion or extension, or opening the mouth may help improve joint visualization. Once the joint is well visualized in the AP position, a metal pointer is placed over the target area – the juncture between the middle and lateral third of the C1 inferior articular process. A skin wheal is raised with 1% Xylocaine overlying the target. A 22–25-gauge, 3.5 inch spinal needle is advanced under intermittent fluoroscopy parallel to the X-ray beam. The needle needs to be kept at the juncture of the middle

Section 2: Interventional Spine Techniques

and lateral third of the joint. If the needle is directed to the medial half of the joint, dural puncture can occur. If the needle is lateral to the joint, vertebral artery puncture can occur. If the superior articular process of C2 is targeted, there is a risk of C2 ganglion penetration. The needle is slowly advanced until the needle abuts bone of the inferior articular process of C1. The needle is then withdrawn a couple of millimeters and redirected inferiorly a couple of millimeters into the joint. Needle position is then checked in the lateral plane. The c-arm is then rotated back to the AP position. Tubing filled with contrast is connected to the spinal needle and 0.2 cc are injected. Contrast should demonstrate an arthrographic pattern (Fig. 23.22). For diagnostic injections, 0.5 cc of 1% Xylocaine or 0.5% bupivacaine is then infused. The double-block paradigm should be followed. For therapeutic injections, 0.8 cc of Celestone Soluspan or dexamethasone mixed with 0.2 cc of 1% Xylocaine are infused. Injection is done until resistance is reached or 1.0 cc of the mixture is infused.

ZYGAPOPHYSEAL JOINT INJECTIONS The zygapophyseal joints are a potential source of axial pain. The joints have been shown to contain nociceptive fibers and mediators.60–62 The prevalence of pain due to the zygapophyseal joints is unknown. Schwarzer et al.63 performed both discography and zygapophyseal joint injections in suffers with chronic low back pain and found pain emanating from these joints in 14%.63 In a second study of 176 sufferers with chronic low back pain, Schwarzer et al.64,65 reported 15% with Z-joint pain based upon diagnostic Z-joint injections utilizing a doubleblock method. In the cervical spine, skilled physical examiners have demonstrated some ability to diagnose Z-joint pain utilizing manual techniques.66 However, in the lumbar spine both history and physical examination have not been reliable in diagnosing Z-joint pain.64,65,67 Radiographic studies also have been unreliable in diagnosing Z-joint pain as abnormalities on imaging studies have been demonstrated in asymptomatic subjects. The current standard for diagnosing Z-joint pain is by diagnostic intra-articular Z-joint injections or medial branch blocks. A double-block paradigm has been recommended to avoid falsepositive diagnostic injection.5,7 The false-positive rate for single diagnostic intra-articular Z-joint injection or medial branch block in the lumbar spine is 38% with a positive predictive value of 31%.7 In the cervical spine the false-positive rate was 27% for single blocks.5 In these studies

the patient had to have definite relief with Xylocaine but 50% relief with bupivacaine. Reproduction of pain with injection is not diagnostic.68 The double-block paradigm was described earlier and should be followed. The correct response is to have longer relief with bupivacaine compared to Xylocaine. If the patient has longer relief with Xylocaine over bupivacaine, the test is a false-positive. False-negative medial branch blocks occurred in 11% of subjects with experimentally induced lumbar Z-joint pain.69 One explanation has been venous uptake of medication with medial branch blockade.69 Additionally, the stricter criteria of 80% relief we propose may increase the false-negative rate. In the presence of Z-joint pain a therapeutic intra-articular injection with corticosteroid may be performed. However, some consider this treatment controversial. At the Penn Spine Center, we routinely offer intra-articular steroid injection prior to considering more aggressive treatments. Of course, the injection is combined with physical therapy that does not stress the joint and, lastly, the patient is expressly prohibited from performing activities that will stress the joint. In the absence of a steroid effect, or if the treatment fails, radiofrequency ablation of the medial branches supplying the involved Z-joint is a viable alternative.

Anatomy The zygapophyseal joints are paired joints in the posterior spinal column and form part of the three-joint complex of the spine. The intervertebral disc is the third joint. The zygapophyseal joints are diathrodial joints with hyaline cartilage, a fibrous joint capsule, synovial membrane, and joint space. The joint capsule blends with the ligamentum flavum at the medial and superior aspects.70

Cervical The cervical pillar is made up of the superior and inferior articular processes of the zygapophyseal joints. From C3 to C7, the superior articular processes are directed upward and backward and the inferior articular processes downward and forward.71 The joints are angled approximately 45 degrees from the coronal plane. The joints are angled 30–50 degrees from the transverse plane.72 The C2–3 Z-joint is oriented more vertical and medial.73 In the cervical spine from C4 to C8, the posterior primary ramus crosses the root of the transverse process. As it crosses the transverse process it divides into the medial and lateral branches. The medial branch curves around the waist of the articular pillar and is covered by tendinous slips from the semispinalis capitis.56 These tendinous slips are equivalent to the mamilloaccessory ligament seen in the lumbar region.56 Articular branches from each of the C4–8 medial branches will innervate the Z-joint above and below.56 At C3, the dorsal ramus divides into a superficial and deep medial branch. The superficial medial branch is the third occipital nerve and innervates the C2–3 Z-joint. The deep medial branch supplies the C3–4 Z-joint and follows the same path around the waist of the articular pillar as more inferiorly located cervical medial branches.

Thoracic

Fig. 23.22 Cervical Z-joint injection. Needle in joint with arthrogram.

The thoracic Z-joints run from C7–T1 to T12–L1. The first thoracic segment more closely resembles the cervical spine and T11–12 resembles the lumbar spine.71 The thoracic articular processes are in the coronal plane with the superior articular process anterior. The joints are rotated from the coronal plane with the lateral aspect anterior and medial aspect of the joint posterior. Quantitative analysis of the thoracic Z-joint shows the approximate rotation from the sagittal to be 16 degrees.72 The rotation from the transverse plane at T6 is approximately 74 degrees.72 Rossi and Pernak74 report the thoracic dorsal ramus courses differently than in the cervical and lumbar spine. The thoracic dorsal ramus crosses the inferior instead of the superior aspect of the 261

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transverse process.74 The initial course of the dorsal ramus is through an osseoligamentous tunnel. The tunnel is formed by the transverse process superiorly, neck of the rib inferiorly, superior costotransverse ligament laterally, and the Z-joint capsule medially.74 The nerve then courses laterally through the space formed by the anterior and posterior lamella of the superior costotransverse ligament.73,75 After exiting this space, the dorsal ramus divides into medial and lateral branches. The medial branch crosses the transverse process and underneath and medial to the multifidus and semispinalis muscles. The medial branch courses through another osseofibrous tunnel along the posteromedial border of the costotransverse joint.74 The medial branch supplies the joint above and below along with the mutlifidus and semispinalis.73 A cutaneous branch is seen with T1–7 medial branches.74

Lumbar In the adult lumbar spine, the joint is oriented between the coronal and sagittal planes with variable curvature of the articular surface.76,77 In the fetus and infant, the joints are oriented in the coronal plane plane.78 During early childhood, the joint becomes curved and biplanar.78 The posterior aspect of the joint becomes more sagittally oriented. In adults, there is considerable individual variation and segmental variation. The joint is most often either hemicylindrical or boomerang-shape – biplanar.78 The larger concave superior articular process is juxtaposed against the convex smaller inferior articular process.78 The lumbar Z-joints are rotated from approximately 50 degrees at L1 to 28 degrees at L5 from the sagittal plan.72 In the transverse plane the lumbar Z-joints are close to 90 degrees.72 Anteromedially and superiorly, the joint capsule blends with the ligamentum flavum.70,78 Laterally, the intertranverse ligament has two layers that are just dorsal and lateral to the ligamentum flavum.79 The ventral layer extends lateral to the intervertebral foramen and ventrally along the vertebral body to the anterior longitudinal ligament.79 Posteriorly, the fibrous capsule is reinforced by a fascicle from the multifidus muscle that runs from the spinous process to the mammillary process.78,79 The multifidus muscle covers the joint posteriorly and has attachments to the superior articular process but not the inferior articular process.79 The fibrous capsule posteriorly is contiguous with the cartilage of the superior articular process. The fibrous capsule blends with fibrocartilage which then transitions to hyaline cartilage.78 The superior and inferior recesses of the joint capsule have loose capsular fibers that are incomplete where the neurovascular bundle enters the joint.78 The inferior recess is larger than the superior recess.70 Large synovially lined adipose tissue fill the joint recesses and project into the joint space as synovial folds or villi.70,78 The folds can be fibrous and compressed between the articular surface as meniscoid inclusions.78 The role of these menisci in pain generation is unclear.80 The superior articular process has a bony process on the dorsolateral aspect called the mammillary process.81 On the dorsal surface of the transverse process is an accessory process.81 The mammilloaccessory ligament runs from the mammillary process to the accessory process.70,81 The band can become ossified and forms a tunnel.70,81 The medial branch of the posterior primary ramus passes through the tunnel. The proximal branch hugs bone, running through the groove formed by the junction of the superior articular process and the transverse process. At this level the medial branch innervates the Z-joint and continues as the descending branch, passing medially and inferiorly to the superior-medial joint capsule below.70,81–83 An ascending branch arises just anterior to the intertransverse fascia and ascends to the posterior aspect of the joint above.70,81 This holds for the medial branches of L1 to L4. For L5, the dorsal ramus travels around the superior articular process of S1 and the sacral ala with the medial branch arising opposite the inferolateral corner of the base of the L5–S1 Z-joint.84 262

Injection technique Intra-articular Cervical A posterior approach has been described.78 The patient is placed in a prone position on the fluoroscopy table with a pillow under the chest, placing the neck in slight flexion. The needle is advanced from an inferior and lateral approach at 45 degrees towards the cervical pillar. Frequent rotation between PA and lateral must be done to avoid inadvertent medial or lateral placement. Directing the needle too medial result in interlaminar penetration with dural or cord puncture. Directing the needle too lateral and ventral could result in vascular penetration. The lateral approach to the cervical Z-joints is simpler to perform, passes through less soft tissue, and is less apt to puncture cord or vertebral artery. In the lateral approach, the patient is placed in the lateral decubitus position to allow visualization of the Z-joints. A towel is placed under the head to place the spine parallel to the fluoroscopy table. Make sure the head is not too high to avoid neck lateral bending with resultant joint space closure. Additionally, avoid shrugging of the shoulders, as the glenohumeral joint will obscure fluoroscopic Z-joint visualization. The neck is prepped and draped in the usual sterile manner. In the lateral view, one counts from the level of the odontoid process to determine the correct level. Once this is established, one has to determine the correct side. In the lateral view, the Z-joints from the right and left side overlap. Before proceeding, the interventionalist must determine which joint is closest to the surface. Failure to determine this can result in catastrophic consequences. Mistakenly targeting the contralateral joint could lead to spinal cord puncture as the needle is passed through the spine to get to the opposite side. To determine which joint is closest, the patient or the gantry angle of the X-ray beam often will have to be rotated forward and backwards on the fluoroscopy table. As the patient is rolled anteriorly, the proximal joint will move anteriorly. As the patient is rolled posteriorly, the proximal joint will roll posteriorly. Once the correct level and side are established, a metal pointer is placed over the midportion of the inferior articular process of the superior vertebra. A skin wheal is raised with a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, though some interventionalists skip this step. A 22–25-gauge, 1.5–2.5 inch spinal needle is inserted parallel to the X-ray beam. Under intermittent fluoroscopy, the needle is advanced to abut upon the midportion of the inferior articular process. With the lateral approach, the needle passes through skin, subcutaneous tissues, and muscle before reaching bone. Touching bone keeps the needle from advancing into the spinal canal. Care must be taken not to advance anterior to the joints as this could result in vertebral artery puncture. This is done by keeping the needle advancing straight down, parallel to the X-ray beam. Once bone is touched, the needle is withdrawn slightly and redirected 1–2 mm caudally into the joint. One may feel the needle walk off the inferior articular process into the joint. Often, there is loss of resistance at the tip of the needle with a sensation of the needle being hugged on the sides by the joint wall. Care must be taken not to advance the needle more than a few millimeters to avoid placing the needle through the joint with subsequent dural puncture or injury to joint cartilage. Once the needle is in the joint, 0.2 cc of non-ionic contrast agent (Isovue or Omnipaque) is injected. An arthrogram confirms proper placement (see Fig. 23.22). If a soft tissue pattern occurs, do not inject additional contrast agent to avoid obscuring the joint line. The needle can be viewed in the lateral and oblique planes to determine whether the needle needs just slight adjustment or a return to the starting position on the inferior articular process. If a return to the starting position is required, the needle may be redirected to a different part of the joint when osteophytic ridging is precluding entrance into the joint. Typically,

Section 2: Interventional Spine Techniques

one redirects to the posterior half of the joint as this is safer. The anterior aspect of the joint is closer to the vertebral artery and spinal nerve. The needle is once again walked 1–2 mm into the joint. Nonionic contrast agent, 0.2 cc, is instilled. Once an arthrogram pattern is obtained, injection of medication can be done. Yet another option is to approach the joint with an anterolateral approach with the patient in the supine position. In a diagnostic injection, the double-block paradigm as described earlier is followed. The patient is blinded to the medication utilized. When comparative blocks are performed, the patient receives either 1% Xylocaine or 0.5% bupivacaine. A volume of 0.5–0.7 cc is utilized. Care must be taken to avoid total volumes of contrast and anesthetic agent greater than 1.0 cc which can lead to capsular rupture and subsequent leakage.85 If the patient has 80% relief, the patient should also perform maneuvers that typically aggravate the pain. If the patient continues with 80% relief, the diagnostic injection is positive. If the patient passes the double-block paradigm, the Z-joint is diagnosed as the source of pain. A therapeutic Z-joint injection may be performed. A therapeutic injection is done with a mixture of 0.2 cc of 1% Xylocaine and 0.8 cc of either Celestone Soluspan or dexamethasone. Therapeutic injections may be repeated at 2-week intervals, with no more than 3–4 in a 6–12-month period. However, therapeutic injections are controversial. Since this chapter is limited to the discussion of techniques, the reader is redirected to the appropriate chapter regarding indications and contraindications.

Thoracic The patient is placed in the prone position on the fluoroscopy table. The back is prepped and draped in the usual sterile manner. To locate the proper level, one should count from C1. The technique as described by Dreyfuss is utilized.86 It is important that the level being targeted is in an AP position; the left and right pedicles should appear symmetric and the spinous process should be directly midline. A skin wheal is raised with 1% Xylocaine overlying the pedicle inferior to the targeted pedicle. For example, if the T5–6 Z-joint is targeted, the skin wheal is raised over the pedicle of T7. A 22- or 25-gauge, 3.5 inch needle is then inserted at 30–45 degrees from the skin surface. The needle is advanced along this plane, targeting the middle to inferior half of the inferior pedicle in the midline of the pedicle. In a T5–6 Z-joint, this would be the pedicle of T6. The spinal needle is kept in the midline of the targeted pedicle. The midline is a line drawn from the twelve o’clock and six o’clock position of the pedicle. By staying in midline, the spinal needle passes through muscle and will then strike bone. If one deviates too medially, there is a risk of dural and spinal cord puncture. If the needle deviates too laterally, there is a risk of puncture of the lung pleura and spinal nerve. Once bone is touched, the c-arm is rotated to the lateral view. The needle should be adjacent or just inferior to the inferior aspect of the targeted Z-joint. If the needle is too cephalad and dorsal to the joint, the needle will need to be withdrawn and positioned inferiorly. If the needle is inferior to the joint, the c-arm is rotated back to the AP position. The AP position is safer for needle advancement, as the line between the twelve and six o’clock positions on the pedicle can be visually maintained. In the AP position, one can rotate the bevel of the needle to face ventrally. This facilitates the needle gliding along bone from the pedicle onto the superior articular process and wedging into the inferior aspect of the Z-joint. The needle can also be directed slightly medially to pierce the dorsomedial capsule.86,87 Fortin and Mckee recommend a gentle bend of approximately 15 degrees of the distal one-half inch of the needle with the bevel directed away from the bend.87 The bend allows the needle to conform to the slope of the joint. The apex of the bend can be utilized as a fulcrum to redirect the needle.87 Correct positioning of the needle should be confirmed on lateral view with the needle in the inferior aspect of the joint.

Non-ionic contrast, 0.2 cc, is then injected. Contrast on the AP view will form a circle filling the inferior and superior capsular recesses. In the lateral view there should be linear arthrogram (Fig. 23.23). Two separate studies have reported on the volume of the thoracic Z-joint. The first suggested the volume of the joint to be less than 0.8 cc.87 The second study reported thoracic Z-joint volumes of 0.4–0.6 cc.88 Dreyfuss et al.88 noted epidural spread occurred in 2/40 joints injected in 9 subjects. To avoid capsular rupture and reduce the risk of epidural spread, the volume injected is only 0.5 cc.86 In a diagnostic injection, 0.5 cc of 1% or 2% Xylocaine or 0.5% bupivacaine is injected. If a diagnostic block is positive, the patient is a candidate for a therapeutic injection, though some prefer comparative blocks to be positive prior to injection of steroid intra-articularly. When radiofrequency ablation is considered, a double-block paradigm should be followed; either comparative or placebo controlled. For a therapeutic intra-articular injection, 0.5–1.0 cc of a 1:1 mixture of anesthetic and steroid is infused. Injection is completed until resistance is reached or 1.0 cc total volume is instilled.

Lumbar Mooney and Robertson first described in the English literature the technique of fluoroscopic intra-articular Z-joint injection.83 The patient is placed on the fluoroscopy table in a prone position. A pillow may be placed under the abdomen to flatten the spine and open up the joint, though many practitioners do not do this. If performing injections unilaterally, the patient can alternatively be placed in the prone–oblique position. The back is prepped and draped in the usual sterile fashion. The lumbar Z-joint are often curved and obliquely oriented.89 The c-arm is rotated into the oblique position to allow visualization of the Z-joints, approximately 45 degrees for the L4–5, L5–S1

A

B Fig. 23.23 Thoracic Z-joint injection. (A) AP view. (B) Lateral view. 263

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Z-joints and 30 degrees for upper lumbar Z-joints.90 Because of the curved appearance, over-rotating the c-arm will result in visualization of the anterior joint space. If a needle is directed to the anterior joint space, the needle will strike the dorsal side of the inferior articular process and not enter the joint.70 The c-arm should be rotated until the posterior wall is just visualized (Fig. 23.24).70,91 A skin wheal is raised with 1% Xylocaine just medial to the joint line of the inferior articular process. With the superior articular process curved around the inferior articular process, entry from lateral to medial will result in the needle tilted away from the joint space and will not allow entrance into the joint. A 22- or 25-gauge, 3.5–5 inch spinal needle is then advanced under fluoroscopic guidance to abut upon the inferior articular process at the inferior aspect of the joint (Fig. 23.25). The needle is then advanced laterally to pierce the inferior subcapsular recess. Alternatively, the superior subcapsular recess can be targeted (Fig. 23.26). The disadvantages of targeting the superior capsular recess are the recess is smaller92 and the spinal nerve is adjacent to the superior aspect of the joint. With the needle situated in the inferior or superior recess, 0.2 cc of non-ionic contrast is infused. Contrast may demonstrate filling in the superior recess, inferior recess, diverticula of the

A

B Fig. 23.26 Lumbar Z-joint-superior approach. (A) Needle in superior capsular recess with image rotated more obliquely demonstrating contrast in superior and inferior capsule. (B) Needle on edge of inferior articular process with contrast in superior and inferior capsular recess.

Fig. 23.24 Lumbar Z-joint oblique view. C-arm rotated until posterior wall just visible.

Fig. 23.25 Lumbar Z-joint: inferior approach. Needle within inferior aspect of joint with contrast in inferior capsular recess, superior capsule, and classic arthrogram. 264

recess,92 linear arthrogram, S-shaped configuration, or any combination of the above. Capsular leakage with epidural spread may also be noted.66,68,75,90,91,93 Small volumes of contrast should be utilized to avoid filling the joint and prohibiting further injection of anesthetic or steroid medication.88,94 Additionally, larger volumes can result in capsular rupture. Destouet et al.77 noted rupture of the superior or inferior recess when injection contrast volumes were 0.5–1.5 cc. Dory92 also noted frequent rupture, most frequently at the inferior recess and medially into the epidural space. Dory injected contrast volumes of 1–3 mL.92 Raymond and Dumas reported no extravasation with total volumes of contrast and anesthetic less than 1.0 cc.95 With confirmation of placement, a diagnostic injection can be done with instillation of 0.5 cc of 2% Xylocaine or 0.5% bupivacaine.7,96 Even with these lower volumes, capsular leakage may occur.68 Injection is completed until resistance is reached – to avoid capsular rupture – or 0.5 cc is infused. Capsular leakage is particularly undesirable in diagnostic injections. Leakage into the epidural space could hypothetically result in anesthetizing the sinuvertebral nerve. A false-positive injection could then occur in the presence of discogenic low back pain. Also, to reduce false-positive diagnostic injection, the double-block paradigm should be utilized. If the patient had the appropriate response with the double-block paradigm, a diagnosis of pain emanating from the zygapophyseal joints can be made. In that scenario the patient may be a candidate for radiofrequency ablation. Some authors would perform an intra-articular Z-joint steroid injection before considering radiofrequency ablation. However, this is controversial. With a therapeutic Z-joint injection, the technique is exactly the same. Instead of just anesthetic agent, 0.5–1.0 cc of a 1:1 mixture of 1% Xylocaine and Celestone Soluspan or Kenalog is instilled. Injection is completed until resistance is reached or a total volume of 1.0 cc is infused. Intra-articular injections are considered more effective than periarticular injections.97

Section 2: Interventional Spine Techniques

Medial branch blocks These are simpler to perform than intra-articular injections. The disadvantages of medial branch blocks are two needle punctures need to be performed and the injections are diagnostic only and carry no therapeutic benefit.

Cervical To anesthetize a cervical zygapophyseal joint from C3 to C7 two medial branches need to be blocked. For example, for the C3–4 joint, the C3 and C4 medial branch is blocked. Two approaches can be used to block the medial branch, a posterior or a lateral approach. In the posterior approach the patient is placed in a prone position on the fluoroscopy table. A pillow is placed under the chest and a cushion under the forehead to place the cervical spine in a neutral position and allow the patient to breathe comfortably. The level to be injected is localized by counting caudally from C1 or C2. The level of interest should be checked to ensure it is in a pure AP view. The waist of the cervical pillar targeted as the medial branch is consistently located here.98 A skin wheal is raised with 1% Xylocaine just lateral to the waist of the cervical pillar. A 22–25-gauge, 2.5–3.5 inch spinal needle is advanced under intermittent fluoroscopy in a slight lateral to medial angle to abut upon the posterior aspect of the cervical pillar waist. Touching bone on the posterior cervical pillar guards against advancing the needle too ventrally. If the needle is recklessly advanced ventrally there is the possibility of spinal nerve, internal jugular vein, and carotid artery puncture. Care must be taken not to advance too medially and superiorly as a dural puncture can occur. Once bone is touched on the posterior cervical pillar, the needle is slightly withdrawn and redirected laterally to abut bone of the lateral waist of the cervical pillar. Needle position is checked in

A

C

the AP and lateral view. Two-tenths of a cubic centimeter of contrast is infused to confirm needle placement and should demonstrate a soft tissue pattern with no vascular flow. Half a cubic centimeter of 1 or 2% Xylocaine or 0.5% bupivacaine is then infused. The advantage of the posterior approach is that bilateral procedures are easily performed without having to reposition the patient. The lateral approach is preferred over the posterior approach as the lateral approach is simpler to perform. Additionally, since the needle passes through less soft tissue, there is less patient discomfort compared to a posterior approach. To perform a bilateral procedure, the patient would have to move from one lateral decubitus position to the other and be re-prepped and draped. However, this is only a minor inconvenience. When using the lateral approach, the patient is placed in a lateral decubitus position on the fluoroscopy table.99 The head is placed on a cushion or towel roll to position the spine in a neutral position. The neck is prepped and draped in the usual sterile fashion. The level to be injected is determined by counting from the odontoid process. A skin wheal is raised with 1% Xylocaine overlying the centroid of the cervical pillar. For example, with a C4 medial branch block, the centroid position of the C4 cervical pillar is targeted (Fig. 23.27A). A 22–25-gauge, 1.5–2.5 inch spinal needle is advanced parallel to the X-ray beam to abut upon the cervical pillar in the centroid position. In the lateral position, the spinal needle passes through skin, subcutaneous tissue, muscles, and then abuts bone. Non-ionic contrast, 0.2 cc, is injected to confirm needle placement. Contrast should demonstrate a soft tissue pattern with no vascular flow. Barnsley and Bogduk99 studied contrast patterns. Contrast was most dense over the centroid target site and covered at least 5 mm along the medial branch. Contrast did not flow anteriorly to the ventral ramus or spinal nerve. Contrast tended to flow posterosuperiorly along the semispinalis capitus muscle and occasionally superior to the multifidus (Fig. 23.27B,C).99

B

D

Fig. 23.27 Cervical medial branch block: lateral approach. (A) Needle in centroid position. (B) Lateral view of contrast with typical soft tissue pattern. (C) Needle in waist of pillar with contrast in typical soft tissue pattern. (D) Oblique view: no contrast into the foramen or epidural space. 265

Part 2: Interventional Spine Techniques

After contrast demonstrates proper placement, 0.5 cc of 1 or 2% Xylocaine or 0.5% bupivacaine is then slowly injected (over 30 seconds). Attention should then be addressed to the adjacent medial branch. To block a cervical zygapophyseal joint from C3 to C7, the two adjacent medial branches need to be blocked. For example, to block the C3–4 Z-joint the C3 and C4 medial branches need to be blocked. To block the C2–3 joint, the third occipital nerve is targeted.99,100 A technique with the patient in the prone position has been described.98,100 In this technique, under PA fluoroscopic guidance the lower half of the C2–3 joint is targeted. Once the posterior aspect of the joint is touched by the needle, the needle is redirected laterally along the lower half of the C2–3 joint, touching bone. The nerve is blocked in three locations: midpoint of the convexity, lower end, and midway between the other two.100 A lateral approach is simpler to perform. The third occipital nerve is blocked in three locations. Injections of 0.5 cc of local anesthetic are performed along a vertical line that bisects the superior articular process of C3 at a point just superior to the inferior subchondral plate of C2, just inferior to the superior subchondral plate of C3, and a point midway between the two points.5 The block is done with the patient in the lateral position on the fluoroscopy table. A towel roll is placed under the head to position the spine in neutral. The C2–3 joint is located. The c-arm may need cranio-caudal tilt and rotation of the patient anteriorly or posteriorly to find the joint space. A skin wheal is raised with 1% Xylocaine overlying the midpoint of the C3 pillar in the lateral view. Along the axis of this point in a cranial and caudal line injections are performed in three positions. A 22–25-gauge, 1.5–2.5 inch spinal needle is advanced parallel to the X-ray beam to abut upon the inferior subchondral plate of C2. Two-tenths of a cubic centimeter of contrast is injected to confirm needle placement. Contrast should demonstrate a soft tissue pattern with no vascular flow. Half a cubic centimeter of 1 or 2% Xylocaine or 0.5% bupivacaine is slowly injected. The needle is then slightly withdrawn and redirected caudally to abut upon the superior subchondral plate of C3. Two-tenths of a cubic centimeter of contrast is infused and should demonstrate a soft tissue pattern with no vascular flow. Half a cubic centimeter of 1 or 2% Xylocaine or 0.5% bupivacaine is then slowly injected. The needle is then slightly withdrawn and redirected cranially at a point midway between the two previous injections. The needle should abut bone. Two-tenths of a cubic centimeter of contrast is then infused to ensure proper placement as previously. Half a cubic centimeter of 1 or 2% Xylocaine or 0.5% bupivacaine is then infused slowly. The needle is withdrawn and a bandage placed. Anesthesia of the third occipital nerve, indicating adequate block, can be tested by checking for numbness in the suboccipital region just lateral to midline.5,98 After diagnostic block, the patient is assessed for pain relief. The patient should perform activities that typically would increase pain. If the patient has 80% relief, the injection is considered positive. As previously mentioned, most practitioners perform a double-block paradigm prior to completing a therapeutic injection or radiofrequency ablation. At the Penn Spine Center, our preference is to use history and examination skills to increase the prevalence of the disorder in the population of patients that may undergo a therapeutic intra-articualr injection. When those skills are employed, a single diagnostic block is sufficient for us to perform an intra-articular glucocorticoid injection. If the patient fails to improve, we use a placebo-controlled paradigm to determine whether radiofrequency ablation is warranted. This conceptual framework is used for cervical, thoracic, and lumbar Z-joint injections and will not be repeated in the following subsections.

Thoracic The technique of thoracic medial branch block is utilized as described by Stolker et al.101 The patient is placed in a prone position on the fluoroscopy table. The c-arm is rotated 20–30 degrees to visualize the juncture of the superior articular process and the transverse process. 266

The rib of same level passes anterior to the juncture of the transverse process and SAP. To block a zygapophyseal joint, the adjacent two medial branches must be blocked. For example, to block the T7–8 Z-joint, the medial branch of T6 and T7 must be blocked. A skin wheal is raised with 1% Xylocaine superior and slightly lateral to the target. A 22–25-gauge, 3.5 inch spinal needle is advanced caudally and slightly inferiorly, targeting the juncture of the SAP and transverse process. Once bone is struck, the needle is checked in the AP plane and lateral planes. Two-tenths of a cubic centimeter of contrast is then instilled and should demonstrate a soft tissue pattern with no vascular flow. Two-tenths to 0.5 cc of 2% Xylocaine is slowly infused. The authors of this technique acknowledge that the course of the medial branch in the thoracic spine has not been adequately studied. They hypothesize the medial branch will follow a similar course in the thoracic spine as it does in the cervical and lumbar spine.101 However, Rossi and Pernak74 state the course of the medial branch passes inferiorly, not superiorly, across the transverse process.

Lumbar To block a lumbar Z-joint the two adjacent medial branches need to be blocked. For example, to block the L4–5 Z-joint, the L3 and L4 medial branches need to be blocked. For L5–S1 Z-joint, the L4 medial branch and L5 dorsal ramus is blocked. The L5 dorsal ramus runs in the groove at the juncture of the SAP of S1 and the sacral ala. Additionally, the L5–S1 Z-joint receives supply from a small branch of the S1 dorsal ramus, though this branch is not considered important to anesthetize the joint.90 The patient is placed in a prone position on the fluoroscopy table. The c-arm is rotated to allow visualization of the juncture between the SAP and transverse process. A skin wheal is raised with 1% Xylocaine superior and lateral to the target point. A 22–25-gauge, 3.5 inch spinal needle is utilized. For larger patients, a 22-gauge, 5 inch spinal needle or two-needle technique is used. Under intermittent fluoroscopic guidance, the spinal needle is advanced until it abuts upon the juncture of the base of the SAP and transverse process (Fig. 23.28A). Avoid placing the needle near the superior border of the transverse process and higher up on the SAP, as this increases the chance for medication to flow around the spinal nerve, foramen, or epidural space.84 The needle bevel should be directed inferiorly and medially to prevent spread to the spinal nerve, foramen, or epidural space.84 Even with excellent technique, there is a 15% incidence of contrast spread extending to the spinal nerve, foramen, or epidural space.84 However, the amount of anesthetic agent that would reach the spinal nerve or enter the epidural space is postulated to be unlikely to be sufficient to anesthetize the spinal nerve or nerve root.84 Confirmation is established by injection of 0.2 cc of contrast, which demonstrates a soft tissue pattern with no vascular flow (Fig. 23.28B,C). Venous uptake of contrast has been demonstrated in medial branch blocks and can result in a false-negative study.69,84 If venous uptake occurs, the needle should be repositioned. Non-ionic contrast infusion should demonstrate no venous uptake. There should be no contrast flow into the foramen, spinal nerve, or epidural space. With proper placement, 0.5 cc of 0.5% bupivacaine or 2% Xylocaine is slowly infused. Speed of infusion has been demonstrated to not affect aberrant flow to the foramen, spinal nerve, and epidural space.84 However, slower infusion tends to be more comfortable for the patient. Attention is then addressed to the next level. The same technique is utilized. After blocking the medial branches supplying a zygapophyseal joint, the patient is assessed 15–20 minutes postprocedure. If the patient has 80% pain relief from pre- to post-block, the patient is asked to perform activities that would typically aggravate symptoms. If the patient continues with 80% relief, the initial injection is considered positive. The patient is asked to keep a pain dairy as previously discussed. The patient then

Section 2: Interventional Spine Techniques

A

C

B

Fig. 23.28 Lumbar medial branch block. (A) Needle at juncture of transverse process and superior articular process on oblique view. (B) AP view of needle placement. (C) Typical soft tissue pattern with instillation of contrast.

returns for a repeat diagnostic injection following the double-block paradigm. Figure 23.29 demonstrates an L5 dorsal ramus injection.

used to treat the radicular pain that can ensue when a cyst is present. This is not treatment for axial pain of Z-joint etiology.

Special situations

Lumbar spondylolysis

Synovial cyst To aspirate a synovial cyst, the same technique as used for Z-joint injections is performed. However, a larger-gauge needle is recommended to facilitate aspiration of the cyst. A 20-gauge spinal needle is usually adequate to aspirate the cyst but still allow advancement into the Z-joint. After contrast confirms placement within the Z-joint, aspiration of the cyst is attempted. A 10 cc syringe is attached to the spinal needle and the plunger pulled back to aspirate fluid. Slightly advancing or withdrawing and rotating the needle may facilitate aspiration, as the needle can abut against bone, cartilage, or joint capsule, inhibiting aspiration. Be careful not to advance the needle through the joint with resultant dural puncture. The fluid aspirated should be consistent with joint fluid – straw colored, clear, and viscous. After aspiration is complete, 0.5 cc of a 1:1 mixture of local anesthetic and steroid is infused. If this technique fails to provide symptom relief, one should consider expanding the cyst beyond its capacity so that it ‘ruptures.’ If this technique is pursued, the patient should be informed that there may be a temporary increase in pain as the cyst expands. This will typically irritate and/or compress the adjacent root until the cyst ruptures. In over 50 cases using this technique no permanent nerve pain has resulted. The success rate remains to be reported, but preliminary observations suggest it is in excess of 60%. Finally, it must be emphasized that either aspiration or cyst rupture is

A

B

In the presence of a pars fracture, injection into the adjacent Z-joint can result in spread of medication into the pars fracture.91,92 Maldague et al.91 demonstrated communication between the Z-joint and pars fracture in 11 subjects. In 9 subjects, contrast extended through a channel from the pars to the adjacent Z-joint. In the presence of bilateral spondylolysis, a channel may communicate with bilateral Z-joints.91 Additionally, channels can occur between a pars fracture and the Z-joint above.91 When injecting a Z-joint adjacent to a pars fracture, one must be cognizant that medication may communicate with the pars fracture. If this occurs, a false-positive diagnostic Z-joint injection may occur. The pars fracture can be a source of low back pain as the pars fractures do contain nociceptive fibers and neuromediators.102,103 However, the exact innervation of pars fractures is unknown. Whether the adjacent medial branch supplies the pars fracture is not known. In the presence of a pars fracture, medial branch blockade may not be specific to pain emanating from the Z-joint. The pars fracture has been injected diagnostically to select patients for surgical treatment.104–106 When performing a pars fracture injection, the patient is placed in a prone position on the fluoroscopy table. The back is prepped and draped in the usual sterile fashion. The carm is rotated to visualize the pars fracture through the neck of the ‘Scottie dog.’ A skin wheal is raised with 1% Xylocaine overlying the superior edge of the fracture. A 22–25-gauge, 3.5 inch spinal needle

Fig. 23.29 L5 dorsal ramus block. (A) Needle at juncture of sacral ala and superior articular process of S1. (B) Contrast demonstrates typical soft tissue pattern on AP view. 267

Part 2: Interventional Spine Techniques

is advanced under intermittent fluoroscopy to abut upon bone at the superior edge of the pars fracture. The needle should be advanced parallel to the X-ray beam. If the needle is too lateral and inferior, the spinal nerve can be contacted. If the needle is too medial and superior, dural puncture can occur. Once bone is touched, the needle is then redirected and advanced 1–2 mm into the fracture. Care must be taken not to advance the needle too deep as dural puncture can occur. One-tenth to 0.2 cc of contrast is then infused and should demonstrate filling within the fracture. Two-tenths to 0.5 cc of 2% Xylocaine is then slowly infused. The patient is taken to the recovery room. After 15–20 minutes the patient is assessed for the degree of pain relief as denoted by the change in the postprocedure VAS rating. In presence of a pars fracture, the interventionalist must be cognizant that diagnostic injections into either the adjacent Z-joint or pars fracture may be at risk for a false-positive result. This may be minimized by limiting injections to small aliquots or mixing the local anesthetic with contrast agent. For example, 0.5 cc of Omnipaque 300 and 0.5 cc of 4% Xylocaine could be mixed to yield a 2% strength Xylocaine injectate. If the anesthetic–contrast mixture begins to leak outside of the intended structure, the injection is stopped. As previously mentioned, the rational use of medial branch blocks to differentiate pain emanating from the Z-joint or pars fracture remains unproven. However, if patients obtained relief and passed the double-block paradigm, they may be candidates for radiofrequency ablation to alleviate back pain. However, if the patient is being selected for surgical treatment of the pars defect such as modified Scott wiring technique,104 medial branch block results would not be helpful. In patients who may undergo surgery for a painful spondylolysis, both intra-articular Z-joint injection and pars fracture diagnostic injections should be done. The patient is blinded to the structure to be blocked and the anesthetic utilized. In random order and on separate days, the adjacent Z-joint and pars fracture should be injected. In the initial step of this evaluation process, the same local anesthetic mixture should be utilized. If the patient has negative Z-joint injections but a positive pars fracture diagnostic injection, the patient then undergoes the double-block paradigm targeting the pars fracture. If the patient has the appropriate response, then the patient may undergo a therapeutic injection or be a candidate for surgical treatment. For a therapeutic injection, 0.5 cc of 1:1 mixture of steroid and local anesthetic is utilized.

SACROILIAC JOINT

Injection technique A modification of the technique described by Hendrix et al. is utilized.123 The patient is placed in a prone position on the fluoroscopy table and the back is prepped and draped in the usual sterile fashion. With the auricular shape of the sacroiliac joint, both the anterior and posterior joint will be seen on fluoroscopy. The c-arm is rotated until a lucent zone is seen at the caudal aspect of the joint (Fig. 23.30). This is the target for injection. A skin wheal is raised with 1% Xylocaine overlying the sacral bony edge adjacent to the lucent zone. A 22–25-gauge, 3.5 inch spinal needle is advanced under fluoroscopic guidance to abut upon the periosteal edge of the sacrum to gauge depth. The needle is then redirected laterally into the caudal aspect of the joint. Two-tenths of a cubic centimeter of contrast is then infused. Contrast should demonstrate an arthrographic pattern with or without filling in the inferior recess (Figs 23.31, 23.32). Diverticula or extravasation through rents in the sacroiliac joint cap-

Fig. 23.30 Sacroiliac joint. Target for injection is the lucent zone at caudal aspect of joint.

Anatomy The sacroiliac joint is an auricular-shaped diarthrodial joint with joint capsule, synovial fluid, hyaline cartilage on the sacral side, and fibrocartilage on the iliac side.107 The fibers of the joint capsule blend with supporting ligaments both anteriorly and posteriorly.108 With aging, ankylosis of the joint begins to occur in 27–50% over the age of 50.108–111 An accessory sacroiliac joint may be present in 13–35.8% of individuals.112,113 The accessory sacroiliac joint when present is at the level of the S2 foramen at the lateral sacral tuberosity and medial to the posterior superior iliac spine.112,113 The innervation of the sacroiliac joint has not been completely delineated. The sacroiliac joint is innervated by the posterior rami of the lumbosacral roots.114 The anterior joint receives innervation from L3–S2 and the superior gluteal nerve.115 The posterior joint innervation has been reported from S1–2115 and L4–S3.116 The S1 level may be the major contributor to the joint.117 Possible autonomic contribution contributes to the complexity of innervation of the sacroiliac joint.118,119 The lumbosacral trunk is just anterior to the joint in the lower third.120,121 The L4 and L5 nerve roots are 1 cm medial to the sacroiliac joint at the level of the pelvic brim.122 The L4 and L5 nerve root are 23 and 26 mm medial to sacroiliac joint and 4.0 cm above the pelvic brim.122 268

Fig. 23.31 Sacroiliac joint injection. Needle in lucent zone with contrast demonstrating arthrogram.

Section 2: Interventional Spine Techniques

the joint capsule. This is one of the reasons for limiting the volume to 2.0 cc.124 Another alternative would be to mix anesthetic and contrast together and inject under continuous fluoroscopy.127 If leakage began to occur, the injection is stopped (Fig. 23.33). A false-negative injection may occur if anesthetic agent does not reach the painful portion of the joint. This may occur if loculations in the joint exist.128 Faulty needle placement could also result in a false-negative or false-positive injection. The radiation exposure to the patient has been evaluated with the Hendrix technique. Skin exposure was 1200–3000 mR/minute. Gonad exposure was 40–60 mR/minute and 10–15 mR/minute for females and males, respectively. In comparison, an AP scout film results in 150–200 mR and 20–30 mR for females and males, respectively. Skin exposure was 500–650 mR.123 Maugars et al.129 reported fluoroscopy time of less than 1 minute to do bilateral sacroiliac joint injections with the Hendrix technique.

SACROCOCCYGEAL AND COCCYGEAL DISC Anatomy A

The distal apex of the sacrum articulates with the first coccygeal segment at the sacrococcygeal disc.71 A synovial joint instead of disc at the sacrococcygeal junction has been reported.128 The first coccygeal segment has small transverse processes and cornu, which articulates with the sacral cornu.71 The coccyx usually consists of four segments that terminates just above the anus.71 The coccyx may have only three or up to five segments.71 The first and second segment often move upon each other and have an intercoccygeal disc. The other coccygeal segments tend to be fused.130

Injection technique

B

Dynamic sitting and standing films helps in determining which level to target first.131,132 The most mobile segment should be targeted first.131,132 If there is no hypermobility detected, the sacrococcygeal disc should be targeted first and the more caudal unfused coccygeal segments next. Reviewing the lateral sacrococcygeal view also helps in planning needle direction and placement. If there is little angulation at the sacrococcygeal junction, little craniocaudal rotation will be needed. If, however, there is significant angulation or displacement of the segment to be injected, the angle and point of entry can be determined. A modification of the technique as described by Maigne et al.

Fig. 23.32 Sacroiliac joint injection: arthrograms. (A) Contrast seen in both anterior joint, posterior joint and inferior recess. (B) Arthrogram with contrast in superior aspect of joint.

sule may be demonstrated.124 Care must be taken not to advance the needle too ventrally through the inferior joint or capsular recess as the lumbosacral plexus is just anterior to the joint.120,121 With confirmation of placement, 1.0–2.0 cc of 2% Xylocaine is infused for a diagnostic injection.124,125 For therapeutic injection, 2.0 cc of steroid mixed with 1.0 cc of local anesthetic is injected. For both, injection is continued until resistance is reached or the full volume of injectate has been infused. For diagnostic injection, pain relief and not pain provocation is considered diagnostic of sacroiliac joint pain.124,126 The patient should do maneuvers that typically aggravate the pain. An 80% decrement in pain is considered positive. The false-positive rate for single sacroiliac joint injections has been estimated at 47%.6 To help minimize a placebo effect, the double-block paradigm may be utilized. Other potential causes of a false-positive injection would be anesthetizing other structures through extravasation of anesthetic through rents in

Fig. 23.33 S1 joint injection under live fluoroscopy with combined anesthetic agent and contrast. When leakage occurred, inferior joint lateral to arthrogram, the injection was stopped. 269

Part 2: Interventional Spine Techniques

is used.131 The patient is place in a prone position of the fluoroscopy table. Sterile gauze is folded and place in the cephalad portion of the gluteal cleft. This serves two purposes. The first is to separate the buttock to allow easier access to the sacrococcygeal or intercoccygeal disc. The second is to allow absorption of the cleansing solution to avoid excess dripping into the perineum. After gauze placement, the sacrococcygeal region is prepped and draped in the usual sterile fashion. For sacrococcygeal disc injection, the c-arm is rotated in a cranial or caudal direction to provide optimal visualization of the sacrococcygeal joint. A skin wheal is raised with 1% Xylocaine overlying the sacral edge of the joint. A 22–25-gauge, 2.5 inch spinal needle is advanced parallel to the X-ray beam under intermittent fluoroscopy to abut upon the edge of the sacral aspect of the joint. During advancement, it is important to keep the needle from veering off to either side of the joint to avoid inadvertent puncture of the rectum (Fig. 23.34). Once bone is touched, the needle is slightly withdrawn and redirected caudally into the sacrococcygeal disc. The c-arm is then rotated to the lateral position. The needle should be seen within the disc but not extending through the disc with risk of perforating the rectum. One-tenth to 2.0 cc of contrast is then injected to confirm needle placement. With a diagnostic injection, 0.1–0.3 cc 2% Xylocaine in then injected. Diagnostic injection is considered positive with 80% decrement in pain with sitting or concordant reproduction of pain with injection of contrast.131 With a therapeutic injection, 0.2–0.5 cc of a 1:1 mixture of local anesthetic and steroid is injected. For intercoccygeal disc injection, the same technique as with sacrococcygeal disc injection is utilized. Frequently, with the angulation at the coccygeal level, the c-arm is caudally rotated to view the edges of the joint. A skin wheal is raised with 1% Xylocaine overlying the inferior edge of the more superior coccygeal segment. A 22–25-gauge, 2.5 inch spinal needle is then advanced to abut upon the inferior edge of the superior coccygeal segment (Fig . 23.35A). The needle is then redirected slightly into the disc. Position is checked in the lateral plane to ensure the needle is within the disc and not through the disc (Fig. 23.35B). One-tenth to 0.2 cc of contrast is then infused to confirm needle placement within the disc (Fig. 23.36). One-tenth to 0.5 cc of 2% Xylocaine is infused for diagnostic injection. For a therapeutic

A Fig. 23.35 Needle in intercoccygeal disc. (A) View (B) Lateral view. 270

Fig. 23.34 Lateral view of sacrum and coccyx demonstrates close proximity of rectum and bowel.

B

Section 2: Interventional Spine Techniques

A

B

Fig. 23.36 Contrast in intercoccygeal disc. (A) AP view.

injection, a 1:1 mixture of local anesthetic and steroid is infused. The sacrococcygeal and intercoccygeal discs hold very little volume. Frequently, there is resistance to injection because of the low volume. Typically, only 0.1 cc of contrast and 0.2–0.3 cc of medication can be infused. A 3 cc volume syringe is utilized. Because of the resistance encountered with injection, great care needs to be taken that the needle is not advanced while injecting. When injecting, the needle is flexed and held by the opposite hand by the hub. Also, one needs to be confident that the needle is within the disc before injecting. If there is any doubt, injection should not be performed.

References

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19. Houten JK, Errico TJ. Paraplegia after lumbosacral nerve root block: report of three cases. Spine J 2002; 2:70–75.

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21. Conners J, Wojack J. Interventional neuroradiology: strategies and practical techniques. Philadelphia: WB Saunders; 1999. 22. Tventen L. Spinal cord vascularity. Acta Radiol 1976; 17:1–16. 23. Stojanovic MP, Vu T, Caneris O, et al. The role of fluoroscopy in cervical epidural steroid injections. An analysis of contrast dispersal patterns. Spine 2002; 27:509–514.

6. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21:1889–1892.

24. Mehta M, Salmon N. Extradural block: confirmation of the injection site by x-ray monitoring. Anaesthesia 1985; 40:1009–1012.

7. Schwarzer AC, Aprill CN, Derby R, et al. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophyseal joints. Pain 1994; 58:195–200.

25. White AH, Derby R, Wynne G. Epidural injections for the diagnosis and treatment of low-back pain. Spine 1980; 5:78–86.

8. Practice guidelines for sedation and analgesia by non-anesthesiologists: a report by the American Society of Anesthesiologists task force on sedation and analgesia by non-anesthesiologists. Anesthesiology 1996; 84:459–471.

26. Stitz MY, Sommer HM. Accuracy of blind versus fluoroscopically guided caudal epidural injection. Spine 1999; 24:1371–1376.

9. Bahn EL, Holt KR. Procedural sedation and analgesia: a review and new concepts. Emerg Med Clin N Am 2005; 23:503–517. 10. Martin ML, Lennox PH. Sedation and analgesia in the interventional radiology department. J Vasc Interv Radiol 2003; 14:1119–1128. 11. Hogan QH. Epidural anatomy examined by cryomicrotome section. Reg Anesth 1996; 21:395–406.

27. El-Khoury GY, Ehara S, Weinstein JN, et al. Epidural steroid injection: a procedure ideally performed under fluoroscopic control. Radiology 1988; 168:554–557. 28. Black MG. Anatomic reasons for caudal anesthesia failure. Anesth Analg 1949; 28:33–39. 29. Tomczak R, Seeling W, Rieber A, et al. Epidurography: comparison with CT, spiral CT and MR epidurography Rofo. Fortschritte auf dem Gebiete der Rontgenstrahlen und der Neuen Bildgebenden Verfahren. 1996; 165:123–129.

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Part 2: Interventional Spine Techniques 30. Kraemer J, Ludwig J, Bickert U, et al. Lumbar epidural perineural injections: a new technique. Eur Spine J 1997; 6:357–361.

60. Giles KG, Taylor JR. Innervations of lumbar zygapophyseal joint synovial folds. Acta Orthop Scand 1987; 58:43–46.

31. Huston CW, Slipman CW. Diagnostic selective nerve root blocks: indications and usefulness. Phys Med Rehabil Clin N Am 2002; 13:545–565.

61. Ashton IK, Ashton BA, Gibson SJ, et al. Morphological basis for back pain: the demonstration of nerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum. J Orthop Res 1992; 10:72–78.

32. Jurmand SH. Corticotherapie peridurale des lombalgies et des sciatiques f ’origine discale. EPU Rhum 1972; 24:5061–5070. 33. Brown FW. Management of diskogenic pain using epidural and intrathecal steroids. Clin Orthop 1977; 129:72–78. 34. Bernat JL. Intraspinal steroid therapy. Neurology 1981; 31:168–171.

63. Schwarzer AC, Derby R, Aprill CN, et al. The relative contributions of the disc and zygapophyseal joint in chronic low back pain. Spine 1994; 19:801–806.

35. Nelson DA. Dangers from methylprednisolone acetate therapy by intraspinal injection. Arch Neurol 1988; 45:804–806.

64. Schwarzer AC, Derby R, Aprill CN, et al. Pain from the lumbar zygapophyseal joints: a test of two models. J Spinal Disorders 1994; 7:331–336.

36. Cicala RS, Turner R, Moran E, et al. Methylprednisolone acetate does not cause inflammatory changes in the epidural space. Anesthesiology 1990; 72:556–558.

65. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–1137.

37. Wagner AL, Murtagh FR. Selective nerve root blocks. Tech Vasc Interv Radiol 2002; 5:194–200. 38. Katz J,ed. Atlas of regional anesthesia. Norwalk, CT: Appleton-Century-Crofts; 1985:124. 39. Chen Y, Derby R, Kim B-J, et al. Current concepts invited review. epidural steroid injections: past, present and future. Spineline 2003; 9:1–19. 40. Morvan G, Mompoint D, Bard M, et al. Direct intra-foraminal injection of corticosteroids in the treatment of cervico-brachial pain. In: Bard M, Laredo JD, eds. Interventional radiology in bone and joint. New York: Springer Verlag; 1988:253–257. 41. Vallee JN, Feydy A, Carlier RY, et al. Chronic cervical radiculopathy: lateralapproach periradicular corticosteroid injection. Radiology 2001; 218:886–892. 42. MacNab I. Negative disc exploration. An analysis of the causes of nerve-root involvement in sixty-eight patients. J Bone Joint Surg [Am] 1971 53:891–903. 43. Haueisen DC, Smith BS, Myers SR, et al. The diagnostic accuracy of spinal nerve injection studies: their role in the evaluation of recurrent sciatica. Clin Orthop Rel Res 1985; 198:179–183.

66. Jull G, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygapophyseal joint pain syndromes. Med J Aust 1988; 148:233–236. 67. Jackson RP, Jacobs RR, Montesano PX. Facet joint injection in low-back pain. A prospective statistical study. Spine 1988; 13:966–971. 68. Schwarzer AC, Derby R, Aprill CN, et al. The value of the provocation response in lumbar zygapophyseal joint injections. Clin J Pain 1994; 10:309–313. 69. Kaplan M, Dreyfuss P, Halbrook B, et al. The ability of lumbar medial branch blocks to anesthetize the zygapophyseal joint. A physiologic challenge. Spine 1998; 23:1847–1852. 70. Jeffries B. Facet steroid injections. spine: state of the art review 1988; 2:409–417. 71. Gardner E, Gray DJ. Vertebral column. In: Garnder E, Gray DJ, O’Rahilly R, eds, Anatomy. A regional study of human structure, 4th edn. Philadelphia: WB Saunders; 1975:509–524. 72. Panjabi MM, Oxland T, Takata K, et al. Articular facets of the human spine. Quantitative three-dimensional anatomy. Spine 1993; 18:1298–1310.

44. Dooley JF, McBroom RJ, Taguchi T, et al. Nerve root infiltration in the diagnosis of radicular pain. Spine 1988; 13:79–83.

73. Dreyfuss P, Lagattuta FP, Kaplansky B, et al. Zygapophyseal joint injection techniques in the spinal axis. In: Lennard TA, ed., Physiatric procedures in clinical practice. Philadelphia: Hanley Belfus; 1995:206–226.

45. Herron LD. Selective nerve root block in patient selection for lumbar surgery: surgical results. J Spinal Disord 1989; 2:75–79.

74. Rossi U, Pernak J. Low back pain: the facet syndrome. Adv Pain Res Ther 1990; 13:231–244.

46. Krempen JF, Smith BS. Nerve root injection: a method for evaluating the etiology of sciatica. J Bone Joint Surg [Am] 1974; 56:1435–1444.

75. Bogduk N, Valencia F. Innervation and pain patterns of the thoracic spine. In: Grant R, ed. Physcial therapy of the cervical and thoracic spine. Edinburgh: Churchill Livingstone; 1988:27–37.

47. Tajima T, Furukawa K, Kuramochi E. Selective lumbosacral radiculography and block. Spine 1989; 5:68–77. 48. Castro WHM, van Akkerveeken PF. Der diagnostische wert der selektiven lumbalen nervenwurzelblockade. Z Orthop 1991; 129:374–379. 49. Van Akkerveeken PF. The diagnostic value of nerve root sheath infiltration. Acta Orthop Scand 1993: 251(suppl):61–63. 50. North RB, Kidd DH, Zahurak M, et al. Specificity of diagnostic nerve blocks: a prospective, randomized study of sciatica due to lumbosacral spine disease. Pain 1996; 65:77–85. 51. Derby R, Bogduk N, Kine G. Review article: precision percutaneous blocking procedures for localizing spinal pain. Part 2. The lumbar neuroaxial compartment. Pain Digest 1993; 3:175–188.

76. Carrera GF, Williams AL. Current concepts in evaluation of the lumbar facet joints. CRC Critical Reviews in Diagnostic Imaging 1984; 21:85–104. 77. Destouet JM, Gilula LA, Murphy WA, et al. Lumbar facet joint injection: indication, technique, clinical correlation, and preliminary results. Radiology 1982; 145:321–325. 78. Taylor JR, Twomey LT. Age changes in lumbar zygapophyseal joints. Observations of structure and function. Spine 1986; 11:739–745. 79. Pedersen HE, Blunck CFJ, Gardner E. The anatomy of lumbosacral posterior rami and meningeal branches of spinal nerves (sinu-vertebral nerves). J Bone Joint Surg [Am] 1956; 38:377–391. 80. Lewin T, Moffett B, Viidik A. The morphology of the lumbar synovial intervertebral joints. Acta Morphol Neerl Scand 1962; 4:299–319.

52. Lutze M, Stendel R, Vesper J, et al. Periradicular therapy in lumbar radicular syndromes: methodology and results. Acta Neurochir (Wien) 1997; 139: 719–724.

81. Bogduk N, Engel R. The menisci of the lumbar zygapophyseal joints. A review of their anatomy and clinical significance. Spine 1984; 9:454–560.

53. Slipman CW, Chow DW. Therapeutic spinal corticosteroid injections for the management of radiculopathies. Phys Med Rehabil Clin N Am 2002; 13:697–711.

82. Lippitt AB. The facet joint and its role in spine pain. Management with facet joint injections. Spine 1984; 9:746–750.

54. Weiner BK, Fraser RD. Foraminal injection for lateral lumbar disc herniation. J Bone Joint Surg [Br] 1997; 79:804–807.

83. Mooney V, Robertson J. The facet syndrome. Clin Orthop Rel Res 1976; 115: 149–156.

55. Daniels DL, Williams VM. Computed tomography of the articulation and ligaments of the occipito-atlantoaxial region. Radiology 1983; 146:709–716.

84. Dreyfuss P, Schwarzer AC, Lau P, et al. Specificity of lumbar medial branch and L5 dorsal ramus blocks. A computed tomography study. Spine 1997; 22:895–902.

56. Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine 1982; 7: 319–330.

85. Hove B, Gyldensted C. Cervical analgesic facet joint arthrography. Neuroradiology 1990; 32:456–459.

57. Dreyfuss P, Rogers J, Dreyer S, et al. Atlanto-occipital joint pain. A report of three cases and description of an intra-articular joint block technique. Reg Anesth 1994; 19:344–351.

86. Dreyfuss P, Tibiletti C, Dreyer S, et al. Thoracic zygapophyseal joint pain: A review and description of an intra-articular block technique. Pain Digest 1994; 4:46–54.

58. Dreyfuss P. Atlanto-occipital and lateral atlanto-axial joint injections. In: Lennard TA, ed., Physiatric procedures in clinical practice. Philadelphia: Hanley Belfus; 1995:227–237. 59. Dreyfuss P, Michaelsen M, Fletcher D. Atlanto-occipital and lateral atlanto-axial joint pain patterns. Spine 1994; 19:1125–1131.

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62. Beaman DN, Graziano GP, Glover RA, et al. Substance P innervation of lumbar spine facet joints. Spine 1993; 18:1044–1049.

87. Fortin JD, Mckee MJ. Thoracic facet blocks: bent needle technique. Pain Physician 2003; 6:513–516. 88. Dreyfuss P, Tibiletti C, Dreyer S. Thoracic zygapophyseal joint pain patterns. A study in normal volunteers. Spine 1994; 19:807–811. 89. Carrera GF. Lumbar facet joint injection in low back pain and sciatica. Description of technique. Radiology 1980; 137;661–664.

Section 2: Interventional Spine Techniques 90. Derby R, Bogduk N, Schwarzer A. Precision percutaneous blocking procedures for localizing spinal pain. Part 1: the posterior lumbar compartment. Pain Dig 1993; 3:89–100. 91. Maldague B, Mathurin P, Malghem J. Facet joint arthrography in lumbar spondylolysis. Radiology 1981; 140:29–36. 92. Dory MA. Arthrography of the lumbar facet joints. Radiology 1981; 140:23–27. 93. Moran R, O’Connell D, Walsh MG. The diagnostic value of facet joint injections. Spine 1988; 13:1407–1410.

113. Ehara S, El-Khoury GY, Bergman RA. The accessory sacroiliac joint: a common anatomic variant. Am J Radiol 1988; 150:857–859. 114. Steindler A, Luck JV. Differential diagnosis of pain low in the back. Allocation of the source of pain by the procaine hydrochloride method. JAMA 1938; 110:106–113. 115. Solonen KA. The sacroiliac joint in the light of anatomical, roentgenological and clinical studies. Acta Orthop Scand 1957; 27(Suppl):1–127.

94. Carrera GF. Lumbar facet joint injection in low back pain and sciatica. Preliminary results. Radiology 1980; 137:665–667.

116. Bernard TN Jr, Cassidy JD. The sacroiliac joint syndrome. Pathophysiology, diagnosis, and management. In: Frymoyer JW, Ducker TB, Hadler NM, et al., eds. The adult spine: principles and practice. New York: Raven Press; 1991:2107–2130.

95. Raymond J, Dumas JM. Intraarticular facet block: diagnostic test or therapeutic procedure. Radiology 1984; 151:333–336.

117. Greenman PE. Clinical aspects of sacroiliac function in walking. J Man Med 1990; 5:25–130.

96. Fairbanks JCT, Park WM, McCall IW, et al. Apophyseal injection of local anesthetic as a diagnostic aid in primary low-back pain syndromes. Spine 1981; 6:598–605.

118. Norman GF, May A. Sacroiliac conditions simulating intervertebral disk syndrome. West J Surg Obstet Gynecol 1956; 64:641–642.

97. Lynch MC, Taylor JF. Facet joint injection for low back pain. A clinical study. J Bone Joint Surg [Br] 1986; 68:138–141. 98. Bogduk N, Marsland A. The cervical zygapophyseal joints as a source of neck pain. Spine 1988; 13:610–617. 99. Barnsley L, Bogduk N. Medial branch blocks are specific for the diagnosis of cervical zygapophyseal joint pain. Reg Anesth 1993; 18:343–350. 100. Bogduk N, Marsland A. On the concept of third occipital headache. J Neurol Neurosurg Psychiatry 1986; 49:775–780.

119. Pitkin HC, Pheasant HC. Sacroarthrogenetic telalgia. 1: a study of referred pain. J Bone Joint Surg [Am] 1988; 70:31–40. 120. Hershey CD. The sacro-iliac joint and pain of sciatic radiation. JAMA 1943; 122:983–986. 121. Albee FH. A study of the anatomy and the clinical importance of the sacroiliac joint. J Am Med Assoc 1909; LIII:1273–1276. 122. Ebraheim NA, Padanilam TG, Waldrop JT, et al. Anatomic consideration in the anterior approach to the sacro-iliac joint. Spine 1994; 19:721–725.

101. Stolker RJ, Vervest ACM, Groen GJ. Percutaneous facet denervation in chronic thoracic spinal pain. Acta Neurochir (Wien) 1993; 122:82–90.

123. Hendrix RW, Lin PJP, Kane WJ. Brief note. Simplified aspiration or injection technique for the sacro-iliac joint. J Bone Joint Surg [Am] 1982; 64:1249– 1252.

102. Eisenstein SM, Ashton IK, Roberts S, et al. Innervation of the spondylolysis ‘ligament.’ Spine 1994; 19:912–916.

124. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37.

103. Schneiderman GA, McLain RF, Hambly MR, et al. The pars defect as a pain source. A histologic study. Spine 1995; 20:1761–1764.

125. Fortin JD, Dwyer AP, West S, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrograpy technique. Part I: asymptomatic volunteers. Spine 1994; 19:1475–1482.

104. Hambly MF, Wiltse LL. A modification of the Scott wiring technique. Spine 1994; 19:354–356. 105. Bradford DS, Iza J. Repair of the defect in spondylolysis or minimal degrees of spondylolisthesis by segmental wire fixation and bone grafting. Spine 1985; 10:673–679. 106. Suh PB, Esses SI, Kostuik JP. Repair of pars interarticularis defect. The prognostic value of pars infiltration. Spine 1991; 16(Suppl):445–448. 107. Bowen V, Cassidy JD. Macroscopic and microscopic anatomy of the sacroiliac joint from embryonic life until the eighth decade. Spine 1981; 6:620–628. 108. Sashin D. A critical analysis of the anatomy and the pathologic changes of the sacro-iliac joints. J Bone Joint Surg [Am] 1930; 12:891–910. 109. MacDonald GR, Hunt TE. Sacro-iliac joints. Observations on the gross and histological changes in the various age groups. Canad MAJ 1952; 66:157–163. 110. Walker JM. Age-related differences in the human sacroiliac joint: a histological study; implications for therapy. J Orthop 1986; 7:325–334. 111. Stewart TD. Pathologic changes in aging sacroiliac joints. A study of dissectingroom skeletons. Clin Orthop Rel Res 1984; 183:188–196. 112. Trotter M. Accessory sacro-iliac articulations. Am J Phys Anthrop 1937; 22: 247–261.

126. Derby R. Point of view. Spine 1994; 19:1489. 127. Slipman CW, Huston CW. Diagnostic sacroiliac joint injections. In: Manchikanti L, Slipman C, Fellows B, eds. Interventional pain management. Low back pain. Diagnosis and treatment. Paducah, Kentucky: ASIPP Publishing; 2002:269–274. 128. Miskew DB, Block RA, Witt PF. Aspiration of infected sacro-iliac joints. J Bone Joint Surg [Am] 1979; 61:1071–1072. 129. Maugars Y, Mathis C, Vilon P, et al. Corticosteroid injection of the sacroiliac joint in patient with seronegative spondyloarthropathy. Arthritis Rheum 1992; 35:564–568. 130. Fogel GR, Cunningham PY, Esses SI. Coccygodynia: evaluation and management. J Am Acad Orthop Surg 2004; 12:49–54. 131. Maigne JY, Guedj S, Straus C. Idiopathic coccygodynia. Lateral roentgenograms in the sitting position and coccygeal discography. Spine 1994; 19:930–934. 132. Maigne JY, Tamalet B. Standardized radiologic protocol for the study of common coccygodynia and characteristics of the lesions observed in the sitting position. Clinical elements differentiating luxation, hypermobility, and normal mobility. Spine 1996; 21:2588–2593.

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PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

Technique of Radiofrequency Denervation

24

Sara Haspeslagh and Maarten Van Kleef

INTRODUCTION History The use of electrical current to create lesions for the treatment of pain began in 1931, when Kirschner introduced it for the treatment of trigeminal neuralgia.1 In 1965, Mullan used direct current to perform percutaneous lateral cordotomy for unilateral malignant pain.2 Later that year, Rosomoff modified this technique and used radiofrequency (RF) current for this treatment.3 An RF current was found to produce more predictable, circumscribing lesions. Several years later, Sweet and Wepsic described their technique for the use of RF lesions of the Gasserian ganglion in the treatment of trigeminal neuralgia.4 In spinal pain, the use of RF current was reported in a series of cases by Shealy (1975).5 He described RF lesioning of the medial branch to treat lumbar facet joint pain. Subsequently, more options for the use of RF lesioning in various spinal pain syndromes were introduced into clinical practice.6–8 The introduction of a small-diameter (22-gauge) temperature monitoring electrode system by Sluijter and Mehta in 19819 increased the safety of the current method used.10 Since then, RF procedures have been widely adopted by many pain practitioners. In addition there have been many new technical developments, such as the improvement of the quality of C-arm image intensifiers. All these developments have contributed to a widespread use of RF lesioning. Recently, a modification of the traditional RF method was introduced by Sluijter et al.11 They used the same output setting of the lesion generator that was used for making heat lesions as in RF lesioning, but they interrupted this output to allow generated heat to be washed out by thermal conductivity and circulation. This technique is called ‘pulsed radiofrequency’ (PRF) and is claimed to be nondestructive. Until now, there are no reports of any sensory or motor loss following this procedure. However, it is too soon to categorically recommend this technique because the mechanism of action is still unknown. Until several double-blind, randomized, controlled trials are conducted this new approach should not be routinely employed.

Physics Radiofrequency current An RF current is applied by an RF lesion generator through an electrode, which is insulated except for the most distal part. This exposed region is the active portion of the electrode. The RF current flows from the electrode tip to the dispersive ground plate, which is placed on the arm or leg of the patient and leads the current back to the RF lesion generator. RF current flows through tissue and results in an electric field. This electric field places an electric force on the ions within tissue electrolytes, causing them to oscillate at a high rate (i.e.

300 000 times per second).12 Tissue heating is created by frictional dissipation of the ionic current within the fluid medium, which heats the electrode.

Lesion size The size of the lesion not only depends on the diameter of electrode and the length of the uninsulated electrode tip, but also depends on tip temperature. This was confirmed in animal studies by Cosman et al. in 1984.13 Bogduk et al. studied not only the size of the lesions, but also the shape of the lesion.14 They performed experimental lesions in egg white and fresh meat. They found that RF lesions do not extend distal to the tip of the electrode, but extend radially around the active electrode tip in a spheroidal shape. Based on these observations, Bogduk suggested that the best placement of the electrode tip was parallel to the target structure. Other research methods involving computerized or mathematical modeling of similar experiments have been used. For example, Moringlane et al. studied experimental RF coagulation with a computer-based on-line monitoring of temperature and power.15 Vinas et al. also studied lesion size in vivo using fresh eggs and in vitro using the subcortical white matter of rabbits.16 Both investigators obtained results that were similar to those reported by Bogduk et al. Once equilibrium temperature is reached (after 20–40 seconds), the size of the lesion does not increase. However, some variables such as circulation effect and the tissue heat conductivity may also produce a variation in lesion size, but are unpredictable.13 Consequently, the lesion size may therefore be variable at different locations within the body.

Radiofrequency lesion generator The modern RF lesion generating system has different functions, including a pulsed RF mode. There is continuous on-line impedance measurement to confirm continuity of the electrical circuit and to detect any short circuits. One of the key components of the system is nerve stimulator function. It is used to confirm the proper position of electrode tip (it indicates the electrode-to-nerve distance) and to permit minor adjustments. To ensure the proximity of the active tip to the sensory fibers, stimulation is performed at 50 Hz. The 2 Hz stimulation is carried out to detect extraspinal muscle contractions that occur when the needle is placed too close to a nerve root motor fiber. Voltage, current, and wattage during an RF procedure are also monitored. Finally, a generator monitors temperature using a thermocouple. This is an important lesion parameter, but the temperature is only measured at the tip of the electrode and not in the more peripheral zones of the lesion area. The usefulness of tip temperature to monitor the lesion size is minimized because the lesion size is dependent on local blood circulation. There is a rapid drop in temperature over the first few millimeters from the electrode tip.13,17

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Effect of radiofrequency current on nerve tissue The effect of RF lesions on nerve tissue is controversial. Letcher and Goldring, in 1968, investigated the effect of RF current and heat on the nerve action potential of the saphenous nerve in cats.18 Delta and C-fibers were blocked before the alpha-beta group by both RF current and heat. Uematsu,19 and subsequently Smith et al.,20 reported quite disparate results. Smith et al. created RF lesions of different temperatures by placing an electrode into the lumbar intervertebral foramina of dogs.20 Indiscriminate damage of both small and large fibers by RF current was observed. Uematsu conducted a histological analysis of feline sciatic nerves that sustained RF thermocoagulation.19 These studies have been criticized because large,14-gauge electrodes were used; in addition, they were placed close to the dorsal root ganglion during open surgery. However, these methods are not comparable to the technique which is commonly used in clinical practice today, since 22-gauge needles where not available at that time.21 In response to this critique, de Louw et al., in 2001, tried to investigate morphological effects of RF lesions as they develop in normal clinical situations.21 A percutaneous RF lesion adjacent to the dorsal root ganglion (DRG) of goats was created with a 22-gauge electrode at a tip temperature of 67°C. Immunocytochemical changes indicative of proliferation and regeneration was observed 2 weeks after the RF lesion was created. These alterations occurred outside the DRG, without interfering with the function of large myelinated fibers.

Effect of pulsed radiofrequency current on nerve tissue Recently, the importance of heat as the definitive mechanism of action RF lesioning has been questioned.11 In 1998, Sluijter et al. investigated isothermic RF lesioning also termed pulsed RF (PRF) treatment.11 Ostensibly, PRF generates its therapeutic effects independent of thermal factors. The pulses are given at a rate of 2 Hz and last 20 msec. The rest period is 480 msec, and this allows the generated heat to be washed out by thermal conductivity and circulation. The mechanism by which pulsed RF treatment effects symptom relief remains unknown. In 2002, Higuchi et al. undertook a study to elucidate this mechanism. They attempted to identify spinal cord neuron activation following the exposure of the dorsal ganglion of rats to PRF currents.22 A significant increase in the number of cFosimmunoreactive neurons in the superficial laminae of the dorsal horn was observed. This finding indicates that PRF current activates painprocessing neurons in the dorsal horn and that this effect is not mediated by tissue heating. This technique is considered to be a safer method of treatment because until now the observations showed no signs of neurodestruction and thus neurological side effects.11,23 Cahana et al., in 2003, compared the acute effects of pulsed versus continuous RF energy on impulse propagation and synaptic transmission in hippocampal slice cultures and on cell survival in cortical cultures of rats.24 In both systems, they found an induction of distance-dependent tissue destruction under the stimulating needle (namely, an inhibition of evoked synaptic activity), but this was more pronounced in the continuous RF group. Thus, they concluded that the acute effects of PRF are more reversible and less destructive in nature than the acute effects of classic continuous RF mode. Nevertheless, the safety, efficacy, and the mechanism of action of pulsed RF current remains unresolved at the present time. Clinical trials still are needed to prove its potential efficacy. 276

RADIOFREQUENCY DENERVATION IN THE CERVICAL REGION Cervical percutaneous radiofrequency denervation of the facet joints Relevant anatomy The cervical zygapophyseal joints are innervated in the same way as the lumbar zygapophyseal joints (Fig. 24.1). The cervical segmental nerves divide into the primary anterior ramus and the primary posterior ramus on exiting the neuroforamen. Immediately, the posterior branch divides into a lateral and a medial branch in the cervical intertransverse space. The medial branches of C4 to C8 run dorsally and medially through the ‘waist’ of their respective articular pillars. They innervate the facet joints at the level of the exiting segmental nerve and at the level below. Because of this multilevel innervation of the facet joints, usually the medial branch procedure is performed at several levels. Furthermore, the medial branches give deep branches to multifidus muscles and superficial branches to semispinal cervical muscles. The anatomy of the innervation of the C2–3 facet joint is distinct from the lower cervical joints. It receives innervation by branches of the greater occipital nerve, which is the continuation of the posterior primary ramus of the C2 segmental nerve. The C3 posterior primary ramus of the segmental nerve gives a medial branch that innervates the C2–3 facet joint, but also gives a branch that forms the third occipital nerve that runs cranially to innervate the skin of the lower part of the occipital region. There is no facet joint between the C1 and the C2 vertebrae.

Procedure Sedation is not employed because of the need for continuous communication between practitioner and patient. Several approaches to

Fig. 24.1 Anatomy of cervical facet joints and their innervation. The medial branches of the posterior primary rami of the segmental nerves C3, C4, and C5 are indicated by red lines, the vertebral artery by the blue line

Section 2: Interventional Spine Techniques

reach the medial branch of the dorsal ramus at the upper and middle cervical area can be used. The most commonly used approach by these authors is the posterolateral approach.25 For this technique, the patient is positioned supine on the operating table, which is tolerated well. The occiput is placed on a headrest and the cervical spine is slightly extended. The C-arm is positioned in a moderately oblique (±30°) location to secure a safe distance between the electrode tip and the exiting segmental nerve. In this position the gantry angle is parallel to the axis of the intervertebral foramen that is upward and slightly caudal. In this position the segmental nerves exit in a plane approximately perpendicular to the monitor screen. The degree of obliquity should be such that the projection of the pedicles is seen a little anterior to 50% of the vertebral body (Fig. 24.2). In the frontal plane, there should be a small angle of the C-arm with the transverse plane. This provides clear visibility of the intervertebral discs and the neuroforamina. In this projection, the medial branch runs over the base of the superior articular process, which is easily viewed. Entry points are marked on the skin, somewhat posterior and caudal to the target points as seen on the monitor, i.e. dorsal from the posterior border of the facet column and slightly caudal. Care should be taken to ensure that the entry point is not too anterior in the neck to avoid important vascular structures such as the carotid artery. The first needle (preferably the most cranial) is inserted in a horizontal plane and in a slightly cranial direction not deeper than 2 cm, so that the needle point is in line with the target point. Then the needle is carefully advanced anteriorly and cranially until bone contact is made with the facet column at the target point (see Fig. 24.2). During the first step of the procedure, several things can go wrong. The needle tip may be projecting over or anterior to the target point without any bone contact. Should the needle then be introduced further and more anteriorly to an imaginary line connecting the posterior aspects of the neural foramina it could make contact with the segmental nerve or even with the vertebral artery. To avoid this, each advancement of the needle should be checked and, if necessary, should be redirected more posteriorly. As the needle is advanced it becomes increasingly difficult to reposition the needle tip to an accurate location. If the needle tip is projecting posterior to the bone of the facet column and is advanced further, there is the possibility that it will pass between the laminae and make contact with the spinal cord. This can occur if the entry point of the needle is too far posterior in the neck. To avoid this, an anteroposterior (AP) check should be made to confirm an ideal starting point. The position of the C-arm in the AP direction should confirm the position of the needle tip adjacent to the concavity (‘waist’) of the articular pillars of the cervical spine at the corresponding level (Fig. 24.3). Once the first needle is in the proper position, the other

Fig. 24.2 Oblique fluoroscopic view of cervical facet joints with three needles aiming for the medial branches of the C3–4, C4–5, and C5–6 facet joints. The red line indicates the position of the pedicles projection a little anterior to 50% of the vertebral body. The green dots indicate the target points.

Fig. 24.3 Antero-posterior fluoroscopic view of the needles aiming for the medial branches of the cervical facet joints C3–4, C4–5, and C5–6. The target points are indicated with green dots. Notice that the needle aiming for the C3–4 medial branch has to be redirected more cranially.

needles are introduced in the same way as described above. The authors prefer to take advantage of the first needle serving as an indicator for the direction and depth for subsequent needles, which accounts for their recommendation of placing all needles before applying RF rather than lesioning a single medial branch and then placing the next needle. The technique is identical for the facet joints from C3–4 until C6–7. The direction of the needle at the C2 level is different. It should be oriented toward the small branches that innervate the C2–3 facet joint and not toward the medial branch, which is the greater occipital nerve. For the RF treatment of this facet joint, the needle should be placed at the arch of C2 at the level of the upper border of foramen C3. When optimal anatomical localization of the needles transpires, an electrical stimulation is performed to confirm correct needle position, i.e. parallel to the medial branch. This can be accomplished by identifying the stimulation thresholds. First, an electrical stimulation rate of 50 Hz should be given and should elicit a response (tingling sensation) in the neck at less than 0.5 volts. Next, a stimulation at 2 Hz is performed to confirm accurate needle position. Contractions of the paraspinal muscles will be noticed. Muscle contractions in the arm indicate needle placement too close to the exciting nerve root. In that case the needle should be repositioned more posteriorly. Once proper positioning of the needle is confirmed, the medial branch of the dorsal ramus is anesthetized with 1–2 mL local anesthetic solution (lidocaine 1–2%). An 80°C radiofrequency thermal lesion is made for 60 seconds at each level. To date, there have been no reported complications from cervical facet joint denervation when the procedure is methodically performed.26 Some postoperative burning pain is described in >30% of patients.27 It disappears spontaneously after 1–3 weeks. One should always bear in mind that there is risk of puncture of the vertebral artery when the needle is positioned anterior to the foramen in the posterolateral approach. A second approach, which is more popular in the United States, is the posterior approach of the facet joint. This was first introduced by Lord et al. in 1995.28 In this technique, the patient is positioned prone on the operating table, with the head flexed (about 5–10°) and with the face resting on a padded ring. This is a ‘tunnel vision’ technique, in which the target points are the posterior aspects of the waists of the articular pillars at the levels to be blocked and are the same as the entry points. The needle is introduced from posterior of the neck to make contact with each of the two nerves supplying the painful joints. When bone contact is made, the C-arm is turned to give a lateral view in which the needle tip should be seen in the posterior aspect of the waist of the articular pillar. A deviation toward the midline should be avoided because of risk of penetration 277

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into the epidural and subarachnoid space. Subsequently, the needle is incrementally advanced until the tip is projecting at the center of the pedicle. Then, a slightly lateral deviation should be made so that the needle tip is in the most lateral aspect of the articular pillar in the posteroanterior view. When this position is confirmed, stimulation is performed as described above to determine the 50 Hz and 2 Hz thresholds. If these are acceptable, local anesthetic is injected and an RF lesion (80°C for 60 sec) is made. At each location two lesions are made: the second one after a rotation of the RF needle over 90° from its first position.

Equipment Different radiofrequency lesioning probes can be used. A SMK-C5 (Sluijter-Mehta Kit, 22-gauge, 50 mm) cannula with a 4 mm active tip or, alternatively, an RCN-6 (24-gauge, 60 mm) needle is used. The advantage of an SMK needle is its ability to measure temperature, but there is the risk of displacement of the needle while inserting the RF probe. The RCN-6 electrode has a connecting tube that allows injection of local anesthetics before lesioning, minimizing potential displacement of the needle once it is positioned. There is no temperature measurement while using the RCN-6 electrode, but this is not thought to be a critical issue, although recently Buijs et al. reported that lesion size is more predictable while measuring the temperature.29 A 10 cm, 22-gauge SMK-electrode with a 4 mm tip is used for the posterior approach. With an SMK probe, an 80°C radiofrequency thermal lesion is made for 60 seconds at each level. With a RCN-6 needle, 20 volts over 60 seconds is applied to the electrode, which should heat the electrode tip to the correct temperature. An alternative is to use a 5 cm or 10 cm curved Racz-Finch radiofrequency thermocoagulation (RFTC) needle (blunt or sharp) with a 10 mm active tip. Individual practitioners have specific beliefs regarding possible advantages of curved needles in comparison to straight needle and of a blunt needle in comparison to a sharp needle, but no definitive answers regarding these issues are available.

Postprocedure care The patient is allowed to go home immediately after the procedure. A feeling of dizziness and vertigo is frequently described, especially after the higher median branch blocks. RF of the third occipital nerve secondarily can partially block the upper cervical proprioceptive afferents and can result in transient ataxia and unsteadiness.30,31 When this situation can possibly occur, patient should be advised not to drive a car or handle other dangerous machinery for the initial 24 hours following the procedure. Some patients report a transient exacerbation of their pain, which they described as burning in nature. It occurs as a result of neuritis caused by the proximity of the RF needle to a large nerve root. This side effect is a self-limiting process and resolves in 2–6 weeks. The patient can take oral analgesics (WHO step 1 or 2) during this period.

Case study A 62-year-old male attended the pain clinic. He complained of an almost continuous pain localized in the cervical area (right > left) in the shoulder not beyond the acromion. Neurological examination showed no abnormalities. X-ray and MRI scan showed severe degenerative change in the midcervical area. On physical examination there was a reduced range of motion on rotation of the head. During palpation there was severe pain elicited on pressure over the facet joints. Test blocks of the facet area were not performed.

278

The authors performed a radiofrequency lesion of the primary dorsal rami of the segmental nerves C3–6 on right and left side. There were no complications after the procedure. Eight weeks after the procedure there was 60% pain relief. Six months after the procedure, the patient still has satisfactory pain relief.

Cervical radiofrequency lesioning of the dorsal root ganglion Relevant anatomy The segmental nerves of C3 to C8 exit through the lower parts of the neuroforamina on the transverse processes just below the level of the facet joints. They pass obliquely forward and downwards and posterior to the vertebral arteries and veins in grooves formed by the anterior and posterior tubercles of the corresponding transverse processes. In these grooves, they lie on the medial parts. Just anterior and inferior to them lie the small ventral roots. The first cervical nerve passes between the posterior arch of C1 and the vertebral artery. The dorsal ramus of the first spinal nerve becomes the suboccipital nerve and supplies the suboccipital muscles. This first cervical nerve has almost exclusively motor fibers and only seldom any significant sensory component. Thus, there is usually no need to block this nerve. The second cervical nerve passes transversely behind the C1–2 joint, and the large dorsal ramus forms the greater occipital nerve, which innervates the posterior scalp.

Procedure Again, this technique is performed without any sedation because of the need of cooperation of the patient. The radiofrequency lesioning of the dorsal root ganglion (RF-DRG) is only performed after a positive diagnostic segmental nerve block (usually several diagnostic blocks are performed). For this procedure, the patient is lying supine on the operating table with a slight extension of the neck. Firstly, the C-arm should be positioned obliquely so that the first three contralateral pedicles are projecting just posteriorly to the anterior line of the vertebral bodies. Secondly, the intervertebral discs should be clearly visible. To do so, the C-arm is orientated in the frontal plane. One should adapt C-arm positioning to have an optimal view of the intervertebral foramen of the level one wants to treat. The axis of the intervertebral foramen points 25–35° anteriorly and 10° caudally. The inclination of the C-arm in the frontal plane should be such that there is no double contour in the caudal aspect of the foramen. Then the target point is identified: it is posterior in the neuroforamen between the caudal and the middle third. This dorsal position is chosen in order to avoid possible damage to the motor fibers of the segmental nerve and to the vertebral artery, which runs anterior to the ventral part of the foramen. The entry point is marked on the skin and is the same as the target point. This technique is a ‘tunnel vision’ technique what means that the entry of the needle is in the direction of the Xrays.32 The needle is than projected on the screen like a dot and the field of vision can theoretically be narrowed down to a tunnel-like diameter (Fig. 24.4). After injection of local anesthetic (lidocaine 1%) into the skin with a 22-gauge subcutaneous needle, a 22-gauge spinal needle or, preferably, a needle with a connecting tube is inserted into the superficial layers of the skin, in the direction of the X-rays so that the electrode is projected on the screen as a dot. Subsequently, the needle is advanced carefully and every step is checked with fluoroscopy. There is the possibility of inadvertent puncture of the segmental nerve. That is why an early check in the anteroposterior (AP) view is done. In this view, the endpoint is the point where the tip of the needle is projecting 1–2 mm lateral to the lateral border of the facet column. Thereafter, only 0.2–0.5 mL of water-soluble dye (Iohexol

Section 2: Interventional Spine Techniques

Fig. 24.6 Lateral fluoroscopic view of the block of the C2 segmental nerve. The target point is the same as the entry point (tunnel vision technique), namely approximately 3 mm posterior to the tip of the dome-shaped space between the laminae of the C1 and C2 vertebrae.

Fig. 24.4 Oblique fluoroscopic view of blocking the C6 segmental nerve. Notice the needle in tunnel vision (projecting as a dot) posterior in the C6 foramen between caudal and middle third of this foramen.

240 mg/mL; Omnipaque® 240) is injected to confirm the proper position of the needle tip close to the segmental nerve and to exclude an accidental intradural or intravascular position of the electrode. When this is confirmed, 0.5 mL of local anesthetic (lidocaine 1–2%) is injected. Alternatively, to perform a radiofrequency lesion, the cannula is advanced until the tip projects into the middle of the facet column (Fig. 24.5). Then the stylet is removed and 0.2–0.5 mL of dye is injected to confirm proximity to the targeted nerve root. The RF probe is now inserted through the cannula. After checking the impedance, electrical stimulation is started at a rate of 50 Hz. The patient should feel a tingling sensation. If the stimulation threshold is felt under 0.4 volts, the needle is withdrawn until the threshold is between >0.4 and <0.65 volts. At the C2 level, a suboccipital tingling has to be confirmed by the patient. Next, the frequency is changed to 2 Hz, and the patient is observed for muscle contractions in the arm and/or hand. These should not occur below a voltage of 1.5 times the 50 Hz threshold. When the thresholds are acceptable, 0.5–1.0 mL of local anesthetic (lidocaine 1–2%) is injected. Subsequently, an RF current is led through the electrode in order to increase the temperature at the tip slowly to 67°C for 60 seconds. As mentioned above, there is the tendency toward using pulsed RF current when treating the DRG because it is believed to be less destructive. With this technique, the stimulation at 50 Hz is started when the needle tip is projecting 2 mm medially to the lateral border of the facet column. An ideal threshold is obtained at <0.3 Hz. Then, a conventional 2 × 20 msec/sec, 45 volt and 120 sec. pulsed RF procedure is performed. The pulsed RF treatment can be repeated a second time if the 50 Hz threshold is lower than the initial threshold after a slight repositioning of the needle.

Fig. 24.5 Anteroposterior fluoroscopic view of RF lesioning of the DRG of the C6 segmental nerve. Notice that the needle tip still has to be inserted more until it is projecting at the middle of the facetal column (target point is indicated with a red dot).

Fig. 24.7 Anteroposterior fluoroscopic view of the block of the C2 segmental nerve, where the tip is projecting halfway across and posterior to the C1–2 joint (atlantoaxial joint) (indicated by a red line). Notice the course of the nerve shown by the injected dye. Notice also that this isn’t a ‘through-the-mouth’ view, but an AP view with hyperextension of the cervical spine.

To perform a diagnostic block and (pulsed) RF procedure of the C2 DRG, the C-arm is positioned straight lateral because of the different anatomy at this level. There is no facet joint and there are no major blood vessels in the direct neighborhood that should be considered. The target point of the DRG of C2 is about 3 mm posterior to the tip of the dome-shaped space between the laminae of the C1 and C2 vertebrae (Fig. 24.6). After injection of a local anesthetic, the needle is inserted and advanced in a tunnel vision technique. The depth of the needle is checked in the AP position (Fig. 24.7) and the needle tip should be projecting halfway across and posterior to the C1–2 joint using a through-the-mouth view. The next steps are identical to those described above for the C3 to C7 DRG. The radiofrequency lesioning of the C8 DRG should be avoided because of the high tendency to develop neuritis and even deafferentation pain. The reason for this occurrence has not been discovered. The pulsed RF technique could be an alternative to avoid this complication.

Equipment For a diagnostic block, it is recommended to use a needle with a connecting tube (for example: an RCN-needle, Radionics), so that once proper positioning of the needle has been attained, contrast medium and local anesthetics can be given without displacement of the needle. For an RF lesioning, either the SMK-50 mm with a 4 mm active tip or the SMK-100 mm with a 5 mm active tip can be used. For the pulsed RF technique, a SMK-C5 with a 4 mm active tip is used. 279

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Postprocedure care The patient can be discharged 1–2 hours postprocedure. Driving or operating dangerous machinery during the first 24 hours after the procedure is prohibited. A side effect that is often seen (40–60%) is a mild burning sensation (some deep neck soreness) in the treated dermatome that subsides spontaneously after 1–3 weeks.33 Some sensory changes, such as a slight hypoesthesia, may occur but invariably disappears within 3–4 months.34,35

Case study A 44-year-old female attending the authors’ pain clinic with a 6month history of pain in her neck radiating to her shoulder, arm, index and middle fingers. The pain in her arm was the most disabling. Physical examination revealed a diminished anteflexion of the cervical spine and paravertebral tenderness over cervical facet joints C3–4, C4–5, and C5–6 on the right side. Neurological examination revealed a positive Spurling test on the right side. Physical examination of both shoulders was normal and radiography of cervical spine showed some minor degenerative abnormalities; in addition, electromyography was also normal. Conservative management (medication, physical therapy, and TENS) gave no meaningful pain relief. In different sessions, the C5, C6, and C7 segmental nerves on the right side were tested. Because of an important decrease (about 50%) of the pain after diagnostic block of the C6 segmental nerve, DRG of C6 was treated with a PRF current for 120 seconds. Two months after the treatment there was an improvement of the pain of 60%. Seven months after treatment there was still the same level of pain relief.

RADIOFREQUENCY DENERVATION IN THE THORACIC REGION Thoracic percutaneous radiofrequency denervation of the facet joints Relevant anatomy In contrast to the lumbar facet joints, the thoracic facet joints are more vertically oriented and almost parallel to the coronal plane (Fig. 24.8). They are oriented perpendicular to the sagittal plane and face directly anterior. The thoracic facet joints are innervated by medial branches of the posterior primary rami of the segmental nerves. Each thoracic facet joint is bisegmentally innervated by the medial branch of the same level and the medial branch of the level above. The thoracic medial branches pass through the intertransverse space and touch the superolateral corner of the transverse process. Then they run medially and inferiorly across posterior surfaces of the transverse processes before entering the posterior compartment of the back and innervating the multifidus muscles.36 In that location they give ascending articular branches to the facet joint. An exception to this pattern occurs at the midthoracic levels (T5–8). Although the curved course remains essentially the same, inflection occurs at a point superior to the superolateral corner of the transverse process. This course is different than that seen with the lumbar medial branches which are fixed at the junction of the superior articular process and the transverse process.37 The T11 and T12 medial branches have the same course as the lumbar medial branches.37 Obtaining a fluoroscopic view is quite difficult for a variety of reasons. In this region one has to contend with overprojection of the ribs, the prominent transverse process that is directed slightly cranial and markedly posterior, and the size and orientation of the pedicles that can make them difficult to visualize. In addition, the orientation of the thoracic facet joints impedes the operator’s ability to differentiate between superior and inferior articular process. 280

Fig. 24.8 Anatomy of the thoracic facet joints and their innervation. Notice that the thoracic facet joints are more vertical and orientated almost parallel to the coronal plane in comparison to the cervical facet joints. The medial branches of the posterior primary rami make their inflection of the curved course at the superolateral corner of the transverse process (indicated by the red lines) and touching it.

Procedure Sedation is avoided as communication between operator and patient must be maintained at all times. In contrast to diagnostic thoracic intra-articular block, which has been well described,38 expert opinion varies on RF lesioning of median branches in the thoracic vertebrae. Nonetheless, the authors describe how they perform an RF lesion of the median branches at the thoracic level. Although the authors embrace this technique some authors have suggested that the needle tip is actually ‘too far anterior’ to the medial branch to result in denervation. The authors use the junction between the superior articular process and the superior border of the transverse process as a target point for thoracic medial branch neurotomy, Stolker et al. reported that with this target site the medial branch of the dorsal ramus was never within reach of the electrodes.39 Based on Stolker’s work, the authors suggest exercising caution regarding categorical acceptance of the technique described here. The C-arm is positioned in the transverse plane and an external radiopaque object such as a clamp is used to identify the proper level. A straight-on AP view of the vertebra at the anticipated target level is obtained. The endplates of the vertebra should be parallel without any visible endplate double contours. Then the C-arm is axially and slightly obliquely rotated in the sagittal plane. This should facilitate the access to the target point that is the junction of the superior articular process and the transverse process. A proposed entry point is marked on the skin and local anesthetics (lidocaine 1%) with a 23-gauge needle are injected. The RF needle is then inserted parallel with the gantry angle (angle of the Carm beam) until bone contact is reached at the junction of the superior articular process and the transverse process (Fig. 24.9). Subsequently, the needle is redirected slightly more cranially and laterally until it is just loses osseous contact. Then the needle position is checked in the lateral view. The needle tip should be just posterior to a line connecting the posterior aspects of the neuroforamina (Fig. 24.10). Stimulation at 50 Hz is now performed. A paravertebral tingling sensation should be perceived with a current with a voltage of less than 0.5 volts. Next, stimulation at

Section 2: Interventional Spine Techniques

The patient can be discharged home a few hours after the procedure provided the vital parameters are normal. Fig. 24.9 Slightly oblique fluoroscopic view of the RF denervation of the medial branches of the T3–4, T4–5, T5–6, and T6–7 facet joints on the right side. The needles make bone contact at the junction of the superior articular process and the transverse process.

Thoracic radiofrequency lesioning of the dorsal root ganglion Relevant anatomy In the higher thoracic segments, it is difficult to reach the dorsal root ganglia because of overlying anatomical structures. Among the obstacles are the wide facet column, articulations of the transverse processes with the ribs and, most importantly, the lungs. The pulmonary structures prevent adopting a very lateral approach, which would have been ideal to allow one to get under the posterior osseous barriers. In successive lower thoracic segments, the anatomy gradually resembles the anatomy of the lumbar spine. This change creates an opportunity for lower thoracic DRG to be reached as if it were a lumbar DRG.

Procedure

Fig. 24.10 Lateral fluoroscopic view of needle tips at the medial branches of the T3–4, T4–5, T5–6, and T6–7 facet joints. The needle tips should be projecting just posterior to a line connecting the posterior aspects of the neuroforamina.

2 Hz should provoke paravertebral muscle contractions at a voltage of ≤1. Stimulation should be negative for anterior nerve root stimulation, which would be perceived as muscle contraction and/or pain in the anterior chest wall or abdominal region depending on the level undergoing RF. When proper needle positioning has been confirmed with fluoroscopic imaging and electrical stimulation, 0.5 mL of lidocaine 1–2% is administered at each level. After local anesthesia has taken effect, RF lesioning is conducted for 60 sec at 20 V. The authors typically RF three levels because of the multisegmental innervation of the facet joints. As was alluded to earlier, the authors use this technique and are attempting to refine it.

Two or more diagnostic blocks at different levels must be performed to identify the segment involved, because of the frequent overlapping of thoracic segmental pain from one segment to another. An intercostal block can be used as a test block of a thoracic segmental nerve.40 The level which provides the best temporary pain reduction is then selected for RF lesioning of the dorsal root ganglion. As described above, in the upper thoracic spine, the classic approach (posterolateral) is not possible because the foraminae face more anteriorly and accurate positioning of the needle is hindered by the angle of the ribs. Therefore, an alternative technique is used to reach the DRG of T7 and above. The patient is placed in a prone position and a dorsal approach is used. The target point is the craniodorsal part of the intervertebral foramen and is thus the same as the target point in the classic dorsolateral approach. The entry point is the midpoint of the pedicle in the posteroanterior view (Fig. 24.11). This entry point is checked in a lateral view where it should aim for the superior dorsal quadrant of the foramina where the DRG should be situated. A small hole is drilled through the lamina of the vertebra under fluoroscopic guidance in the posteroanterior view using a 16-gauge Kirschner wire and local anesthesia. A potential danger is the piercing of the facet joint. Then, an RF cannula is inserted through the burr hole into the proper position, which is checked in the lateral view and should be in the craniodorsal part of the intervertebral foramen (Fig. 24.12). The stylet of the cannula is replaced with an RF probe and stimulation at

Equipment For a diagnostic block a 10 cm CMK needle (with a connecting tube) is used. For an RF lesioning, a SMK-C10 cannula with a 5 mm active tip can be used. Alternatively, a 10 cm with 10 mm active tip RaczFinch radiofrequency thermocoagulation (RFTC) needle can be used. When using the latter needle, a 20-gauge angiocatheter and an RFTC electrode are necessary.

Postprocedure care As with any RF procedure there is always the possibility of postprocedure exacerbation of pain. A complication unique to the thoracic region is a pneumothorax. Proper technique and the use of fluoroscopic guidance for the placement of the needle will minimize the risk of this complication. The patient must be warned of the possibility of the development of a pneumothorax and should return to the hospital if shortness of breath or pain with inspiration develops.

Fig. 24.11 Anteroposterior fluoroscopic view of a RF lesioning of the T8 DRG. The entry point is the midpoint of the pedicle (indicated by a green line; the pedicle is indicated by a red line) in the posteroanterior view. Notice the introduction needle is in tunnel vision. 281

Part 2: Interventional Spine Techniques

Fig. 24.12 Lateral view of the RF lesioning of the T8 DRG where the proper position of the RF cannula is the craniodorsal part of the intervertebral foramen. Notice the introducer needle (indicated with a red line).

50 Hz is carried out. The patient should feel tingling sensations in the selected dermatome using a 0.4–1.0 V stimulus. Stimulation at 2 Hz should not give contractions of the intercostal muscles at a stimulation threshold below 1.5 times the sensory threshold. After satisfactory placement is achieved, 0.4 mL of contrast medium (Omnipaque) is injected to exclude intradural or intravascular spread. When correct position has been confirmed, 1–2 mL of lidocaine 1–2% is injected and a 60 second, 67°C lesion is made. One could consider performing PRF lesioning (pulses of 2 Hz and 20 msec during 120 seconds), but this technique has not yet been proven to be less destructive or as effective as RF lesioning. At the lower levels the same approach can be used as at the lumbar level. The needle position, the stimulation, and the lesion parameters are identical. This technique is described under RF denervation in the lumbar region.

Diagnostic blocks were performed at the T6, T7, and T8 levels with each block performed during a separate visits. Diagnostic block at the level T7 on the right side provided complete relief of pain. A radiofrequency lesion of the T7 dorsal root ganglion was performed using a standard orthopedic drill (AO drill). There was complete relief of pain after this procedure for 4 months. Four months later the patient underwent an identical procedure with excellent pain relief.

RADIOFREQUENCY DENERVATION IN THE LUMBAR REGION Lumbar percutaneous radiofrequency denervation of the facet joints Relevant anatomy The lumbar facet joints are all almost vertically oriented (Fig. 24.13). The upper lumbar facet joints are more oriented in the sagittal plane and they rotate to a more oblique angle in the lower lumbar region. The upper facet joints are more curved than the lower joints, which are more flat. The facet joint is innervated by the medial branch of the posterior ramus of the spinal nerve. As it exits from the intervertebral foramen, the spinal nerve divides into an anterior primary

Equipment A 10 cm SMK 22-gauge cannula with 5 mm active tip and an RF probe can be used. This needle can be manually curved to perform the parasagittal approach. For the dorsal approach, a 16-gauge Kirschner wire can be used the make a burr hole into the lamina.

Postprocedure care One of the most important complications is the possibility of damage to the nerve root or spinal cord during needle placement. Another common complication is neuritis. Again, there is a slight possibility of a pneumothorax and/or hemothorax. These particular complications should be described in detail to any prospective candidate for RF lesioning. Other possible complications include infection, increased pain, bleeding, and bruising. The authors typically discharge patients a few hours after undergoing procedures. It cannot be overemphasized that the absence of a pneumothorax should be clinically determined. If any doubt remains, radiographs are mandatory.

Case study A 55-year-old woman was referred by the neurology service to the authors’ pain clinic. She worked for a cleaning company. For almost 2 years she had progressive, continuous pain which began in the upper thoracic region and referred symptoms to just under the right breast. Neurological examination and MRI scan from the thoracic region were normal. There were mild degenerative changes of the midthoracic vertebrae. A trial of medication was tried with little in the way of success. These included gabapentin, amitriptylline and venlafaxin. Other therapies included transcutaneous nerve stimulation and physical therapy. These were equally ineffectual. 282

Fig. 24.13 Anatomy of the lumbar facet joints and their innervation. The medial branches of the posterior primary rami of the segmental nerves L1, L2, and L3 are indicated by red lines.

Section 2: Interventional Spine Techniques

ramus and a posterior primary ramus. At approximately 5 mm from its origin, the posterior primary ramus divides into medial, lateral, and intermediate branches. The medial branch supplies the facet joint at its own level and the next lower level. The medial branch runs in a dorsal and caudal direction and lies in a groove on the base of the superior articular process in direct contact with the base of the superior surface of the transverse process. Each medial branch also supplies the multifidius, interspinales, and intertransversarii mediales muscles and the ligaments and periosteum of the neural arch. The anatomy of the L5–S1 facet joint is different. The transverse process of S1 is replaced by the ala of the sacrum and thus the median branch of L5 runs at the junction between the sacral articular process and the upper sacral border. Also, in some circumstances there is a branch from the S1 nerve exiting the posterior opening of the first sacral foramen. It courses cephalad and innervates the L5–S1 facet joint. Consequently, in certain patients the only way to completely denervate the L5–S1 facet joint would be to conduct RF at three locations, affecting the medial branches of L4, L5, and S1.

Procedure Since continuous verbal feedback from the patient is required during the stimulation and heating phases, sedation is not employed. The patient assumes a prone position on the fluoroscopic table. A pillow is placed under the abdomen to diminish the physiological lumbar lordosis. Firstly, targeted levels are identified and a straight AP projection is obtained. Then, the C-arm is axially rotated until there are no visible double contours of the caudal endplate of the middle vertebra. The middle vertebra of the levels to be treated is used as the reference point prior to the searching for the optimal position of the C-arm. Subsequently, the C-arm is rotated to an approximately 15° oblique view until the spinous processes are projecting off the midline but well inside the contralateral facet joints. Then, the entry point should be marked over the target point, which is the point at the junction of the superior articular process and transverse process. To perform a diagnostic block, the target point should be approximately 1 mm under this junction to avoid inadvertent spread of local anesthetic to segmental nerves, thereby creating the potential for a false-positive result. After injection of local anesthetic (lidocaine 1%) into the skin, the needle is inserted at the entry point and slowly advanced using a tunnel vision technique until the tip makes osseous contact. For a diagnostic block, the position of the needle is then checked in the lateral view, which should be at the level of the inferior part of the intervertebral foramen in line with the facet joint column. When accurate positioning is confirmed and following a negative aspiration, 1 mL of local anesthetic (lidocaine 1%) is injected at each level. To perform an RF lesioning of

Fig. 24.14 Oblique fluoroscopic view of two needles in tunnel vision, aiming for the medial branches of the L3–4 and L4–5 facet joints on the left side.

Fig. 24.15 Lateral fluoroscopic view of RF lesioning of the medial branches of the L3–4, L4–5 and L5–S1 facet joints. Notice that the tips of the needles are in line with the facet joint column and are projecting at the level of the inferior part of the intervertebral foramen about 1 mm dorsal to the level of the line connecting the posterior aspects of the intervertebral foramina.

the medial branch, after making bone contact with the needle tip, the needle is redirected slightly more cephaled until bone contact is lost and immediately the target point is reached (Fig. 24.14). Then, the Carm is rotated into the lateral view to check the position of the needle tip, which should be in line with the facet joint column and at the level of the inferior part of the intervertebral foramen about 1 mm dorsal to the level of the line connecting the posterior aspects of the intervertebral foramina (Fig. 24.15). It should be a little deeper and more cranial than the position of the needle for the diagnostic block. When this position is confirmed, the impedance is checked and, if acceptable, stimulation at 50 Hz is conducted. The patient should feel new pressure or tingling in the back at a voltage of <0.5 V. If sensations are felt in the ipsilateral extremity, the needle tip is too close to the segmental nerve. It is imperative the needle be slightly withdrawn and stimulation at 50 Hz checked again. Subsequently, settings are changed so that stimulation occurs at 2 Hz. The patient should experience localized contractions of the multifidus muscle and not of muscles of the leg. These local contractions can be palpated by the operator. Similarly, any contractions that occur in the leg may be detected by the operator or the assistant if a hand is placed over the muscles innervated by the exiting nerve root. If the patient perceives pain and/or contractions in the extremity or if muscular contractions are detected by an operator then the needle must be repositioned. After accurate positioning of the needle tip is attained and a negative aspiration is demonstrated, 1 mL of local anesthetic (lidocaine 1%) is injected at each level. RF lesioning of 20 V (approximately 67°C) is performed for 60 seconds. The fluoroscopic view for the L5–S1 facet joint and thus the median branch of the L5 is different from the other lumbar levels because of the difference in anatomy. The L5 medial branch lies at the junction between the superior sacral articular process and the upper border of the sacrum. Since there is no pedicle at this level to use as a radiological landmark, the C-arm is positioned so that the junction is seen as a round, curved transition. The C-arm is rotated slightly obliquely (about 15°). The identified target point is the curve of the transition and is the same as the entry point. The needle is thus placed in tunnel vision (Fig. 24.16). The depth of the needle is checked in the lateral position and the tip must project over the posterior border of the facetal column. Thereafter, the rest of the procedure is the same as described before.

Equipment A 22-gauge, 10 cm SMK needle with a 5 mm active tip can be used to perform an RF lesioning. Another possibility is to use a 10 cm, 20-gauge blunt RFTC needle with a 10 mm active tip and a 16-gauge 283

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Procedure Fig. 24.16 More anteroposterior fluoroscopic view while aiming for the medial branch that innervates the L5–S1 facet joint. Notice that the needle aiming at the nerve of this joint is in tunnel vision and that the upper needles (aiming for the medial branches of the L3–4 and L4–5 facet joints) are not.

angiocatheter as an introducer. However, no clinical studies have been published using the latter mentioned equipment. For a diagnostic procedure, a needle with tubing is preferred (for example: a 10 cm 22-gauge pole RC needle). When a PRF lesioning is performed, a 10 cm SMK cannula and a SMK-TC 10 RF probe can be used.

Postprocedure care The patient is allowed to go home immediately after the procedure. Driving a car or handling dangerous machinery is proscribed for the first 24 hours. In some instances there will be a transient numbness of the ipsilateral extremity because of overflow of local anesthetics into the intervertebral foramen. The overall incidence of minor complications per radiofrequency site was found to be only 1%.41 For up to 2 weeks after the procedure there may be burning pain perceived in the lower extremity (neuritic pain) or there can be more localized pain lasting in excess of 2 weeks. Invariably, these are short-lived side effects and will resolve spontaneously. Other possible side effects include infection, bruising, and muscle spasms.

Case study A 64-year-old man presented to the authors’ pain clinic with a major complaint of low back pain with radiation into the bilateral inguinal region and into the dorsal thighs. These symptoms had been present for 2 years with failure to improve with classic rehabilitation measures including medication and physical therapy. Physical examination revealed limited extension of the lumbar spine and pain on extension. Furthermore, there was pain elicited with paravertebral pressure to the lower lumbar region. Neurological examination was normal. Radiography of the lumbar spine revealed a facet arthrosis of the right L4–5 and L5–S1 facet joint and less so on the left side. Diagnostic block of the median branches of the right L4, L5, and S1 posterior primary rami was performed with 1 mL of lidocaine 1% at each level. Thirty minutes after the procedure, the patient reported approximately 70% pain intensity relief. One week later, an RF lesion of these median branches was performed. At 8-weeks follow-up the patient reported complete relief of pain.

Lumbar radiofrequency lesioning of the dorsal root ganglion Relevant anatomy The lumbar dorsal root ganglion (DRG) is situated in the cranial part of the intervertebral foramen. The DRG lies more dorsally in the upper lumbar levels compared to the lower lumbar levels. 284

Sedation is not employed. The procedure is performed with the patient in prone position on a fluoroscopic table with a pillow under the abdomen to diminish the physiological lumbar lordosis and facilitate the approach. A straight AP view is secured and the targeted segmental level is identified using a radiopaque object such as a clamp. Then, the C-arm is axially rotated to give a view of the targeted vertebra without any double contour of the endplate. Subsequently, the C-arm is rotated obliquely, approximately 20–25°, so that the spinous processes are projecting just medially to the contralateral facet column. Then, the entry point is marked and is the same as the target point (Fig. 24.17). The target point is different for a diagnostic segmental block in comparison to an RF of the DRG. For a diagnostic block, the target point is 1–2 cm distal to the DRG. The target point for an RF lesioning of the DRG is approximately 1 mm caudad to an imaginary line that bisects the pedicle. After infiltration of the skin with local anesthetics (lidocaine 1%), the needle is inserted and slowly advanced using a tunnel vision technique. The depth of the needle should be checked following each advancement. This is best viewed using a lateral projection. If this is not done, the root can be inadvertently irritated or even injured. In this lateral view, the needle tip should rest within the cranial part of the intervertebral foramen and only 1 mm past the posterior aspect of this foramen (Fig. 24.18). To do a diagnostic block of the segmental nerve, which is always performed before any RF lesioning, the needle should also be in the cranial part of the intervertebral foramen, but at the ventral border. Even using meticulous technique does not guarantee that the root will not be touched by an advancing needle. The authors routinely warn the patient that this may happen and that they should Fig. 24.17 Oblique fluoroscopic view (approximately 20–25°) to perform an RF lesioning of the L5 DRG on the left side. Notice that the spinous processes are projecting just medially to the contralateral facet column. The target point (indicated by a red dot) is approximately 1 mm caudal to an imaginary line that bisects the pedicle (indicated by a blue line).

Fig. 24.18 Lateral fluoroscopic view of the needle tip while performing an RF lesioning of the L5 DRG. The needle tip should be projecting in the cranial part of the intervertebral foramen and only 1 mm past the posterior aspect of this foramen.

Section 2: Interventional Spine Techniques

not be concerned. If the patient experiences a sudden jolt of pain in the ipsilateral radicular dermatome the needle should be immediately withdrawn a millimeter or two. The next step is to check the needle position by injecting contrast medium. Turn the C-arm in an AP projection, where the needle tip should be projecting within the contours of the vertebra and inject a small volume of dye. Only the exiting nerve should be seen and there should be no flow of contrast into the epidural space (Fig. 24.19). For a diagnostic block, more than 1 mL of local anesthetic (lidocaine 1%) is injected. To perform an RF or PRF lesioning of the DRG, stimulation at 50 Hz is first conducted. It should give a tingling sensation in the leg in the appropriate dermatome at a threshold <0.5 V. Subsequently, the 2 Hz threshold is searched for and should occur at less than 150% of the previously established 50 Hz threshold. In the lumbar region, the PRF lesioning of the DRG is preferred as it may be less destructive than RF lesioning. The authors create a lesion over 120 seconds using pulses of 2 × 20 msec/sec at 45 V. If the impedance is >400 Ohms, 1 mL

Fig. 24.19 Anteroposterior fluoroscopic view of an RF lesioning of the L5 DRG. Notice that the needle tip is projecting within the contours of the vertebra. A small volume of dye is injected and is revealing the L5 exiting nerve.

of lidocaine 1% should be injected before the lesioning. The tip temperature should not exceed 42°C. If this occurs, the voltage should be lowered to 40°C. Prior to performing this intervention, the spine clinician should be aware that there is level two evidence that RF lesioning of a lumbar DRG is not effective.42

Equipment For a diagnostic block, a 10 cm 22-gauge needle can be used. An example is the pole RC needle. To perform an RF lesioning, a 100 mm SMK cannula and SMK-TC 10 RF probe can be used.

Postprocedure care Patients should be warned that local anesthesia can create a temporary weakness of the lower extremity following a diagnostic block. Consequently, standing or walking for 45–60 minutes after the procedure is potentially dangerous. At 15–30 minutes after the diagnostic block, its analgesic effect should be tested. If there is pain relief of >50%, a PRF treatment can be planned. The patient can go home immediately after an RF lesioning. Patients should be warned that there can be a burning pain for a few weeks and that the beneficial effect of the treatment may be delayed for several weeks (6–8 weeks).

THE SYMPATHETIC SYSTEM Stellate ganglion block Relevant anatomy The cervical paravertebral sympathetic trunks consists of preganglionic fibers originating in the anterolateral horn of the first and second thoracic spine segments (Fig. 24.20). They innervate the head and the neck. These preganglionic fibers travel with the ventral roots of

Fig. 24.20 Anatomy of the stellate ganglion, indicated by a red line. 285

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T1 and T2 as white communicating rami and then join the sympathetic chain cephalad and synapses either at the inferior or middle or superior cervical ganglion. The inferior cervical ganglion is called the stellate ganglion and all preganglionic fibers either synapse here or pass through this ganglion. Then the postganglionic fibers run cranially following a course along the carotid arteries or go to the cervical plexus or upper cervical nerves as gray communicating rami to innervate neck structures. The preganglionic fibers that will innervate the upper extremity originate in the T2 and T8 or T9 spine segments and travel with the ventral roots of T2–8 as white communicating rami to join the sympathetic chain. Subsequently they pass cephalad and make synapses at the second thoracic, the first thoracic, the stellate, or the middle cervical ganglion (occasionally). Some of the postganglionic fibers form the subclavian perivascular plexus. However, most of these fibers travel to the anterior spinal nerves of C5–T1 as gray communicating rami and join the anterior spinal nerves to form the brachial plexus. Often, the inferior cervical ganglion and the upper thoracic ganglion are fused to form the stellate ganglion. Sometimes the middle cervical ganglion is also fused with the stellate ganglion. The stellate ganglion usually lies on the lateral border of the longus colli muscle anterior in the neck between the base of the seventh cervical transverse process and the first rib. The classic approach to block the stellate ganglion is at the C6 level, namely at the Chaussignac’s tubercle. The ganglion is limited medially by the longus colli muscle, laterally by the scalene muscles, inferiorly by the pleura, anteriorly by the subclavian artery, and posteriorly by the transverse processes.43 Sympathetic innervation of the upper extremity is provided by the stellate ganglion through gray communicating rami of C7, C8, and T1 and occasionally from C5 and C6. However, the T2 and T3 gray communicating rami also can innervate the upper extremity but don’t always pass through the stellate ganglion (they are then called ‘Kuntz’s nerves’) and thus aren’t blocked by blocking the stellate ganglion. That is often the reason why the stellate ganglion block fails to provide adequate relief of the sympathetically mediated pain of the upper extremity.

Procedure There is no need for sedation of the patient. On the contrary, it is not recommended to perform this procedure on a sedated patient because it can be catastrophic. Every sudden, uncontrolled movement of the patient can dislocate the needle and can cause unintentional injection in the important nearby structures such as the carotid artery or the spinal canal. An intravenous line can be provided before starting the blockade to have a safe access for injection of resuscitative drugs if needed. The use of the C-arm is optional, but practical to check and confirm proper needle positioning. The anterior approach at C6 is the most commonly used approach, but it can give an insufficient block of the sympathetic innervation of the upper extremity (see above). The patient is lying supine on a fluoroscopic table with a pillow under the shoulders to slightly hyperextend the neck. In this manner, the landmarks are easier to locate and the esophagus on the left side will be located more medially and thus away from the needle insertion point. The target point is the same as the entry point and is the Chaussignacs’ tubercle (C6) approximately 1–2 cm from the midline. This tubercle can be palpated and is located at the medial border of the sternocleidomastoid muscle lateral to the cricoid cartilage. Palpation of the tubercle is best done with the index finger, and most of the time this finger is also used to retract the carotid artery laterally away from the needle entry point. 286

Then the needle is inserted just medially to the index finger towards the junction between the tubercle and the C6 vertebral body. Local injection of the skin is done with lidocaine 1%. The needle is aimed downwards perpendicular to the fluoroscopic table until bone contact is made. This bony contact is expected at a depth of 2.0–2.5 cm. Pneumothorax can be avoided with careful placement of the needle: control the direction and advance the needle gradually. The needle position can then be checked with fluoroscopy in the anteroposterior position (Fig. 24.21) and in the lateral view after injection of watersoluble dye. Of course, this injection of dye is only performed when the aspiration test has proven to be negative: i.e. no aspiration of cerebrospinal fluid or blood. When proper needle position is confirmed following the spread of the contrast medium, local anesthetic (lidocaine 1%) can be injected gradually using 0.5 mL as a test injection. After every 3–4 mL of local anesthetic, careful re-aspiration should be done to exclude dislocation of the needle point. At least 5 mL of local anesthetic fluid is needed to block the stellate ganglion, but this volume does not guarantee that Kuntz’s nerves (T2 and T3) will be blocked. A volume of at least 10 mL is probably needed to block all the sympathetic innervation of the upper extremity including the anomalous Kuntz’s nerves. To provide a long-lasting blockade, radiofrequency thermocoagulation can be used. When the stellate ganglion block is performed as a diagnostic block to predict the effect of an RF lesioning, only 2–3 mL of local anesthetic solution should be used, otherwise it is not a good predictor. After correct placement of the electrode tip, stimulation is performed at 2 Hz and at 50 Hz to exclude close proximity to the phrenic nerve, the recurrent laryngeal nerve, or the segmental nerve of C7. When no stimulation of these nerves occurs and the injection of contrast dye reveals the characteristic spread, 2 mL of lidocaine 1% is injected and a 60-second, 80°C lesion is made. An alternative method to the C6 anterior approach is the C7 anterior approach. These two methods are comparable, however the C7 anterior approach is more technically challenging because the C7 transverse process is not easily palpable. It is due to this anatomic issue that the authors recommend the use of fluoroscopy. Nevertheless, the advantage of this approach is the fact that a smaller volume (only 4–6 mL) of local anesthetic can be used to provide complete blockade of the sympathetic innervation of the upper extremity. The disadvantage of this technique is that the risk of pneumothorax is much greater.

Equipment To perform a stellate ganglion block, a 23- or 24-gauge 4–6-cm needle can be used. A side line tubing is recommended because it guarantees

Fig. 24.21 Anteroposterior fluoroscopic view of a diagnostic block of the right stellate ganglion after injecting dye.

Section 2: Interventional Spine Techniques

the stability of the needle tip during the aspiration and the injection (for example: a 60 mm 24-gauge Pole RC needle). A 22-gauge SMK needle of 50 mm with a 4 mm active tip can be used to perform a radiofrequency thermolesion.

Postprocedure care Correct placement of the block can be confirmed when an ipsilateral Horner’s syndrome is seen: miosis, ptosis, and enophthalmia. Conjunctival injection, nasal congestion, and facial anhidrosis are also signs that can be seen. The blockade of the sympathetic innervation of the upper extremity will reveal temperature differences between the blocked arm and the contralateral arm (raised skin temperature in the ipsilateral arm) and visible engorgement of the veins on the ipsilateral hand and forearm. Ten to fifteen minutes after a diagnostic block, the effect can be evaluated and the patient can go home with an accompanying person.

Thoracic sympathetic block Relevant anatomy The preganglionic fibers of the thoracic sympathetic chain originate from the anterolateral horn of the respective thoracic spine segments and travel with the thoracic segmental nerves through the intervertebral foramen.44 As white communicating rami, they synapse with postganglionic fibers in the thoracic sympathetic ganglia. Most often, there are 10 pairs of thoracic sympathetic ganglia lying paravertebrally and at the posterolateral surface of the thoracic vertebral bodies. Sometimes 11 pairs of ganglia can be found. Some of the postganglionic fibers return to their respective somatic nerves as gray communicating rami and go to the regional vasculature, the sweat glands, and the pilomotor muscles of the skin. Some of them go to the cardiac plexus and go up or down the sympathetic trunk to end in more distant ganglia. As mentioned above, the first thoracic ganglion is fused with the lower cervical ganglion to form the stellate ganglion. The difficulty in blocking the thoracic sympathetic chain is related to, on one hand, the proximity of the pleura directly lateral and anterior to the ganglia and, on the other hand, the proximity of the segmental nerves.

Procedure45 There is no need for sedation. The patient is lying on a fluoroscopic table in a prone position. Ideally, there should be a pillow under the chest so that the thoracic spine is slightly flexed. The C-arm can be used to check the needle position. The entry point of the needle should be just below and approximately 4 cm to the spinous process of the vertebra one level above the level to be blocked. The needle is inserted and a local anesthetic (lidocaine 1%) skin wheal is made. The needle tip is directed towards the lamina until bone contact is made. Then the needle is laterally ‘walked off ’ the lamina until a loss of resistance is observed. This is the sensation one should expect while passing through the costotransverse ligament. After this loss of resistance, the needle should be advanced another 0.5–1.0 cm. There are several possible complications at this point. First, there is the possibility to enter the pleura and in doing so causing a pneumothorax. This should be avoided by keeping the needle tip medially as close as possible to the vertebral body. Secondly, it is possible to enter the intraspinal space when the needle tip is positioned too medially. Thirdly, the needle tip could be making contact with the segmental vertebral nerve and causing paresthesia in the respective dermatome. When

this occurs, the needle should be withdrawn and redirected a little bit more cephalad. When the aspiration test is negative for blood, cerebrospinal fluid, or air, approximately 5 mL of local anesthetics (lidocaine 1–2%) can be injected. Longer-lasting pain relief can be provided by radiofrequency lesioning. Until now, no randomized, controlled trials have been performed to prove the efficacy of the radiofrequency lesioning of the thoracic sympathetic chain.

Equipment A 23- or 24-gauge, 4–6 cm needle can be used (for example: a 60 mm 24-gauge Pole RC needle).

Postprocedure care After the procedure with local anesthetics, the patient should be observed for several hours and vital parameters should be checked. When these parameters are stable, the patient can go home but has to be instructed to come back to the hospital within half an hour if shortness of breath should occur because of the possibility of a developing and evolving pneumothorax.

Lumbar sympathetic block Relevant anatomy The lumbar sympathetic chain consists of two paravertebral trunks that are connected segmentally by preganglionic neurons (Fig. 24.22). These preganglionic fibers follow their corresponding nerves as white communicating rami and communicate in the paravertebral ganglia with postganglionic efferents and with efferents to the pelvic viscera. Some postganglionic fibers directly pass the ganglia and go to the ganglia in the aortic plexus and the superior and inferior hypogastric plexuses. The postganglionic fibers leave the sympathetic chain as gray communicating rami. Some go to the L1 nerve (iliohypogastric and genitofemoral nerve), others go to the L2–5 nerves, and the rest go to the upper three sacral nerves and end in the lumbosacral plexus. There is a great variation in number and position of the ganglia of the sympathetic chain. Most often four ganglia on each side are found. Often, there is a fusion of the L1 and L2 ganglia.

Procedure Sedation should not be employed. The patient lies in a prone position on a radioscopic table. A straight AP projection is obtained. Next, the obliqueness is adjusted. The spinous processes should project over the contralateral facet column, which is usually at about a 35° oblique angle. The target point is

Fig. 24.22 Anatomy of the lumbar sympathetic chain. This is a crosssectional view where the two paravertebral sympathetic trunks are seen (indicated with a black line).

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Fig. 24.23 Oblique fluoroscopic view (approximately 35–40°) of an RF block of the lumbar sympathetic chain. The target point of the needles are approximately 1 mm lateral to and a little caudad to the middle of the concavity of the vertebral body. Notice the two needles at their target points in tunnel vision at the L4 and the L5 vertebrae.

approximately 1 mm lateral to and a little caudal to the middle of the concavity of the vertebral body (Fig. 24.23). This point is often obstructed by the transverse process. Therefore, the C-arm is rotated axially to move the transverse process upwards so that visualization of the target point is unobstructed. After local infiltration of the skin with lidocaine 1%, the needle is inserted and advanced using a tunnel vision technique. The depth is checked on the lateral view. The needle tip should be at the anterior border of the vertebra (Fig. 24.24). In the AP view, the needle tip should be projecting within the lateral border of the vertebra and over the facet column (see Fig. 24.24). During the procedure, the patient is asked to report paresthesias, especially when the L4 level is treated, because of the possibility of making contact with the L3 ramus and thus the genitofemoral nerve. When the needle is in the right position, 1–2 mL of water-soluble contrast medium is injected and should spread cranially and caudally. A lateral spread of the dye at the L4 level suggests dispersal within the psoas muscle. When this happens, the needle should be redirected more anteriorly or medially. In the lateral view, the dye should spread at the anterolateral border of the vertebra in a linear fashion (Fig. 24.25). For an RF lesion, the next step is to perform sensory stimulation at 50 Hz. The patient should only feel a little pressure or warmth in the back, but not in the inguinal region or groin because this suggests the proximity of the needle tip to the genitofemoral nerve. Using motor stimulation of up to 2 or 3 volts should not trigger fasciculations or induce inguinal or groin pain. When the correct position is confirmed and a negative aspiration obtained, then 1–2 mL of local anesthetic (lidocaine 1%) is injected and an RF lesion (90 seconds, 67°C) is performed. At the L5 level, the lateral approach could be more difficult because of the overprojection of the iliac crest. At this level the position of

Fig. 24.25 Lateral fluoroscopic view of RF lesioning of the lumbar sympathetic chain after injecting dye. The needle tips are projecting at the anterior borders of the vertebrae. Notice that the dye is spreading toward the anterolateral border of the vertebra in a linear fashion.

the C-arm should be less oblique but more axially rotated to move the visualization of the iliac crest downwards. The endpoint of the needle tip at the L5 level is at the junction of the anterior one-third and posterior two-thirds of the vertebral body.

Equipment For a diagnostic block, a 14.5 cm 20-gauge SMK needle can be used. For the RF lesion, a 15 cm SMK Thermocouple RC probe or a 15 cm curved blunt needle with a 10–15 mm active tip and a 16-gauge angiocatheter can be used.

Postprocedure care Bed rest is not required after this procedure. There are no restrictions to daily activities provided the patient is not planning to participate in extreme exertional activities. After approximately 15 minutes, the block with local anesthetic should be checked. If there is an improvement of the usual pain, an RF lesioning is planned. After the RF treatment, there is the possibility of postoperative discomfort for approximately 1 week. There is also a possible delay of effect of the treatment for several weeks.

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Fig. 24.24 Anteroposterior fluoroscopic view of RF lesioning of the L4 and L5 sympathetic ganglia. The needle tips are projecting within the lateral border of the vertebrae and over the facet columns. 288

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22. Higuchi Y, Nashold BS Jr, Sluijter M, et al. Exposure of the dorsal root ganglion in rats to pulsed radiofrequency currents activates dorsal horn lamina I and II neurons. Neurosurgery 2002; 50(4):850–855.

38. Gray D, Bajwa Z, Warfield C. Facet block and neurolysis. In: Waldman SLR, Ross A, et al, eds. Interventional pain management. Philadelphia: WB Saunders; 2001:446–483.

23. Sluijter M, Van Kleef M. Characteristics and mode of action of radiofrequency lesions. Cur Rev Pain 1998; 2:143–150.

39. Stolker R, Vervest A, Groen GJ. Electrode positioning in the thoracic percutaneous partial rhizotomy: an anatomical study. Pain 1994; 57:241–251.

24. Cahana A, Vutskits L, Muller D. Acute differential modulation of synaptic transmission and cell survival during exposure to pulsed and continuous radiofrequency energy. J Pain 2003; 4(4):197–202.

40. Dooley JF, McBroom RJ, Taguchi T, et al. Nerve root infiltration in the diagnosis of radicular pain. Spine 1988; 13(1):79–83.

25. Sluijter M. The medial branch procedure. In: Sluijter M, ed. Radiofrequency. Part 2: thoracic and cervical region, headache and facial pain. Meggen (Switzerland): FlivoPress SA; 2003:99–110. 26. Van Kleef M, Sluijter M. Radiofrequency lesions in the treatment of pain of spinal origin. In: Gildenberg P, Tasker R, eds. Textbook of stereotactic and functional neurosurgery. New York: The McGraw-Hill; 1998:1585–1599. 27. van Suijlekom HA, van Kleef M, Barendse GA, et al. Radiofrequency cervical zygapophyseal joint neurotomy for cervicogenic headache: a prospective study of 15 patients. Funct Neurol 1998; 13(4):297–303.

41. Kornick G, Kramarich S, Lamer T, et al. Complications of lumbar facet radiofrequency denervation. Spine 2004; 29(12):1352–1354. 42. Geurts JW, van Wijk RM, Wynne HJ, et al. Radiofrequency lesioning of dorsal root ganglia for chronic lumbosacral radicular pain: a randomised, double-blind, controlled trial. Lancet 2003; 361(9351):21–26. 43. Moore D. Stellate ganglion block. Springfield, IL: 1954. 44. Pitkin G. Cervical and thoracic nerves. Philadelphia: JB Lippincott; 1946. 45. Rai P, Rauck R, Racz G. Autonomic nerve blocks. St. Louis: Mosby-Year Book; 1996.

28. Lord SM, Barnsley L, Bogduk N. The utility of comparative local anesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophyseal joint pain. Clin J Pain 1995; 11(3):208–213.

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PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

Discography

25

Richard Derby, Sang-Heon Lee and Byung-Jo Kim

INTRODUCTION Discography was developed in the late 1940s for diagnosing lumbar intervertebral disc herniation.1,2 In contemporary practice, discography refers to provocation discography in which the most important component is the evaluation of pain reproduction caused by pressurizing the disc with contrast medium. Discography is conceptually an extension of clinical examination, tantamount to palpating for tenderness.3 A precision injection of contrast dye into the disc nucleus stimulates nerve endings4 (via two mechanisms: chemical stimulus from contact between contrast dye and sensitized tissues, and a mechanical stimulus resulting from fluid-distending stress). Discography is a potential solution to the diagnostic dilemma concerning which patients to treat surgically and at what segmental level. In 1995, the North American Spine Society stated that discography, especially followed by CT scanning, may be the only study capable of providing a diagnosis or permitting precise description of the internal anatomy of a disc and the integrity of disc substructures.5 Although new diagnostic imaging tools have been developed and are widely used, discography is still practiced. Discography remains particularly useful in problematic cases unresolved by MRI or myelography and in patients for whom surgery is contemplated.6 In this chapter, the technical considerations and complications of discography are discussed.

INDICATIONS AND CONTRAINDICATIONS According to the position statement on discography by the North American Spine Society:5 Discography is indicated in the evaluation of patients with unremitting spinal pain, with or without extremity pain, of greater than 4 months’ duration, when the pain has been unresponsive to all appropriate methods of conservative therapy. Before discography, the patients should have undergone investigation with other modalities which have failed to explain the source of pain; such modalities should include, but not be limited to, either computed tomography (CT) scanning, magnetic resonance imaging (MRI) scanning and/or myelography. The single purpose of discography is to obtain information. Disc morphology is not diagnostic; it does not indicate whether a given disc is responsible for a patient’s pain. However, it is reassuring if a disc proven to be symptomatic on other grounds also happens to be morphologically abnormal. The prime indication for discography is to establish a diagnosis of discogenic pain when therapy is to be directed at that disc. A parallel application is to identify asymptomatic discs. When a single disc is found to be symptomatic in the presence of adjacent asymptomatic discs, focused surgical therapy can be

entertained. Patients with symptomatic or abnormal discs at multiple levels constitute a greater surgical challenge. Congenital anomalies of the vertebrae or nerve roots and postoperative spinal abnormalities constitute relative contraindications to discography. Such conditions require greater care and dexterity to negotiate the abnormal anatomy to access the target disc and avoid injury to surrounding structures. In the case of cervical discography, spinal cord compression constitutes an absolute contraindication to discography. In such cases neurologic features are key, and information about discogenic pain is immaterial to management. Moreover, the uncertainty of the relationship between the prolapsed disc and the spinal cord and resistance of the disc to passage of a needle only invites morbidity.

PREPROCEDURAL EVALUATION AND PATIENT PREPARATION Preprocedural evaluation A thorough patient evaluation is performed before discography. The evaluation should include the general medical status and a detailed history, including previous medical conditions and allergies. Symptom onset, pain nature and distribution, pain duration and frequency, injury type, previous medication and surgery, and posture or movements that aggravate or diminish pain should also be recorded. In most cases of lumbar discography and all cases of thoracic and cervical discography an MRI or CT scan should be reviewed prior to discography. Further, since false-positive rates increase with somatization, psychometric testing should be included. Prior to the procedure, the clinician should explain the nature of the procedure, its risks and complications, and what to expect. It is important that patients recognize and report any reproduction of accustomed pain and distinguish this pain from other pain. Subjects should be instructed in the use of pain scales for pain intensity responses. Unless the patient is able to describe the nature and intensity of provoked pain, the procedure has no value. In this regard, it is advantageous to have a trained observer independently monitor patient pain responses while an operator concentrates on technical aspects of the procedure.

Patient preparation Since the disc is avascular, there is an increased risk of disc space infection and most discographers use prophylactic antibiotics.3 Animal studies have shown that intradiscal and intravenous antibiotics prevent discitis, and prophylactic intravenous antibiotics 20 minutes prior to the procedure are recommended.7,8 In addition, many discographers add 2–6 mg/mL of a cephalosporin antibiotic to 291

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the nonionic contrast solution.8 All procedures should be performed under sterile conditions, including sterile scrub and double gloves. At best, discography is uncomfortable; at worst, it can be very painful. For this reason, it is recommended that patients be sedated with the intravenous injection of either midazolam (2–5 mg) or intermittent does of 10–30 mg of propofol. Patient response should be monitored and the dosage titrated to establish a level of sedation permitting the patient to be conversant and responsive after needle placements, yet tolerant of procedural discomfort. The main disadvantage is that midazolam and propofol frequently cause procedural amnesia, and the patient report of experienced pain when asked at a later date is unreliable. In addition, patients taking significant narcotics for pain control should be given a preoperative dose of narcotic (e.g. 50–100 ␮g fentanyl) to reduce pain intolerance and withdrawal hypersensitivity. Although respiratory depression is uncommon using this protocol, subjects are monitored with pulse oximetry and a blood pressure cuff. Supplemental oxygen is administered by nasal cannula.

TECHNIQUE OF LUMBAR DISCOGRAPHY Patient position The patient lies in a prone oblique position on a fluoroscopy table. Elevating the target side approximately 15° allows the fluoroscopy tube to remain in a more AP projection and reduce radiation scatter. If required, a folded towel or soft wedge may be placed under the patient’s flank to prevent side bending of the lumbar spine. On the side selected for puncture, a wide area of the skin of the back is prepped and draped from the costal margin to the mid-buttock and from the midline to the flank. The puncture side should be opposite the patient’s dominant pain to eliminate confusion between pain reproduced during contrast injection and the pain of penetrating the outer anulus fibrosus.

Disc puncture Prior to injection, a fluoroscopic examination of the spine is performed to confirm segmentation and determine the appropriate level for needle placement. Using AP view, the beam should be parallel to the inferior vertebral endplate. After selecting the target disc using AP view, the fluoroscopic beam is axially rotated until the facet joint space is located midway between the anterior and posterior vertebral margins. In this view, the insertion point is 1 mm lateral to the lateral margin of the superior articular process (Fig. 25.1). The insertion point is marked on the skin. Since the distance between the opposite superior articular processes increases at lower

Fig. 25.1 Oblique view of lumbar spine (*, needle insertion point; P, pedicle; FJ, facet joint). 292

Fig. 25.2 Safe triangle for needle insertion (NR, nerve root outlined by contrast media; SAP, superior articular process; EP, endplate).

levels, the usual distance from the midline increases from about 3–4 cm at the T12–L1 level to 6–7 cm at the L5–S1 level. Because of the iliac crest and increased interfacetal distance, at the L5–S1 level the fluoroscopy tube is rotated only far enough to bring the facet joint space approximately 25% of the distance between the anterior and posterior vertebral margins. Prior to needle placement, the skin, subcutaneous tissues, and deep muscular tissues along the needle trajectory are infiltrated with local anesthetic (1% lidocaine). Techniques vary depending upon the number of needles used. The single-needle technique has the advantage of a single needle insertion and perhaps shorter procedure duration, but the risk of disc infection may be higher. To avoid potential neural injury, the needle should be directed into the safe triangle. The borders of the safe triangle include the nerve root for the superior tangential border, the vertebral endplate of the target disc for inferior border, and the lateral margin of the superior articular process for the medial side line (Fig. 25.2). To minimize nerve trauma, one should use a needle with a short, noncutting bevel or blunt-pointed tip with a side port.

Puncture of T12–L1 through L4–L5 intervertebral discs In the double-needle technique, a styletted 25-gauge, 6-inch needle is placed into each disc through a 20-gauge 3.5-inch introducer needle under fluoroscopic guidance. To protect the discographer’s hand from radiation exposure, forceps may be used to grasp the introducing needle. The introducer needle is advanced parallel to the fluoroscopic beam using an oblique fluoroscope view (Fig. 25.3).

Fig. 25.3 The introducing needle should proceed parallel to the fluoroscopic beam using an oblique fluoroscope view.

Section 2: Interventional Spine Techniques

Discography Needle Introducer Needle

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Fig. 25.4 The ideal position of needle when the needle contacts the disc is on the line between midpoint of pedicles at AP (A) and posterior vertebral margin at lateral view (B) (P, pedicle).

A slight ‘hockey-stick’ bend at the end of the introducer needle can improve navigation. If bony obstruction is encountered, the physician should confirm whether the needle has contacted the superior articular process or the vertebral body. If necessary, the needle may be slightly withdrawn and its trajectory modified. The introducer needle can be either advanced just over the lateral edge of the superior articular process or advanced to the margin of the disc. At the L5–S1 level, advancement may proceed just over the lateral edge of the superior articular process. When the introducer or discogram needle contacts the disc margin, the ideal position in the AP projection is on a line drawn between the midpoints of the pedicles above and below (Fig. 25.4A). In no case should one advance the introducer or discogram needle medial to the inner pedicle margins before contacting the intervertebral disc. In the lateral view the needle should contact the disc between the posterior vertebral margins (Fig. 25.4B). After confirming introducer needle position with a lateral view, a 25-gauge, 6-inch needle is advanced into the center of the disc through the introducing needle while monitoring by lateral view. A slight ‘hockey-stick’ bend on the end of the discogram needle facilitates navigation. When the needle contacts the disc, position should be checked using AP and lateral views. Contact with the anulus fibrosus is characterized by the perception of firm but resilient resistance, and frequently the patient experiences a momentary, sharp, or sudden aching sensation in the back or the buttock. The needle is then advanced to the center of the disc. Needle position must be monitored and checked by both AP and lateral imaging.

L5–S1 intervertebral disc Due to increased facetal width and the presence of the iliac crest diacrest, puncture of the lumbosacral disc is more challenging. Instead of a direct lateral approach, once the introducer needle is advanced to the anterior border of the superior articular process of S1, a slight curve or ‘hockey-stick’ bend is needed to advance the discogram needle in a medial and slightly posterior direction around the SAP to contact the disc just anterior to the vertebral margin as viewed in the lateral fluoroscopy projection. Less experienced operators may find an 18/23-gauge needle combination easier to direct than the 20/25-gauge combination used for upper levels. Longer needle combinations may be required in muscular or obese patients. The fluoroscopy tube is rotated until about 1–2 cm of the L5–S1 disc

B

Fig. 25.5 (A) Oblique view of L5–S1 discography. The inner needle is advanced slightly under direct fluoroscopic vision, and the guide needle is simultaneously retracted slightly. (B) Lateral view. The inner needle should contact the disc 2–3 mm anterior to the vertebral margin.

is visualized between the superior articular process of S1 and the sacral ala (Fig. 25.2). Using the oblique fluoroscopic view, the guide needle is introduced toward the bony notch between the sacral ala and superior articular process of S1 until the needle tip lies immediately adjacent to the anterolateral aspect of the superior articular process of the sacrum (Fig. 25.5A). The needle tip should not be handled directly, but should be wrapped in sterile gauze. The distal 2–3 cm of the needle should be bent in a direction opposite the bevel. The degree of curve is determined by the operator on the basis of how much deflection is required in the patient at hand for the needle to approach the target disc center. In a lateral fluoroscopic projection, the 25-gauge discogram needle is passed through the guide needle while the guide needle is held firmly in position. The inner needle is advanced until the tip emerges from the guide needle. The inner needle is advanced under direct fluoroscopic vision. As it emerges, the guide needle is retracted slightly (Fig. 25.5A). This unsheathes the procedure needle, which should be turned so that the curve or bend bows the introducer needle in a medial and posterior direction through the safe triangle. Once the needle encounters the anulus fibrosus, its position is checked and confirmed in both AP and lateral fluoroscopy views. In the lateral view the needle should contact the disc 2–3 mm anterior to the vertebral margin (Fig. 25.5B) and in the AP view the needle should ideally be on a line bisecting the midpoint of the L5 and S1 pedicles. If the inner needle fails to curve medially it will not pass toward the center of the disc, and may strike the ventral ramus. As a result, the needle course must be monitored. If the needle fails to track medially and posteriorly, the needle should be removed and its curvature accentuated. Should the procedure needle meet with bony obstruction, the fluoroscope should be turned to determine whether the superior articular process or the vertebral body has been encountered. If the vertebral body has been encountered, the course of the needle can be corrected by withdrawing it slightly and rotating the needle appropriately. If the needle is blocked by the superior articular process, the inner needle is retracted into the guide needle and the pair are advanced to the lateral edge of the S1 superior articular process. The inner needle may then be directed toward the disc as described above. The ideal final needle position is in the disc center; however, there is leeway. In severely degenerated discs the needle position is not as critical, since contrast medium will spread throughout the disc. Ideally, the needle should be within 4–5 mm of the center on AP and lateral fluoroscopy. 293

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Provocation using pressure manometry Provocation Once the needle tip has been properly placed in the center of the nucleus pulposus, nonionic contrast medium mixed with antibiotic is injected into each disc at slow velocity using a controlled injection syringe with digital pressure readout. The total volume injected should probably be limited to 3.5 mL. Although a few severely degenerated discs will accept more volume, the incidence of false-positive pain responses may increase. If one cannot achieve 50 psi above opening pressure at 3.5 mL due to the degree of disc degeneration or a leak through the endplates or anulus, a dynamic pressure of 50 psi above opening can usually be achieved by more rapid injection. In general, however, the media should be injected as slowly as possible. Higher injection speeds may cause rapid pressure elevations leading to increased pressure differences between the nucleus pulposus and manometer and between the dynamic and static pressures. At 0.05 mL/sec (one revolution of the Merit monometer) the difference between static and dynamic pressures is minimal. The intrinsic disc pressure is the pressure required to start the flow of contrast medium into the nucleus (opening pressure) resulting from osmotic forces within the disc resisted by anulus tension and the tension of the anterior and posterior longitudinal ligaments. Typical opening pressures are 5–25 psi, depending on the degree of nuclear degeneration. An opening pressure >30 psi usually indicates that the needle tip is within the inner anulus. In this case, the needle tip should be repositioned. The disc is slowly pressurized by injecting 0.5 mL increments through a syringe attached to a pressure measuring device. At each 0.5 mL increment, the injection pressure, location of contrast medium, and any pain response are recorded. At a slow injection speed, the dynamic pressure more closely reflects the real intradiscal pressure than the static pressure taken without pressure applied to the injecting syringe. Injection continues until one of the following end points is reached: subject pain = 6/10, intradiscal pressure >50 psi above opening in a disc with a grade 3 annular tear or 80–100 psi in a normal-appearing nucleogram, or a total of 3.5 mL of contrast medium has been injected.

Imaging The appearance of the normal nucleus following the injection of contrast medium is unmistakable: the contrast medium assumes a lobular pattern or a bilobed ‘hamburger’ pattern (Fig. 25.6A). A variety of patterns may occur in abnormal discs.9 Contrast medium may extend into radial fissures of various lengths but remain contained within the disc (Fig. 25.6B), or it may escape into the epidural spaces through a torn anulus (Fig. 25.6A).

In some cases (Fig. 25.6C), the contrast medium may escape through a defect in the vertebral endplate.3 However, none of these patterns alone is indicative of whether the disc is painful; that can be ascertained only by the patient’s subjective response to disc injection. Immediately after discography, CT–discography may be performed to define fissures extending to the outer third of the anulus and extending circumferentially within the anulus fibrosus. Radial annular tears can be found by discography, but only the postdiscogram CT axial view clearly shows the location and size of fissures within the anulus fibrosus.3 Sachs et al.10 developed the Dallas discogram scale, in which annular disruption is graded on a 4-point scale. Grade 0 describes contrast medium contained wholly within a regular nucleus pulposus. Grades 1 to 3 describe the extension of contrast medium along radial fissures into the inner third, middle third, and outer third of the anulus fibrosus, respectively. Aprill and Bogduk11 proposed a modified Dallas description scale which includes grade 4, distinguished from grade 3 by the spread of contrast medium circumferentially within the substance of the anulus fibrosus and subtending a >30° arc at the disc center.

Interpretation The most important information obtained from discography is whether the patient’s pain is reproduced. There is no alternative or superior means of determining if a disc is the source of a patient’s pain. Conceptually, discography is an extension of clinical examination, tantamount to palpating for tenderness. It is only the inaccessibility of a disc to palpation that requires the use of needles. In this regard, it is critical that the criteria for a painful disc be rigorously satisfied. Internal control observations are mandatory: a disc cannot be deemed the source of a patient’s pain if stimulating other discs or other structures in the same region reproduce similar pain. Assessing patient response to discography requires measuring the pain reproduced by injection. Pain may be characterized by three components: intensity, location, and character. If the location and character of pain provoked during discography are similar to or the same as the patient’s clinical symptoms, the criteria for concordant pain are satisfied. The intensity of pain is measured by the patient (e.g., by using a numerical rating scale) and by observed pain behaviors. The intensity of provoked pain, however, is dependent on stimulus intensity. In simple terms, the harder one pushes on the syringe the more likely the disc is to hurt. By measuring intradiscal pressures, stimulus intensity can be quantified and standardized, permitting more reliable comparisons among patients and discographers. While injection pressures may be manually estimated, use of a controlled inflation syringe with digital pressure readout is more precise.

LT L4/5

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Fig. 25.6 The appearance of the nucleus following the injection of contrast media. (A) The contrast medium assumes either a lobular pattern or a bilobed (‘hamburger’) pattern (black arrowhead) as a normal nucleogram. Contrast medium escaped into the epidural space through a radial fissure at L5–S1 level (white arrow). (B) Contrast medium extended into radial fissures (arrow) but remain contained within the disc. (C) The contrast medium escaped through a defect in the vertebral end plate (white arrowheads). 294

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Adding pressure monitoring to provocative discography improves interobserver reliability and, as a result, reproducibility. A positive discogram requires an abnormal disc, pain response =6/10 (numeric rating scale; NRS), pressure level =50 psi, pain described by the participant as ‘familiar,’ and at least one negative control disc. One must, however, be aware that transient pain is often provoked when fissures are suddenly opened. In most cases, such pain should not be used as evidence of a true-positive response unless pain >6/10 is sustained for more than 30 seconds. Most experienced discographers will perform a confirmatory re-pressurization once a suspected positive response is provoked. If re-pressurization does not again provoke significant concordant pain at 50 psi or less above opening pressure, then the initial response will remain indeterminate. These criteria for positive response were reconfirmed in a study performed in 13 normal asymptomatic volunteers.11a,11b When the operational criteria for discography were set to pressure =50 psi and evoked pain intensity >4, the expected false-positive rate was <10%. However, a false-positive rate of zero could be secured either if the pain score was held at 4 and the injection pressure lowered to 20 psi, or if the pressure was held at 50 psi and the required pain score was raised to 6. To increase discography specificity, local anesthetic may be injected into the positive disc in an effort to obtain prolonged relief of pain from that disc (analgesic discography). In a preliminary study investigating the reliability of analgesic discography, 78% of patients showed significantly prolonged pain relief after local anesthetic injection. Those patients underwent fusion surgery and were followed to observe surgical outcome (T. Alamin, personal communication, 2004). In addition to these criteria for positive discography, disc anulus sensitivity may also be graded. Using the protocol of Derby et al.,12 four disc categories may be defined: (1) chemical discs, which provoke pain at 15 psi above opening pressure, (2) mechanical discs, which provoke pain at pressures between standing and lying, or 15–50 psi above opening pressure, (3) indeterminate discs, which provoke pain at 51–90 psi above opening pressure, and (4) normal discs, with no pain provocation. If a disc is painful at >50 psi, the response cannot be considered clinically significant, since it is difficult to distinguish from the effect of mechanically stimulating a normal or subclinically symptomatic disc.13 Excessive stimulation involving pressures >50 psi above opening pressure and uncontrolled, high injection speeds increase false-positive responses.

TECHNIQUE OF CERVICAL DISCOGRAPHY Patient position The patient is placed on the fluoroscopy table in a supine position. Extension of the neck may help improve disc access, and can be achieved by elevating the upper trunk and placing a cushion or a triangular sponge under the shoulders. The head is gently lowered and rested on a small supporting sponge, and the chin is extended. Rotating the head to the left may help move the trachea and esophagus toward the left. While the side to be punctured in lumbar discography is that opposite the patient’s dominant pain, a right-sided approach is used for cervical discography because the esophagus lies to the left in the lower neck. The skin of the right anterior and anterolateral neck is prepped from the mandible to the supraclavicular region. Sterile drapes are applied with their margins overlapping the sternocleidomastoid muscles.

Disc puncture Midline approach The disc level to be studied is identified by fluoroscopy. Most discographers use the AP view and count both upwards from the C7–T1 level and downwards from the C2–3 level. Counting down from the C2–3 level using the lateral fluoroscopic view is more accurate. The lateral views of lower cervical segments are usually attenuated by the

Midline approach Lateral approach

scm

ij

T

t

t

ic e

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scm ic

ij

lc D sc

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Fig. 25.7 Needle trajectories for midline and lateral approaches. In the midline approach, the needle will pass through the platysma muscle, between carotid sheath and airway, longus colli muscle and intervertebral disc. In the lateral approach, the needle will pass through the lateral neck muscles, posterior to internal jugular vein, 1–2 mm anterior to uncinate process.

overlying shoulders. To optimally visualize these segments, longitudinal, downward traction of the bilateral upper limb is often necessary. Once the levels are identified, the fluoroscopy tube is rotated in a cephalad–caudal direction to bring the endplates parallel to the beam. Pressure is applied with the index finger to the space between the trachea and the medial border of the sternocleidomastoid. Firm but gentle pressure will displace the great vessels laterally and the laryngeal structures and trachea medially. Below C4, the right common carotid artery and the internal carotid artery above C4 artery are palpated. The fingers are insinuated until they encounter the anterior surface of the vertebral column. The patient is monitored closely for vasovagal signs, which may be caused by compression of the catrotid artery during manual displacement with needle entry.14 The spinal needle or metal instrument can be used as a guide for needle insertion. The instrument is placed on the skin parallel to the disc space using fluoroscopic guidance and a marker pen is used to draw the lines on the skin over the intervertebral disc spaces. The needle entry point should be medial to the medial border of the sternocleidomastoid, and not through that muscle. The declination of the sternocleidomastoid ensures that at C3–4 the puncture point lies more laterally and will avoid the pharynx, whereas at C7–T1 it will be more medial and avoid the apex of the lung. One should use the shortest needle possible to reach the center of the target disc. Longer needles are more difficult to hold and direct and easier to inadvertently pass through the disc. A 23- or 25-gauge, 2.5-inch spinal needle is typically used for the procedure. With the point of the needle just medial to or under the index finger, both the needle and index finger can be moved in unison. The trachea is pushed medially by the fingernail of the index finger, and when the needle overlies the disc at a 20–40° angle, the needle is introduced through the skin directed toward the anterior lateral aspect of the disc (Fig. 25.7). In some patients, the discs can be directly palpated and the finger moved almost perpendicular to the disc center. Patients with short, thick necks or a large, immobile larynx are a challenge. On contact with the anulus, the patient may experience transient pain. The needle is advanced into the substance of the disc under direct AP fluoroscopic visualization. All movements of the needle should be slow and deliberate. One must be very careful not to pass the needle through the disc and into the epidural space or spinal cord. Use of a short needle may be helpful. Novice discographers may want to touch the anterior 295

Part 2: Interventional Spine Techniques

Fig. 25.9 For the midline approach, the fingernail of the left index finger applies firm pressure to push the great vessels laterally and the trachea medially. The medial border of the sternocleidomastoid is a relative skin surface marker.

Fig. 25.8 Needle insertion point. The target insertion point is 1–2 mm medial to the anterior margin of the uncinate process using an oblique view (UP, uncinate process).

disc body just above or below the disc margin to help judge the depth of penetration. Once the needle is passed several millimeters into the disc, the lateral view is used to guide further advancement.

Lateral approach Although in the medial approach the needle traverses the same tissue plane used by surgeons to gain access to the cervical intervertebral disc during open and percutaneous surgical procedures, many nonsurgeon interventionists have been trained to use a more lateral approach. In this approach, the disc level is identified by fluoroscopy, and the AP view is adjusted until the vertebral endplates of the target level show parallel lines on the fluoroscopic image. The fluoroscopic beam is then axially rotated until the anterior margin of the uncinate process is moved approximately one-quarter of the distance between the anterior and posterior lateral vertebral margins. In this view, the target insertion point is 1–2 mm medial to the anterior margin of the uncinate process (Fig. 25.8). The skin entry point will be over the lateral neck muscles and posterior to the great vessels or trachea (Fig. 25.9). Pressure displacement of the great vessels is difficult and usually not done. However, this anatomic region is highly vascular and one should carefully observe patients for signs of hematoma during and after the procedure. A 25-gauge, 2.5-inch spinal

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needle is directed toward the anterior aspect of the uncinate process and should enter the disc 1–2 mm anterior to the process, then slowly advanced to the center of the disc. One should use a needle no longer than is required to reach the center of the target disc. Before injection of contrast, the needle position within the disc is confirmed with both AP and lateral fluoroscopic images (Fig. 25.10). At C7–T1 the medial approach is preferred to avoid puncturing the apex of the lung.

Provocation and interpretation The utility of discography for solving puzzling presentations of atypical pain resulting from cervical lesions has been demonstrated. In such cases, MRI did not disclose the pain-producing lesion.14,15 Normal cervical discs accept fairly small volumes (0.25–0.5 mL) and intradiscal injection of normal discs is not painful.15,16 Schellhas et al.15 studied the accuracy of discography and MRI in the identification of source(s) of cervical discogenic pain. The results showed that discographically normal discs were never painful, significant cervical disc anulus tears often escape MRI detection, and that MRI cannot reliably identify the sources of cervical discogenic pain.15 Pain questioning and fluoroscopic imaging are performed as in lumbar discography. However, pressure-controlled injections are usually

Fig. 25.10 The needle placement. AP (A) and lateral (B) views demonstrating the needle tip (arrowhead) in the center of discs.

Section 2: Interventional Spine Techniques

not used. If the tip of the needle has been correctly placed in the center of the disc, a 1 mL or 3 mL syringe containing contrast media is attached. Manual syringe pressure is increased slowly until the intrinsic disc pressure is exceeded. Volumes as small as 0.2 mL may cause visible separation of the vertebrae, which should be monitored by fluoroscopy. Concordancy and pain intensity are recorded at 0.2 mL increments. Use of an NRS can help the patient quantify the intensity of pain experienced relative to the intensity of pain during the injection of adjacent discs. In healthy adults, the intervertebral discs of the cervical spine have a structure similar to that of the lumbar discs, consisting of an anulus fibrosus and nucleus pulposus. However, it has been observed that in the first and second decades of life before complete ossification occurs, lateral tears occur in the anulus fibrosus. Tears are most probably induced by motion of the cervical spine in the bipedal posture.17 In childhood, the uncovertebral joints begin to undergo an ongoing transformation.18 Tears in the lateral part of the disc tend to enlarge toward the medial aspect of the intervertebral disc. The development of such tears, uncinate fissures, through both sides may result in a complete transverse splitting of the disc. Such a process may be observed in the second and third decades of life in the lower cervical spine when the intervertebral disc is split in the middle into equal halves.17 These uncinate fissures are a normal finding, and rarely will one see a ‘normal’ nucleogram. A normal cervical disc offers firm resistance, and accepts less than 0.5 mL of solution with little discomfort at the time of distention. In most patients there will be transient pain when the uncinate fissures fill with contrast (Fig. 25.11). Pain provocation should be ignored unless persistent, concordant, and significant pain can be reproduced by repeated gentle manual pressurizations. Approximately 1 mL of injected contrast medium is usually enough to opacify the nucleus and fill lateral or posterior annular fissures. A positive response requires provocation of significant (>6/10) concordant pain during a confirmatory repeat injection of another 0.1– 0.2 mL of contrast medium. One should also consider retesting adjacent levels to compare pain intensities and concordance of pain. It is not uncommon to provoke concordant pain at multiple levels. In addition, one often will cause separation of the endplates during pressurization, and this movement may cause pain secondary to a symptomatic z-joint. A convincing, positive response to disc stimulation is one in which the patient reports exact or similar reproduction of pain on stimulation of a given disc, stressing one or two adjacent discs is painless or evokes pain totally foreign to the patient’s previous experience. Any other pattern of response is not held to be reliably indicative that the

A

B

Fig. 25.11 Cervical nucleogram. (A) Postinjection AP view. All needles were placed in the center of the discs. Contrast medium extended into uncinate recesses. Extension of contrast media to uncinate recesses are common after adolescence with maturation of cervical disc. (B) Postinjection lateral view.

stimulated disc is the source of the patient’s pain. It is common for a patient to have two symptomatic discs, but under those circumstances, one should still identify an adjacent disc that is asymptomatic. Without an asymptomatic ‘control’ disc, there is no evidence that the patient can discriminate between a symptomatic and asymptomatic discs, and there is no evidence that what is reported as disc pain is not simply the pain of needles felt in the back or the neck. Patients may also simply comply with the operator’s expectation that there should be pain. Although the authors agree in principle, in the common occasion when more than four discs provoke concordant pain, performing additional levels (usually the C2–3 or C7–T1) may be inappropriate. In addition to provocative testing, analgesic discography may be a useful technique for the evaluation of chronic cervical pain.14 Patients whose clinical pain pattern is reproduced or provoked during the injection of contrast media may benefit from analgesic discography. Once a painful disc has been identified in the course of discography, and once all discographic radiographs have been taken, 0.5 mL of bupivacaine can be injected into the disc to test pain relief. The patient’s accustomed pain should be relieved by this action. The duration of relief should be monitored and recorded by the patient. Relief of accustomed pain for a period consistent with the expected duration of action of the local anesthetic agent used constitutes strong evidence that the disc in question is the pain source. In practice, however, pain relief following multiple-level provocation discography is difficult to assess. Analgesic discography is probably best evaluated at a separate session, and only the one disc in question should be injected with local anesthetic. Finally, there are some patients who cannot tolerate the procedure. In these cases, little or no useful information may be obtained except that either the patient has a low pain tolerance or the operator performing the procedure is inept.

TECHNIQUE OF THORACIC DISCOGRAPHY Patient position The patient lies in a prone position on the fluoroscopy table. A wide area of the skin of the upper back is prepped and draped from the midline to the lateral wall of the chest on the side selected for puncture. As a rule, the side to be punctured is that opposite the patient’s dominant pain.

Disc puncture The current standard technique of thoracic discography was described by Shellhas et al.19 in 1994. Prior to the procedure, a fluoroscopic examination of the thoracic spine is performed to confirm segmentation and determine the safest and most accessible route to each disc. After the discographer selects the target disc on AP view, the fluoroscope is rotated in a cephalad–caudal direction to align the endplates. The fluoroscopic beam is then rotated ipsilaterally until the corner of the intervertebral disc space is visualized between the superior articular process and the costovertebral joint. Typically, this degree of ipsilateral rotation will superimpose the tip of the spinous process on the edge of the contralateral vertebral body. In this view, the insertion point is just lateral to the interpedicular line (Fig. 25.12) and approximately 3 cm lateral to the spinous process. Prior to needle placement, the skin and subcutaneous and deep muscular tissues along the trajectory of each needle are infiltrated with local anesthetic. Most discographers prefer a single-needle technique using either a 23- or 25-gauge, 3.5-inch needle. A slight bend placed on the end of the needle will facilitate changing directions by needle rotation. The trajectory of the needle is roughly parallel and behind the rib as it passes anterior to attach to the spine at the costovertebral joints. One aims at a round to square section of the posterior lateral disc that can be seen through a 1–3 mm opening between the superior articular process and the rib (Fig. 25.13). The needle should be advanced in short 297

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following end points is reached: the subject experiences pain greater than 6/10 or 7/10, intradiscal pressure reaches a firm end point, or a total of 2.5 mL of contrast medium has been injected.

Imaging

Fig. 25.12 Target point for needle insertion at thoracic spine (oblique view) (SAP, superior articular process; P, pedicle; CVJ, costovertebral joint; EP, endplate).

increments and the direction changed as necessary by needle rotation. If one stays behind the rib there is no chance of penetrating the lung. Although passage of the needle behind the rib is usually uneventful, passage of the needle between the rib and superior articular process may be difficult. The needle often contacts either the superior articular process or the body of the rib, and it is often difficult to tell which structure obstructs needle advancement. The bend on the needle can be rotated one way or the other and readvanced to assist a needle direction change and allow passage through the small aperture. Once the needle has passed anterior to the superior articular process using a lateral fluoroscopic view, the needle bend is turned posteriorly to facilitate advancing the needle in a more posterior direction (Fig. 25.13).

Provocation and interpretation Provocation Once the tip of needle has been properly placed in the center of the nucleus pulposus, nonionic contrast medium mixed with antibiotic is slowly injected into each disc in 0.2–0.5-mL increments under direct fluoroscopic observation. If firm resistance to injection is encountered before the nucleus opacifies, the needle may be embedded in the anulus or in the cartilage of a vertebral endplate. At 0.2–0.3 mL increments, pain response including behavior, NRS pain intensity, and concordance should be evaluated. At any incremental injection volume, one should record the presence of morphologic abnormalities such as grade 1–3 annular tears or endplate defects. Injection is continued until one of the

A

298

B

The appearance of the normal thoracic nucleus following contrast medium injection varies, but is usually either a diffuse, elongated homogeneous pattern or a lobulated pattern. Contrast medium may extend into one or many radial fissures in various locations and may remain contained within the disc, or escape into the epidural spaces through an outer annular tear. Vertebral endplate defects may allow contrast medium to flow into the vertebra or the vertebral veins. Following discography, computerized tomography (CT–discography) is often performed to define the exact location and size of annular fissures and protrusions.

Interpretation The most important information obtained from discography is whether the patient’s pain is reproduced. Assessing the patient’s response to discography requires evaluating pain evoked by injection. Pain may be characterized by three components: intensity, location, and character. Pain intensity is reported by the patient as an NRS score and observed pain behaviors are used. If the location and character of pain provoked during discography is similar to or the same as the patient’s clinical symptoms, the criteria for concordant pain are satisfied. a positive discogram requires an abnormal disc, pain response =6/10 (NRS), pain described by the participant as ‘familiar,’ and at least one negative control disc.

POSTPROCEDURAL CARE Patients are carefully examined for vital signs and any evidence of subcutaneous bleeding or hematoma immediately after discogram, and again 30 minutes later. After the second postprocedure check, patients are advised of any possible side effects to watch for during the next several days and are allowed to leave the department on the same day. The patient should be warned to expect postprocedure discomfort, including difficulty swallowing after cervical discography and lingering back pain after lumbar discography. One should also inform the patient that there will probably be a flare-up in usual symptoms that lasts 2–7 days, but infrequently can last for an indefinite period of time. The patient should be instructed to call if he or she experiences fever, chills, or severe (or delayed) onset of pain. Patients are contacted by telephone 48–96 hours after discography to screen for any possible complications or side effects.

Fig. 25.13 The needle placement. AP (A) and oblique (B) views demonstrating the needle tip (arrowhead) in the center of discs.

Section 2: Interventional Spine Techniques

POTENTIAL RISKS AND COMPLICATIONS Lumbar discography The main complications of lumbar discography include infection (e.g. discitis) and neural injury.20 Discitis following lumbar discography has been more frequently documented and studied than cervical discitis. Causative organisms have been identified as Staphylococcus aureus, S. epidermis, and E. coli,21,22 suggesting inoculation with surface organisms or misadventure through bowel perforation. To prevent discitis, prophylaxis with antibiotics before and after the procedure may be used; however, this practice remains controversial. To avoid infection, stringent attention to aseptic technique is critical. Some authors consider discitis a rare complication of lumber discography,23–25 whereas others have found overall rates of 2.3% per patient and 1.3% per disc7 or 0.1% per patient and 0.05% per disc.22 Discitis incidence is higher for single, large-gauge needles and much lower for doubleneedle techniques.26 The authors have avoided discitis in all but one case in over 2000 lumbar discograms over a 10-year period. Animal studies have shown that intradiscal8 and intravenous7 antibiotics prevent discitis. The recommended regimen is 1 mg of cefazolin per mL of contrast medium injected into the disc at the time of discography.8 However, many discographers use 3–6 mg cefazolin (or equivalent antibiotic) per mL of contrast. Even with prophylactic antibiotics, epidural abscess after discography have been reported.27,28 Striking a ventral ramus is a potential hazard, but may be avoided by careful attention to correct technique. Any needle should be prevented from straying beyond its required and intended course. Fortunately, in a conscious patient, contact with the ventral ramus will be indicated by severe, sharp lancinating pain, which is an indication to withdraw and redirect the needle. Penetration of the intervertebral foramen or the lumber nerve roots should never be a problem, for the needle should never be permitted to stray behind the midpoint of the target disc. Other complications include spinal cord or nerve root injury, cord compression or myelopathy, urticaria, retroperitoneal hemorrhage, nausea, convulsions, headache, and most commonly, increased pain.5 Disc herniation following discography is very rare,29 and there is little evidence that discography damages the disc.30 Freeman et al.31 recently reported no histological damage following needle insertion into sheep discs.

Cervical discography Major neural structures are not along the course of the needle to the target disc. However, one must be aware that it is possible to pass a needle through the disc and into the spinal cord. Unrecognized, the injection of contrast could traumatize the spinal cord. Using the shortest needle possible to reach the center of the disc, touching the anterior vertebral margin to confirm needle depth, and checking the lateral fluoroscopic view prior to injection will minimize this risk. During injection, the operator’s second hand should be used to brace the needle hub to prevent inadvertent overpenetration of the needle. Penetration of viscera such as the pharynx and esophagus is not a problem per se, but increases the risk of infection such as epidural abscess, retropharyngeal abscess, and discitis.22,32–34 Introduced organisms may be external, or from the pharynx or esophagus if penetrated. The reported incidence of cervical discitis is 0.1–0.5%.22,33 The most common presentation is severe exacerbation of axial pain, usually beginning 5–21 days following the procedure.22 Although the patient usually experiences chills, fever is an inconsistent finding. Administering preoperative intravenous antibiotics and adding antibiotics to the contrast solution will help minimize this risk. However,

significant increases in pain following cervical discography should be investigated with tests that include a minimum of sedimentation rate and C-reactive protein. Any elevation in the former should be investigated with a contrast-enhanced MRI scan. Passage of a 23- or 25-gauge needle though the carotid artery may occur in patients with heavy, short necks where displacement of the medial structures is difficult. Although this event may result in a hematoma, the swelling usually causes minor discomfort to the patient. Continued bleeding due to a genetic- or medication-related bleeding disorder could cause airway obstruction. Cervical discography is not an inherently unsafe procedure and can be performed with few complications when performed in sterile conditions by those well experienced with cervical disc injections.35

Thoracic discography The main complications of thoracic discography include pneumothorax, discitis, and neural injury. Pneumothorax can complicate cervical, thoracic, or lumbar discography, but usually occurs in the thoracic spine with traumatic pleural puncture during discography, paravertebral block,36 or needle biopsies.37 Since Shellhas et al.19 described, and experts quickly adopted, the technique of accessing the thoracic disc behind the rib, pneumothorax has been a rare event. A small traumatic pneumothorax after percutaneous needle procedures without other significant injuries can be treated conservatively and usually does not need chest tube insertion.38 The complications with infection or neural injury at thoracic spine should be similar to those of the lumbar spine. To prevent discitis at thoracic spine, stringent attention to aseptic technique is critical, and prophylaxis with antibiotics before and after the procedure may be used.

CLINICAL TRIALS: LITERATURE REVIEW Discography has been proposed as a potential solution to the diagnostic dilemma concerning which patients to treat surgically and at what segmental level. Lumbar discography for the diagnosis of abnormalities involving intervertebral discs has been used extensively as a diagnostic tool for evaluating low back pain (LBP) since the 1950s. Although new diagnostic imaging tools have been developed and are widely used, discography is still practiced. Discography remains particularly useful in problematic cases unresolved by MRI or myelography, and for patients for whom surgery is contemplated.6 In 1992, Osti and Fraser39 compared MRI with discography in disc disease and found that, using the current standard techniques, MRI failed to demonstrate some structural changes in the anulus that were visualized by discography. A similar result was obtained in a comparison of high-resolution CTs with discography.40 Several studies have demonstrated that MRI cannot reliably predict which discs are painful upon discography, at least not to the level of confidence required to rely solely on MRI for surgical decision making.41,42 A high intensity zone (HIZ) in the posterior anulus visualized by MRI has been proposed as a marker for painful discs.11,43 While highly specific, the sensitivity of this finding is only 26%, limiting the usefulness of the HIZ in selecting patients for surgery.44 While numerous papers have examined the usefulness of discography, some physicians still question its reliability.45,46 Critics point towards mismatches between morphological features and clinical complaints and false-positive rates. Discography, especially combined with CT scanning, is exquisitely sensitive for identifying morphologic disc abnormalities, and the frequency of discography-detected abnormal discs in the LBP population is quite high. For example, Grubb et al.29 found that in 78% of their patients with LBP, discography afforded positive findings for abnormality at one or more levels, 299

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whereas plain radiography and myelography demonstrated no such disease. Brodsky and Binder23 also found that discography revealed abnormalities in many patients with normal-appearing myelograms. The frequency of morphologic abnormalities revealed via discography in the back pain population is high, and increases with age,47,48 putatively due to painless degenerative changes.48 In addition, the location of an annular tear and the location of pain appear to be uncorrelated.49 Discrepancies between morphological appearance and pain provocation have also been described.50 Millete and Melanson51 reported retrospectively that concordant pain was evoked by injection in only 37% of patients with a morphological abnormality documented by discography. Antti-Poika et al.52 reported only a 52.8% concordant pain provocation rate in discs where discography showed abnormal morphological changes. There have been some reports that only anulus tears may be reliably associated with pain provocation, and that other degeneration patterns were not necessarily associated with a pain response. It is clear that abnormal morphological structures revealed by discography are considered too non-specific to be clinically useful, and that positive results should be limited to those eliciting concordant pain.46,53 Several series of asymptomatic patients have shown abnormal morphological findings using discography and CT–discography.53–55 Sachs et al.10 reported a 13% incidence of abnormal disc structure detected by postdiscography CT scanning without pain provocation in a large series of patients. Several authors have also discussed that severe back pain may be elicited by discography in patients without a prior history of such pain.45,54,55 Early work by Holt55 reported a 36% rate of positive discography in asymptomatic subjects, although this study contained methodological flaws. These findings were subsequently refuted by Walsh et al.,53 who demonstrated a 0% rate of positive discography in asymptomatic volunteers and established reproducible criteria for positive discography. Walsh studied 10 asymptomatic subjects and 7 patients with chronic LBP. Criteria for a positive result included 3/5 pain intensity (using a pain thermometer), similar distribution of pain, two types of pain behavior assessed by videotape review, and structural degeneration. Antti-Poika et al.52 reported in a prospective study of 279 injected discs in 100 patients that injection elicited concordant pain in >13% of patients with normal disc anatomy. Caragee et al.54 expanded on Walsh’s study of asymptomatic subjects by examining a cohort without LBP but with clinical characteristics closely matching those of patients with LBP. Results showed that, in individuals with normal psychometrics without chronic pain, the rate of false positives is very low if strict criteria are applied, and that false-positive rates increase with abnormal psychometrics and increased annular disruption. The authors have recently studied the reliability of discogram using precise criteria for positive discography (e.g. reproducible NRS pain over 6/10 with <50 psi intradiscal pressure and <3.5 mL total volume) in 13 volunteers including normal asymptomatic participants. No false-positive results were recorded for examined discs. Pressurecontrolled manometric discography coupled with precise criteria for positive discography can afford no false positives for the diagnosis of discogenic LBP in patients with normal psychometrics. Surgical fusion has been used for pain relief in discogenic LBP unresponsive to conservative therapy. The identification of exact pain generators has been challenging, and many studies have investigated the reliability of discography for determining pain sources in LBP patients. Colhoun et al.56 studied 195 patients with axial pain and reported that of 137 patients with a discogram positive for disc disease and provoked concordant pain, 89% derived significant, sustained clinical benefit from operation. Twenty-five patients showed morphologic disc abnormalities, but no provocation of concordant 300

pain on discography. Among this group, only 52% had clinical success. Blumenthal et al.57 reported that 74% of patients with internal disc disruption returned to work following anterior lumbar fusion performed based upon discography. In a multicenter surgical and nonsurgical outcome study after pressure-controlled discography, Derby et al.12 stated that precise prospective categorization of positive discographic diagnoses may predict treatment outcomes, surgical or otherwise, thereby greatly facilitating therapeutic decision-making. In addition, patients with highly sensitive discs at low pressure appear to achieve significantly better long-term outcomes with interbody/combined fusion than with intertransverse fusion. Finally, although imperfect, discography is relatively safe, shows substantial sensitivity for identifying painful discs, and may predict surgery-related outcomes.

SUMMARY Lumbar discography has been widely used for evaluating discogenic LBP. However the diagnostic power of discography remains controversial.58 Walsh et al.53 showed that the use of strict criteria for a positive test, including review of videotaped responses, affords excellent accuracy for the diagnosis of discogenic LBP. When excluding patients with somatization, applying more precise criteria for determining a positive level, and using a manometric grading scale, the specificity of lumbar discography increases 80–100%.3 Based on these data, Caragee et al.45 concluded that in individuals with normal psychometrics without chronic pain, false-positive rates increase with abnormal psychometrics and increased annular disruption, and that the rate of false positives is very low if strict criteria are applied. False-positive rates of 40–50% in discogram studies of patients without a history of LBP have been obtained.54,59,60 Since these studies, there have been advances in discography techniques and diagnostic criteria. One important recent advance has been the introduction of pressure-controlled manometric discography, which permits control of intradiscal pressure and the rate of contrast dye injection. Previous discogram studies assessing falsepositive rates have limitations which include use of manual injections, uncontrolled injection rates, unrecorded and/or unreported opening and dynamic pressures, volumes, and maximal volumes. The authors have examined the diagnostic power of lumbar discography in select participants without present low back symptoms using advanced discogram techniques and criteria (R Derby et al., unpublished work, 2004). Results have shown that when using pressure-controlled techniques and precise criteria for positive discography (e.g., reproducible VAS pain > 6/10 with <50 psi intradiscal pressure, and <3.5 mL total volume) no false positives may be obtained for the diagnosis of discogenic LBP. Accordingly, discographers should carefully scrutinize positive responses obtained without pressure-controlled manometric discography and precise criteria. Strict attention and adherence to operational criteria reduces the risk of false-positive responses.13 The authors recommend positive criteria for lumbar pressure-controlled manometric discography as follows: numeric rating scale of pain above 6/10, <50 psi intradiscal pressure above opening pressure, <3.5 mL total volume, and at least one negative control disc. Further, cervical discography is a safe and valuable diagnostic procedure if done by the highly trained and competent interventionist with expertise in the procedure.14 It is not a screening procedure but rather a confirmatory one. Even MRI is a useful adjunct to cervical discography; there are some MRI patterns that cannot be considered pathologic, and discography is required to diagnose discogenic pain syndrome.61 In a ‘select group’ of patients with chronic intractable neck pain but negative or indeterminate imaging findings who are being considered for surgical intervention, it can help localize the

Section 2: Interventional Spine Techniques

symptomatic level and potentially benefit the patients by surgical intervention.62 Finally, thoracic discography can be performed safely by experienced interventionists as a reliable tertiary diagnostic procedure to determine if degenerated discs on MR studies are related to clinical complaints.19 It can reveal the true source of pain and thus lead to precise and effective treatment.63

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4. O’Neill C, Derby R. Percutaneous discectomy using nucleoplasty. In: International 21st course for percutaneous endoscopic spinal surgery and complementary techniques. Zurich, Switzerland: 2003. 5. Guyer RD, Ohnmeiss DD. Lumbar discography. Position statement from the North American Spine Society Diagnostic and Therapeutic Committee [see comments]. Spine 1995; 20:2048–2059. 6. Greenspan A, Amparo EG, Gorczyca DP, et al. Is there a role for discography in the era of magnetic resonance imaging? Prospective correlation and quantitative analysis of computed tomography–discography, magnetic resonance imaging, and surgical findings. J Spinal Disord 1992; 5:26–31. 7. Fraser RD, Osti OL, Vernon-Roberts B. Iatrogenic discitis: the role of intra-venous antibiotics in prevention and treatment. An experimental study. Spine 1989; 14:1025–1032. 8. Osti OL, Fraser RD, Vernon-Roberts B. Discitis after discography. The role of prophylactic antibiotics. J Bone Joint Surg [Br] 1990; 72:271–274. 9. Adams MA, Dolan P, Hutton WC. The stages of disc degeneration as revealed by discograms. J Bone Joint Surg [Br] 1986; 68:36–41. 10. Sachs BL, Vanharanta H, Spivey MA, et al. Dallas discogram description. A new classification of CT/discography in low-back disorders. Spine 1987; 12:287–294.

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41. Simmons JW, Emery SF, McMillin JN, et al. Awake discography. A comparison study with magnetic resonance imaging. Spine 1991; 16:S216–S221.

11b. Derby R, Kim BJ, Lee SH, et al. Comparison of discographic findings in asymptomatic subject discs and the negative discs of chronic LBP patients: can discography distinguish asymptomatic discs among morphologically abnormal discs. Spine J 2005; 5:389–394.

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12. Derby R, Howard MW, Grant JM, et al. The ability of pressure-controlled discography to predict surgical and nonsurgical outcomes. Spine 1999; 24:364–371; discussion 371–372. 13. Endres S, Bogduk NC. Lumbar disc stimulation. In: International spinal injection society practice standards and protocols. San Francisco: ISIS; 2003. 14. Singh V. The role of cervical discography in interventional pain management. Pain Physician 2004; 7:249–255. 15. Schellhas KP, Smith MD, Gundry CR, et al. Cervical discogenic pain. Prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers. Spine 1996; 21:300–311; discussion 311–312. 16. Smith GW, Nichols P Jr. The technique of cervical discography. Radiology 1957; 68:718–720. 17. Dvorak J. Epidemiology, physical examination, and neurodiagnostics. Spine 1998; 23:2663–2673. 18. Taylor JR, Twomey LT. Acute injuries to cervical joints. An autopsy study of neck sprain. Spine 1993; 18:1115–1112. 19. Schellhas KP, Pollei SR, Dorwart RH. Thoracic discography. A safe and reliable technique. Spine 1994; 19:2103–2109. 20. Thomas PS. Image-guided pain management. Philadelphia: Lippincott-Raven; 1997. 21. Agre K, Wilson RR, Brim M, et al. Chymodiactin postmarketing surveillance. Demographic and adverse experience data in 29 075 patients. Spine 1984; 9:479–485. 22. Guyer RD, Collier R, Stith WJ, et al. Discitis after discography. Spine 1988; 13:1352–1354. 23. Brodsky AE, Binder WF. Lumbar discography. Its value in diagnosis and treatment of lumbar disc lesions. Spine 1979; 4:110–120. 24. Simmons EH, Segil CM. An evaluation of discography in the localization of symptomatic levels in discogenic disease of the spine. Clin Orthop 1975; 108:57–69.

43. Schellhas KP, Pollei SR, Gundry CR, et al. Lumbar disc high-intensity zone. Correlation of magnetic resonance imaging and discography. Spine 1996; 21:79–86. 44. Saifuddin A, Braithwaite I, White J, et al. The value of lumbar spine magnetic resonance imaging in the demonstration of annular tears. Spine 1998; 23:453–457. 45. Carragee EJ, Chen Y, Tanner CM, et al. Provocative discography in patients after limited lumbar discectomy: A controlled, randomized study of pain response in symptomatic and asymptomatic subjects. Spine 2000; 25:3065–3071. 46. Resnick DK, Malone DG, Ryken TC. Guidelines for the use of discography for the diagnosis of painful degenerative lumbar disc disease. Neurosurg Focus 2002; 13:1–9. 47. Smith SE, Darden BV, Rhyne AL, et al. Outcome of unoperated discogram-positive low back pain. Spine 1995; 20:1997–2000; discussion 2000–2001. 48. Vanharanta H, Sachs BL, Ohnmeiss DD, et al. Pain provocation and disc deterioration by age. A CT/discography study in a low-back pain population. Spine 1989; 14: 420–423. 49. Slipman CW, Patel RK, Zhang L, et al. Site of symptomatic annular tear and site of low back pain: is there a correlation? Spine 2001; 26:E165–E169. 50. Maezawa S. Muro T. Pain provocation at lumbar discography as analyzed by computed tomography/discography. Spine 1992; 17:1309–1315. 51. Milette PC, Melanson D. A reappraisal of lumbar discography. J Can Assoc Radiol 1982; 33:176–182. 52. Antti-Poika I, Soini J, Tallroth K, et al. Clinical relevance of discography combined with CT scanning. A study of 100 patients. J Bone Joint Surg [Br] 1990; 72: 480–485. 53. Walsh TR, Weinstein JN, Spratt KF, et al. Lumbar discography in normal subjects. A controlled, prospective study. J Bone Joint Surg [Am] 1990; 72:1081–1088. 54. Carragee EJ, Tanner CM, Khurana S, et al. The rates of false-positive lumbar discography in select patients without low back symptoms. Spine 2000; 25:1373–1380; discussion 1381.

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62. Parfenchuck TA, Janssen ME. A correlation of cervical magnetic resonance imaging and discography/computed tomographic discograms. Spine 1994; 19:2819– 2825.

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INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

IDET Technique

26

Daniel Southern and Gregory E. Lutz

INTRODUCTION Intradiscal electrothermal therapy (IDET) is a recently proposed and investigated treatment for intractable discogenic pain. There is good evidence that IDET denatures collagen and causes changes in disc protein.1 Yet, these changes do not alter the fundamental biomechanics of the intact motion segment.2 Relatively speaking, it is a minimally invasive technique when compared to fusion or total disc arthroplasty. An important attribute of this treatment is that it does not preclude the future application of these more invasive treatments while the corollary is not true. Once disc replacement or fusion is undertaken, IDET is no longer a viable treatment option at that disc level. Although IDET is a ‘minimally invasive’ intervention, this must not be construed to mean that the procedure is simple to perform or without potential deleterious side effects or complications. Both of these issues can be mitigated and optimal outcomes can be realized if meticulous technique is used. It is important to keep in mind the definition of technique: the systematic procedure by which a complex or scientific task is accomplished. The presentation of such a systematic, step-by-step approach is the aim of this chapter. By adhering to this approach, technical facility in clinical application is attained with every expectation of maximizing successful outcomes. There exists an interplay between technique and clinical experience whereby good technique impacts clinical experience and vice versa. Undeniably, experience cannot be adequately transmitted through the generation of even the best written manuscript. On the other hand, the hard-earned hindsight that experience provides and which alters the basic procedure is teachable as technique. The technique presented here is tempered with our idiosyncratic experience to which, it is hoped, the future practitioner will add their own.

RELEVANT ANATOMY AND THE IDET PROCEDURE Intradiscal electrothermal therapy entails the threading of a blunttipped thermal catheter through the disc with the goal of traversing the entire posterior anulus midway between endplates. Various aspects of the anatomy of the normal and degenerative disc conspire against the physician attempting to do so. There are small regional variations in disc structure due to the different demands placed upon them in the cervical, thoracic, and lumbar spine. As the main target of the IDET procedure, the lumbar disc will be the focus of discussion. The intervertebral discs are interposed between adjacent vertebral bodies accounting for approximately 25% of the height of the column. The three main functions of the disc are to allow movement

between spinal segments, serve as shock absorbers, and transmit the axial load of the body. The disc is composed of a tough outer anulus and a central nucleus pulposus. The nucleus is a remnant of the embryologic notochord. It is composed of semifluid ground substance and irregularly placed collagen fibers. When compressed, the gelatinous nucleus deforms and distributes load forces in all directions. The anulus is designed to contain these forces. It is composed of 10–20 fibrous lamellae arranged in concentric rings around the nucleus. Coincidental with the eccentric location of the nucleus, which is closer to the posterior anulus, there is a reduction in lamellar thickness posteriorly when compared to its anterior and lateral portions. Lumbar flexion places a stress on this relatively vulnerable area. Two design features of the disc offset this weakness. First, like the lumbar vertebral bodies, the lumbar disc is kidney shaped with a slight concavity to its posterior border. This concavity increases the surface area of the posterior anulus and serves to strengthen it against distractive and compressive forces. It also increases the length the catheter must navigate as well as the acute angle of the posterolateral corners that must be negotiated to cover the posterior anulus. The passage of the catheter is more difficult as a result of increased resistance from the greater length and sharper angles. Also, this concavity must be considered when attempting to judge the proximity of the catheter to the thecal sac on a lateral fluoroscopic view prior to beginning the heating protocol. It may appear from this lateral orientation that the catheter is well contained within the substance of the anulus if its position is compared to the most dorsal extent of the vertebral body when, in fact, it has escaped at the turn around the posterolateral corner. When this transpires, the catheter will bridge the concavity of the posterior anulus instead of following its contour and, yet, appear to be safely within its confines. Secondly, each lamella consists of obliquely oriented parallel collagen fibers. The direction of this obliquity is rotated 90° in adjacent lamellae so that the fibers between any two adjacent lamellae form a rough ‘X’ shape. This configuration contributes to the integrity of the anulus under similar forces. While the majority of lamellae form complete rings around the circumference of the disc, as many as 50% of the lamellae at the posterolateral corners are incomplete.3 Where a lamella ends, the superficial and deep rings approximate or fuse together (Fig. 26.1). Advancement of the blunt catheter tip past these fusion points may account for some of the difficulty of passing around the posterolateral corner. The tip, which tracks easily between lamellae when traveling within the anulus, may be unable to penetrate the fused lamellae at the terminus of the layer it is following. Covering the entire nucleus and a portion of the annular ring is a layer of hyaline and fibrocartilage known as the vertebral endplate. It is bordered by the slightly raised perimeter of the vertebral body

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anulus that can develop into radial tears extending through the anulus to the epidural space of the spinal canal. Increasing fibrillation of the lamellae is associated with similar defects.5 Circumferential tears of the anulus are the result of splitting between lamellar layers (Fig. 26.2). Fibrotic change within the disc resulting from simple aging or scar formation following injury increases the possibility of obstruction to catheter passage and makes proper placement more difficult. Disruption of the lamellae with attendant loss of smooth tracking of the catheter between layers also increases the resistance to catheter passage. Defects in the nucleus and anulus may capture the advancing catheter tip and redirect it along paths of reduced resistance. These often lead to the epidural space as in complete radial tears or into dead ends such as the PLL or vertebral endplate. The physician performing the IDET procedure is, in large measure, dependent upon patient anatomy for proper catheter placement; never more so than in the degenerated disc. Strategies for dealing with these problems are discussed below.

Discontinuous lamella Indistinct annular–nuclear border

Superior articular processes

Spinous Fig. 26.1 Illustration of process normal lumbar disc.

called the ring apophysis. The endplate is securely attached to the disc with the fibers of the inner lamellae being continuous with the fibrocartilage of the endplate. In contrast, the outer annular fibers attach directly to the bony ring apophysis of the vertebral body and serve as the main ligamentous connection between segments. This function is aided by the anterior and posterior longitudinal ligaments (PLL). The PLL is intimately connected to the posterior anulus and serves to separate it from the dural sac. Both PLL and outer anulus are richly supplied with nerve fibers and are common tissue sources of back pain. With aging, the water content of the disc diminishes and the disc becomes more fibrous. Collagen content of both the nucleus and anulus increases4 and the disc becomes increasingly less pliant as a result. The inner anulus expands at the expense of the nucleus and the boundary between them becomes less distinct. With dehydration the nucleus becomes less able to transmit forces equally and certain sections of anulus are subjected to disproportionately greater axial loads. Defects occur at the transition zone between the nucleus and Annular tears – radial – circumferential

Very indistinct annular–nuclear border

PATIENT SELECTION The suitable candidate for IDET is a patient with a confirmed discogenic source of back pain without predominant leg symptoms unresponsive to aggressive conservative care including medications, activity modification, injection therapy, and an exercise program (Table 26.1). The need to deliver these treatments thoroughly and with expertise prior to considering IDET cannot be overemphasized. If the judgment has been made that there has been failure to progress, standing X-ray and recent magnetic resonance imaging (MRI) of the lumbosacral spine is required. Acceptable abnormalities for the performance of IDET may include disc space narrowing, disc desiccation and degeneration, or a small, contained disc protrusion. The presence of a high-intensity zone lesion does not preclude employing IDET. These images should also be scrutinized for abnormalities that could lead to the prohibition of the performance of IDET. Higher grade (II–IV) spondylolisthesis, especially isthmic and traumatic cases, will require flexion and extension plain views to rule out instability in the motion segment. Spondylolisthesis also increases the importance of ruling out nondiscogenic causes of axial low back pain. Pain greater with extension versus flexion of the spine with findings on imaging of central canal encroachment or fluid-filled zygapophy-

Table 26.1: IDET Criteria INCLUSION Axial back pain > leg pain (no pain below knee) 6-month failure to respond to conservative care (PT, NSAIDs/analgesic meds, epidural injections, activity/lifestyle modification) Confirmed discogenic source of pain (discogram positive for concordant pain at low pressure and volume)

Protrusion Osteophyte

EXCLUSION

Fig. 26.2 Illustration of degenerative disc with disruption of annular fibers. 304

Disc height < 50% at symptomatic level Large (>5 mm) disc protrusion Severe central canal stenosis Pars fracture High grade (II–IV) spondylolisthesis Lack of annular disruption on discogram at symptomatic level in presence of Schmorl’s node

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seal joints could support the diagnosis of stenosis and facet arthropathy, respectively. A positive discogram without evidence of annular disruption in the presence of a prominent Schmorl’s node may point to the node as the pain generator rather than the anulus. Short of a radical placement of the IDET catheter tip in the node itself, conventional IDET is not indicated. Performing the high heat protocol with a standard catheter placement within the anulus has been shown in a histologic study not to affect the adjacent endplate.1 Fractures of the pars, significant central canal stenosis, large disc protrusions (>5 mm extrusion beyond the posterior border of the vertebral body), extrusions, and sequestered fragments are all relative contraindications for the procedure. Patients with prior history of fusion who return with adjacent symptomatic discs or those with multiple symptomatic levels may be suitable candidates (Table 26.2). In experience of the authors, patients tolerate single-visit, three-level IDETs without prolongation of the recovery period. Patients who have had prior partial discectomy and fusion may also be candidates though the fusion mass or instrumentation may prevent an acceptable approach to the disc. Similarly, prior chemonucleolysis, laser decompression, or nucleoplasty at the symptomatic level does not preclude IDET as long as other inclusion criteria, especially adequate preservation of disc height, are present. These intradiscal procedures may increase annular fibrosus with consequent difficulty of catheter placement. A repeat IDET procedure on the same disc may be considered in certain cases. Patients who initially respond with greater than 50% relief, but then have return of similar axial low back pain or those whose lack of response is felt to be due to less than ideal catheter placement may benefit from a second IDET at the same level. With increased experience in performing the procedure, the surgeon finds fewer patients filling the latter category. Further studies are needed to judge the efficacy of repeat procedures, but in the authors’ limited experience, selected patients often experience clinically significant decreases in symptoms. Six months postprocedure is the minimum period required to judge clinical outcome and is necessary prior to consideration of a repeat IDET. The symptomatic disc should have preserved disc height >50% with reproduction of concordant pain at low pressure and volume on provocative discography. Postdiscography CT reveals an abnormal discogram with disc disruption associated with a radial tear extending to the outer anulus (see Fig. 26.13A below). Extravasation of contrast dye into the extra-annular space indicating full-thickness annular disruption is not uncommon and is not a contraindication for IDET. Patient selection should not rely solely on the results of the

Table 26.2: IDET Potential Indications SYMPTOMATIC LEVEL With <5 mm disc protrusion With/without high-intensity zone With/without Grade V annular disruption (extravasation of contrast beyond anulus) Status post: Percutaneous disc decompression (chemonucleolysis, laser decompression, nucleoplasty) Discectomy Instrumented/noninstrumented fusion IDET MULTIPLE SYMPTOMATIC LEVELS

discogram. Discography is just one step in the evaluative process and invariably follows a thorough history and physical exam after failure to improve with rehabilitation measures. In general, IDET should be considered in patients in whom fusion is to be avoided. The procedure fills a notable gap in the treatment of discogenic low back pain between nonoperative care outlined above and spinal fusion. Further clinical studies are needed to better define the exact patient subsets that are responsive to IDET.

Informed consent A knowledgeable patient serves as a clinical ally. Carefully explaining the procedure, its indications, risks and potential benefits can increase the percentage of successful outcomes and patient satisfaction. The patient’s expectation of a ‘cure’ for back pain must be tempered with information about the natural history of low back pain unresponsive to rehabilitation measures. Symptomatic relief should be the stated clinical goal. The postoperative recovery period including a timeline for the use of a lumbosacral orthosis, progressive advancement of functional activities and a physical therapy program should be reviewed in detail. It is necessary to describe to the patient potential complications including infection and nerve injury. Reassurances may be given that, by all reports, complication rates are very low.6 Saal and Saal reported no adverse events in their prospective uncontrolled study of 62 patients.7 A 2-year follow-up study by Lee of 62 patients reported no complications.8 There are anecdotal reports of bacterial discitis, thermal root injury, and catheter breakage due to kinking. One case report documents a catheter misplacement within the spinal canal resulting in cauda equina syndrome.9 Measures used to prevent these complications include sterile technique, antibiotic prophylaxis, avoidance of oversedation during the procedure, and a graduated heating protocol. Bleeding is also a concern which is addressed with documenting a normal coagulation parameters prior to the procedure. Reviewing, along with the patient, the clinical indication for the procedure is helpful. As with any surgical procedure, the first step toward a successful outcome is meticulous attention to patient selection and their expected outcome.

PREOPERATIVE PREPARATION The patient should be instructed to stop all nonsteroidal antiinflammatory drugs (NSAIDs) and aspirin-containing compounds 1 week prior to the procedure. The use of anticoagulant medications must be stopped prior to the performance of IDET. An exception is the prophylactic use of 81 mg of aspirin daily in high-risk cardiac patients where the risk of a cardiac event is considered to be greater than the risk of bleeding. Whether the risk of discontinuation of these agents is worth the potential benefit of the procedure is a decision that requires input from the physician managing the relevant medical problem, the surgeon planning to perform IDET, and the patient. In general, when a decision has been made to proceed, the patient is instructed to stop coumadin, antiplatelet drugs such as clopidogrel, and aspirin 5 days prior and nonselective NSAIDs including COX2 selective drugs 48 hours prior to the procedure. Low molecular weight heparins such as enoxaparin need to be discontinued 24 hours prior. An INR of 1.1 or less and a platelet count of greater than 50 000 should be documented in the chart on the day of the procedure. Bleeding times for chronic antiplatelet medication use are advisable. Medications that treat hypertension, diabetes, and cardiac disease may be taken on the day of the procedure. Comorbid medical conditions must be under acceptable control. Acute infections of any type are a contraindication to the procedure. 305

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Allergies to iodine or latex should be clearly marked on the chart so that gadolinium10 and latex free gloves and syringes can be used, respectively. The patient is allowed liquids but no solid food on the day of the procedure. The use of sedative medications precludes driving until the day following the procedure. Arrangements should be made for a relative or friend to accompany the patient to and from the hospital.

Equipment and set-up The following is a list of the necessary set-up and equipment prior to performing an intradiscal electrothermal procedure: ● ● ● ● ● ● ● ●

Skin marker; Radiopaque straight edge; Sterile drapes and preparation materials; 1% lidocaine 27-gauge 1.5˝/ 25-gauge 2.5˝ needles for local anesthesia; #11 scalpel; Gen II 6˝ 17-gauge introducer with gray hub × 4; SpineCATH × 4. Or:

● ● ● ●

Gen II 9˝ 17-gauge introducer with black hub × 4; SpineCATH XL × 4; Sterile connector cables for SpineCATH; Smith + Nephew Ora-50™ S Electrothermal Spine Generator. Or:

●

Smith + Nephew 20S Spine Generator.

Side of approach Immediately prior to the procedure, the postdiscography CT scans, MRI, and standing radiographs of the spine should be reviewed. Special attention should be paid to the number of lumbar segments and the presence of any congenital anomaly of the lumbosacral spine which may lead to misplacement of the introducer needle. Placement and configuration of suspected symptomatic annular tears should be noted and used to decide the side of approach to optimize catheter coverage of these areas. While covering the entire posterior anulus is optimal, often, for various reasons which will be discussed, this is not possible. In these cases, it is the authors’ experience that placing the catheter across the suspected lesion in the outermost reaches of the involved anulus provides the best results. In the majority of patients, the initial approach is from the contralateral side of such a lesion. Entering on the same side as a posterolateral radial tear means having to traverse the longest possible route through the disc to reach the suspected area. Satisfactory catheter placement over such a long distance can be difficult. However, in some patients whose discograms clearly show a large radial annular tear, the ipsilateral approach may be preferred. In these cases, the contralateral approach will often result in the catheter escaping through the annular defect. If multiple levels are to be treated, the choice of approach is considered for each level. Unlike discography, there need be little concern for avoiding an approach from the side of symptomatic pain. Catheter placement across the entire posterior anulus of the symptomatic level is the goal of the procedure. Ideally, this is accomplished from a unilateral approach. However, there are numerous situations that may require a bilateral approach to achieve this goal. Large tears can easily grab the catheter tip and redirect it along the line of tear. Major disruption of the posterior anulus can result in repeated failure to contain the catheter within the annular space. Fibrotic scarring due to advanced degeneration may obstruct catheter passage. 306

Annular septums that prevent advancement across the midline are believed to occur in numerous cases. Redirecting the catheter and/ or repositioning of the introducer may allow the operator to ‘drive’ around these obstacles. If not, a two-step procedure using a bilateral approach may be necessary and may be performed without interruption of the procedure as discussed below.

PATIENT POSITION AND MARKING THE SKIN Prone positioning is preferred to allow access to both sides of the spine if so needed. A pillow is placed under the belly of the patient to reduce lumbar lordosis and facilitate a clear approach to lower lumbar segments. The patient is placed on the table so that the chosen side of approach is away from the physician. This is done so that the camera is not interposed between the physician and the operative field. A change of approach mid-procedure will result in this awkward positioning which is dealt with by moving the camera in and out to adjust the needles. After the patient has been placed prone on the table, anteroposterior (AP) scout fluoroscopic views are taken to confirm the target level. Wide views to include T12 may be needed to count down to the correct interspace. Cross-table lateral views can also be helpful, especially if there is a pronounced lordosis. Once the target level is in view, it is necessary to ‘square up’ the angle of view with the interspace. The inferior endplate at the target level should be seen on end so that it appears as a thin horizontal line. The camera is tilted toward the head (‘cephalic tilt’) to align the proximal and distal edges of the endplate to obtain this view. The amount of tilt will be greater with lower levels and increasing lordotic curve. A radiopaque straight edge is then laid on top of the inferior endplate and a line is drawn across both sides of the back (Fig. 26.3). This will facilitate contralateral introducer placement and cut down

Fig. 26.3 AP fluoroscopic view of straight edge across inferior endplate of L5 vertebral body.

Section 2: Interventional Spine Techniques

Fig. 26.4 Oblique fluoroscopic view showing ‘Scotty Dog’ appearance of lumbar posterior elements with radiopaque marker ventral to L5 SAP.

Fig. 26.5 Oblique fluoroscopic view of introducer ventral to L5 SAP. Note radiolucent triangle formed by superior articular process of S1, the inferior endplate of L5, and the iliac crest.

on fluoroscopic exposure should a bilateral approach become necessary. Next, the camera is tilted towards the side of approach to obtain oblique views of the spine showing the classic ‘Scotty Dog’ appearance of the facet joints, pedicle, and transverse process. The camera is rotated until the superior articular process (SAP), the ‘ear’ of the dog, is approximately in the middle of the disc space (Fig. 26.4). At the L5–S1 level, the iliac crest will be obstructing the approach to the disc in this view. To open up a window, the camera needs to be rotated back towards the AP view and/or tilted in a cephalic direction until an upside-down radiolucent triangle appears composed of the edges of the superior endplate, the SAP, and the iliac crest (Fig. 26.5). The skin is marked slightly lateral to the SAP in the oblique view. Marking immediately lateral to it may prevent adequate medial placement of the introducer within the disc. This difficulty can be reduced by aligning the SAP within the middle of the disc on the oblique view. It will be noted that the skin markings for L4–5 and L5–S1, when approaching from the same side, will often be within a few centimeters or less of each other. Indeed, it is sometimes possible to use a single puncture to approach both levels. The economy of this approach, however, must not be chosen if it will compromise optimal placement of the introducer as this is the key to a successful approach to the difficult L5–S1 disc.

surgical field. Should a change in the side of approach become necessary, the wide placement of the under-drapes allows easy exposure of the opposite side by simply moving the over-drape. Prior to covering the patient with the over-drape, a grounding pad is placed on the thigh. The chosen site should be cleaned with alcohol to ensure good contact between skin and pad. Patients with abundant body hair may need to have the grounding site shaved. The head of the C-arm and the side of the table are also draped to prevent contamination of the surgical field with cross-table lateral positioning of the camera. The patient is now given mild i.v. sedation. The choice of medications should be those the anesthesiologist is comfortable using and invariably include midazolam and, often, propofol. General anesthesia is contraindicated and not given under any circumstances. It is an essential safeguard of the procedure that the patient be able to self-monitor for and report signs of nerve root irritation. During the course of the procedure, i.v. fentanyl may be used for analgesia as needed. The skin is anesthetized using a short-acting amide local anesthetic such as lidocaine. The bevel of a 27-gauge needle is inserted in the epidermis and approximately 0.5 cc of 1% lidocaine is injected to raise a small weal. Using the needle in a ‘down-the-tube’ approach following the angle of the camera to the target, several milliliters are used to anesthetize the dermis. A longer, 3.5˝, 25-gauge needle can then be used to anesthetize the deeper fascia and muscle tissue down to the level of the superior articular process (SAP). Care must be taken in especially thin patients in whom the neuroforamen may be reached by a 2.5˝ needle not to anesthetize the exiting nerve root or spinal nerve. This is avoided by touching down on the SAP as opposed to placing the needle tip lateral to it. Several milliliters of local anesthesia are injected with the needle at its full depth and several more may be used as it is slowly withdrawn. Clinical experience has shown that the application of generous amounts of local anesthetic (4–6 mL of 1% lidocaine) to the paraspinal tissues makes passage of the larger introducer needles much more comfortable, thereby reducing the need for excessive intravenous sedation.

PATIENT PREP, SEDATION, AND ANESTHESIA The patient should be prepped and draped in sterile fashion. Both sides of the patient’s back around the line marked through the inferior endplate should be cleaned with three passes of a betadine sponge. Small under-drapes are placed to form a rectangular operative field so that there is an adequate window of access to both sides of the back. The larger over-drape contains a smaller, precut rectangle which should be positioned so that the marked approach is centered in the

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PLACING THE INTRODUCER The introducer comes in either a beveled or diamond-shaped tip. An arrow on the hub indicates the face of the bevel. The diamondshaped tip (Gen II – Smith & Nephew/Oratec) was developed out of concern that the bevel tip (Gen I) increased the risk of spinal nerve damage (Fig. 26.6). Both are 17-gauge with a screw-in stylet and come in 6˝ and 9˝ sizes. The larger size is designed for use with an extra-long catheter. Making a slight bend in the needle increases the ability to direct or ‘drive’ it into the optimum location in the disc. This is done by holding the introducer with a gauze 4 × 4 with the forefinger behind the tip and the thumb below it on the shaft. Pressing gently but firmly with the thumb will bend the tip slightly upwards. The direction of bend should be toward the arrow on the introducer hub. With the bend, the stylet should still be able to be removed without difficulty. A number 11 scalpel is used with a short stab over the skin mark to facilitate passing the introducer through the tough epidermis without undue force. The introducer is also inserted along the angle of the camera with the bend facing the patient’s midline. The larger gauge of the introducer allows a greater feel of the tissues it passes through. The operator will be able to clearly identify dermis, subcutaneous fat, fascia, and muscle. Using the oblique fluoroscopic view as a guide, the introducer is aimed at the SAP. To avoid the exiting spinal nerve which

Fig. 26.6 Photo of SpineCATH, top, with Gen II 17-gauge introducer needle and screw-in stylet, bottom.

A

B

passes laterally in oblique fashion across the superior endplate and disc, the introducer should hug the SAP’s ventral edge in order to stay medial to the nerve. To accomplish this, the needle is advanced until it gently touches down on bone. By withdrawing slightly, rotating 180° in a caudal direction away from the exiting nerve root so that the bend faces away from the spine, and readvancing, the tip can be made to slide off the ventral edge. Once it has cleared the SAP, the introducer is rotated back, again in a caudal direction, completing a turn around the facet joint (see Fig. 26.5). It is important to always rotate the needle in a caudal direction to minimize the chance of contact with the exiting nerve root. Before advancing the introducer, the placement must be checked on an AP view. The tip should be seen lateral to the medial border of the inferior pedicle. Otherwise, there is danger of puncturing the thecal sac. If it does so, withdrawal and lateral redirection are necessary. A cross-table, lateral, view is checked next for cephalocaudad orientation. The alignment of the introducer should be parallel to the disc space. Any deviation from the midpoint between the two endplates is noted and corrected as the introducer is advanced using the lateral view. At this point in the procedure, the patient should be awake and alert for any symptoms of nerve root irritation. A 17gauge needle can, obviously, be injurious to the anulus and exiting nerve root. Proper alignment of the introducer prior to entering the disc will minimize the chance of nerve injury as well as the need for multiple passes through the anulus. As the tip contacts the posterior anulus, resistance to advancement will increase slightly, together with a ‘gummy’ feel indicating penetration into annular fibers. The patient may experience discomfort or pain in the form of deep localized axial back pain as the anulus is breached and this reaction can be taken as confirmatory. Reports of sharp leg pain below the knee indicates close proximity to the exiting spinal nerve. This is more likely to occur with superolateral positioning of the tip on its approach. The introducer should be withdrawn and redirected in a medial and/or inferior manner before further advancement. From this point, AP and lateral fluoroscopic views are checked frequently while advancing into the nucleus of the disc. Unlike standard discographic technique, the tip of the introducer should be placed slightly more anterior and off center so that it lies within the ipsilateral anterior quadrant of the disc. Optimal positioning will be seen as tip placement just lateral to the midline of the disc on AP and

C

Axial

Fig. 26.7 AP and lateral fluoroscopic views of correct needle position within disc (A,B). Illustration showing correct positioning of the tip in the ipsilateral anterior quadrant of the disc (C). 308

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approximately three-fourths of the way across the diameter of the disc on lateral views (Fig. 26.7). This will allow for the passage of the catheter into the mid- to outer annular rings. Correct introducer placement is one of the keys to the IDET procedure. All subsequent steps in the procedure will be affected by it. Suboptimal positioning of the introducer leads to suboptimal catheter positioning. Taking the time to place the introducer correctly will be rewarded by increasing the chance of a successful outcome. Placement at the L5–S1 level is complicated by the intervening iliac crest. Advancing the introducer between the crest, SAP, and inferior endplate requires a steeper cephalocaudal angle with lesser angulation away from the sagittal midline than at more superior levels. The net result is increased difficulty securing adequate medial positioning within the disc. Increasing the bend placed in the needle will help. Once the tip is past the SAP, the needle is rotated so that the bend curves medially. Marking the skin as lateral from the SAP as the confines of the radiolucent triangle will also facilitate greater medial placement. In addition, the steepness of the approach limits the window for passage into the outer anulus between the endplates. Osteophytic spurs of the endplates or hypertrophy of the ring apophysis have greater potential to obstruct advancement. Again, the bend in the needle is used to navigate around them. Often, rotation to take advantage of the bend along with leverage applied to the heavy-gauge needle will enable the tip to glance off a bony prominence. Make sure the bevel opening of the needle is facing posteriorly within the plane of the disc by turning the arrow on the needle hub. Once optimal positioning is achieved, unscrew and remove the stylet in preparation for placing the catheter.

THREADING THE CATHETER The SpineCath (Smith & Nephew/Oratec) comes in two sizes (SpineCATH, SpineCATH XL). Both have working distal lengths of 5˝. The proximal portion is either 6.8˝ or 9.8˝ for overall lengths of 11.8˝ (30 cm) for the SpineCATH and 14.8˝ chest (37.5 cm) for the SpineCATH XL. The SpineCATH XL used with the corresponding Gen II XL introducer can be very helpful in larger patients. The longer catheter and introducer are distinguished by their black hubs. Both versions have a plastic-coated wire core which serves as the heating element and which is surrounded by insulation proximal to the distal heating coil. The width of the working portion is 0.038˝ (approximately 1 mm). The distal heating coil is marked by radiopaque marks 2.2˝ (5.5 cm) apart. Prior to performing the heating protocol, both marks must be clearly seen on the fluoroscope distal to the end of the introducer to avoid heating the introducer and damaging the tissue through which it passes. There are hash marks on the proximal portion of the catheter, approximately a centimeter apart, two of which are thicker than the others and mark the points at which the radiopaque marks emerge from the tip of the introducer. These hash marks should not be used, however, in lieu of fluoroscopic visualization to determine when the radiopaque marks of the heating coil are safely out of the introducer. Before using the SpineCATH, it should be tested to ensure that it is functional. On the sterile field, connect the catheter to its cable so that the white stripe on the hub aligns with the white dot on the cable plug. There will be an audible click when the cable plug is correctly inserted into the catheter hub. The other end of the cable is handed off the sterile field and plugged into the generator. Make sure the generator is plugged in and the power is turned on using the On/Off switch on the rear panel. The thumbwheel on the rear panel needs to be set on 2 for SpineCATH procedures. (The 20S generator designed to replace the 50S has probe recognition and setting the thumbwheel is not needed [Fig. 26.8]). Check that the Actual

Fig. 26.8 The 20S Electrothermal Generator with catheter attached.

Temperature is recording the temperature of room air (18–26°). The impedance should be between 85 and 230 ohms. Disconnect the catheter from its cable before placing it in the introducer. Both versions of the SpineCATH have an angled tip to facilitate driving within the disc. The direction of the angle corresponds to a white stripe on the long axis of the hub. The hub may be used to facilitate rotation of the catheter tip. It should not be used to advance the catheter. Holding the catheter by the proximal shaft when advancing limits the amount of traction that may be developed and decreases the incidence of kinking. The catheter is inserted into the introducer with the white stripe facing the patient’s spine. Initial AP views are best to show the catheter advancing towards the contralateral anterior anulus before turning posteriorly with the contour of the disc. It is important to make sure that the tip of the catheter exits the introducer in a manner that is parallel to the disc space (Fig. 26.9). Once tracks are made in the anulus, the catheter will follow the path of least resistance so that redirecting the catheter that is heading towards the endplate will be difficult. Any deviation of the catheter in a cephalic or caudal direction may be adjusted with rotation of the white stripe on the hub in the appropriate direction. Advancing the catheter is a slow, gentle process accomplished in 1 cm increments with repeated fluoroscopic images to check the progress. As the catheter passes the anterolateral corner, the direction of advance will be more or less ‘head-on’ into the camera on an AP view. Switching to a cross-table lateral view will be more helpful in showing the progress of the catheter through the disc. Similarly, returning to an AP view as the catheter passes the posterolateral corner will provide a better view of catheter advancement. With greater experience, the catheter may be safely advanced mostly by feel, reducing the number of camera angles needed. Otherwise, it is important to maintain a clear view of the catheter tip as it moves through the disc. Again, holding the catheter by the proximal shaft as it is advanced will increase sensitivity to changes in resistance to catheter passage and reduce the incidence of kinking when obstacles are encountered. A kink is a permanent bend in the shaft of the catheter (see Fig. 26.15A below). Kinks result from continued force against resistance preventing catheter advancement. Any change in resistance should prompt a fluoroscopic view in several planes to adequately assess the advancement and position of the tip. Bowing of the catheter may occur parallel to the needle and is poorly visualized on a single plane. 309

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A

B

Typical locations of increased resistance within the disc include the posterolateral corner, the posterior midline, and sites of annular tears. Loss of resistance usually indicates escape of the catheter tip into the extra-annular or epidural space (Fig. 26.10). This occurs in excessively degenerated discs where the general integrity of the anulus is compromised. Focal annular tears can serve as paths of least resistance and may redirect the catheter along the lesion into inappropriate areas. Obstacles include the superior and inferior endplates, the anterior and posterior longitudinal ligaments, and scar tissue within the disc. When meeting increased resistance, the initial strategy to avoid kinking the catheter will be a gentle rotation of the catheter back and forth a few degrees while advancing a few millimeters. This maneuver should be followed with a fluoroscopic view to check for tip advancement even if there is little resistance. Should there be no advancement or if continued resistance is encountered, needle repositioning will be required. Repositioning the needle involves withdrawing the catheter, rotating the tip, and readvancing. Unfortunately, the ability to drive the catheter within the disc is limited due to the confined space inside the disc, disc anatomy, and equipment design. The blunt catheter tip has limited ability to puncture the anulus and most often follows the nuclear/annular interface. The tougher anulus deflects and serves to guide the catheter along this interface. Where the anulus is discontinuous due to defects such as radial tears, it loses this guide function, allowing the catheter, as mentioned, to track along paths of lesser resistance. It is quite common, for example, for a radial tear to catch the catheter and direct it external to the anulus or into the PLL, especially when the approaching tip forms an obtuse angle with the tear. The nature of the disc space limits the ability to drive around these points in cephalocaudal directions as it is most limited in this plane. Changing the catheter’s position in the AP plane is, generally, more productive. To accomplish this usually involves a considerable withdrawal of several centimeters or complete retraction of the tip back within the introducer followed by rotation and readvancement. Failing this, it may be necessary to change the point of attack of the tip on the annular/nuclear interface by repositioning the introducer within the disc. In general terms, retracting the introducer towards the center of the disc will cause the catheter to travel a smaller diameter whereas advancing it away from the disc center will create a path 310

Fig. 26.9 AP fluoroscopic view of catheter advancement. Proximal radiopaque mark is still within the introducer (A) and exited (B).

of larger diameter. Despite these maneuvers, it may be impossible to correct the catheter position or bypass an obstacle. Prior to abandoning an approach, if the catheter is judged to be safely positioned within a portion of the posterior anulus, a heating protocol may be performed. (Care must be taken to make sure that both radiopaque marks have exited the introducer.) The benefit of heating before trying a contralateral approach is twofold. First, this portion of the anulus may not be accessible from the contralateral side and, second, following heating, the surgeon may find that the catheter can be successfully advanced, thus obviating the need for the contralateral approach. Several unsuccessful attempts to traverse such an obstacle should prompt consideration of a 180° change in the direction of the catheter’s advancement. Most commonly this is done by changing the side of approach to the disc. Having prepped the contralateral side prior to beginning the procedure will facilitate this change by simply moving the sterile drapes to frame the new operative field. Locate the new entry site by measuring a similar distance from the midline as that of the initial approach along the horizontal line through the inferior endplate drawn at the beginning of the procedure. The introducer is guided through the anulus on the opposite side and into the nucleus. As mentioned, the camera will come between the physician and the operative field when obliqued to view the extrapedicular approach. Moving the camera in and out to allow needle adjustments may be necessary. The catheter is then inserted and advanced in the opposite direction along the posterior anulus. Although changing the side of approach is the most common method, there are case reports of the so-called ‘pig-tail’ technique in which a 180° redirection of the catheter is done without moving the introducer.11 The catheter is made to turn in a sharply acute angle when exiting the introducer so that it doubles back and advances in the opposite direction. The sharp turn out of the introducer gives a curled appearance reminiscent of a pig’s tail, prompting the name. This technique has the advantage of preserving a unilateral approach and avoiding the necessity of a double puncture of the posterior anulus. The acute angle between the catheter and introducer may, however, create a problem with catheter removal with increased risk for catheter shearing. Concern over these potential complications limit the use of the technique, especially in inexperienced hands.

Section 2: Interventional Spine Techniques

Fig. 26.10 Lateral fluoroscopic view of catheter tip beyond posterior border of epidural space.

Optimal placement of the catheter is obtained when its position is deemed adequate on two planes of view, the AP and lateral. A specialized view that somewhat replicates the axial view of the disc seen on a standard CT of the spine is obtained with extreme caudal tilt of the fluoroscopy camera. The truest axial views are seen at the lowest lumbar segments with this technique. Known as the ‘CT view,’ it is

LEFT

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A

helpful in defining the extent of circumferential coverage of the anulus. The heating coil, bounded by the distal and proximal radiopaque marks, should be seen to traverse the posterior anulus and its two posterolateral corners (Fig. 26.11). Postdiscography CTs of the target disc are helpful when assessing catheter position and should be available for review during the procedure. Lateral fluoroscopic views may show the catheter to be dorsal to the posterior edge of the vertebral bodies, raising concern for epidural placement. Lateral CTs, by showing the extent of disc bulging, can confirm safe placement within the disc. X-ray exposures of the cross-table fluoroscopic view can help to assess the location of a poorly visualized catheter and rule out placement in the epidural space (Fig. 26.12). Axial CTs may be consulted when considering placement across radial tears, especially in the hard to reach far lateral corners of the posterior anulus. If the heating coil of the catheter cannot be placed to cover the entire posterior anulus, yet covers a significant portion, consideration should be given to performing the heating protocol with the catheter in place prior to withdrawing and using a bilateral approach. With the catheter in place, preparation is made for the delivery of thermal energy. The generator (model Ora-50™ S) is turned on. The AutoTemp mode is used if the generator is so equipped (AutoTemp label will be seen in the center of the generator faceplate). If not, the Temperature Control mode is used. The mode button is pressed once for AutoTemp mode and twice for Temperature Control mode. In the AutoTemp mode, the Set Power button will display P90, indicating a peak temperature of 90°C. Peak temperature can be adjusted to 80, 85, or 90 degrees (P80, P85, or P90) using the Set Power button. All the heating protocols start at 65°C and increase 1 degree every 30 seconds until the maximum temperature is reached. The maximum temperature is sustained for 4–6 minutes. Lower heat protocols reach the maximum temperature sooner and are shorter in duration. The P90 protocol lasts 17 minutes. The cable is reattached to the hub of the catheter. It is important to check that both radiopaque marks are clearly outside the introducer. Check that impedance is in the normal range (85–230 ohms) indicating that the power circuit is complete. Impedance should be checked periodically during the procedure. Pressing the RF button once or, if using a foot pedal, stepping on the pedal once will initiate the delivery of energy and commence

B

Fig. 26.11 AP (A) and CT scan (B) fluoroscopic views of intradiscal catheter placement at L4–5 showing optimal coverage of the posterior anulus on CT view (B). 311

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Fig. 26.12 Lateral X-ray exposure view showing catheter tip beyond posterior border of vertebral body.

eter hub. First the catheter is removed, followed by the introducer. The technique for removal is a back and forth rotation of the catheter as it is retracted through the introducer (‘a lot of wiggle with a little pull’). Resistance to retraction of the catheter may indicate the needle biting into the catheter. To avoid shearing the catheter, it should be advanced a centimeter, rotated, and then gently withdrawn. Continuing resistance will require removing the catheter and introducer as a single unit. The special case of a catheter kink causes concern due to weakening of the catheter at the kinked section. Further advancement or manipulation of the kinked catheter is ill-advised. Careful withdrawal of the catheter from the disc is indicated. Prior to withdrawal, a heating protocol may be performed without further damage to the integrity of the catheter if it is deemed to be in an acceptable treatment position. When treating with a kinked catheter, it is necessary to verify catheter function by confirming normal ranges for Impedence and Actual Temperature readings. To withdraw a kinked catheter, the introducer tip should be carefully retracted a few millimeters while ensuring that the tip remains in the disc. This is followed by cautious withdrawal of the catheter. Stop immediately if any resistance is felt. If there is resistance on withdrawal, the introducer and catheter should be withdrawn as a unit. Using excessive force on withdrawal or continued manipulation may sever the catheter within the disc. At the conclusion of the procedure, sterile compression dressings should be placed over the entry site. The patient is discharged home accompanied by a friend or family member following a period of postprocedure observation.

POSTPROCEDURE the heating protocol. The generator will emit an audible tone and a blue light on the panel will light when thermal energy is delivered. It is good practice to note that Actual Temperature readings coincide with Set Temperatures. Temperature may be adjusted using the Set Temperature buttons. Note that the temperature cannot exceed peak temperature. During the procedure, the patient should be monitored for pain. It is extremely important that the patient be alert and able to selfmonitor for signs of nerve root irritation during the procedure. General anesthesia is contraindicated. It is expected that the procedure will reproduce familiar axial back pain. Severe back pain or pain radiating into the lower extremity may indicate dangerously high temperatures in the outer wall of the anulus adjacent to the thecal sac and/or nerve root. Generally speaking, tolerable back pain with radiation into the buttock and thigh but not below the knee is of little concern. Pain radiating below the knee is a sign of nerve root or cauda equina injury and will require reducing the set temperature or repositioning the catheter. The patient should be instructed, when questioned, on the importance of making this distinction between above and below the knee prior to the procedure. Do not attempt to move the catheter in any direction while RF energy is being delivered. In the event of severe pain or signs of nerve root irritation, the heating protocol should be stopped immediately. Pressing the RF button or stepping on the pedal once will pause the delivery of energy. The catheter should be repositioned before resuming the procedure. If symptoms of nerve root irritation persist, repositioning by changing the side of approach can be trie d if not already attempted. Otherwise, the procedure should be abandoned. At the conclusion of the heating protocol, the generator will cease emitting sound and the blue light will go out, indicating cessation of energy delivery. The cable is disconnected from the cath312

Many patients will experience an increase in their typical back pain following the procedure. NSAIDs and mild opiates (hydrocodone) are used for symptomatic relief. This procedure-related discomfort subsides over the course of several days to a week with most patients returning to their typical level of symptoms by the end of the first or second week. Generally, symptom improvement is gradual and occurs over the course of 3–5 months. Preparing the patient for an extended recovery period prior to the procedure will help the patient to remain calm and optimistic. A brief period (1–3 days) of bed rest is followed by relative rest in which vertical sitting or walking is limited to 10–20 minutes. Driving is not allowed in the first 48 hours. Resumption of driving begins with short rides of 20–30 minutes for the first 6 weeks. Return to work in 1 week with these restrictions is permitted for sedentary work. Recovery typically takes 6–12 weeks during which time the activity of the patient must be restricted to maximize healing in the treated disc. A corset-type lumbosacral orthosis is worn during the day for approximately the first 6 weeks to remind the patient of proper body mechanics and to limit activities and range of movement (ROM). The patient should be instructed to avoid back flexion, extension, and rotation. Lifting is limited to 10 pounds. No sports activities including running, biking, golfing, tennis, skiing, etc. are allowed in the first month. Physical therapy is not usually started before 6–8 weeks. Daily exercises initially include hamstring and piriformis stretching. Pulling the knees to the chest is done with each knee in turn as well as both together. If the patient tolerates extension and prone lying, butt/glut squeezes are performed prone over a pillow. Progression to stabilization exercises includes proper pelvic bracing while performing ‘dying bug’ and ‘superman’ routines, abdominal curls, and wall slides. Patients are encouraged to begin a graduated walking pro-

Section 2: Interventional Spine Techniques

gram. Backstroke-only swimming and standard stationary bike riding are also permitted. The patient is graduated to advanced stabilization exercises for the back and progressive resistance exercises for the limbs 3–4 months postoperatively. Resumption of athletic pursuits begins 4–6 months postoperatively and is graduated on an individual basis.

Case history 1 A 29-year-old man developed chronic bilateral axial low back pain following a rear-end auto accident as the seat-belted driver. He was unable to sit or stand longer than 15 minutes and ambulated with pain. MRI showed a small (<5 mm), contained central protrusion at L5–S1 without neural compression. On physical examination there was restriction in lumbosacral range of motion with a normal neurologic examination. Provocative discography reproduced severe concordant back pain with 1 cc of contrast at 15 psi. Postdiscography CT showed a posterior midline, grade III radial tear (Fig. 26.13A). Excellent introducer placement was obtained from the right side. The catheter was directed circumferentially along the posterior anulus without obstruction or redirection. CT and lateral fluoroscopic views confirmed adequate coverage of the midline annular tear (Fig. 26.13B,C) The standard high heating protocol was performed without significant back or leg pain. At the conclusion of the procedure, the catheter and introducer were withdrawn without incident. At 9-month follow-up, the patient reported significant decreases in pain and disability with improved sitting and standing tolerances. He was able to walk without pain.

Case history 2 A 47-year-old man presented with a 7-year history of persistent left-sided axial back pain without radiation to the legs aggravated by lifting, prolonged sitting, and standing. His symptoms were unresponsive to therapeutic exercise or injections. He received only minimal relief from a combination of NSAIDs and narcotics. An MRI showed Grade I L5–S1 spondylolisthesis with high-intensity zones at the L3–4 and L4–5 discs. Reproduction of concordant pain at low

A

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pressure and volume was found at L3–4. Postdiscography CT scan revealed a left posterolateral tear extending to the outer anulus. Proper introducer needle placement was obtained using a standard extrapedicular approach from the right side. The catheter was passed circumferentially into the disc with a sudden loss of resistance after passing the left posterolateral corner. The tip of the catheter was clearly within the epidural space on lateral views, confirming the impression of catheter escape through a radial tear. Retraction and redirection of the catheter was unsuccessful in traversing the tear. The catheter was then reinserted after retraction of the introducer in an effort to bypass the tear by finding a more interior line of passage within the disc. This maneuver produced the same result. Finally, the catheter was retracted so that the tip was just contained within the posterolateral corner of the disc. The proximal radiopaque mark was concealed within the introducer in this position. The introducer was then withdrawn sufficiently to clearly reveal both marks within the disc (Fig. 26.14). A medium heating protocol was then performed beginning at 65°C and progressing to a maximum of 85°C. It was determined that a less than optimal coverage of the annular tear had been obtained from the right side and an approach from the left side was attempted. The catheter was threaded as far as the posterior midline before further advancement was met with insurmountable resistance. Repeated attempts to advance past the midline resulted in kinking of the catheter (Fig. 26.15A). Lateral fluoroscopic views appeared to show the catheter positioned just beyond the posterior border of the vertebral body (Fig. 26.15B). A heating protocol was begun cautiously. Within the first minute, the patient experienced sharp back and foot pain. The protocol was stopped and the procedure was discontinued. The catheter was removed via the introducer without incident. Following the procedure the patient reported no symptoms in the lower extremity and was discharged home after a stable neurologic exam. One month postprocedure, the patient reported a decrease in visual numeric back pain score from 8 to 2, a decrease in Roland Morris Disability score from 18 to 3, with increases in sitting, standing, and walking tolerances. He no longer required medications for pain symptoms.

C

Fig. 26.13 Case history 1. (A) Postdiscogram CT scan of L5–S1 disc showing midline posterior annular tear. (B) Lateral and (C) CT views of intradiscal catheter placement. 313

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A

B

B

References 1. Shah RV, Lutz GE, Lee J, et al. Intradiscal electrothermal therapy: a preliminary histologic study. Arch Phys Med Rehabil. 2001; 82(9):1230–1237. 2. Lee J, Lutz GE, Campbell D, et al. Stability of the lumbar spine after intradiscal electrothermal therapy. Arch Phys Med Rehabil. 2001; 82(1):120. 3. Marchand F, Ahmed AM. Investigation of the laminate structure of lumbar disc anulus fibrosus. Spine 1990; 15:402–410. 4. Adams P, Muir H. Qualitative changes with age of proteoglycans in human lumbar discs. Ann Rheum Dis 1976; 35:289–296.

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Fig. 26.14 Case history 2. Right side approach. AP and lateral (A,B, respectively) fluoroscopic views showing retraction of the introducer needle and both radiopaque marks of the catheter within the disc.

Fig. 26.15 Case history 2. Left side approach. AP fluoroscopic (A) view showing catheter tip at posterior midline with a kink in the catheter. Lateral fluoroscopic view (B) showing catheter tip extending into extra-annular space. Note the absence of clearly visible kinking on the lateral view.

7. Saal JA, Saal JS. Intradiscal electrothermal treatment for chronic discogenic low back pain: a prospective outcome study with minimum 1-year follow-up. Spine 2000; 25:2622–2675. 8. Lee M, Lutz G, Lutz C, et al. Intradiscal electrothermal therapy (IDET) for the treatment of chronic lumbar discogenic pain: a minimum 2 year clinical outcome study. Data presented at American Academy of Physical Medicine and Rehabilitation Annual Assembly, 2003, Chicago, IL. 9. Hsia AW, Isaac K, Katz JS. Cauda equina syndrome from intradiscal electrothermal therapy. Neurology 2000; 55:320.

5. Buckwalter J. Aging and degeneration of the human intervertebral disc. Spine 1995; 20:1307–1314.

10. Slipman CW, Rogers DP, Isaac Z, et al. MR lumbar discography with intradiscal gadolinium in patients with severe anaphylactoid reaction to iodinated contrast material. Pain Med 2002; 3(1):1–7.

6. Heary RF. Intradiscal electrothermal annuloplasty: The IDET Procedure. J Spinal Disord 2001; 14(4):353–360.

11. Narvani AA, Tsiridis E, Ishaque MA, et al. ‘Pig tail’ technique in intradiscal electrothermal therapy. J Spinal Disord 2003; 16(3):280–284.

PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

Technique for Chemonucleolysis of Lumbar Disc Herniation

27

Mark D. Brown

INTRODUCTION Chemonucleolysis is a method for the dissolving of displaced nucleus pulposus of the spinal intervertebral disc (Fig.27.1).1 Chymopapain, a non-specific proteoglycanase derived from the fruit of papaya plants, remains the only clinically proven substance for the purpose of treating displaced discs in humans and animals by chemonucleolysis.2 The technique of chemonucleolysis was perfected over a period of more than 40 years primarily for the use of chymopapain although other agents including the enzymes collagenase3 and chondroitinase ABC4 have been studied for this purpose.

BACKGROUND/HISTORY The non-specific proteolytic action of chymopapain is destructive to delicate microvascular tissues which can result in severe neurologic complications5 and therefore is very dangerous if injected into the wrong places in the spine. Consequently, a very specific and safe technique for injecting this enzyme into the intervertebral disc has evolved for what would seemingly be an easily performed procedure.6–8 Chymopapain not only has the potential for severe local tissue toxicity but it is also very allergenic dispite its wide use in food additives. As much as 3% of the North American population has been sensitized

Fig. 27.1 Illustration of the chemonucleolysis procedure for injecting a proteolytic enzyme into a herniated lumbar intervertebral disc. The solid arrows depict the flow enzyme. The white arrow shows the disc in the spinal canal.

to papaya enzymes. During the early clinical experience with this enzyme there were several preventable fatalities and severe neurologic complications in humans following chymopapain injection.9 Given the fact that potential catastrophic complications, such as paralysis and fatal systemic anaphylactic reaction, are preventable by adherence to a refined and proven technique for chemonucleolysist, it behoves the clinician who performs this procedure to be intimately familiar with and adhere to the technique which is described here.

INDICATONS/CONTRAINDICATIONS Patient selection is of paramount importance for the safe outcome of the chemonucleolysis procedure.10 Candidates for chemonucleolysis are otherwise healthy individuals who suffer from lumbar disc displacement causing primarily radicular pain, with or without mild to moderate neurologic deficit(s), who have not responded to an adequate course of medical rehabilitation and interventional spine treatment. Pregnant patients, children under the age of 16, those with uncontrolled medical conditions, and psychologically impaired individuals are not candidates for this procedure. It is contraindicated to inject patients with a history of allergy to papaya fruit, pervious injection with chymopapain, or with IgE antibody to chymopapain. Patients who suffer from severe and/or progressive neurological deficits or cauda equina syndrome are not candidates for chymopapain, but should be operated upon as an emergency. Relative contraindications for this procedure are patients who require large amounts of narcotic medications, morbidly obese individuals, and smokers. Recurrent disc herniations at previously operated levels should not be injected with chymopapain.11 Ideal candidates for the procedure have a one-level lumbar disc herniation primarily causing leg pain, who have not responded to 6 weeks of conservative care, which may have included one to three selective nerve root injections and who do not have any of the contraindications listed above. They are patients who are in good health or would be cleared for surgery by their internist and would likely experience some relief of pain following a surgical disc excision. Patients should be informed of the nature, benefit and risks of chemonucleolysis compared to surgical disc excision. Although chemonucleolysis fails and surgery is required in 20% of patients compared to reoperation rate of less than 10% with laminectomy, the severe complication rate is 10 times more with surgery as compared to chymopapain injection.12 Patients should be informed of the high rate of satisfactory outcomes achieved with prolonged observation and no treatment at all for proven symptomatic lumbar disc displacement.13 Chemonucleolysis with chymopain does not adversely effect the outcome from subsequent surgical disc excison.11 Confirmation of the diagnosis of proven symptomatic lumbar disc displacement should almost always be made with a good-quality magnetic resonance imaging study (MRI).14 315

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placed into the spinal canal whereas the sequestered fragment of disc is completely displaced into the spinal canal at various distances from the disc space (Fig. 27.2). Understanding the degree of disc displacement and the type of disc rupture is important in determining the potential effectiveness of the chemonucleolysis technique. For example, patients who suffer from leg pain as the result of a bulging disc are more likely to have some component of lateral recess spinal stenosis responsible for their pain, a condition that must be addressed by surgery and is not amenable to dissolution of the disc, a procedure which may actually exacerbate the condition. MRI is also very useful in determining what component of the patient’s symptoms are the result of spinal stenosis versus disc displacement, especially when viewing the T2weighted images. Herniated or prolapsed discs that are contained within an intact anulus fibrosus are the best discs to inject because the injected enzyme physically stays in the disc space. However noncontained extruded and sequestered discs are also amenable to chemonucleolysis if the injection is performed carefully. This will be addressed further in the description of the actual injection technique. Massive disc displacement with almost complete compromise of the spinal canal is not a contraindication for chemonucleolysis as long as it is not causing severe or progressive nerve injury. Additionally, central disc displacement causing primarily low back pain can be successfully managed by chemonucleolysis.17

TECHNIQUE

Fig. 27.2 Sagittal MRI views showing examples of progressively displaced intervertebral discs. Top left is a bulging disc, top right a herniated disc, bottom left is an extruded disc, and bottom right a sequestered disc fragment.

As emphasized throughout this text, it is absolutely imperative to identify a displaced disc that is compressing a spinal nerve that corresponds to the patient’s symptoms and signs. Remember that totally asymptomatic individuals may have a herniated disc on MRI.15 The use of a contrast-enhanced MRI to detect suspected intrathecal tumors or underlying disc space infections should be considered if the patient has progressive and severe night pain with sleep disturbance or if the first MRI shows abnormal signal intensities in the disc or vertebral body suspicious for infection. Careful note of the level and side of the disc herniation on the MRI scan is important and the actual MRI films should be available in the treatment suite at the time of the injection to confirm the site to be injected. The added benefit of the MRI scan availability at the time of injection is to aid the physician in the selection of the trajectory of the insertion of the needle into the proper disc space, as will be explained in the explanation of the technique later in this chapter. MRI is the only imaging technique that can distinguish among the various degrees of disc displacement,16 i.e. contained disc displacement with the anulus fibrosus intact, bulging and prolapsed discs versus noncontained discs, extruded and sequestered discs where the nucleus pulposus has displaced through the ruptured anulus fibrosus into the spinal canal. An extruded nucleus pulposus is partially dis316

Patient preparation for the procedure is important. Determination of the presence of IgE antibody to chymopapain is an important precaution to prevent injection of potentially allergic individuals.18 In North America there is a commercially available test, ChymoFast™, to determine even traces of IgE in the serum. Skin testing has not proven to be helpful in screening patients who are susceptible to an anaphylactic reaction to chymopapain.19 Pretreatment of the patients with H1 and H2 histamine receptor blockers to ameliorate the severe consequences of a systemic allergic reaction have not been proven to be effective. H1 blockers such as diphenhydramine must be given in such high doses for an extended period of time prior to exposure to antigen that the patient becomes sedated and difficult to manage as an outpatient. Administration of corticosteroids as H2 histamine blockers must be given for at least 24 hours prior to chymopapain injection and their effectiveness in preventing a full-blown anaphylactic reaction has not been proven. When given in large doses they are not without complications, such as gastrointestinal bleeding or making the patient susceptible to infection. For these reasons the author does not advocate the use of H1 and H2 blockers in preparation of the patient for chemonucleolysis with chymopapain.18 Commercially available chymopapain for injection in humans is not currently available in the United States. It is available in Europe and Australia. The drug should be available with a back-up vial in case of mishap in handling, and the expiration date of the vial should be checked prior to use. The procedure can be performed in an ambulatory surgery center, a regular operating room, or a special-procedures radiology suite. Sterile conditions, anesthesia capability, and good-quality bi-planar fluoroscopy are the minimal requirements for the procedure. Chemonucleolysis with chymopapain should be performed under local anesthesia with careful supplemental intravenous sedation so that the patient can alert the physician if the needle stimulates a spinal nerve. It has been estimated that needle penetration of a nerve occurs in 7% of patients undergoing the procedure under general

Section 2: Interventional Spine Techniques

10 cm

margin of the skin. In an individual of average size, the mark should be closer to 10 cm and in a large individual closer to 12 cm. This mark should be superior to the iliac crest (see Fig. 27.3). Prepare the skin with an antiseptic solution and drape appropriately. The previously made marks on the skin will not wash off during the preparation of the skin. Inject 1 mL of 0.5% lidocaine subcutaneously at the point of insertion of the spinal needle at the lateral mark just superior to the iliac crest. Under fluoroscopic control, insert a 15-cm in length, 18-gauge needle with stylus in place at an angle of 45° to the sagittal plane following the angle of the slope of the L5–S1 disc as previously determined on fluoroscopy and marked on the skin with the indelible pen (usually between 30° and 60° caudad) and enough superior to the iliac crest for the needle to clear it on a trajectory toward the center of the disc (Fig. 27.6). Keep the bevel of the needle pointed lateral and insert it to the posterior lateral corner of the disc with fluoroscopic guidance. Insert the needle slowly when nearing the disc to avoid injuring the exiting L5 spinal nerve just distal to the L5 pedicle. If the patient complains of nerve pain radiating down the side of the leg, back the needle out and take a slightly different trajectory to avoid the nerve (Fig. 27.7). When the tip of the 18-gauge needle reaches the posterior lateral corner of the L5–S1 disc, remove the stylus and rotate the needle so that the bevel faces the disc space and

8

anesthesia.18 Penetration of the neural elements may lead to inadvertent intrathecal injection of the enzyme where neurological damage may occur. The incidence of catastrophic neurologic complications was higher in patients undergoing the procedure under general anesthesia versus local anesthesia.18 General anesthesia masks the early symptoms of systemic allergic reaction at a time when it is critical to initiate administration of epinephrine.20 Some agents utilized in induction and maintenance of general anesthesia enhance histamine release during an anaphylactic reaction, thus making the reaction more severe.21 It is therefore important to perform the procedure under local anesthesia with the patient alert enough to relate the symptoms of a systemic allergic reaction and to warn the operator if the injection needle is touching a nerve, so that the operator can redirect it. An anesthesiologist should insert a large-bore intravenous access line and administer conscious sedation and be prepared with a syringe containing 1:200 000 dilution of epinephrine. The patient is positioned in a lateral or prone position (operator’s preference). The author’s preference is the left lateral decubitus position with a bolster under the left side between the ribs and iliac crest (Fig. 27.3). Tape the patient in the true lateral position. Bring the bipolar fluoroscopy unit into play and line up the disc space that is to be injected. Have the patient’s MRI scan in the room and review it just before doing this to confirm the appropriate level. You must be able to clearly see the bony end-plates of the disc to be injected in both an anterior–posterior and lateral projection before proceeding. The L5–S1 disc is the most difficult of the lumbar discs to inject from the posterolateral approach because one must clear the iliac crest, compensate for the forward slope of the disc, and avoid the L5 spinal nerve where it exits the foramen and traverses the disc. For an L5–S1 injection, line up the angle of the slope of the disc space with a marker under lateral fluoroscopic projection and mark this angle on the flank with a sterile gentian violet marker (Fig. 27.4). Palpate the spinous processes in the midline of the spine and make a mark 10–12 cm to the right, the distance being dictated by the size of the patient and the estimate made on the transverse view of the MRI scan (Fig. 27.5). Beginning on the sagittal line of the disc to be injected in the transverse view of the MRI scan, draw a second line beginning at the center of the disc at a 45° angle and determine how many centimeters lateral to the sagittal plane the line intersects at the

Fig. 27.4 Illustration of fluoroscopic view within the circle with a metal ruler on the skin to determine the angle of forward inclination of the L5–S1 disc space so that a pen mark can be placed on the skin corresponding to this angle.

12 10 8

Fig. 27.3 Illustration of patient in lateral decubitus position with a bolster under the left flank, tape securing the patient to the table, a pen mark showing the iliac crest and a mark 10 cm lateral to the midline of the spine just above the iliac crest.

Fig. 27.5 Transverse MRI image L5–S1 disc space with triangulation markers showing the posterior lateral projection at 45° angle from the sagittal plane beginning 10 cm lateral to the midline as determined by the scale on the scale seen on the right-hand side of the MRI with each notch representing one centimeter. 317

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30˚

Fig. 27.6 Illustration of angle of insertion of needle into the L5–S1 disc from the posterior lateral approach, just over the iliac crest, beginning 11 cm lateral to the midline on the right side, with a 45° angle to the sagittal plane and inclination of 30° caudad.

45˚ 11 cm

Fig. 27.7 Illustration of the proximity of the L5 spinal nerve (arrow) to the line of trajectory of the needle into the L5–S1 disc from the posterior lateral approach.

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2

3

insert a 20-cm length, 22-gauge needle with stylus in place through the 18-gauge needle with the bevel pointed caudally (Fig. 27.8). The bevel of the needle will act like a rudder and turn the needle as it is inserted around the corner of the L5 vertebral endplate and into the center of the disc. Take permanent X-ray films in the AP and lateral projections to confirm that the tip of the 22-gauge needle is in the center of the L5–S1 disc (see Fig. 27.8). In 1986, Fraser22,23 performed a study in animals to determine the cause of discitis following chemonucleolysis. He demonstrated convincingly that the two-needle technique described above prevented the introduction of skin microorganisms into the disc because the 22-gauge needle did not penetrate the skin. The 18-gauge needle is stiff enough to take a straight trajectory which is required from the site of skin penetration to the corner of the disc. The 22-gauge needle is also pliable and can easily bend around the corner of the vertebral endplate into the disc, thus facilitating the entry into the L5–S1 disc, which must be approached from an angle to clear the iliac crest. The two-needle technique for disc injection is far superior to the use of one needle for ease of insertion, prevention of infection, and to help avoid penetrating the nerve root. Injection of a small amount of X-ray contrast into the disc was originally recommended to confirm that the needle was properly placed and to assure that the contrast did not enter into the epidural or intrathecal space. Studies of the effect of chymopapain and X-ray contrast media injected into the intrathecal space of nonhuman primates caused a severe reaction which was worse than either agent injected alone. Injection of X-ray contrast in addition to chymopapain adds another agent to which the patient may have an allergy. For these reasons, the author stopped using X-ray contrast in the chemonucleolysis technique.

4

1 2 and 3

318

Fig. 27.8 Illustration of the two-needle technique with the 22-gauge needle being inserted through the 18-gauge needle into the L5–S1 disc. Note the orientation of the bevel of the needle at each stage of injection.

Section 2: Interventional Spine Techniques

The enzyme is then reconstituted with sterile saline without preservatives according to directions. One to three milliliters of enzyme is then injected very slowly, until resistance is met in the case of contained discs. If the patient experiences an inordinate amount of pain on injection, stop so as to not displace disc fragments further into the spinal canal from the disc space. Most patients will experience some pain from the increased intradiscal pressure on injection. If no back pressure is felt on the syringe when injecting noncontained discs, do not inject more than 3 mL. If one injects very slowly, the positively charged chymopapain will bind with the negatively charged disc matrix, and this may not enter into the spinal canal. The risk of an intrathecal disc herniation is remote. However, injection of a disc that has previously been operated upon is not recommended because of the adhesions between the disc and the adjacent dura. In such cases there is a greater chance of the intradiscally injected enzyme entering into the subarachnoid space.24 Following the injection of chymopapain into the disc, the needles are removed, a small dressing is applied to the needle hole in the skin and the patient is turned into the prone position on the table and vital signs observed for at least 20 minutes for tachycardia, hypotension, urticaria, pruritus, or wheezing, all signs of systemic allergic reaction. If any or all of these symptoms or signs occur, a 1:200 000 dilution of epinephrine should be injected by the anesthesiologist by the intravenous route as rapidly as elevations in blood pressure will allow until the reaction has subsided. In the absence of an allergic reaction in the first 20 minutes following the injection of chymopapain, the likelihood of a reaction occurring is remote.20 The patient is then taken to a recovery area and monitored until the sedation has worn off and the patient can independently ambulate and void. The patient is given appropriate analgesic pain medication and allowed to go home. Fewer than 1 in 20 patients must be admitted to the hospital for pain control. The pain response varies widely in intensity and duration from patient to patient in the post-chemonucleolysis period after chymopapain.25 The author has seen patients who have had dramatic relief of leg pain in the procedure room and have been able to travel long distances the next day. Other patients experience an initial increase in leg and or back pain which subsides slowly over the next 6 weeks. Those patients who do not obtain relief from the injection will usually be evident by 2 weeks post-treatment. Patients who have a slow recovery but are gradually improving each day are reassured and followed. If a patient experiences any increase in neurologic deficit(s) or a new deficit, surgery is recommended as soon as the situation dictates.

References 1. Smith L. Chemonucleolysis. Personal history, trials, and tribulations [review]. Clin Orthop 1993; 287:117–124. 2. Gogan WJ, Fraser RD. Chymopapain. A 10-year, double-blind study. Spine 1992; 17:388–394. 3. Brown MD, Tompkins JS. Chemonucleolysis (discolysis) with collagenase. Spine 1989; 14:321–326. 4. Fry TR, Eurell JC, Johnson AL, et al. Radiographic and histologic effects of chondroitinase ABC on normal canine lumbar intervertebral disc. Spine 1991; 16: 816–819. 5. Agre K, Wilson RR, Brim M, et al. Chymodiactin post-marketing surveillance. Spine 1984; 9:479–485. 6. Brown MD. Chemonucleolysis with disease: techniques, results, case reports. Spine 1976; 1:115–1120. 7. Kitchel SH, Brown MD. Complications of chemonucleolysis [review]. Clin Orthop 1992; 284:63–74. 8. Abdel-Salam A, Eyres KS, Cleary J. A new paradiscal injection technique for the relief of back spasm after chemonucleolysis. Br J Rhematol 1992; 31:491–493. 9. Nordby EJ, Wright PH, Scholfield SR. Safety of chemonucleolysis. Adverse effects reported in the United States, 1982–1991 [review]. Clin Orthop 1993; 13: 122–134. 10. Brown MD. Intradiscal therapy: chymopapain or collagenase. Chicago: Yearbook Medical Publishers; 1983:173. 11. McCulloch JA. Chemonucleolysis. JBJS 1977; 59B:45. 12. Bouillet R. Treatment of sciatica. A comparative survey of complications of surgical treatment and nucleolysis with chymopapain. Clin Orthop 1990; 251:144–152. 13. Weber H. Lumbar disc herniation: a controlled, prospective study with ten years of observation. Spine 1983; 8:131. 14. Brown MD. The pathophysiology and diagnosis of low back pain and sciatica. AAOS Instructional Course Lectures 1992; 41:205–215. 15. Boden SD, Davis DO, Ding TS, et al. Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects. JBJS 1990; 72A:403–408. 16. Herzuq RJ. The radiologic evaluation of lumbar degenerated disc disease and spinal stenosis in patients back or radicular symptoms. AAOS Instructional Course Lectures 1992; 41:193–203. 17. Garreau C, Dessarts I, Lassale B, et al. Chemonucleolysis: correlation of results with the size of the herniation and the dimensions of the spinal canal. Eur Spine J 1995; 4:77–83. 18. Brown MD. Update on chemonucleolysis. Spine 1996; 21:62S–68S. 19. Pinkowski JL, Leeson MC. Anaphylactic shock associated with chymopapain skin test. A case report and review of the literature [review]. Clin Orthop 1990; 260:186–190. 20. Hall BB, McCullough JA. Anaphylactic reactions following the intradiscal injection of chymopapain under local anesthesia. JBJS 1983; 65A:1215. 21. Kelly J, Patterson R. Anaphylaxis: course, mechanism, and treatment. JAMA 1974; 227:1431. 22. Fraser RD. Discitis following chemonucleolysis. Spine 1986; 11:679.

SUMMARY/CONCLUSION

23. Fraser RD, Osti O, Vernon-Roberts B. Discitis after discography. JBJS 1987; 69B:26–35.

The late John McCulloch was able to treat more than 2000 patients by chemonucleolysis with chymopapain without the occurrence of a major morbidity or fatality.24 Most of the technique described in this chapter was perfected from his experience. It is highly unlikely that a similar record of safety could be obtained in a similar number of patients undergoing surgery for lumbar disc displacement.

24. McCulloch JA. Chemonucleolysis: experience with 2000 cases. Clin Orthop 1980; 146:128–135. 25. Brown MD, Tompkins JS. Pain response post-chemonucleolysis or disc excision. Spine 1989; 14:321–326.

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PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

Automated Percutaneous Lumbar Discectomy: Technique

28

Giuseppe Bonaldi

INTRODUCTION Automated percutaneous lumbar discectomy (APLD) was introduced in 1985 by Gary Onik et al.1–3 Since the 1960s, many different techniques for percutaneous removal of the nucleus pulposus or its protruding components have been proposed; they may achieve the goal in different ways, with different types of instruments, with or without fiberoscopic vision, or different types of energy (radiofrequency [RF], laser, coblation, etc.).4–12 The basic principle, shared by most percutaneous intradiscal decompressive procedures, including APLD, is that in an enclosed space a reduction in volume, even partial, confers a much greater reduction in pressure; this leads to decreased pressure upon the nerve root, and relief of sciatica, even without a radiographically evident reduction in total disc volume.13 After weeks or months, the partial vacuum causes the protruded portion of nucleus pulposus (or other disc material) to move away from the nerve root back towards the center of the disc, pushed by partially intact fibers and ligaments of the outer anulus; this process, along with regeneration of a more fibrous nucleus pulposus, favors restoration of the inner fibers of the anulus and decreases the tendency to further protrusion towards the spinal canal. The success of the procedure depends to a great extent on selecting lesions to treat: the protruding nucleus pulposus must be at least partially contained by the external fibers of the disc, without a large extrusion and migrated or sequestrated fragments.14–16 For decades, minimally invasive treatments for disc protrusions have been opposed by the surgical community, despite the high preference of patients to undergo a less intrusive intervention. APLD seems to have suffered the drawback of having been the first nonchemical, nonmanual procedure to be used worldwide, as the technique was met with fierce opposition. It would be fair to state that 20 years ago, surgeons were not ready to embrace percutaneous procedures. Now that the neurosurgical and orthopedic communities have accepted the concepts of intradiscal decompression and minimally invasive procedures,17 other techniques less effective than APLD dominate the field. In all likelihood, this relationship stems from the fact that APLD is still burdened with old, biased, and superficial judgments that are in part substantiated by poorly conducted studies.18,19 In most published series good results range from 60% to 85%,20–26 depending on patient selection criteria, while poor results are reported in the only two randomized and controlled studies.18,19 In 1993, Revel et al. reported a 37% success rate at 1 year in a study comparing APLD and chemonucleolysis.18 Chatterjee et al., 2 years later, found a 29% success rate with APLD when compared to open surgery.19 However these studies, like others reporting low percentages of good outcomes,27–29 have limitations and features that make the patient populations and technical conditions not really suitable for a comparison, and their results unreliable. First, the numbers of

patients are low: 32 treated by one operator19 and 69 treated by many operators in a multicenter study.18 The authors do not state how experienced the operators were, i.e. how many APLD procedures each had already performed. The technical learning curve for APLD is longer than one might expect. It is only after many procedures are performed that the surgeon can obtain sufficient quantities of nucleus pulposus, and from the correct location of the disc. For example, the L5–S1 level is approached safely and reliably only by operators having performed a minimum of 40–50 procedures at higher levels. It is highly likely that the operators in the two studies mentioned above were much more experienced in open surgery or chemonucleolysis. As well, these investigators did not have access to some of the technique modifications that are described later in this chapter. Another critical issue relates to the population of patients that are being compared. It is undeniable that adhering to specific inclusion and exclusion criteria is crucial to obtain good results with APLD, chemonucleolysis, and open surgery. However, there is little overlap between the indications for open surgery or chemonucleolysis and those for APLD. Consequently, there is a huge inherent limitation in randomized trials attempting to compare APLD to either chemonucleolysis or open surgery. The patients recruited in the two trials mentioned above are likely to have extruded, noncontained protrusions, which are not good indications to perform APLD. In almost 20 years, a minimum of 170 000, and very likely many more, procedures have been performed. It is reasonable to state that APLD ‘opened the way’ to the concept of minimally invasive spine surgery, and that the concept and the technique itself have stood the test of time. APLD is an effective and safe method to obtain an intradiscal decompression, for relief of discogenic radicular or low back pain. It remains the percutaneous procedure that removes the largest amounts of nuclear material from within the intervertebral disc. Another great advantage, when comparing APLD with physical techniques that blindly destroy the disc (such as laser, RF or Coblation®), is that the surgeon can verify directly and visually the quantity of disc material removed, and its ‘quality’ as well. The extracted nucleus pulposus can be observed as it passes through the transparent tubing that connects to a filter. How much nucleus is taken out and how degenerated it is are important procedural and prognostic pieces of information. For example, viewing the quantity of removed nuclear tissue and comparing that to the amount that was anticipated to be extracted from interpreting the preoperative imaging provides critical information to determine whether the probe worked in the correct intranuclear location. Observing blood coming from the disc could suggest the presence of unexpected degeneration, or of painful granulation tissue inside the disc, or prompt arrest of the procedure so as not to damage the endplate cartilage. Aspirated disc material can also be sent for histology or microbiology in selected cases. 321

Part 2: Interventional Spine Techniques

APLD achieves a very good compromise between low invasiveness and the need to obtain discal decompression. Its clinical results remain among the most satisfying when dealing with minimally invasive percutaneous treatments.

SAFETY One of the appeals of percutaneous procedures, other than obtaining a high proportion of good results in properly selected cases, is the limited associated tissue destruction. While open surgery is effective, it has well-known disadvantages, including epidural scarring, damage to bone, denervation of paraspinal muscles with consequent segmental instability, long postoperative inactivity, and the feared ‘failed back-surgery syndrome.’ Patients who experience this latter phenomenon are often untreatable and can be severely disabled. Indeed, they represent the best advertisement for the benefits of minimally invasive procedures, particularly given the high tendency of disc protrusions to self-heal. When considering the issue of side effects and complications, it appears that APLD is an extremely safe technique. Of course, that assumes that the surgeon performing the technique has the experience and ability to convert it into a safe procedure. If the nucleotome is improperly placed, it can easily cut dura, nerve roots, vessels, and other soft tissues. However, once the nucleotome is safely within the disc, i.e. isolated from surrounding neural and vascular structures, it is unable, unlike other devices, to cut its way out of the disc space to cause injury to those structures. The operator must at every moment be absolutely sure of the anatomical position of the operating instruments. Obviously, a key prerequisite is the ability to view two-dimensional fluoroscopic images and reconstruct a threedimensional anatomic picture in the mind’s eye of the operator. To achieve this objective the operator must have a perfect knowledge of radiological projections and a large amount of experience. The mortality rate of the procedure is zero. Lesions of nerve roots, vessels, or the ureter are possible;30–32 however, as previously emphasized, with thorough knowledge of and attention to radiographic landmarks for proper probe positioning, vascular, neural, or dural injuries are very unlikely. The only major reported injury following APLD occurred in Mexico and resulted in a cauda equina direct lesion. It is quite likely that there was little if any attention directed to the radiographic landmarks that allow the surgeon to stay out of a potentially harmful pathway;33 moreover, the procedure was performed under general anesthesia, definitely contraindicated, for the reasons explained later. A posteriorly placed colon can insinuate behind the psoas muscle.34,35 For this reason the preoperative imaging studies, both computed tomography (CT) or magnetic resonance imaging (MRI), must be carefully examined to exclude the presence of such an anatomical condition, since bowel in the path of the instruments could be perforated, with the risk of peritoneal or disc infection or local abscess formation. If not available, a planning CT scan of the whole abdomen through the disc space of interest with large field of view (FOV) must be obtained. When the L5–S1 disc is being removed, two scan slices (at the L4–5 and L5–S1 levels) should be obtained because the entry point for the L5–S1 placement is at the L4–5 level to avoid the iliac crest. In addition, this preoperative, planning CT can provide other valuable information. At the L5–S1 level, special attention should be paid to the bifurcation of the iliac vessels; at upper levels, the scan ensures that the lower pole of the kidney or the sulcus of the pleural space will not be traversed. Beginning in June 1987, in our institution more than 1250 patients (accounting for more than 1450 discs) were treated. We observed and reported an overall complication rate of less than 0.9%.36 There were no injuries to nerve roots, dura mater, ureters, major vessels, or

322

bowel. We suspect this extremely low complication rate stemmed from our singular use of only local anesthesia, with or without light sedation, and the avoidance of general anesthesia. There was one acute hematoma in the iliopsoas that occurred following injury to a small artery and which resolved without sequelae in approximately 1 month. Among the side effects observed were two cases of discitis, resulting in a rate of 0.16 %, similar to the rate published in large series of discography.37–39 Since discitis is a major complication, special care must be taken during skin prep and draping. We also use prophylactic antibiotics and typically give 2 g of intravenous cephalosporin to cover Streptococcus epidermidis. It should be emphasized that some of the potential complications and side effects one could observe following open surgery have never been reported following APLD. Advantages of APLD when compared to other percutaneous technologies are the internal cutting action of the device and its blunt external portion that obviates damage to structures other than the nucleus pulposus. Of course, these factors dictate that the inherent morbidity of APLD is lower than that of other percutaneous disc removal methods.

INSTRUMENTATION Automated percutaneous lumbar discectomy utilizes a probe called Nucleotome® (Fig. 28.1), manufactured by Clarus Medical, LLC, for removal of the nucleus pulposus. The probe tip, excluding the handle, is 20.2 cm long and has an outer diameter of 2.2 mm. The blunt tip is an extremely important safety feature. Once the probe is inserted, the lack of a sharp end prevents it from piercing through the outer limits of the disc, even with an inadvertent hard push. This feature is unique and not a component of other instruments such as laser, RF probes, or manual biopsies, thus essentially removing the risk of lesion of vessels or other abdominal structures. The negative

Nucleus pulposus

H2O

Vacuum

H2O

Aspirated nucleus

Fig. 28.1 The Nucleotome® probe has a blunt, rounded tip. Internal irrigation and cutting functions are incorporated. The aspirated nucleus pulposus enters the side port, and is resected by a pneumatically driven ‘guillotine blade’, which has a reciprocal, not rotary movement.

Section 2: Interventional Spine Techniques

pressure for aspiration is generated by a console. A vacuum is created that draws nuclear material into the side port, which is located a few millimeters proximal to the distal tip of the probe. The cutting blade for fragmentation of nucleus pulposus aspirated through the port, works with a reciprocal, not rotatory motion. This type of movement is a safety feature because the ‘guillotine’ blade is contained within the probe. Consequently, only the nuclear material that is drawn into the port can be cut. The blade is pneumatically driven by a pressure pulse, generated by the same console that creates the vacuum that draws nuclear material into the side port. The console also controls the cut rate and the flow of irrigation fluid to the probe. Internal irrigation with sterile saline is a vehicle for easy aspiration. The reciprocal movement of the internal cutting blade also sequences the introduction of liquid inside the disc, to prevent accumulation of nuclear material and consequent clogging inside the probe, or an excess infusion of fluid within the disc. The cutting rate knob on the console allows for adjustment of between 60 and 180 cuts per minute. At the beginning of the procedure, the maximum cutting rate should be used to cut smaller pieces of disc and prevent the instrument from clogging. As the decompression proceeds, the amount of disc material aspirated diminishes, allowing the surgeon to ratchet down the cutting rate. This will allow more time for the negative pressure to draw disc material through the port before it is resected. The fluids and solid material aspirated from the inner disc and exiting through the metallic probe are ultimately deposited into a filter in a disposable collection bottle. To reach that location the extracted nuclear tissue traverses a transparent plastic tube. Throughout this journey the nuclear material is clearly visible. As alluded to previously, there are tangible benefits that can be realized by real-time monitoring of the disc material as it flows through the transparent aspiration line, mainly the possibility to verify in which positions of the probe inside the disc the largest quantities of nuclear material are extracted. Moreover, the nucleus pulposus collected in the filter is available for quantitative and macroscopic qualitative evaluation, or even for histology examination. The operator must also use the transparent line to check for air: an excessive amount mixed with little or no nuclear material indicates a leak somewhere in the system, which decreases the effectiveness of the suction. The most common cause is an inadequate seal on the cannula, which allows air to be sucked into the disc space. This usually does not happen because anulus and extradiscal soft tissues make a seal around the probe and prevent air from being sucked into the disc. However, if anulus and tissues have less resilience because the patient is older, air will be sucked through the cannula preventing aspiration of the disc and thus rendering the procedure less effective (or longer); in these cases the straight cannula can be replaced with the larger, curved one. If the cannula is not the cause, the air leak may be emanating from the fluid delivery line or even the probe. If a check of the fluid delivery line does not reveal the problem and all maneuvers fail to stop the leak, place the trocar back through the cannula and change both the cannula and the probe. A sequence of devices is used for introduction of the probe inside the disc. After local anesthesia, the first device is positioned in the center of the disc. It is a flexible, 18-gauge stainless steel guide wire with a trocar point. Unlike bevel-pointed needles, a trocar point does not have a sharp cutting effect, thus limiting the risk of vessel or nerve injuries; these structures are more likely deviated by the trocar point rather than resected. In addition, unlike beveled needle tips, the symmetric trocar point follows a straight trajectory, without deflections that would render a precise positioning more difficult. This is particularly applicable when driving the instrument in relatively resistant tissues such as the anulus fibrosus. Moreover, the blunt trocar device is more difficult to push through soft tissues,

which gives the surgeon a much better feeling of the tissue actually met and traversed, and allows for easy recognition of the muscular fasciae, anulus fibrosus, and nucleus pulposus. Once the guide wire is positioned correctly, a cannula with a dilator inside is passed over the guide wire. The dilator is designed to protect soft tissues from surgical trauma; this prevents both bleeding and postoperative muscle spasm. Each single kit contains both a straight cannula, with an outer diameter of 2.8 mm, and a curved cannula, with an outer diameter of 3.8 mm. The reason for a larger diameter in the latter is that it is internally coated by a Teflon layer, which reduces friction and favors sliding of the flexible but straight probe. Once the cannula is positioned against the outer fibers of the anulus, the dilator is removed from the cannula and replaced by a trephine. An incision in the anulus fibrosus is made by means of the trephine, which is a few millimeters longer than the cannula; the same flexible trephine is designed to function with both the straight and curved cannula.

PATIENT POSITIONING AND SELECTION OF ENTRY ROUTE The procedure can be performed with the patient in either the prone or lateral decubitus position. When the prone position is used, bolsters are placed underneath the patient’s abdomen to open the disc spaces posteriorly. This will provide for easy access and for better transmission of the decreased pressure in the center of the disc, consequent to the aspirating action of the probe, to the herniating nucleus pulposus. For the same reason, the patient is flexed when in the lateral decubitus position, which is the approach of preference for addressing pathology of the L5–S1 disc. The entry route, as usual with every lumbar percutaneous approach to the disc space, is posterolateral (Fig. 28.2). Correctly positioning the guiding trocar is crucial to the result. The trocar must be placed with its tip in the midline in frontal view, at the junction of the middle and posterior thirds of the disc in lateral view, where the normal nucleus lies (Fig. 28.3). This location corresponds to the initial working position of the probe. In cases of large, posterior protrusions invading the spinal canal, it is preferable to aim for a more posterior position of the probe. The best and safest way to accurately place the trocar is to choose a path that passes anteriorly and laterally tangent to the posterior zygapophyseal complex, i.e. with the trocar touching the anterolateral surface of the superior articular process (see Fig. 28.2). The usual skin entry point for such a route is 10 cm from the spinous processes. The operator can use the preoperative CT scan to accurately and easily geometrically derive the proper skin entry site. Once the skin target has been determined, a skin wheal is raised. Immediately thereafter, a 22–25-gauge spinal needle is inserted more posteriorly than the anticipated route to the disc, with the aim to touch the posterior facets. Local anesthetic is injected at this location and the needle is gradually withdrawn toward the skin, allowing for anesthetization of the underlying spinal musculature. It is critical that local anesthetic is not deposited anterior to the articular processes, which can anesthetize the exiting root. General anesthesia is contraindicated for this procedure since the chance of nerve root injury is much greater under those circumstances. The 22-gauge, 15 cm long needle can also be used to test if the trajectory from the skin to the anulus is accurate. Which side to begin the procedure depends upon the side of the patient’s symptoms. We usually select the side of the patient’s symptoms. There are two compelling reasons to do so: first, to place the nucleotome probe as close to the herniation as possible, particularly when the herniation is lateralized; second, to avoid the possibility of bilateral symptoms in the event of complications. In rare 323

Part 2: Interventional Spine Techniques Probe Herniated nucleus

Nucleus pulposus

Vertebral bodies

Exiting roots

Transverse processes

Spinous processes

Annulus fibrosus

L4 Trocar Disc

L5

Discs

Entry point Cannula S1

A

B

c

Fig. 28.2 The correct path of the devices from the skin entry point to the center of the disc is anteriorly tangent to the superior articular facet (A, axial view; B, oblique view; C, lateral view).

Fig. 28.3 The tip of the trocar must be placed at the junction between middle and posterior third of the disc in lateral view. The anteroposterior view must confirm the correct position in the midline. In addition, the trocar must be ideally parallel to the endplates in both views.

circumstances a contralateral approach is preferred. First, if a correct trocar positioning inside the disc becomes impossible. That situation can arise when the trocar repeatedly abuts the exiting nerve root, precluding safe advancement into the anulus. Anatomic circumstances that can lead to this scenario are a conjoined nerve root, flattened root compressed by the herniation, and in particular at L5–S1, the normal position of the exiting L5 root. When a conjoined nerve root is present, both roots can exit from a single foramen. The superior root takes a more caudal and inferior course, which places it in the 324

line of a correctly placed trocar. In addition, in case of a far lateral herniation, it is possible that the nerve root is in an abnormal position and pushed posteriorly to close the space between the nerve and the anterior surface of the facet. The second reason to use the contralateral side is when the patient does not tolerate lying with the ipsilateral side superior. A third factor is when an anatomical variant precludes entry. For instance, an L5–S1 approach is not possible from the side of a monolateral transitional vertebra, with sacralization of the transverse process, or if there is a risk of posteriorly placed colon,

Section 2: Interventional Spine Techniques

behind the psoas muscle, as shown by the preoperative CT scan with large field of view (FOV). In the latter case, considering that the leftsided sigmoid colon is more mobile, the surgeon can let gravity assist, positioning the patient on his/her right side; under this condition the left colon falls away from the entry route of the instruments. It must be emphasized that the prone position increases the risk of piercing posteriorly placed bowel. The procedure is monitored fluoroscopically, with use of a C-arm. A comprehensive knowledge and extremely precise use of the radiological projections and landmarks is a prerequisite to performing this procedure. Such knowledge will dramatically impact the outcome and the probability of realizing a side effect or complication. An incorrect projection means that the probe is actually working away from the place where it is supposed to, not effectively aspirating nucleus or, worse, damaging vital or functionally important structures. The crucial radiographic rules are as follows: The projections must be perfect, i.e. strictly lateral and anteroposterior. A correct lateral view is defined by a superposition of the posterior articular facets and of the posterior wall of the vertebral bodies, which clearly appears as a single line. In a correct anteroposterior view the spinous process is exactly midway between the pedicles. The X-ray beam must be parallel to the vertebral body endplates in the lateral view; if this is not so, the endplates will not be seen distinctly, and it will be impossible to tell where in the disc space the devices are positioned in a cephalocaudal direction. Once the endplates are seen distinctly, modifying the cephalocaudal inclination of the beam, it is important to place the disc of interest in the center of the fluoroscopic image, otherwise the parallax created by the fan-shaped X-ray beam coming from a point source can mislead the viewer into thinking that the needle tip is in the correct position when it is not (Fig. 28.4). Of course, as always in radiology, the position of a device must be confirmed in two orthogonal projections, i.e. the tip of the trocar will be in the center of the disc only if this condition is confirmed by the two correct lateral and anteroposterior views, as defined above.

Radiopaque objects as seen under fluoroscopy

Surface of the image intensifier

NUCLEOTOME PLACEMENT AND ASPIRATION OF THE NUCLEUS PULPOSUS As with the needle for local anesthesia, the operator should start, in lateral view, with a posterior trajectory until the trocar hits the bone of the articular facets; then, the trocar is worked anteriorly with tiny movements, until it slides along the anterior surface of the articular complex (actually, over the anterolateral surface of the superior articular facet) (see Fig. 28.2). The closer to this superior articular process the instrumentation is, the less likely the operator is to touch the nerve root. Then, the trocar is pushed toward the posterior profile of the disc, corresponding to the posterior somatic walls, always parallel to the vertebral endplates. When the tip of the trocar reaches the posterior profile of the disc, a gritty, hard but elastic (definitely different from bone and soft tissues) tactile sensation is felt, corresponding to the anulus fibrosus (Fig. 28.5). If the operator does not feel the anulus, the trocar must be withdrawn and replaced more posteriorly; under no circumstances should the operator push the trocar anterior to the posterior profile of the disc. In this situation, the path of the trocar would be too anterior, rendering it impossible to achieve correct trocar placement. Moreover, the risk of injuring nerve root, bowel, inferior vena cava, aorta, or iliac arteries would be escalated. If one attempts to position the trocar more posteriorly, but is precluded because of the articular complex, then a more lateral skin entry point must be used. The described trajectory brings the needle and eventually the nucleotome dorsal to the nerve, which is coursing from the upper portion of the foramen anteriorly and inferiorly (see Fig. 28.5). If the patient is going to experience radicular pain from the needle placement, it will usually occur when the needle is placed too high in the foramen or anterior to the posterior vertebral body’s line. If the nerve root is touched, the patient experiences radicular symptoms, usually a sensation described as a sudden ‘electrical shock’ which may be experienced as distal as the foot, depending on the root that has been abutted. In contrast, the pain originating directly from the nociceptive fibers of the external anulus is less intense and never goes down distal to the knee. If the patient describes a radicular sensation, the trocar must be withdrawn and replaced, even if that requires the skin entry point be modified. In general, moving the entry point 1–1.5 cm in either direction is enough to change the trajectory and obtain a painless trocar placement. All major redirections of the trocar require that it be withdrawn into the subcutaneous space before readvancement, because the fascial planes create a point of fixation that does not allow for major path corrections. Consequently, if the trocar is

Posterior vertebral body line Ganglion

Radiopaque objects X-ray tube (source)

Fig. 28.4 Effect of the parallax created by the diverging X-rays on the position of objects seen under fluoroscopy. Two radiopaque objects are seen. The one in the central beam is projected where it actually is. The offcenter one is projected lateral to its actual position (indicated by the dotted line and arrow).

Exiting nerve root

Trocar Disc

Posterior vertebral body line

Fig. 28.5 The nerve root exits underneath the pedicle at the top of the foramen and courses anteriorly and inferiorly. Under fluoroscopy in lateral view, the trocar’s tip must be at the posterior vertebral body line (PVBL) when the anulus is felt. 325

Part 2: Interventional Spine Techniques

not withdrawn a sufficient distance, further attempts of trocar placement will only result in trocar bending. When the anulus is reached, as determined by its tactile quality, and the 18-gauge trocar touches the posterior vertebral body’s line and is midway between and parallel to the vertebral body endplates, the anteroposterior view should be checked (Fig. 28.6) and this represents a major safety feature. It confirms that the 18-gauge trocar is outside the spinal canal and consequently will not traverse the thecal sac as it is advanced into the disc space. In this anteroposterior view, the tip of the trocar should be lateral to a vertical line connecting the medial borders of the pedicles, thereby confirming its correct position outside the spinal canal. Once confirmed, the trocar can be safely advanced into the center of the disc using this anteroposterior view. The fluoroscope is then repositioned to obtain a lateral view, allowing the surgeon to confirm that the trocar’s tip is correctly placed on both anteroposterior and lateral views (see Fig. 28.3). If the trajectory is too anterior, the trocar tip is visible in the center of the disc on the anteroposterior view, but extends ventral to the center of the disc on the lateral view. Since we want to be as close as possible to the disc herniation, no placement that has an anterior trajectory is acceptable. When the trajectory is posterior, the trocar tip will appear to be in the center of the disc on the anteroposterior view, but posterior to the center of the disc on the lateral view. Since the nucleus pulposus is situated slightly posterior to the center of the disc and we want to be as close to the herniation as possible, a posterior trajectory placement is not only acceptable, but preferred (as previously stated, ideally at the junction between middle and posterior third of the disc). Once the trocar is in the correct position, the dilator and cannula are placed over the trocar and advanced until the anulus is reached. The dilator is then removed, and the cannula is pushed the extra few millimeters to rest on the anulus. At this point, the biopsy stop is brought down to the skin. Later in the procedure, this marker will indicate whether the cannula has been withdrawn or pushed into the anulus. The fluoroscopic beam is now reoriented perpendicular to the cannula, in an oblique view, to confirm that the cannula has reached the anulus (Fig. 28.7). Due to the oval shape of the disc, the tip of the cannula could overlap the margins of the disc on the anteroposterior and lateral views and still not be against the anulus. In this circumstance, if the trephine is used and the cannula is not absolutely against the anulus, the adjacent nerve root could be inadvertently

Ideal line joining medial borders of pedicles

Exiting nerve root

Trocar

326

Fig. 28.6 In the Pedicles anteroposterior view, after the trocar has touched the anulus at Disc the posterior vertebral body line, as shown in Sacrum Figure 28.5, the trocar’s tip must absolutely lie lateral to the vertical line joining the medial borders of the pedicles; this confirms that the trocar is outside the spinal canal and it will not traverse the thecal sac when pushed to advance into the disc space.

90⬚

Fig. 28.7 An oblique X-ray view, perpendicular to the cannula, confirms that the cannula itself is abutting the anulus fibrosus, without any gap in which the nerve root could slide and be cut by the trephine.

injured. When the oblique view confirms that the cannula is resting on the anulus, the dilator is exchanged with the trephine while keeping cannula and trocar in place. During this maneuver the cannula must be pushed firmly against the anulus to prevent the root from insinuating itself between the cannula and the anulus. The trephine is placed against the anulus, which is then incised. Just prior to using the trephine, lightly tapping the anulus with the trephine ensures that a portion of nerve root has not been trapped by the cannula. Patients with a chronic disc disease may experience intense, nonradicular pain when the cannula and the trephine are pushed against the annulus, probably because of sprouting of nociceptive fibers that can accompany degeneration of a disc. If the patient cannot tolerate such pain, before incision with the trephine, a long, 22-gauge needle is inserted in the space between cannula and trocar, and 0.5 ml of 1% plain lidocaine are injected at the site of incision of the anulus. Now that the incision is made, the trocar and trephine can be removed. While accomplishing this, the cannula must be held firmly so as not to lose the newly created hole. The nucleotome is then placed into the disc. Once the aspiration probe is seen to be in the correct position in anteroposterior and lateral views, the port of the instrument is rotated toward the area of the herniation, the nucleotome console is turned on, the footswitch pressed, and the disc aspiration is initiated. As much disc material as possible is aspirated, while gradually moving the probe back and forth. Once no more additional disc material can be retrieved with the port in the direction of the herniation, turn the port to a new area and repeat the back-and-forth motions along the entire length of the nucleus. The cannula can be angled to obtain material from other areas of the disc. During the initial 5–7 minutes, use the straight cannula to aspirate centrally and anteriorly. A curved cannula should be utilized for the rest of the aspiration phase of the procedure, which usually does not take more than 12–15 minutes. The curved cannula that is provided with the surgical kit is particularly helpful in reaching the L5–S1 disc, especially when the approach is partially covered by the iliac crest. It also enhances

Section 2: Interventional Spine Techniques

the range of movement of the probe inside a disc, resulting in the aspiration of greater amounts of nucleus pulposus. This advantage is extremely important when in the more posterior or posterolateral positions, where the nerve root is compressed. For this reason the curved cannula is used at every discal level. During aspiration, the probe is constantly moved in a double rotation-type maneuver, therefore creating successively larger and larger arcs of motion. During this action, the port is maintained in a position that is external to these virtual circles. Ultimately, at least two large tunnels are excavated in the disc. Since the disc is avascular, the fluid flowing from the aspiration line should not be bloody. If the fluid has a red tinge, the most likely explanation is the presence of a gap between the cannula and the anulus that allows blood to be sucked into the disc from the surrounding soft tissues. Be aware that you will aspirate blood whenever you retrieve the probe into the cannula or during each exchange of the probe or cannula (for instance, after withdrawing the probe to purge clogged extracted tissue or exchanging the curved for the straight cannula). One final cause of a haemorragic return is enlargement of the hole in the anulus that may occur near the end of the procedure; angling of the cannula to reach various portions of the disc can widen the initial annular opening. It is through this increased aperture that blood is aspirated inside the disc. When treating discogenic back pain, aspiration is never stopped before blood starts coming from the disc (from granulation tissue or endplate cartilage). Observing blood in the tube suggests the possibility of subsequent scarring. It is always possible to achieve this result when using the ‘double rotation’ technique. It is likely the good results of APLD for discogenic pain are achieved by lowering the pressure within the disc and by stimulating scar formation. The latter ultimately reinforces the anulus with more fibrous tissue and diminishes the motion in cases of symptomatic microinstability. It is reasonable to assume that discogenic pain can be improved or cured thanks to removal of nodules of innervated, painful ‘granulation’ tissue. These areas may be evident on MRI as zones of high signal, usually in the posterior annulus;40 since granulation tissue is vascularized, early bleeding occurs during aspiration. Bleeding is not, however, necessary when treating patients for relief of root compression; aspiration is stopped when the amount of disc material coming from the probe greatly decreases. When treating radicular pain, at the end of the procedure, the side port of the probe is positioned close to the protruding parts of the disc in the neural foramen in an attempt to aspirate the protruding material itself. This ‘topographical’ criterion must guide the aspiration. It is important to keep in mind that the probe is not positioned to work only in the center of the disc, but should be directed to look for the main bulk of the nucleus pulposus and its protruding components. As long as the preprocedural MRI or multiplanar reformatted CT scan indicate that the height of the disc is preserved, at least a moderate amount of nuclear material must be removed. In general, the less degenerated, i.e. yellowish, the nucleus material appears, the more quantity must be aspirated. If, after an apparently correct first positioning of the probe inside the disc, nuclear material does not come freely, the probe must be moved to locate it. Treatment proceeds until nucleus is found and removed. If the instrument becomes obstructed, the probe must be removed from the cannula and flushed with normal saline to remove the clogging material. The probe is withdrawn into the cannula once no more material can be aspirated. Both the cannula and probe are removed, as a single unit. This maneuver prevents the port of the probe from inadvertently injuring any structures during removal. In addition, by retracting the probe into the cannula first, the dissipation of any negative pressure that was created in the disc is prevented.

After withdrawal, 80 mg methylprednisolone acetate (DepoMedrol®) and 1 ml bupivacaine 0.5% are injected in the disc. This is easily accomplished by passing an 18-gauge needle over an 0.8 mm Kirschner wire that had been left in place as a guide. The author’s experience is that adding an intradiscal glucocorticoid infusion results in a more rapid convalescence, and postoperative pain relief will be realized much earlier. Since introduction of the probe requires a miniscule skin incision, a suture is not necessary to end the procedure.

PERCUTANEOUS DISCECTOMY AT THE L5–S1 LEVEL The height of the iliac crests is the crucial factor determining the difficulty of a percutaneous approach at the L5–S1 level. High iliac crests cover the disc space, and consequently the entry route must come from a more cephalad starting point. There are instances in which straight instrumentation will not enter the disc correctly, i.e. parallel to the vertebral bodies’ endplates. For this reason the procedure is usually easier in women because of their wider and gently sloping iliac crests. Three other situations in which the procedure is more difficult should be anticipated. First, the narrower the disc space, the more difficult the procedure becomes. Second is the presence of a spondylolisthesis. Lastly, the smaller the space between the transverse process of L5 and the sacrum, the more difficult the procedure. Prior to beginning a decompression at the lumbosacral junction, the anteroposterior radiography should be reviewed to ascertain whether there is a transitional vertebra, an enlarged transverse process, the degree of disc height decrement, and the relationship of the iliac crest to the annular entry site. Performing the procedure with the patient lying in the lateral decubitus position increases the probability of correctly entering the L5–S1 disc. A soft silicon gel cushion or other similar prop wedged just superior to the iliac crest will laterally flex and lower the iliac crest on the entry side, thus opening an access trajectory to the L5–S1 disc (Fig. 28.8). Owing to the upward convex curve of the iliac crests, the more lateral the skin entry point is selected, the steeper from above (i.e. the less parallel to the endplates) the trajectory to the disc space will be. However, if too medial a starting point is chosen, the nucleotome will terminate in a too ventral (anterior) location within the disc. If the correct intradiscal position cannot be achieved with a straight cannula, the curved one should be substituted for it. Although placement of the curved cannula is technically demanding, it offers a palpable benefit. When oriented correctly, the curve of the cannula allows the trocar and the probe to enter the plane of the disc (i.e. parallel to the endplates), despite an angled approach from above of the devices (Fig. 28.9). When it is anticipated that the trocar will enter the disc following a suboptimal path, either because the trajectory is too anterior or not parallel to the endplates, the curved cannula can be brought down over the trocar to the anulus. Then, the trocar can be withdrawn and the cannula can be slid along the anulus or angled to the anulus at the appropriate degree to achieve the correct trajectory. The trocar can then be reinserted into the disc. If the angle of the trocar in relation to the disc space is too steep, it is not possible to place the trocar within the disc. In this case, the trocar can be firmly anchored against the anulus or endplate and the curved cannula advanced to the disc. Again, if it is kept against the disc or endplate, the cannula can be appropriately moved or angled to allow the trocar to enter the disc. Once the trocar is correctly placed, the dilator is removed and the trephine is placed over the trocar and through the cannula. The trephine and trocar are then both removed and the probe is 327

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Trocar L4 L5

Discs

Fig. 28.8 The L5–S1 disc space is more easily approached in the lateral decubitus position. A soft silicon gel cushion is positioned under the patient’s hip and used to tilt the pelvis and to bend the lumbar spine in order to lower the iliac crest on the entry side, thus uncovering the disc from the iliac crest.

Straight cannula with trocar

L5–S1 disc

Fig. 28.9 The angle to the L5–S1 disc space is too great, because of the slope of the iliac crest: a straight cannula would lead the trocar to a course not parallel to the endplates, Curved entering high and cannula going down to touch with the superior endplate trocar of the sacrum (left). Sacrum Properly maneuvered, as described in the text, the curved cannula allows a more favorable positioning of the devices in the disc space, i.e. acceptably parallel to the endplates (right).

placed through the cannula into the disc. If the curved cannula was required to deposit the probe parallel with the endplates, it can be subsequently used to reach posterior aspects of the disc (Fig. 28.10). Indeed, the reach it achieves is superior to that offered by a straight cannula. It is sometimes difficult to pass the curved cannula through the lumbar fascia, because of the larger diameter and bigger step down from the edge of the cannula to the dilator. If so, it may be necessary to dilate the tract first with the straight cannula and dilator. At L5-S1, the disc is aspirated using the same concepts and methods that apply to more cephalad intervertebral discs. In favorable anatomy, an alternative method for placement of the trocar in the L5–S1 can be used. The path to the disc is found centering the X-ray beam over the L5–S1 disc space in the anteroposterior view. The fluoroscopic unit is then angled in the cephalocaudal direction until the endplates of the disc are visible as single superior and inferior entities, indicating that the entry angle is parallel to the 328

Probe

Curved cannula

Fig. 28.10 After positioning of the probe in the L5–S1 disc space as described in the text and in Figure 28.9, the curved cannula can be turned with an anterior convexity, so that the probe will be directed to work and aspirate in a position more posterior than it would be allowed by a straight cannula.

endplates. The X-ray beam is then angled toward the lateral view, and as it is moved in an oblique orientation, the L5–S1 facet joint moves across the disc space and the iliac crest starts to overlap the anterior portion of the disc. When the beam is at approximately a 45° angle, a triangular window at the center of the disc space is seen (Fig. 28.11). This triangle is bounded laterally by the iliac crest, medially by the anterior surface of the superior articular process of S1, and superiorly by the inferior endplate of the L5 vertebra. Once this view is obtained and centered on the screen, the trocar, with use of a holder, is inserted in bull’s-eye fashion through the middle of the triangle. When done properly the trocar will appear as a single dot. The trocar should then be advanced using real-time imaging until it touches the outer annular fibers.

POSTOPERATIVE CARE We routinely perform APLD on an outpatient basis. At the conclusion of the procedure, observation is needed for about 2 hours before discharging the patient home. Prescriptions are provided for a 2-week supply of a nonsteroidal antiinflammatory agent, and for diazepam at

Section 2: Interventional Spine Techniques

L5

Fig. 28.11 In an oblique view, a triangle free from bony structures indicates the path to the L5–S1 disc; the triangle is bounded by the iliac crest, the anterolateral surface of the superior articular Superior facet of S1, and the articular facet of S1 inferior endplate of L5. The needle, appearing Iliac crest in the central beam as a single dot, will be pushed easily in the center of the disc space.

usually believed. A ‘topographic’ criterion must guide the operator, who must maneuver the aspiration probe inside the disc looking for the nuclear material where it is and not ending the procedure until a significant amount of it is extracted. In this respect a great advantage of Onik’s method is the possibility to visually and directly verify quantity and quality of extracted nuclear material. Among minimally invasive percutaneous treatments, APLD probably achieves the best compromise between low invasiveness and entity (quantitative and topographic) of discal decompression.

References 1. Onik G, Helms CA, Ginsburg L, et al. Percutaneous lumbar diskectomy using a new aspiration probe. Am J Neuroradiol 1985; 6:290–293. 2. Maroon JC, Onik G. Percutaneous automated discectomy: a new method for lumbar disc removal. J Neurosurg 1987; 66:143–146. 3. Onik G, Maroon JC, Helms CA, et al. Automated percutaneous discectomy: initial patient experience. Radiology 1987 162:129–132.

bedtime for 2–3 days. Patients are encouraged to move, stand, and walk on day three. Driving or prolonged sitting is proscribed for a 2–3-week interval. After APLD, early activity is not only possible but also useful. It is imperative to avoid muscle atrophy and general deconditioning. Repetitive forward flexion, prolonged car driving, prolonged sitting, and lifting heavy weights is prohibited for 3–4 weeks. Limb pain resolution may take weeks, owing to ‘remodeling’ of the disc and regression of inflammation at the surgical site. Progressive return to heavy activities or sports is usually possible at 4–6 weeks. A procedure that does not result in substantial relief of pain should not be considered a failure until at least 6 weeks have passed. During the convalescence phase, rehabilitation measures applied by experienced physical therapists may be useful, not before 3 weeks after the intervention. Among the concepts that need to be learned are maintaining a positive attitude, recognizing the difference between symptoms of a residual herniation and those of a healing process, and proper biomechanics. The only noteworthy side effect is the possibility of increased back pain. Most patients with a surgical wound have pain, and that applies to percutaneous discectomy. Injury to skin, muscle, fascia, and anulus will occur; a correct operative technique usually avoids injury to the endplates, but this may occur when treating patients for back pain. Patients are warned that they may experience new back pain for up to 3–4 weeks. Patients should be encouraged to maintain as much mobility as possible despite the presence of back pain.

SUMMARY Automated percutaneous lumbar discectomy is a minimally invasive intradiscal decompressive technique proposed in 1985 by Gary Onik, referred to as ‘automated’ since it is characterized by the use of a mechanical probe, working by means of a ‘suction and cutting’ action for removal of the nucleus pulposus. The method achieves a high degree of clinical efficacy for relief of not only radicular but also of low back pain. Results are particularly favorable in some subgroups of patients, such as elderly people, patients previously operated on, and patients suffering from ‘discogenic’ low back pain. Complication rates are extremely low (less than 1%) and usually mild from the clinical point of view, followed by complete recovery; a correct operative technique rules out the risk of any major, particularly neurological, complication. A thorough technique is also mandatory to obtain a good intradiscal and root decompression, and the learning curve is longer than

4. Smith L, Garvin PJ, Jennings RB. Enzyme dissolution of nucleus pulposus. Nature 1963; 198:1398–1400. 5. Smith L. Enzyme dissolution of nucleus pulposus in humans. JAMA 1964; 187:137– 140. 6. Choy DS. Percutaneous laser disc compression (PLDD): twelve years’ experience with 752 procedures in 518 patients. J Clin Laser Med Surg 1998; 16:325–331. 7. Friedman WA. Percutaneous discectomy. An alternative to chemonucleolysis? Neurosurgery 1983; 13:542–547. 8. Hijikata S, Yamagishi M, Nakayama T, et al. Percutaneous nucleotomy: a new treatment method for lumbar disk herniation. J Toden Hosp 1975; 5:5–13. 9. Hijikata S. Percutaneous nucleotomy: a new concept technique and 12 years’ experience. Clin Orthop 1989; 238:9–23. 10. Kambin P, Gellmann H. Percutaneous lateral discectomy of the lumbar spine. A preliminary report. Clin Orthop 1983; 174:127–132. 11. Schreiber A, Suezawa Y. Transdiscoscopic percutaneous nucleotomy in disc herniation. Orthop Rev 1986; 15:75–78. 12. Yeung AT. The evolution of percutaneous spinal endoscopy and discectomy: state of the art. Mt Sinai J Med 2000; 67:327–332. 13. Shea M, Takeuchi TY, Wittenberg RH, et al. A comparison of the effects of automated percutaneous diskectomy and conventional diskectomy on intradiskal pressure, disk geometry, and stiffness. J Spinal Disord 1994; 7:317–325. 14. Milette PC. The proper terminology for reporting lumbar intervertebral disk disorders. Am J Neuroradiol 1997; 8:1859–1866. 15. Fardon DF, Milette PC. Nomenclature and classification of lumbar disc pathology. Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001; 26:E93–E113. 16. Fardon DF, Milette PC. Nomenclature and classification of lumbar disc pathology. Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. American Society of Neuroradiology, 2003; www.asnr.org 17. Haines SJ, Jordan N, Boen JR, et al. Discectomy strategies for lumbar disc herniation: results of the LAPDOG trial. J Clin Neurosci 2002; 9:411–417. 18. Revel M, Payan C, Vallee C, et al. Automated percutaneous lumbar discectomy versus chemonucleolysis in the treatment of sciatica. A randomized multicenter trial. Spine 1993; 18:1–7. 19. Chatterjee S, Foy PM, Findlay GF. Report of a controlled clinical trial comparing automated percutaneous lumbar discectomy and microdiscectomy in the treatment of contained lumbar disc herniation. Spine 1995; 20:734–738. 20. Castro WH, Jerosch J, Hepp R, et al. Restriction of indication for automated percutaneous lumbar discectomy based on computed tomographic discography. Spine 1992; 17:1239–1243. 21. Moon CT, Cho J, Chang SK. Availability of discographic computed tomography in automated percutaneous lumbar discectomy. J Korean Med Sci 1995; 10:368–372. 22. Dullerud R, Amundsen T, Lie H, et al. CT-diskography, diskomanometry and MR imaging as predictors of the outcome of lumbar percutaneous automated nucleotomy. Acta Radiol 1995; 36:613–619. 23. Dullerud R, Amundsen T, Lie H, et al. Clinical results after percutaneous automated lumbar nucleotomy. A follow-up study. Acta Radiol 1995; 36:418–424.

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Part 2: Interventional Spine Techniques 24. Grevitt MP, McLaren A, Shackleford IM, et al. Automated percutaneous lumbar discectomy. An outcome study. J Bone Joint Surg [Br] 1995; 77:626–629.

32. Flam TA, Spitzenpfeil E, Zerbib M, et al. Complete ureteral transection associated with percutaneous lumbar disk nucleotomy. J Urol 1992; 148:1249–1250.

25. Sortland O, Kleppe H, Aandahl M, et al. Percutaneous lumbar discectomy. Technique and clinical result. Acta Radiol 1996; 37:85–90.

33. Onik GM, Maroon JC, Jackson R. Cauda equina syndrome secondary to an improperly placed nucleotome probe. Neurosurgery 1992; 30:412–415.

26. Bernd L, Schiltenwolf M, Mau H, et al. No indications for percutaneous lumbar discectomy? Int Orthop 1997; 21:164–168.

34. Hopper KD, Sherman JL, Luethke JM, et al. Retrorenal colon in the supine and prone patient. Radiology 1987; 162:443–446.

27. Shapiro S. Long-term follow-up of 57 patients undergoing automated percutaneous discectomy. Neurosurgery 1995; 83:31–33.

35. Prassopoulos P, Raissaki M, Daskalogiannaki M, et al. Retropsoas positioned bowel: incidence and clinical relevance. J Comput Assist Tomogr 1998; 22:304–307.

28. Lee SH, Lee SJ, Park KH, et al. Comparison of percutaneous manual and endoscopic laser diskectomy with chemonucleolysis and automated nucleotomy. Orthopäde 1996; 25:49–55.

36. Bonaldi G. Automated percutaneous lumbar discectomy: technique, indications and clinical follow-up in over 1000 patients. Neuroradiology 2003; 45:735–743.

29. Ramberg N, Sahlstrand T. Early course and long-term follow-up after automated percutaneous lumbar discectomy. J Spinal Disord 2001; 14:511–516. 30. Schreiber A, Suezawa Y, Leu H. Does percutaneous nucleotomy with discoscopy replace conventional discectomy? Eight years of experience and results in treatment of herniated lumbar disc. Clin Orthop 1989; 238:35–42. 31. Stern MB. Early experience with percutaneous lateral discectomy. Clin Orthop 1989; 238:50–55.

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37. Collis JS Jr, Gardner WJ. Lumbar discography. Analysis of 600 degenerated disks and diagnosis of degenerative disk disease. JAMA 1961; 178:67–70. 38. Collis JS Jr, Gardner WJ. Lumbar discography. An analysis of one thousand cases. J Neurosurg 1962; 19:452–461. 39. Feinberg SB. The place of discography in radiology as based on 2320 cases. Am J Roentgenol Radium Ther Nucl Med 1964; 92:1275–1281. 40. Aprill C, Bobduk N. High intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. Br J Radiol 1992; 65:361–369.

PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

Laser

29

Johannes Hellinger and Stefan Hellinger

INTRODUCTION Although many patients benefit from surgical discectomy with or without a fusion, these open procedures are associated with known risks, including early or late failures secondary to symptomatic adhesions, pseudoarthrosis, and adjacent level instability.1 These complications have prompted the development and introduction of less invasive percutaneous intradiscal procedures that have the ability to chemically or mechanically remove intradiscal nuclear material. Chemonucleolysis using the intranuclear injection of chymopapain was introduced several decades ago and a variety of other intradiscal and endoscopic procedures have followed. Among the intradiscal procedures are endoscopic nucleotomy, nucleoplasty (coblation), percutaneous lumbar discectomy methods of decompression. Most of the devices removed nuclear material using mechanical incision by surgical instruments or suction, but in 1986 Choy et al.2 introduced nonendoscopic percutaneous laser disc decompression and nucleotomy (PLDN) with the Nd:YAG laser (wavelength 1064 nm). Even though the 1064 nm wavelength Nd:YAG laser technique in this context is not to be understood as the use of soft laser technology,3 many consider this first introduction of intradiscal laser technology a pioneering achievement.

Fig. 29.1 Controlled vaporization of a disc. Note the zone of thermocoagulation surrounding the defect. (Courtesy W. Siebert, M.D.)

PRINCIPLES

3000

B 2000 Pressure

Several postulates have been proposed to explain why intradiscal laser decompression can help relieve pain caused by a herniated disc. The first and more apparent reason is the potential beneficial effect of lowering the intradiscal pressure by vaporizing nuclear material. The Nd:YAG 1064 nm irradiation of discal tissue creates a small vaporization defect lined with a carbonized margin (Fig. 29.1)4 and minimal ablation of disc tissue.5 Greater ablation is possible with the Nd:YAG laser 1320 nm with a pressure drop of up to 55.6% recorded (Fig. 29.2).6 This reduction in pressure appears to be independent of age or the degree of disc degeneration.7 Even though the amount of tissue removed and the ablation defect is less than that achieved with a mechanical discectomy, clinical results are similar using the Nd:YAG laser. Laser ablation may have other beneficial effects. Some believe that laser provides benefits other than mechanical decompression. One such potential beneficial effect is the shrinkage of collagen fibrils caused by laser-generated heat8–10 followed by a subsequent reduction of intradiscal volume. We postulated this mechanism after observing sudden shrinking of a resected meniscus irradiated by the Nd:YAG laser 1064 nm.8 Our basic studies showed a reduction in disc diameter up to 14% in explanted bovine discs, even though comparative studies8 using the holmium:YAG laser caused 1% or less diameter shrinkage. Consistent with our findings regarding disc shrinkage (Fig. 29.3), Turgut et al.11

A

1000

0 10’ Initial pressure

Laser shot

23’ Control

Fig. 29.2 Intradiscal pressure reduction after intradiscal irradiation by Nd:YAG laser (modified from Choy et al.6).

demonstrated water loss, and proteoglycan and collagen changes in animal discs following laser treatment. Kosaka et al.12 showed size reduction of several millimeters of extruded discs by open surgical Nd:

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A

B

YAG laser disc decompression and intraoperative monitoring. As well, Mayer13 documented disc shrinkage on video during endoscopic Nd: YAG laser-assisted percutaneous discectomy and Grönemeyer14 with computed tomography (CT) intraoperatively. Reductions in the density of disc protrusions and extrusions have been documented with CT scans performed on the first postoperative day following Nd:YAG PLDN.15 Brat et al.16 similarly documented reduced size of extrusions on postoperative magnetic resonance imaging (MRI) scans. Similar findings were seen on MRI myelograms performed on the first postoperative day17 where improved cerebrospinal fluid (CSF) flow was demonstrated at the site of the previously constricted dural sac (Fig. 29.4). The authors concluded that the improved CSF flow was the evidence of reduced venous congestion, reduced arteriole compression, and reduced dural sympathetic nerve fiber compression. Because only minimal venous congestion will adversely affect dorsal root neurons18 and compression often occurs at two adjacent segments,19 proximal and distal root decompression over two segments is recommended. Contrary to open and most percutaneous surgical disc interventions, the Nd:YAG 1064 nm laser technique may not cause postoperative instability.20 On the contrary, Wittenberg and Steffen21 have even reported an increase in translation stability of spinal segments, which they felt was due to a change of collagen tissue formation.22 Scar tissue was seen at 6 weeks intradiscally, but takes a year to mature.10 Thal et al.22 reported a late shrinking effect of the intervertebral disc without any detectable increased segmental movement. Finally, another theoretical but unproven potential beneficial side effect of the heat generated during laser ablation is the destruction of nociceptors in the outer anulus, destruction of nociceptors that follow the ingrowth of vascular tissue into radial and concentric annular tears, and the denaturing of inflammatory chemokines.

SAFETY OF USE Siebert23 in the lumbar spine and Schmolke et al.24 in the cervical spine have provided safety data for the Nd:YAG 1064 nm laser system. At an irradiation time of one shot per second at 20 watts the laser beam will penetrate to a depth of 6 mm in disc tissue. When the laser beam was not directed at the endplate or within the spinal canal, temperatures above the coagulation threshold of proteins were not reached in either the endplate or the epidural tissue adjacent to the disc. Their findings prompted the recommendation that a posterolateral approach be used to access the dorsolateral third of the lumbar and thoracic disc and an anterior approach involving the ventral third of the cervical disc. Based on the experimental studies, the recommended maximal dose per disc is 1600 joules in the lumbar spine, 1000 joules in the thoracic spine, and 300–400 joules in the cervical spine. 332

Fig. 29.3 Diameter shrinkage of bovine discs and local shrinking effect (arrow) after intradiscal Nd:YAG 1064 nm shooting up to 750 joules (15 watts, 1 sec).

Pilot studies showed that patients under regional anesthesia and analgesic sedation will empirically tolerate single shots of 15 watts at 1 second intervals in both the lumbar and thoracic spine, and in the cervical spine 20 watts every 0.3 seconds with a 5 second interruption after five shots. During the past 15 years, the authors have gradually reduced the lumbar dose to 900–1000 joules without any difference in clinical outcome. Although endplate injury has been reported during the use a holmium:YAG laser, we have observed no cases of endplate injury using the Nd:YAG laser 1064 nm. We have, however, seen sporadic edematous lesions in the adjacent vertebrae, but these lesions are often seen after open surgery as well and are of uncertain clinical significance.

Alternative laser technology Carbon dioxide lasers have a wavelength that is very effective in shrinking the disc;25 however, using the Nd:YAG 1320 nm wavelength requires higher dosing to cause disc shrinkage comparable to the Nd:YAG 1064 nm laser. Such higher doses by 1320 nm can cause damage to both endplates in 8% of cases26 and thus its use in disc decompressions is limited. The KTP laser is very similar to the Nd:YAG laser in both its mode of action and its effect,27,28 but basic research is significantly less than for the Nd:YAG 1064 nm laser. The diode laser uses 890–980 nm wavelengths and will shrink an intervertebral disc to the same degree as the Nd:YAG 1064 nm laser. Using a wavelength of 940 nm, we validated the shrinking effect of this laser29 and also showed that a reduced dose could provide sufficient decompression yet still avoid thermal damage to the endplates. The holmium:YAG laser with a 2100 nm wavelength may not be suitable as a pulsed laser when used for nonendoscopic intradiscal use.30 The somewhat larger ablated volume compared to the Nd: YAG 1064 nm laser is less than 10 milligrams,31 and therefore of dubious clinical importance. Furthermore, there is 90% less disc shrinkage, and the apparent scattering may increase the risk of endplate damage.32

INDICATIONS AND PATIENT SELECTION We define pain by its quality, quantity, topology, and chronology and classify discogenic pain as causing local, pseudoradicular, radicular, medullary, or autonomic symptoms. In addition, pain symptoms may be associated with neurological deficits such as dysesthesias, hypo- or hypersensitization, or even paralysis. The cause of these pain syndromes can be diagnosed by a characteristic history and physical examination substantiated by MRI or CT evidence of disc bulging, protrusions, extrusions, or sequestrations.33,34 Abnormal structural findings alone without corresponding symptoms are not, however, a reason for surgical intervention.35

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Patients who fail 6 weeks of conservative care and continue to have disabling discogenic pain are first offered Nd:YAG PLDN before an open surgical procedure. Although progressive neurologic deficits, paralysis, conus medullaris, and cauda syndrome require immediate intervention, the severity of pain most often dictates when we determine that surgery will be offered. With the exception of a patient with a hemostatic disorder or untreated infection, there are few contraindications to discal laser intervention. Because shrinkable collagen fibers are always present in the fibrous ring, even age is not a contraindication. In fact, as long as we clinically believe the patient’s axial or extremity pain is due to a disc bulge, protrusion, or extrusion and it is seen on a CT or MRI scan, the patient will be offered laser decompression. In particular, laser decompression is not contraindicated when a disc protrusion is aggravating the pain of spinal instability or is contributing to stenosis.36 Furthermore, many patients who have unrelieved pain for over 6 weeks will begin to develop somatization symptoms, but unlike other authors20,37 we believe these symptoms are not a contraindication to surgery. In addition, although many physicians including Siebert20 and others16,37,38 prefer restricting percutaneous laser decompression to patients with monoradicular pain, the authors have shown that patients with monoradicular pain alone account for only 20% of patients presenting with discogenic pain.4 Consequently, the authors believe that axial pain alone is not a contraindication to the performance of laser disc decompression, similar to radiofrequency (RF) application. Finally, the authors do not routinely use discography to confirm the source of pain,39 but will use discography to help position the cannula during the operation.

In practice, the majority of patients who are offered a percutaneous laser decompression have mono- or polyradicular pain associated with a disc bulge, protrusion, or contained and noncontained extrusions. When selection is limited to patients with radicular pain, patients who will eventually require an open procedure may be less than 10%4,40 and more than 90% would choose the procedure again for a recurrence in pain. In a consecutive prospective series, 85% of the operated patients had either protrusions or contained extrusions and 15% had noncontained extrusions with either caudal, cranial or buttonhole dislocations. The failure rate was 3% in the protrusioncontained extrusion group and even though the failure rate in the noncontained extrusions was 20%, open surgery was avoided in four of the five cases. Although most surgeons rarely operate on sequestered fragments that are free-floating in the epidural space, many sequestered fragments remain within the protrusion or trapped in the fibrous ring.41 Furthermore, when there is both a free-floating epidural sequestered fragment and a foraminal disc protrusion, decompression of the protrusion alone may provide enough radicular pain relief such that the patients are satisfied. In the authors’ series of 3970 lumbar Nd:YAG PLDN procedures between 1989 and 2002 there were seven patients with both protrusions and free-floating sequestered fragments. Six of the seven patients were satisfied with their outcome following discal decompression alone, and only three had residual local axial pain. Two patients with dorsiflexor foot weakness had full recovery. Finally, most consider cauda equina syndrome as a contraindication for percutaneous disc decompression.20,42 The authors have, however,

A

B

Fig. 29.4 (A) Pre- and (B) postoperative MRI myelogram with evidence of improved dural sac contours and cerebrospinal fluid flow. 333

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successfully performed Nd:YAG PLDN on 30 cases of cauda equina syndrome. Moreover, in only one case of a recurrent herniation with a free-floating sequestered fragment was open surgery necessary.43 While this chapter has emphasized lumbar disc disorders, it should be understood that laser decompression may also be considered for symptomatic disc herniations in the cervical and thoracic spine.44

9. After removal of the needle, digital compression is applied to the puncture site and a bandage applied. 10. Dressings are next applied and the patient is fitted with a soft neck brace for 24 hours. 11. A Philadelphia collar brace is worn for 6 weeks postprocedure at discharge, and NSAIDs are given to control pain.

TECHNIQUE

Thoracic

In the lumbar and thoracic spine, the patient is positioned in the lateral decubitus position with the painful side up, and a posterolateral approach is used. In the cervical spine, the patient’s neck is placed in hyperextension and access is made on the right side between the vessels and the trachea. Local anesthetic is infiltrated in the skin and subcutaneous muscles, and analgesic sedation is given by the anesthetist. Direct and continuous fluoroscopic visualization using intermittent anteroposterior (AP) and lateral projections is used during needle insertions. Because the 400–600 μ bare fiber of the Nd:YAG laser extends 2 mm beyond the cannula tip. The laser beam penetrates to a depth of 6 mm. Accurate and specific placement within the disc is important. Although rarely needed, puncture laser osteotomy45 through the edge of the vertebral body, osteophyte, or superior articular process will facilitate access to the intervertebral disc. On rare occasions, transdural puncture will be needed to access the L5–S1 disc.

1. The patient is in the lateral decubitus position on the operating table with the painful side facing upwards. 2. Local anesthetic infiltration of skin, subcutaneous tissue, paravertebral muscles and the small vertebral joints in the affected segment or in several levels is performed with 30–50 mL mepivacaine 0.5%. 3. In addition to local anesthetic infiltration, sedation by an anesthetist is used to eliminate acute pain during the puncture procedure. 4. Adjustment of the c-arm allows for progressive cephalad counting of vertebrae from L5 to determine the segment to be treated. 5. In the anterolateral projection, a 1.8 mm needle is inserted 6–8 cm paravertebrally on the affected side under intermittent c-arm imaging towards the affected intervertebral disc. 6. After advancing past the costal head under continuous c-arm imaging, the intervertebral intradiscal space is reached at an angled position of about 45°. 7. Following puncture, an AP image of the needle penetrating the middle third is taken. 8. Exchange the stylet for the clamping device with the bare fiber extending 2 mm beyond the needle tip. Irradiate with maximum 1 second per shot, 15 watts per shot up to 900–1000 joules. 9. Continuously check for lower extremity pain or muscle contraction during the administration of laser. 10. Interactive verbal contact with the patient regarding pain is a requirement. If pain is described, pause for up to 5 seconds or reduce the irradiation time while increasing the number of shots to reach the total number of joules. 11. Remove the needle and apply a bandage. 12. Patient should now be placed in the supine position. Monitoring of peripheral neurological findings is conducted. 13. A fluoroscopic view of the thorax is taken to rule out pneumothorax. After 4 hours, a chest X-ray is performed. 14. When analgesic sedation subsides, mobilization with a bridging brace with raised thoracic support pad is made after a plaster cast impression.

Technical procedure for nonendoscopic percutaneous laser disc decompression and nucleotomy Cervical 1. The patient is placed in a supine position with the shoulders supported in order to bring the midcervical spine into the extended position. An anesthetist administers conscious sedation to a level that the patient is comfortable with but can communicate with the surgeon. 2. Using continuous fluoroscopic visualization, 10 mL of 1% mepivacaine is infiltrated into the skin and subcutaneous tissue between the carotid artery and the trachea to the depth of the intervertebral disc. 3. Using a lateral fluoroscopic projection, the appropriate cervical level is identified. 4. The endplates of the desired intervertebral disc are brought into a parallel view by tilting the fluoroscopy tube in a cephalad–caudad direction. 5. Using direct fluoroscopic imaging and while the index finger displaces the trachea medially and the carotid artery laterally, a 1.8 mm external diameter needle is directed into the ventral onethird of the disc and directed towards to the superior endplate. The final needle position should be approximately 2 mm ventral from the center of the disc. Manual depression of the shoulders may be necessary to visualize the C6–7 or C7–T1 interspace. 6. The needle is manually fixated and the stylet is exchanged for the laser cable which will have the bare laser fibers extending 2 mm beyond the needle tip. 7. Deliver 60 laser shots of 0.3 seconds each, 20 watts in series of five at 5-second intervals. Between intervals, allow the irradiated area to cool. Permanent images are recorded to document needle position. 8. While delivering each series, continuously check for motor stimulation in upper and lower extremities and maintain verbal contact with the patient so that he or she will report sensations or pain in the extremities. 334

Lumbar 1. The patient is in the lateral decubitus position on the operating table with the symptomatic side facing upward with hips and knees slightly flexed. 2. The skin, subcutaneous paravertebral muscles, and dorsal rami of the vertebral nerve are infiltrated with 50–70 mL of mepivacaine 0.5% depending on the number of segments involved. 3. Adjust the c-arm to enable the 1.8 mm special needle to be inserted while using an oblique view onto the relevant vertebral intradiscal space followed by posterolateral insertion 6–8 cm laterally to the spinous processes into the disc under continuous c-arm control. An AP view is used to determine whether the needle tip is in the posterior third of the disc. 4. Replace the stylet with the bare fiber marking and clamping device. The bare fiber will extend 2 mm beyond the needle tip, which determines the irradiation zone in the disc.

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5. It is not uncommon to encounter difficulty when treating an L5– S1 disc herniation due to a high iliac crest and/or pronounced sacral inclination. Nevertheless, we can perform this procedure almost exclusively with the semirigid 1.8 mm needle and the stylet without injuring the L5 nerve root. A curved needle has not been used so far by us. 6. Using a conventional approach, one should attempt to position the needle in the posterior third of the intervertebral disc. Using a straight laser application, the nonparallel action of the laser beam has not resulted in any serious consequences in our experience. 7. If insertion into the L5–S1 intervertebral space is unsuccessful, puncture laser osteotomy can be performed after deep analgesic sedation. A total application is made of up to 300 joules, one shot per second, 15 watts, while exerting mechanical pressure on the needle. 8. Following correct placement of the needle, replace the stylet with the bare fiber. 9. Following application of a series of laser shots with a maximum of 1 second and 15 watts, the needle length is changed on reaching about 750 joules by withdrawing it about 2 mm. This is done under continuous c-arm control, again with verification of proper needle placement. 10. During the procedure, the motor response in the foot and perioperative pain are constantly monitored. If the patient expresses pain, we briefly pause the laser shot application for up to 5 seconds. 11. It is usually possible to puncture 2–3 intervertebral discs from a single access site. For this purpose, the needle tip must be shifted subcutaneously to the respective segment under continuous radiographic guidance. 12. After a total dose of 900–1000 joules, the needle is removed, and a bandage is applied. 13. Patient should be placed supine until the analgesic sedation subsides. Then the lower extremities are repositioned such that there is 90° hip and 90° knee flexion. 14. The patient is fitted on the same day with a brace prepared from a plaster cast impression. The brace is to be worn daily for 6 weeks. Physical therapy is used only for peripheral paralysis during this interval.

CLINICAL EXPERIENCE A multicenter prospective study has been conducted. There was a total of 4977 patients, including 316 with cervical and 38 thoracic discogenic pain syndromes treated by laser between November 23, 1989, and January 12, 1999. Among the parameters recorded were pain symptomatology, clinical findings, neurological findings, imagebased diagnosis and, increasingly, with the computerized spine motion test, integrated dorsal muscle electromyelogram (EMG). Patients with prior intervertebral disc surgery were also enrolled from the outset.46 The proportion of these patients remained unchanged at 20% over the years. Based on many years’ experience with open disc and spine surgery,47 the polysegmental use of nonendoscopic percutaneous laser disc decompression and nucleotomy with the Nd:YAG laser 1064 nm was introduced.44 Ninety percent of patients were followed up at 6 weeks, while the remaining 10% were questioned by telephone interview. This scheduled survey period of 6 weeks was considered the optimal timeframe48 as it allowed for scar formation of lacerated intervertebral discs.10 The results have remained consistently good over the years. Subjective outcome is positive in 80% of lumbar spine cases, 86.5%

for cervical spine cases, and 90% for thoracic spine. Visual analogue pain ratings demonstrate a decrease of 80% (p < 0.01). Objectively, a 90% improvement in lumbar spine patients was observed, as evidenced by the change in the straight leg raising test from the first postoperative day onward. This remains an impressive testimony to the success of intradiscal laser treatments (p < 0.01). These findings have been confirmed in follow-up examinations at up to 4 years.4,40 More recently, these findings have been demonstrated in up to 8 years’ follow-up.49 Regression of paralysis in all spinal regions was noted to be over 90%. Computerized measurements of spinal mobility have also revealed marked improvement.4

COMPLICATIONS The complication rate is an important criterion for the choice of spinal intervention. Therefore, complications need to be discussed. We will disclose our 15 years of experience of PLDN with the Nd:YAG 1064 nm combined with findings in the literature.50

Technical problems Due to technical problems with the laser tool, one cervical and one lumbar intervention had to be repeated the following day. In another case, the intervention was aborted as fluoroscopy failed during a lumbar intervention. In total, the error quota resulting from technical failure of the laser and X-ray machines was 0.06%. Thoracic interventions thus far have proceeded without complications. Besides the somewhat unpleasant feeling of a repeated intervention, patients did not experience adverse consequences. A needle break has been described by Ascher following the use of a special needle. However, despite the broken needlepoint remaining in the fatty tissue, no negative effects were reported. Lastly, a single incident of a broken laser fiber point has also been reported.

Problems following the puncture of the discal region Due to severe cervical spondylosis in the adjacent disc, two of 800 cervical discs were not punctured. In one case, a laser osteotomy was necessary to obtain access. Injuries to the vertebral arteries, trachea, and esophagus did not occur. However, cases of trachea and esophagus injuries have been published, though the incidence is rare. In comparison to open anterior surgical approaches, the risk is significantly smaller. With percutaneous laser interventions, vascular injuries are rare, while damage to the esophagus has been recorded as between 0.03% and 0.07%. Pneumothoraces have been reported, but no serious long-term sequelae. Due to an unsuccessful T5–6 disc puncture, one patient was not laser treated. No puncture-related complications occurred. In the lumbar spine region, five cases resulted in a prevertebral needle placement. No adverse consequences resulted from this complication. In over 8000 punctured discs, this equates to a complication rate of 0.062%. If access needs to be obtained in the pathological segment, laser osteotomy may be necessary in 0.25% of the cases. Bone injuries did not occur and never negatively influenced the results. When the L5–S1 disc was inaccessible from a posterolateral approach, three cases were performed using a transdural puncture without complications. No nerve root lesions were reported using this technique. Nerve root injury rate of more than 0.46% has been reported with percutaneous nucleotomy (PLD), percutaneous endoscopic discectomy (PED), percutaneous endoscopic laser discectomy (PELD), automated percutaneous lumbar discectomy (APLD), and percutaneous fenestration (PF). The diameter of these aforementioned puncture instruments utilized is significantly larger than the 335

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diameter of the puncture tube used for the PLDN (18 gauge to 2 mm exterior diameter). Retroperitoneal vessel damage from Nd: YAG laser was reported in 3%. In 0.15% of the cases, damage to the transverse process was described. In comparison to an open microscopic nucleotomy, nerve root damage occurs in up to 8% by open procedure while the rate of nerve root injury with Nd:YAG PLDN is estimated to be significantly lower.

Hematoma51 In the cervical region, three incidents of episternal hematoma were observed without long-term consequences. A frequency of up to 11% has been reported in open procedures. With repeated puncture attempts in the lumbar spine, one large hematoma was observed. In 1.7% of patients, a psoas hematoma developed after APLD and PF interventions. Unlike open procedures that are fatal in up to 1% of epidural bleedings, these interventions do not affect the spinal canal, and no fatalities occurred.

Intra-abdominal injuries The most serious complication was a perforation of the ileum. Though the patient was initially free of complaints, he suffered the symptoms of an acute abdomen 2 days after the operation. Subsequently, he required a laparotomy with resection of the small bowel. Histologically, a laser beam-related defect was identified in the small intestine. We suspect the bare fiber penetrated the abdominal cavity where the marking sticker dissolved. It became evident that this resulted in a lesion of the peritoneal lining of the small intestine. As no retroperitoneal signs were noted postprocedure, it is improbable that the laser beam itself penetrated the peritoneal cavity. In comparison to microsurgical discectomies, the incidence of abdominal injuries, including vessels and the ureter, is 1 in 3000. This case has never been reported in any other study, and is clearly the exception. Thus, the statistical frequency of this complication is similar to that of other microsurgical discectomies. There are reported injuries to the sigmoid colon following open L4–5 microdiscectomies. These cases have resulted in a discitis. Ten cases of injuries to the intestine during conventional discectomies have been described. Injuries to the ileum during open operations usually occur when treating the L4–5 segment.

Vasovagal reactions Only three vasovagal reactions during procedures of the cervical spine have been documented. In all cases, the intervention was technically successful. Besides the effect of the local anesthetic, the cause of this could also be irritation of the carotid sinus during the puncture of the discal region. In cases of cervical discographies, this pathomechanism has resulted in cases of death. In the lumbar spine, one patient’s intervention had to be aborted after 300 joules. Nonetheless, the clinical result was very good.

Infections An intradiscal abscess formation was observed after a lumbar percutaneous laser disc decompression and nucleotomy procedure. The open re-operation was successful in resolving the abscess. Although another case was clinically suspected to be a discitis, no bacterial infection could be verified. Our incidence of infection was 0.08%. Based on numerous reports totaling 8000 completed discs, the infection rate is estimated to be 0.1%. In open discotomies, the rate of infection has been reported to be between 0.2% and 8.5%. In a multicenter study, other intradiscal operation procedures were evaluated. The incidence of spondylitis was reported to be 0.3–1.5%. 336

No infections occurred in the thoracic region. A Staphylococcus albus infection of the cervical spine resulted in the paresis of the arm, and required open surgery. There was complete resolution of the paresis. In another instance, an S. aureus intradiscal abscess led to quadriplegia. Anterior fusion and laminectomy resulted in almost complete retrogression of the quadriplegia. After 356 completed cervical cases, the rate of infection in cervical laser decompression is 0.5%. This infection rate is still significantly lower than in both anterior (2%) and posterior (1.4–2%) open approaches. One case of a deep cervical soft tissue infections with the Nd:YAG PLDN procedure was described. In contrast, 0.1–0.7% of soft tissue infections occur with anterior-approach operations on the cervical intervertebral disc. These infection rate statistics prompted prophylactic antibiotic dosing. Following a case of S. aureus infection, all patients received a preoperative 1-day dose of antibiotics. Since initiating this prophylaxis, no further infections have occurred.

Thromboembolic complications Three cases of thromboembolic complications following a lumbar procedure will be discussed. In one case, a deep vein thrombosis developed after a progressive peroneal palsy. The patient underwent conservative treatment for several weeks. Both the pain syndrome and paresis were successfully treated, though the PLDN intervention resulted in a pulmonary embolism 1 week later. In a second case of a large disc extrusion at L5–S1, a nonlethal pulmonary embolism occurred 6 weeks after intervention. In the last case of a successful multisegmental decompression for severe spinal stenosis resulting in knee extension weakness, footdrop, and plantarflexion weakness, a deep vein thrombosis occurred in the lower leg. It is estimated that, in comparison to open operation procedures, thromboembolic complications are exceptionally rare with percutaneous laser decompression. By comparison, thromboembolic events occur in 5.6% of open cervical spine cases and in 26.5% of lumbar spine cases, especially when general heparinization was not utilized. The patients undergoing laser decompression can immediately be mobilized on the day of surgery. This greatly reduces the risk of thromboembolic complications.

Neurological complications In the cervical region, neurological deficits occurred after the two infections discussed previously. This corresponds to a rate of 0.5%. Both cases resolved with appropriate treatment and therapy. The rate of neurological injuries is significantly lower than in open interventions. With the Nd:YAG laser no direct injury of neural structures in the cervical spine is known. No neurological deteriorations occurred during thoracic interventions. In the region of the lumbar spine we got five footdrops, four deteriorations of preexisting footdrop and, in one case, a new footdrop developed after the procedure. The cause of this new one has not been identified. Two other instances of footdrop resolved after conservative therapy. In another case, improvement of the dorsiflexion weakness occurred after an open intervention. There were no cases of plantarflexion weakness postoperatively. Temporary L3 myotomal weakness was seen in six cases after polysegmental procedures. In all cases, the weakness vanished within 6 months. Two cauda equina syndromes were observed. In one of these cases, the patient’s symptoms resolved after removal of an intradiscal abscess. In the other cauda equina case, a 56-year-old re-PLDN patient developed urinary retention after a multisegmental decompression. This could not be cured. Despite the fact that the conus medullaris and cauda equina syndrome are quite rare, the patient should be appropriately informed of the potential risks involved in this intervention.

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In comparison to other percutaneous operation procedures, nerve injuries were described in five of 3194 patients. Neurological injuries have been reported after chemonucleolysis, including paraplegia, conus medullaris, and cauda equina syndrome at a rate of 0.06%. In open procedures of the lumbar spine, different rates of neurological deficits have been described. It is important to recognize that conus medullaris and cauda equina syndromes, paraplegia, and other severe complications can occur. Horner’s syndrome was not an uncommon occurrence following cervical procedures. A slow improvement of Horner’s symptoms occurred after the regional local anesthetic wore off. In one case of a lumbar PLDN at L5–S1, a sympathectomy effect was noted with increased warmth in the ipsilateral lower extremity. This required 6 months to resolve. In rare cases, the Nd:YAG PLDN left a neuropathic pain in the region of the knee, the lower leg, and the foot without a radicular component despite the resolution of the positive straight leg raise test. These exceptionally unpleasant sensations usually fade away after 6–12 weeks. An intensive pain therapy program is required when these occur. The cause has not been identified with certainty. Reinnervation pain after long-standing or extensive nerve root damage could possibility be a cause.

Stability damage, damage of the endplates Thus far, no particular reactions of the endplates have been observed after the utilization of the Nd:YAG laser with a wavelength of 1064 nm. Edema in the bordering vertebral bodies was rarely seen, unlike in open nucleotomy cases.

DISCUSSION It is believed that the Nd:YAG laser 1064 nm exhibits two mechanisms of action for eliminating discal sources of pain and weakness. One is an effect of the kind observed following open intraspinal decompression: mechanical relief of the compressed intraspinal structures such as the venous plexus, spinal arteries, radicular arteries, and neuronal structures such as the nerve root and long tracts. This mechanism of action is based on the combination of intradiscal pressure reduction by vaporization and the shrinking phenomenon with maximal pressure relief in the spinal canal. Relieving venous congestion is of paramount importance in this respect, since only slight increases cause changes in dorsal spinal ganglion synapses.18 Multisegmental decompression is preferred by the authors to reduce venous stasis. This has been substantiated by the studies of Porter and Ward19 on the significance of two-level pathology. The second mechanism of action of the Nd:YAG laser is the destruction of the nociceptors in the posterior fibrous ring for pain relief. Equally as important is the destruction of the budding nerve fibers during neovascularization of the intervertebral disc tissue. The denaturation of pain-activating kinins from the torn intervertebral tissue is a factor that should not be underestimated. The experimental principles described in vitro, in vivo, and in clinical research now leave no doubt as to the efficacy of the Nd:YAG laser 1064 nm on the tissue of the intervertebral disc52 and thus on pathological manifestations in the form of clinical syndromes, despite a very mixed database. This confusion is due to incorrect quotations,42 combining results obtained with different types of lasers,53 and even incorrect scientific statements.23 It has been repeatedly asserted that there are psychological effects resulting from laser application that account for positive results. To date, no literature has substantiated this concept. Others question whether the procedure is genuinely effective for the patient or merely a ‘gimmick’ activity,54 placebo, or even nonsense. We believe

that the clinical results of the megastudy and the evaluation of the meta-analysis impressively refute those claims.5

LASER SELECTION The use of lasers naturally requires the necessary knowledge of laser physics and the ability to select an appropriate laser. Positive results can only be achieved if the right laser is used with a suitable wavelength. Experimental and clinical results have shown that the ideal choice is the Nd:YAG laser 1064 nm. The Nd:YAG laser 1320 nm also provides good results, but requires at least a threefold higher dose. Unfortunately, this higher dose can result in damage to the adjacent vertebrae. The holmium:YAG laser is less suitable for nonendoscopic operations because of the more mechanical effects, i.e. those performed only through percutaneous needle puncture.6 Based on our experimental studies and clinical experience, this technique should only be used in open or endoscopic intervertebral disc operations in an assistive mode and under visual control.30 The recently developed diode laser with wavelengths of around 940 nm (890–980 nm) has the greatest thermal effect with a very good shrinking mechanism. This has been shown by experimental research conducted by our own research group. In a prospective, randomized, single-blind clinical study, it provided the same results as the Nd:YAG laser 1064 nm without an increase in complications.29,55 Regrettably, cases in which much too high doses were used have also been reported, resulting in severe damage to the adjacent vertebrae. The same applies for the KTP laser which, when the correct fiber tip is chosen for straight shooting, provides good results without damaging the adjacent vertebrae. Nonendoscopic laser types used: KTP 532 side firing Diode 890–980 straight firing Nd:YAG 1064 straight firing Nd:YAG 1320 straight firing Ho:YAG 2100 side firing Ho:YAG 2100 straight firing

SUMMARY In a large number of patients, discogenic vertebrogenic pain syndromes can be eliminated or reduced to a tolerable level. The success rate of patient satisfaction is 80% for the lumbar spine, 86.5% for the cervical spine, and 90% for the thoracic spine. With a complication rate to date of 0.66% as demonstrated by meta-analyses, the procedure appears to be safe. Because of its absorption spectrum, the Nd:YAG laser 1064 nm has been shown in experimental studies to offer the best preconditions for inducing a radical drop in pressure by vaporizing disc tissue. The sudden drop in pressure in the spinal canal due to the shrinking effect associated with the thermal action, accompanied by shortening of the collagen fibrils in the intervertebral disc structure, is to be regarded as an even more important process. Additional effects include the increased stability of the moving segment and the destruction of nociceptors and nerve fibers in the posterior fibrous ring as well as the vascularized intervertebral disc in the degeneration process. Also not to be neglected is the denaturing of pain-inducing intervertebral disc-generated kinins. Since exact studies on the penetration depth of the Nd:YAG 1064 nm laser beam and heat convection have not produced any evidence of damage when using the correct dose, the Nd:YAG laser 1064 is currently the laser2,8,10,20,31,53,56,57 of choice for intradiscal intervertebral disc decompression and nucleotomy.49,53,57–60 337

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References 1. Kiskimäki I., Seitsala S, Östermann H, et al. Reoperations after lumbar disc surgery. Spine 2000; 25:1500–1508. 2. Choy DSJ, Case RB, Ascher PW. Percutaneous laser ablation of lumbar disc. Ann Meet Orthop Res Soc 1987; 1:19. 3. Miriutora NF. Laser therapy in the treatment of discogenic neurological manifestations of spinal osteochondrosis. Vopr Kurortol Fizioter 2000; 3:30–33. 4. Kornelli H, Hellinger J. Der computerisierte Spine-motion-Test mit integrierte perkutane Rückenmuskel-EMG prä- und postoperativ nach perkutaner Laserdiskusdekompressio und nukleotomie. Schmerz 1998; 12(Suppl 1/98):63. 5. Hellinger J, Stern S. Nonendoskopische PLDN-Nd-YAG 1064 nm – Eine 10-Jahres- Bilanz als Megastudie und Metaanalyse. Newsletter Dornier Med Tech, 2000; S2. 6. Choy DSJ, Ascher PW, Saddekni S, et al. Percutaneous laser disc decompression. Spine 1992; 17:949–956. 7. Yonyzawa T, Matomura K, Atsumi K, et al. Laser nucleotomy: a preliminary study for vaporizing the degenerated nucleus. Laser in der Orthopädie, Symp. Hannover, Germany, 1991:19–20.09. 8. Hellinger J. Technical aspects of percutaneous cervical and lumbar laser disc decompression and nucleotomy. Neurol Res 1999; 21:99–102. 9. Hilbert J, Braun A, Papp J, et al. Erfahrungen mit der perkutanen Laserdiskusdekompression bei lumbalem Bandscheibenschaden. Orthop Prax 1995; 31:217–221. 10. Skuginna A, Reinicke J. Open discectomy after failed percutaneous laser disc decompression; histological results [abstract]. III. Barcelona: Kongress effort; 1997:581. 11. Turgut M, Acikgöz, B, Klinc S, et al. Effects of Nd-YAG laser on experimental disc degeneration. Acta Neurochir (Wien) 1996; 138:1348–1354. 12. Kosaka R, Onomura T, Yonyzawa T, et al. Laser nucleotomy – a case report of open procedures. J Japan Spine Res Soc 1992; 3:249. 13. Mayer HM. Percutaneous endoscopic laser discectomy. Internat. Symposium ‘New Developments in Knee and Spine Surgery.’ Munich, Germany, 1991: 21–22.11. 14. Grönemeyer D. CT-guided lumbar laser nucleotomy [abstract]. Internat. Symposium ‘New Developments in Knee and Spine Surgery.’ Munich, Germany, 1991: 21–22.1. 15. Hellinger J, Linke DR, Heller HJ. A biophysical explanation for Nd-YAG percutaneous laser disc decompression success. J Clin Laser Med Surg 2001; 19:235–238. 16. Brat H, Bouziane F, Lambert J, et al. CT-guided percutaneous laser-discdecompression (PLDD): prospective clinical outcome. Laser Med Sci 2003; 18 (Suppl 2):16. 17. Wuttge R, Hellinger J, Hellinger S. Pre- and postoperative MR-myelography of PLDN. In: Brock M, Schwarz W, Wille C, eds. Spinal surgery and related disciplines. Bologna: Monduzzi; 2000:895–898. 18. Sugawara O, Atsuta Y, Iwahara T, et al. The effects of mechanical compression and hypoxia on nerve root and dorsal root ganglia. Spine 1996; 21:2089–2094. 19. Porter RW, Ward D. The significance of two-level pathology. Spine 1992; 17:9–15. 20. Siebert W. Percutaneous laser disc decompression: the European experience. Spine 1993; 7:103–133. 21. Wittenberg RH, Steffen R. Minimal-invasive Therapie lumbaler Bandscheibenvorfälle. Bücherei d Orthop 1997; 68:23–24. 22. Thal DR, Werkmann K, Leheta F, et al. Effects of Nd-YAG laser radiation in cultured porcine vertebral tissue. SPIE 1996; 2623:212–231. 23. Siebert W. Corrigendum. Percutaneous laser discectomy of cervical disc: preliminary clinical results. J Clinical Laser Med Surg 1996; 14:354. 24. Schmolke S, Kirsch L, Barth A. Gosse: Infrarot-Thermographie und Bestimmung des Ablationsvolumens bei zervikaler Lasernukleotomie. In: Matzen KA, Hrsg. Therapie des Bandscheibenvorfalls. München: Zuckschwerdt; 1998:193–201. 25. Kolarik J, Nadvornik B, Rozhold O. Photonucleolysis of intervertebral disc and its herniation. Zbl Neurochir 1990; 51:69–71. 26. Grasshoff H, Mahlfeld K, Kayser R. Komplikationen nach perkutaner Laserdiskusdekompression (PLDD) mit dem Nd-YAG-Laser. Lasermedizin 1998; 14:3–7. 27. Knight M, Patko JA, Wan S. KTP-523 laser disc decompression – 6 years experience [abstract]. Fifth Intern. Congr. IMLAS. Sevilla, Spain, 1998. 28. Liebler WA. Percutaneous laser disc nucleotomy. Clin Orthop 1995; 310:56–58. 29. Paul M, Hellinger J. Nd-YAG (1064) versus diode (940 nm) PLDN: a prospective randomised blinded study. In: Brock M, Schwarz W, Wille C, eds. Spinal surgery and related disciplines. Monduzzi; Bologna: 2000:555–558.

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30. Hellinger J. Holmium-YAG-assistierte offene Nukleotomie. Laser Med Surg 1995; 11:86–87. 31. Schlangmann BA, Schmolke S, Siebert WE. Temperatur- und Ablationsmessungen bei der Laserbehandlung von Bandscheibengewebe. Orthopäde 1996; 25:3–9. 32. Casper GD. Results of a prospective clinical trial of the holmium-YAG laser disc decompression utilizing a side-firing fiber: four year follow-up [abstract]. Fifth Intern. Cong. IMLAS. Sevilla, Spain, 22–25.4, 1998. 33. Hellinger J, Manitz U. Vertebragene Syndrome bei degenerativen Wirbelsäulenerkrankungen. Med Akt 1981; 6:274–278. 34. Hellinger J. Zur Nosologie und Therapie zervikaler vertebraler Syndrome bei degenerativen Erkrankungen. Z Orthop 1981; 119:595–596. 35. Weishaupt D, Zanetti M, Hodler J, et al. Imaging of the lumbar spine: prevalence of intervertebral disk extrusion and sequestration, nerve root compression, endplate abnormalities and osteoarthritis of the joints in asymptomatic volunteers. Radiology 1998; 209:661–666. 36. Choy DS, Ngeow J. Percutaneous laser disc decompression in spinal stenosis. J Clin Laser Med Surg 1998; 16(2):123–125. 37. Ohnemeiss DD, Guyer RD, Hochschuler SH. Laser disc decompression. The importance of proper patient selection. Spine 1994; 19:2054–2058. 38. Gangi A, Dietemann JL, Ide C, et al. Percutaneous laser disk decompression under CT and fluoroscopic guidance: indications, technique and clinical experiment. Radiographics 1996; 16:89–96. 39. Grasshoff HR, Kayser N, Mahlfeld D. Diskographiebefund und Ergebnis der perkutanen Laserdiskusdekompression (PLDD): Fortschr Röntgenstr 2001; 173: 191–194. 40. Evermann H, Stern S. Four years follow up non-endoscopic percutaneous laser disc decompression (PLDD) [abstract] Fifth Intern. Coug. IMLAS. Sevilla, Spain, 22–25.08, 1998. 41. Messing-Jünger AM, Bock WJ. Lumbale Nervenwurzelkompression. Ein cooperatives Projekt zur Qualitätssicherung in der Neurochirurgie. Zbl Neurochir 1995; 19:26–56. 42. Schmolke S, Gossè F, Rühmann O. Die perkutane Laser-Diskusdekompression. In: Matzen KA, Hrsg. Therapie des Bandscheibenvorfalls. München: Zuckschwert; 1997:223–231. 43. Hellinger J. Borderline indications for lumbar Nd-YAG-PLDN. Intern. 21. Course for percutaneous endoscopic spinal surgery and complementary techniques. 23–24.01.03 Zürich, Schweiz, 2003. 44. Hellinger J. Nonendoskopische perkutane Laserdiskusdekompression und Nukleotomie. Med Bild 1995; 5:49–56. 45. Hellinger J. Die Laserosteotomie als Zugangsmöglichkeit zur lumbalen und zervikalen perkutanen Nukleotomie. Laser Med Surg 1992; 8:105. 46. Hellinger J. Nd-YAG-Laser-YAG PLDN in postnucletomy syndrome. In: Brock M, Schwarz W, Wille C, eds. Spinal surgery and related disciplines. Bologna: Monduzzi; 2000:277–280. 47. Kähn R, Hellinger J, Graner H, et al. Klinisch- neurologische, röntgenologische und elektrodiagnostische Nachuntersuchungsergebnisse des lumbalen Bandscheibenvorfalls. Beitr Orthop Traumatol 1979; 17:703–705. 48. Berendse GAM, Berg SGM, Kessels AHF, et al. Randomized controlled trial of percutaneous intradiscal radiofrequency thermocoagulation for chronic discogenic back pain. Spine 2001; 26:287–292. 49. Stern S. Eight years follow up non-endoscopic percutaneous laser disc decompression (PLDD) – high-tech tool for intradiscal pain therapy or placebo? Tenth Intern. Congr. IMLAS. Luxembourg, 19–21.6, 2003. 50. Hellinger J. Komplikationen der nonendoskopischen perkutanen Laserdiskusdekompression und Nukleotomie (PLDN) mit dem Neodym-YAG-Laser 1064 nm. Orthop Praxis 2002; 38:335–341. 51. Grumme TH, Kolodziejcyk D. Komplikationen in der Neurochirurgie. Berlin: Blackwell; 1994:121–202. 52. Anders JO, Pietsch S, Staupendahl G. Kritische Betrachtung der Indikationen des Holmium:YAG- und des Neodym:YAG-Lasers in der orthopädischen Chirurgie anhand einer In vitro-Studie. Biomed Tech (Berl) 1999; 44:83–86. 53. Zweifel K, Panoussopoulos A. Laser und Bandscheibenchirurgie. In: Berlin HP, Müller G, Hrsg. Angewandte Lasermedizin. Landsberg [ecomed]. III-3.11.3:12–16, 1996. 54. Mayer HM, Müller G, Schwetlick G. Lasers in percutaneous disc surgery: beneficial technology or gimmick? Acta Orthop Scand 1993; 64(Suppl 251):38–44. 55. Menchetti PPM, Longo L. Diode laser treatment of migrated disc. Laser Med Sci 2003; 18(Suppl 2):17.

Section 2: Interventional Spine Techniques 56. Choy DSJ, Altman P, Trokel SL. Efficiency of disc ablation with lasers of various wavelengths. J Clin Laser Med Surg 1995; 13:153–156. 57. Siebert W, Bise K, Breitner S, et al. Die Nucleus-pulposus- Vaporisation- Eine neue Technik zur Behandlung des Bandscheibenvorfalls? Orthop Praxis 1988 12:73.

59. Castro WHM, Halm H, Schinkel V. Neodymium-YAG-1064nm Laservaporisation von lumbalen Bandscheiben: Klinische Frühergebnisse. Aachen: Laser Shaker, 1992:187. 60. Hellinger J. Ein neuer Weg der Bandscheiben-Chirurgie. Ärztl Praxis 1992; 44:21–22.

58. Berendsen B-T, Schlangmann B, Schmolke S. Percutaneous laser disc decompression (PLLD): fundamental experiments and clinical findings [letter]. Dornier 1995; 1:20–22.

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CHAPTER

Spinal Cord Stimulation for Chronic Pain Management Implantation Techniques

30

Giancarlo Barolat

INTRODUCTION The fact that electricity might beneficially affect painful conditions has been known since antiquity.1–4 Spinal cord stimulation (SCS) was introduced by Shealey in 1967.5 Initially, the electrodes were placed over the dorsal columns in the subarachnoid space through a laminectomy. Subsequently, the electrodes were implanted, always through a laminectomy, between the two layers of the dura or epidurally. Some authors demonstrated efficacy of the procedure even with electrodes implanted ventrally to the spinal cord.6–8 This did not prove to be a practical way of conducting spinal cord stimulation and was subsequently abandoned. In 1975, Dooley described percutaneous implantation of electrodes in the dorsal epidural space. Manufacturers involved in the early stages of SCS included Medtronic, Avery, Cordis, Clinical Technology Corporation. Initially, the stimulating systems were only radiofrequency (RF)driven passive receivers. In the mi-1970s, Cordis introduced the first pulse generator powered by a lithium battery. This was then followed by the Itrel pulse generator manufactured by Medtronic. In the first stages, stimulation was delivered through a unipolar electrode. Subsequently, bipolar arrays were made available. Many different types of percutaneous and plate-type arrays were developed. In all of them, however, the contact combinations were hardwired, and could no be reprogrammed after the pulse generator was implanted. A very important advance stemmed by the collaboration of Joseph Waltz and the Neuromed company in the early 1980s; they produced the first percutaneous quadripolar electrode with contact combinations that could be reprogrammed noninvasively through the external transmitter.9,10 In the late 1970s, there was a surge of enthusiasm for spinal cord stimulation among neurosurgeons in Europe and in the US. Thousand of patients with almost any type of painful condition were subjected to SCS. Poor patient selection, technical problems with the implanted equipment, and implantation by surgeons with minimal experience and commitment, resulted in a large number of patients with poor results; in the early 1980s the procedure fell into disrepute and was viewed with skepticism. Only a few dedicated neurosurgeons continued to apply this procedure for pain management. Gradually, in the past 10 years, the procedure has regained acceptance in the management of chronic nonmalignant pain; its role is currently firmly established in the armamentarium of the pain specialist as proven by several reports in the literature. The procedure has been acquired by other specialties, first among them anesthesiologists specializing in pain management. Other specialties have also demonstrated interest in the procedure, although to a lesser extent, such as rehabilitation medicine and orthopedic surgery. Interestingly, a large percentage of the SCS implants currently performed in Europe (particularly in

Italy and Spain) are performed by vascular surgeons for the management of peripheral vascular disease. Because of the emerging complexity of the structures being involved by the stimulation, the term ‘dorsal column stimulation,’ which was originally applied to this procedure, has been in general replaced by the term ‘spinal cord stimulation.’ Spinal cord stimulation, even though not considered an extremely technically demanding surgical procedure, commands extreme care in the details of the planning and of the execution. One has to be extremely fastidious about the correct positioning of the electrode(s), both in the longitudinal and transverse direction in the spine, about the position of the pulse generator, about the location of the subcutaneous wires and about the hook-up of the whole system. If only one of the various factors is not optimal, the effectiveness of the whole procedure might be negated. This chapter will discuss the various available hardware solutions and some of the technical details of surgical implantation.

CURRENTLY AVAILABLE EQUIPMENT Currently available equipment for SCS consists of electrodes, pulse generators, radio receivers, and transmitters.

Electrodes There are two main types of electrodes, the catheter-type (otherwise commonly referred to as ‘percutaneous’ leads) and the plate-type (otherwise commonly referred to as ‘laminotomy’ or ‘surgical’ leads) (Fig. 30.1). Percutaneous electrodes are commonly used both for trial stimulation or for permanent implantation. The most commonly used electrodes are either quadri- or octopolar. The general trend is to utilize one or two quadripolar electrodes for limb pain, and one or two octopolar electrodes for axial pain. A percutaneous electrode recently introduced by Advanced Bionics (Sylmar, CA) has 16 electrical contacts. The electrodes might be connected directly to the pulse generator/receiver, or they can be connected to an intermediate subcutaneous extension which, in turn, interfaces with the pulse generator/receiver. Plate-type electrodes require surgical implantation under direct vision (Fig. 30.2). The amount of actual bony removal varies and is often limited to a small portion of the lamina and spinous process. The simplest quadripolar plate electrode is the Medtronic Resume and Resume-TL, and the Advanced Neuromedulation Systems Lamitrode 4 (Medtronic Inc., Minneapolis, MN; Advanced Neuromedulation Systems, Plano, TX), with all four contacts arranged linearly in one paddle. The Medtronic Specify and the ANS Lamitrode 44 have eight contacts arranged in two parallel columns. Another electrode (ANS Peritrode) consists of two smaller paddles, each with two contacts; this configuration allows

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Fig. 30.1 Some of the currently available spinal cord stimulation electrodes.

Spinal cord

Plate electrode inserted in the dorsal epidural space (transparent bony structures)

nal cord levels. By inserting multiple parallel electrodes, various configuration matrices can be constructed that allow creating extremely focused electrical fields. Placement of percutaneous electrodes must be performed under fluoroscopic guidance (Fig. 30.4). This requires wearing heavy shielded garments and potentially exposes the implanting physician to non-negligible levels of radiation. The plate electrodes require open surgical intervention. Bony removal can be very limited. In the thoracic area the lower two-thirds of the spinous process and a small portion of the lamina usually have to be removed. In the cervical area, bony removal is often not necessary, and this is particularly true when placing electrodes at the C1–2 level. Most ‘laminotomy’ implants can be done through a small (1–1.5") skin incision. By advancing the electrode in a cephalad or caudal direction, one can explore at least three spinal levels in the thoracic and 4–5 in the cervical spine. (Fig. 30.4) Multiple arrays or different electrode configurations can

Fig. 30.2 Schematic drawing of a dual-plate electrode in the dorsal epidural space or of one dual octopolar plate electrode.

the surgeon to place the paddles in two different locations or with two different orientations and therefore offers a greater degree of flexibility. Plate electrodes with one or two columns of eight contacts are also available (ANS Lamitrode 88 and Lamitrode 8). With modern technology, both types of electrodes are safe and effective ways of delivering electrical stimulation to the spinal cord. The percutaneous technique is appealing because it allows one to insert the electrode without muscle dissection and bony removal (Fig. 30.3). This is a substantial advantage when one wants to perform a trial stimulation to assess candidacy for a permanent implant. Percutaneously placed electrodes can also be advanced over several segments in the epidural space, thus allowing testing of several spi342

A pair of percutaneous electrodes inserted in the dorsal epidural space (transparent bony structures)

Fig. 30.3 Schematic drawing of two parallel octopolar percutaneous electrodes in the dorsal epidural space.

Fig. 30.4 Anteroposterior X-ray view of two implanted percutaneous electrodes.

Section 2: Interventional Spine Techniques

be also constructed by utilizing more than one plate electrode. In the author’s experience, the main advantage of plate electrodes resides in their greater inherent stability in the dorsal epidural space and lesser propensity to migrate. Plate electrodes are the only option in case of previous spine surgery at the planned implant levels. The pattern of stimulation–induced paresthesiae provided by plate electrodes might be superior to the ones produced by the percutaneous electrodes. In a randomized, prospective study, North et al. proved that the performance of plate electrodes significantly exceeded that of percutaneous electrodes.10 Concordance of stimulation paresthesiae with pain was statistically better for plate electrodes. Plate electrodes are electrically more efficient. This is due to the fact that all the current is directed toward the dura instead of being dispersed circumferentially, as in the percutaneous electrodes. Plate electrodes therefore have a lower current requirement. Another advantage of plate electrodes with two columns of contacts lies in the fact that, unlike two parallel percutaneous electrodes, the relation among the electrical contacts is fixed and completely predictable. Some situations clearly command one of the two methods (i.e. a percutaneous system in the case of an outpatient percutaneous trial, or a plate electrode in the case of prior spine surgery). In most other situations, the choice is usually dictated by individual preferences and patterns of practice. A skilled implanter can usually achieve a similar stimulation matrix with either a plate or a percutaneous electrode. The differences between plate and percutaneous electrodes is likely to become more blurred with the development of miniaturized plate electrodes that can be introduced epidurally through a percutaneous device

Pulse generators/receivers See Figure 30.5 Stimulation consists of rectangular pulses delivered to the epidural space through the electrodes. Two types of systems are currently available. The totally implantable pulse generators contain a lithium battery in the pulse generator. They are activated and controlled by

Advanced Bionics

Medtronic

Medtronic

Advanced Neuromodulation Systems

Fig. 30.5 Currently available fully implantable pulse generator and patient programmer.

outside transcutaneous telemetry and, once activated, do not require any patient input to function. They can also be turned on and off through a small magnet. Lifespan of the battery greatly varies with usage and with the utilized parameters (voltage, rate, pulse width, etc.). Most patients can expect, under average use, the battery to last 2.5–4.5 years. Available lithium-powered pulse generators allow stimulation to be given in increments of 0.1 V. and with rates up to 130 Hz. The Precision pulse generator, manufactured by Advanced Bionics, contains a rechargeable lithium battery. The battery is recharged by wearing an outside recharger while the stimulator is in use. The interval between charges varies with usage time and power requirements and can be expected to be in the order of at least several days under normal utilization. Lithium-powered pulse generators make up the majority of implanted spinal cord stimulator. Radiofrequency-driven systems, instead, consist of a passive receiver, implanted under the skin, and the transmitter which is worn outside of the body. An antenna, which is applied to the skin in correspondence of the receiver and connected to the transmitter, transmits the stimulation signals transcutaneously. In order for the system to function, the transmitter has to contain charged alkaline batteries and the antenna must make adequate contact with the receiver. This requires the patient to wear the outside system in order to receive the stimulation. RF-driven systems can deliver stimulation with a rate up to 1400 Hz, and can be customized to deliver more power than the corresponding lithium-powered systems. Both systems have advantages and disadvantages. The main disadvantage of the RF systems is the inconvenience of having to wear the antenna and the radio receiver. The problem might go beyond pure inconvenience in individuals who have handicapped motor function in the upper extremities and cannot properly go through all the steps required to make the external unit function properly. Other patients, particularly individuals affected by a complex regional pain syndrome type 1, might not tolerate the antenna taped to the skin. The equipment cannot be worn while swimming or showering, and severe perspiration might make proper contact of the antenna problematic. Besides these considerations, the patient has to worry about changing batteries on a regular basis and making sure that the proper coupling exists between the antenna and the receiver at all times. These inconveniences are obviated by a lithium-powered system that runs automatically without any patient intervention. The RF system is usually reserved for patients who have greater power requirements and who would have to undergo replacement of the lithium-powered pulse generator with an unacceptably high frequency. The advent of the rechargeable lithium battery might redefine this requirement and the indications for an RF system. The distribution of the electrical fields within the intraspinal structures is affected by the position of the electrode array as well as the polarity of the individual contacts. In order to generate an electrical field, one must have at least one negative contact activated (cathode) and one positive contact activated (anode). With the ANS and Medtronic systems, each contact can be either on or off. The Advanced Bionics System, instead, allows each electrical contact to be activated in fractional increments, thus allowing an almost seamless change in the distribution of the electrical field.

WHAT STRUCTURES ARE BEING STIMULATED The spinal canal contains several nervous and non-nervous structures that, when stimulated electrically, give rise to a variety of responses. The electrical properties of the intraspinal contents can be characterized as the ones of an nonhomogeneous conductor (Fig. 30.6) Knowledge of the different type of responses and their 343

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correlation with the underlying anatomical substrate is extremely important in implementing strategies for spinal cord stimulation.11,12 The width of the cerebrospinal (CSF) space is the most important factor in determining the stimulation parameters, particularly the perception and discomfort thresholds (Fig. 30.7). Dorsal root fibers in general have a lower stimulation threshold than dorsal column fibers and this is particularly evident with increasing thickness of the CSF layer. This is due in large part to the fact that dorsal root fibers have a very high conductivity at their entry into the spinal cord. Stimulation of the large myelinated afferent fibers at the intraspinal level can occur in four different areas: the dorsal root, the dorsal root

Vertebra 0.04 s/m Dura mater 0.03 s/m CSF 1.7 s/m

Ventral root Ganglion

Dorsal root Epidural space 0.04 s/m

Spinal cord -Gray matter 0.23 s/m -White matter Longitudinal 0.60 s/m Transverse 0.083 s/m

Fig. 30.6 Schematic drawing of the various intraspinal structures as they relate to spinal cord stimulation.

entry zone, the dorsal horn, and the dorsal columns. Electrical activation of these structures elicits tingling paresthesiae that are always ipsilateral to the stimulating electrode. If the stimulation voltage is increased, discomfort and pain occur. Clinically, it is extremely important to differentiate activation of the segmentary large myelinated afferents (dorsal root/entry zone/dorsal horn) versus activation of the ascending long tracts in the dorsal columns. Activation of the segmentary afferents causes paresthesiae located in the radicular dermatome at the level of the electrode. For electrodes in the thoracic area, this usually means paresthesiae along the anterior chest wall. With electrodes placed at T12 or L1 the usual pattern is paresthesiae along the anterior aspect of the thigh or in the inguinal area. In the cervical spine, paresthesiae will be elicited in various segments of the upper extremity. The stimulation threshold for the segmentary system is lower than the one for the dorsal columns, and usually ranges 0.1–0.5 volts Differentiating between stimulation of the dorsal root, dorsal root entry zone, or dorsal horn can be exceedingly difficult. One can assume dorsal root stimulation can be expected if the electrode is placed laterally in the spinal canal. On the other hand, stimulation of the dorsal root entry zone and/or dorsal horn is more likely if the electrode is placed near midline, and segmentary paresthesiae are rapidly followed by activation of the dorsal columns with a small voltage increment. Stimulation of the longitudinal fibers of the dorsal columns is characterized by ipsilateral paresthesiae occurring in areas of the body caudal to the level of the electrode The exact distribution of the paresthesiae varies with the level of the electrode and with some degree of interindividual variability. In some individuals, activation of the dorsal columns gives rise to a smooth tingling sensation which is uniformly distributed in all the dermatomes caudal to the implanted electrode. This is usually the hallmark of upcoming good therapeutic effects. Other individuals, fortunately a minority, perceive the stimulation with a patchy distribution, affecting separate body segments that are not connected by paresthesiae. Individuals that exhibit this pattern of distribution of the paresthesiae, unfortunately, almost never experience any meaningful pain relief.

Spine levels

Correlation between perception threshold and thickness of the CSF space dorsal to the cord C1–2 C3 C4 C5 C6 C7 T1 T2 T3–4 T5 T6 T7 T8 T9 T10 T11 T12 L1

Thickness of dorsal CSF layer

C5 C6

T5 T6

T11 T12 0

344

C4

Perception threshold

0.5

1 Volts

1.5

2

0

2

4 mm

6 Fig. 30.7 Perception threshold and dorsal cerebrospinal fluid thickness at various spine levels.

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Activation of the dorsal columns usually occurs at a threshold that is at least 0.5–1.0 volt higher than the segmentary pathway. A thicker dorsal CSF space usually favors more selective activation of the segmentary sensory system as opposed to the dorsal column fibers. It is common to observe that, initially, systems are simultaneously activated, but after a few weeks the stimulation pattern is confined to a segmentary band. For this reason electrode placement in the upper thoracic spine (where the CSF space is the widest) seldom results in satisfactory long-term stimulation of the dorsal lemniscal pathway. When stimulating the intraspinal structures epidurally, most commonly one observes a mixture of dorsal column, dorsal root entry/ zone, dorsal root stimulation. This is true particularly with electrodes placed in the low thoracic–upper lumbar area (T11–12, L1) where the spinal cord tapers into the conus medullaris and the cauda equina nerve roots are a prominent component of the intraspinal structures. Stimulation of the motor structures results in muscle contractions. Activation of the segmentary motor system (ventral root/motor neurons) results in muscular contractions in the somatic distribution of the stimulated segment. Activation of the descending corticospinal pathways, instead, causes muscle contractions in segments caudal to the level of the electrode. With laterally placed electrodes, stimulation of the segmentary motor system can occur at a threshold equal to or lesser than the one for large myelinated afferents. This invariably results in unpleasant contractions that can completely mitigate the benefits of the stimulation. In the vast majority of patients, stimulation over the dorsal columns does not result in activation of the motor system unless the stimulation is increased to a much higher voltage. The author, however, has occasionally seen patients in whom, even with a perfectly placed midline electrode, activation of the motor system occurred simultaneously with the sensory system. In these instances, selective stimulation of the dorsal column cannot be successfully performed.

OPERATIVE TECHNIQUE Intraoperative anesthetic management Electrode implantation can be performed either under monitored anesthesia (local anesthetic and intravenous sedation) or under general anesthesia. Unlike SCS for movement disorders or for peripheral vascular disease, the exact distribution of the stimulation-induced paresthesiae is crucial in pain management. Consequently, it is crucial to test an awake and cooperative patient if the best results are to be achieved. When the procedure is performed under general anesthesia, one can rely only on the radiological position and on evoked motor or sensory responses. However, when the procedure is performed under general anesthesia, one cannot obtain information about the specific details of the distribution of the paresthesiae or as to whether there is concomitant motor stimulation at the therapeutic threshold. Percutaneous electrode placement is always performed with local anesthesia and intravenous sedation. Plate electrode implantation can be performed either under monitored or general anesthesia. Unless there are medical contraindications, it is the author’s preference to perform the implantation of the stimulator under general anesthesia and then to wake up the patient intraoperatively to perform the sensory testing of the electrode positioning. Percutaneous and plate electrode implantation under general anesthesia is required at the C1–2 level. Anesthetic management during implantation performed under monitored anesthesia is of crucial importance to the success of the procedure. Working with an uncooperative patient or one who is too sedated to be able to answer questions during the testing might result

in complete failure of the procedure or, even worse, in accidental neural injury. The procedure should be accomplished with minimal discomfort for the patient. The patient should be fully awake and cooperative during the testing phase. With keen attention to detail and good cooperation with the attending anesthesiologist, these goals can be satisfactorily reached in the majority of the patients. Generous anesthetic infiltration with a long-acting agent minimizes the requirements for intravenous sedation. Whether the procedure is percutaneous or through a laminotomy, the periosteum must be generously infiltrated. The dura is often painful when first touched by an instrument or the needle. The pain is usually sharp and localized to the stimulated site. Dural pain, however, usually habituates quickly, and only minimal/moderate discomfort is usually perceived upon further dural manipulations or needle insertions. Some authors have advocated injecting local anesthetic (1% lidocaine or 0.25% bupivacaine) in the epidural space. This results in analgesia to painful pinprick and reduces local anesthetic requirements without preventing the patient from warning that the needle may be piercing the dura. This technique has been shown not to affect the electrical stimulation of the large myelinated fibers in the spinal cord and therefore does not jeopardize the reliability of the intraoperative testing. Excessive use of intravenous benzodiazepines must be avoided because the duration of their effect can be unpredictable and the patient may remain confused at the wake-up test. The key medication during this procedure is propofol (Diprivan, Stuart Pharmaceuticals, Wilmington, DE). This is an intravenous hypnotic agent which has a rapid onset of action when given intravenously and whose effects last only a few minutes. The best way of administering it is through intermittent boluses or continuous infusion. The patient usually wakes up promptly and lucidly when the drug is discontinued. Despite the fact that with increasing dosage propofol will eventually cause respiratory depression, a regimen can usually be found where the patient is adequately sedated without excessive respiratory depression. Constant interaction between the surgeon and the anesthesiologist is imperative.

Percutaneous electrode placement Most commonly, the procedure is performed in the prone position. If the patient is unable to tolerate that position the procedure can also be performed in the lateral decubitus or seated position. Although feasible, the lateral decubitus position makes intraoperative fluoroscopic assessment more problematic. In some centers, the procedure is routinely performed with the patient in a sitting position. An advantage of this latter position is enhanced patient comfort and increased ability to obtain a thoracolumbar kyphosis, which facilitates insertion of the needle in the epidural space. The patient is positioned in a comfortable prone position on a padded fluoroscopy table. A certain degree of kyphosis, as obtained by inserting a pillow underneath the abdomen, facilitates electrode insertion. It is very important to make sure that the trunk (for thoracolumbar placement) and/or neck (for cervical placement) are in a neutral position without any rotation. Several considerations determine the level of electrode insertion. Since at least 3” of the lead body must lie within the epidural space in order to assure maximal stability of the electrode and minimize unwanted dislodgment, the insertion must be at least two spine segments below the desired target. For cervical placement, electrode insertion should be performed below the T1–2 level in order to avoid the risk of damaging with the needle the cervical cord enlargement. Most commonly, implantation for a pain problem in the lower part of the body usually entails electrode insertion at T12–L1 or L1–2 while implantation for an upper extremity target requires insertion at T2–3 or T3–4.

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The fluoroscopy equipment is commonly utilized in both the anteroposterior (AP) and lateral planes at the time of needle insertion. This will allow monitoring of the depth of penetration and the laterality of the needle. The Tuohy needle is inserted with as shallow an angle as one possibly can obtain. While in the thoracic area this can be accomplished with either a midline or paramedian approach; in the upper lumbar area a paramedian approach is required. Besides lessening the risk of a dural puncture, a shallow trajectory greatly facilitates the subsequent insertion of the electrode in the epidural space. An excessively steep angle of entry of the electrode into the epidural space will also increase the risk of electrode fracture or dislodgment. A paramedian needle insertion is always more desirable, not only because it allows a more shallow angle of needle placement, but also because it avoids placing the electrode between two adjacent spinous processes. During lordotic extension of the trunk, the electrode can be pinched between the two spinous processes, leading to premature electrode fatigue and fracture. A specific tactile feedback occurs when the needle engages the ventral surface of the lamina. When this is perceived, gentle wiggling of the needle hub will produce slight movement of the needle shaft but not of the needle tip. If entry in the interlaminar space proves to be extremely difficult, one can attempt to increase the degree of spine flexion to open up the interlaminar space; other options include changing the angle of approach or trying a different level. If the ligamentum flavum is calcified (as often happens in the thoracic spine), one can gently tap the needle to force it through; occasionally the only way to insert the needle through a calcified ligament is through an open laminotomy. Of the several methods that are available to identify the epidural space, the tactile feedback that ones perceives when the tip of the needle enters the epidural space is important, but can be missed and cannot be completely relied upon. The most common method is the loss of resistance using a low-friction syringe (and not the usual disposable plastic syringes). After several needle insertions at one spine level, however, the loss of resistance method may loose its reliability. The insertion of a guide wire through the needle provides invaluable information as to the degree of penetration into the spinal canal. If the needle tip is in the interspinous ligament and has not completed penetrated the ligamentum flavum, the wire cannot be advanced. Advancement of the wire is possible only if the needle tip is in the paraspinal muscles or within the spinal canal. The pattern of advancement and the location of the wire under fluoroscopic imaging usually clarify its position. Once the electrode is in the spinal canal, one has to be certain that it is positioned in the epidural and not subarachnoid space. Even though this might seem obvious and easily recognizable, there are instances in which it is more difficult. For example, when multiple attempts are needed to achieve seemingly proper needle placement, the ability to differentiate electrode location may be compromised. This is especially true if the arachnoid has been previously pierced and CSF has escaped and pooled in the dorsal epidural space. When the electrode is in the subarachnoid space, much less resistance is encountered when moving the guide wire (or the electrode), particularly for lateral movements. The wire seems almost to be ‘floating’ and undergoes large shifts of direction; this contrasts with epidural placement, where electrode movements are more discrete and obtained only with specific manipulations. The same type of wire/electrode movement can, however, be experienced epidurally if the dural sac has significantly collapsed because of CSF escape. Another helpful clue occurs during stimulation. When electrical current is delivered into the subarachnoid space, motor or sensory responses are elicited at a much lower threshold than that which occurs epidurally. 346

When the epidural space is satisfactorily identified, the electrode is gently inserted under fluoroscopic guidance in the AP plane. Removal of the electrode once it has been inserted through the tip of the needle has to be accomplished with the utmost care. It is very easy to catch the electrode in the needle and shear it at the junction of the insulation with the electrical contacts. If the electrode does not slide without any resistance (even minimal), the needle and the electrode should be removed altogether. Every time the electrode is withdrawn through the needle, it should be thoroughly inspected for minute breaks in the insulation, which would demand its disposal. Alternatively, a sleeve can be inserted over the guide wire in the epidural space. The guide wire is then removed and the electrode inserted through the sleeve. This obviates the risk of shearing the electrode during its manipulations. The electrode is then steered in the epidural space to the desired location. Should the targeted location prove to be less than two spinal segments from the electrode insertion, the electrode should be withdrawn and repositioned at a more caudal level. Frequently, the electrode curves around the dural sac and slides in the ventral epidural space. In the AP projection this might be undistinguishable from a proper midline dorsal location. A gentle lateral curve of the electrode shortly after its entry in the epidural space should raise the suspicion that the electrode is actually going around the spinal sac. Absolute confirmation of the ventral location arises from the stimulation, which elicits mostly motor contractions. Alternatively, observation in the lateral plane readily discloses the anterior position of the electrode tip. If more than one electrode is inserted, all the needles should be inserted before passing the electrodes into the epidural space. Needle insertion might shear an already implanted electrode. In addition, it is often possible to insert two electrodes simultaneously and advance them synchronously in the epidural space while maintaining their relative position and spacing. In other situations it might be convenient to insert a guide wire parallel to the electrode to block its passage to an unwanted location. The electrode is then guided to the desired location. Some electrodes have a removable wire stylet that can be bent. Other electrodes are inherently stiffer and must be slightly bent to help in steering. Patience, persistence, and frequent use of the fluoroscopic unit are the keys to successful electrode placement. Once in place, the electrode must be secured to the interspinous ligament to minimize dislodgment. Various anchors exist to facilitate this process.

Plate electrode placement Patient positioning Two basic positions can be utilized: prone or semilateral. The prone position allows a more straightforward understanding of the spatial relations and is one that the surgeon is usually more familiar with for spine surgery. However, the potential difficulty in airway management precludes any type of substantial intravenous sedation. This position is therefore contraindicated with cervical implantations under monitored anesthesia. The prone position can safely be utilized for implantation under general anesthesia. In the semilateral position the patient lies comfortably in a benchpark type position, allowing the operative field to include the spine as well as the flank, abdomen or buttock for the pulse generator implant. If the pain is predominant on one side, the patient is asked to lie on the least affected side. In this position, airway management is safer than in the prone decubitus and the anesthesiologist feels more comfortable waking up and extubating the patient intraoperatively. One has to be aware that, because of variable degree of rotation of the

Section 2: Interventional Spine Techniques

body, 3-D spatial rapport and angles may vary; this can render 3-D visualization of the operated structures less intuitive. This problem is compounded in the cervical area since one has both rotation and flexion/extension of the spine. In the author’s experience of more than 2000 implanted plate electrodes, the semilateral position has proven to be superior for implants in which the patient is awakened intraoperatively. The prone position is always utilized in the case of electrode placement at C1–2 (under general anesthesia).

Strategies at different spine levels In the planning phase of the procedure, the implanting surgeon must be aware of the varying angulation of the spinous processes at the different spine levels. The surgeon must also be aware of the correlation between the various spine levels and the patterns of stimulationinduced paresthesiae.12,13

Thoracic – upper lumbar area Prior to the surgery, an X-ray is taken in the operating room with metallic markers placed on the skin at the level of the planned incision. This allows for a precise marking of the entry level. Alternatively, one can localize the level with fluoroscopic imaging. In the lower thoracic – upper lumbar area the incision is usually placed over the interspinous gap. If placed over the spinous process it usually has to be lengthened. In the mid – upper thoracic area, instead, the incision can be placed either over the interspinous gap or over the spinous process itself (depending on the location of the incision, the bone removal technique may vary.). In a thin individual the incision is usually about 1" in length. Even in large individuals, the incision seldom needs to be more than 2" long. Different considerations apply if one is implanting in an area where a previous laminectomy has been performed. Subperiosteal dissection is usually limited to the upper half of the spinous process inferior to the desired ligamentum flavum and to at least the inferior two-thirds of the spinous process superior to it. Parts of the superior spinous process are incrementally removed until the ligamentum flavum is visualized. In the lower thoracic – upper lumbar area this usually requires removal of inferior one-third of the spinous process. In the mid thoracic area the whole spinous process must be removed (due to the acute angle and significant overlapping of the spinous processes). A slightly different strategy can be adopted in the mid – upper thoracic spine. The incision can be made over the spinous process and removal encompasses the lower one-third of the superior process. Removal continues through the upper half of the inferior spinous process and lamina until the epidural space is exposed. With this approach the exposed epidural space lies directly under the incision instead of being slanted in a cephalad direction. This makes it possible to insert an electrode either in a caudal or cephalad direction. Following removal of the ligamentum flavum, the electrode(s) is inserted in the dorsal epidural space; the patient is then awakened and, when mentally clear, intraoperative testing begins.

Mid – low cervical area The patient is placed in the semilateral position with the neck slightly flexed. The skin incision is usually about 1" long. Even with a short skin incision one can reach 3–4 levels by extending the dissection of the subcutaneous tissues and by stretching the skin edges with a Gelpi retractor. The neck should be positioned so that it is flexed but not excessively rotated laterally. Even though some neck rotation is inevitable, extreme rotation increases substantially the difficulty of the procedure.

It is important to study in detail the anatomy of the spinous processes on the spine X-ray immediately before starting the procedure. Once inside the cervical fascia, one can palpate the spinous processes and try to recognize them based on the radiographic features. Because of the neck rotation, finding the midline in the cervical area is usually more difficult than in the thoracic area. The alignment may substantially vary even between two adjacent spinous processes and the plane from one spinous process to the next might be different; one could therefore be misled and wander off midline in the lateral regions of the neck. One has to be aware of the fact that, especially at C3–4 or C4–5, the spinous processes are small and the ligamentum flavum can be extremely thin. When the neck is flexed, one could inadvertently enter the spinal canal. It is not unusual in the cervical spine to be able to remove the ligamentum flavum and have adequate access to the epidural space without having to perform any bone removal.

C1–2 This placement is indicated in some patients with motor disorders or in pain management when the pain is in the jaw area and/or in the neck – shoulder – upper extremity(ies). The patient is under general anesthesia and is placed in the prone position with the head held in a Mayfield head-holder (Fig. 30.8). The cervico-occipital junction is flexed as much as possible to open the C1–occiput space but the cervicothoracic junction is kept straight without angulation. An incision of 1–1.5" is placed at the cervico-occipital junction, over the arch of C1. After exposing the arch of C1 and the superior aspect of the C2 lamina, the ligamentum flavum between C1 and C2 is removed. Complete subperiosteal dissection is then carried out underneath the arch. If the C1 arch is particularly thick, it is undermined and thinned with a 45° Kerrison rongeur. The electrode(s) is then passed in a caudal direction under the arch of C1 and then under the C2 lamina. No electrical contact should lie above the arch of C1, in correspondence of the cisterna magna. At this level the distance between the electrode and the cord makes it almost impossible to stimulate the spinal cord. Intraoperative testing is carried out relying on motor responses. Stimulation is applied at 1–2 Hz with increasing voltage until motor contractions are elicited. At this level a midline electrode usually triggers contractions in the neck and shoulder muscles bilaterally. A more laterally placed electrode produces motor stimulation in the ipsilateral upper extremity. By sliding the electrode laterally one can precisely fine-tune the degree of lateralization of the stimulation. At this level, sensory stimulation usually follows closely the motor stimulation.

Implantation of the radio receiver/pulse generator There are two types of spinal cord stimulation systems: (1) those with three parts, namely the electrode, an extension cable and the radio receiver/pulse generator, and (2) those with two parts only, namely the electrode and the radio receiver. In this latter situation, the electrode extension is long enough to connect directly to the radio receiver/ pulse generator. The position of the pulse generator/receiver is crucial. If placed in an uncomfortable position, the unit will eventually have to be moved to a different location. The most common placement sites include the abdomen, the fat pad in the posterior iliac area, the infraclavicular area and the lateral chest wall area (Fig. 30.9).

Posterior iliac area This location is typically the most convenient region for the stimulating unit. The exact site of the placement is crucial, and it is at the 347

Part 2: Interventional Spine Techniques Occipital bone

C1 C2

A-P X-ray

Electrode(s) pointing in a caudal direction

Lateral X-ray

Head held in Mayfield Head-holder

Incision

Fig. 30.8 Most common locations for implanted pulse generators/receivers.

presence of the underlying iliac wing acts as a stabilizing element. Even if the patient loses a large amount of body fat, the posterior iliac area does not change dramatically (unlike the abdominal adipose tissue). This area is also ideal for placement of radiofrequency receivers. The presence of the underlying iliac wing provides a firm background and allows the antenna to consistently make good contact with the implanted unit. The radio receiver/pulse must not be placed low in the buttock, since that location would make sitting extremely uncomfortable.

Abdomen

Fig. 30.9 Patient position and schematic rendition of dual-plate electrode placement at C1–2.

level of the fat pad present laterally in the posterior iliac area, usually slightly below the iliac crest level. The main advantage of this location lies in the fact that, independently from the size of the patient or his/her body fat, the implant tends to remain stable without excessive motion. The subcutaneous tissue in that location is firm, and the

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The abdomen, due to its large surface, is a natural candidate for implantation. For many patients, abdominal placement of the unit is adequate. The problem occurs when the patient has a large adipose tissue or, worse, loose abdominal wall tissues. In this case, it is extremely difficult to secure the stimulator to a firm surface. In this scenario, the unit tends to migrate, tilt, or actually flip onto itself. When the abdominal wall tissues are loose, even suturing the electrode to the abdominal fascia will not assure proper stabilization. A similar situation occurs when a previously implanted patient loses a significant amount of weight. The position of the belt line must be identified, since placing the unit exactly under the belt line will most likely be perceived as uncomfortable and will eventually lead to a revision.

Section 2: Interventional Spine Techniques

Lateral chest wall

Motor testing

This location is suitable only for small radiofrequency transmitters. The main advantage is that the firm underlying rib cage allows excellent contact between the radio receiver and the antenna. The main disadvantage lies in the fact that the receiver could rub against one or more ribs and/or the forearm and become a source of discomfort.

The patient must not be paralyzed at the time the testing is carried out. Only short-acting muscle relaxants can therefore be given at the beginning of the procedure, if necessary. Stimulation must be given at a rate of 1–2 Hz. The elicited motor contractions are observed and/or recorded through surface electrodes. The goal is to place the electrode where one can trigger motor contractions in the desired extremity. This will assure that the stimulation-induced paresthesiae will also be perceived in the affected extremity. The mere fact that motor contractions are elicited in the desired limb, of course, is no guarantee that the paresthesiae later will be perceived exactly in the painful area. Motor stimulation is therefore not nearly as reliable as direct patient’s sensory feedback. Motor stimulation is usually performed in cases when the implant is installed under general anesthesia and prior to patient awakening. This allows one to minimize repositioning of the electrode with an awake patient.

Infraclavicular area This location can be utilized exclusively with cervically implanted electrodes. It is an excellent location for both RF and lithium-powered systems. The presence of the underlying rib cage facilitates contact between the antenna and the radio receiver. A potential problem with this location, particularly in females, is that, in some instances, the unit tends to migrate caudally and lodge in the breast area. Even securing the unit to the subcutaneous tissues with nonreabsorbable sutures may not provide a solution. The author has actually secured the unit to the bone by drilling a whole through the clavicle and suturing the unit to it. The subcutaneous pocket is made with either blunt (fingers, Kelly clamps) or sharp (scissors, cutting coagulator) dissection. When preparing the pocket for an RF system, one must make sure that the thickness of the subcutaneous tissue above the receiver is not more than 0.5–1". A thicker layer might impede transmission of the RF signals from the antenna to the receiver and prevent activation of the system. The pocket must be only slighter larger than the implanted unit in order to prevent its migration. Attention must be paid to having the whole unit (including the connectors) completely within the pocket and not crossing underneath the skin incision. The excess cable should be looped behind the unit, so that it would not be damaged if the subcutaneous pocket were to be tapped with a needle to aspirate fluid. The unit can be secured to the underlying tissues with nonreabsorbable sutures. If one is concerned about a high risk of migration or tilting of the unit (in patients with large adipose tissue and/or loose subcutaneous tissues), the unit should be placed in a Dacron pouch which can then be secured with multiple sutures to both the deep and superficial subcutaneous layers. This maneuver will minimize, but not completely eliminate, the risk of migration/tilting. Placement under the fascia is sometimes indicated, particularly in thin patients or in subjects who cannot tolerate the bulging of the implant under the skin. The subfascial plane is often vascular, because of the vascularization of the underlying muscles, and adequate hemostatis must be secured prior to closure. Careful securing of the implant is also mandatory to prevent migration of the unit in the subfascial plane.

Intraoperative testing If the procedure is performed under monitored or local anesthesia, the patient is woken up after the electrode(s) is placed in the desired position. The patient must be fully awake, cooperative, and with normal cognitive abilities before starting the intraoperative testing. Failure in this respect will inevitably result in incorrect positioning of the electrode. It is extremely important to assure that the patient is comfortable during the stimulation trial. When testing, the implanter must be aware of the different responses that stimulation of the various intraspinal structures will elicit. The strategy for electrode placement in both the transverse and longitudinal direction varies according to the pain topography and intraoperative elicited responses.12 As a general rule, one wants to achieve a complete paresthesia coverage of the painful area at the lowest possible stimulation threshold and with the least amount of extraneous stimulation. If the implantation is performed under general anesthesia, one can rely on three factors.

Somatosensory evoked potentials Some authors have advocated the utilization of intraoperative somatosensory evoked potentials to help localize the correct position of the electrode. The author does not have any personal experience with the utilization of this modality.

Intraoperative radiological localization Intraoperative localization, either by plain X-ray or by fluoroscopy, can be useful to locate the spine level and lateralization of the electrode. One must be aware, however, that only with extreme lateral position of the electrode in the spinal canal, can any correlation be made between electrode location and lateralization of paresthesiae. It is well known that the physiological midline of the spinal cord does not always correspond with the radiological midline. A midline electrode placement is one in which the X-ray shows a centrally placed lead and motor stimulation elicits bilaterally symmetrical motor contractions.

CONCLUSIONS By utilizing proper surgical techniques, implantation of spinal cord stimulation systems can be accomplished safely and effectively. The reliability and the complexity of the systems has increased in the past few years, and technical hardware-related problems are less common now. The electrodes remain the weak part of the system, particularly the ones implanted in the cervical area. Due to the greater mobility of the neck, electrodes implanted in the cervical area tend to migrate or break with greater frequency then in other locations. Spinal cord stimulation has risen to the role of one of the most effective procedures available today for the long-term management of some chronic pain conditions.

References 1. Diascorides T. The Greek herbal of Diascorides. Translated by J. Goodyear, ed. London: Oxford University Press; 1934. 2. Galen C. De usu partium. English translation by M. Tallmadge, ed. Ithaca, NY: Cornell University Press; 1968. 3. Kellaway P. The part played by electric fish in the early history of bioelectricity and electrotherapy. Bull Hist Med 1946; 20:112–137. 4. Stillings D. A survey of the history of electrical stimulation for pain to 1900. Med Instrum 1975; 9:255–259. 5. Shealy CN, Mortimer JT, Reswick JB. Electrical inhibition of pain by stimulation of the dorsal columns. Preliminary clinical report. Anesth Anal Cur Res 1967; 46:489–491. 6. Hoppenstein R. Electrical stimulation of the ventral and dorsal columns of the spinal cord for relief of chronic intractable pain. Surg Neurol 1975; 4:187–194.

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Part 2: Interventional Spine Techniques 7. Larson SJ, Sances A, Cusick JF, et al. A comparison between anterior and posterior implant systems. Surg Neurol 1975; 4:180–186.

11. Barolat G, Zeme S, Ketcik B. Multifactorial analysis of epidural spinal cord stimulation. Stereotactic Functional Neurosurg 1991; 56:77–103.

8. Lazorthes Y, Verdie JCL, Arbus L. Stimulation analgesique medullaire anterieure et posterieure par technique d’implantation percutanee. Acta Neurochir 1978; 40:253–276.

12. Barolat G, et al. Mapping of sensory responses to epidural stimulation of the intraspinal neural structures in man. J. Neurosurg 1993; 78:233–239.

9. Waltz JM, Andreesen WH. Computerized percutaneous multi-level spinal cord stimulation in motor disorders. Appl Neurophys 1982; 45:73–92. 10. North RB, Kidd DH. A prospective randomized comparison of spinal cord stimulation electrode design. Acta of the 8th World Congress, The Pain Clinic. Tenerife, Spain, May 6–8 1998:p. 57.

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13. Barolat G. Experience with 509 plate-electrodes implanted epidurally from C1 to L1. Stereotactic Functional Neurosurg 1993; 61:60–79.

PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

Intrathecal Therapies and Totally Implantable Drug Delivery Systems

31

Mouchir Harb and Elliot S. Krames

INTRODUCTION The discovery of opioid receptors in 19711 and their subsequent isolation in nerve tissue in 19732 in brain tissue3 and the spinal cord were foundational to the idea of using intraspinal opioids for pain control. In 1976, intrathecal opioid infusion was first reported in animals.4,5 Subsequently, intrathecal and epidural morphine was used in humans in 1979.6,7 Both modes of intraspinal delivery were effective in effectively controlling chronic nonmalignant and cancer pain.8 The discovery of a pain processing and modulating role for gamma-aminobutyic acid (GABA) receptors, adrenergic receptors, glutamate receptors, and calcium channels, amongst others, at both spinal and supraspinal levels, expanded intrathecal therapy to include non-opioid agents for intrathecal analgesic application. The treatment of chronic nonmalignant pain, like the treatment of cancer pain, requires that the treating physician understands the mechanism underlying the patient’s pain, the psychological and behavioral factors operant in perpetuating that pain, and the appropriate treating modalities to manage the diagnostic specific pain syndrome.9 It is important to know that there are no syndrome-specific therapies and there are many therapies to choose from for the management of chronic pain conditions. Because there are many therapies to treat chronic pain, from noninvasive to more invasive therapies, caregivers should choose therapies using a logical approach or algorithm to those choices. Fig. 31.1 is an example of a pain treatment continuum or algorithm of care that we use in our practice for patients with nonmalignant pain. This continuum of care starts with exercise at the bottom of the ladder moving up, by order of invasiveness and cost, towards more invasive therapies including implantable technologies and neuroablative therapies. This continuum of care should be placed in context by the

PAIN CONTROL Neuroablation Spinal analgesia Spinal cord stimulation Strong opioid medications Weak opioid medications Cognitive and behavioral therapies Adjuvant medications Physical and occupational therapies Over the counter medications Exercise PAIN

Fig. 31.1 The pain treatment continuum.

reader and should not be considered guidelines to care. It is important to emphasize that spinal analgesia is a costly and an invasive therapy and therefore should be applied only when less invasive and less costly therapies have failed, including sequential systemic opioids trials.

INDICATIONS FOR INTRATHECAL THERAPY Initially, intrathecal therapy was only used for patients with cancer-related pain syndromes, but over the years the indications for intrathecal therapy have expanded.10 Newer indications include neuropathic pain syndromes,11 failed back surgery syndrome (FBSS),12,13 complex regional pain syndromes,14 and head and neck pain.15 Intrathecal therapy is invasive and expensive treatment for chronic pain and should only be applied when certain criteria are applicable. These inclusion criteria for intrathecal therapy include: 1. Failure of less costly and less invasive therapies including spinal cord stimulation (SCS), when applicable; 2. Objective pathology exists that is concordant with the pain complaint; 3. Further surgical interventions are not indicated; 4. No serious untreated drug habituation exists; 5. There are no psychological barriers to successful outcome; 6. There are no absolute contraindication for implantation; and 7. A trial, ruling in efficacy and ruling out toxicity, has been performed. It is also important, when choosing therapies for cancer and noncancer pain, to know whether the patient’s pain is primarily nociceptive in nature, whether the pain is primarily neuropathic in nature, or whether the pain is of a mixed neuropathic/nociceptive nature. For example, when choosing pharmaceutical therapies, patients with primarily nociceptive pain usually respond to opioid and NSAID therapies. Patients with primarily neuropathic pain may or may not respond to opioid or NSAID therapies but may respond to adjuvant medications such as tricyclic antidepressants, Ca2+ channel blocking agents, the anticonvulsant medications (Na+ channel blocking agents, GABA-ergic medications, NMDA receptor). Likewise, when choosing implantable technologies for pain control such as spinal cord stimulation (SCS) or intrathecal therapy with opioids, it is equally important to know if the patient’s pain is nociceptive, neuropathic, or mixed nociceptive/neuropathic. Neuropathic pain is amenable to spinal cord stimulation for pain, while nociceptive pain is not. Intrathecal opioid therapy is useful for nociceptive pain, but minimally useful for patients with primary neuropathic pain. Intrathecal therapy with non-opioids such as local anesthetics, alpha-adrenergic agents or voltage sensitive, N-type calcium channelblocking agents have been shown to be effective with neuropathic pain syndromes. Because intrathecal therapies are moderately efficacious

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for neuropathic pain syndromes when using admixtures of opioids and non-opioids there exists no clear-cut boundaries when choosing between SCS or intrathecal analgesic therapies for neuropathic pain syndromes. Fig. 31.2 is a Venn diagram that presents clear-cut diagnoses which respond to intrathecal opioids alone and those that respond to spinal cord stimulation alone. The overlapping gray area represents diagnoses that will respond to both therapies. Intrathecal therapy with opioids and non-opioids alike is only indicated when trials of sequential, long-acting, potent opioids have failed. Failure is not defined as failure to provide analgesia but is defined as intolerable and intractable side effects with all long-acting opioids trialed. If the patient tolerates high doses of any given opioid without analgesic effect and has no side effects, that patient has opioid nonresponsive pain and most probably will not respond to intrathecal opioid therapy alone. This patient, having tried all appropriate therapies for the pain, is a candidate for intrathecal admixture therapies with opioids/local anesthetics/alpha-adrenergic agents/voltage sensitive, N-type Ca2+ channel-blocking agents, in some form of combination as will be outlined below. There are some minor points to remember when designing intrathecal therapies and systems for patients with chronic, nonmalignant pain when compared to patients with end-of-life, terminal pain. Patients with nonmalignant pain will live long lives not cut short by their disease and therefore are candidates for continuous, totally implanted intrathecal systems (catheter and pump). Patients with terminal illness, with less than 3 months to end of life after failure of conservative therapies tried, might be candidates for intrathecal therapies but, because of a shortened life expectancy, should be implanted with a spinal catheter or catheter/port alone, connected to an external pump. Those with terminal illness with life expectancies greater than 3 months are candidates for totally implanted systems.

TRIALS FOR INTRATHECAL THERAPY When a patient meets all criteria for intrathecal analgesia delivery and that patient has failed conservative therapies as outlined in Figure 31.1, that patient should undergo a trial for intrathecal therapy. We, in our practice, do not perform ‘single-shot,’ intrathecal or epidural trials since ‘single-shot’ trials are associated with strong non-

• Lump radioculopathy • Cervical radioculopathy • Mononeuropathy • Intercostal neuralgia peripheral vascular disease

• Reflex sympathetic dystrophy • Causalgia • Failed back surgery syndrome • Arachnoiditis • Diabetic neuropathy • Alcoholic neuropathy • AIDS-releted neuropathy • Slump pain • Phantom limb pain • Postherpetic neuralgia • Spinal cord injury • Plexus neuropathies

specific or placebo effects. In order to mitigate non-specific or placebo responses, and thus avoiding implanting an expensive device in the wrong patient, trials should be as long as logistically possible. It is our belief that continuous external delivery of agents through an implanted intrathecal catheter for as long as possible is the only trial that can possibly mitigate these strong, non-specific, placebo responses. We call this implanted intrathecal catheter/external pump trial a ‘functional trial.’ This ‘functional trial’ not only may mitigate strong placebo responses, but allows for continuous sequential trialing of multiple agents and mimics the final implanted drug delivery system. We perform most of our functional trials on an outpatient basis, Medicare patients being the exception because of reimbursement issues. Medicare will only reimburse for outpatient intrathecal trials for patients with malignant pain and will not reimburse for intrathecal trial outpatient services (home infusion, nursing, etc.) for patients with nonmalignant pain. For our trials, we surgically implant an FDA approved intrathecal catheter, anchoring the catheter to the perispinous fascia, and attaching the catheter to a tunneled, externalized subcutaneous epidural catheter system (Dupen Catheter®) Bard Access systems, Salt Lake City, Utah). All patients are given preoperative antibiotics with a broad-spectrum antibiotic, usually cephalexin for 72 hours, to cover for Staphylococcus aureus and S. epidermidis infections. After implantation and tunneling, the Dupen catheter system exit site is covered with an antibiotic-coated dressing (Bio-Patch, Johnson and Johnson, NJ) and then covered by a clear plastic dressing. The entire system is attached to an external pump system with two intervening 0.22 micron filters. Patients are instructed to lead a normal lifestyle at home, performing activities of daily living as they would normally do. If the patient tolerates the initial drug and dose without analgesia, the dose is adjusted by programming the pump to accelerate delivery. Because existing external pumps are programmed to deliver rates at 0.1 increments, starting as low as 0.1 cc/hour, we usually deliver our desired hourly dose at the flow rate of 0.2 cc/hour. If we delivered the desired hourly dose in 0.1 cc/hour, then our next choice for increase is 0.2 cc/hour, a doubling of the dose. When we start at 0.2 cc/hour and wish to increase to 0.3 cc/hour, then we only increase our dose by 50%.

• Diffuse cancer pain • Osteoporosis • Visceral pain • Axial somatic pain • Head, neck pain • Multiple sclerosis

The circle on the left lists chronic pain syndromes that respond to spinal cord stimulation. The circle on the right lists pain syndromes that respond to the intraspinal administration of opioid medications. The shared area in the middle of the Fig. 31.2 Venn diagram of the trialing of spinally overlapping circles lists pain syndromes that respond to either spinal cord stimulation or spinally administered opioids. administered analgesia.

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If the patient does not tolerate the initial drug trialed and is in need of trial of a second agent, only the drug reservoir, the existing tubing and the first 0.22 micron filter which is proximal to the more distal filter (filter nearest the catheter exit site) is changed. Because it is known that infection rates of these systems is proportional to the ‘fiddle-factor’ in personnel handling the systems, we adopt a handsoff policy to system changes and dressing changes. We first change the dressing of the system within 48 hours of surgery and then, unless the dressing becomes wet, we only change the dressing, once every 7 days. We recommend that only physicians or nurses familiar with this system be involved in dressing changes. Biopatch® is left unchanged for 7 days unless saturated with blood. A reduction of pain by 50% and/or improved function with reduced systemic intake of opioids indicates a successful trial. Evaluation for efficacy of spinal analgesia should be individualized, taking into consideration analgesic improvement and/or improvement in function, as well. For examples, a patient who reports a 50% pain relief but refuses to increase function is, in our estimation, a trial failure. Another patient who reports only a 30% reduction in pain and not a 50% reduction in pain but is more alert and cognitively more functional is a patient for whom intrathecal therapy should be considered. To prevent withdrawal during the trial we give the patient 50% of the orally administered dose as an equivalent intrathecal dose, allowing continued oral intake of 50% of the original oral or systemic dose. Each subsequent day the oral dose is decreased by 20% and the intrathecal dose is increased by 20%.

Fig. 31.4 Medtronic Isomed fixed-rate pump.

IMPLANTABLE DRUG DELIVERY SYSTEMS The first drug delivery system approved for the delivery of intraspinal analgesics was the Infusaid, model #400 pump, which is no longer manufactured. This pump was a nonprogrammable, fixedrate flow pump. Today, there are other FDA approved fixed-rate pumps including the Codman, model 400 pump (Fig. 31.3) and the Medtronic, Isomed Pump (Fig. 31.4). These pumps utilize a charging fluid that remains a fluid at room temperature, but becomes a gas exerting pressure on a metal bellows that extrudes drug at a fixed rate when implanted into a patient. Other fixed-rate pumps used outside of the USA includes the Esox®, Archimedes®, Micromedes®, and the Anschutz pump®, all of which are fixed-rate pumps. Some new fixed-rate pumps are being developed by other companies and are not approved by the FDA in the USA today. An example is the AccRx Pump being developed by Advanced Neuromodulation Systems of Plano, Texas (Fig. 31.5).

Fig. 31.5 AccRx, a fixed-rate pump in trials, manufactured by Advanced Neuromodulation Systems, Plano, Texas.

Fig. 31.3 Codman model #400 fixed-rate pump.

Because the rate of all of these fixed-rate pumps is preset and nonprogrammable, dosing changes are made by changing concentrations of the drug. Medtronic’s Synchromed® system is the only totally implantable and programmable pump that is approved in the USA and Europe. Other companies, including Codman (a Johnson and Johnson company), Advanced Neuromodulation Systems, and Advanced Bionics (a Boston Scientific company), are developing totally programmable intrathecal delivery systems. Rate and therefore dose of drug are externally programmable (Fig. 31.6).

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Fig. 31.6 Medtronic Synchromed pump, a fully programmable pump.

Besides increasing or decreasing a continuous rate of delivery of the drug, the Synchromed® system can be programmed to deliver drug in different configurations that includes programming a single bolus of drug, a timed bolus of drug, a complex continuous delivery of drug, and a continuous delivery of drug.

INTRATHECALLY ADMINISTERED OPIOIDS Morphine remains the gold standard for intrathecal analgesic therapy. It has an extensive history, with an ample literature for intrathecal therapy, more than any other opioid.16 It is the only opioid approved by the Food and Drug Administration (FDA) for intrathecal analgesia. Other opioids are used for intrathecal therapy when patients are intolerant to intrathecal morphine and include hydromorphone,17 meperidine,18 methadone,19 fentanyl,20 sufentanil,20 and buprenorphine.21 The latter is a partial agonist that is used intrathecally in Europe. These agents are not labeled for intrathecal therapy and are not approved by the FDA, but are used empirically, based on efficacy and safety reported in the literature. Morphine’s analgesic efficacy is well reported. A prospective survey by Kumar et al. of 16 patients (mean follow-up, 29±12 months) found that intraspinal morphine reduced pain scores for all types of pain by an average of 57%. Surprisingly, the greatest efficacy was found in patients with neuropathic pain and mixed nociceptive/neuropathic pain when compared to nociceptive pain (75% and 61% reductions, respectively).22 A national outcomes registry for low back pain collected prospective data on 136 patients using intraspinal infusion via implanted devices, 81% of whom received morphine. After 12 months, the Oswestry Low Back Pain Disability Scale ratings improved by 47% in patients with back pain and by 31% in patients with leg pain.23 The dose of intrathecal morphine is highly individualized and depends on the age of the patient and the systemic dose before the initiation of intrathecal therapy. In general, a patient with neuropathic pain requires a higher dose and elderly patients require lower doses than patients who are younger to achieve analgesia. The intrathecal opioid’s time to onset and duration of action, uptake and distribution, availability to supraspinal centers, and central nervous system (CNS) side effects are all governed by the opioid’s relative (to morphine) lipophilicity and its receptor affinity.24 354

Morphine’s low lipid solubility, high hydrophilicity, and high receptor affinity translates clinically to slow onset of action but prolonged analgesic action. Because of this hydrophilicity of morphine, it remains in the cerebrospinal fluid (CSF) longer and therefore is available to ascend to supraspinal centers through bulk flow of the CSF. Because morphine mixes in the CSF and is carried from low spinal centers to higher spinal centers and supraspinal centers, the position of the catheter tip within the thecal sac is relatively unimportant to provide segmental analgesia. On the other hand, this hydrophilicity of morphine increases the risks for CNS supraspinal side effects such as nausea, vomiting, sedation, and respiratory depression. Intrathecal morphine delivery is associated with side effects. Both elevated concentrations of morphine-3-glucuronide, a metabolite of morphine in plasma, and an elevated plasma or CSF morphine3-glucuronide over morphine-6-glucuronide ratio may play a pathogenic role in the development of the cutaneous dysesthesias, hyperalgesia, and allodynia and/or myoclonus seen with the longterm delivery of high-dose intrathecal morphine.25 It seems that morphine-3-glucuronide might exert this neuroexcitatory effect by indirect activation of the N-methyl-D-aspartate (NMDA) receptor, an inotropic glutamate receptor.26 Some patients might not tolerate morphine, but may tolerate hydromorphone, a relatively hydrophilic (to morphine) but more lipophilic agent than morphine. In some patients, supraspinal effects such as nausea and vomiting might be severe. In such cases, more lipophilic compounds which do not mix in the CSF such as fentanyl, sufentanil, or methadone might be chosen. During the course of intrathecal therapy some patients, in spite of a good response to the drug during the trial, might develop tolerance to the drug’s analgesic effects, develop intolerance to the drug and resultant side effects, or develop opioid resistant pain syndromes. If side effects, such as confusion, nausea, vomiting, generalized pruritus, constipation, urinary retention, sexual dysfunction, peripheral edema, hyperalgesia, etc., do occur, pharmacologic treatment of the side effect should be tried before switching to another agent. If this strategy fails, then switching to another agent is warranted, as there is incomplete cross-tolerance among opioids. Intrathecal morphine delivery is known to be associated with hypothalamic–pituitary dysfunction. In a study conducted in Belgium, Abs et al.27 examined hypothalamic–pituitary axis function in 93 patients with non-cancer pain. Seventy-three patients received intrathecal morphine with a mean dose of 4.8 mg/day for a mean duration of 26.6 months. A 20-patient comparison group had comparable pain syndromes but was not treated with intrathecal morphine. A majority of patients of both genders in the intrathecal morphine group developed hypogonadotropic hypogonadism. Fifteen percent also developed central hypocortisolism and/or growth hormone deficiency, compared to none in the control group. Further, decreased libido occurred in 96% of men and 69% of women who received intrathecal opioids, compared with 10% and 20% of men and women, respectively, in the controlled group. Hormone replacement therapy ameliorated decreased libido in 10 of 14 males and 7 of 12 premenopausal females. The authors suggested further investigations to determine the need for systematic endocrine evaluations and replacement therapy in patients treated with long-term intrathecal morphine. Hydromorphone is a mu agonist that is 8–10 times more lipid soluble28,29 and 5–10 times more potent than morphine. It is a hydrogenated ketone of morphine. Although it is not FDA approved, it is increasingly being used for intrathecal therapy.30,31 Hydromorphone is stable when contained in an infusion system (SynchroMed) and held at 37°C for 4 months.32 Because of its higher lipophilicity than morphine, hydromorphone has a quicker onset of action, a shorter duration of action and, for the same reason, fewer supraspinal side effects because of less rostral spread.

Section 2: Interventional Spine Techniques

Because of the incomplete cross-tolerance among opioids, switching from morphine to hydromorphone is a consideration when morphine use is associated with too many side effects or poor analgesia. The initial dose of hydromorphone should be 50% of its equianalgesic dose to morphine (equianalgesia is 1:5–10) and should be titrated higher until analgesia is achieved. Hydromorphone is not only successful in delivering intraspinal analgesia33 but also has a lower incidence of side effects than morphine when given epidurally. In the retrospective study comparing intrathecal morphine to hydromorphone by Anderson et al.,30 37 patients received intrathecal hydromorphone after either inadequate analgesia or unmanageable side effects occurred during treatment with intrathecal morphine sulfate alone. Pain scores improved during the 10 months’ mean follow-up after changing to hydromorphone. Drowsiness and nausea lessened after patients were switched from morphine to hydromorphone and leg edema subsided temporarily, but eventually reoccurred after extended hydromorphone exposure A known complication of intrathecal therapies is the development of intrathecal granuloma, an intradural but extramedullary mass associated with either high dose or high concentration of intrathecally delivered agents. This complication of intrathecal analgesia will be discussed later in this chapter. In contrast to morphine, hydromorphone exposure intrathecally was not associated with the development of catheter tip granuloma in a sheep model when daily doses, equianalgesic to doses of morphine that produced granulomas, were given.34 However, hydromorphone when used in humans is known to be associated with the development of tip granuloma. In an initial report, the formation of inflammatory masses at the catheter tip was reported in 9 patients who received hydromorphone, either alone or mixed with other drugs.35 A subsequent review of the same report and database and an additional six case reports identified was published with the number of new cases reported in the literature to be 15.36 It still is unclear whether these 15 reported cases of granuloma were due to the intrathecal hydromorphone delivered or due to other agents since all patients had, at one time or another, other agents, either alone or in combination with hydromorphone, in their pumps. The neuroexcitatory side effects of opioids, e.g., hyperalgesia, are not reported to be more frequent with hydromorphone than morphine, although hydromorphone-3-glucuronide is a more potent neuroexcitant than morphine-3-glucuronide37 which could be responsible for these symptoms. Meperidine is a phenyl piperidine derivative with physical characteristics, molecular weight, and pK similar to those of local anesthetics. Because meperidine is more lipid soluble than morphine and hydromorphone it has a quicker onset and more segmental action (localized effect at the segment of the spinal cord delivered) than either morphine or hydromorphone. Meperidine is the only member of the opioid family that has clinically important local anesthetic activity in doses used for analgesia. Because of this quality of meperidine, it is the only opioid in current use that is active as a sole agent for spinal anesthesia (not analgesia). Surgical procedures to the lower limbs, inguinal area, perineum or c-section have been performed using spinal meperidine alone.38,39 Meperidine has been used for labor analgesia and found not to increase c-section deliveries.40 A 0.5 mg/kg intrathecal dose of meperidine produces anesthesia for up to 6 hours or longer.38 A dose of 1 mg/kg or a total dose of 100 mg has been associated with respiratory depression, bradycardia, and hypotension.18,41 There is limited literature on the use of continuous intrathecal meperidine via implantable infusion pumps. In a case report by Harvey et al.42 a woman with chronic low back who failed other

medical interventional treatment modalities achieved significant pain relief using a continuous intrathecal meperidine infusion. Another case report also showed similar success.43 According to Chrubasik et al., the dose of meperidine should be 25–30 times higher than morphine to maintain equianalgesia.44 A dose of up to 60 mg per day appears to be safe.45 Methadone. In a survey by Hassenbusch and Portenoy, 2–4% of respondents cited use of this opioid.46 Methadone is more lipid soluble than morphine, hydromorphone, and meperidine, and therefore does not produce noticeable migration within CSF to supraspinal centers. Methadone, based on this lipophilicity, should have fewer supraspinal side effects than morphine when given intrathecally. The L-isomer of methadone has mu agonist activity and D-isomers have noncompetitive antagonism of NMDA receptors.47 In vitro studies suggest that methadone induces desensitization of the delta opioid receptor by uncoupling the receptor from its underlying Gprotein. This delta opioid activity is critical for the development of morphine-induced tolerance and dependence. Animal studies showed that D-methadone reduces the development of morphine tolerance and NMDA-induced hyperalgesia by virtue of its NMDA receptor antagonist activity.48 Studies of the prolonged use of intrathecal methadone for cancer and non-cancer pain showed overall effectiveness between 37.5% and 80% for those populations studied based on greater than 50% reduction49–51 in pain or pain reduction combined with improved scores on quality of life questionnaire.19 These studies involved both cancer and non-cancer patients. Methadone was administered at total daily dosages of 5–60 mg and the duration of treatment ranged from 3 days to 37 months. Fentanyl is an opioid analgesic which preferentially binds to mu receptors. It is highly lipophilic and has a fast onset of action in the order of 5 minutes with a peak analgesic effect of approximately 20 minutes, when given epidurally. Due to lipophilicity, its effect is largely segmental, although continuous intrathecal infusion is associated with receptor saturation and mixing in the CSF. It is equipotent when given epidurally or intravenously.52 As fentanyl is 75–100 times more potent than morphine sulfate, lower doses are needed to produce similar analgesia. Thus, considerations for side effects must be made, especially since fentanyl side effects have been noted to be more severe than those of morphine sulfate. Cephalad spread of fentanyl which could lead to respiratory depression does occur, but less so than morphine. Although it is uncertain whether fentanyl’s exact location of action is systemic or spinal, the systemic mode of action appears to be favored by some.53 While scientific data on epidural and intrathecal fentanyl are evolving, there does appear to be a role for fentanyl in treating both acute and chronic pain processes. Two retrospective studies on intrathecal fentanyl have been reviewed. One study of 122 patients examined the complications associated with implantable drug delivery systems. This study included two patients with the combination of fentanyl and bupivacaine54 and neither of these patients experienced serious adverse events. In another study, eight patients out of a total of 29 patients with intrathecal therapy received intrathecal fentanyl, 10.5–115 mcg/ day for a mean duration of 31 months.55 The authors reported a 68% reduction in pain and an overall satisfaction of 3.25 on a scale of 1 (poor) to 4 (excellent) in all eight patients. Sufentanil is an anilino piperidine with a lipid partition coefficient 1000 times higher than that of morphine. Therefore, it has a much more rapid onset of action, and a much shorter duration of action than morphine when delivered intrathecally. Due to being extremely lipid soluble, it largely diffuses into the central neural tissue when administered intrathecally, leaving less 355

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bulk drug available for rostral movement, and thus fewer central side effects such as nausea, vomiting, itching, urinary retention, and respiratory depression. Because of this lipid solubility, after intrathecal administration, sufentanil concentrations in the CSF decrease more quickly when compared to morphine. The mean residence time in the CSF, i.e., the time required to eliminate 63.2% of the drug, is approximately 0.9 hours after injection of 15 mcg sufentanil56 while that of morphine (0.05 mg/kg) is 2.3 hours.57 The higher affinity of sufentanil to mu opioid receptors when compared to morphine gives sufentanil a potential benefit in delaying the development of tolerance to the drug. It has been postulated that agents with high efficacy and receptor reserve, i.e. sufentanil, should produce less tolerance than agents of lower efficacy and lower receptor reserve, i.e. morphine.58 Rats develop, over time, less tolerance to intrathecal sufentanil when compared to morphine. Also, sufentanil requires the occupancy of fewer mu receptors to produce antinociception than does morphine. In a survey performed by Hassenbusch and Portenoy,46 nearly 20% of pain clinicians have used either fentanyl or sufentanil in intrathecal drug delivery systems; however, there are no clinical data of long-term use of intrathecal sufentanil in humans. It is known that in humans a 10 mcg bolus of intrathecal sufentanil produces analgesia within 5 minutes with a duration of about 19 minutes.59 Because of its high lipophilicity, this agent is used when more hydrophilic drugs produce excessive supraspinal side effects. When converting morphine to sufentanil in an implanted pump, we, based on the potency ratio of sufentanil to morphine, arbitrarily use a dose conversion of 1 mcg of sufentanil to 1000 mcg (that is 1 mg of morphine) as shown in Table 31.1. Animal toxicology studies of intrathecal sufentanil have shown no detectable pathological effects on spinal cord histology. However, in a study performed in sheep, which have relatively smaller intrathecal spaces, a rather large dose of 7.5 mcg/kg of sufentanil did produce demonstrable neurotoxic changes. These authors did demonstrate a low-grade inflammatory response to the intrathecal catheter itself and concluded that the response was thought to represent a foreign body response.60 Because of its high lipophilicity, the catheter tip position for the delivery of both fentanyl and sufentanil probably plays an important role in delivering the required analgesic effect when the pain syndrome is segmental.

INTRATHECALLY ADMINISTERED NON-OPIOIDS (ADJUVANTS) Intrathecally administered opioid therapy certainly belongs irrevocably to our clinical armamentarium for pain control in cancer and nonmalignant pain patients. As stated previously, in the USA, morphine remains the only analgesic approved by the FDA for intraspinal use. Because many patients develop tolerance to their opioid analgesic,

Table 31.1: Equianalgesic opioid conversion (mg) Oral Morphine

Epidural

100

10

60

20

2

Meperidine

3000

1000

100

Fentanyl

2–[K.E.L. 1]

1

Sufentanil

2–[K.E.L.2]

0.1

Hydromorphone

356

Parenteral

300

Intrathecal 1 0.25 10

0.1

0.01

0.01

0.001

have neuropathic pain, or develop these pain syndromes during their intraspinal opioid therapy, it has become clear that intraspinal opioid therapy alone is not sufficient to provide adequate analgesia for many patients. This has led scientists and clinicians to look for other intraspinal pharmacological solutions for these opioid-resistant pain syndromes. Based on widespread clinical use and literature, the use of bupivacaine, the alpha2 agonist, clonidine, and the neuron-specific Ca2+ channel blocking agent, ziconotide, should not be considered investigational, but should be used in some form of accepted continuum of intrathecal clinical care. Most recently, in February of 2005, the FDA has approved the intrathecal use of Ziconotide (Prialt®, Elan Pharma, San Diego, California, USA) for chronic pain. The intraspinal use of other agents, such as the alpha2 adrenergic receptor drug tizanidine, opiate peptides such as DADLE or DPDPE, or other spinally active analgesic agents such as somatostatin or octreotide, NSAIDs, NMDA receptor antagonist, etc., are all investigational and should be used only with protocols accepted by an investigational review board (IRB). Bupivacaine. Local anesthetics are the most common adjuvant agents used with opioids for intrathecal therapy. By the year 2000, more then 20% of patients with intrathecal therapy for pain control had local anesthetics in their implantable pumps. According to this survey of implanting physicians, 60% of the responding physicians used morphine–bupivacaine combinations.46 Bupivacaine HCl has been shown to be stable and compatible with the Medtronic SynchroMed implantable pump, maintaining 96% of its initial concentration with chronic exposure to the system after 12 weeks at 37°C.61 Further, Trissel et al.62 in a stability study, showed that combinations of morphine sulfate, 5 mg/mL plus bupivacaine, 2.5 mg/mL, or morphine sulfate, 50 mg/mL plus bupivacaine, 25 mg/ mL, packaged in 20 mL aliquots in plastic syringes and maintained at 4°C or 23°C for 60 days or −20°C or 37°C for 2 days remained stable. In other words, the morphine remained stable at, or greater than, 97% and the potency of bupivacaine remained greater than 95%, after the study. Frozen samples exhibited microparticulates upon thawing, suggesting that freezing of morphine–bupivacaine combinations should be avoided. Bupivacaine is the intrathecal local anesthetic most widely used in humans. Other local anesthetics including tetracaine and lidocaine have been tried but their use has been abandoned due to their relative known toxicity.63 Recently, ropivacaine has been tried in humans;64 however, it offers little advantage over the less expensive bupivacaine. Human postmortem studies and the long-term usage of bupivacaine do suggest clinical safety of the long-term infusion of low doses of intrathecal bupivacaine.65 There are, however, reports in the anesthesia literature of permanent neurological sequelae, specifically the cauda equina syndrome, when some local anesthetics, specifically 5% lidocaine, are used for spinal anesthesia, particularly when delivered through small-bore intrathecal catheters.66 It is unclear, as reported by the authors, whether this complication was drug related, catheter related, technique related, or a combination of these. The positive analgesic response with the use of local anesthetic– opioid combinations intraspinally, for the treatment of cancer and non-cancer-related pain, has been previously reported.67,68 Deer et al., in a retrospective study of 109 patients, 25 with cancer pain and 84 with nonmalignant pain, studied the effect of the addition of bupivacaine intrathecally to patients who did not receive analgesia with their intrathecal opioids alone (morphine, mean dose of 8 mg/day, or hydromorphone, mean dose 1.5 mg/day).69 All patients who had a poor response to the opioid alone, who were switched to opioid–bupivacaine combinations, reported significantly lower pain

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scores and experienced a mean opioid dose reduction of 23. In a nonrandomized, noncontrolled prospective study, performed by van Dongen et al.,70 it was found that in 5 of 20 cancer patients with inadequate analgesia with morphine alone, the addition of bupivacaine (5–21.6 mg) improved pain relief. However, in the study, the doses of morphine were relatively low (1.2–7.2 mg/day). Recently, Mironer et al., in a randomized, double-blind, multiple-phase, crossover trial, comparing intrathecal morphine or hydromorphone alone to morphine and or hydromorphone with the addition of bupivacaine, found a statistically significant improvement in quality of life scores, but no change in pain scores, in the group with the addition of bupivacaine, when compared to the group with opioids alone.71 Lundborg et al. reported on their clinical experience using intrathecal bupivacaine infusion for three patients with complex regional pain syndrome.72 These 3 patients received bupivacaine at an average dose of 54 mg/ day, maximum of 90 mg/day, and were followed for an average of 374 days during their infusion for an average of 1900 days. Although there was a moderate decrease in pain, there was no improvement in allodynia, edema, or trophic changes. Clonidine is a centrally acting alpha2 adrenergic receptor agonist used intrathecally or epidurally in both animal studies and in humans. It has been shown to provide potent analgesia whether used alone or in combination with intraspinal opioids. Further, clonidine appears to block the release of substance P at the presynaptic receptor and blocks the firing of the second-order nociceptive neuron. Clonidine acts primarily at the spinal cord level where norepinephrine receptors are found. However, it is known that clonidine also works at supraspinal levels at the rostroventral medulla and the locus ceruleus of the midbrain when given systemically. Clonidine is not approved for clinical use in the USA; however, its use is widespread and safety has been established. Because of this, and because of a significant literature on its use, this agent for intrathecal use should not be considered experimental. Some authors have found that the combination of clonidine with an opioid works synergistically and thus the combination provides better analgesia at lower doses than if the drugs were given alone.73,74 Daily intrathecal dosages in humans have ranged from 3 mcg/kg to 60 mcg/kg. Studies in different animals and humans have demonstrated no neuropathology after intraspinal clonidine.75 The main side effect of clonidine, when given intrathecally, is hypotension. Humans may also experience decreases in heart rate but no metabolic changes. Other side effects of intrathecal clonidine include dry mouth, drowsiness, dizziness, and constipation. Sudden withdrawal of clonidine can precipitate agitation and rebound hypertension.76 Some authors believe that clonidine may be useful in facilitating a ‘spinal opioid holiday’1 in patients who have become tolerant to high doses of opioids.77 Clonidine may also be effective in neuropathic pain78 and sympathetically mediated pain syndromes.79 Clonidine has been used safely in numerous patients and is stable with various agents. It is stable in a titanium reservoir infusion pump (SynchroMed, Medtronic, Inc., Minneapolis, Minn., USA) in concentrations of 0.05 mg/mL and 1.84 mg/mL, in combination with morphine sulfate at a concentration of 2 mg/mL and 20 mg/mL at 37°C for 90 days and 54 weeks, respectively.80 When an admixture of morphine sulfate, bupivacaine hydrochloride, and clonidine hydrochloride was incubated in SynchroMed-EL pumps (Medtronic, Minneapolis, Minnesota, USA) at 37°C for 90 days or stored in glass vials at 4°C and at 37°C, as controls, the concentrations remained at greater than 96% of the original concentrations.81 A color change from colorless to light yellow between days 30 and 60 did not affect the solution’s stability. No particulate matter and no clinically significant changes in osmolality were observed during this 90-day study period.

As stated above, there are more than enough clinical data reported in the literature to include clonidine as an agent that could be used in some patients for intrathecal therapies. It is the opinion of these authors that clonidine should no longer be considered experimental. Hassenbusch et al. reported a 20-month prospective phase I/II cohort study of 31 patients (6 with cancer pain, 25 with nonmalignant pain) who received intrathecal clonidine alone at dosages between 144 and 1200 mcg (mean 872 mcg).82 Twenty-two patients achieved greater than 50% pain and symptom reduction without intolerable side effects. At 6 months, 77.3% (17/22) achieved continued good pain relief, and 59% of the total group were considered long-term successes (mean follow-up 16.7 months). Clonidine dosages did not change significantly over time in this group. Poor long-term outcomes were related to inadequate pain relief (n=4), intolerable side effects such as hypotension (n=2), impotence, lethargy, and malaise (n=1 each). A retrospective survey of Ackerman et al. observed that only 2 of 10 patients treated with clonidine alone (doses 75–950 mcg/day) had good pain relief after 7–11 months of intrathecal therapy.83 The addition of clonidine (75–950 mcg/day) to either morphine 0.15–15 mg/ day (5 patients) or hydromorphone 200–800 mcg/day (10 patients) similarly yielded very limited effect; only 3 of these patients achieved long-term pain relief (7–11 months). Although the results from this study and that of Hassenbusch et al.82 appear to contradict each other, it should be noted that Ackerman and colleagues’ report was retrospective in nature and their group was not homogeneous, since many patients received either many drugs over time and/or more than one drug at a time during the therapy period. Siddall et al., in a randomized, prospective study, compared the efficacy of intrathecal administration of saline, morphine (0.2–1 mg), clonidine (50–100 μg), and the combination of clonidine and morphine.84 In phase I of the study, each patient received saline, clonidine, and morphine in a random sequence. One dose per day of each drug was titrated over 3 days until the occurrence of either analgesia (defined as a >50% reduction from baseline pain score) or side effects. During phase II of the study, each patient received a combination consisting of 50% of the final dosage of morphine combined with 50% of the final dosage of clonidine. The authors compared the proportion of those patients who had a positive response at any time during the assessment. Five of 15 patients responded positively to saline, 3 of 15 responded to the largest dosage of clonidine alone, 5 of 15 responded to the largest dosage of morphine alone, and 7 of 15 to the combination of one-half the largest dosage of clonidine plus one-half the largest dosage of morphine. These data suggest that morphine and clonidine is a worthwhile combination to achieve improvement in analgesia. In a prospective study, Uhle et al. reported on 10 patients with neuropathic pain syndromes who received clonidine at an average of 44 mcg/day in combination with morphine sulfate or buprenorphine.85 All patients had a 70–100% reduction in pain after the addition of clonidine to either morphine or buprenorphine. Four of eight patients with non-neuropathic pain syndrome also appeared to benefit from the addition of clonidine. The most frequent adverse effects noted in this study were hypotension, fatigue, dry mouth, and impaired bowel (N=10, 4, 3, 1 patients, respectively). Tizanidine is an alpha2 agonist used clinically as a muscle relaxant. It appears to have a potential role as an intrathecal analgesic drug. In a dog model, Kroin et al.86 reported that tizanidine and clonidine at dosages of 3.0–18.0 mg/day yielded equivalent analgesia using a thermal withdrawal test, but that clonidine, when compared to tizanidine, was associated with greater toxicity (hypotension, bradycardia, and bradyarrhythmias). A further toxicity study of 3–6 mg/day in dogs was performed and these authors found no significant side effects or 357

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differences in spinal cord histopathology between the 3 mg/day and 6 mg/day groups. Kawamata et al.87 studied the effects of clonidine and tizanidine on a rat model of neuropathic pain. Sprague-Dawley rats were chronically implanted with lumbar intrathecal catheters, and the sciatic nerve was loosely ligated. Twenty-one to 28 days after surgery, the rats received intrathecal clonidine (0.3, 1.0, and 3.0 μg) and tizanidine (1.0, 2.0, and 5.0 μg), and the antihyperalgesic effects of thermal and mechanical stimuli were examined. In addition, changes in blood pressure and heart rate, sedation level, and other side effects after intrathecal administration of drugs were studied. The authors found that the administration of 3.0 micrograms of intrathecal clonidine or 5 micrograms of tizanidine significantly reversed both thermal and mechanical hyperalgesia. The administration of 3.0 micrograms of intrathecal clonidine, but not 5.0 micrograms of tizanidine, significantly decreased mean blood pressure and heart rate and produced urinary voiding. A greater sedative effect was produced by the clonidine when compared to the tizanidine. The authors concluded that the antihyperalgesic dose of intrathecal clonidine and the antinociceptive doses produced several side effects. Intrathecal tizanidine at the dose that reversed hyperalgesia would be preferable for neuropathic pain management because of absence of hypotension and bradycardia and lower incidence of sedation. Ziconotide is an omega-conopeptide, a synthetic form of the cone snail peptide, varpi-conotoxin MVIIA. Ziconotide is a neuron-specific, N-type voltage-gated calcium channel blocking agent with an analgesic and neuroprotective effect.88 Spinally administered ziconotide blocks neurotransmitter release from primary nociceptive afferents to prevent pain signal propagation to the brain. It has an advantage over intrathecal morphine in that it is a non-opioid and tolerance does not developed after its prolonged use. Although it has been used extensively in humans, ziconotide is approved by the FDA for clinical intrathecal use. Ziconotide is indicated for both nociceptive and neuropathic type of pain. It has been shown to be effective not only for chronic pain but also for acute postoperative pain. Atanassoff et al.89 performed a randomized, double-blind pilot study in patients undergoing elective total abdominal hysterectomy, radical prostatectomy, or total hip replacement. After intrathecal injection of local anesthetic and before surgical incision, a continuous intrathecal infusion of either placebo or 1 of 2 doses of ziconotide (0.7 mcg/hour or 7 mcg/hour) was started and continued for 48–72 hours postoperatively. Thirty patients received the study drug and 26 of them were evaluable for efficacy. It was found that the mean daily patient-controlled analgesia (PCA) morphine equivalent consumption was less in patients receiving ziconotide than in placebo-treated patients. The visual analogue scale of pain intensity (VASPI) scores during the first 8 hours postoperatively were remarkably lower in ziconotide-treated than in placebo-treated patients. In 4 of 6 patients receiving the high dose of ziconotide (7 mcg/hour), adverse events such as dizziness, blurred vision, nystagmus, and sedation led to discontinuation of the study drug infusion. After ziconotide discontinuation, these symptoms resolved. In a double-blind, placebo-controlled, short-term trial of ziconotide in 257 patients with non-cancer pain by Presley et al.,90 31% of the ziconotide-treated patients reported significantly lower pain scores, compared to 6% of the placebo-treated patients. Moderate to complete pain relief was achieved in 43% of patients in the ziconotide arm versus 18% in the placebo arm. Patients who received ziconotide also decreased their systemic opioid intake and reported improved quality of life compared to patients who received placebo. Staats et al., in a double-blind, placebo-controlled, randomized trial,91 studied 111 patients (ages between 24 to 85 years) with cancer or AIDS pain with VASPI score of 50 mm or greater. Patients 358

were randomly assigned in a 2 to 1 ratio to receive ziconotide or placebo treatment. Intrathecal ziconotide was titrated over 5–6 days followed by a 5-day maintenance phase for responders and crossover of nonresponders to the opposite treatment group. Pain relief was moderate to complete in 53% of patients in the ziconotide group compared to 17.5% in the placebo group. Five of 111 (4.5%) patients receiving ziconotide achieved complete pain relief. In spite of being a promising analgesic, ziconotide, like all analgesics, is not free of side effects, and side effects increase with a rapid titration of the agent and decrease with reduction in dose.91 Adverse events associated with intrathecal ziconotide have included vestibular disorders such as nystagmus, abnormal gait, nausea/vomiting and dizziness, urinary retention, blurred vision, diplopia, memory impairment, and orthostatic hypotension.90–92 Apparently, these side effects do decrease over time. In the study by Penn and Paice93 involving the use of intrathecal ziconotide in three patients with both neuropathic and nociceptive pain mechanisms, in dosages between 0.2 mcg/hour and 5.3 mcg/hour, significant pain relief was achieved. Side effects seen included nausea, diarrhea, nystagmus, dysmetria, sedation, confusion, and hallucinations. With intrathecal ziconotide doses of 0.9 mcg/hour or greater, much more serious side effects occurred including disorientation, agitation, and in two of three patients, unresponsiveness, which only resolved at some point after intrathecal ziconotide was discontinued. Midazolam. Midazolam is a GABA-alpha receptor agonist. GABAergic neurons appears to have a modulatory effect on pain processing both at the spinal and supraspinal levels. At the supraspinal level, the GABAergic neurons appear to have a tonic inhibitory effect over the descending noradrenergic inhibitory neurons. In contrast to that, at the spinal level, GABAergic neurons have an antinociceptive effect. Intrathecal midazolam works on the spinal GABA receptors to potentiate this analgesic effect. Midazolam has been used as a sole drug for intrathecal therapy for the management of postoperative pain.94 In animal studies, it has been shown that the antinociceptive analgesic effect of intrathecal midazolam can be reversed by naloxone; more specifically, this analgesic effect of intrathecal midazolam was blocked by delta-selective antagonists in rats.95 Midazolam has been shown to have a synergistic analgesic effect when given with bupivacaine intrathecally, and in animals this synergistic analgesic effect was demonstrated, giving midazolam with clonidine and with NMDA and AMPA receptors antagonists in rats.96,97 Because of conflicting reports of different toxicities in differing animal models, the use of midazolam, although used emperically by some in humans, continues to be controversial. Toxicity has not been associated with the intrathecal infusion of midazolam in studies on rats,96 cats,98 pigs and sheep;99 however, there has been, in contrast to these studies in rats, cats, pigs and sheep, evidenced toxicity with the intrathecal infusion of midazolam in rabbits.100 For a detailed review of preclinical safety issues with midazolam see the excellent review by Yaksh and Allen.101 In a prospective study by Rainov et al., 26 patients received a combination of various intrathecal agents as follows: four patients received midazolam 0.4 mg/day plus morphine sulfate 0.5 mg/day, clonidine 0.03 mg/day, and bupivacaine 1.0 mg/day; four patients received morphine/bupivacaine/midazolam; and two patients received morphine/ midazolam.102 Overall, 19/26 patients (73%) achieved good to excellent pain relief, 6/26 patients (23%) achieved sufficient pain relief, and one patient reported poor pain relief. No information was provided regarding outcomes according to drug combination received on-study. Baclofen is a GABA-beta agonist that has been used to treat spasticity since 1984. Intrathecal baclofen is FDA approved for the

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treatment of spasticity caused by upper motor neuron disease; however, questions remain as to whether baclofen is an analgesic when given intrathecally. Baclofen is stable alone or in combinations with clonidine when placed into intrathecal pump systems.103

Other non-opioid agents used intrathecally Other agents shown to be effective for the relief of pain when given intrathecally include neostigmine,104,105 adenosine,106,107 and octreotide.108,109 Neostigmine is an acetylcholinesterase (Ach) inhibitor which increases the availability of acetylcholine at the neuromuscular and the dorsal horn level. Since muscarinic receptor2 agonists produce antinociception in rats,110 and because muscarinic receptors have been detected at the level of the substantia gelatinosa and to a lesser extent in laminae III and V of the dorsal gray matter of the spinal cord, it was felt that neostigmine would be an effective analgesic if given intraspinally in humans. Neostigmine does produce analgesia in humans; however, its use is associated with an extremely high incidence of nausea and vomiting.105 Endogenous adenosine may be involved in the mediation of the spinal antinociception induced by descending adrenergic fibers originating from the locus ceruleus. This antinociceptive effect is blocked by intrathecal aminophylline (an adenosine receptor antagonist).111 Kekesi et al.106 reported that adenosine has little antinociceptive efficacy during continuous intrathecal administration, but appears to potentiate the effect of endomorphin-1. Eisenach et al.107 compared intrathecal adenosine with intravenous adenosine for chronic neuropathic pain in seven patients with hyperalgesia and allodynia. In intrathecal group, spontaneous pain was not relieved; however, evoked dysesthesias such as allodynia and mechanical hyperalgesia were markedly reduced. Five of seven patients developed back pain after the induction of adenosine. Octreotide (Sandostatin), a synthetic octapeptide derivative of somatostatin, has been found to be beneficial in the treatment of chronic pain, although the mechanisms underlying its therapeutic effect are not completely understood. Somatostatin is distributed in the substantia gelatinosa. It has been shown to have analgesic effect without adverse effects if given intrathecally, but the high cost, more than US$20 000.00 per year, prevents its widespread use.113 In a recent double-blinded study, octreotide was found to exert primarily an antihyperalgesic rather than analgesic effect on visceral pain perception.112

SELECTION OF DRUGS FOR LONG-TERM INTRATHECAL INFUSION In year 2000, an expert panel of physicians was convened to review what was known about common practices of European and American physicians using intrathecal agents and to review what was known about the drugs that were being used by these physicians up to 1999. This Polyanalgesic Consensus Conference 2000 published their review of common and experimental intrathecal agents and proposed guidelines for the appropriate use of these agents.112 Most recently a second expert panel, the Polyanalgesic Consensus Conference 2003, convened to review newer information since 1999 and to modify the 2000 guidelines. The purposes of this expert consensus panel were to: review the medical literature since 1999 pertaining to intraspinal agents; update the algorithm for intraspinal drug selection; propose guidelines for optimizing drug concentration and dosing during therapy; develop consensus regarding the evidence required to support use of a drug for long-term intrathecal infusion; and clarify existing regulations and guidelines pertaining to the use of compounded drugs for intrathecal administration.113 Regarding guidelines for intrathecal therapy, the panel suggests six lines of approach (Fig. 31.7).

According to the recommendations of this expert panel, firstline therapy, a Line-1 approach, includes morphine, the only opioid approved by the FDA for long-term intrathecal administration, and hydromorphone, which is supported by an extensive medical literature28–34 and clinical experience. In order to avoid the risk of the development of catheter tip granuloma, the panel recommends an upper limit for drug dosage and concentration as shown in Table 31.2. If side effects come before efficacy, or if efficacy is not established at the highest recommended dose with either morphine or hydromorphone (as shown in Table 31.2), the panel recommends switching to the alternate drug on Line-1 or moving to Line-2 therapy. The latter approach, moving to Line-2 therapy, is appropriate if the pain is neuropathic in nature. Some of the experts on the panel endorsed the idea of omitting Line-1 completely and moving to Line-2 if the patient has severe neuropathic pain that had not responded to systemically administered opioids. Line-2 includes morphine or hydromorphone combined with either bupivacaine or clonidine. The hypotensive side effects associated with clonidine makes bupivacaine more favorable over clonidine. Some physicians prefer to resort directly to a Line-2 approach with patients with mixed or neuropathic pain. There are no solid data, however, to support this approach, nor are there data to support the usage of bupivacaine or clonidine for intrathecal monotherapy. If patients do not respond to the agents in Line-2, in any combination, or are intolerant to the side effects of the agents in Line-2, the panel recommends moving to the Line-3 approach of using 3drug combinations, the addition of both clonidine and bupivacaine to either morphine or hydromorphone. If the analgesic response to this 3-drug combination with morphine is inadequate, then the panel recommends moving to hydromorphone plus bupivacaine and clonidine before moving to Line-4 therapies. Line-4 therapies include the lipophilic opioids, fentanyl and sufentanil, the GABA-alpha agonist, midazolam, and the GABAbeta agonist, baclofen. The strategy here, basically, is to switch opioid treatment from morphine or hydromorphone to fentanyl or sufentanil. Baclofen is approved for a long-term infusion for spasticity. Data, however, do support its use as an analgesic agent for intrathecal therapy. Although the data for their safety and efficacy are limited, intrathecal fentanyl and sufentanil have been used in clinical practice.20,53 As stated before, the high lipophilicity of these agents minimizes their diffusion to rostral pain centers. Therefore, the supraspinal side effects induced by these agents are less than those induced by the more hydrophilic agents such as morphine or hydromorphone. In the United States, midazolam is not available commercially as a preservative-free compound for intrathecal therapy.101 There are few data and limited experience to suggest the intrathecal infusion of drugs in Line-5, which includes neostigmine, adenosine, and ketorolac, and Line-6, which includes ropivacaine, meperidine, gabapentin, buprenorphine, octreotide and others. Drugs in Line-5 have some degree of preclinical evaluation including toxicity evaluation; drugs in Line-6 have little or no preclinical investigation and minimal or no clinical experience to warrant suggestion of their use by the panel.

COMPOUNDING OF DRUGS FOR INTRATHECAL DELIVERY Because many physicians use off-labeled analgesic agents for intrathecal delivery, and because many of these agents are not manufactured in concentrations necessary for intrathecal use, many physicians rely on the compounding of these off-labeled analgesics 359

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Fig. 31.7 Amended guidelines of the Polyanalgesic Consensus Conference, 2003. (Used with permission of the authors.)

for their practices. The Polyanalgesic Consensus Conference 2003113 felt it necessary to guide this part of the physician’s practice [compounding] to assure that patients would not be hurt by poor practice. According to the American Society of Health System Pharmacists

Table 31.2: Recommended intrathecal dosages and concentrations Drug

Dosage (mg/day)

Concentration (mg/mL)

Morphine

15

30

Hydromorphone

10

30

Bupivacaine

30

38

Clonidine

1.0

2.0

Recommended intrathecal dosages and concentrations106 to prevent the formation of intrathecal tip granuloma. These recommendations represent general recommendations of the expert consensus panel and are dependent upon the specific patient and the clinical experience of the physician; thus, maximum dosage and/or concentration may vary from these.Re volorem num voloreet ut vullamc ortisim zzriliscilit prate

360

(ASHSP),114 compounding is defined as the process of mixing of ingredients to prepare a medication for patient’s use, including dilution, admixture, repackaging, reconstitution, and other manipulations of sterile products. Morphine sulfate is the only available, commercially packaged, preservative free, FDA approved opioid for intrathecal use, while baclofen is the only available, commercially packaged, preservative free, FDA approved spinal antispasmodic for intrathecal use and ziconotide is the only available, commercially packaged, preservative free non-opioid intrathecal analgesic that is FDA approved. Most other intrathecal agents, in concentrations that are needed for monotherapy or combination therapy, require compounded formulations from compounding pharmacies. The United States Pharmacopoeia (USP)115 and the ASHSP have issued standards for compounding sterile products. These standards also apply to the compounding of solutions for intrathecal drug delivery. According to these standards, all sterile compounded and preservative free preparations, administered via an intrathecal delivery system, are classified as, at least, level 2 (medium risk), and many are classified as level 3 (high risk) preparations.114,115 The Polyanalgesic Consensus Conference 2003 suggests a set of considerations that need to be respected when preparing com-

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pounded formulations for intraspinal delivery.113 The following is a list of does and don’ts when compounding intrathecal agents: 1. Avoid preservatives, antioxidants, and solubility enhancers, as they may be neurotoxic and/or may be incompatible with the delivery system. 2. Use products that are compatible with the delivery system. 3. Use a pH that is physiologically appropriate and is consistent with the drug solubility and delivery system, generally in the range of pH 4 to 8. 4. In order to avoid exposing spinal tissues to the drug for a prolonged period of time, use solutions that are ideally isotonic with normal CSF (approximately 300 mOsm/L), so that the drug in solution can distribute evenly and quickly in the CSF. 5. Prepare the solution in a manner that does not alter the solubility of the constituents within the solution. Solubility enhancers should be avoided as they may be neurotoxic or incompatible with the delivery system. 6. Verify the chemical and physical stability of the preparation under relevant conditions in accordance with the USP and ASHSP applications. 7. Verify the stability of the preparation in accordance with the USP and the ASHSP publications. 8. Ensure appropriate control of bacterial endotoxins (pyrogens). Bacterial endotoxins are safety concerns, even for products that are sterilized, because sterilization does not remove endotoxins.

THE SIDE EFFECTS OF INTRASPINAL ANALGESIC THERAPY Patients might or might not tolerate a drug well during its administration for the screening trial. However, during therapy, patients may develop intolerance or tolerance to the drug. Should side effects of intrathecal delivery (nausea and vomiting, urinary retention, generalized pruritus, constipation, oversedation, confusion, paranoia, hyperalgesia/myoclonus syndrome, Meniere’s-like symptoms, nystagmus, the development of tip granuloma, or herpes reactivation) develop during therapy, an attempt should be made to manage these problems pharmacologically, if possible, before switching to another spinal agent. Although respiratory depression is a known consequence of the use of intrathecal opioids in the opioid-naive patient, it is rarely seen in patients who are receiving intrathecal agents because most of these patients have had extensive systemic exposure to opioid use. As stated above, there is incomplete cross-tolerance of one opioid agonist to other opioid agonists. Therefore, patients who have side effects from one intrathecal agent may not have the same side effects with another drug at equivalent doses.

Gastrointestinal complications Constipation. The incidence of constipation from intrathecal delivery of opioids is less than when the opioids are given systemically.116 The management of intrathecal opioid induced constipation is the same as the management of systemic opioid induced constipation using stool softeners and gentle laxatives. If this approach does not resolve the problem, one should consider switching to another opioid or, if possible, lowering the dose of the opioids. Nausea and vomiting. Opioids are thought to induce nausea and vomiting by a direct action on the chemoreceptor trigger zone (CTZ), an area of the hindbrain, which is outside the blood–brain barrier. This is supported by evidence showing that ablation of the CTZ prevents the induction of vomiting by opioids.117 The mechanism of action of opioids in emesis is, however, complicated. Biphasic dose–response curves have been reported and, in certain circumstances, opioids can

have antiemetic actions.118 Vomiting as a side effect of intrathecal administration of opioids is infrequent; however, should it happen, antiemetic therapy usually will resolve the problem. If nausea and vomiting persist, the clinician should use an agent that has less spread to supraspinal centers when given intrathecally. Agents that have less spread to supraspinal centers are agents of greater lipophilicity, including methadone, fentanyl, and sufentanil. Urinary retention is an early common side effect of intrathecally administered opioids in males, especially elderly males, and is infrequent in females. Urinary retention is most common when therapy is first initiated, but fortunately resolves spontaneously with continued therapy. Bethanechol (Urecholine) is the agent of choice for urinary retention.116 It is indicated for the treatment of acute postoperative and postpartum nonobstructive (functional) urinary retention and for neurogenic atony of the urinary bladder with retention. Dosage must be individualized, depending on the type and severity of the condition to be treated. The usual adult oral dose ranges from 10 to 50 mg three or four times a day. The effects of the drug appear in 30–90 minutes and persist for approximately 1 hour. If necessary, the effects of the drug can be abolished promptly with atropine. Should urinary retention persist, in spite of adequate pharmacologic therapy, decreasing the dose of intrathecal medication would be the next step, and if that does not work, perhaps changing agents from a hydrophilic agent to a lipophilic agent would be appropriate. Pruritus a fairly common side effect. The incidence of this opioid side effect is higher in opioid-naive patients than in those patients who are opioid tolerant. The use of antihistamines may ameliorate the problem; however, using opioid antagonists or partial antagonists, in combination with opioids in the pump, has been suggested as a possible solution.45

Central nervous system side effects Sedation, dizziness, and memory problems are not unusual and are related to the rostral spread of the opioids within the CSF. If these side effects develop and become a serious problem, using a more lipophilic opioid might ameliorate the problem. Although, in our practice, the use of modafenil and other psycho-stimulants have helped some of our patients to overcome the sedating side effect. Sexual and endocrine dysfunction. The prevalence of these side effects is quite high in patients who are receiving intrathecal opioid therapy. In a study of 73 patients, the majority had hypogonadotropic hypogonadism, 13% developed central hypocorticism, and 17% growth hormone deficiency. These abnormalities affected the sexual function in this group of patients.27 Leg and pedal edema. These side effects are not infrequent in patients receiving intrathecal opioid therapy. In a study by Aldrete and da Silva et al.,119 five out of 23 patients (21.7%) who received intrathecal opiates for longer than 24 months developed pedal or leg edema. However, the symptoms improved by the discontinuation or reduction of the dose; the most effective treatment was elevation of the legs and dose reduction. The use of diuretics with elastic stockings can be helpful in overcoming this side effect. In our experience, the incidence of peripheral edema is greater with the use of hydrophilic agents such as morphine or hydromorphone than with lipophilic agents such as fentanyl, sufentanil, and methadone. Consequently, if peripheral edema develops and does not respond to diuresis, we switch hydrophilic agents to lipophilic agents. Tolerance is a phenomenon in which exposure to a drug results in the diminution of effect, either desired or undesired, or the need for a higher dose to maintain the effect, desired or undesired. Tolerance can be considered an adaptation process which may be traced back to cellular and molecular levels. Receptor mechanisms of tolerance 361

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include downregulation and upregulation of numbers of receptors. Also, there is evidence that the higher the intrinsic activity of the opioids at only one receptor site, fewer receptors are needed in order to induce a potent analgesic effect; therefore, the incidence of tolerance is less. Drugs with high intrinsic activity include sufentanil and fentanyl.120 NMDA receptor activation through protein kinase, phospholipase C translocation, and activation of nitric oxide synthetase also contributes to the formation of tolerance.120,121 If titrating the dose up does not resolve the problem, changing into a new opioid or giving the patient a ‘holiday’ from opioid intrathecal therapy should be considered.

Although intrathecal therapy is helpful for patients with chronic intractable pain that fails to respond to other modalities of therapy, this treatment modality is not free of complications. Complications of intrathecal therapy may be divided into surgical complications, complications related to the drug delivery system, and iatrogenic complications.

Hematoma is a collection of blood in the surgical wound and seroma is a collection of the serum in a wound. A hematoma might develop secondary to the tissue trauma of surgery or the nonmeticulous attention to homeostasis. After surgery, and because the body abhors a vacuum, most newly created pump pockets do develop a fluid collection or seroma that may last for up to 1–2 months post implantation. These fluid collections are self-limiting and usually are of no clinical significance. Patient reassurance is usually the only treatment necessary. If fluid collection is excessive and bothersome to the patient, an abdominal binder usually will decrease the size of the seroma and promote healing. If infection is suspected (rubor, dolor, calor), an aspiration for Gram-stain, and culture-and-sensitivity should be performed. Restated, Gram-stains must show bacteria to differentiate from simple seroma. All seroma contain large amounts of white blood cells. If there is a proven bacterial contamination of the wound, the patient should be placed on intravenous antibiotics with antibiotic irrigation of the pocket itself.

Surgical complications

Infections

Bleeding. Bleeding may occur despite meticulous surgical incisions and dissection. In order to minimize this, the surgeons screen their patients appropriately for coagulopathies, especially in cancer patients undergoing chemotherapy who may have low platelet counts or in those patients taking excessive amounts of NSAIDs. Patients who are pharmacologically anticoagulated or those who have physiologic coagulopathies are not candidates for these procedures until anticoagulation is corrected and bleeding parameters return to normal. In spite of good surgical evaluative and technical skills, surgical bleeding is often unavoidable. A good rule for the implantation surgeon to follow is to close a wound only after carefully inspecting the wound area for active bleeding. Wound bleeding provides a good medium for the growth of bacteria, leading to postoperative infections. Since the technique for catheter implantation of drug delivery systems passes through the epidural space, bleeding may occur within the epidural space without the surgeon being aware of it. This bleeding, if significant, could lead to epidural hematoma, spinal cord compression, and a cauda equina syndrome leading to paralysis with bowel and bladder dysfunction. The surgeon should expect this complication if the patient complains of persistent back pain and tenderness, urinary incontinence, anal sphincter tone weakness and fecal incontinence. The diagnosis of epidural hematoma is confirmed with emergent MRI or CT with contrast of the spine. Epidural hematoma is a neurosurgical emergency which may require evacuation. To avoid postoperative bleeding, patients should be screened for coagulopathies. Cancer patients and some patients with comorbid disease such as bleeding dyscrasia or liver disease might be thrombocytopenic, and some patients with chronic pain might be on nonsteroidal antiinflammatory agents. Physicians must be aware of all of the possible causes of surgical and postsurgical bleeding and take steps to correct them appropriately. Patients with thrombocytopenia should receive platelet transfusion preoperatively and patients on NSAIDs must have their medications discontinued 72 hours before surgery and 12 days before surgery, if the patient is taking aspirin. Patients who are on warfarin should have their medication stopped, if appropriate, at least 4 days prior to the planned surgery. If not appropriate, the patient should be placed on an agent such as enoxaperin (Lovenox) for 4 days prior to surgery after discontinuing warfarin. The enoxaperin can be discontinued safely 12 hours before surgical time. The meticulous attention to hemostasis intraoperatively is also an important measure to prevent postoperative bleeding.

Appropriate preoperative antibiotics, and strict adherence to intraoperative external measures, help minimize the problem of postoperative infection. Since most postoperative infections are caused by the Gram-positive cocci, S. aureus and S. epidermidis, agents specific for these bacteria, such as the cephalosporins or vancomycin, should be used preoperatively. If a postoperative infection does occur and is superficial and not deep, systemic antibiotics should be used to prevent deepening of the infection to involve the pump pocket itself. If the infection does involve the implanted catheter or the pocket of the implanted pump, removal of the entire system is mandatory to prevent epidural abscess or meningitis. The development of epidural or intrathecal infections mandates the immediate removal of the system. In case of intrathecal infection, attention should be paid to meningeal irritation signs and consultation with an infectious disease consultant is recommended. Remember, not all fever spikes in the first 72 hours after implantation of an intrathecal catheter means meningitis. In our experience, a good percentage of patients with newly implanted intrathecal catheters do develop fever spikes within the first 72 hours after implantation. These noninfectious fevers, probably a foreign body reaction to the implanted catheter, may be associated with a slightly stiff neck due to the CSF leakage, and may be associated with headache. In these cases, CSF withdrawn from the side port of the pump will be negative for bacteria, but will be positive for a mild to moderate leukocytosis, a spinal response to the implanted foreign body. If the CSF culture is negative for bacteria, the physician should take a wait and see attitude before starting antibiotics unnecessarily.

Complications

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Hematoma and seroma

CSF leakage Leakage of CSF around the catheter as it enters the dural sac is a frequent occurrence after intrathecal catheter placement. Fortunately, CSF leakage is a self-limiting occurrence. CSF leakage usually resolves within a week after catheter implantation. However, should the problem persist, resulting in either a postural headache or leakage of CSF from the skin suture site which might require an epidural blood patch as a treatment option of PDPH, care should be taken when this procedure is performed. This autologous blood patch is prefereably done one level below the entrance level of the catheter to avoid catheter damage and should be performed under fluoroscopy to prevent catheter damage. If CSF leakage persists with formation of a subcutane-

Section 2: Interventional Spine Techniques

ous CSF collection (hygroma), aspiration of the CSF collection must be avoided to prevent development of an infection. Aspiration does not cure the problem of the leak and fistula between the thecal sac and subcutaneous collection. Instead, applying an abdominal binder that increases pressure in the pocket might decrease CSF drainage and may help the fistula to close spontaneously. If that fails, surgical intervention might be indicated to close the fistula.

Spontaneous malpositioning of the pump Accumulation of fluid in the pump pocket such as CSF traveling from the thecal sac along the catheter to the pump pocket prevents healing of tissues, prevents capsule formation around the pump, and increases movement of the pump within the pocket. The pump, if you will, becomes a ‘floating pump.’ If a capsule does not form snuggly around the pump or if the pump is not suture-anchored to a strong tissue plane, the pump may flip over, which may lead to kinking, obstruction, or even separation of the catheter. Also, a pump flipped over in its pocket is impossible to fill. If one cannot rectify this problem by digital manipulation, a surgical revision of the pump pocket, decreasing the size of the pocket, is indicated.

Complications related to the intrathecal delivery system Complications related to the intrathecal delivery system are not unusual, but may be prevented. These complications include complications of the implanted pump or catheter system or both. Pump complications include battery failure or breakdown of the internal workings of the pump, if the pump is a programmable one. Nonprogrammable pumps, by virtue of their simplicity, usually do not break down. Catheter complications include system dislodgements, catheter kinks, breaks, shears, or obstruction. Catheter complications are heralded by a sudden loss of pain control or spasticity control, or sudden withdrawal symptoms. Examination of the catheter system under fluoroscopy and/or X-ray examination of entry site and tip site is warranted to diagnose this problem. If the system appears to be intact, a dye study of the system should be performed to discern any small breaks in the system. One must remember that there is dead space within the catheter system, containing drug, and these drugs may be of high concentrations. If one pushes a high-concentration drug within the dead space by injecting dye through the pump side port, untoward and unintended complications may arise due to inherent toxicities of the drug ‘pushed.’ To prevent this, one should aspirate all of the drug out of the dead space before injecting dye through the side port. If it is expected that one might not be able to aspirate from the side port at the time of the dye study, then all concentrations of drug in the pump should be diluted way in advance of the study to prevent toxic levels of the drug or drugs from being injected intrathecally. An alternative to this strategy for detection of breaks within the system, in programmable pumps, is to drain the pump of drug in advance of the study, and, after an appropriate time interval, inject the side port, or as Medtronic, Inc. (Minneapolis, Minnesota) recommends, filling the pump with an isotope, then programming the pump to deliver the isotope while observing the system by nuclear medicine scanning. Pump ‘breakdown’ is most usually heralded by a sudden loss of pain or spasticity control, sudden withdrawal syndrome, or an observed discrepancy between observed residual volume and expected residual volume at the time of refill. Pump breakdowns do occur and may be related to faulty manufacturing or damage by a nonapproved drug placed within the pump, which might damage the internal catheter system. Diagnosis of a faulty motor/rotor, within the pump, is made by real-time, fluoroscopic observation of motor/rotor performance.

The programmable pump is programmed to bolus inject over a relatively short period of time. The motor/rotor is observed under fluoroscopy to either move or not. If the rotor, after programming of a bolus, does not move, there is breakdown of the pump.

Iatrogenic complications Iatrogenic complications may be related to errors in formulating admixtures of drugs, refilling pumps with wrong medications, technical errors in refilling pumps, or errors in programming pumps. Infection, as it relates to poor sterile technique, is also an iatrogenic complication. Medications injected into the pocket surrounding the pump instead of into the pump requires immediate aspiration of the drug from the pocket and close observation for an appropriate period of time to rule out drug overdose from systemic uptake of the drug into systemic circulation. To avoid ‘dumping’ medication into the pump pocket, one should always aspirate drug after partial filling to assure that there is no sanguinous material in the aspirate. Programming errors that lead to serious consequences include programming wrong concentrations or wrong rates of administration. Also, remember that it is important to correctly calculate a ‘bridge bolus’ after changing concentrations of the drug infused.

Catheter tip granuloma In 1991, North et al. first reported a granulomatous region associated with the intrathecal catheter tip causing mass effect and neurologic dysfunction.122 In a literature review on the subject by Coffey and Burchiel, in November of 2000, 41 cases, 16 from the literature and 25 reported to Medtronic, Inc. and to the FDA, were identified.35 The mean duration of therapy in these cases was 24.5 months. Most cases were located in the thoracic region. Intrathecal drugs involved included morphine or hydromorphone, either alone or mixed with other drugs in 39 out of the 41 cases. Thirty patients underwent surgery to relieve spinal cord or cauda equina compression. Eleven of the patients were nonambulatory and one died due to pulmonary embolism. Microscopically, the masses were composed of chronic inflammatory cells with variable degrees of granuloma formation. In these cases, there was a region of central necrosis resembling an abscess that contained no polymorphonuclear leukocytes. Although tissue stains for microorganisms were uniformly negative, intraoperative cultures were positive in three cases, thought to be a secondary process. Yaksh et al., observing masses in humans and in two species of animals, suggested a probable relationship existing between the mass formation and opioid dose and concentration.123 Some authors have suggested placing catheter tips below the conus medullaris to avoid catastrophic complications caused by granulomatous mass formation over the spinal cord. However, in a case report by Fernandez et al.,124 a patient placed on hydromorphone, 110 mg per day with a concentration of 400 mg/mL, developed a catheter tip granuloma in the sacral region. In this case, the catheter was placed caudally into the lumbosacral region. This patient presented with saddle anesthesia and bowel/bladder incompetence, and after surgery, the patient was left permanently disabled.

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Part 2: Interventional Spine Techniques 111. Han BF, Zhang C, Qi JS, et al. ATP sensitive potassium channels and endogenous adenosine are involved in spinal antinociceptive produced by locus coeruleus stimulation. Acta Physiol Sinica 2002; 54:139–144. 112. Bennett G, Burchiel K, Buchser E, et al. Clinical guidelines for intraspinal infusion: report of an expert panel. J Pain Symptom Manage 2000; 20;S37–S43. 113. Hassenbusch S, Portenoy R, et al. Polyanalgesic Consensus Conference 2003: an update on the management of pain by intraspinal drug delivery – report of an expert panel. J Pain Symptom Manage 2004; 27(6):540–563. 114. American Society of Health System Pharmacists ASHP. Guideline on quality assurance for pharmacy-prepared sterile products. Am J Health Syst Pharmacol 2003; 60:1440–1446. 115. USP. General chapter 797: pharmaceutical compounding sterile preparations. US Phamacopeia 2004; Jan 1. 116. Naumann C, Erdine S, et al. Drug adverse events and system complications of intrathecal opioid delivery for pain: origins, detection, manifestations and management. Neuromodulation 1999; 2:92–107. 117. Wang SC. Emetic and antiemetic drugs. In: Root WS, Hofmann FG, eds. Physiological pharmacology, II. New York: Academic Press; 1965:255–328.

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118. Barnes NM, Bunce KT, Naylor RJ, et al. The actions of fentanyl to inhibit druginduced emesis. Neuropharmacology 1991; 30:1073–1083. 119. Aldrete JA, da Silva JMC. Leg edema from intrathecal opiate infusions. Eur J Pain 2000; 4:361–365. 120. Freye E, Latasch L. Development of opioid tolerance – molecular mechanisms and clinical consequences. Anasthesiol Intensivemed Notfallmed Schmerzther 2003; 38(1):14–26. 121. Hsu MM, Wong CS. The roles of pain facilitatory systems in opioids tolerance. Acta Anaesthesiol Sin 2000; 38(3):155–166. 122. North RB, Cutchis PN, Epstein JA, et al. Spinal cord compression complicating subarachnoid infusion of morphine: case report and laboratory experience. Neurosurgery 1991; 29:778–784. 123. Yaksh TL, Hassenbusch S, Burchiel K, et al. Inflammatory masses associated with intrathecal drug infusion: a review of preclinical evidences and human data. Pain Med 2002; 3:300–312. 124. Fernandez G, Madison-Michael L, Feler CA. Catheter tip granuloma associated with sacral region intrathecal drug administration. J Neuromodulation 2003; 6:225–228.

PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

Vertebroplasty

32

Amit S. Bhargava and Curtis W. Slipman

SCREENING OF PATIENTS REFERRED FOR VERTEBROPLASTY Before considering vertebroplasty, one must perform a through history, physical examination, and review appropriate investigations including radiographic analysis. This information should be able to differentiate between the source of pain being vertebral compression fracture or other back problems such as disc herniation, facet arthropathy, or spinal stenosis.1 History should include the site of pain, cause, inciting event, date of origin, exacerbating factors, alleviating factors, analgesic use, and activities of daily living. The patient should be screened for allergies, medications, medical problems, and conditions which may prevent the patient from lying prone during the procedure. The origin of pain may coincide with minor trauma and is typically exacerbated during activity, movement, or while weight bearing, and is relieved by lying down. Physical examination will reveal a tender site corresponding with the fracture level. If multiple vertebral compression fractures are present, the origin of pain will be elicited by careful clinical examination and analysis of radiographic studies.1,2 Magnetic resonance imaging (MRI) is helpful in patients with multiple fractures and usually reveals edema within the marrow space of the vertebral body that is best visualized on sagittal T2-weighted images. Bone scans can also differentiate the symptomatic level from incidentally discovered fractures.3 Bone scan imaging may be indicated when considering vertebroplasty therapy for patients suffering from multiple vertebral compression fractures of uncertain age or in patients with nonlocalizing pain patterns. We do not, however, routinely perform bone scans.4 Blood investigations should include complete blood and platelet counts, measurement of prothrombin time, partial thromboplastin time, International Normalized Ratio, activated clotting time, and complete metabolic panel.5,6

CONSULTATION Because most vertebral compression fractures occur in the older age group, the initial consultation should include family members involved in the patient’s care. The time of reporting for the procedure, postprocedure care, and time of discharge from the hospital should be explained. Informed consent must include a through explanation of the procedure, methods, the physician’s prior history of complications, and the expected outcome based on the physician’s own outcome data. The patient should also be informed that the addition of material (barium, tungsten or tantalum) to make the bone cement material opaque technically makes the cement a non-FDA-approved material.1,7

One should carefully temper unrealistic patient expectations. In general, the patient can be told to expect a higher chance of a favorable outcome if his or her fracture is subacute, but a diminished success rate if the fracture is old.

Timing Early studies performed vertebroplasty only after conventional treatment (medication and rest) had failed.8 Later series have advocated treatment as early as weeks or days if the patient requires narcotic medication or admission to hospital secondary to pain. Others have recommended vertebroplasty within 4 months.3 Although late treatment is unlikely to be successful, there are case reports of patients being successfully treated after a few years.9 Even though some believe it is a reasonable indication,1 there are insufficient data to categorically support the treatment of painful tumor infiltration without fracture. In addition, it is unclear whether to treat before or after radiation therapy. Injection of cement into the vertebral body will likely dislodge marrow elements that could potentially be absorbed into the blood stream. This concern for causing metastatic dissemination suggests that vertebroplasty should be performed only after radiation therapy. Prophylactic vertebroplasty is neither widely accepted nor approved for osteoporotic vertebral compression fractures and no studies have been done to substantiate the utility of this practice.1

TECHNIQUE 1. Pre-procedure planning. MRI, computed tomography (CT), and X-ray images of the fracture are evaluated in all views specifically looking for the angle of approach to the vertebra through the pedicle. Because normal anatomy (Fig. 32.1) is altered by the fractures, the approach to the body of the vertebra through the pedicle is altered. This altered bone architecture must be carefully analyzed by reviewing all the available radiological films. Specifically, the cortical margins of the bone are reviewed in anteroposterior (AP), lateral, and axial views to preplan the pathway of the trocar to the exact target area within the vertebral body. The angle will be altered based on the characteristics of the fractured vertebra. The vertebra may be approached through one pedicle or both pedicles. If the angle of insertion is achieved in such a way that the tip of the trocar is in the center of the body, then one may use a single-pedicle approach. If the trocar lies on one side of the body of vertebrae, then the other pedicle may be used to approach the other side of the vertebral body. 2. Prior food and medication. For procedure performed in the morning, the patient is informed not to eat or drink after midnight, but is allowed to take medications. When conscious, sedation is used

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A

Thoracic vertebra

Lumbar vertebra

B

Thoracic vertebra

Lumbar vertebra

for a procedure to be done later in the day, and the patient should not drink or eat for a minimum of 4 hours beforehand. Diabetics and other chronic medical illness management including the timing of anticoagulants should be coordinated with the primary care physician. 3. Prophylactic antibiotics. Intravenous antibiotics (cefazolin 1 g) are given 30 minutes before the procedure. Ciprofloxacin 500 mg orally twice a day may be given, if the patient is allergic to other medications and should be started 12 hours before the procedure and continued 24 hours after completion of the procedure.6 We do not give any prophylactic antibiotics and prescribe antibiotics postoperatively for a week. 4. Position of patient. The patient is placed in a prone position for surgery in the thoracic and lumbar region and supine for cervical region.3 It is critical to confirm the level of pain and fracture under fluoroscopy before beginning vertebroplasty.1 Applying pressure with the thumb or palm of the hand over each spinous process or side-to-side movement of the spinous process will often elicit tenderness. As the patient is awake during the procedure and placed in a prone position, the patient should be made comfortable with padding and arm supports. 5. Anesthesia. Percutaneous vertebroplasty is performed using local anesthesia typically combined with neuroleptanalgesia2,3,5,10,11 or general anesthesia.10,11,12 The authors use a combination of intravenous midazolam (Versed; Roche, Manate, Puerto Rico) and fentanyl (Sublimaze; Abbott Laboratories, North Chicago, IL).13,14 Dosages are based on patient size and condition and can be titrated during the procedure based on the patient’s response. 368

Fig. 32.1 Pedicles. (A) Axial view. (B) Lateral view.

General anesthesia is rarely used for this procedure. Two to 3 ml of 1% solution of lidocaine injected into the marrow through the needle will relieve pain, which some patient may experience when cement is injected into the bone.6,15 6. Prepping and draping. The skin is prepared with iodine and then draped. As the position is checked many times in AP and lateral views, the field of procedure should be well protected with sufficient drapes. 7. CT scan versus C-arm fluoroscopy. Vertebroplasty is performed using biplanar fluoroscopy,3,11 C-arm fluoroscopy, and dual-guidance CT.3,16 CT is only used for extremely difficult cases, such as tumor destruction of the posterior vertebral wall6 or vertebra plana.17 When using a single-plane C-arm fluoroscopy all the movements during the procedures should be confirmed in two planes, AP and lateral. 8. Approach to the vertebral body. Cervical vertebroplasty has been done with transoral approach,18,19 lateral, and anterolateral approach.20 The authors do, however, have concerns about the transoral approach. This technique necessitates traversing the oropharynx which is riddled with bacteria ready to flourish in the vertebral body. Consequently, we prefer the anterolateral approach used by Deramond in the first described vertebroplasty procedure.21 As osteoporotic fractures are rare in the cervical area, vertebroplasty is rarely done in the cervical region except for conditions such as tumors. During the needle placement one must be careful to avoid the carotid artery and internal jugular vein.6 Both structures are displaced laterally and the esophagus and trachea medially to reach the body of cervical vertebrae (Fig. 32.2).

Section 2: Interventional Spine Techniques Approach to vertebral body Trachea Esophagus ICA Jugular vein

Fig. 32.2 Cervical body, anterior.

The thoracic and lumbar vertebral bodies are usually approached through one or, most commonly, both pedicles.2,8,21–27 Various approaches are used including a costovertebral,5 paravertebral, posterolateral, or anterolateral (cervical) approach. The parapedicular or transcostovertebral28 approach is used when a transpedicular approach cannot be used because of small pedicles, a fractured pedicle, or tumor invading the pedicle. Like most physicians, the authors prefer the transpedicular approach instead of the parapedicular approach, which may increase the chance of both a pneumothorax and that a paraspinous hematoma may not be controlled with application local pressure.6 The posterolateral approach increased the risk of injuring the exiting nerve root and segmental artery,6 and has largely been abandoned although some authors recommend it for lumbar vertebrae.20,23,28 There are many companies which supply cement and delivery equipment: Parallax Medical Inc./Arthrocare Corporation; Cook Group Inc.; Interpore Cross International Inc.; Interpore Cross International Inc./American OsteoMedix Corp.; Medtronic Inc./ Medtronic Sofamor Danek; Orthofix International NV/Orthofix Inc.; Stryker Corp.; Tecres SPA.29 These sets contain stylets, needles, tubing, injectors, and injector barrels, but the end result is the same. The equipment allows one to inject cement into the anterior part of the vertebral body. Some authors have, however, modified the equipment and technique,30–33 and before these sets were available, operators recommended using 1 mL syringes for injection of cement.7,11,17,24

Fig. 32.3 Injecting local anesthetic.

Fig. 32.4 Needle is inserted and viewed on the monitor with the clamp holding the needle.

9. Needle insertion. Mark a point on the skin after viewing the fractured vertebra in the anteroposterior and lateral views. This is the planned insertion site of the cannula. The initiation site should correspond with superolateral aspect of the pedicle. It should not be near the inferior or medial margins of the pedicle. Local anesthetic is infiltrated into the skin, subcutaneous tissue, and up to the periosteum of the pedicle. We inject 2–3 mL of lidocaine 1% with 25-gauge 1.5 inch needle for local anesthesia (Fig. 32.3). A small incision is made using a No. 11 knife blade and the introducer needle from the set is inserted (Fig. 32.4). A 15-gauge needle is used for cervical vertebrae and 10-gauge for thoracic and lumbar vertebrae.3 Currently, even thinner needles (13-gauge) are being used.6 The needle entry site is localized in the AP view. The authors use a diamond-tipped needle to start the entry. During the procedure, one must confirm all the movements and steps in both the AP and lateral fluorosopic views. The needle is held with forceps to minimize radiation exposure to the operator.6 After confirming the position, the vertebroplasty needle is advanced through the superior-lateral cortex of the pedicle (Fig. 32.5).

Fig. 32.5 Initial tap into the pedicle.

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The vertical and horizontal diameter of the pedicle increases from upper thoracic to lower lumbar vertebrae (Table 32.1). Proximally, in the sagittal plane, the direction of the pedicle is more oblique. (Fig. 32.6) The authors start with a diamond-tipped needle and then change it to beveled needle to make directional adjustments.7 The bevel of the needle is directed so that the tip is pointed laterally to avoid the spinal canal. The needle is directed anteriorly, medially, and inferiorly through the pedicle to reach the anterior third of the vertebral body in the midline in the sagittal plane. Incremental changes in position of the needle are observed in the AP and lateral views to ensure that the proper pathway is being pursued. In osteoporotic bones it may be easy to advance the needle by hand, but in cases where the bone is dense, as in pathologic fractures, a mallet is necessary to advance the needle.6 While advancing the needle by hand the direction of needle may change, and using the mallet may keep the needle advancing in the direction wanted. We invariably use

Table 32.1: Vertical and horizontal pedicle diameter Pedicles

T3

L4

Vertical diameter

0.7 cm

1.5 cm

Horizontal diameter

0.7 cm

1.6 cm

A

B

370

Thoracic vertebra

Thoracic vertebra

a mallet to advance the needle as this provides much greater control of the needle direction. As the needle is slowly advanced through the pedicle, we are hypervigilant about the location of the needle tip and the orientation of the needle. At no point do we want to breach the medial wall and subject the patient to the risk of cement extravasation into the spinal canal. When we reach the anterior part of the pedicle on lateral view, the trocar should be just lateral to the medial border of the pedicle on anteroposterior view. This ensures we are not going to break the medial wall of the pedicle. In addition, we do not want to fracture the roof or the base of the pedicle and inadvertently pierce an exiting nerve root. Advancing the needle through the lateral border of the pedicle will deposit cement intramuscularly. We have experienced this latter scenario on a few occasions and it is not associated with any adverse effects. Theoretically, it is conceivable that the needle could be placed too close to the aorta if the needle breaks through the lateral margin of the left pedicle, but this is a highly unlikely event. It is also important to be sure that the angle of inclination will allow the needle to ultimately rest in the anterior one-third of the vertebral body. To obtain ideal terminal position, it is critical that one repeatedly rechecks the cephalocaudal tilt while traversing through the pedicle. It is very difficult to re-orient the angle of inclination once the needle has passed through the pedicle and enters the vertebral body. If the angle of inclination is too steep then gentle downward pressure on the hub will minimize this angle, especially if the needle is still within the pedicle. We emphasize the term ‘gentle’ since osteoporotic bone can easily fracture if aggressive motions are used. If such gentle pressure does not achieve the intended result, a beveled needle can be

Lumbar vertebra

Lumbar vertebra

Fig. 32.6 (A) Direction of insertion of the trocar and cannular (axial view). (B) Approach to vertebra on lateral view.

Section 2: Interventional Spine Techniques

substituted for the diamond-tipped needle. The bevel can be rotated so that the needle courses in the direction of choice. After the needle is observed to enter the vertebral body using a lateral view, the AP perspective does not need to be checked until the cement is injected. An AP view is needed at three points during the procedure: when planning where to insert he needle, checking the progress of the needle as it courses through the pedicle, and then later when cement is injected. Once the needle is in the vertebral body it should be rotated so that the tip is opening medially. 10. Biopsy. If a biopsy is required, it is done by introducing the needle coaxially34 or thorough the needle. The biopsy is done before the cement is injected.1 The authors introduce a thinner biopsy cannula through cannula already through the pedicle. Biopsy kits are commercially available and the biopsy needle size is compatible with the vertebroplasty cannula. After the trocar and cannula have been placed in the vertebral body through the pedicle, the trocar is removed. The biopsy needle is inserted through the vertebroplasty cannula. The biopsy needle is longer than the vertebroplasty cannula and precaution should be taken not to pierce the anterior cortex. The authors initially stop the vertebroplasty cannula in the posterior third of the vertebral body. The biopsy needle is then inserted and advanced through the vertebroplasty cannula in a rotating motion and then pulled out. After the biopsy is obtained, the trocar is reinserted into vertebroplasty cannula and it is advanced anteriorly to the target area. 11. Another needle may be placed in the contralateral pedicle in the manner mentioned above for bipedicular approach. 12. Venography can be done after achieving the correct position with the needle.10,28 Contrast dye is injected into the vertebral body and leakage can be visualized under fluoroscopy. Because the viscosity of the contrast material and bone cement is so different, venography may not be an accurate assessment of the embolization risk.6 In fact, venography is seldom used in Europe and is only done in United States to discover the potential leak sites. Some authors, however, continue to defend its use,2,35,36 while others have either seldom7,37,38 or never used venography.39,40 Embolization of vascular lesions may be done by microfibrillar collagen after venography.2 13. Cement preparation. Bone cement, approved by FDA specifically for vertebroplasty with radio opaque material already incorporated, is available. There are two kinds of cement, slow set or fast set. The authors prefer the fast-set cement. Prior to starting the procedure we place the monomer in a refrigerator. Cooling the liquid slows the set time, allowing a few extra minutes to complete the procedure. Once the monomer and cement powder are mixed, a chemical reaction ensues that cannot be aborted, which ultimately results in hardening of the mixture. Once this reaction has progressed beyond a certain point it becomes impossible to advance cement through the delivery apparatus. So, cooling of the monomer decreases the kinetic energy and slows the chemical reaction time, thereby providing a few extra minutes to the potential cement delivery time. Some interventional spine physicians have suggested altering the monomer to powder ration as a method of altering the set time. We do not do this and do not advocate such a solution. Using polymethyl methacrylate (PMMA) for vertebroplasty is considered off-label use although it is off-label only because of the ratio of monomer to cement powder. But before one modifies the cement preparation, one must first understand that the mechanical properties of the cement would be inextricably altered. Second, and probably most important, is that the amount of free or unbound monomer would likely increase, which could lead to increased complication due to intravascular monomer uptake.

The typical concentration is 0.40 mL of PMMA powder (SimplexP; Stryker-Howmedica-Osteonics) combined with 6 g of sterile barium sulfate powder, tantalum,3,11 or tungsten (Figs 32.7, 32.8).10 The barium sulfate powder is included to better visualize the PMMA under fluoroscopy. The safety of the procedure depends on cement leakage rather than the type of cement used.41 In addition, before adding the 10 mL liquid monomer, one can add 1 g of tobramycin antibiotic to reduce the chance of disc space infection.5,25,42,43 Some authors, including ourselves, recommend not adding antibiotics to PMMA unless the patient is immunocompromised.6,17 After the barium is added to the powder, the polymer is added to the monomer using a 10 cc syringe and an 18-gauge, 5” needle. The tube is closed and the mixture is shaken vigorously for 45 seconds. Open mixing should be avoided to maintain a sterile environment. While one is mixing the cement, an assistant connects the long, flexible tube for delivery to the injector barrel. The bone cement preparation is mixed until a doughy, cohesive consistency (similar to toothpaste) is obtained. We delay the polymerization process by

Fig. 32.7 Mixing PMMA and barium.

Fig. 32.8 Preparing cement. 371

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cooling the polymer in the refrigerator for an hour before the procedure and this gives additional working time.6,44 In limited circumstances, slow-set cement Cranioplastic type 1 Slow Set (Codman/Johnson & Johnson, Berkshire, UK), at room temperature can be used.6,35 Rapid-set material has the advantage as it rapidly sets in case of leaks, as seen with these procedures. If a cement leak is observed on fluoroscopy, one can stop for a few minutes till the fast cement hardens and blocks that area. As the leaking area is blocked by the hardening cement, more cement may be reinjected. One should look for cement flowing into the opposite direction to the area where the previous cement had already hardened. The cement will rapidly polymerize and will plug the leak in 1–2 minutes and further cement can be injected, which is not possible with slow-setting cement. In addition, slow-setting cement stays liquid longer in the body and thus could potentially leak for a longer time and may leak along the needle tract when the needle is pulled out.6 Once mixing is completed, the bone cement is slowly poured into the injector tube (Fig. 32.9). The injector device is attached and rotated till the cement starts pouring from the tip of the flexible tube (Figs 32.10, 32.11). One can see the consistency of the cement

Fig. 32.9 Pouring cement into the chamber.

Fig. 32.10 Connecting the rotator. 372

at the end (Fig. 32.12). The flexible tube is connected to the needle inserted earlier into the vertebral body (Fig. 32.13). 14. Cement injection. The paste-like cement is slowly injected into the vertebral body under constant fluoroscopic control with help of the injector device (Fig. 32.14). The amount of cement injected is monitored under fluoroscopy and the quantity can be measured from the labeled injector tube. The objective is to fill the anterior two-thirds of the vertebral body as seen on the lateral view. If required, further cement can be injected from the contralateral pedicle cannulation.3 At times, the cement does not flow according to the plan. The cement may pool in front of the needle, and the cannula may be repositioned by slightly moving anteriorly or posteriorly. If the cement is moving into the anterior part of the vertebral body, the cannula can be withdrawn slightly and one can then inject more cement. If the cement is flowing to the posterior or lateral part of the vertebral body, the inserting device can be rotated in the opposite direction to create a negative pressure. In some cases, cement may

Fig. 32.11 Connecting the delivery tube.

Fig. 32.12 Checking the consistency of the cement.

Section 2: Interventional Spine Techniques

in both AP and lateral views. If it is considered safe to proceed with the procedure, the needle position should be adjusted. Another needle can also be placed from the contralateral pedicle. 16. Removal of the needle. The stylet should be repositioned into the needle before removal of the needle whenever possible to prevent cement leak.3 The authors prefer not to place the trocar as that may lead to unmonitored injecting of cement. We leave both cannulas in the vertebral body till the cement is injected from the cannula. If one cannula is pulled out before the cement is injected into the second pedicle, then one is potentially providing a route for cement to leak from the first pedicle. 17. Dressing. Local pressure is applied at the skin puncture site to prevent any bleeding. The puncture site is closed with steristrips and a sterile dressing applied.

Postprocedure Fig. 32.13 Connecting the delivery tube to the needle.

The cement polymerizes in 1 hour and the patient remain recumbent in supine position for that duration. The patient may be discharged after an hour of monitoring.5 At our center, we discharge patients after keeping them for 1 hour postprocedure, or if medically required we admit them overnight. The patient is discharged with narcotic medication to be used on an as-needed basis and is prescribed Keflex for a week. If the patient is allergic, ciprofloxacin is prescribed. The patient is not given any brace on discharge.

Multiple compressions Multiple-level vertebral compression fractures may be treated by percutaneous vertebroplasty. It is less cumbersome to stagger needles by alternating between right and left pedicles.2 However, there may be additional stress on the adjacent vertebrae.49 If there are multiple compression fractures, one should treat the most painful fracture first.1 No more than two should be treated on a particular day. It is the authors’ preference to treat a single vertebral fracture per day to ensure monomer toxicity risk is minimized. Incidence of venous extravasation of cement or fat50 increases with multiple-level treatment.

Repeat vertebroplasty Fig. 32.14 Ready to inject with hands out of the radiation field.

fortuitously flow to the opposite side of the vertebral body and injection through the second pedicle may not be required. Vital signs should be monitored looking for hypotension, as cement injection has been known to cause hypotension in patients undergoing joint replacement surgery.45,46 15. Amount of cement. Total volume of cement injected is commonly 2–8 mL.3,6 Outcome, however, is not related to the amount of cement injected, and even 2 mL of cement injected has been reported to provide pain relief.47 Only a small amount of bone cement (≈15% volume of fill) is necessary to restore compressive stiffness of the damaged vertebral body to its value before damage.48 The injection of cement is stopped whenever epidural or paravertebral opacification is observed or when the cement reaches the dorsal quarter of the vertebral body.3 If extravasation of cement is seen, further injection of cement is stopped. The extravasation is evaluated

If the recurrent pain arises from a vertebra previously treated with vertebroplasty, repeat percutaneous vertebroplasty offers therapeutic benefit.37 Repeat vertebroplasties may be approached from the pedicle opposite the previous insertion.37,51

AVOIDANCE OF COMPLICATIONS The complications are minimal if precautions are taken.52

Leakage of cement Leakage of cement can cause neurologic injury or pulmonary emboli.53–56 One can, however, prevent cement leaks by using high-resolution fluoroscopy (or rarely CT), adequate cement opacification, and by interrupting or terminating the procedure on first recognition of a leak. Biplanar fluoroscopy is not required but does make visualization in two projections simpler and faster. One must visualize the vertebra in two planes numerous times. The authors use a uniplanar machine which is rotated at every step to obtain anteroposterior and lateral views. Sterile barium sulfate is added to bring the barium quantity to 30% by weight, making the cement opaque for visualization under fluoroscopy. Presently, FDA approved premixed cement for vertebroplasty is available commercially. Terminating injection when 373

Part 2: Interventional Spine Techniques

early leakage of cement is visualized limits the size of the leak and usually prevents it from becoming significant. Venography has been used to observe leakage but it does not accurately predict the leak of cement.14 If there is leakage into the spinal canal with neurological deficit, a neurosurgeon or spinal surgeon should be consulted.57,58 The cement emboli can leak into the valveless veins of the vertebrae and migrate into the paraspinal plexus which drains into the azygous vein. The azygous veins empty in to the right atrium of the heart, after which blood then flows to the lungs. Asymptomatic leakage of the cement routinely occurs and a patient with mediastinal problem had an MRI of chest done at our center. Small emboli of cement were observed in the lungs and he had previous history of percutaneous vertebroplasty. This patient probably had asymptomatic multiple microemboli of cement. The PMMA cement emboli were not the source of his problem.

Pain exacerbation At times the pain may exacerbate due to local ischemia or increased pressure. A CT scan be immediately obtained to ensure no leakage. Otherwise, the pain usually resolves in a few hours or a few days.14 We discharge all patients with narcotic medication (oxycodone) to be used on an as-needed basis. If radicular pain occurs secondary to leakage into the neural foramen, within 10–20 minutes we inject 10 cc of 0.2% lidocaine followed by 100–200 cc of pressurized saline perfusion.59,60 During the injection, the patient may feel some pressure, but the surgeon should be aware of this and slow or stop injection if significant radicular pain occurs.

Bleeding The cannula is removed after adequate filling of the vertebra. Venous bleeding may be observed at the needle entry sites and local pressure for 3–5 minutes will minimize the bleeding.6

Occupational dose mitigation Secondary radiation, particularly scatter radiation from the patient and leakage radiation from the radiograph tube, is the primary source of operator and medical staff exposure. Techniques to reduce exposure to the operator include shielding devices, which are placed directly on the patient to provide maximum shielding to the operator’s hands and upper body. Additionally, a lead apron can be placed between the surgeon and the patient. Exposure on injecting cement with 1 mL syringe and vertebroplasty kit is the same.61 Through the use of radiation-reducing procedures, such as pulsed fluoroscopic operation at 4 pps, radiograph tube positioning under the patient table, and use of lead sheets on the patients and lead aprons placed between the surgeon and the patient, more than 6700 vertebroplasty vertebrae procedures may be safely performed by a single operator per year. Polymethyl methacrylate vapor levels to which medical personnel are exposed during percutaneous vertebroplasty are well below the level typically considered hazardous. However, it is important to note that some individuals may experience adverse effects, such as asthma, coughing, nausea, and decreased appetite, when exposed to levels6 typically considered to be acceptable.62–64

References 1. Stallmeyer MJ, Zoarski GH, Obuchowski AM. Optimizing patient selection in percutaneous vertebroplasty. J Vascul Intervent Radiol 2003; 14(6):683–696. 2. Amar AP, Larsen DW, Esnaashari N, et al. Percutaneous transpedicular polymethylmethacrylate vertebroplasty for the treatment of spinal compression fractures. Neurosurgery 2001; 49(5):1105–1114; discussion 1114–1115.

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3. Gangi A, Guth S, Imbert JP, et al. Percutaneous vertebroplasty: indications, technique, and results. Radiographics 2003; 23(2):e10. 4. Maynard AS, Jensen ME, Schweickert PA, et al. Value of bone scan imaging in predicting pain relief from percutaneous vertebroplasty in osteoporotic vertebral fractures. Am J Neuroradiol 2000; 21(10):1807–1812. 5. Hodler J, Peck D, Gilula LA. Midterm outcome after vertebroplasty: predictive value of technical and patient-related factors. Radiology 2003; 227(3):662–668. 6. Mathis JM, Wong W. Percutaneous vertebroplasty: technical considerations. J Vascul Intervent Radiol 2003; 14(8):953–960. 7. Kallmes DF, Jensen ME. Percutaneous vertebroplasty [Review]. Radiology 2003; 229(1):27–36. 8. Jensen ME, Evans AJ, Mathis JM, et al. Percutaneous polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral body compression fractures: technical aspects. Am J Neuroradiol 1997; 18(10):1897–1904. 9. Kaufmann TJ, Jensen ME, Schweickert PA, et al. Age of fracture and clinical outcomes of percutaneous vertebroplasty. Am J Neuroradiol 2001; 22(10):1860–1863. 10. Barr JD, Barr MS, Lemley TJ, et al. Percutaneous vertebroplasty for pain relief and spinal stabilization [see comment]. Spine 2000; 25(8):923–928. 11. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful vertebral body fractures in cancer patients. J Neurosurg 2003; 98(1 Suppl):21–30. 12. White SM. Anaesthesia for percutaneous vertebroplasty. Anaesthesia 2002; 57(12):1229–1230. 13. Brown DB, Gilula LA, Sehgal M, et al. Treatment of chronic symptomatic vertebral compression fractures with percutaneous vertebroplasty. Am J Roentgenol 2004; 182(2):319–322. 14. Mathis JM. Percutaneous vertebroplasty: complication avoidance and technique optimization. Am J Neuroradiol 2003; 24(8):1697–1706. 15. Sesay M, Dousset V, Liguoro D, et al. Intraosseous lidocaine provides effective analgesia for percutaneous vertebroplasty of osteoporotic fractures. Can J Anaesthes 2002; 49(2):137–143. 16. Gangi A, Kastler BA, Dietemann JL. Percutaneous vertebroplasty guided by a combination of CT and fluoroscopy. Am J Neuroradiol 1994; 15(1):83–86. 17. Peters KR, Guiot BH, Martin PA, et al. Vertebroplasty for osteoporotic compression fractures: current practice and evolving techniques. Neurosurgery 2002; 51(5 Suppl):96–103. 18. Gailloud P, Martin JB, Olivi A, et al. Transoral vertebroplasty for a fractured C2 aneurysmal bone cyst [Case Reports. Letter]. J Vascul Intervent Radiol 2002; 13(3):340–341. 19. Martin JB, Gailloud P, Dietrich PY, et al. Direct transoral approach to C2 for percutaneous vertebroplasty. Cardiovasc Intervent Radiol 2002; 25(6):517–519. 20. Cotten A, Boutry N, Cortet B, Assaker R, et al. Percutaneous vertebroplasty: state of the art. Radiographics 1998; 18(2):311–320; discussion 320–323. 21. Galibert P, Deramond H, Rosat P, et al. [Preliminary note on the treatment of vertebral angioma by percutaneous acrylic vertebroplasty]. [French] Neuro-Chirurgie. 1987; 33(2):166–168. 22. Appel NB, Gilula LA. ‘Bull’s-eye’ modification for transpedicular biopsy and vertebroplasty. Am J Roentgenol 2001; 177(6):1387–1389. 23. Cortet B, Cotten A, Boutry N, et al. Percutaneous vertebroplasty in the treatment of osteoporotic vertebral compression fractures: an open prospective study. J Rheumatol 1999; 26(10):2222–2228. 24. Deramond H, Depriester C, Galibert P, et al. Percutaneous vertebroplasty with polymethylmethacrylate. Technique, indications, and results. Radiol Clin N Am 1998; 36(3):533–546. 25. Kallmes DF, Schweickert PA, Marx WF, et al. Vertebroplasty in the mid- and upper thoracic spine. Am J Neuroradiol 2002; 23(7):1117–20. 26. Kim AK, Jensen ME, Dion JE, et al. Unilateral transpedicular percutaneous vertebroplasty: initial experience. Radiology 2002; 222(3):737–741. 27. Martin JB, Wetzel SG, Seium Y, et al. Percutaneous vertebroplasty in metastatic disease: transpedicular access and treatment of lysed pedicles – initial experience. Radiology 2003; 229(2):593–597. 28. Garfin SR, Yuan HA, Reiley MA. New technologies in spine: kyphoplasty and vertebroplasty for the treatment of painful osteoporotic compression fractures. Spine 2001; 26(14):1511–1515. 29. http://sis.windhover. com/windbuy/lpext.dll/ windbuy/iv/2001/ 2001800190.htm 30. Al-Assir I, Perez-Higueras A, Florensa J, et al. Percutaneous vertebroplasty: a special syringe for cement injection. Am J Neuroradiol 2000; 21:159–161.

Section 2: Interventional Spine Techniques 31. Heini PF, Allred C. The use of a side-opening injection cannula in vertebroplasty: a technical note. Spine 2002; 27(1):105–109.

49. Berlemann U, Ferguson SJ, Nolte LP, et al. Adjacent vertebral failure after vertebroplasty. A biomechanical investigation. J Bone Joint Surg [Br] 2002; 84:748–752

32. Murphy KJ, Lin DD, Khan AA, et al. Multilevel vertebroplasty via a single pedicular approach using a curved 13-gauge needle: technical note. Can Assoc Radiol J 2002; 53(5):293–295.

50. Aebli N, Krebs J, Davis G, et al. Fat embolism and acute hypotension during vertebroplasty: an experimental study in sheep. Spine 2002; 27:460–466.

33. Schallen EH, Gilula LA. Vertebroplasty: reusable flange converter with hub lock for injection of polymethylmethacrylate with screw-plunger syringe. Radiology 2002; 222(3):851–855.

51. Gilula L. Is insufficient use of polymethylmethacrylate a cause for vertebroplasty failure necessitating repeat vertebroplasty? [comment]. Am J Neuroradiol 2003; 24(10):2120–2121; author reply 2121–2122.

34. Minart D, Vallee JN, Cormier E, et al. Percutaneous coaxial transpedicular biopsy of vertebral body lesions during vertebroplasty. Neuroradiology 2001; 43(5):409–412.

52. McGraw JK, Cardella J, Barr JD, et al. SIR Standards of Practice Committee. Society of Interventional Radiology quality improvement guidelines for percutaneous vertebroplasty. J Vascul Intervent Radiol 2003; 14(7):827–831.

35. McGraw JK, Heatwole EV, Strnad BT, et al. Predictive value of intraosseous venography before percutaneous vertebroplasty [see comment]. J Vascul Intervent Radiol 2002; 13(2 Pt 1):149–153.

53. Harrington KD. Major neurological complications following percutaneous vertebroplasty with polymethylmethacrylate: a case report [see comment]. J Bone Joint Surg [Am] 2001; 83-A(7):1070–1073.

36. Peh WC, Gilula LA. Additional value of a modified method of intraosseous venography during percutaneous vertebroplasty. Am J Roentgenol 2003; 180(1):87–91.

54. Kang JD, An H, Boden S, et al. Cement augmentation of osteoporotic compression fractures and intraoperative navigation: summary statement. Spine 2003; 28(15): S62–S63.

37. Gaughen JR Jr, Jensen ME, Schweickert PA, et al. The therapeutic benefit of repeat percutaneous vertebroplasty at previously treated vertebral levels [see comment]. Am J Neuroradiol 2002; 23(10):1657–1661. 38. Phillips FM. Minimally invasive treatments of osteoporotic vertebral compression fractures. Spine 2003; 28(15):S45–S53. 39. Vasconcelos C, Gailloud P, Beauchamp NJ, et al. Is percutaneous vertebroplasty without pretreatment venography safe? Evaluation of 205 consecutives procedures. Am J Neuroradiol 2002; 23(6):913–917. 40. Wong W, Mathis J. Is intraosseous venography a significant safety measure in performance of vertebroplasty? J Vascul Intervent Radiol 2002; 13(2 Pt 1):137–138.

55. Mousavi P, Roth S, Finkelstein J, et al. Volumetric quantification of cement leakage following percutaneous vertebroplasty in metastatic and osteoporotic vertebrae. J Neurosurg 2003; 99(1 Suppl):56–59. 56. Yeom JS, Kim WJ, Choy WS, et al. Leakage of cement in percutaneous transpedicular vertebroplasty for painful osteoporotic compression fractures. J Bone Joint Surg [Br] 2003; 85(1):83–89. 57. Lee B-J, Lee S-R, Yoo T-Y. Paraplegia as a complication of percutaneous vertebroplasty with polymethylmethacrylate: a case report. Spine 2002; 27(19):E419–E422.

41. Mathis JM, Barr JD, Belkoff SM, et al. Percutaneous vertebroplasty: a developing standard of care for vertebral compression fractures. Am J Neuroradiol 2001; 22(2):373–381.

58. Shapiro S, Abel T, Purvines S. Surgical removal of epidural and intradural polymethylmethacrylate extravasation complicating percutaneous vertebroplasty for an osteoporotic lumbar compression fracture. Case report. J Neurosurg 2003; 98(1 Suppl):90–92.

42. Hiwatashi A, Moritani T, Numaguchi Y, et al. Increase in vertebral body height after vertebroplasty. Am J Neuroradiol 2003; 24(2):185–189.

59. Jarvik JG, Kallmes DF, Mirza SK. Vertebroplasty: learning more, but not enough. Spine 2003; 28(14):1487–1489.

43. Peh WC, Gilula LA. Percutaneous vertebroplasty: indications, contraindications, and technique. Br J Radiol 2003; 76(901):69–75.

60. Kelekis AD, Martin J-B, Somon T, et al. Radicular pain after vertebroplasty: compression or irritation of the nerve root? Initial experience with the ‘cooling system.’ Spine 2003; 28(14):E265–E269.

44. Chavali R, Resijek R, Knight SK, et al. Extending polymerization time of polymethylmethacrylate cement in percutaneous vertebroplasty with ice bath cooling. Am J Neuroradiol 2003; 24(3):545–546. 45. Kaufmann TJ, et al. Cardiovascular effects of polymethylmethacrylate use in percutaneous vertebroplasty [see comment]. Am J Neuroradiol 2002; 23(4):601–604. 46. Vasconcelos C, Gailloud P, Martin JB, et al. Transient arterial hypotension induced by polymethylmethacrylate injection during percutaneous vertebroplasty. J Vascul Intervent Radiol 2001; 12(8):1001–1002. 47. Belkoff SM, Mathis JM, Jasper LE, et al. An ex vivo biomechanical evaluation of a hydroxyapatite cement for use with vertebroplasty. Spine 2001; 26(14):1542–1546. 48. Liebschner MA, Rosenberg WS, Keaveny TM. Effects of bone cement volume and distribution on vertebral stiffness after vertebroplasty. Spine 2001; 26(14):1547–1554.

61. Kallmes DF, Roy SS, Piccolo RG, et al. Radiation dose to the operator during vertebroplasty: prospective comparison of the use of 1-cc syringes versus an injection device. Am J Neuroradiol 2003; 24(6):1257–1260. 62. Cloft HJ, Easton DN, Jensen ME, et al. Exposure of medical personnel to methylmethacrylate vapor during percutaneous vertebroplasty. Am J Neuroradiol 1999; 20(2):352–353. 63. Kirby BS, Doyle A, Gilula LA. Acute bronchospasm due to exposure to polymethylmethacrylate vapors during percutaneous vertebroplasty. Am J Roentgenol 2003; 180(2):543–544. 64. Nimmagadda U, Salem MR. Acute bronchospasm associated with methylmethacrylate cement. Anesthesiology 1998; 89:1290–1291.

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PART 2

INTERVENTIONAL SPINE TECHNIQUES

Section 2

Interventional Spine Techniques

CHAPTER

Kyphoplasty Technique

33

Amir H. Fayyazi and Frank M. Phillips

INTRODUCTION Pathologic vertebral compression fractures (VCFs) are a leading cause of disability and morbidity in patients with osteoporosis, multiple myeloma, and bone metastases.1–4 The consequences of these fractures include pain and often progressive vertebral collapse with resultant spinal kyphosis. Osteoporotic VCFs have been shown to adversely affect quality of life, physical function, mental health, and survival.4–6 These effects are related to the severity of the spinal deformity and are, in part, independent of pain.4,5 In recent years, researchers have highlighted the reduced quality of life, functional limitations, and impaired pulmonary function associated with spinal kyphotic deformity from osteoporotic VCFs.3,4,7–9 Kyphosis can lead to reduced abdominal space with poor appetite and resultant nutritional problems.4,10 By shifting the patient’s center of gravity forward, kyphotic deformity not only increases the risk of additional fractures,11 but also may lead to poor balance which potentially increases the risk of accidental falls.12,13 The ideal surgical treatment of VCFs should address both the fracture-related pain and the kyphotic deformity. It should be accomplished in a minimally invasive fashion without subjecting the patient to inordinate risks or excessive surgical trauma. Over the past decade, percutaneous vertebroplasty, involving the injection of polymethylmethacrylate (PMMA) into a fractured vertebral body, has been popularized. Substantial alleviation of pain has been reported in a majority of patients treated with vertebroplasty for osteopenic VCF.14–22 Although effective at relieving vertebral fracture pain, vertebroplasty is not designed to address the associated sagittal plane deformity. Kyphoplasty involves the penetration of the vertebral body with a trochar followed by insertion of an inflatable balloon tamp (IBT). Inflation of the balloon tamp restores the vertebral body back towards its original height, while creating a cavity to be filled with bone void filler. This technique was first performed in 1998. Early results of kyphoplasty suggest significant pain relief as well as the ability to improve the collapsed vertebral body’s height.23–29 The kyphoplasty procedure was designed to address vertebroplasty’s shortcomings such as high rates of cement leakage, although they rarely manifest with symptoms, and inability to correct fracture deformity. As the balloon tamp is inflated in the fractured vertebral body, the vertebral endplates are pushed apart reducing the fracture, and cancellous bone is pushed away from the balloon creating a cavity surrounded by compacted cancellous bone.30–32 The creation of an intravertebral cavity may decrease the potential for cement leakage by allowing for low-pressure, controlled placement of ‘doughy’ cement into the cavity and by creating a dam effect by densely compacting bone around the cavity.

PMMA has been the most common bone void filler used in both vertebroplasty and kyphoplasty. This acrylic cement has a long history of clinical use for the fixation of metal and plastic joint replacements and for the fixation of pathological fractures.33,34 When used to treat vertebral compression fractures, PMMA is usually modified (for example, addition of more barium sulfate, addition of antibiotics, alteration of monomer to powder ratio), in part to attain a viscosity that allows percutaneous insertion into vertebrae while minimizing risk of extravertebral leaks. In April, 2004, the United States FDA approved a formulation of PMMA for use in kyphoplasty procedures.

KYPHOPLASTY PATIENT SELECTION Indications and contraindications The main indications for kyphoplasty are painful or progressive osteoporotic or osteolytic vertebral compression fractures. Contraindications include systemic pathologies such as sepsis, prolonged bleeding times, or cardiopulmonary conditions that would preclude the safe completion of the procedure. In certain vertebra plana fracture configurations with height loss greater than 80% of the prefracture height, kyphoplasty may be technically difficult. The feasibility of the procedure should be assessed on the merits of the case. Patients with true burst fractures or fractures associated with neurologic findings are not candidates for percutaneous vertebral augmentation procedures. Generally, we do not advocate cementing more than three vertebral levels in one procedure because of the potential for deleterious cardiopulmonary effects related to pulmonary embolization (fat or cement) or to cement monomer.

Surgical timing The optimal timing of kyphoplasty treatment is uncertain. In a patient with an acute VCF and relatively minor vertebral collapse, the senior author (F.M.P.) will attempt a trial of conservative care during which serial radiographs are obtained. Kyphoplasty is recommended if there is progressive collapse of the vertebral body, if the pain attributed to the VCF is incapacitating, or if the pain attributed to the VCF does not respond to a reasonable period of conservative care. With advanced kyphosis at the time of presentation after a VCF, immediate kyphoplasty treatment may be considered to improve sagittal alignment. In the authors’ experience, earlier kyphoplasty may also be warranted for fractures at the thoracolumbar junction, fractures due to steroid-induced osteoporosis, and fractures occurring in vertebra with extremely low bone mineral density (i.e. a T score of ≤ 4 SD), which are predisposed to progressive collapse and deformity. To improve reliability and the extent of fracture reduction, one might consider performing kyphoplasty soon after fracture. Some studies

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suggest improved fracture reduction when kyphoplasty is performed earlier.24,26 However, the appropriate duration of nonoperative treatment prior to consideration of kyphoplasty has not yet been established.

the pedicle allowing cannulation through an extrapedicular approach. Despite the smaller size of the thoracic pedicle, the costovertebral attachment results in a much larger effective pedicle size (Fig. 33.2)

Preoperative evaluation

KYPHOPLASTY SURGICAL TECHNIQUE

Before proceeding with kyphoplasty, the physician must confirm that the patient’s back pain is indeed caused by a VCF. This determination requires careful correlation of the patient’s history and clinical examination with radiographic documentation of an acute or nonhealed VCF. The possibility of other spinal pathologies such as tumors or degenerative spondylosis must be considered as potential causes of back pain and deformity. A thorough neurologic examination is essential to rule out neurologic compromise. Pain radiating around the trunk in a dermatomal manner may accompany VCFs. Pulmonary function should be evaluated in those patients in whom advanced kyphosis may have led to respiratory difficulty. Preoperative planning for kyphoplasty includes imaging studies to confirm the fracture, estimate the duration of the fracture, and define the fracture anatomy. Lateral radiographs are particularly useful to plan the trajectory for any percutaneous procedure. Magnetic resonance imaging (MRI) can visualize bony edema, which indicates acute fracture, as well as help rule out infection or tumor involvement. Malignant causes of VCF are usually characterized by an illdefined margin, signal enhancement, and pedicle involvement as well as by paravertebral soft tissue mass.35 Sagittal MRI images with short tau inversion recovery (STIR) sequences highlight the marrow edema changes associated with acute VCFs. STIR sequence MRI has proven useful in determining the acuteness of a VCF.

Anesthesia

SURGICAL ANATOMY Understanding the anatomy of the spinal column and correlating spinal anatomy with intraoperative fluoroscopic images is essential to performing kyphoplasty. The mediolateral pedicle diameter is significantly smaller than the superior–inferior diameter. In the thoracic spine, the pedicle diameters are smallest in the midthoracic region especially at T5–7. The pedicle size appears to decrease as one descends from the upper thoracic segment to the middle segment and later increases in the lower segments. In the lumbar spine, the pedicle diameter increases gradually in the caudal segments. Also, in the majority of patients, the L1 pedicle diameter is smaller than the T11 or T12 pedicle diameter. The orientation of the pedicle is important in planning an appropriate trajectory for kyphoplasty. The medial inclination in the transverse plane appears to be greatest in the upper thoracic segments (T1–3), and becomes a straight anterior trajectory in the middle to lower thoracic spinal segments (Fig. 33.1). In the lumbar spine, the medial orientation of the pedicles increases slightly from L1 to L5. In the thoracic spine, the attachment of the ribs to the corresponding vertebral body (i.e. costovertebral joint) protects the lateral side of

Fig. 33.1 In the thoracic spine, the pedicles have less of a medial inclination (arrows), so that an extrapedicular approach will allow for better medialization of the IBTs. 378

Although the procedure may be performed under conscious sedation, the authors prefer to use general anesthesia for patients undergoing kyphoplasty. Advantages of general anesthesia include easier airway management, elimination of patient discomfort during the procedure, and elimination of patient motion that might impair fluoroscopic imaging.

Intraoperative positioning The patient is positioned prone on a table in the operating room or on a spinal frame with cushioned bolsters in the radiology suite. We prefer to use a Jackson frame which enhances the natural extension of the spine and also allows for biplane fluoroscopy. Alternatively, the patient can be placed on a radiolucent table with rolls placed beneath the chest and hips. The face, elbows, and legs should be well padded.

Fluoroscopic imaging The authors have found simultaneous biplanar fluoroscopy to be advantageous by allowing orthogonal visualization without having to move the C-arm. The ability to visualize the pedicles in both anteroposterior (AP) and lateral views is essential to performing the procedure. Fluoroscopic images confirming the patient’s anatomy must be obtained prior to initiating vertebral cannulation. In the AP view, the superior and inferior endplates are parallel to the fluoroscopic beam and are each

Costovertebral attachment

Fig. 33.2 The costovertebral attachment results in a much larger effective pedicle size in thoracic vertebrae.

Section 2: Interventional Spine Techniques

visualized as a single cortical shadow, the spinous process is centered in the vertebral body, and the pedicles are symmetric and positioned in the upper half of the vertebral body (Fig. 33.3A). In the lateral view, the endplates are also parallel and the pedicles are superimposed (Fig. 33.3B), Alternatively, the fluoroscope can be rotated 10– 20° for a pedicle en-face view, the view down the path of the pedicle (Fig. 33.3C) In this position, the pedicle is visualized directly and can be cannulated by paralleling the pathway of the X-ray beam.

spine, the transpedicular route may not allow for adequate medial placement of the instruments, which may limit optimal IBT inflation. The extrapedicular approach is an alternative that may allow for better medialization of the tools. The extrapedicular approach takes advantage of the costovertebral complex and allows entry through a more lateral starting point. An alternative far lateral approach to the lumbar vertebra has also been described; however, this technique has not been widely adopted.

Surgical approaches

Surgical technique

Bilateral transpedicular and extrapedicular approaches have been described for accessing the vertebral body during kyphoplasty. Most kyphoplasty procedures are performed by accessing the vertebral body through a transpedicular approach. In the upper and midthoracic

When using the transpedicular approach, the initial instrument should dock on the lateral aspect of the facet joint overlying the lateral aspect of the pedicle on the AP fluoroscopic image (Fig. 33.4). With

Starting position

Pedicles in upper half of vertebral body Endplates parallel Spinous process equidistant between pedicles

A

Endplates parallel

Pedicles superimposed

B

C Fig. 33.3 (A) In a centered AP view, each endplate is visualized as a single cortical shadow, the spinous process is centered in the vertebral body, and the pedicles are symmetrical and positioned in the upper half of the vertebral body. (B) In a centered lateral view, the endplates are parallel, and the pedicles are superimposed. (C) When the fluoroscope is rotated 10–20°, a pedicle en-face view, the view down the path of the pedicle, is visualized. Figures A and B courtesy of Kyphon Inc., Sunnyvale CA, USA.

Fig. 33.4 With the transpedicular approach, the initial instrument should dock on the lateral aspect of the facet joint overlying the lateral aspect of the pedicle on the AP view (center). Lateral and axial views are shown (top and bottom, respectively). 379

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the extrapedicular approach, the initial instrument is docked at the junction of the transverse process, rib head, and lateral pedicle wall (Fig. 33.5). The tip of the instrument appears outside of the lateral pedicle wall on the AP image. Unless an appropriate starting point is chosen, the balloon tamps cannot be positioned correctly, decreasing the success of the reduction. Once the docking position is selected on the AP view, the position of the starting point must be checked on the lateral view to confirm the appropriate trajectory toward the collapsed vertebral body.

Transpedicular

Pedicle cannulation During a transpedicular approach, the Jamshidi needle is advanced down the pedicle and into the posterior aspect of the vertebral body. At first, resistance to the passage of the needle is noted because of the cortical bone of the facet. As the needle enters the cancellous bone of the pedicle, the resistance decreases. Orthogonal fluoroscopic views are required as the needle advances through the pedicle. With both transpedicular and extrapedicular approaches, as the needle is advanced, the tip should remain lateral to the medial pedicle wall on the AP image until it reaches the posterior aspect of the vertebral body on the lateral image (Fig. 33.6). This technique ensures that the instrument remains outside of the spinal canal. Once the vertebral body is entered, the tip of the instrument may be medialized as Midpedicle

Final position

Extrapedicular

Midpedicle

Final position

Fig. 33.6 With both transpedicular and extrapedicular approaches, as the needle is advanced (Midpedicle), the tip should remain lateral to the medial pedicle wall on the AP image (center) until it reaches the posterior aspect of the vertebral body on the lateral image (Final position, top). Axial views are also shown (bottom). Fig. 33.5 With the extrapedicular approach, the initial instrument is docked at the junction of the transverse process, rib head, and lateral pedicle wall. Lateral, AP, and axial views are shown (top, center, and bottom, respectively). 380

Section 2: Interventional Spine Techniques

is appropriate but should not cross the midline. The Jamshidi needle should be advanced 1–2 mm past the posterior vertebral body margin.

Placement of working cannulae Fig. 33.9 On the AP view, the tip of the drill should approach the middle of the vertebral body but not cross midline. Courtesy of Kyphon Inc., Sunnyvale CA, USA.

The inner stylet is removed from the introducer needle, and a guide wire is placed into the vertebral body. After the working cannula is advanced over the guide wire into the posterior aspect of the vertebral body under biplanar fluoroscopic guidance, the guide wire is removed (Fig. 33.7). It is important to limit the number of passes through the pedicle as multiple attempts at cannulation create potential paths for cement leakage.

Vertebral body preparation A drill or bone tamp is used to prepare the vertebral body for placement of the IBTs. Under lateral fluoroscopy, the drill or tamp should be advanced to within 2–4 mm of the anterior cortex without perforating the cortex (Fig. 33.8). On the AP view, the tip of the drill should approach the middle of the vertebral body (Fig. 33.9). Once the drill is removed, a dull guide pin can be used to palpate the anterior cortex to confirm that there is no perforation. The vertebral body is now ready for expansion.

Fig. 33.7 The working cannula is advanced over the guide wire into the posterior aspect of the vertebral body under biplanar fluoroscopic guidance, and the guide wire is removed. Courtesy of Kyphon Inc., Sunnyvale CA, USA.

Inflatable balloon tamp inflation The bilateral IBTs are placed anteriorly in the vertebral body. To create a cavity within the vertebra and to reduce the fracture deformity, the IBTs are inflated in 0.5 cc increments while using visual (radiographic), volume, and pressure controls (digital manometer). Inflation continues until vertebral body height is restored, the IBT contacts a vertebral body cortical wall, the IBT reaches the maximal pressure rating without spontaneous decay, or maximal balloon volume is reached (Fig. 33.10). Four- or six-millimeter-sized balloons are available. We prefer to use 6 mm balloons in larger vertebral bodies (T12–L5) and 4 mm balloons in the midthoracic spine.

Cement application After the IBTs are withdrawn, a bone filler cannula is used to place partially cured PMMA into the cavity within the fractured vertebral body. To minimize the risk of cement extravasation, the authors allow the cement to become quite viscous prior to placement in the vertebral body. The bone filler device (BFD) filled with cement is positioned anteriorly in the intravertebral cavity created by IBT inflation. As the plunger is advanced, cement is expelled and fills the intravertebral cavity in a retrograde fashion. Cementing should be discontinued if extravertebral extravasation occurs or when cement reaches the posterior 25% of the vertebral body. The cement volume should approximate the volume of the intravertebral cavity. The judicious use of live fluoroscopic imaging is critical during cementing (Fig. 33.11). If cement extravasation occurs, usually through a fractured endplate or vertebral cortex, placing a small amount of viscous cement into the cavity and reinflating the balloon can salvage this situation. This maneuver will line the cavity walls with cement, effectively preventing further extravasation when the remainder of the cavity is filled with cement.

Postoperative care Postoperatively, the authors prefer to keep patients prone until they are alert. Once the patients have recovered from the anesthesia, they are mobilized by first sitting on the side of the bed and ambulating later that evening. Most patients are discharged home within a day of the procedure.

A

B

Fig. 33.8 Under lateral fluoroscopy, the drill (A) or tamp (B) should be advanced to within 2–4 mm of the anterior cortex without perforating the cortex. Courtesy of Kyphon Inc., Sunnyvale CA, USA.

COMPLICATIONS AND PREVENTIVE MEASURES Errors in patient selection Poor clinical outcomes may be predicted for kyphoplasty unless careful attention is given to patient screening and work-up. Treating old, healed VCFs is unlikely to affect the patient’s symptoms. The VCF must be confirmed as the likely pain generator if either 381

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Fig. 33.11 The cement volume should approximate the volume of the intravertebral cavity. The judicious use of live fluoroscopic imaging is critical during cementing. Courtesy of Kyphon Inc., Sunnyvale CA, USA.

A

by activity or changing positions and that is localized to the area of the radiographically documented fracture suggests the fracture to be responsible for the patient’s symptoms. In contrast to acute fracture pain, the back pain of chronic kyphosis typically worsens as the patient remains erect for periods of time and is not typically exacerbated by changes in position. The existence of multiple fractures may complicate the diagnosis, so that advanced imaging studies such as MRI or computed tomography (CT) with bone scans are usually required to identify recent fractures. Sagittal T1-weighted MR sequences can distinguish acute or nonhealed fractures from healed fractures. Edema associated with acute VCFs produces low signal intensity, whereas more chronic fractures tend to produce signals that are similar to those of nonfractured vertebrae. As mentioned in the Preoperative Evaluation section, sagittal STIR (heavily T2-weighted) MRI sequences are the most sensitive way to distinguish marrow fat from marrow edema. In STIR-MR images, edema in acute fractures produces high-intensity signal.36–38 On bone scan analyses, recently fractured vertebrae show an increased uptake of 99mTc compared to nonfractured vertebrae. CT plus bone scans may be used when MR images cannot be obtained.

B

C

Fig. 33.10 Inflation continues (A–C) until vertebral body height is restored, the IBT contacts a vertebral body cortical wall, the IBT reaches maximal pressure rating without spontaneous decay, or the maximal balloon volume is reached. Courtesy of Kyphon Inc., Sunnyvale CA, USA.

vertebroplasty or kyphoplasty is being considered. This determination usually requires a combination of clinical findings suggestive of fracture pain and confirmatory imaging studies. VCF pain often increases with weight-bearing activities and eases with recumbency. On history, the presence of abrupt onset of pain that is aggravated 382

Vertebral body access complications With either the transpedicular or the extrapedicular approach, care must be taken to avoid injuring surrounding tissues while accessing the vertebral body. The risk of injury to the neural elements increases if the medial pedicle wall is breached. Accessing the vertebral body caudal to the pedicle may place the segmental vessels and nerve roots at risk. Anterior or lateral perforation of the vertebral cortices with instruments may result in vascular injury or injury to structures in the thoracic or retroperitoneal spaces. Multiple attempts at cannulating the vertebral body should be avoided because of the increased risk of cement leaks through these additional tracts.

Cement complications The majority of complications reported for vertebral augmentation procedures relate to extravertebral cement extravasation. Cement may leak out of the vertebral body directly through deficiencies in the vertebral body cortex or via the venous system. If PMMA extravasates

Section 2: Interventional Spine Techniques

outside of the vertebral body, complications related to mechanical or thermal injury of adjacent anatomic structures may occur. The risk of local cement leakage is likely affected by cement injection pressure and cement viscosity as well as the ability of the bone, particularly the vertebral body cortex, to resist cement leakage. In addition to the risks of local cement leakage, systemic exposure to cement has been associated with cardiovascular collapse.39,40 It has been hypothesized that pressurization of PMMA into cancellous bone predisposes to embolization of cement, methylmethacrylate monomer, and bone marrow contents to the lungs with resulting adverse cardiopulmonary sequelae.39–42 This theorized result is certainly a cause for concern during vertebral augmentation procedures when high-pressure PMMA injection into vertebral bodies is performed. Extravertebral cement extravasation commonly occurs during vertebroplasty with reported leak rates of up to 65%;14 however, clinical sequelae of the leakage have been infrequently reported. In contrast, the reported rate of cement extravasation with kyphoplasty is typically less than 10%.23,26–29,43 With kyphoplasty, the creation of an intravertebral cavity surrounded by compacted bone allows for the placement of higher-viscosity cement under lower pressure compared to the injection conditions needed for vertebroplasty.

Failure of reduction The deleterious effects of spinal kyphosis on physical function, mental, respiratory, and gastrointestinal health are well established.3–5,9,44–46 Kyphoplasty attempts to reduce the fracture and associated deformity in a reliable and predictable fashion. Some degree of fracture reduction has been achieved in more than 60% of treated fractures.27,28 Factors that seem to limit reduction achieved with kyphoplasty include partial healing of bone, suboptimal placement of the IBT, and collapse of vertebral endplates after IBT removal and before cement placement. In cases where healed bone limits IBT expansion and fracture reduction, high IBT pressures at low balloon volumes and distorted IBT inflation shapes will be observed. To improve reduction of partially healed bone, the authors have developed a technique combining kyphoplasty with percutaneous osteotomy. Regarding positioning, if the IBT is placed too far laterally in the vertebral body, balloon contact with the lateral vertebral body cortex early during inflation limits the surgeon’s ability to continue inflation and optimize vertebral endplate elevation. This difficulty may be salvaged by the use of directional balloon tamps that preferentially inflate in a medial direction; however, this situation is best prevented by creating an appropriate channel for IBT placement. In cases where loss of endplate reduction occurs with balloon deflation, it may be possible to maintain reduction with unilateral bone tamp inflation elevating the endplate while placing cement on the opposite side.

SUMMARY Kyphoplasty is a technically demanding procedure offering a much needed treatment option for patients with symptomatic VCFs that do not respond to medical therapy or that are associated with progressive kyphosis. Rapid pain reduction, improved quality of life, and often fracture reduction have been observed in several consecutive case series.23,25–28,43,47 Further study is required to determine the optimal time for surgical intervention, to refine the patient selection criteria, and to delineate specific long-term effects of correcting vertebral deformity.

References 1. Barrick MC, Mitchell SA. Multiple myeloma. AJN 2001; 101(Suppl)(4):6–12. 2. Schachar NS. An update on the nonoperative treatment of patients with metastatic bone disease. Clin Orthop 2001; (382):75–81.

3. Lyles KW, Gold DT, Shipp KM, et al. Association of osteoporotic vertebral compression fractures with impaired functional status. Am J Med 1993; 94(6):595–601. 4. Silverman SL. The clinical consequences of vertebral compression fracture. Bone 1992; 13(Suppl 2):S27–S31. 5. Gold DT. The clinical impact of vertebral fractures: quality of life in women with osteoporosis. Bone 1996; 18(3 Suppl):185S–189S. 6. Gold DT, Lyles KW. Fractures: effects on quality of life. In: Rosen CJ, Glowacki J, Bilezikian JP, eds. The aging skeleton. San Diego, CA: Academic Press; 1999:632. 7. Leidig G, Minne HW, Sauer P, et al. A study of complaints and their relation to vertebral destruction in patients with osteoporosis. Bone Miner 1990; 8(3):217–229. 8. Pluijm SM, Tromp AM, Smit JH, et al. Consequences of vertebral deformities in older men and women. J Bone Miner Res 2000; 15(8):1564–1572. 9. Schlaich C, Minne HW, Bruckner T, et al. Reduced pulmonary function in patients with spinal osteoporotic fractures. Osteoporos Int 1998; 8(3):261–267. 10. Ross PD, Davis JW, Epstein RS, et al. Pain and disability associated with new vertebral fractures and other spinal conditions. J Clin Epidemiol 1994; 47(3):231–239. 11. Lindsay R, Silverman SL, Cooper C, et al. Risk of new vertebral fracture in the year following a fracture. JAMA 2001; 285(3):320–323. 12. White AA 3rd, Panjabi MM, Thomas CL. The clinical biomechanics of kyphotic deformities. Clin Orthop 1977 128:8–17. 13. Keller TS, Harrison DE, Colloca CJ, et al. Prediction of osteoporotic spinal deformity. Spine 2003; 28(5):455–462. 14. Cortet B, Cotten A, Boutry N, et al. Percutaneous vertebroplasty in the treatment of osteoporotic vertebral compression fractures: an open prospective study. J Rheumatol 1999; 26(10):2222–2228. 15. Cortet B, Cotten A, Boutry N, et al. Percutaneous vertebroplasty in patients with osteolytic metastases or multiple myeloma. Rev Rhum Engl Ed 1997; 64(3):177–183. 16. Cyteval C, Sarrabere MP, Roux JO, et al. Acute osteoporotic vertebral collapse: open study on percutaneous injection of acrylic surgical cement in 20 patients. AJR Am J Roentgenol 1999; 173(6):1685–1690. 17. Deramond H, Depriester C, Galibert P, et al. Percutaneous vertebroplasty with polymethylmethacrylate. Technique, indications, and results. Radiol Clin North Am 1998; 36(3):533–546. 18. Evans AJ, Jensen ME, Kip KE, et al. Vertebral compression fractures: pain reduction and improvement in functional mobility after percutaneous polymethylmethacrylate vertebroplasty: retrospective report of 245 cases. Radiology 2003; 226(2):366–372. 19. Gangi A, Kastler BA, Dietemann JL. Percutaneous vertebroplasty guided by a combination of CT and fluoroscopy. AJNR Am J Neuroradiol 1994; 15(1):83–86. 20. Grados F, Depriester C, Cayrolle G, et al. Long-term observations of vertebral osteoporotic fractures treated by percutaneous vertebroplasty. Rheumatology 2000; 39(12):1410–1414. 21. Hodler J, Peck D, Gilula LA. Midterm outcome after vertebroplasty: predictive value of technical and patient-related factors. Radiology 2003; 227(3):662–668. 22. Jensen ME, Evans AJ, Mathis JM, et al. Percutaneous polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral body compression fractures: technical aspects. AJNR Am J Neuroradiol 1997; 18(10):1897–1904. 23. Rhyne A 3rd, Banit D, Laxer E, et al. Kyphoplasty: report of eighty-two thoracolumbar osteoporotic vertebral fractures. J Orthop Trauma 2004; 18(5):294–299. 24. Wong WH, Reiley MA, Garfin SR. Vertebroplasty/kyphoplasty. J Women’s Imaging 2000; 2(3):117–124. 25. Theodorou DJ, Theodorou SJ, Duncan TD, et al. Percutaneous balloon kyphoplasty for the correction of spinal deformity in painful vertebral body compression fractures. Clin Imaging 2002; 26(1):1–5. 26. Phillips FM, Ho E, Campbell-Hupp M, et al. Early radiographic and clinical results of balloon kyphoplasty for the treatment of osteoporotic vertebral compression fractures. Spine 2003; 28(19):2260–2265. 27. Lieberman IH, Dudeney S, Reinhardt MK, et al. Initial outcome and efficacy of ‘kyphoplasty’ in the treatment of painful osteoporotic vertebral compression fractures. Spine 2001; 26(14):1631–1638. 28. Ledlie JT, Renfro M. Balloon kyphoplasty: one-year outcomes in vertebral body height restoration, chronic pain, and activity levels. J Neurosurg 2003; 98(1 Suppl):36–42. 29. Dudeney S, Lieberman IH, Reinhardt MK, et al. Kyphoplasty in the treatment of osteolytic vertebral compression fractures as a result of multiple myeloma. J Clin Oncol 2002; 20(9):2382–2387. 30. Garfin SR, Yuan HA, Reiley MA. New technologies in spine: kyphoplasty and vertebroplasty for the treatment of painful osteoporotic compression fractures. Spine 2001; 26(14):1511–1515.

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Part 2: Interventional Spine Techniques 31. Lane JM, Johnson CE, Khan SN, et al. Minimally invasive options for the treatment of osteoporotic vertebral compression fractures. Orthop Clin North Am 2002; 33(2):431–438, viii. 32. Phillips FM, Wetzel FT, Lieberman I, et al. An in vivo comparison of the potential for extravertebral cement leak after vertebroplasty and kyphoplasty. Spine 2002; 27(19):2173–2178; discussion 2178–2179. 33. Jang JS, Lee SH, Rhee CH. Polymethylmethacrylate-augmented screw fixation for stabilization in metastatic spinal tumors. Technical note. J Neurosurg 2002; 96(1 Suppl):131–134. 34. Bauer TW, Schils J. The pathology of total joint arthroplasty. I. Mechanisms of implant fixation. Skeletal Radiol 1999; 28(8):423–332.

40. Rudigier JF, Ritter G. Pathogenesis of circulatory reactions triggered by nervous reflexes during the implantation of bone cements. Res Exp Med (Berl) 1983; 183(2):77–94. 41. Markel DC, Femino JE, Farkas P, et al. Analysis of lower extremity embolic material after total knee arthroplasty in a canine model. J Arthroplasty 1999; 14(2):227–232. 42. Orsini EC, Byrick RJ, Mullen JB, et al. Cardiopulmonary function and pulmonary microemboli during arthroplasty using cemented or non-cemented components. The role of intramedullary pressure. J Bone Joint Surg Am 1987; 69(6):822–832.

35. Shih TT, Huang KM, Li YW. Solitary vertebral collapse: distinction between benign and malignant causes using MR patterns. J Magn Reson Imaging 1999; 9(5):635–642.

43. Coumans JV, Reinhardt MK, Lieberman IH. Kyphoplasty for vertebral compression fractures: 1-year clinical outcomes from a prospective study. J Neurosurg 2003; 99(1 Suppl):44–50.

36. Do HM. Magnetic resonance imaging in the evaluation of patients for percutaneous vertebroplasty. Top Magn Reson Imaging 2000; 11(4):235–244.

44. Leech JA, Dulberg C, Kellie S, et al. Relationship of lung function to severity of osteoporosis in women. Am Rev Respir Dis 1990; 141(1):68–71.

37. Mathis JM, Barr JD, Belkoff SM, et al. Percutaneous vertebroplasty: a developing standard of care for vertebral compression fractures. AJNR Am J Neuroradiol 2001; 22(2):373–381.

45. Kado DM, Browner WS, Palermo L, et al. Vertebral fractures and mortality in older women: a prospective study. Arch Intern Med 1999; 159(11):1215–1220.

38. Phillips FM, Pfeifer BA, Lieberman IH, et al. Minimally invasive treatments of osteoporotic vertebral compression fractures: vertebroplasty and kyphoplasty. Instr Course Lect 2003; 52:559–567.

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39. Pinto PW. Cardiovascular collapse associated with the use of methylmethacrylate. AANA J 1993; 61(6):613–616.

46. Cooper C, Atkinson EJ, Jacobsen SJ, et al. Population-based study of survival after osteoporotic fractures. Am J Epidemiol 1993; 137(9):1001–1005. 47. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful vertebral body fractures in cancer patients. J Neurosurg 2003; 98(1 Suppl):21–30.

PART 3

SPECIFIC DISORDERS

Section 1

Medical Spinal Disorders

CHAPTER

Medical Radiculopathies

34

Andrew J. Haig

Sciatica – This is often associated with rheumatism and gout, but is also frequently brought on by catching cold. Occasionally it is due to accumulations in the bowels, or to diseases of the bones through which the nerve makes its exit. The painful points are usually found back of the trochanter or most projecting point of the thigh bone, at certain spots in the thigh about the knee and ankle joints. Medicology, a medical text published in 1905.1 How dumb could those old guys have been? Sciatica is caused by the spine. Disc herniation, spinal stenosis, fracture, tumor … Didn’t they ever examine the patient? This chapter will show that they were not so dumb. Despite our obsession with spinal imaging and spinal injections, all that radiates does not come from the spine. All that denervates does not come from the spine, either. The author will follow through on the history of sciatica, look at the differential diagnosis, and then take a look at the clues on history and physical examination that can give us a hint. Finally, the author will evaluate diagnostic tests that might help detect causes of sciatica and denervation.

HISTORY AND EPIDEMIOLOGY Sciatica is a constant. It has been present throughout the ages. With humility, it should be noted that it is not sciatica, but the medical theories and treatment that have changed over the years … and not always to the benefit of the patient. Theories of etiology are varied across cultures and time. The equivalent of Medline in the late 1800s was an annual compilation of published research presented by the United States Surgeon General. A search on the term sciatica results in numerous ‘hits’ – articles discussing the presentation and treatment of sciatica as a self-limiting cold ‘settling’ in the back, or flu ‘residing’ in the sciatic nerve. The 1905 general medical text Medicology doesn’t even mention trauma as an etiology.1 Around the turn of the last century the field of physical medicine and rehabilitation was born. A fringe group who espoused electrical treatments of medical problems ranging from cancer to the common cold held their first annual meeting in 1890.2 Though scorned by the medical establishment, this specialty gained popularity with the people, in part due to its apparent success in treating sciatica and back problems. As medicine advanced, management of back pain became more focused on basic scientific theory than pragmatic outcomes. New theoretical ‘causes’ for back pain and sciatica resulted in alarmingly unchallenged treatments. For example, long before the disc was implicated in sciatica, it was popular to blame sciatica on entrapment of the nerve in the piriformis muscle or on irritation from the sacroiliac joint. In 1928, Yeomans claimed success with surgical treatment of hundreds of people with sciatica and nerve damage that he

related to the sacroiliac joint.3 Almost certainly, a number of these people – at least the ones with neurologic deficits – had lumbar disc herniation, a syndrome that would not be discovered for more than a decade. His patients typically recovered and were ‘cured’ in spite of his well-meaning, but wrong, interventions. Mixter and Barr are rightly credited with proving that sciatica comes from disc herniations.4 But there is history behind this history. In the authors’ first years of practice at the University of Vermont, his senior partner Phillip Davis would often tell the story of Mixter and Barr’s first patient. This Vermonter had excruciating pain down the leg. His small-town doctor told him that it was likely ‘one of those cartilage tumors in the spine’ but that he would get better if he only waited. The disgusted patient ignored his doctor and went for a second opinion at the prestigious Harvard Medical School, where Mixter and Barr performed the first of millions of possibly unnecessary operations, paving their way to fame. More recent literature on the natural history of sciatica show us that, even today, physicians with high-sounding theoretical constructs and a big podium often win out over common sense and clinical insight. The NHANES survey of American health indicates that about 13% of noninstitutionalized adults have back pain of more than 2 weeks duration, and about 9% of these have sciatica with back pain.5 A lifetime prevalence of 1.5% can be calculated from these studies. But other studies show that up to 40% of people suffer from sciatica in their lifetime.6,7 Regardless of the numbers, from a physician standpoint, sciatica is a very common patient complaint. The author will present numerous nonspinal causes for sciatica. Since back pain is so common, there is a good chance they could coincide with sciatica. Since one-third or more of the population has abnormalities on an MRI, there is even a good chance that back pain, disc changes, and an unrelated cause of sciatica coincide. The risk of error is even greater when one realizes that MRI also misses some spinal causes of sciatica.

DIFFERENTIAL DIAGNOSIS Jeffrey Saal coined the term ‘pseudo-radicular syndrome’ for the nonspinal disorders that cause sciatica-like pain.8 The causes of pseudoradicular syndrome can be divided into musculoskeletal causes, focal neuropathies, and neuromuscular diseases. Among the musculoskeletal causes (Table 34.1), Galm et al.9 have shown that sacroiliac pain occurs in about one-third of persons with disc herniations, and that treatment of the sacroiliac joint in these people results in relief of pain. Trochanteric bursitis is another cause of similar pain that often occurs after onset of sciatica from disc herniation.10 Swezy11 found trochanteric bursitis in 31 of 70 persons referred for evaluation of sciatica or back pain. Most think of hip arthritis in the differential diagnosis of radiculopathy in older persons. In younger persons, avascular necrosis of the femoral head, 385

Part 3: Specific Disorders

Table 34.1: The Differential Diagnosis of Radiculopathy INTRINSIC SPINAL CAUSES

FOCAL NEUROMUSCULAR CAUSES—Cont’d

Cord compression at or above the suspected area Disc herniation Spinal stenosis Spondylolisthesis Segmental hypermobility Ganglion cyst Tumor Fracture Failed spine surgery syndrome Arachnoiditis Facet joint Bent spine syndrome Posterior primary ramus syndrome

Vibration hand (‘white finger’) syndrome Lumbar plexus Tumor Aneurysm Pelvic organ enlargement Sciatic nerve lesions Piriformis syndrome Blunt, sharp, or chronic trauma Baker’s cyst Peroneal nerve lesion at the fibular head Tarsal tunnel syndrome Anterior tarsal tunnel syndrome Femoral neuropathy Lateral femoral cutaneous (meralgia paresthetica) Obturator, gluteal, cluneal, and other odd neuropathies

MUSCULOSKELETAL CAUSES Neck Myofascial pain Glenohumeral joint pain Acromioclavicular joint pain Lateral epicondylitis Low back Sacroiliac joint pain Trochanteric bursitis Anserine bursitis Hip arthritis Avascular necrosis of the femoral head Diffuse arthritis Shin splints Hamstring strain FOCAL NEUROMUSCULAR CAUSES Brachial plexus Tumor Stretch Thoracic outlet syndrome Upper limb focal neuropathies Carpal tunnel syndrome Ulnar neuropathy Multiple radial nerve locations

slipped capital femoral epiphysis, and other unusual hip arthritides can fool the unwary. Paraspinal muscle inadequacy-related to previous surgery,12 deconditioning, stretch of the dorsal root,13 or focal myopathy14,15 is increasingly being reported as a cause of pain. Focal neuromuscular disorders are not uncommon. Most worrisome are tumors and infections causing compression of the nerves or plexus. Bicknell and Johnson16 pointed out a number of characteristics of neoplastic plexopathies. They are characteristically painful; in the brachial plexus, more than 70% involve the lower trunk and are mainly due to axillary lymph node infiltration. In contrast, lumbosacral plexus neoplasms cause neuropathy by direct infiltration. They also favor the lower plexus, with 31% lumbar and 51% sacral plexus. With a history of cancer treatment the differential diagnosis is often radiation plexopathy versus tumor.17,18 Painless and progressive weakness is the hallmark of radiation plexopathies, which typically occur in the upper trunk of the brachial plexus and in the lower part of the lumbosacral plexus. In the lumbar area, radiation plexopathy is usually bilateral but asymmetrical.16 The presence of lymphedema suggests that there has been radiation damage, but does not rule out tumor. The classic electrodiagnostic finding of myokymia is related to radiation, but again does not rule out tumor. 386

NEUROMUSCULAR DISEASES Diffuse polyneuropathy Mononeuritis multiplex Inflammatory radiculopathy/plexopathy Myopathy Myoneural junction disorder SYSTEMIC CAUSES Cardiac ischemia Aortic aneurysm Pulmonary embolism and other lung diseases Gastrointestinal disorders Genitourinary disorders Metabolic disorders (e.g. sickle cell, porphyria) Fibromyalgia Polyarthritis PSYCHIATRIC DISORDERS Anxiety/hyperventilation Hysteria Malingering Munchausen syndrome

Infectious causes are typically obvious because of their systemic presentation. But they can be missed. Tuberculosis deserves special attention because of the rise in immune disorders such as AIDS and the increasing resistance to antibiotics. The slow-growing nature of tuberculosis may result in a missed diagnosis.19 Focal neuropathies masquerading as radiculopathy are not uncommon. Some, such as carpal tunnel syndrome, meralgia paresthetica, or peroneal nerve lesion at the fibular head, are relatively straightforward to diagnose once the clinician is aware of the possibility. The association of these lesions with neck and back pain is termed the ‘double crush syndrome.’ It is debated whether the presence of two compressions (e.g. neck and ulnar nerve) is coincidental or whether one lesion predisposes to the other.20 Other focal neuropathies such as thoracic outlet syndrome or piriformis syndrome are quite controversial. For both of these disorders part of the controversy has to do with language. For example, some will call a tender tight piriformis muscle ‘piriformis syndrome’ while others reserve this term for nerve irritation caused by the muscle. Thoracic outlet syndrome should properly be divided into ‘true neurogenic thoracic outlet syndrome’ in which there is objective electrodiagnostic evidence of nerve involvement, vascular thoracic outlet syndrome in which a vein or artery is clearly causing dysvascular pain,

Section 1: Medical Spinal Disorders

and ‘disputed thoracic outlet syndrome’ in which there is a subjective sense that the thoracic outlet is involved. Even when language is clear, the diagnosis of these disorders is not simple. Despite its long history in the literature, as late as 1989 there had not been a single unequivocal, electrodiagnostically proven case of piriformis syndrome.21 Subsequent cases have shown that the syndrome exists.22 Fishman believes that it is very common, based on a somewhat circuitous but reasonable argument that electrodiagnostic F-waves disappear in certain positions in people with certain complaints.23 Thoracic outlet syndrome clearly exists, based on a number of electrodiagnostic, vascular, and surgical observations. Nerves, arteries, or veins can be entrapped by a number of structures in the neck and shoulder, ranging from the classic cervical rib to the scaleneus muscles to anomalous fibrous bands. But some think it is exceedingly rare, while others think it is common. The controversy is further befogged by the fact that a key article published by Urschel,24 one of the great proponents of thoracic outlet surgery, has been found to include misrepresentations.25 Many of the focal neuropathies that can mimic radiculopathy are uncommon. They are typically found when an alert clinician detects a classic presentation or when the MRI is negative despite neurogenic complaints. Neuromuscular diseases are frequently confusing to spine clinicians. In the author’s prospective masked study of 150 older persons with low back pain, spinal stenosis, or no spinal symptoms prescreening was conducted for polyneuropathy, alcohol, and diabetes. Despite this, eight subjects thought by a clinician to have spinal stenosis were found on electrodiagnostic testing to have a neuromuscular disease.26 These included undetected diabetic neuropathy, but also a statin myopathy and Charcot-Marie-Tooth disease. Similar to spinal disorders, neuromuscular diseases can cause weakness, sensory loss, and pain. They may actually predispose to back pain due to their effect on spinal stability and limb biomechanics.27 Even when there is a spinal disorder, the prognosis from invasive treatment is poorer in these people.28 It is beyond the scope of this chapter to review all neuromuscular diseases. Some observations are useful, however. Diabetes and alcohol are the two most common causes of polyneuropathy in developed countries. Diabetes can present with neuropathy before the disease itself is detected. Alcohol use is notoriously underreported, especially among women with back pain.29 Congenital neuropathies and myopathies are often unrecognized by the back pain patient, as they develop slowly, and family members often have the same impairments. Inflammatory and congenital myopathies often present with back and hip pain.30 One interesting myopathy requires special attention by spine clinicians. The ‘bent spine syndrome,’ also called camphylocormia or, in the cervical region, ‘dropped head syndrome’ is a focal myopathy of the paraspinal muscles.14,15 The typical presentation sounds strangely like spinal stenosis, as the patient can ambulate for a short time, but the back begins to ache and tire. After a rest the patient can continue ambulation. Attentive inspection of the MRI will show fatty replacement (as opposed to atrophy) of the paraspinal muscles. Electromyogram of the paraspinal muscles will confirm the diagnosis. It has been shown by the author that the disability caused by bent spine syndrome actually relates to the presence of a hip flexion contracture. Correction of hip flexion contracture in one patient allowed him to assume a more typical myopathic extended spine posture, and increased his ambulation ability tenfold.31 Systemic disorders commonly present to the primary care physician as back pain. The spine physician does not see these very often, probably because of good screening on the part of the primary care

physician. While any of the disorders listed in Table 34.1 could be detected by the specialist, most interesting are a number of disorders that can cause both pain and psychiatric disease. Chronic pain with psychiatric presentation is so common in the spine clinician’s practice that a medical tie between the two is often not considered. The prototype disease is acute intermittent porphyria. But thyroid disease, chemical toxicities, sickle cell disease, metabolic derangements, and numerous other disorders can cause both psychiatric and peripheral nerve complaints. Of course, purely psychiatric complaints such as hysteria or malingering do occur, as well. Although high lumbar disc herniations – L2, 3, or 4 nerve root irritation – are really spinal disorders, they deserve special attention. They are often missed because the physician is looking solely for sciatica as the complaint from disc herniations. These lesions comprise only about 5% of disc herniations. They seldom present with pain below the knee, but instead typically cause anterior thigh pain. Albert et al.32 collected 141 surgically proven high lumbar disc herniations. They found that the examination for weakness is often negative, although the iliopsoas can be of some help. The only accessible high lumbar reflex, the patellar reflex, remains intact in about 50% of surgically proven lesions. The straight leg raise test is negative, and the ‘reverse straight leg raise’ test thought to be specific for high lesions is also negative in about half of cases. More concerning, MRI misses about half of these lesions, which are more often hidden in the lateral recess. Fortunately, electromyography including a systematic paraspinal examination appears to miss very few upper lumbar lesions.33

PHYSICAL EXAMINATION Many, but not all, useful physical examination tests for back pain have been subjected to validation trials.34–36 Most components of the ‘manual physical examination’ used to evaluate segmental changes in the spine have not shown good reliability, despite the fact that the manual therapy which is based on such evaluations probably is effective.37 While this is specifically true, in general it is not difficult to find a musculoskeletal diagnosis. Finding peripheral musculoskeletal causes is a matter of thinking and taking the time to examine the patient. One simply asks the patient where he or she is tender, and confirms this location by palpation. The problem comes in patients who have been told that their problem is spinal. They attribute bone, joint, or ligament findings to the spine. Some hints include lateral hip pain or pain on lying on the side (trochanteric bursitis), groin pain, especially getting in and out of a car (hip arthritis), and complaints of pain emanating from the sacral sulcus when combined with five or more sacroiliac joint provocation maneuvers38 and point towards the sacroiliac joint as a cause of pain.39 Focal neuropathies are somewhat more difficult to differentiate from radiculopathies on physical examination, especially when they are not severe. Classically, hand pain that does not go above the wrist is more likely a focal median or ulnar neuropathy. If the problem is neurologically severe enough, the physical examination should be normal in muscles that share the same nerve root, but not the same nerve. A comprehensive strength examination should find these contradictions. Table 34.2 lists selected muscles that share the same root, but not the same nerve. Perhaps the most important pair is the extensor hallucis longis and the tensor fascia lata. L5 is the most common lumbar radiculopathy. Toe weakness in the presence of back pain suggests an L5 radiculopathy. Since polyneuropathy, peroneal neuropathy, bunions, and discoordination can affect extension of the great toe, it is important to always test the tensor fascia lata to see if the lesion is proximal and in another nerve. This is done by having the patient sit with knees 387

Part 3: Specific Disorders

Table 34.2: Selected Muscles that Share the Same Root but Different Nerves Root

Muscle 1

Confirmation Muscle

C5

Biceps, musculocutaneous N

Rhomboids, nerve to rhomboids

C6

Biceps, musculocutaneous N

Supraspinatus, suprascapular N

C7

Triceps, radial N

Flexor carpi radialis, median N

C8

Extensor indicis, radial N

Flexor pollicis longus, anterior interosseous N

T1

Abductor digiti quinti, ulnar N

Abductor pollicis brevis, median N

L2–4

Quadriceps, femoral N

Adductors, obturator N

L5

Extensor hallucis longis, peroneal N

Tensor fascia lata, superior gluteal N

S1

Gastrocnemus, tibial N

Gluteus maximus, inferior gluteal N

N, nerve.

together and ankles apart. Resisted pressure laterally and simultaneously on the ankles is a remarkably sensitive finding. While it is true that a recovering radiculopathy may have good hip muscle strength, but still have distal weakness, this pattern of weakness should raise suspicion. The physical examination for neuromuscular diseases may be clear or may still result in confusion. Numbness in a stocking distribution or symmetrical weakness may be helpful. In congenital neuropathies the classic high arches, and in myopathies the proximal weakness and myalgia, may be appreciated. More useful is a high index of suspicion based on history. In persons with diabetes, alcoholism, or other disorders known to cause polyneuropathy, there should be a presumption that any neurologic deficit is not caused by the spine until proven otherwise.

DIAGNOSTIC TESTING The single most important test in differentiating nonspinal causes of radiculopathy is electrodiagnostic consultation (EDX). It is the only test that can diagnose polyneuropathy, myopathy, or neuromuscular junction disorders. EDX is also sensitive to spinal causes of radicular pain, and in fact may be more sensitive and specific than MRI to the clinical syndrome of spinal stenosis.40,41 In contrast to imaging studies, there is little overlap between the asymptomatic and symptomatic populations. EDX costs less than MRI and patients tolerate it as well as or better than MRI, with essentially no long-term side effects. EDX findings that suggest a nonspinal cause for radicular pain include needle examination showing findings in a nonroot distribution and nerve conduction studies showing slowing, either diffusely or across an area of possible nerve damage. Axonal neuropathies have distal, rather than radicular findings. Mononeuritis multiplex will show lesions outside of the area in question. Nonanatomic radiculopathies will often show diffuse, rather than focal paraspinal abnormalities. Where there is a question of polyneuropathy, study of an uninvolved limb and of the thoracic paraspinal muscles should be considered. There are some cautions about EDX. Since S1 probably does not innervate the paraspinal muscles it is impossible to differentiate an S1 radiculopathy from a mild sacral plexopathy. A more severe peripheral nerve lesion anywhere would result in decreased sensory nerve amplitude. Classically, radiculopathies are proximal to the dorsal root ganglion, but contrary to common thought, about 10% of S1 radiculopathies due to spinal disorders may be distal to the S1 ganglion. The EDX consultant must build an index of suspicion about possible peripheral nerve causes of radiculopathy. A good screen includes 388

5 lower limb muscles plus quantified paraspinal needle exam for the low back, or 7 upper limb muscles for the neck.42,43 Work the author has recently concluded shows the great importance of a quantified paraspinal examination, which is the single most sensitive and specific electrodiagnostic test for spinal stenosis and probably other spinal disorders.21,26 It also includes a sensory and a motor study, or alternatively an H-wave. With any index of suspicion, a test of the upper limbs (for a lumbar complaint) or lower limbs (for a cervical complaint), or the thoracic paraspinals (for a difficult radicular complaint) is useful. Imaging of the apparently affected part may be useful. Anesthetic injections into the affected part may also confirm a diagnosis. Blood tests such as a blood count and sedimentation rate are useful, but often need to be followed by a more detailed rheumatologic or metastatic work-up.

SUMMARY All that radiates is not sciatica, and all that is neurogenic is not discogenic. Given the high prevalence of back pain along with the high prevalence of disorders that can mimic sciatica, the spine clinician must remain constantly aware of the possibility of a cause outside of the spine. The key is to have a high index of suspicion. An abnormal MRI is not proof that the complaint emanates from the spine. Some warning signs include: ● ● ● ● ● ● ● ●

History suggesting a comorbid disorder that can cause neuropathy; Distal bilateral pain; High arches; Pain that does not go above the wrist or ankle; Diffuse hyporeflexia; Tenderness away from the spine; Groin pain; Pain that does not go away with spinal treatments. Sciatica – apply belladonna ointment to seat of pain. Poultices applied very hot. Sulpher applied to painful part is very effective, after which the limb or part should be enveloped in flannel. … also amenable to treatment with electricity … have fifty of these pills made: Sulphate iodine … phosphate iron … Strychnine. … Take one after each meal. … The use of these tonics will tend towards a cure, but the disease is very obstinate, and strict observances of hygiene precautions is imperative.1 Medicology

Section 1: Medical Spinal Disorders

References 1. Wood JP. Medicology (or) home encyclopedia of health. A complete family guide. New York: University Medical Society; 1905. 2. Gritzer G, Arluke A. The making of rehabilitation. A political economy of medical specialization, 1890–1980. Berkeley, CA: University of California Press; 1985. 3. Yeoman W. The relation of arthritis of the sacro-iliac joint to sciatica. Lancet 1928; 2:1119–1122. 4. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934; 211:210. 5. Deyo RA, Tsui-Wu YJ. Descriptive epidemiology of low back pain and its related medical care in the United States. Spine 1987; 12:264. 6. Svensson HO, Anderson GBJ. Low back pain in 40–47 year old men: I. Frequency of occurrence and impact on medical services. Scand J Rehabili Med 1982; 14:47. 7. Frymoyer JW, Pope MH, Clements JH, et al. Risk factors in low-back pain. An epidemiological survey. Bone Joint Surg (Am) 1983; 65(2):213–218. 8. Saal JA, Dillingham MF, Gamburd RS, et al. The pseudo-radicular syndrome: lower extremity peripheral nerve entrapment masquerading as lumbar radiculopathy. Spine 1988; 13:926–930. 9. Galm R, Frohling M, Rittmeister M, et al. Sacroiliac joint dysfunction in patients with imaging-proven lumbar disc herniation. Eur Spine J 1998; 7(6):450–453. 10. Tortolani PJ, Carbone JJ, Quartararo LG. Greater trochanteric pain syndrome in patients referred to orthopedic spine specialists. Spine J 2002; 2(4):251–254. 11. Swezey RL. Pseudo-radiculopathy in subacute trochanteric bursitis of the subgluteus maximus bursa. Arch Phys Med Rehabil 1976; 57(8):387–390.

23. Fishman LM, Anderson C, Rosner B. BOTOX and physical therapy in the treatment of piriformis syndrome. Am J Physical Med Rehabil 2002; 81(12):936–942. 24. Urschel HC Jr. Management of the thoracic-outlet syndrome. N Engl J Med 1972; 286(21):1140–1143. 25. Wilbourn AJ, Lederman RJ. Evidence for conduction delay in thoracic-outlet syndrome is challenged. N Engl J Med 1984; 310(16):1052–1053. 26. Haig AJ, Tong HC, Yamakawa KSJ, et al. Spinal Stenosis, back pain, or no symptoms at all? A masked study comparing radiologic and electrodiagnostic diagnoses to the clinical impression. Arch Phys Med Rehabil 2006; 87(6):897–903. 27. Ingram CM, Harris MB, Dehne R. Charcot spinal arthropathy in congenital insensitivity to pain. Orthopedics 1996; 19(3):251–255. 28. Cinotti G, Postacchini F, Weinstein JN. Lumbar spinal stenosis and diabetes. Outcome of surgical decompression. J Bone Joint Surg (Br) 1994; 76(2):215–219. 29. Booker EA, Haig AJ, Geisser ME, et al. The relationship between alcohol use and performance in persons with chronic back pain disability. Am J Phys Med Rehabil 2001; 80:8. 30. Haig AJ. The complex interaction of myotonia and low back pain. Spine 1991; 16:580–581. 31. Haig AJ, Tong HC, Kendall R. The bent spine syndrome: myopathy + biomechanics = symptoms. In review, Spine J, October, 2004. 32. Albert TJ, Balderston RA, Heller JG, et al. Upper lumbar disk herniations. J Spinal Disord 6(4)351–359. 1993; 33. Haig AJ, Yamakawa K, Hudson DM. Paraspinal electromyography in high lumbar and thoracic lesions. Am J Phys Med Rehabil 2000; 79(4):336–342.

12. Sihvonen T, Herno A, Paljarvi L, et al. Local denervation atrophy of paraspinal muscle in postoperative failed back syndrome. Spine 1993; 18(5):575–581.

34. van den Hoogen HM, Koes BW, van Eijk JT, et al. On the accuracy of history, physical examination, and erythrocyte sedimentation rate in diagnosing low back pain in general practice. A criteria-based review of the literature. Spine 1995; 20(3): 318–327.

13. Fisher MA, Kacr D, Houchin J. Electrodiagnostic examination, back pain, and entrapment of posterior rami. Electromyogr Clin Neurophysiol 1985; 25:187.

35. Andersson GBJ, Deyo RA. History and physical examination in patients with herniated lumbar discs. Spine 1996; 21(24S):105–185.

14. Ricq G, Laroche M. Acquired lumbar kyphosis caused in adults by primary paraspinal myopathy. Epidemiology, computed tomography findings, and outcomes in a cohort of 23 patients. Joint, Bone, Spine: Revue du Rhumatisme 2000; 67(6): 528–532.

36. Deyo RA, Rainville J, Kent DL. The rational clinical examination: What can the history and physical examination tell us about low back pain? JAMA 1992; 268: 760–765.

15. Laroche M, Ricq G, Delisle MB, et al. Bent spine syndrome: computed tomographic study and isokinetic evaluation. Muscle Nerve 2002; 25(2):189–193. 16. Bicknell JM, Johnson SF. Widespread electromyographic abnormalities in spinal muscles in cancer, disc disease, and diabetes. Univ Mich Med Center J 1976; 42:124–127. 17. Kori SH, Foley KM, Posner JB. Brachial plexus lesions in patients with cancer: 100 cases. Neurology 1981; 31:45–50. 18. Jaeckle KA, Young DF, Foley KM. The natural history of lumbosacral plexopathy in cancer. Neurology 1985; 35:8–15. 19. Myllyla VV, Sutinen S, Kotaniemi A. Radicular symptoms in tuberculosis. A case report. European Neurology 1976; 14(2):90–96. 20. Bednarik J, Kadanka Z, Vohanka S. Median nerve mononeuropathy in spondylotic cervical myelopathy: double crush syndrome? J Neurology 1999; 246(7):544–551. 21. Haig AJ, Wallbom A. Low back pain and electromyography. New England J Med 2001; 344(12):1644. 22. Papadopoulos EC, Khan SN. Piriformis syndrome and low back pain: a new classification and review of the literature. Orthoped Clin N Am 2004; 35(1):65–71.

37. Najm WI, Seffinger MA, Mishra SI, et al. Content validity of manual spinal palpatory exams – A systematic review. Complement Alternat Med 2003; 3(1):1. 38. Fortin JD, Falco FJ. The Fortin finger test: an indicator of sacroiliac pain. Am J Orthoped (Chatham, NJ) 1997; 26(7):477–480. 39. Slipman CW, Sterenfeld EB, Chou LH, et al. The predictive value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehabil 1998; 79(3):288–292. 40. Haig AJ, Tong HC, Yamakawa KSJ, et al. The sensitivity and specificity of electrodiagnostic testing for the clinical syndrome of lumbar spinal stenosis. Spine 2005; 30(23):2667–2676. 41. Haig AJ, Geisser ME, Tong HC, et al. Electromyographic and magnetic resonance imaging measurements in older persons with lumbar spinal stenosis, low back pain, and no back complaints. (In revision, JBJS August 2005.) 42. Dillingham TR, Lauder TD, Andary M, et al. Identifying lumbosacral radiculopathies: an optimal electromyographic screen. Am J Phys Med Rehabil 2000; 79(6):496–503. 43. Dillingham TR, Lauder TD, Andary M, et al. Identification of cervical radiculopathies: optimizing the electromyographic screen. Am J Phys Med Rehabil 2001; 80(2):84–91.

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PART 3

SPECIFIC DISORDERS

Section 1

Medical Spinal Disorders

CHAPTER

Spondyloarthropathies

35

Joanne Borg-Stein and Bonnie Bermas

INTRODUCTION

GENERAL CLINICAL FEATURES

Spondyloarthropathy (SpA) refers to the clinical family of disorders that are characterized as inflammatory rheumatic disorders with manifestations in the vertebral column, peripheral joints, and extraarticular structures. These disorders frequently manifest initially with back complaints. For example, back complaints are the first symptoms in 75% of patients with ankylosing spondylitis and may be present in 89% of patients with undifferentiated spondyloarthropathy.1,2 Given the high prevalence of axial spine complaints in this population, it is of critical importance to the spine clinician to be aware of these diagnoses. The spine specialist must be familiar with characteristic aspects of the patient history, physical examination, laboratory data, and diagnostic imaging. It is the purpose of this chapter to provide a comprehensive overview of the different categories of spondyloarthropathy, including pathology, diagnostic criteria, imaging, extra-articular manifestations, and treatment.

In general, spondyloarthropathies demonstrate the following clinical features:

DEFINITION AND CLASSIFICATION The spondyloarthropathies are a cluster of overlapping and interrelated chronic inflammatory rheumatic disorders which include ankylosing spondylitis (often considered the prototype), reactive arthritis, arthritis associated with psoriasis, arthritis associated with Crohn’s disease and ulcerative colitis, Reiter’s syndrome, and undifferentiated spondyloarthropathy.3 These disorders are often referred to as the seronegative spondyloarthropathies, which are considered together since they share clinical, epidemiologic, and imaging features. The spondyloarthropathies usually have a negative rheumatoid factor (seronegativity), association with HLA-B27, familial clustering, predominant axial and peripheral joint involvement, and extra-articular manifestations.4

EPIDEMIOLOGY AND GENETICS Spondyloarthropathies are a group of diseases heavily influenced by genetic factors, particularly HLA. There is a clinical spectrum of these disorders. Undifferentiated spondyloarthropathy is the most common disorder; with ankylosing spondylitis (AS) being second most common. The estimated incidence is likely more common than previously realized as newer classification systems have been developed. Prevalence of SpA is correlated with the presence of HLA-B27 in a particular population.5,6 Both men and women are affected. In ankylosing spondylitis, males are disproportionally affected in a 3:1 ratio.7 Psoriatic arthritis affects men and women equally.8 Postvenereal Reiter’s syndrome is more common in men, whereas postdysenteric Reiter’s syndrome equally affects men and women.9,10

● ● ● ● ● ●

A tendency to affect spinal joints, causing sacroiliitis and spondylitis; Peripheral arthritis, typically oligoarticular and asymmetric; Inflammation of bony insertions for tendons and ligaments (enthesitis or enthesopathy); Usually a young age at onset; Negative tests for rheumatoid factors; and Familial predisposition and a strong association with a genetic polymorphism of the major histocompatibility complex (MHC), HLA-B27.7,11,12

PATHOLOGY Enthesopathy The ‘enthesis’ is the region of insertion of a tendon, ligament, capsule, or fascia into bone. The enthesis is now understood to be a complex structure that extends into the bone and marrow cavity.13 Recent work suggests that the entheseal fibrocartilage is the major target of the immune response and the primary site of the immunopathology.14 The bone marrow demonstrates edema and contains cellular infiltrates. T lymphocytes are abundant in these areas with a preponderance of CD8+ cells.15 Pathologic studies have demonstrated inflammatory infiltration and destruction which affect the whole anulus fibrosus, not just the enthesis of the intervertebral disc.16

Synovitis Patients with spondyloarthropathy may have peripheral arthritis, typically mono- or oligoarticular, and often affecting one or both knees. Microscopic analysis reveals fibrin, synovial cell proliferation, lymphocytes, and plasma cells in the synovium.17 A more recent hypothesis suggests that bacterial antigens and microorganisms in a susceptible HLA-B27-postitive patient may interact to produce inflammation and arthritis in ankylosing spondylitis.18 It is well established in reactive arthritis that synovial fluid demonstrates bacteria-specific T-cell responses to the bacterium that causes the arthritis.19,20

Sacroiliitis Studies of the sacroiliac joint reveal evidence of synovitis, osteitis, and enthesitis. Biopsy and autopsy specimens demonstrate pannus formation, myxoid marrow, superficial cartilage destruction, intra-articular fibrous strands, new bone formation, and bony ankylosis. Biopsy 391

Part 3: Specific Disorders

samples demonstrate cellular infiltrates of T lymphocytes, with both CD4+ and CD8+ cells.21,22 Contrast-enhanced magnetic resonance imaging (MRI) studies of the sacroiliac joints in inflammatory back pain can demonstrate the following: sacroiliitis is more often bilateral in AS (84%) than in undifferentiated SpA (48%); the dorsocaudal parts of the synovial joint and the bone marrow are the most frequently inflamed structures early in the disease; in contrast, the entheses and ligaments are more commonly involved in later stages.23

DIFFERENTIAL DIAGNOSIS The differential diagnosis of sacroiliitis is narrow and is summarized in Table 35.1.7 Spinal pain and restriction may also be caused by diffuse idiopathic skeletal hyperostosis (DISH). In contrast to SpA, DISH usually presents with later age of onset, normal sedimentation rate, larger and more flowing ligamentous ossifications (syndesmophytes), and the absence of sacroiliitis.24

DIAGNOSIS The classification criteria for AS were reassessed in 1984 and are referred to as the ‘modified New York criteria for ankylosing spondylitis.’ The criteria include both clinical and radiographic categories.25,26 The three clinical criteria include:

● ●

Low back pain and stiffness of longer than 3 months’ duration, improved with exercise but not relieved by rest; Limitation of motion of the lumbar spine in both the sagittal and frontal planes; and Limitation of chest expansion relative to normal values corrected for age and sex.

The two radiologic criteria include: ● ●

Sacroiliitis with more than minimum abnormality bilaterally; and Sacroiliitis of unequivocal abnormality unilaterally.

‘Definite AS’ is present in the presence of one clinical criterion and one radiologic criterion. ‘Probable AS’ is diagnosed if three clinical criteria are present or one radiologic criterion.

Table 35.1: Spondyloarthropathies SPONDYLOARTHROPATHIES AS Reiter’s syndrome (reactive arthritis) Psoriatic arthritis Inflammatory bowel disease Acne-associated arthritis or SAPHO syndrome Intestinal bypass arthritis INFECTIOUS Pyogenic infections Tuberculosis Brucellosis Whipple’s disease OTHER Hyperparathyroidism Paraplegia Sarcoidosis (rare)

392

Clinical features of AS are heralded by chronic low back pain and stiffness as the initial symptoms in 75% of patients.27 Often, the symptoms develop spontaneously and progress insidiously. Buttock pain that radiates into the thigh may be erroneously blamed on sciatica. This pain may reflect involvement of the sacroiliac joints.28,29 A history of nocturnal back pain, diurnal variation with prolonged morning stiffness, and improvement with exercise should raise the suspicion of an inflammatory etiology to chronic back pain. A good response to nonsteroidal antiinflammatory drug (NSAID) therapy and an age younger than 40 also increase the likelihood of inflammatory back pain.30 Another, less common presentation of AS may be enthesitis or peripheral arthritis, mono- or oligoarticular.31 The enthesitis may involve the Achilles or plantar tendon insertions. The knee is often involved in the arthritis. These findings are not unique to AS. The differential diagnosis may include Reiter’s syndrome or reactive arthritis.

Physical examination

Ankylosing spondylitis

●

Clinical features

The earliest physical examination finding is often tenderness in the region of the sacroiliac joints or pain on provocative test maneuvers such as hip hyperextension and sacral compression tests. The two most sensitive maneuvers are pressure over the anterior-superior iliac spines and pressure over the lower half of the sacrum.32 As the disease progresses, physical examination findings will reflect restricted ranges of motion. As an example, reduced chest expansion is measured from maximal exhalation to maximal inhalation at the level of the fourth intercostal space. An expansion of less than 2.5 cm is considered abnormal.27 The restricted motion reflects fusion of the costovertebral joints. Schober’s test and finger-to-floor test will also become abnormal. The Schober’s test is performed by marking the fifth lumbar vertebra and a point in the midline 10 cm above. The patient is then asked to flex forward maximally while maintaining the knees straight. The distance between the two points exceeds 15 cm in normal individuals.1

Laboratory studies Laboratory studies in AS are often non-specific. Acute-phase reactants such as erythrocyte sedimentation rate and C-reactive protein are often elevated, but are not specific for AS and do not necessarily reflect disease activity.33,34 A mild normochromic normocytic anemia may be present. Serologic tests for lupus and rheumatoid arthritis should be negative. HLA-B27 is present in approximately 90% of Caucasian patients and 50–60% of African-American patients with AS.3 It is present in only 6% of the general population.

Undifferentiated spondyloarthropathy, Reiter’s syndrome, and reactive arthritis The spondyloarthropathy family of diseases share common features. As a spine specialist, it is most important to diagnose the presence of a spondyloarthropathy, rather than the specific type. The classification criteria for SpA is based on clinical features, as there are no specific confirmatory blood tests. There are two sets of clinical criteria that have been developed and validated in Europe and are used widely. These are the European Spondyloarthropathy Study Group (ESSG) and the multiple-entry criteria by Bernard Amor.1

Section 1: Medical Spinal Disorders

The European Spondyloarthropathy Study Group criteria To consider the diagnosis of spondyloarthropathy according to the ESSG criteria, a patient must demonstrate one of two entry criteria: ● ●

Inflammatory spinal pain; or Synovitis, either asymmetric or predominantly in the lower limbs.

Table 35.2: Clinical features scored in the Amor classification

● ● ● ●

Onset before 40 years of age; Insidious onset; Duration longer than 3 months; Morning stiffness; and Improvement with exercise.

Indications for the designation of synovitis are: ● ● ● ● ●

Soft tissue swelling; Warmth over a joint; Joint effusion; Decreased active and passive range of motion; and Symptoms are worse after rest.

There are other features which can be considered if a patient has one or two of the entry criteria. These include: ● ● ● ● ● ● ●

Positive family history; Psoriasis; Inflammatory bowel disease; Urethritis, cervicitis, acute diarrhea; Alternating buttock pain; Enthesopathy; and Sacroiliitis.

The ESSG criteria have been evaluated in many studies, including those in Europe, Brazil, and Alaska.35–38

The Amor criteria The Amor criteria are a series of items which are weighted with a point scoring system.1,39,40 In order to qualify for a diagnosis of spondyloarthropathy, a patient must score a total of at least six from among the list of features detailed in Table 35.2.

Specific diagnoses The Amor and ESSG criteria are for the diagnosis of spondyloarthropathy in general. The criteria for the subtypes of spondyloarthropathy are less well defined.

Reactive arthritis Inflammatory arthritides developing after a distant infection are labeled reactive.41 Inciting organisms may be: Chlamydia, Yersinia, Salmonella, Shigella, Campylobacter, Clostridium difficile, Brucella, and Giardia.42 The infection should have occurred within 6 weeks of clinical presentation of the arthritis. The presence of HLA-B27 renders the host susceptible; however, there is an interplay between HLA-B27 and environmental/infectious triggers in the development of reactive arthritis.43

Reiter’s syndrome Reiter’s syndrome represents one example of reactive arthritis. The classic triad of uveitis, urethritis, and arthritis defines Reiter’s syndrome. The pathogenesis is similar to reactive arthritis since both

Score

Night pain or morning stiffness of the thoracic or lumbar spine

1

CLINICAL

Indications for the designation of spinal pain as ‘inflammatory’ are: ●

Feature

Asymmetrical oligoarthritis

2

Buttock pain (uni- or bilateral)

1 or 2

Sausage-like toe or digit

2

Heel pain

2

Iritis

2

Nongonococcal urethritis or cervicitis within 1 month prior to arthritis

1

Acute diarrhea within 1 month prior to arthritis

1

Presence or h/o psoriasis, balanitis, inflammatory bowel disease

2

Sacroiliitis (grade >2 if bilateral; grade >3 if unilateral)

2 or 3

HLA-B27 present and/or family h/o spondyloarthropathy

2

Clear-cut response to NSAIDs

2

RADIOLOGIC

GENETIC

RESPONSE TO TREATMENT

are triggered by an infectious agent and are more common in those patients with the HLA-B27 gene.44 Not all patients present with all three features of the triad. The American College of Rheumatology requires peripheral arthritis (longer than 1 month’s duration) in association with urethritis or cervicitis.45

Undifferentiated spondyloarthropathy Among patients who meet ESSG or Amor criteria for spondyloarthropathy, there is a large group that does not fit into the above discrete categories. These patients are labeled as undifferentiated spondyloarthropathy.1 In a recent study from Spain,46 68 patients with the diagnosis of undifferentiated spondyloarthropathy (uSpA) were followed for 2 years. At the end of this period, 75% retained the diagnosis of uSpA; disease remission occurred in 13%; ankylosing spondylitis 10%; and psoriatic arthritis 2%. In addition, a subset of patients with uSpA may be found to have reactive arthritis.47

Arthritis associated with psoriasis Psoriasis is a chronic autoimmune disorder affecting the skin and can be associated with inflammatory arthritis. Ten to forty percent of patients with psoriasis develop a chronic inflammatory arthritis. Psoriatic arthritis (PSA) occurs as a result of interplay of genetic, immunologic, and environmental factors.48,49 Clinically, PSA may resemble RA, except that PSA patients are seronegative and express cytokines preferentially at the enthesis in addition to the synovium. The most common presentation is either oligoarthritis or symmetric polyarthritis. There are several proposed subtypes: monoarthritis and 393

Part 3: Specific Disorders

oligoarthritis, polyarthritis, arthritis of distal interphalangeal joints with nail changes, arthritis mutilans, and spondylitis.6,50 This is often associated with flexor tenosynovitis. Axial spinal involvement of sacroiliitis and spondylitis does occur in PSA but usually occurs after years of illness, and is not a common presenting complaint.8

Enteropathic arthritis Enteropathic arthritis refers to inflammatory arthritis in association with inflammatory bowel disease, ulcerative colitis, or Crohn’s disease.51 Conversely, two-thirds of patients with spondyloarthropathy show subclinical histologic signs of gut inflammation and approximately 6% will go on to develop inflammatory bowel disease.52 In a study by de Vlam et al.,53 39% of 103 consecutive patients followed in a gastroenterology clinic for ulcerative colitis or Crohn’s disease had enteropathic arthritis. Ninety percent met criteria for spondyloarthropathy, while 10% fulfilled criteria for ankylosing spondylitis. An additional 18% had asymptomatic sacroliliitis.6 Approximately 25% of patients with enteropathic arthritis have axial disease. Peripheral joint arthritis occurs more frequently in patients with enteropathic colitis compared with AS. Please refer to Table 35.3 which represents a summary of some of the key clinical aspects of the differential diagnosis of systemic causes of arthritis. This may clarify the recognition of systemic arthritis for the practicing spine specialist.1

Radiographic imaging in spondyloarthropathies Seronegative spondyloarthropathies including ankylosing spondylitis, psoriatic arthritis, reactive arthritis, Reiter’s syndrome, enteropathic arthritis, and undifferentiated spondyloarthropathy share common clinical and radiographic features. Synovial joint inflammation and enthesitis may involve the axial or appendicular skeleton, or both. The main musculoskeletal features include: sacroiliitis, spondylitis, and peripheral joint lesions. Sacroiliitis is the hallmark feature which unifies the group.54 The distribution of joint involvement may give a clue to diagnosis. For example, ankylosing spondylitis primarily involves the axial joints and enthesis, with less consistent findings in the appendicular skeleton,55 and psoriatic arthritis distinctively may involve the interphalageal joints.56 Multiple imaging modalities are available to assess seronegative spondyloarthropathies, provide early diagnosis, and possibly follow disease activity.

Radiographic assessment Standard radiographs are still the appropriate first images to obtain in practice. Radiographic features common to all spondyloarthropathies include: erosion, periostitis, bone proliferation at the entheses, and normal bone mineralization.54 Radiographic analysis of early sacroiliitis may demonstrate erosions on the iliac side of the joint. Latestage radiographic appearance is one of SI fusion and ankylosis.57 The shortcomings of plain radiography for the diagnosis of sacroiliitis include the large variability in interpretation among radiologists, and the relative insensitivity in early sacroiliitis.58

Scintigraphy (bone scan) Bone scanning is well documented as a modality to identify hyperemia and joint inflammation that may not be apparent radiographically. Quantitative bone scanning has approximately 80% predictability for detection of active sacroiliitis. This compares to 100% for MRI.59 Periarticular radionuclide uptake around peripheral joints and at the entheses are demonstrated with bone scan.60 The problem with scintigraphy is that it is non-specific and must be correlated with other clinical and radiologic investigations. Single photon emission computed tomography (SPECT) has improved localization of areas of increased uptake and may be a useful supplement.54

Computed tomography Computed tomography (CT) scanning is superior to plain radiography for visualization of early sacroiliac erosions and sclerosis.61 The true synovial sacroiliac joint is the inferior two-thirds, with the superior one-third being ligamentous. Comparison of CT with MRI scanning suggests that CT is superior for evaluation of chronic bone changes in the ligamentous portion of the joint; however, it is insensitive for detection of inflammatory changes in the subchondral bone.62 In addition, CT should be considered if further information about spinal fracture or bony canal stenosis is needed. A recent study demonstrates efficacy of CT-guided sacroiliac injections for treatment of sacroiliitis.63

Magnetic resonance imaging Magnetic resonance imaging (MRI) has emerged as a sensitive and detailed modality for imaging of spondyloarthropathy. MRI is excellent at depicting the normal sacroiliac joint and clearly separates the

Table 35.3: Differential diagnosis of some systemic causes of arthritis

394

Reiter’s syndrome

Rheumatoid arthritis

Gonococcal arthritis

Psoriatic arthritis

Age

Young

Middle

Young

Middle

Gender

Male > female

Female > male

Female > male

No effect

Onset

Abrupt

Insidious

Abrupt

Insidious

Joint number

Oligoarthritis

Polyarthritis

Monoarthritis or oligoarthritis

Oligoarthritis

Symmetry of arthritis

No

Yes

No

No

Sausage digits

Yes

No

No

Yes

Back pain

Yes

No

No

Yes

Urethritis

Yes

No

Yes

No

Skin lesions

Palms and soles in 10%

Subcutaneous nodules

Pustular, nodular, or vesicular

Psoriasis

Gonococcus

No

No

Yes

No

Section 1: Medical Spinal Disorders

3. Check specialized tests of chest expansion and lumbar range of movement; and 4. Take specific imaging.

synovial and ligamentous compartments. The tissue resolution permits visualization and evaluation of bone marrow, synovium, articular cartilage, ligaments, tendons, muscles, entheses, and various stages of inflammation. MRI can identify joint effusion, synovitis, bone marrow edema, and bone erosions.54 In patients with a high clinical likelihood of spondyloarthropathy and negative standard radiography, MRI (especially with gadolinium enhancement) provides excellent radiation-free evidence of sacroiliitis and enthesitis.64

Systemic features of spondyloarthropathies One of the distinguishing features of the spondyloarthropathies is their systemic nature. In contrast to other etiologies of back pain, patients with spondyloarthropathies may experience systemic symptoms such as fever, malaise, and weight loss. Patients may have increased levels of inflammatory markers such as an erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Moreover, they may have extra-articular manifestations of their disease. Below is a discussion of the most common extra-articular findings in patients with spondylitis.

Musculoskeletal ultrasound Currently, ultrasound is best applied to the evaluation of small peripheral joints since they are superficial and accessible. Early enthesitis may be demonstrated on ultrasound.54

DIAGNOSIS OF SPONDYLOARTHROPATHIES

Ocular Eye involvement can occur in all of the spondylotic variants. The most common finding is uveitis, and this can be seen in 25–40% of patients who have ankylosing spondylitis.65 Symptoms include eye pain, blurred vision, and photosensitivity. The eye can appear red and injected. In cases in which uveitis is suspected, patients should immediately be referred to an ophthalmologist, as the diagnosis can

As an overview, there are four basic steps to follow if a clinician suspects the diagnosis of spondyloarthropathy (Fig. 35.1): 1. Suspect the disease if back pain characteristics are ‘inflammatory;’ 2. Take additional history, physical examinations, labs;

Inflammatory arthritis that is asymmetric or predominantly lower extremity? and/or Back pain of insidious onset of >3 months’ duration associated with morning stiffness and improvement with activity?

No

Unlikely to be a spondyloarthropathy

Yes

Evidence of psoriasis or inflammatory bowel disease? No

Yes

One or more of the following? Radiographic evidence of sacroiliitis Enthesopathy Dactylitis Buttock pain (unilateral or alternating) Urethritis or cervicitis Family history Iritis Acute diarrhea or nongonococcal urethritis within 1 month of onset

Consider enteropathic or psoriatic arthritis

Yes

No Unlikely to be a spondyloarthropathy

Likely to be a spondyloarthropathy

Evidence of spondylitis? (inflammatory spinal pain and limitation of movement) No Evidence of chlamydial infection? (i.e. elevated antichlamydial antibody titers) No Reactive arthritis/ Reiter’s syndrome

Probably reactive arthritis/Reiter’s syndrome

Yes Probably ankylosing spondylitis

Yes Chlamydial-associated reactive arthritis

Fig. 35.1 An algorithm of the four basic steps to follow if a clinician suspects the diagnosis of spondyloarthropathy. 395

Part 3: Specific Disorders

only be made by slit-lamp examination. The treatment generally includes topical nonsteroidal eye drops or steroid drops. In severe or refractory cases, systemic immunosuppression and aggressive treatment with disease-modifying agents is necessary. While most patients will recover, severe cases can result in visual loss. A less common ocular manifestations of the spondylotic variants includes Sjögren’s syndrome and optic neuritis.66

Spondylitis Functional Index (BASFI) and the Dougados Functional Index (DFI).77 More recently, the World Health Organization Disability Assessment Schedule II (WHODAS II) was shown to be useful for evaluating functional capacity in patients with ankylosing spondylitis.78 The BASDAI focuses on pain, joint involvement, and swelling while the BASFI, DFI, and the WHODAS II assess functional impairment.

Gastrointestinal

Prognostic indicators

Gastrointestinal involvement, in particular bowel inflammation and ulceration, can be seen in all of the spondylotic variants. Up to 44% of patients with ankylosing spondylitis have gastrointestinal involvement.67 Gut inflammation in patients with ankylosing spondylitis is histologically similar to the lesions found in Crohn’s disease.68 Moreover, in one series subclinical sacroiliitis was found in 24% of patients with inflammatory bowel disease.69 Therefore, patients with spondylitis should be monitored for symptoms suggestive of occult inflammatory bowel disease and, conversely, patients with documented inflammatory bowel disease should be monitored for spondylitis.

In addition to functional assessment, various disease characteristics portend prognostic outcome. In particular, worse outcome is found in persons who have disease onset prior to age 16, hip joint involvement, peripheral joint involvement (in particular a sausage digit), decreased range of motion of the lumbar spine, high ESR, and poor response to nonsteroidal antiinflammatory drugs.79 One should examine patients for active inflammation of the peripheral joints. Laboratory testing should include ESR and CRP, CBC with differential, platelet count, and an assessment of baseline renal and liver function. The renal and liver function should be assessed because of the potential of hepatorenal toxicity of many of the medications in use. An elevated ESR and CRP suggest that ongoing active inflammation is occurring.

Cardiac Aortitis and aortic root disease that can sometimes lead to valvular dysfunction is the most common cardiac lesion found in patients with ankylosing spondylitis. In one case series, 82% of patients with ankylosing spondylitis had evidence of either aortic root disease or valvular disease. Valve regurgitation was found in close to half of the patients and many of these patients went into heart failure or required valve replacement therapy.70 Conduction abnormalities affecting the atrioventricular node and myocardial involvement are found less commonly.71

Skin There have been reports of an association between vitiligo and the spondyloarthropathies. In men, circinate balanitis can also occur.72,73

Pulmonary In patients who have thoracic spine and costovertebral joint involvement, decreased chest wall expansion during inspiration can lead to decreased lung capacity and dyspnea. This can lead to recurrent infections as well.74 In addition, patients can develop fibrobullous disease of the upper lobes.75

Genitourinary tract In both male and female patients with ankylosing predominately spondylitis, Chlamydia trachomatis infection is common and seen in patients who are HLA-B27 positive.76

Patient management The management of patients with spondylotic variants should first include a functional evaluation. Treatment modalities include physical therapy, pharmacologic agents, spinal injections, surgery, and complementary therapies.

Functional assessment This functional evaluation should include a functional assessment and an evaluation of how much fixed damage has been done to the spine and the joints. Patients with spondylitis can develop functional impairment leading to long-term disability. Various assessment tools can be used but the most common are the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), the Bath Ankylosing 396

Physical therapy One of the mainstays of therapy for spondylitis is exercise and physical therapy. The theory is that even in cases of spinal fusion and severe restriction in range of motion of the spine, physical therapy and exercise can maximize function and maintain as much mobility as possible. In Europe, spa therapy is included as part of the treatment regimen.80 Unfortunately, there are few well-designed studies that clearly demonstrate long-term efficacy of physical therapy. In one metaanalysis, group physical therapy was better than home exercise in decreasing pain and stiffness.81 In another study, recreational exercise for longer than 200 minutes a week was shown to decrease pain and stiffness, but not to improve HAQ scores in patients with disease for less than 15 years. In patients with longer-standing disease, 5–7 days a week of back exercises decreased pain and had a modest improvement of HAQ scores.82

Pharmacologic management For many years, treatment of the spondylotic variants, in particular ankylosing spondylitis and Reiter’s syndrome, was almost exclusively limited to nonsteroidal antiinflammatory drugs, analgesics, and occasionally steroids. Other disorders that present with spondylitis as part of the disease, such as inflammatory bowel disease and psoriatic arthritis, were more likely to be treated with systemic agents for the extraspinal manifestations. Occasionally, disease-modifying antirheumatic drugs such as sulfasalazine and methotrexate were used, but with limited enthusiasm. More recently, however, with the advent of biologics, there has been interest in being more aggressive with the treatment of the spondylotic variants. There is growing evidence that these agents may arrest the progression of these disorders. Below is a discussion of the treatment of spondylotic disorders with NSAIDs, sulfasalazine, methotrexate, biologics, and the more experimental therapies such as palidronate and thalidomide.

Nonsteroidal antiinflammatory drugs and COX-2 inhibitors Historically, the most commonly used NSAID has been indometacin.83 This was based upon the sense that this medication was more

Section 1: Medical Spinal Disorders

effective than other antiinflammatory agents although controlled studies have failed to substantiate this finding.84 In general, any of the nonsteroidals may be used to treat the pain and inflammation of the spondylotic variants. Phenylbutazone was once used with high frequency in patients with ankylosing spondylitis but is no longer used secondary to its high toxicity. In those patients who are intolerant of NSAIDs or who have had gastrointestinal toxicity from NSAIDs, the COX-2 inhibitors can be used. Both the NSAIDs and the COX-2 inhibitors can unmask occult colitis in these patients, so the treating healthcare provider should be aware of the potential for gastrointestinal toxicity. Moreover, the COX-2 inhibitors have been associated with increased risk of cardiovascular disease and should be used judiciously.

Sulfasalazine Sulfasalazine has been used for many years in the treatment of inflammatory bowel disease and for rheumatoid arthritis. The data on its utility in spondylitis are murkier. While inflammatory markers such as the C-reactive protein clearly improve with sulfasalazine it is unclear whether the spondylitis and those symptoms benefit. It is particularly beneficial for patients who have extraspinal manifestations of spondylitis such as psoriatic arthritis, peripheral arthritis, and inflammatory bowel disease. Dosing is in the range of 2000–3000 mg a day. The major toxicity is bone marrow or liver toxicity.85

Methotrexate Methotrexate was approved in the early 1980s for use in rheumatoid arthritis. It has also been used for the treatment of inflammatory bowel disease and psoriatic arthritis. The efficacy of this medication in spondylitis is less clear. In one double-blind, placebo-controlled study of ankylosing spondylitis, there was no benefit of methotrexate treatment compared with placebo.86

Tumor necrosis factor-alpha antagonists The new biologic agents, especially those directed against tumor necrosis factor-alpha, have only been used recently for the treatment of spondylotic variants but represent a large advance in the pharmacologic therapy of ankylosing spondylitis. Those that are approved include etanercept, infliximab, and adalimumab. These agents have been shown to be effective in the treatment of patients with ankylosing spondylitis. Both infliximab and etanercept have been shown to cause a rapid and significant improvement in BASDAI scores and improvement in morning stiffness, spinal pain, and inflammatory markers such as the ESR and CRP.87,88 As these agents are used with greater frequency and earlier in the course of the disease, it will be interesting to see whether they can impact disease outcome. They do have significant toxicities including either the exacerbation of underlying demyelinating processes or the reactivation of tuberculosis, including atypical forms.

Corticosteroids Systemic corticosteroids are of limited use in patients with ankylosing spondylitis and are generally not used.85

Corticosteroid injections Sacroiliac injections can provide short-term relief in patients with AS.89 Improvement can last up to 15 months and in one study the average length of improvement in 66 patients receiving CT-guided intra-articular corticosteroids was 10±5 months.90

Experimental therapy Thalidomide has been used for refractory ankylosing spondylitis. In one open label study minimal improvement in joint symptoms and function was observed. Further studies need to be performed before this medication is used on a regular basis.91 Pamidronate has been studied in a few open label trials. Long-lasting improvement in pain, stiffness, and function were found although several patients developed arthralgias and myalgias after the infusions. Further studies need to be done before accepting the utility of this medication in treating spondylitis.92

Complementary therapy There are limited data on the use of complementary therapy in the treatment of spondylitis. In one case study, chiropractic manipulation was helpful in a patient with advanced ankylosing spondylitis. However, given the degree of fusion found in patients’ spines, caution should be used.93

Surgery Some patients with spondylotic variants will require surgery. Hip arthroplasty and spinal surgery are the most common. Risks particular to persons with ankylosing spondylitis are postoperative heterotopic ossification. Spinal surgery is rarely used for the treatment of ankylosing spondylitis because the auto-fusion the patients experience circumvents the benefit of many spinal surgical procedures. In the case of instability, fusion has been used. Persons presenting for evaluation of lower back pain, especially in the area of the sacroiliac joints, may be presenting with spondylitis. Morning stiffness and systemic symptoms may be present. Once the diagnosis of spondylitis is suspected, patients should be monitored for extra-articular manifestations. While standard therapy has included physical therapy and nonsteroidal antiinflammatory drugs, more recently the biologics and other agents are being evaluated. These newer therapies may hopefully lead to earlier treatment that will circumvent the spinal fusion that can be so debilitating in these disorders.

CASE STUDIES Case study 1 A 28-year-old male who has a 10-year history of ankylosing spondylitis comes to the office. He has ongoing pain in his neck and the feeling of malaise. He has shortness of breath with walking short distances. He also has new onset of eye pain and blurry vision. His family history is notable for a mother with AS. On exam, Schober’s reveals an expansion of 1 mm, chest expansion is 1 cm, and he has minimal rotation (30° in either direction) of his neck. He is currently taking nonsteroidals but is wondering about other treatment options. Laboratory testing reveals an elevated ESR and CRP. What further work-up needs to be done? This case illustrates the systemic nature of ankylosing spondylitis and the spondylotic variants. The key features of his presentation are the shortness of breath and eye symptoms. These should prompt further work-up. He needs to have a chest X-ray to rule out pulmonary fibrosis and possibly pulmonary function tests. He also needs to be referred to an ophthalmologist for a slit-lamp examination because of the risk of uveitis. After these extraspinal conditions are ruled out, one could consider therapy with a disease-modifying agent such as sulfasalazine or tumor necrosis factor blockade. 397

Part 3: Specific Disorders

Case study 2 A 33-year-old woman is referred for pain in her lumbar area. The pain is not radiating and she has no neurological symptoms. She feels that after she gets up in the morning and showers, she loosens up. She feels better as the day goes on and she moves around. She is concerned because she is recently married and would like to start a family and she is not sure that she would be able to handle an infant with her current level of pain. On examination, her Schober’s test shows her lumbar spinal extension is 3 cm, chest expansion is normal, and she has no peripheral joint involvement. Plain radiographs of her back are negative. What should the next diagnostic work-up be? MRI of the sacroiliac joints is more sensitive than plain radiographs in detecting erosions. In this case, her history of profound morning stiffness and improvement with activity in conjunction with the findings on physical examination are quite suggestive of a spondylotic variant. This patient should have MRI of her sacroiliac joints.

SUMMARY

16. Bywaters EGL. Pathology of the spondyloarthropathies. In: Calin A, ed. Spondyloarthropathies. Orlando: Grune & Stratton; 1984:43–68. 17. Chang CP, Schumacher HR. Light and electron microscopic observations on the synovitis of ankylosing spondylitis. Semin Arthritis Rheum 1992; 22:54. 18. Granfors K. Do bacterial antigens cause reactive arthritis? Rheum Dis Clin North Am 1992; 18:37–48. 19. Hermann E. T cells in reactive arthritis. APMIS 1993; 101:177–186. 20. Urgrinovic S, Mertz A, et al. A single monamer from the Yersinia 60-kD heat shock protein is the target of HLA-B27 restricted CTL response in Yersinia-induced reactive arthritis. J Immunol 1997; 159:5715–5723. 21. Braun J, Bollow M, Neure L, et al. Use of immunohistologic and in situ hybridization techniques in the examination of sacroiliac joint biopsy specimens from patients with ankylosing spondylitis. Arthritis Rheum 1995; 38:499. 22. Bollow M, Fischer T, Reisshauer H, et al. Quantitative analyses of sacroiliac biopsies in spondyloarthropathies: T cells and macrophages predominate in early and active sacroiliitis – cellularity correlates with the degree of enhancement detected by magnetic resonance imaging. Ann Rheum Dis 2000; 59:135.

Spondyloarthropathies are a family of disorders that frequently manifest with back and spine complaints. These disorders are associated with psoriasis and inflammatory bowel disease. Other systemic symptoms are seen, including uveitis and lung disease. Practitioners who treat patients with spine disorders should be aware of these diseases and consider them in the differential diagnosis of patients who present with back pain. Systemic symptoms, the presence of an elevated CRP and ESR, and a positive HLA-B27 can be helpful in diagnosing these disorders. Imaging studies such as radiographs and magnetic resonance imaging may be helpful in establishing the ankylosing spondylitis. These patients may be treated with traditional NSAIDs and, in some cases, patients may benefit from rheumatic disease-modifying antirheumatic drugs.

23. Muche B, Bollow M, Francois RJ, et al. Anatomic structures involved in earlyand late-stage sacroiliitis in spondylarthritis: a detailed analysis by contrastenhanced magnetic resonance imaging. Arthritis Rheum. 2003; 48:1374–1384.

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69. Queiro R, Maiz O, Intxausti J, et al. Subclinical sacroiliitis in inflammatory bowel disease: a clinical and follow-up study. Clin Rheumatol 2000; 19:445–449. 70. Roladan CA, Chavez J, Wiest PW, et al. Aortic root disease and valve disease associated with ankylosing spondylitis. J Am Coll Cardiol 1998; 2:1397–1404. 71. Lautermann D, Braun J. Ankylosing spondylitis – cardiac manifestations. Clin Exp Rheumatol 2002; 20:S11–S15. 72. Padula A, Ciancio G, La Civita L, et al. Association between vitiligo and spondyloarthritis. J Rheumatol 2001; 28:313–314. 73. Angualo J, Espinoza LR. The spectrum of skin, mucosa and extra-articular manifestations. Baillieres Clin Rheumatol 1998; 12:649–666. 74. Hunningnake GW, Fauci AS. Pulmonary involvement in the collagen vascular diseases. Ann Rev Respir Dis 1979; 119:471–503. 75. Rumanak WM, Firooznia H, Davis MJ, et al. Fibrobullous disease of the upper lobes: an extraskeletal manifestations of ankylosing spondylitis. J Comput Tomogr 1984; 8:225–229. 76. Lange U, Teichmann J. Ankylosing spondylitis and genitourinary infection. Eur J Med Res 1999; 4:1–7. 77. Ruof J, Sangha O, Stucki G. Comparative responsiveness of 3 functional indices in ankylosing spondylitis. J Rheumatol 1999; 26:1959. 78. Van Tubergen A, Landewe R, Heuft-Dorenbosch L, et al. Assessment of disability with the World Health Organization Disability Assessment Schedule II in patients with ankylosing spondylitis. Ann Rheum Dis 2003; 62:140–145. 79. Amor B, Santos RS, Nahal R. Predictive factors for the long-term outcome of the spondyloarthropathies. J Rheumatol 1994; 21:1883. 80. Van Tubergen A, Hidding A. Spa and exercise treatment in ankylosing spondylitis: Fact or fancy? Best Pract Res Clin Rheumatol 2002; 16:653–666. 81. Dagfinrud H, Kvien TK, Hagen K. Physiotherapy interventions for ankylosing spondylitis. Cohrane Database Syst Rev 2004; (4)CD002822. 82. Uhrin A, Kuzis S, Ward M. Exercise and changes in health status in patients with ankylosing spondylitis. Arch Intern Med 2000; 160:2969–2975. 83. Harrison TR, Wilson JD. Ankylosing spondylitis and reactive arthritis. In: Jeffers HD, Boynton SD, eds. Principles of internal medicine, 12th ed. New York: McGraw-Hill: 1991:1453. 84. Barlle-Gualda E, Figueroa M, Ivorra J, et al. The efficacy and tolerability of aceclofenac in the treatment of patients with ankylosing spondylitis: a multicenter controlled clinical trial. Aceclofenac Indomethacin Study Group. J Rheum 1996; 23:1200–1206. 85. Dougados M, Dijkmans B, Khan M, et al. Conventional treatments for ankylosing spondylitis. Ann Rheum Dis 2002; 61:11140–11150. 86. Roychowdhury B, Bintly-Bagot S, Bulgen DY, et al. Is methotrexate effective in ankylosing spondylitis? Rheumatology 2002; 41:1330–1332. 87. Braun J, Brandt J, Listing J, et al. Long-term efficacy and safety of infliximab in the treatment of ankylosing spondylitis: an open, observational, extension study of a three-month, randomized, placebo-controlled trial. Arthritis Rheum 2003; 42:2224–2233. 88. Gorman JD, Sack KE, Davis JC. Treatment of ankylosing spondylitis by inhibition of tumor necrosis factor alpha. N Engl J Med 2002; 246:1349–1356.

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91. Wei JC, Chan TW, Lin HS. Thalidomide for severe refractory ankylosing spondylitis: a 6-month open-label trial. J Rheumatol 2003; 30:2627–2632. 92. Maksymowych WP, Jhangri GS, Leclercq S, et al. An open study of pamidronate in the treatment of refractory ankylosing spondylitis. J Rheumatol 1998; 25:714– 717. 93. Rose KA, Kim WS. The effect of chiropractic care for a 30-year-old male with advanced ankylosing spondylitis: a time series case report. J Manip Phys Ther 2003; 26:E1–E9.

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PART 3

SPECIFIC DISORDERS

Section 1

Medical Spinal Disorders

CHAPTER

Spine Infections: An Algorithmic Approach

36

Gregory A. Day and Ian B. McPhee

INTRODUCTION Late diagnosed or misdiagnosed spine infections may have serious consequences. The commonest organisms causing spine infection are pyogenic bacteria. Other bacteria, Mycobacterium species, and fungi are infrequent causes of spine infection. Adverse outcomes can be anticipated in spine infections involving more virulent organisms or immunocompromised hosts. The range of spinal infections from hematogenous spread includes childhood discitis, spondylodiscitis and epidural abscess, and excludes open trauma to the spine. Other iatrogenic spinal infections including adult discitis, spondylodiscitis, and facet (zygapophyseal) joint septic arthritis resulting from postdiscectomy/laminectomy, postinjection/aspiration, or instrumentation of the spine are discussed separately. Successful management encompasses early diagnosis, appropriate antimicrobial medication, and surgical management if the patient develops neurological deficit, has an unstable spine, or fails conservative management. This algorithmic approach to the management of spinal infections presents the clinician with clinical paths to aid in the management of a potentially serious condition.

CHILDHOOD DISCITIS Pathogenesis, etiology, and natural history The natural history of childhood discitis varies from neonates/infants to young children to teenagers.1

Neonate/infant and young children discitis A high proportion of negative disc cultures in infants and toddlers has prompted some authors to state that childhood discitis may be either inflammatory or infective. Infective childhood discitis usually results from hematogenous seeding of organisms. The intervertebral disc is avascular even in infants.2 It has been postulated that pediatric spine infections commence in the microarterioles of the vertebrae3 because the nutrient arteries have been demonstrated to be a more direct route for the spread of infection to the vertebral column than its venous drainage.3 This theory proposes that spinal infection in infants and toddlers starts in a very similar way to the development of metaphyseal osteomyelitis in long bone infection. Terminal arterioles arising from the circumferential vessels fed from the extraperichondrial arterial plexus and from nutrient metaphyseal arteries penetrate the hyaline cartilage endplates of the vertebral bodies and terminate adjacent to the intervertebral disc in neonates up to 1 year of age.2,4,5 Venous drainage follows the same route. Blood-borne bacteria can be delivered directly to the intervertebral disc during bacteremia.6 The pediatric host cannot mount a response to invading organisms within an avascular disc, allowing the organisms to multiply unim-

peded. Pyogenic bacteria release proteolytic enzymes, leading to destruction of the intervertebral disc. Spread of infection to the vertebral body in infants is limited by the cartilage-capped endplates. However, with further progression, the hyaline cartilage-capped endplates may be destroyed, allowing the invading organisms direct access to the vertebral body.7 Infants have widespread anastomotic connections between intraosseous arterioles within the vertebral body.8 Disappearance of these anastomoses later in childhood increases the risk of vertebral bone necrosis and subsequent osteomyelitis through microthrombosis. Vertebral osteomyelitis is present in 25% of cases. Spread to the epidural space is rare in young children but has been reported in previously well males.9

Early teenage discitis The anatomy of the adolescent spine is similar to a skeletally mature spine after the growth plates fuse to the vertebral body, and spine infections follow a similar pathogenesis.

Clinical presentation – history and clinical features Childhood discitis is uncommon. The clinical presentation can be subdivided into three distinct age groups – neonates/infants, young children, and early teenagers. Infants and young children present acutely with malaise and a limp or refusal to bear weight on one leg.10 Brown et al.11 report an insidious onset of symptoms in young children with typical late presentation. Viral or bacterial infections often precede childhood discitis. A history of recent mild spinal trauma is sometimes elicited. Seventy-eight percent of cases involve the lumbar spine.12 Fifty percent to 57% of young children present with backache.10,13 Teenagers present with spinal and occasionally abdominal pain.14 The commonest clinical signs are trunk stiffness and a loss of the normal lumbar lordosis.11 Paravertebral muscle spasm and hamstring tightness are common. Some children may present with a totally rigid lumbar spine. Spinal tenderness is easier to detect in children old enough to communicate verbally. A minority (28%) of children with discitis are febrile (>37.9°C).12 If the disease progresses to spondylodiscitis (which includes vertebral osteomyelitis), up to 79% have an elevated temperature.12 Neurological deficit in this age group is rare.

ADULT PYOGENIC SPONDYLODISCITIS Pathogenesis, etiology, and natural history Spondylodiscitis may complicate generalized septicemia or result from a distant focus such as vegetation of a heart valve or florid skin infection. Blood-borne adult pyogenic spondylodiscitis originates in the endplate of the vertebra (rather than the intervertebral disc), 401

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most likely in the capillary loop or postcapillary venous channels, spreading secondarily to the intervertebral disc. Pyogenic bacteria secrete proteolytic enzymes, causing necrosis of bone and intervertebral disc. Individuals at risk include those affected by: ● ● ● ● ● ● ● ● ● ●

Postprocedural, including postspinal injection and postdiscectomy; Advancing age – more than one-half of recently reported spinal infections involve subjects 50 years and older; Chronic malnutrition and chronic alcoholism; Diabetes; Immune deficiency including HIV infection, steroid and cancer therapy, immunosuppression and organ transplantation; Intravenous drug abuse; Chronic disease such as rheumatoid arthritis, psoriasis, and sickle cell disease; History of malignancy; Renal failure; Distant infection, including endocarditis/heart valve vegetation and skin infection.

Infection of males has a slight preponderance,15 with a male:female ratio ranging up to 1.8:1. If the patient has been previously well and the organism is indolent, the spondylodiscitis can be arrested at an early stage with nonoperative management. If the patient has been previously unwell and the organism is more virulent, the natural history of spondylodiscitis is of worsening local sepsis, sometimes spreading paravertebrally. Infection may spread to form a psoas abscess and extend to its insertion at the lesser trochanter of the proximal femur. Epidural spread also occurs. The spinal cord or cauda equina may be compressed by an enlarging abscess, usually at one spinal level. The microvascular circulation from the anterior spinal artery to the spinal cord/cauda equina is also disturbed by the presence of microvascular thrombosis as a result of persisting adjacent infection.16 Prolonged immobilization with osteopenia and progressive vertebral osteomyelitis with bone destruction predispose to pathological fracture. The resultant angular kyphosis or posteriorly displaced bone fragments into the spinal canal may contribute to neurological compromise. Mortality has been reported in 10–16% of adults with pyogenic spondylodiscitis.17–19

Clinical presentation – history and clinical features Patients typically present with insidious onset of unremitting spinal pain and loss of spinal movement. The clinical presentation can be classified into acute, subacute and chronic, depending on the virulence of the organism and the ability of the affected individual to mount a response.20 A history of malaise, anorexia, fevers, weight loss, and night or resting spinal pain is common. Most have a diminished range of movement and mild tenderness over the spinous process of the affected vertebra early in the disease. Paravertebral muscle spasm is common. Torticollis in cervical spine infection and bizarre posturing from thoracic and lumbar spine infection may be related to psychological factors, but a large psoas abscess or neurological compromise should be excluded. Rigors are uncommon and are manifest by a spiking elevation in temperature. With more-advanced spinal infection, neurological deficit is present in 29–51% of spondylodiscitis.17,18,21–23 Two-thirds of patients with paralysis from spinal infection have central cord syndrome and onethird have anterior cord syndrome.21 Neurological deficit is most common at the cervical spine level and least common at the lumbar level. 402

Factors associated with neurological deficit include diabetes mellitus, advancing age, steroid therapy, organ transplantation, chronic inflammatory conditions, and intravenous drug abuse.18

ADULT PYOGENIC DISCITIS Pathogenesis, etiology, and natural history True adult pyogenic discitis usually follows surgical intervention. The incidence following discography is 0.5–1% and following any type of spinal procedure 0.4–4%.24 It has been reported after every type of spinal procedure including laminectomy, discectomy, arthrodesis, discography, chemonucleolysis, myelography. and lumbar puncture. Discitis complicates discectomy in 0.4–2.8% of patients.24,25 Microdiscectomy using a microscope was reported to reduce the rate of discitis24 but others have found no difference in infection rate.26 It is probably due to direct inoculation of the organism into the avascular intervertebral disc although some believe that it results from aseptic inflammation.24 During the stage of suppuration, the invading organisms multiply and a surrounding inflammatory response is mounted by the host. In a similar manner to spondylodiscitis, the bacteria secrete proteolytic enzymes, leading to necrosis of the intervertebral disc and endplates. Again, the amount of disc destruction depends on the virulence of the invading organism and the resistance of the host. In a previously well patient, the discitis may be locally contained with little treatment, when the invading organism is indolent. However, the infection may spread to the vertebral endplates and beyond if the organism is virulent or in an immunocompromised individual. Should this occur, the pathogenesis and natural history of discitis is similar to that of adult pyogenic spondylodiscitis (Fig. 36.1).

Clinical presentation – history and clinical features Pain is expected following a surgical procedure or injection.24 The clinical course of postprocedural discitis is often reflected by early relief of symptoms due to the surgical procedure, typically Potential pathological seguence Hematology (embolic or bacteremic) spread

Primary source: Kidney Upper respiratory tact Skin Bowel

Infection

Disc

Iatrogenic: Discography Nucleotomy Myelography Metal/material insertion into the intervertebral disc Vertebral bodies

Destruction

Spread

Paravertebral

Epidural space

Psoas abscess

Epidural abscess

(Extra spinal)

Surgical implantation

Neuology

Fig. 36.1 Potential pathological sequence.

Collapse

Fracture

Deformity Kyphosis Instability

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followed by recurrence of similar spinal pain 1–4 weeks after the procedure (range, 2 days to 10 weeks).27 The constant, throbbing pain that subsequently develops is often out of proportion to the clinical picture. Unlike postoperative deep wound infection, the surgical skin incision/scar is normal in more than 90% of cases.24 Most patients with postprocedural discitis have only a very mildly elevated temperature. They eventually develop malaise, anorexia and weight loss. Clinically, patients develop marked paravertebral muscle spasm and stiffness of the affected spine. Fewer than 15% of patients develop a new or worsening neurological deficit from the spread of infection.24,28

Prolonged surgical time may result in excess wound edema or ischemic/necrotic wound edges from prolonged skin edge retraction. Both complications allow virulent bacteria or normal skin flora to enter the wound. Skin flora of low virulence including Acinetobacter baumani, Peptiostreptococcus, Corynebacterium, coagulase-negative Staphylococcus, and Propionibacterium acnes have been cultured from postoperative surgical wounds in elective orthopedic surgery.34 Although S. aureus and methicillin-resistant S. aureus (MRSA) are the commonest hospital-based organisms responsible for early deep wound infection, some wound infections involve more than one organism and include indolent types of bacteria from normal skin flora.

POSTOPERATIVE DEEP WOUND INFECTION Pathogenesis, etiology, and natural history Early wound complications of spine surgery Early postoperative infections occur less frequently following discectomy (0.5–1%) than instrumented posterior spine arthrodesis (up to 12.9%).29 Laminectomy alone has been reported to result in a 1.5% wound infection rate. When arthrodesis is added, the risk increases 50%, and with the addition of instrumentation it increases 100%.29 The preoperative nutritional status of the patient is an important factor in the incidence of wound dehiscence and subsequent infection.30–32 Generally, patients have a better chance of uncomplicated postoperative wound healing with a plasma albumin level of greater than 3.5 g/dL and a total lymphocyte count of greater than 2000 cell/ mm3.12 Preoperative radiation increases the risk of early wound complication in patients with spinal tumours.29,32 Risk factors for early wound complications include prolonged intraoperative time (>4 hours), massive blood loss, blood transfusions, large wound hematomas, posterior rather than anterior approach, and large numbers of operating theater personnel.33 Staphylococcus aureus accounts for approximately 60% of all infections. Other organisms implicated in primary and postprocedural pyogenic spinal infections are shown in Table 36.1. Patients with immune deficiency are susceptible to the rarer fungal organisms including those shown in Table 36.2. Superficial wound infection may extend to involve deeper tissues, including the intervertebral disc, following spinal surgery.

Table 36.1: Other Organisms Implicated in Primary and Postprocedural Pyogenic Spinal Infections Actinomyces

Aerobacter

Bacteroides

Brucella

Enterobacter

Escherichia coli

Klebsiella

Proteus

Pseudomonas

Salmonella

Serratia

Streptococcus

Table 36.2: Rarer Fungal Organisms Aspergillus

Candida

Coccidioides

Cryptococcus

Histoplasma

Nocardia

Late infection and late hematogenous seeding The range of organisms isolated from late infection of the spine following instrumented spine arthrodesis is similar to that of early wound infection. Embolization or bacteremia from the bladder, kidney, respiratory tract, skin, or bowel may result in hematogenous seeding in spinal instrumentation some time after surgery. Late infection can also follow intravenous drug abuse.35 The bacteria remain dormant for a period of time and secrete a glycocalyx which promotes their adherence to the metal of the spinal instrumentation and shields the organisms from lymphocytes and antibiotics.36–38 When the host develops an intercurrent illness and natural immunity is depressed, late spinal infection may develop. It is manifest as an initial suppurative phase with abscess formation, followed by reactive granulation tissue when the host mounts a response to the infection. Pyogenic bacteria secrete proteolytic enzymes, leading to necrosis of surrounding soft tissue and bone. Symptoms have usually developed by this stage and the patient may develop a painful swelling about the spinal instrumentation. Should the infection remain undiagnosed, a sinus may develop. Superficial drainage to the skin is not common in late pyogenic infection.

Sterile inflammation Hematoma formation and sterile bursae are frequently evident between prominent metal and the skin in thin patients with posteriorly instrumented spinal arthrodesis. Corrosion and metal fretting with release of particulate metal from micromotion between coupled spinal instrumentation results in a sterile inflammatory response, even after solid arthrodesis.39,40 In most cases, cultures of the fluid and tissue adjacent to the metal implants are negative. Where bacteria can be cultured from the interface membrane, it is hypothesized that the metal particles and resultant inflammation may potentiate late infection due to activation of indolent organisms or hematological embolization.

Clinical presentation – history and clinical features Deep spinal wound infection can be manifest in three clinical scenarios – early, delayed, and late. Early deep wound infection may follow a superficial wound infection from anterior or posterior spine surgery. The incidence of erythema, cellulitis, wound dehiscence, or purulent discharge before the onset of deep wound infection is up to 93%.29 Less than a one-third are noted to have a temperature of greater than 37.5°C at diagnosis. Delayed and late deep wound infections are reportedly due to or associated with intraoperative inoculation of indolent bacteria/fungi in the presence of metal fretting or from true late hematogenous seeding in spinal instrumentation. When intraoperative inoculation of indolent organisms occurs, some early wound erythema is often noted.29,41,42 Diagnosis is often made by exclusion. 403

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Clinical symptoms include spinal pain, malaise, anorexia, and subjective swelling within the spinal wound.43

EPIDURAL SPACE INFECTION Pathogenesis, etiology, and natural history Epidural infection is relatively rare but the incidence may be increasing due to a greater number of spinal procedures, epidural catheterization for pain control, intravenous drug abuse, and immunocompromised patients.23,44 Although they are distributed circumferentially around the spinal cord/cauda equina, anterior epidural space infection is more likely to be associated with spondylodiscitis than a posterior infective focus. Posterior foci usually result from hematogenous spread and are associated with frequent venous puncture for steroid or antiinflammatory injection and acupuncture.45 Epidural space infections are more common in the thoracic and lumbar spines, and tend to spread rapidly, often spanning a number of spinal segments at the time of diagnosis. Neurological compromise and even paralysis can occur early in the course of the infection, being manifest in days rather than in weeks, as is sometimes the case in spondylodiscitis. A combination of neural compression and microvascular thrombosis of the vessels of the spinal cord are thought to be responsible. Neurological deficit has been described in 19–80% of cases.23,45 Rarely, other infections occur within the spinal canal, including subdural abscess and spinal cord abscess.

Clinical presentation – history and clinical features Epidural infections affect patients of all ages (including children) and may present with signs of overwhelming infection including septicemia, bleeding diathesis, abrupt onset of paraplegia, and even adult respiratory distress syndrome with minimal overt signs of spinal infection. In contrast to spondylodiscitis, high fevers and rigors are noted early in the course of the infection. Affected individuals often have severe constitutional symptoms of malaise and anorexia. Neck rigidity is often seen in cervical epidural space infection. Meningeal irritation and radicular pain are often present. Classically, neurologic deficit is evident within 7–10 days of the onset of infection. Progressive neurologic deficits are present in 19–37% of cases,23,46 and are commoner in the thoracic spine (60% of these cases) than the cervical spine (33.3% of cases),46 although McHenry et al. report a higher incidence from cervical spine infection.18

PRIMARY AND POSTPROCEDURAL FACET JOINT INFECTION Pathogenesis, etiology, and natural history Even though the capsule of the lumbar facet joint has anterior perforations, paraspinal and intradural extension of the abscess is exceedingly rare.47,48 The sepsis is contained within the joint in most cases and causes localized spinal pain until drained. Severe neurological sequelae have not been reported in joint sepsis following facet joint infection.

Clinical presentation – history and clinical features Suppurative facet joint arthritis is rare with less than 50 reported cases.47 The clinical features can mimic spondylodiscitis. It is a very rare complication following facet joint injection with only three cases 404

reported to date.49 Because facet joint injection is gaining popularity in the therapeutic management of low back pain in Western medicine, an increase in incidence should be expected. Most patients undergoing this procedure have localized spinal pain with or without radiation. Often, the patient will have immediate benefit of pain relief while the local anaesthetic is effective. Postinjection suppurative arthritis is difficult to diagnose in the early stages because it is recognized that under normal circumstances, it may take up to 10 days for locally injected steroids to have a dampening effect on the pain. Pain localization usually occurs only when the infection is established. Patients with undiagnosed postinjection suppurative facet joint arthritis continue to deteriorate, with severe unremitting back pain.

DIAGNOSIS There is no single diagnostic test for spinal infection.

Plain radiology Childhood discitis In the earliest stages of infection, loss of cervical or lumbar lordosis is seen on lateral plain radiographs.7 A reduced disc height and erosion of adjacent vertebral endplates is present in up to 76% childhood discitis of 2 weeks duration.7,12 Long-standing infection leads to scalloping of the vertebral endplates. Late angular kyphosis may develop from destruction of either the vertebral body or the growth plates or both. The differential diagnosis of childhood discitis includes vertebra plana secondary to eosinophilic granuloma, bone tumors, and Scheuermann’s kyphosis in adolescents. Plain radiographs of the spine can distinguish among these conditions at presentation in most cases.

Pyogenic spondylodiscitis Depending on the nature of the invading organisms and the general condition of the patient, plain radiological changes appear from 2 weeks to 3 months after the onset of infection.50 Progressive narrowing of the disc space and irregularity and loss of the sharp, straight outline of the adjacent vertebral endplates is demonstrated better on lateral radiographs.51 Subchondral endplate lysis or defects may follow. Evidence of bone repair is manifest by hypertrophic or sclerotic bone formation adjacent to the vertebral endplate. With progression of the disease, paravertebral soft tissue swelling is evident on anteroposterior (AP) radiographs. A psoas abscess may form, changing the profile of the psoas shadow on AP radiographs. If gas is demonstrated in the soft tissues, anaerobic bacteria are usually responsible. With progressive osteomyelitis, bone destruction of the vertebral bodies may cause a pathological fracture,50 acute angular kyphosis or, less commonly, scoliosis. Pyogenic spondylodiscitis may heal by late bony or fibrous ankylosis (Fig. 36.2).

Axial and spiral CT Pyogenic spondylodiscitis The demonstration of end-plate irregularities, erosions, and sclerosis in adjacent vertebral bodies helps to differentiate spondylodiscitis from most secondary spine tumors. Secondary spinal tumors usually involve the pedicle or the posterior aspect of one or sometimes many vertebral bodies. Apart from multiple myeloma, primary spine tumors (osteoid osteoma, osteoblastoma, and giant cell tumor) usually involve the posterior elements of a vertebra. Multiplanar (spiral) CT is the investigation of choice to demonstrate the presence and extent of paraspinal/psoas abscesses, because MRI sagittal plane sequences are usually limited laterally to the tips of the transverse processes. Spiral CT imaging has the added advantage

Section 1: Medical Spinal Disorders

A

B

of providing the clinician with a 3-D view of the vertebral bodies of the infected spine.50,51 CT-guided percutaneous spinal biopsy allows for precise direction and localization of the infected disc or paravertebral abscess. MR imaging is superior in differentiating among epidural blood, pus, or tumor (Fig. 36.3).

Nuclear medicine (scintigraphy) Nuclear medicine studies are very sensitive in identifying spinal infection before changes occur on plain radiographs. Increased blood flow to soft tissue and bone occurs as the host mounts a vascular response to an invading spinal organism. Nuclear medicine studies are sensitive to this vascular response 2–3 days after a pyogenic infection commences. They are also useful in identifying remote infections in bone, joint, and soft tissue, especially in childhood infection. Techniques include Technetium 99 (Tc-99m), Gallium 67 citrate (Ga-67), and Indium 111 labeled leukocyte (In111-WBC) scan. Gallium is an analog of ferritin which is secreted by leukocytes. In111-WBC scans have a low sensitivity (17%).50,51 Ga-67 SPECT images are accurate in diagnosing spinal osteomyelitis in up to 91% of cases. Combined accuracy of Technetium 99 and Gallium 67 citrate scans is as high as 94%.50 Technetium 99 scanning is recommended in very young children when discitis is suspected and exact localization is difficult from history and clinical examination. The scan appearance may show a high probability of infection as early as 3–5 days after clinical symptoms develop.52,53 During the healing phase

Fig. 36.2 A 67-year-old female. Staphylococcus L1–2 spondylodiscitis. Pathological fractures of each vertebra with resultant slight angular kyphosis.

of infection, the Gallium-67 scan may become negative although the Technetium-99 scan remains positive.54 For this reason, Gallium-67 scan alone has been recommended for follow-up studies of disc space infections.55 The authors’ preferred recommendation is follow-up MRI with gadolinium, except when general anesthesia is required for children. Under these circumstances, follow-up Technetium-99 and Gallium-67 scans are both considered (Fig. 36.4)

Magnetic resonance imaging Magnetic resonance imaging (MRI) is the investigation of choice in assessment of early spondylodiscitis.50 It allows for multiplanar imaging. It has a specificity of up to 94% in distinguishing among discitis, vertebral osteomyelitis, epidural, paraspinal and prevertebral abscess, transverse myelitis, and spinal cord or intradural suppuration with a sensitivity of up to 97%,56,57 when gadolinium is added for enhancement. Early infection can be detected on T1-weighted sequences, in which decreased signal intensity in the intervertebral disc and the adjacent vertebral bodies from edema is evident. The intranuclear cleft is nearly always demonstrable (94%)51 in normal discs and is not visible in discitis. Signal hyperintensity of the disc on T2-weighted images, combined with loss of disc height, is useful in identifying the infected disc. After discography or facet joint blocks, injected fluids demonstrate low signal intensity on T1-weighted sequences and high signal intensity on T2-weighted sequences, occasionally mimicking purulent fluid. T2-weighted images demonstrate increased signal 405

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B

Fig. 36.3 Staphylococcus spondylodiscitis. Endplate irregularity and lytic erosion of vertebra, and disc destruction.

Fig. 36.4 Scintigraphy. Staphylococcus L1–2 spondylodiscitis. (The same 67-year-old female as in Fig. 36.2.) 406

Section 1: Medical Spinal Disorders

intensity within the bone marrow of adjacent vertebral endplates in spondylodiscitis due to inflammatory changes. Axial plane gradient echo sequences are useful in distinguishing between normal and infected vertebral bodies. Fat suppression techniques are useful for differentiating inflammatory areas in the vertebral bodies from fatty marrow in older individuals. Fat suppression also distinguishes between epidural suppuration and epidural fat. Epidural abscesses demonstrate high signal on T2-weighted sequences and may be isointense with cerebrospinal fluid (CSF). Proton densityweighted sequences demonstrate a darker image for CSF than pus. Gadolinium enhances images when tissue is hypervascular, and can help distinguish infection from scar tissue, tumor, CSF, and chronic degenerative changes. Enhancement of the disc, vertebral endplates, and bone marrow on postgadolinium sequences is highly suggestive of pyogenic spondylodiscitis.50,58,59 Gadolinium is especially useful when the spinal cord or dural sac is compressed by abscess, distinguishing pus from surrounding edema fluid.50 The signal from the spinal cord may be hyperintense under compression but acute changes are felt to be reversible. Persisting spinal cord hyperintensity usually reflects cord ischemia or myelomalacic change.60 One favored protocol for MRI of cervical spine infections involves:60 ● ● ● ●

Sagittal T1-weighted sequences; Sagittal fast spin-echo fat-saturation T2-weighted sequences; Axial T1-weighted sequences; and Gadolinium-enhanced sagittal and axial fat-saturation T1-weighted images.

MRI is more difficult to interpret following surgery which involves bone grafting. Also, postoperative enhancement of the uninfected disc is common.50 In the first few days after surgery, paravertebral edema and slight enhancement of the bone graft–vertebra interface is evident on T2-weighted sequences. By 4 weeks postsurgery, a noninfected bone graft and adjacent vertebrae enhance irregularly. The bone graft normally demonstrates high signal intensity on

A

B

T2-weighted sequences for 1 year following surgery. This enhancement eventually reduces as the bone graft incorporates into the adjacent vertebral bodies. When infection intervenes, the bone graft usually displays a hyperintense, uniform enhancement. Stainless steel causes more artifact than titanium on all sequences, and its use may preclude MRI as a useful tool for diagnosing postoperative infection. Some conditions are difficult to distinguish from spondylodiscitis on MRI. Severely degenerative discs with acute fibrovascular infiltration demonstrate decreased signal on T1-weighted images and increased signal on T2-weighted sequences in the subchondral endplates. These degenerate discs, however, demonstrate reduced T2-weighted disc signals in the less hydrated nucleus pulposus. Inflammatory spinal conditions have similar signal changes to infection on all MRI sequences. They include ankylosing spondylitis, rheumatoid arthritis, sarcoid disease, gout, and calcium pyrophosphate crystal deposition. Gouty lesions (very rare) are usually sharply delineated and are associated with punched-out lesions of the endplate. If a spinal infection is less vascular, for example a granuloma, then MRI may not distinguish the infection from tumors which rarely cross a disc space (multiple myeloma and lymphoma).60 In these cases, there is an indication to perform spinal biopsy (Figs 36.5, 36.6).

Laboratory studies Leukocytosis is usually indicative of infection but can often be absent or minimal in patients with pyogenic vertebral osteomyelitis. Elevated leukocyte counts are evident in 13–60% of cases.46 Elevation of erythrocyte sedimentation rate (ESR) is sometimes minimal in spine infection, but a vast majority of patients with discitis demonstrate a raised ESR at some stage.24 The sensitivity for using ESR as a postprocedural index of infection ranges 73–100%.24,46 The specificity ranges 38–62%.24 The ESR peaks 4 days after surgery and returns to normal levels between 14 and 42 days after surgery, depending on the extent of surgery and the amount of spinal instrumentation.24

Fig. 36.5 MRI T2-weighted sequence. A 71-year-old male. Early T12–L1 staphylococcal spndylodiscitis, reported as acute Schmorl’s node. 407

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B

Fig. 36.6 CT coronal, axial. The same 71-year-old male as in Fig. 36.5, 6 months after the previous MRI, demonstrating disc and vertebral destruction, minor epidural abscess.

C-reactive protein (CRP) is nearly always elevated when inflammation or infection occurs and is an excellent indicator of the degree of infection/inflammation. The sensitivity for using CRP as a postprocedural index of infection is 64–100%;24 the specificity is 62–96%.24 CRP levels demonstrate a faster return to normal following surgery compared to ESR.24 CRP levels fall with the leukocyte count. The magnitude of spinal surgery/instrumentation also determines how quickly the CRP level returns to normal. It is recommended that both ESR and CRP be serially monitored to gauge the efficiency of treatment of spinal infections.24 Blood cultures are reported to be positive in 25% of spinal infections61 in adults and up to 50% in childhood discitis,62 if taken at the time of a rigor.

Diagnostic procedures CT-guided percutaneous biopsy accurately predicts the invading organism in 37% of childhood discitis7 and 60–70% of adult cases.62 Cultures may be negative if the patient has been previously administered antibiotics. Histological examination will exclude tumors and foreign body granulomas. Gram stain and acid-fast stain as well as cultures for aerobic, anaerobic, fungal, and TB cultures of fresh material will maximize the chances of an accurate diagnosis. Bacterial cultures should be maintained for a minimum 10 days to detect indolent organisms. The volume of material obtained reflects the degree of accuracy in diagnosis. A tissue core obtained through a Craig biopsy needle or a TruCut (Baxter Travenol) needle generally provides more material than a fine needle aspiration, unless forced aspiration is applied as the needle is withdrawn. An open surgical

408

biopsy has a higher yield for the confirmation of a positive bacterial culture62 and is obligated if CT-guided aspiration fails to grow an organism and the patient does not respond to antistaphylococcal antibiotics (Fig. 36.7)

MANAGEMENT Nonoperative The management of spinal infection changed in the 1940s and 1950s with the introduction of penicillin and other antibiotics. The traditional treatment prior to this was rest in bed and immobilization. Today, treatment of individual spinal infections depends on the nature of the invading organism, the host resistance, and the stage of spinal infection at the time of diagnosis (acute, subacute, chronic). Ideal nonoperative management involves establishing the diagnosis, isolating the causative organism, providing or restoring nutrition to the host to fight the infection, maintaining spinal stability, eliminating the invading organism initially with intravenous antibiotics, and detecting early neurological deficit. Broadly, definitive antibiotic medication management commences after procuring positive cultures and sensitivities of the invading organisms. The duration of antibiotic therapy is variable. For pyogenic infections, intravenous antibiotics are continued empirically for approximately 6 weeks. The patient’s reaction to the infection is monitored by serial white cell count, ESR, and C-reactive protein. Oral antibiotics are generally ceased when the ESR has returned to less than 20.63 Failure of nonoperative treatment is high in immunocompromised patients –18/57 HIV positive and 42/57 intravenous drug abusers.64

Section 1: Medical Spinal Disorders

Suspected infection of spine

Haematologic investigations White cell count ESR CRP

+

Secondary imaging: CT MRI

Plain x-ray

+

–

Scintigraphy

–

Discharge

CT guided biopsy Histology Gram stain C/8 – up to 1+ days to include anaerobic cultures + Fig. 36.7 Diagnosis of spine infection.

Probable/confirmed infection

Specific infections Childhood discitis Childhood discitis can usually be treated nonoperatively. In the past, no difference has been reported in the outcome for infants receiving antibiotics and those treated with bed rest alone.65–69 Immunocompetent infants who are systemically well are more likely to respond to this management. However, prolonged or recurrent symptoms can occur in children not initially receiving intravenous antibiotics.70 For this reason, intravenous antibiotics are now recommended for initial management.2,5,11,71,72 Recommendations for the ideal length of an intravenous antibiotic course range from 1 to 8 weeks.5,6,11,12 Generally, intravenous antibiotics are administered for up to 2 weeks followed by oral antibiotics for up to 6 weeks. Response to antibiotic treatment is monitored by weekly white cell count, ESR, and C-reactive protein. Patients should be followed up for at least 12–18 months after resolution of spinal pain and malaise. The indications for repeat radiological assessment include a recurrence of symptoms or failure of the ESR and CRP to return to normal. Narrowing of the disc space and vertebral endplate sclerosis are expected;5 however, 20% infants and 30% older children demonstrate spontaneous fusion.10,66 If an infant develops vertebral osteomyelitis, an extreme form of angular kyphosis may develop.1 As bone necrosis is rare in infantile discitis, the only explanation is that the vertebral growth plates are destroyed as a result of the infection. The indications for considering surgical debridement of the disc/vertebrae are continuing septicemia during an antibiotic course or progressive neurological deficit.11,73 An updated algorithm for investigating/managing childhood discitis is: 1. Initial leukocyte count, differential, ESR and CRP; 2. Blood cultures;

3. Spinal biopsy recommended only for failure of conservative management or for immunocompromised or immunosuppressed patients; 4. Rest in bed without spinal immobilization for immunocompetent infants; 5. Empiric antistaphylococcal parenteral antibiotics for 2–6 weeks (or when the CRP returns to <10) followed by oral antibiotics until the ESR returns to <15; 6. Indications for surgical debridement are: A. Septicemia not controlled by antibiotics; B. The development of a neurological deficit.

Pyogenic discitis and spondylodiscitis Nonoperative treatment including rest and antibiotics is indicated for patients without neurological deficit or progressive spinal deformity. Prognostic factors for successful nonoperative management include age under 60 years, immunocompetence, a decreasing ESR, and infection involving an organism other than S. aureus. Ninety percent patients treated nonoperatively are pain free and 75% have a bony or short fibrous union within 2 years of the onset of infection.28 However, longer-term outcomes in larger series portray a poorer outcome, with up to 75% having severe chronic spinal pain and an inability to work.18 Indications for surgical debridement are failure of nonoperative treatment manifest by continuing sepsis, development of a neurological deficit, or increasing/significant spinal deformity. Hodgson and Stock popularized anterior debridement and bone grafting for spinal tuberculosis in 1960 following publication of successful outcomes in terms of spinal stability and alignment.74 Subsequently, others reported successful outcomes following anterior debridement and bone grafting for pyogenic and fungal infections.17,21,75,76 A costotransversectomy approach to the thoracic spine may be indicated for unilateral abscess drainage or in a fragile patient. Thoracic

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endoscopically assisted abscess drainage or spinal debridement may be indicated in unwell or older patients with comorbidities. However, mixed outcomes from minimally invasive techniques for spinal debridement have been reported with an increased complication rate and conversion to an open procedure.24 Minimally invasive techniques may have an impact on surgical debridement for spine infection in the future. Anterior surgery involves thorough debridement of the disc and vertebral bodies back to normal bleeding bone and anterior reconstruction with bone graft. Tricortical iliac crest or middle third of fibula bone grafting is recommended in adults. Rib graft is useful in children. Vascularized rib and iliac crest grafts unite to the host spine faster than free bone grafts.77 Disadvantages of using vascularized bone grafts are the protracted surgical time and the number of theater personnel required. Fresh frozen cortical allografts are indicated for a large defect created by spinal debridement. Harvesting a very large piece of tricortical iliac crest may create donor site pain, although back-filling the defect with a bone graft substitute is now popular as it may reduce future donor site pain. Fresh frozen cortical allografts should be supplemented with autogenous cancellous bone graft. Recently, successful outcomes have been reported following anterior reconstruction using titanium cages or mesh filled with autogenous cancellous bone graft.78,79 Posterior spinal instrumentation is recommended following extensive anterior debridement, to correct/minimize kyphosis and to allow early patient ambulation.80,81 Posterior stabilization is often delayed following anterior debridement if medical, hematological, and nutritional interventions are thought to be helpful in optimizing the patient’s recovery, if initial surgery is protracted, or if the patient is not robust enough to continue the procedure. Limited data on the outcomes following simultaneous debridement and anterior instrumentation in the thoracic and lumbar spines are available.78,82–84 Both patients in one report had complications,78 one subsequently dying of sepsis and the other developing recurrent osteomyelitis and subsequent angular kyphosis. Anterior debridement and instrumentation has better results if performed in the

cervical spine.85–87 Outcomes following all types of surgery are satisfactory in 79%18 and depend on the absence of residual neurological deficits. Mortality from spondylodiscitis treated with or without surgery ranges from 3% in patients who are neurologically intact17 to 16%15,17,18 who are neurologically impaired. Advancing age, neurological deficit, immune incompetence, delay in diagnosis, and the presence of diabetes mellitus are the commonest factors identified causing mortality.15,17,18 McHenry et al.18 reported mortality in five of seven neurologically impaired patients in 253 cases of spondylodiscitis. The other two remained significantly disabled. The recovery of neurological function following surgical debridement varies according to whether the deficit is complete or incomplete prior to surgery. Carragee reported that of 33 patients with neurological deficits, nine developed a complete spinal cord lesion of whom four recovered completely and three incompletely.17 Of 21 patients with incomplete spinal cord lesions, only nine recovered completely. Additionally, new postoperative neurological deficits developed in three patients, all subsequently resolving completely.17 Others have reported similar percentages of postoperative recovery of neurological function.15 McHenry et al. reported outcomes of 253 infected spines with a median age of 60 years. Neurological improvement or recovery was reported in 86 of 109 patients treated surgically.18 When neurological decompression was completed via an anterior approach, 83% had a satisfactory outcome, and when completed via a posterior approach, 57% had a satisfactory outcome (p =0.067).11 Carragee reported 8% of surviving patients having chronic severe spinal pain at minimum 2 years follow-up following treatment for vertebral osteomyelitis.17 Causes of chronic spinal pain included pseudarthrosis, kyphosis at the level of the infection, and rheumatoid arthritis in other spinal joints. Hadjipavlou et al. reported residual spinal pain in 64% of those treated nonoperatively versus 26% following surgical debridement and arthrodesis.46 Spontaneous bony ankylosis occurred in 35%.46 McHenry et al.18 reported relapse of infection in up to 14% with a mean follow-up of 6.5 years, with 75% of relapses occurring within 12 months of the initial infection. Factors associated with relapse include inadequate surgical debridement or drainage of a

Management of vertebral column infection Spondylodiscitis Osteomyelitis

Epidural abscess

Major. Epidural abscess – single vertebral level Extensive bone destruction Deformity Neurology Instability

Minor. Minimal destruction of endplates +/– disc narrowing No deformity No neurology No cord compression

Neurological or major compression

Yes No psoas abscess

Psoas abscess

Conservative Rx Resolved

Sx Mini-invasive Failed

Resolved

Failed

Anterior debride Reconstruct/graft Drain psoas abscess +/– Anterior spinal instrumentation Deformity Instability

410

Decompression laminectomy over length of abscess

Posterior instrumentation and fusion

Fig. 36.8 Management of vertebral column infection.

Section 1: Medical Spinal Disorders

sinus, suboptimal antibiotic therapy, the presence of gross vertebral destruction, and recurrent bacteremia. The presence of a relapse of spinal pain is regarded as a red flag sign of relapse of the spinal infection.18 About one-half of the surviving patients return to work and reasonably normal activities of daily living following treatment for spondylodiscitis (Fig. 36.8).88

Epidural abscess/infection Staphylococcus is the usual cause. MRI confirmation is critical for early diagnosis and treatment. Nonoperative management is preferred only if the patient is not septicemic and has no neurological deficit (rare), if the patient is not expected to survive surgery, or if complete spinal cord paralysis has been present for 48 hours.89 Urgent surgical drainage results in the best neurological recovery.9,23,45,89 Hadjipavlou et al.46 reported 100% neurological recovery following paraparesis. If epidural granulation tissue rather than pus was found, the neurological recovery was also 100%.46 However, recovery of neurological deficit was evident in only 18% of all cases including complete paralysis following surgery. Single-level epidural abscess anterior to the spinal cord/cauda equina is best treated with corpectomy/abscess debridement followed by strut bone grafting and stabilization by anterior instrumentation. Multiple-level epidural abscess noted posterior to the neural elements can be treated by either multilevel lamino-foramenotomy or contiguous laminectomy, followed by clinical assessment of spinal stability. Supplementary posterolateral bone grafting is only required for multiple-level contiguous laminectomy. Posterior instrumentation is required only infrequently if deformity is present/imminent. Mortality has not recently been reported following childhood epidural abscess;9 however, morbidity from neurological deficit is 18%.9 Mortality in adults ranges from 5% to 23%.9,90 The presence of a low platelet count of less than 100 × 109/L is associated with a poorer outcome.45

Postoperative spinal infections Generally, it is recommended that spinal instrumentation be removed if the patient exhibits uncontrollable local or general sepsis or if the posterior arthrodesis is radiologically united when wound debridement is undertaken.91–93 Recommendations for the management of early postoperative spine infection include thorough wound debridement with up to 9 liters pulsatile lavage irrigation and parenteral antibiotics.27 Satisfactory outcomes have been reported when the instrumentation is left in situ, if debrided back to healthy viable tissue. If necrotic tissue is present, repeat wound debridement is recommended and delayed primary closure is inevitable.29,42 The use of continuous irrigation with antibiotic-laden fluid for a period of 5 days postoperatively combined with primary wound closure is successful.91,93 Antibiotic impregnated polymethylmethacrylate beads are beneficial when repeated surgical debridement is required for severe spinal infection.94 If severe vertebral osteomyelitis complicates late infection, it can only be effectively treated by a ‘radical’ debridement of a pedicle screw tract/other vertebral element, back to normal bleeding bone. A large defect in the pedicle and vertebral body may sometimes result from debridement. Supplementary autogenous bone grafting of the large defect should be beneficial. If the spinal infection is severe, delayed primary closure is advantageous.29 If the posterior bone graft is not sound when debridement for infection is undertaken, stability of the potentially unstable spine may be regained through the use of external orthoses and/or delayed spinal instrumentation through a clean surgical field. Simultaneous debridement/exchange posterior instrumentation for spinal infection has not been reported.

Facet joint infection Because the diagnosis is invariably delayed, it is difficult to eradicate by nonoperative means. Good results are reported following surgical joint debridement.48 Noninstrumented posterolateral arthrodesis is indicated following extensive facet joint debridement or when the contralateral facet joint is subluxed on preoperative imaging.

PROPHYLAXIS Postoperative spinal infection Postprocedural spine infection rates range from 0.7% to 11.9%.29 Risk factors for iatrogenic infection include postoperative bowel and bladder continence, posterior approach, procedure for resection of tumor, morbid obesity (BMI greater than 35),95 arthrodesis and the use of spinal instrumentation.29,33,96,97 Using prophylactic gentamicin or cephalosporin reduces postdiscectomy wound infections by 100%, from 2% to 1%.98,99 A recent meta-analysis confirms the efficacy of prophylactic antibiotics in spine surgery.100 The British Society for Anti-Microbial Chemotherapy Working Party recommends a first- or second-generation cephalosporin for adequate infection prophylaxis.101 Exceptions include patients who are allergic to these antibiotics or are known to be colonized or infected with MRSA. These patients should receive vancomycin or teicoplanin plus gentamicin. Single doses at induction of anesthesia are adequate unless the procedure extends beyond 4 hours, in which case 50% of the initial dosage of intraoperative antibiotics should be administered every 4 hours. Although there are no reports regarding the ideal duration of postoperative prophylactic antibiotic administration, there is no demonstrable benefit from continuing intravenous antibiotics longer than 24 hours.102

Prophylaxis following interventional procedures Interventional procedures on intervertebral discs uncommonly result in discitis (lumbar discography,103 chemodiscolysis with chymopapain, nucleodiscectomy (ONIK), and laser discectomy.104 A 1% infection rate follows cervical discography.25,105 Septic arthritis of a facet joint following a diagnostic facet joint injection is exceedingly rare.49 It is recommended that patients undergoing percutaneous procedures have a single dose of antibiotics at the time of intervention. Choices of antibiotics are the same as those for open procedures.

Prevention of discitis following spinal surgery Rhode reported success in totally preventing postoperative discitis by leaving a gentamicin-containing absorbable sponge within the disc following microdiscectomy in 1134 consecutive patients.99 His previous 508 consecutive patients had no prophylaxis and 3.7% developed discitis. Intraoperative irrigation with bacitracin-loaded saline is less effective, reducing the rate of postoperative discitis to 0.2–1.2%.43,99 The incidence of postoperative discitis following prophylactic parenteral gentamicin or cephalosporin administration varies from 0% to 0.5%.99 Experimentally, antibiotics are unable to arrest the progression of established discitis in a sheep model.106 However, the incidence of discitis in this sheep model was zero when 1 g of cefalozin was administered intravenously 30, 60, and 120 minutes prior to an intradiscal injection of 20 Staphylococcus epidermidis in 0.1 mL of Conray 280. Cefalozin was detected in the anulus fibrosus only if the antibiotic was given 30 minutes prior to the procedure and not when it was administered 60 or 120 minutes earlier. Results are similar in human discs with the highest intradiscal levels of antibiotics being recorded 30 minutes after the parenteral 411

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administration of antibiotic.107 Antibiotics which are known to penetrate the nucleus pulposus include aminoglycosides, glycopeptides, and clindamycin.99 Those that do not penetrate the nucleus pulposus include penicillins and cephalosporins. The current recommendation for antibiotic prophylaxis is to administer a single intravenous dose of an appropriate antibiotic 30 minutes prior to the surgical procedure, unless surgery lasts longer than 4 hours.24,99 At this point, an extra dose equaling 50% of the first dose of antibiotic is recommended.101

Wound irrigation and protection Saline irrigation has not been definitively proven to be of benefit in reducing the incidence of wound infection, although wound contamination is reduced.99 The use of iodinated occlusive sticky surgical drapes has not been demonstrated to lower deep wound infection in hip surgery.108 There are no similar reports involving spine surgery.

Wound drainage systems Little evidence for or against use of drains is reported.99 There is probably a good indication to use drains in patients with a bleeding diathesis or when surgery is complicated by excessive bleeding to prevent possible neurological complications from an excessively large wound/epidural hematoma.

TUBERCULOUS SPINAL INFECTION Tuberculous infection is still prevalent world-wide, accounting for about one-third of all bone and joint infections. Three and one-half million die of tuberculosis annually.109 Three percent of tuberculosis infections involve the skeleton, of which one-half involve the spine. Three-quarters of spine infections involve the thoracic region and 20% are in the lumbosacral spine. Tuberculosis is endemic in some Asian, African, and Central American countries and is more prevalent in patients infected with the human immunodeficiency virus.109

Pathogenesis and natural history Tuberculous infections progress slowly as the organisms are often indolent. Three species of Mycobacterium are known to infect humans: M. tuberculosis, bovis, and africanum.109 They are all strict aerobic organisms and invade the lungs of humans. Miliary spread of the bacilli can occur to all organs. Bacilli invade the vertebral body through the microvenous circulation adjacent to the vertebral endplate. Spinal tuberculosis is manifest most commonly in the thoracolumbar junction which parallels the entry of the renal veins. A granuloma can form under the anterior longitudinal ligament and spread to a number of spinal segments (anterior granuloma) before detection.109 Primary granulomatous lesions have also been reported in the laminae, pedicles, facet joints, and even spinous processes– appendiceal lesions.109 The pathogenesis of tuberculous and pyogenic spondylodiscitis is different. Typically, bacilli start a slow inflammatory response with the formation of a tuberculous granuloma in the vertebral endplate. It caseates centrally and forms an abscess. The untreated abscess may extend in any direction. Paravertebral extension and swelling are common. Paravertebral and psoas abscesses may become large and eventually a ‘cold’ abscess may result. A sinus then develops, usually just below the groin or above the iliac crest and occasionally on the medial side of the thigh or even the popliteal fossa. In the neck, large abscesses are more common in children than adults, sometimes causing compression of adjacent structures.109 The abscess may also extend into the spinal canal. Bacilli do not produce proteolytic enzymes. The intervertebral disc is not destroyed in the same way as pyogenic spinal infections. The 412

vertebral endplate is a temporary barrier to the spread of infection but the intervertebral disc is eventually involved. Tuberculous spondylodiscitis usually results in a fibrous ankylosis. When osteomyelitis becomes established, pathological fracture of the vertebral body may eventually result in angular kyphosis, which is commonest in the thoracic spine. The spinal canal may be further compromised by sequestration of vertebra and disc or by dislocation of one spinal segment. Contiguous vertebral involvement can be evident in spinal tuberculous infection. Neurological deficits can result from neural compression or stretching from spinal fracture/angulation as well as (1) thecal compression by an epidural granuloma, (2) intramedullary or intradural tuberculous infection (rare), (3) microvascular compromise, or (4) tuberculous meningitis.109 Neurological deficits are present in 10–60% of tuberculous spondylitis at presentation.109

Clinical features Presentations are variable, depending on the age and general condition of the patient, the delay in diagnosis, and the presence of neurological deficits. Symptoms include fever, anorexia, weight loss, and night sweats. Eventually, the patient complains of an insidious onset of spinal pain. The patient may have angular kyphosis, draining sinuses, torticollis, stridor and even dysphagia at presentation. The leukocyte count is normal and the ESR elevated above 20 mm/hour in at least 80% of patients.109 The Mantoux (tuberculin skin) test is nearly always positive. Definitive diagnosis only follows positive culture of a CT-guided needle, or occasionally open, biopsy of the spine. Positive cultures may not be evident for a number of weeks following biopsy. More recently, polymerase chain reaction (PCR) techniques have hastened diagnosis.

Radiology Fine calcification is often noted initially in the paravertebral soft tissue swelling over 2–3 segments. Early occult changes in the trabecular pattern of the vertebra adjacent to the infected endplate are best seen on CT. MRI sequences are no different from any other type of spinal infection. Low signal intensity is noted in the bone marrow on T1-weighted sequences and high signal intensity on T2-weighted sequences. Gadolinium enhances the image signals in areas of bone infection. Spinal cord tuberculomas and tuberculous arachnoiditis (radiculomyelitis) are manifest by loculated abscesses in the subarachnoid space, which may eventually be obliterated by granulomatous invasion. Technetium bone scans are negative in 35% cases and gallium scans can be negative in up to 70%. Late radiological features of spinal tuberculosis include pathological fracture, angular kyphosis, and gross intervertebral disc destruction.

Nonoperative management Antituberculous chemotherapy, rest, and enhanced nutrition are recommended for most patients. Neurologically intact patients have a 93% good outcome, according to the Medical Research Council (MRC). The latest MRC recommendation for therapy is isoniazid and rifampicin, although other drugs including pyrazinamide, streptomycin, and ethambutol have proven to be just as effective. Chemotherapy is usually continued until the ESR has returned to normal and the radiological features demonstrate quiescence of the infection.

Surgery Indications for surgery parallel those for pyogenic infection. Although patients with mild neurological deficit have been reported to have up to 79% improvement with chemotherapy alone, more recent

Section 1: Medical Spinal Disorders

reports have demonstrated up to 94% improvement when surgery is performed as early as possible, followed by chemotherapy.109 Early debridement and bone graft of all tuberculous spinal cases by an anterior approach has always been preferred in Hong Kong.74 Long-term results from this treatment are superior to nonoperative management in terms of spinal stability and alignment, with less angular kyphosis. Most recent reports have emphasized better outcomes when the anterior bone graft is combined with anterior instrumentation, although posterior instrumentation is equally effective.109,110 Whether anterior or posterior instrumentation with bone graft is used, better spinal alignment is maintained long-term following instrumentation.109 A costotransversectomy approach was preferred 50 years ago but is now used only when the patient is fragile.

FUNGAL SPINE INFECTIONS Fungi reported to cause spine infections in humans are summarized in Table 36.2. Fungi are slow-growing, indolent, and non-caseating organisms. They are capable of widespread dissemination throughout the body and spinal involvement sometimes plays only a minor part. Spinal infection often causes a paucity of symptoms, and a late presentation can mimic tuberculous spine infection. Aspergillus spinal osteomyelitis has been reported following organ transplantation and chemotherapy.111,112 Spinal infection is rare, with 50 reported cases113 and results in death if untreated.111 Treatment with amphotericin B of 1 mg/kg/day initially, followed by antifungal medication for 12 weeks up to 3 years is considered ideal treatment.114 The mortality rate following antifungal medication and surgical debridement is 25%114 and neurological deficits are noted in 30%.113 Only 60 cases of Candida vertebral osteomyelitis have been reported.115 Candida albicans is the commonest species involved (62%). Nearly all cases involve the lower thoracic or lumbar spine. Most cases have back pain for longer than 1 month, one-third have an elevated temperature at presentation, and about 20% have neurological deficits. Eighty-five percent of cases have a good outcome following treatment with amphotericin and surgical debridement.115 Coccidioides spine infection is uncommon and typically affects immunocompromised individuals. Spinal involvement usually follows disseminated disease in 100 reported cases.116–119 Neurological deficit is evident in 20% cases. Mortality is reported in 20% following treatment with amphotericin and surgical debridement. Long-term antifungal therapy is recommended.116 Cryptococcal spine infection is uncommon.120,121 There is difficulty radiologically differentiating cryptococcal from tuberculous spine infection. All patients succumb without antifungal medication. Fluconazole, flucytosine,120 and amphotericin B121 have recently been successful in terms of patient survival. Neurological recovery may also follow this treatment with three of five recovering neurological function completely.121 Histoplasma spondylodiscitis is rare and also difficult to separate radiologically from tuberculous infection. Ketoconazole medication and surgical debridement were successful in a single case. Another case presented with complete paralysis.122 Nocardia asteroides spondylodiscitis is rare, with 11 reported cases.123 Successful outcomes have been reported following surgical debridement and long-term antifungal medication.123

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57. Ozuna R, Delamarter R. Pyogenic vertebral osteomyelitis and postsurgical disc space infections. Orthop Clin N Am 1996; 27:87–94.

87. Przybylski G, Sharan A. Single-stage autogenous bone grafting and internal fixation in the surgical management of pyogenic discitis and vertebral osteomyelitis. J Neurosurg 2001; 94S:1–7.

58. Boden S, Davis D, Dina T, et al. Postoperative diskitis: Distinguishing early MR imaging findings from normal postoperative disk space changes. Radiology 1992;1 84:765–771. 59. Grand C, Bank W, Baleriaux D, et al. Gadolinium enhancement of vertebral endplates following lumbar disc surgery. Neuroradiology 1993; 34:503–505. 60. Ruiz A, Donovan-Post J, Sklar E, et al. MR imaging of infections of the cervical spine. MRI Clin N Am 2000; 8:561–579. 61. Weisz R, Errico T. Spinal infections. Diagnosis and treatment. Bulletin Hospital for Joint Diseases 2000; 59:40–46. 62. Tay B, Deckey J, Hu S. Spinal infections. J Am Acad Orthop Surgeons 2002; 10:188–197. 63. Collert S. Osteomyelitis of the spine. ACTA Orthopaed Scand 1977; 48:283.

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64. Rezai A, Woo H, Errico T, et al. Contemporary management of spinal osteomyelitis. Neurosurgery 1999; 5:1018–1025.

88. Jiminez-Mejias M, Colmenero J, Sanches-Lora F, et al. Postoperative spondylodiskitis: Etiology, clinical findings, prognosis and comparison with nonoperative pyogenic spondylodiskitis. Clin Infect Dis 1999; 29:339–345. 89. Sampath P, Rigamonti D. Spinal epidural abscess: A review of epidemiology, diagnosis and treatment. J Spinal Dis 1999; 12:89–93. 90. Rigamonti D, Liem L, Sampath P, et al. Spinal epidural abscess: contemporary trends in etiology, evaluation, and management. Surg Neurol 1999; 52:189–197. 91. Soultanis K, Mantelos G, Pagiatakis A, et al. Late infection in patients with scoliosis treated with spinal instrumentation. Clin Orthop 2003; 411:116–123. 92. Clark C, Shufflebarger H. Late-developing infection in instrumented idiopathic scoliosis. Spine 1999; 24:1909–1912.

Section 1: Medical Spinal Disorders 93. Richards B. Delayed infections following posterior spinal instrumentation for the treatment of idiopathic scoliosis. J Bone Joint Surg 1995; 77A:524–529.

109. Khoo L, Mikawa K, Fessler R. A surgical revisitation of Pott distemper of the spine. Spine J 2002; 3:130–145.

94. Glassman S, Dimar J, Puno R, et al. Salvage of instrumented lumbar fusions complicated by surgical wound infection. Spine 1996; 21:2163–2169.

110. Yilmaz C, Selek H, Gurkan I, et al. Anterior instrumentation for the treatment of spinal tuberculosis. J Bone Joint Surg 1999; 81A:1261–1267.

95. Olsen M, Mayfield J, Lauryssen C, et al. Risk factors for surgical site infection in spinal surgery. J Neurosurg 2003; 98(Suppl 2):140–155.

111. Andriole V. Infections with Aspergillus species. Clin Inf Dis 1993; 17:S481– S486.

96. Roberts F, Walsh A, Wing P, et al. The influence of surveillance methods on surgical wound infection rates in a tertiary care spinal surgery service. Spine 1998; 23:366–370.

112. Patterson T, Miniter P, Patterson J, et al. Aspergillus antigen detection in the diagnosis of invasive aspergillosis. J Infect Dis 1995; 171:1553–1558.

97. Capen D, Calderone R, Green A. Perioperative risk factors for wound infection after lower back fusions. Orth Clin N Am 1996; 27:83–86. 98. Mastronardi L, Tatta M. Intraoperative antibiotic prophylaxis in clean spinal surgery: a retrospective analysis in a consecutive series of 973 cases. Surg Neurol 2004; 61:129–135. 99. Rohde V, Meyer B, Schaller C, et al. Spondylodiscitis after lumbar discectomy. Spine 1998; 23:615–620.

113. Vinas F, King P, Diaz F. Spinal Aspergillus osteomyelitis. Clin Infect Dis 1998; 28:1223–1229. 114. Salvalaggio P, Bassetti M, Lorber M, et al. Case report: Aspergillus vertebral osteomyelitis after simultaneous kidney–pancreas transplantation. Transplant Infect Dis 2003; 5:187–189. 115. Miller D, Mejicano G. Vertebral osteomyelitis due to Candida species: case report and literature review. Clin Inf Dis 2001; 33:523–530.

100. Barker F. Efficiency of prophylactic therapy in spinal surgery: A meta-analysis. Neurosurgery 2002; 51:391–401.

116. Wrobel C, Chappell E, Taylor W. Clinical presentation, radiological findings, and treatment results of coccidioidomycosis involving the spine: a report on 23 cases. J Neurosurg 2001; 95(1 Suppl):33–39.

101. Brown E, Pople I, de Louvois J, et al. Spine update: Prevention of postoperative infection in patients undergoing spinal surgery. Spine 2004; 29:938–945.

117. Herron L, Kissel P, Smilovitz D. Treatment of coccidioidal spinal infection: Experience in 16 cases. J Spinal Dis 1997; 10:215–222.

102. Dimick J, Lipsett P, Kostuik J. Spine update: antimicrobial prophylaxis in spine surgery: basic principles. Spine 2000; 25:2544–2548.

118. Kushwaha V, Shaw B, Gerardi J, et al. Musculoskeletal coccidioidomycosis. A review of 25 cases. CORR 1996; 332:190–199.

103. Fraser R, Osto O, Vernon-Roberts B. Discitis after discography. J Bone J Surg 1987; 69B:26–35.

119. Zeppa M, Laorr A, Greenspan A, et al. Skeletal coccidioidomycosis: imaging findings in 19 patients. Skeletal Radiol 1996; 25:337–343.

104. Zeiger H, Zampella E. Intervertebral disc infection after lumbar chemonucleolysis: report of a case. Neurosurg 1986; 18:616–621.

120. Cook P. Successful treatment of cryptococcal osteomyelitis and paraspinous abscess with fluconazole and flucytosine. South Med J 2001; 94:936–938.

105. Zeidman S, Thompson K, Ducker T. Complications of cervical discography: analysis of 4400 diagnostic disc injections. Neurosurg 1995; 37:414–417.

121. Govender S, Mutasa E, Parbhoo A. Cryptococcal osteomyelitis of the spine. JBJS (Br) 1999; 81:459–461.

106. Fraser R, Osti O, Vernon-Roberts B. Iatrogenic discitis: the role of intravenous antibiotics in prevention and treatment, an experimental study. Spine 1989; 14: 1025–1032.

122. N’dri Oka D, Varlet G, Kakou M, et al. Spondylodiscitis due to Histoplasma duboisii. Report of two cases and review of the literature. Neurochirurgie 2001; 47:431–434.

107. Boscardin J, Ringus J, Feingold D, et al. Human intradiscal levels with cefazolin. Spine 1992; 17(Suppl):145–148.

123. Graat H, Van Ooij A, Day G, et al. Nocardia farcinica spinal osteomyelitis. Spine 2002 27:E253–E257.

108. Chiu K, Lau S, Fung B, et al. Plastic adhesive drapes and wound infection after hip fracture surgery. Aust NZ J Surg 1993; 63:798–801.

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Section 1

Medical Spinal Disorders

CHAPTER

Nonosseous Spinal Tumors

37

M. Sean Grady, James Schuster and Thomas Metkus

INTRODUCTION Only 15% of primary central nervous system (CNS) tumors are intraspinal.1 Nonosseous spinal tumors represent a collection of pathologic entities that are difficult to differentiate from each other based on clinical findings, and more importantly are sometimes difficult to distinguish from the much more common degenerative spinal disorders. Obviously, it is important to make this distinction when evaluating patients with spinal disorders, but the ready availability of high-resolution imaging has removed the majority of suspense in making these distinctions. However, a basic understanding of the pathophysiology of spinal tumors and the key elements in the history and physical examination that help differentiate them from degenerative spinal pathologies are essential to avoid delayed or erroneous diagnosis. A suspicion of a spinal tumor may lead to earlier spinal imaging, as well as more comprehensive imaging to include portions of the spine that would otherwise not be imaged. We cannot overemphasize the importance of evaluating the history and physical examination for inconsistencies and ‘red flags’ such as a history of systemic malignancy, family history of syndromic tumors (neurofibromatosis, von Hippel – Lindau), nocturnal or recumbent pain, unusual radicular or medullary (burning, dysesthetic, nonradicular, as with a syrinx) symptoms, spasticity or other pathologic reflexes, bowel/bladder/sexual involvement. One additional difficulty in differentiating spinal tumor types from each other is that because the majority of symptoms are from compression, symptomatology in general is more related to the level of the lesion that the identity of the lesion itself. However, as will be discussed in subsequent sections, there is a regional predilection for each tumor and some lesions have distinct clinical findings secondary to associated pathologic changes (i.e. a syrinx associated with an intramedullary tumor). Our intention with this chapter is to give a concise and organized summary of nonosseous spinal tumors in addition to suggesting a rational approach to differentiating these lesions from more common spinal pathologies. Nonosseous spinal tumors can be generally separated in three general categories: (1) extradural (55–60%), arising in the epidural space or in vertebral bodies; (2) intradural/extramedullary (30–40%); and (3) intramedullary (5–10%).2 These distinct categories are somewhat oversimplified as some tumors can span more than one compartment. Additionally, while metastasis can be found in all groups, the vast majority are extradural.

little or no bone involvement (Fig. 37.1).3 Schwannomas and meningiomas can be wholly or partially extradural but these tumors will be covered in the section on intradural/extramedullary tumors. Other more unusual causes of extradural spinal cord compressions include benign angiolipomas.4 Epidural lipomatosis is an infrequent cause of epidural spinal cord compression associated with chronic steroid use.5 Finally, epidural abscess can present as a mass lesion with or without associated discitis and osteomyelitis (Fig. 37.2).

INTRADURAL/EXTRAMEDULLARY TUMORS The majority of intradural/extramedullary (ID-EM) tumors (90%) are either nerve sheath tumors or meningiomas. Other less common lesions include paragangliomas, metastasis, congenital/developmental lesions (dermoid, epidermoid, lipoma, neurenteric cyst, arachnoid cyst), granulomatous/inflammatory disease (sarcoidosis, tuberculoma), and infection (subdural empyema). The clinical features of intradural/extramedullary tumors generally reflect the slow-growing nature of these tumors and are more

EXTRADURAL TUMORS Tumors arising in and from bone will be discussed in other sections of this book. The majority of extradural tumors, with or without bone involvement, are metastatic in nature. Lymphomas are somewhat unique in that they can present with only epidural involvement and

Fig. 37.1 Sagittal T1 MRI with contrast showing compression of the thecal sac from extradural lymphoma.

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Fig. 37.2 Axial T1 MRI with contrast showing epidural abscess with associated discitis.

dependent on location within the spinal axis rather than specific pathology. Upper cervical and foramen magnum lesions often arise ventrally and can present with long tract signs as well as headaches and a syndrome of distal arm weakness, hand clumsiness, and intrinsic hand muscle wasting.6,7 Local/regional pain is a common initial symptom in both nerve sheath tumors and meningiomas. Because of the origin of nerve sheath tumors, they are more likely to also have radicular symptoms.8,9 These regional/radicular symptoms generally precede compressive cord symptoms. Hand and arm weakness as well as local and/or radicular sensory disturbances, and long tract signs, are common in mid and lower cervical lesions. Lateralizing asymmetry including Brown-Séquard type of findings (ipsilateral motor and proprioceptive and contralateral sensory derangement) can also be seen.10 Other less common presenting syndromes include hydrocephalus (thought to be related to increased cerebrospinal fluid [CSF] protein which alters absorption)11 and subarachnoid hemorrhage from schwannomas.12 Thoracic-level lesions often present with variable amounts of back pain and a predominance of long tract signs including: spasticity, weakness, numbness, and sensory gait ataxia. Bowel and bladder symptoms are generally a late finding. Lesions in the cauda equina present very commonly with back and radiating leg pain except for lipomas. Early sphincter disturbances are more common in lesions at the conus or cauda equine.13

Multiple nerve sheath tumors are seen in patients with neurofibromatosis, with neurofibromas predominating in NF1 and schwannomas predominating in NF2. Multiple schwannomas can occur in patients without a recognized genetic predisposition. Approximately 2.5% of nerve sheath tumors show malignant degeneration,9 with more than half associated with neurofibromatosis. Malignant nerve sheath tumors have a very poor prognosis. Most nerve sheath tumors are predominantly intradural; however, 30% show extension along the nerve root sleeve in a dumbbell fashion. Schwanommas with extradural extension (dumbbell schwannomas) often show a smooth expansion of the bony foramen (Fig. 37.3). Extramedullary tumors by definition displace the cord by magnetic resonance imaging (MRI) and myelogram. MRI has become the imaging modality of choice for spinal lesions. The MRI appearance of schwannomas can help differentiate them from meningiomas in that schwannomas are somewhat hypointense to spinal cord on T1 and hyperintense on T2 (Fig. 37.4).2 Enhancement tends to be heterogeneous and a predominantly peripheral pattern of enhancement is not uncommon. This may be due to cystic, hemorrhagic, or necrotic changes. Nerve sheath tumors that are predominantly intradural are usually amenable to complete resection and have a low recurrence rate with complete resection.10 The nerve fibers of origin of the tumor often have to be sectioned to allow complete resection. This rarely results in significant neurologic deficit even at the cervical or lumbar level, as adjacent roots may have assumed some of the neurologic function.8,14–16 However, intraoperative nerve monitoring/stimulation helps guide intraoperative decision-making.

Meningiomas Meningiomas and nerve sheath tumors occur at approximately the same incidence in adults. However, there is an extreme gender bias, as approximately 80% of spinal meningiomas occur in women in the fifth to seventh decades of life.2 Almost 80% occur in the thoracic spine but they are also found in the upper cervical spine and foramen magnum. Almost all meningiomas are completely intradural; however,

Nerve sheath tumors Nerve sheath tumors consist of neurofibromas and schwannomas which have a common cell of origin, the myelin-producing Schwann cell. The distinction is ultimately histopathological, as neurofibromas expand the involved nerve in a fusiform fashion with nerve fibers intermingled in the substance of the tumor. Schwannomas arise in a more eccentric, globoid fashion with a more discrete attachment to the nerve. Nerve sheath tumors account for approximately 40% of intradural/extramedullary tumors in adults, with an annual incidence of 0.3–0.4 per 100 000.9 Men and women are affected equally, and generally within the fourth to sixth decades of life. Most solitary schwannomas are nonsyndromic and are distributed proportionally throughout the spine. 418

Fig. 37.3 Axial T1 MRI showing schwannoma extending and expanding the right neural foramen.

Section 1: Medical Spinal Disorders

removed in 90% of cases. Recurrence rates range 3–23%.17,18 One potential recurrence risk is the extent to which involved dura can be removed. In dura that cannot easily be removed, extensive coagulation is also used. It is unclear if there is a significant difference in recurrence rates between these two methods.18 Often, resection of involved dura aids in removal in accessible areas (dorsal). Dural involvement more ventral is difficult to remove safely and effectively and is probably better coagulated.

Other neoplastic process

Fig. 37.4 Sagittal T2 MRI showing hyperintense schwannoma compressing the thoracic spinal cord.

as many as 10% have an extradural component. The MRI appearance of meningiomas as compared to schwannomas tends to be isointense to spinal cord on T1 and T2 sequences with a tendency towards more homogeneous enhancement (Fig. 37.5). An enhancing dural tail by MRI is also suggestive of a meningioma. Calcification is also a common finding. In general, spinal meningiomas can be completely

As stated previously, metastatic lesions predominate in the extradural space. However, metastasis can be intradural (4%) and should be considered especially in the patient with a known history of systemic malignancy.19 Paragangliomas are rare benign tumors that are histologically related to other nonadrenal paraganglion tumors such as carotid body and glomus jugulare tumors. They tend to be very vascular, well-circumscribed tumors arising from the filum terminale or cauda equine.20 Radiographically, they are difficult to distinguish from filum ependymomas. The histologic determination of neurosecretory granules betrays the neural crest origin of these tumors. Many of the non-neoplastic extramedullary lesions are often developmental in nature and are often associated with other abnormalities including cutaneous lesions and sinus tracts. In addition to presenting as mass lesions, they can be associated with spinal cord tethering. Inclusion-type cysts (dermoid, epidermoid, neurenteric) can also present with recurrent episodes of meningitis. Epidermoids and dermoids are generally developmentally retained ectodermal implants. However, epidermoid tumors were also documented to occur when nonstyleted lumbar puncture needles were used.21 Both have linear growth rates like skin as opposed to the exponential growth rate of neoplasm. Epidermoids are lined by stratified squamous epithelium and the contents include keratin, cellular debris, and cholesterol. They tend to be isointense to CSF by MRI but show diffusion restriction in comparison to arachnoid cysts.21 Dermoids are lined by squamous epithelium but also include dermal appendage organs (hair follicles and sebaceous glands). Their contents are similar to epidermoids but also contain hair and sebum. Their appearance by MRI is variable but classically show patterns similar to fat signal.22 Dorsal arachnoid cysts in the thoracic spine can present as extramedullary mass lesions.23 A neurenteric is a cyst formed by failure of separation of the gastrointestinal tract from the primitive neural crest because of the neural connection with the spinal canal, which may be via a sinus tract or a fibrous band. Neurenteric cysts have a high incidence of associated vertebral anomalies or anterior vertebral defects.24,25 Inflammatory or infectious processes such as sarcoid, tuberculoma, or subdural empyema can present as intradural lesions.26–28

INTRADURAL/INTRAMEDULLARY TUMORS

Fig. 37.5 Sagittal T1 MRI with gadolinium showing the typical homogeneous enhancement of a high cervical meningioma.

Intradural/intramedullary (IM-ID) spinal cord lesions only represent 5–10% of spinal tumors. The majority are either astrocytomas or ependymomas which together make up 95% or ID-IM tumors.29,30 In adults, regional pain is the most common initial presentation, which may precede diagnosis by several months to years.31 The location of the tumor dictates the distribution and progression of symptoms. Upper extremity symptoms occur in cervical lesions, while thoracic lesions produce spasticity and sensory disturbances. Numbness in the lower extremities often progresses from distal to proximal. Conus lesions often present with back pain, leg pain, and early sphincter disturbances.2,10 419

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Astrocytomas Astrocytomas of the spinal cord can occur at any age but predominate in the first three decades of life. They account for 90% of spinal cord tumors in patients less than 10 years old, and 60% in adolescents. The majority of these tumors (60%) are found in the cervical and thoracic regions. There is an associated syrinx in approximately 20% of cases. Spinal cord astrocytomas have a higher incidence in neurofibromatosis. Histologically, most adult spinal astrocytomas are fibrillary in nature. Pilocytic astrocytomas are more common in pediatric cases. Approximately 25% of adult spinal astrocytomas are malignant.31–33 Astrocytomas are hypo- to isointense on T1 and hyperintense on T2. They appear as focal enlargements of the spinal cord and even the lower-grade lesions can have significant enhancement (Fig. 37.6).2

Ependymoma Ependymomas are the most common intramedullary tumors in adults. They occur predominantly in the third through sixth decades of life with a slight male predominance. They commonly occur in the conus and cauda equina where myxopapillary histology predominates.2 These tend to be low grade but can, however, be more aggressive in younger patients and may be refractory to resection if they heavily encase the nerve roots. Symptoms are present 1 year before diagnosis in 82% of cases.10 Intramedullary ependymomas are more commonly found in the cervical cord and frequently (65%) have an associated syrinx.34 There is an association between NF2 and spinal ependymomas. Contrast enhancement is generally intense by MRI with variable homogeneity (Fig. 37.7).

Hemangioblastoma Hemangioblastomas are histologically benign tumors of vascular origin. The peak incidence is in the fourth decade of life. Approximately 25% are associated with von Hippel–Lindau syndrome.35 This is an autosomal dominant condition associated with brain/spine hemangioblastomas, retinal angiomas, and renal cell carcinoma. By MRI, they often show an intensely enhancing nodule associated with a cyst or syrinx. By angiography, they show a robust vascular blush.

Fig. 37.7 Axial T1 MRI with contrast showing a contrast-enhancing spinal ependymoma.

must be considered in patients with a history or suspicion of a systemic malignancy.39 Lipomas occur often in conjunction with spinal dysraphism. Of those not associated with dysraphism, they occur with no sex predominance in the second to fifth decades of life. They often present with ascending mono- or paraparesis. At the conus level they present with early sphincter disturbances and less frequently with pain. They often have intramedullary and extramedullary components.40 By MRI, they show a classic fat pattern. Vascular lesions such as cavernous malformations (Fig. 37.8) or arteriovenous malformations (AVMs) can present with acute onset of symptoms, especially with recurrent hemorrhage.41

Miscellaneous ID-IM lesions Other primary neoplasms found much less commonly in the spinal cord include gangliogliomas,36 subependymomas,37 and oligodendrogliomas.38 Intramedullary metastasis is extremely rare but, again,

Fig. 37.6 Sagittal T2 MRI showing focal expansion of the spinal cord by an astrocytoma. 420

Fig. 37.8 Axial MRI showing a hemosiderin ring around a spinal cavernous malformation.

Section 1: Medical Spinal Disorders 9. Conti P, et al. Spinal neurinomas: retrospective analysis and long-term outcome of 179 consecutively operated cases and review of the literature. Surg Neurol 2004; 61(1):34–43; discussion 44. 10. Schwartz TH, McCormick PC. Spinal cord tumors in adults. In: Winn HR, ed. Youman’s textbook of neurosurgery. Philadelphia: WB Saunders; 2001:4817–4833. 11. Prasad VS, et al. Intraspinal tumour presenting as hydrocephalus in childhood. Childs Nerv Syst 1994; 10(3):156–157. 12. Parmar H, et al. Spinal schwannoma with acute subarachnoid hemorrhage: a diagnostic challenge. Am J Neuroradiol 2004; 25(5):846–850. 13. Bagley CA, Gokaslan ZL. Cauda equina syndrome caused by primary and metastatic neoplasms. Neurosurg Focus 2004; 16(6):e3. 14. Kim P, et al. Surgery of spinal nerve schwannomas. Risk of neurologic deficit after resection of involved root. J Neurosurg 1989; 71(6):810–814. 15. Celli P. Treatment of relative nerve roots involved in nerve sheath tumors: removal or preservation? Neurosurg 2002; 51(3):684–692. 16. Miura T, et al. Resection of cervical spinal neuroma including affected nerve root: recovery of neurologic deficits in 15 patients. Acta Orthop Scand 1998; 69(3):280–282.

Fig. 37.9 Sagittal T1 MRI showing a cervical syrinx.

17. Solero CL, et al. Spinal meningiomas: review of 174 operated cases. Neurosurgery 1989; 25(2):153–160. 18. King AT. et al. Spinal meningiomas: a 20-year review. Br J Neurosurg 1998; 12(6):521–526. 19. Perrin RG, Livingston KE, Aarabi B. Intradural extramedullary spinal metastasis. A report of 10 cases. J. Neurosurg 1982; 56(6):835–837.

A syrinx not associated with tumor can be seen post-traumatically and in association with a Chiari malformation type 1 (Fig. 37.9). Inflammatory processes such as multiple sclerosis and transverse myelitis can often have presentations similar to mass lesions in the spine.42 In addition to presenting as extramedullary lesions, granulomatous conditions such as sarcoid and tuberculoma can present as intramedullary lesions.43,44

CONCLUSIONS Fortunately for the general population, spinal cord tumors are relatively rare. Unfortunately, as with other rare conditions, their diagnosis is often delayed, as their distinct signs and symptoms blend into a background of much more common degenerative and musculoskeletal disorders. Retrospectively, in almost every case there are ‘red flags’ in the history and physical examination (nocturnal/recumbent pain; unusual radicular, regional or medullary symptom; crossed sensory/motor finding; sphincter disturbance; spasticity) that, if detected, would have led to earlier diagnosis, as these complaints and findings often predate diagnosis by several months to years. Our goal with this chapter has been to provide a general overview of nonosseous spinal cord lesions to aid clinicians in the early diagnosis and management of these lesions.

References 1. Kopelson G, et al. Management of intramedullary spinal cord tumors. Radiology 1980; 135(2):473–479.

20. Sundgren P, et al. Paragangliomas of the spinal canal. Neuroradiology 1999; 41(10):788–794. 21. Lai SW, et al. MRI of epidermoid cyst of the conus medullaris. Spinal Cord 2005; 43(5):320–323. 22. Krishna KK, et al. Dermoid of the conus medullaris. J Clin Neurosci 2004; 11(7):796–797. 23. Wang MY, Levi AD, Green BA. Intradural spinal arachnoid cysts in adults. Surg Neurol 2003; 60(1):55–56. 24. Lippman CR, et al. Intramedullary neurenteric cysts of the spine. Case report and review of the literature. J Neurosurg Spine 2001; 94(2):305–309. 25. Singhal BS, et al. Intramedullary neurenteric cyst in midthoracic spine in an adult: a case report. Neurol India 2001; 49(3):302–304. 26. Bernaerts A, et al. Tuberculosis of the central nervous system: overview of neuroradiological findings. Eur Radiol 2003; 13(8):1876–1890. 27. Bose B. Extramedullary sarcoid lesion mimicking intraspinal tumor. Spine J 2002; 2(5):381–385. 28. Greenlee JE. Subdural empyema. Curr Treat Options Neurol 2003; 5(1):13–22. 29. Bowers DC, Weprin BE. Intramedullary spinal cord tumors. Curr Treat Options Neurol 2003; 5(3):207–212. 30. Kane PJ, et al. Spinal intradural tumours: Part II – Intramedullary. Br J Neurosurg 1999; 13(6):558–563. 31. Houten JK, Cooper PR. Spinal cord astrocytomas: presentation, management and outcome. J Neurooncol 2000; 47(3):219–224. 32. Banczerowski P, et al. Primary intramedullary glioblastoma multiforme of the spinal cord: report of eight cases. Ideggyogy Sz 2003; 56(1–2):28–32. 33. Santi M, et al. Spinal cord malignant astrocytomas. Clinicopathologic features in 36 cases. Cancer 2003; 98(3):554–561. 34. Koyanagi II, et al. Diagnosis of spinal cord ependymoma and astrocytic tumours with magnetic resonance imaging. J Clin Neurosci 1999; 6(2):128–132.

2. Van Goethem JW, et al. Spinal tumors. Eur J Radiol 2004; 50(2):159–176.

35. Huang JS, Chang CJ, Jeng CM. Surgical management of hemangioblastomas of the spinal cord. J Formos Med Assoc 2003; 102(12):868–875.

3. Chamberlain MC, Kormanik PA. Epidural spinal cord compression: a single institution’s retrospective experience. Neurooncol 1999; 1(2):120–123.

36. Jallo GI, Freed D, Epstein FJ. Spinal cord gangliogliomas: a review of 56 patients. J Neurooncol 2004; 68(1):71–77.

4. Samdani AF, et al. Spinal angiolipoma: case report and review of the literature. Acta Neurochir (Wien) 2004; 146(3):299–302; discussion 302.

37. Shimada S, et al. Subependymoma of the spinal cord and review of the literature. Pathol Int 2003; 53(3):169–173.

5. Clancey JK. Spinal epidural lipomatosis: a case study. J Neurosci Nurs 2004; 36(4):208–209, 213.

38. Aman RA, et al. Intramedullary oligodendroglioma: a case report. Gan To Kagaku Ryoho 2000; 27 (Suppl 2):571–573.

6. Goodridge AE, et al. Hand wasting due to mid-cervical spinal cord compression. Can J Neurol Sci 1987; 14(3):309–311.

39. Kaya RA, et al. Intramedullary spinal cord metastasis: a rare and devastating complication of cancer – two case reports. Neurol Med Chir (Tokyo) 2003; 43(12):612–615.

7. Hirano H, et al. Foramen magnum and upper cervical cord tumors. Diagnostic problems. Clin Orthop 1983; (176):171–177. 8. McCormick PC. Anatomic principles of intradural spinal surgery. Clin Neurosurg 1994; 41:204–223.

40. Kulkarni AV, Pierre-Kahn A, Zerah M. Conservative management of asymptomatic spinal lipomas of the conus. Neurosurgery 2004; 54(4):868–873; discussion 873–875.

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41. Sandalcioglu IE, et al. Intramedullary spinal cord cavernous malformations: clinical features and risk of hemorrhage. Neurosurg Rev 2003; 26(4):253–256.

43. Prelog K, Blome S, Dennis C. Neurosarcoidosis of the conus medullaris and cauda equina. Australas Radiol 2003; 47(3):295–297.

42. Krishnan C, et al. Transverse myelitis: pathogenesis, diagnosis and treatment. Front Biosci 2004; 9:1483–1499.

44. Torii H, et al. Intramedullary spinal tuberculoma – case report. Neurol Med Chir (Tokyo) 2004; 44(5):266–268.

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Section 2

Osseous Spinal Tumors ■ i: Physiology and Assessment

CHAPTER

Bone Biology

38

Robert J. Pignolo and Frederick S. Kaplan

GENERAL PRINCIPLES Organization of bone Macroscopically, the skeleton is composed of flat bones (e.g. bones of the skull) and long bones (e.g. tibia), based on development and growth occurring through an intramembraneous process or endochondral and intramembraneous processes, respectively.1 From a gross anatomical perspective, individual bones are made up of varying proportions of cortical (compact) and trabecular (cancellous) tissue, depending on location, and reflecting specific structural and functional differences. Compact bone is 80–90% mineralized tissue by volume, whereas trabecular bone is only 15–25% mineralized. Thus, trabecular bone has a much larger interface with soft tissue such as bone marrow, vascular, and connective tissue. In general terms, skeletal specialization is dictated by the relative abundance of cortical and trabecular tissue within specific bones; that is, cortical tissue accounts mainly for mechanical and protective functions while metabolic and cellular renewal functions are attributed mostly to trabecular tissue. Microscopically, the hard tissue of bone is composed of a mineralized matrix and cellular elements that give rise to, maintain, and remodel bone. The bony matrix is composed of hydroxyapatite crystals associated with type-I collagen fibers and noncollagenous proteins. The predominant mineral composition of bone (95% of its mineral weight) is Ca10(PO4)6(OH)2, hydroxyapatite, with carbonate and other small impurities. Type I collagen accounts for about 90% of the total protein in bone with absorbed plasma proteins and proteins synthesized by bone-forming cells accounting for the remaining noncollagenous component. Bony matrix glycoproteins and proteoglycans serve to stabilize the mineral crystal. Before mineralization the organic matrix, called osteoid, is laid down by active osteoblasts and becomes mineralized soon after deposition. However, osteoid can accumulate under conditions such as rickets and chronic renal failure, when adequate calcium and/or phosphate ions become limiting. The lamellar structure of adult bone forms from the alternating orientation of collagen fibers, allowing the greatest density of collagen per volume of bone tissue. Lamellae can be found in parallel sheets on the flat surfaces of periosteum and trabecular bone, or concentrically located around channels containing blood vessels in socalled Haversian systems. Deviation from this preferred arrangement of collagen is found in woven bone where fibers are oriented loosely and randomly. Woven or immature bone is found under conditions of rapid bone formation, as occurs with growth, fracture healing, tumor formation, and in some metabolic bone diseases.

Cellular elements Osteocytes are bone-forming cells that become trapped in the bony matrix, and are produced and are found embedded within bone in small lacunae. These cells have many long processes, formed before

matrix calcification, that interconnect with processes from bonelining cells or other osteocytes and collectively make up a network of canaliculi. The periosteocytic space includes both the lacunae and this network, serving as a reservoir for calcium-containing extracellular fluid. The surface area of adult bone represented by periosteocytic space is 7–35 times the surface area of all lung capillaries and thus can be considered a sizeable bed for exchangeable bone calcium. Despite their restricted environs, osteocytes continue to function as bone-forming cells at the surface of lacunae. In addition, they may serve as mechanosensors in the activation of local remodeling events under endocrine/paracrine and autocrine control. The ultimate fate of the osteocyte is probably death by phagocytosis during bone resorption. Under the influence of fibroblast growth factors, bone morphogenetic proteins and Wnt proteins, bone marrow mescenchymal stem, or stromal cells differentiate into osteoblast precursors and finally bone-lining osteoblasts that produce osteoid. Osteoblasts respond to receptor-mediated signals such as parathyroid hormone, prostaglandins, estrogens, and vitamin D3 to regulate synthesis of bony matrix. They also are intimately involved in bone remodeling, expressing both activating (e.g. colony stimulating factor-1 [CSF-1], receptor for activation of nuclear factor kappa B ligand [RANKL]) and inhibitory (e.g. osteoprotegerin, a decoy RANK receptor) factors of osteoclastogenesis (see Remodeling in the Spine below). Osteoclasts are giant multinucleated cells whose precursors are bone marrow monocytes/macrophages derived from hematopoietic stem cells and whose sole function is bone resorption.2 They are typically located in contact with a calcified bone surface within Howship’s lacunae. Their so-called zone of contact with bone is a ruffled membrane bounded circumferentially by an actin ring that serves to seal off the underlying bone as a discrete resorbing compartment. Specific attachment of osteoclasts to matrix components occurs through αvβ3, αvβ5, and α2β1 integrin receptors. The ruffled membrane contains both a proton ATPase and coupled chloride channel that acidifies the sealed-off bone resorbing compartment while maintaining electrical neutrality across the membrane. This is made possible by carbonic anhydrase within the cell and a HCO3–/ Cl– exchanger on the basolateral membrane. RANK, the receptor for RANKL, and the macrophage-colony stimulating factor receptor are also located on the basolateral membrane, both being required for osteoclast differentiation.

Ossification in the spine As in long bones, ossification in the spine occurs through an endochondral process.3 Mesenchymal cells give rise to prechondroblasts which then become progressively embedded within their cartilaginous matrix in lacunae. Now designated as chondrocytes, they continue to proliferate and then enlarge progressively to become hypertrophic, 423

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eventually undergoing apoptotic cell death. As cartilage cells die, and presumably under the influence of vascular endothelial growth factor (VEGF), the area is invaded by blood vessels. Osteoblasts move onto the cartilage surface and deposit bone in this area of primary spongiosa. Osteoclasts or chondroclasts remove residual cartilage, which is then replaced by bone in the secondary spongiosa. This process is largely responsible for initial replacement of the embryonic cartilage template, fracture repair, and the growth/elongation of bones. Subsequent new bone formation is dictated by mechanical, humoral, or local signals and occurs by a remodeling process that continuously attempts to match bone architecture with function.

VERTEBRAL MORPHOGENESIS AND EMBRYOLOGICAL DEVELOPMENT Cartilage models Neural crest cells contribute to the branchial arch derivatives of the craniofacial skeleton, and the lateral plate mesoderm gives rise to the limbs. However, it is the paraxial mesoderm that gives rise to most of the axial skeleton, including the vertebral bodies, as well as the nonbranchial arch derivatives of the craniofacial skeleton. Mesenchymal cells condense to form regions with positional identity, which ultimately represent the future skeletal outline. The fate of mesenchymal cells within condensations dictates whether ossification occurs via an intramembranous or endochondral process. The former occurs as the result of osteoblast differentiation in the calvarium, maxilla, mandible, and subperiosteal bone-forming region of long bones. It is mediated by the transcription factors CBFA1/RUNX2 and osterix (OSX).4–7 Endochondral ossification requires differentiation of mesenchymal cells into chondrocytes, creating cartilage models of the remaining skeleton that serve as templates for bony replacement. Chondrocyte differentiation is influenced by members of the SOXfamily of transcription factors.5–8 Cartilage models develop by interstitial and appositional growth until they take on the characteristic shapes and sizes of those intended bones. Patterning of the endochronal skeleton occurs even in the absence of eventual bone formation. Regulation of cartilage differentiation and growth in proper spatial sequence is essentially sufficient to complete a correctly shaped skeleton and this concept is supported by the phenotype of mice harboring two null alleles for the gene encoding CBFA1/RUNX2.5,6 Despite the lack of osteoblast differentiation in these mice, a nearly intact skeleton is formed with accurately placed and correctly shaped skeletal elements, albeit consisting totally of cartilage.

MESENCHYMAL CONDENSATION AND CHONDROCYTE DIFFERENTIATION Through a complex series of events during the fourth week of human development, segmented somites derived from paraxial mesoderm come to straddle the neural tube and notochord bilaterally. Mesenchymal cells within the somites eventually surround the notochord and form structures called sclerotomes. It is the sclerotome cells that differentiate into chondrocytes, forming the cartilage models of vertebral bodies. The notochord finally emerges as the nucleus pulposus within the intervertebral discs. The dorsal migration of sclerotome cells around the neural tube give rise to the neural arches of the vertebrae. The regulation of events leading up to the formation of somites is thought to be tightly controlled by cell–cell interactions involving the Notch1 receptor and its ligands, which are also transmembrane 424

molecules.9,10 Vertebral defects in mice can be seen as the result of somite condensation and patterning errors when the gene for Notch1 or one of its ligands is inactivated.8,11–13 Mutations in specific Notch1 ligands also occur in humans and are associated with the vertebral abnormalities found in the recessive form of spondylocostal dysostosis (semivertebrae) and Alagille syndrome (butterfly vertebrae).14–16 Disruption of sclerotome cell differentiation, and thus chondrocyte differentiation, also has profound effects on vertebral column formation. The notochord-secreted cytokine, Sonic hedgehog, is an important regulator of sclerotome cell differentiation. Its inactivation in mice leads to skeletal development without a vertebral column and posterior rib regions.17,18 Spinal deformities in mice and humans have also been reported to occur with mutations in PAX1, a transcription factor thought to be at least partly inducible by Sonic hedgehog.19,20

OSTEOBLAST DIFFERENTIATION AND BONE FORMATION Regulatory pathways Transcriptional control mechanisms regulate osteoblastogenesis. Examples of early transcriptional regulators include the homeodomain proteins (e.g. Msx-2, Dlx-2, Dlx-5, BAPX1), steroid receptors, as well as the helix-loop-helix (HLH) proteins Id, Twist, and Dermo. The HLH proteins play important roles in the proliferation of osteoprogenitor cells, but repress osteoblast differentiation and must be down-regulated before a mature bone cell phenotype can be expressed.21 The activating protein cFOS is also expressed in osteoprogenitor cells, resulting in osteosarcomas if overproduced, but is not detected in mature osteoblasts.22 A similar theme is true for some of the homeodomain transcription factors, where mesenchymal precursors abundantly express them, but mature bone-forming cells do not.23,24 In contrast, the runt homology domain proteins (e.g. Runx2/ Cbfa1) and the zinc finger protein Osterix and others activate genes expressed in the mature osteoblast, such as osteocalcin and osteopontin (Fig. 38.1).6,7,25–27 Null mouse mutants of Runx2 and Osterix result in inhibition of bone formation and perinatal mortality, demonstrating their requirement in osteogenesis.6,7 Runx2 also plays important roles in the maturation of chondrocytes, cartilage mineralization, and endothelial cell migration necessary for vascular invasion.28–30 Runx2 mediates its plethora of effects by interaction with diverse coregulatory proteins, including CBFβ1, Wnt pathway regulator LEF1, and TGF-β/BMP responsive SMAD proteins, to name a few.31–38 Temporal expression of Runx2 followed by Osterix is thought to be essential for the later stages of osteoblast differentiation.7 Hormonal regulation of osteoblast differentiation includes steroid as well as polypeptide signaling molecules. Glucocorticoids enhance the differentiation of bone marrow stromal cells to osteoblasts in vitro, but in vivo have negative effects on bone that contribute to osteoporosis by inducing apoptotic cell death.39–41 Vitamin D3, sex steroids, adrenomedullin, and leptin all have osteogenic or anabolic effects on bone.42–50 Retinoic acid contributes to skeletal development in the embryo and also plays a role in postnatal bone formation.51–53 Among the polypeptide hormones, PTH and PTHrP have stimulatory effects on osteoprogenitor cells and regulatory effects on differentiation, both mediated by coupled G protein interactions with their receptors.54–61

Osteoprogenitor cells Osteoprogenitor cells can arise from stem cells in a variety of tissues. There are as yet no unique identifying markers for the mesenchymal stem cell (MSC) that gives rise to bone, fat, cartilage, and muscle.

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Histone Collagen TGFβ1 Osteopontin

Stem cell

BMPs TGFβ

Mesenchymal stem cell

BMPs Osteoprogenitor

BMPs Collagen Osteocalcin Osteopontin Collagenase Other NCPs Mineralization

Alk Phos BSP Collagen

PTH

Pre-osteoblast

IGF-l, PGE2 Vitamin D Steroids

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Runx2 Osx Adipocyte

Chondrocytes Myocytes Fibroblasts

Bone marrow stroma contains highly proliferative cells that will form single colonies or colony-forming units-fibroblasts (CFU-Fs) and are thought to contain mesenchymal stem cells that can be distinguished from early hematopoietic precursors.62–65 Stromal cells grown in vitro are heterogeneous with respect to the capacity for differentiation, and only a low percentage of all CFU-Fs have stem cell properties.62,63,66,67 Further, only a small fraction of CFU-Fs are bone-forming cells.68,69 Although a specific osteoprogenitor marker has not been identified, antibodies have been developed (e.g. STRO-1, SP-10, SH2, HOP26) that recognize some subsets of precursor cells.70–77 Mesenchymal differentiation may proceed by a multistep hierarchical process with greater cell lineage restriction to terminal cell types at each subsequent step.78 This idea is supported by identification of bipotential adipocyte-osteoblast precursors, and has suggested that there may be an inverse relationship between adipocyte and osteoblast differentiation.79,80 A related observation is the transdifferentiation of bone to fat cells, or fat to bone cells.81–84 Depending on the local cellular environment, ‘committed’ MSC progeny may also dedifferentiate into another lineage.85 Thus, plasticity may be a common phenomenon; however, at least some reports suggest that cell fusion events may confound this paradigm.86–90 Figure 38.1 shows a simplified scheme for osteoblast differentiation. MSCs similar to those found in bone marrow have been found in adult peripheral blood, fetal cord blood, fetal liver, tooth pulp, muscle satellite cells, and extramedullary adipose tissue and have osteogenic potential.91–100 Multipotent adult progenitor cells (MAPCs) derived from bone marrow can contribute to most somatic cell types, including skeletal tissue.101,102 Pericytes can also be induced toward the osteogenic lineage.103

Osteogenic growth factors Osteogenic growth factors have been described as signaling polypeptides that function in the bone microenvironment to regulate skeletal metabolism. These factors may be secreted by bone-forming cells, stromal cells, cells of the hematopoietic system, or by cells at distant sites whose products are released into the circulation and act systemically on bone. Bone morphogenetic proteins (BMPs), members of the transforming growth factor β (TGF-β) superfamily, are produced by skeletal and extraskeletal tissues. BMP-2, -4, and -6 are secreted by osteo-

Bonelining cell

Osteocyte

Fig. 38.1 Stem cell commitment and differentiation of osteoblasts. Cell types are indicated by boxes. Important regulatory factors are listed above arrows and transcription factors below arrows. Typical markers of later maturation stages are given above the block arrows. The dotted, double-sided arrow denotes possible transdifferentiation. Only representative examples of regulatory and other factors are shown (NCPs, noncollagenous proteins).

blasts and play an autocrine role by enhancing the differentiated function of bone-forming cells.104 BMPs induce the differentiation of cells toward the osteoblast lineage, increase the terminally differentiated pool of osteoblasts, and induce endochondral ossification and cartilage formation in concert with Indian/Sonic hedgehog.105–107 BMPs interact with three distinct serine/threonine kinase receptors which, after dimerization, can signal through at least eight different Smads that become phosphorylated and/or heterodimerize to regulate transcription.108–110 Smads have activating and inhibitory functions, and also mediate signals initiated through TGF-β and activin receptors. BMPs and TGF-β signaling may also use Smad-independent pathways that rely on Ras or MAP kinase.111 Suppression of BMP activity occurs at several levels, including nonsignaling pseudoreceptors, inhibitory Smads, Smurf-mediated ubiquitination and degradation of signaling Smads, intracellular Smad binding proteins, and extracellular BMP antagonists such as noggin, chordin, follistatin, and twisted gastrulation.112 TGF-β1, -β2, and -β3 are polypeptides synthesized by bone cells and function as mitogens for preosteoblasts, stimulatory factors for collagen synthesis, and inducers of osteoclast apoptosis.113 The effect of BMPs on osteoblast differentiation is inhibited by TGF-β, and transgenic mice overproducing TGF-β are, in fact, osteopenic.114,115 Like BMPs, TGF-β signals through distinct serine-threonine kinase receptors that activate specific Smads to regulate transcription.110,111 Insulin-like growth factors (IGFs) are produced in a variety of tissues and have been characterized as IGF-I and IGF-II, both sharing similar properties but the former being more potent. IGFs116 stimulate proliferation of the osteoblastic lineage, prevent apoptosis of mature osteoblasts, and enhance net type I collagen abundance by stimulation of transcription and inhibition of collagen protein degradation. IGF-I knockout mice have decreased bone formation while those overexpressing IGF-I have enhanced bone formation.117,118 In humans, IGF-I has a generalized anabolic effect on musculoskeletal tissue with stimulation of bone remodeling.119 Parathyroid hormone (PTH) induces IGF-I synthesis in osteoblasts, and the anabolic effects of PTH on bone is diminished in the absence of IGF-I.117 Steroids decrease IGF-I expression and this may, in part, explain glucocorticoid-induced bone loss.120 β-catenin in association with specific transcription factors can regulate BMP and TGF-β signaling.121 The so-called Wnts prevent the degradation of β-catenin. Low-density lipoprotein receptor-related 425

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protein 5 (LPR5) is a coreceptor for Wnt that is required for optimal signaling with resultant accumulation of β-catenin.122 BMP-stimulated osteoblasts and stromal cells express LRP5 and knockout mice lacking LRP5 are osteopenic.123 In humans, inactivating mutations in LRP5 cause decreased bone mass, while other mutations in LRP5 cause a high bone mass phenotype.124,125 Fibroblast growth factor (FGF) 1 and 2 stimulate osteoblast proliferation and in vivo are important in the maintenance of bone mass. FGF null mice display low numbers of osteoblasts and decreased bone formation.126 Conversely, systemic FGF2 increases the preosteoblast pool that ultimately forms mature bone.127 FGF receptor signaling is essential for chondrogenesis and normal skeletal and limb development, with an activating mutation in FGF receptor-3 causing achondroplasia associated with dwarfism and early closure of cranial sutures.128 Platelet-derived growth factor (PDGF) has activities similar to those of FGF.129

Synthesis of bony matrix The extracellular matrix of bone is composed predominantly of type I collagen, noncollagenous proteins, and mineral in the form of hydroxyapatite. Osteoid also contains serum-derived proteins, including albumin and α2-HS-glycoprotein. Bone-forming cells secrete proteoglycans, glycosylated proteins with and without cell attachment function, and γ-carboxylated (gla) proteins. In early bone formation, a chondroitin sulfate proteoglycan (versican) and the glycosaminoglycan hyaluronan are secreted and may delineate areas of future bone deposition.130 Versican is eventually replaced by two chondroitin sulfate proteoglycans, decorin and biglycan, each containing leucine-rich tandem repeat sequences. One possible function for these leucine-rich repeat proteins is their ability to bind and regulate TGF-β family members in the extracellular milieu.130 Biglycan-deficient transgenic mice have underdeveloped trabecular bone.131 The most abundant noncollagenous glycoprotein secreted by bone cells is osteonectin, with putative functions in osteoblast proliferation and matrix mineralization. Other glycoproteins mediate cell attachment and have been designated members of the SIBLING family (e.g. fibronectin, osteopontin, bone sialoprotein).132 All members contain the cell consensus sequence RGD (Arg-Gly-Asn) that binds to integrin cell surface molecules. Although most members of the SIBLING family are found in other tissues, bone sialoprotein is specific to mineralized tissue.133 The bone-specific gla-containing protein osteocalcin may function as an inhibitor of mineral deposition, as judged by osteocalcindeficient mice who have increased bone mineral density.134 Similarly, mice deficient in the matrix gla protein (MGP), found in many connective tissues, develop extracellular sites of calcification.135 Bone mineral contains numerous impurities and is a carbonatesubstituted hydroxyapatite with solubility properties that enable its constituent imperfect crystals to serve as a reservoir for calcium, phosphate, and magnesium ions.135 While the mineral content provides mechanical rigidity and load-bearing strength, the organic matrix provides elasticity, flexibility, and microstructural organization largely secondary to the presence of type I collagen.135 Extracellular matrix vesicles released from chondrocytes and osteoblasts accumulate calcium and phosphate ions, enzymes that degrade inhibitors of mineralization, and components of a nucleation core that induce apatite formation.133 It is unclear if there is an association of vesicle mineral with mineral in the collagen matrix or if the matrix vesicle directly provides a calcium and phosphate reservoir that supports mineralization initiated in collagen fibrils. In either case, the first stable crystal formed is followed by the addition of ions and

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ion clusters that allows for the expansion of crystal structure with addition of secondary nucleation sites.136 Removal of noncollagenous protein from matrix, particularly phosphoprotein, inhibits crystal nucleation and apatite formation.137 Alkaline phosphatase may contribute to enhanced mineralization by increasing the local phosphate concentration, removing phosphate-containing inhibitors of apatite growth, or modifying phosphoproteins to control their function as potential nucleators.133 Growth of mineral crystals is primarily dictated by the collagen matrix template. Noncollagenous proteins that bind crystals can also influence the extent and direction of mineral deposition.133 The presence of ions other than calcium and phosphate may influence bone apatite crystal growth, size, and solubility, and they include magnesium, strontium, cadmium, carbonate, and fluoride.133

MECHANISMS OF BONE RESORPTION Osteoclast differentiation Cells of the mononuclear/phagocytic lineage give rise to osteoclasts. Early precursors are committed to the myeloid series by the action of transcription factors PU-1 and MiTf. The lineage is further narrowed to monocytic cells by macrophage-colony stimulating factor (M-CSF).2,138 Proliferation and survival of monocytic cells, with concomitant RANK receptor expression, is mediated by M-CSF. The presence of RANKL is then required for commitment to the osteoclast differentiation program. Osteoclastogenesis depends on the association of M-CSF and RANKL, found on stromal cells and osteoblasts, with their receptors on monocytes/macrophage cells.2,138 Subsequent fusions of preosteoclasts result in the formation of giant multinucleated cells containing 4–20 nuclei and expressing characteristic markers of mature osteoclasts. The osteoclast membrane has lost several macrophage markers and is lacking Fc and C3 receptors, but retains phagocytic non-specific esterases, lysozyme synthetic function, and CSF-1 receptors.2,138 Osteoclasts are distinguishable from macrophages by the abundance of RANK, vitronectin (integrin αvβ3) receptors, and calcitonin receptors. Osteoclasts undergo an estrogen-promoted apoptotic cell death after a cycle of resorption.2,138

Regulation of osteoclast activity Resorption by osteoclasts may be stimulated by local or systemic factors that expand the pool of committed osteoclastic precursors or activate mature osteoclasts. Locally produced cytokines and hormones may exert more profound effects on normal bone resorption and remodeling than systemic hormones. The key regulators of osteoclastic bone resorption are RANK ligand and its two confirmed receptors, RANK and osteoprotegerin (OPG). OPG is a member of the TNF receptor superfamily that lacks a transmembrane domain and, as such, is a secreted molecule. OPG regulates osteoclast activity by serving as a decoy receptor for RANKL.138–141 The only other known ligand for OPG is TRAIL which, like RANKL, is also a type II membrane-bound TNF homolog. The significance of OPG–TRAIL interaction is unknown. Deficiency of OPG in mice causes increased osteoclast formation, activity, and survival that results in destruction of growth plates, loss of trabeculae, decreased bone strength, and reduced bone mineral density (BMD).142,143 Parenteral administration of OPG causes a decrease in the number of active osteoclasts with a concomitant increase in BMD.144 In vitro, OPG abrogates osteoclast formation mediated by M-CSF and RANKL, in the absence of osteoblasts or stromal cells.139,140 OPG also inhibits osteoclastogenesis induced by a diverse group of osteotropic hormones.138–141 Finally, there is a direct

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effect of OPG on isolated mature osteoclasts due, in part, to limiting osteoclast survival. RANKL expression is obligatory for osteoclastic resorption and physiologic bone remodeling (Fig. 38.2). Membrane-bound RANKL is more potent than soluble forms and mature osteoblasts express RANKL constitutively.145–147 Knockout mice lacking RANKL are devoid of osteoclasts and exhibit osteopetrosis with occlusion of the marrow cavity.148 The bone-resorbing activity and survival of mature osteoclasts is greatly increased by exposure to recombinant RANKL in the absence of stromal cells or osteoblasts.138–141 The signaling receptor for RANKL is RANK, a transmembrane protein that is sufficient to induce, upon RANKL binding, all downstream signals for osteoblast differentiation as well as later activation of mature osteoclasts. Mutations in the RANK gene that cause constitutive activation have been detected in familial expansile osteolysis, resulting in osteolytic lesions and osteopenia.149,150 Engineered mice lacking RANK have severe osteopetrosis secondary to the absence of osteoclasts.151,152 M-CSF or CSF-1 is required for normal osteoclast formation in the neonatal period and in rodent models of osteopetrosis there is impaired CSF-1 production. CSF-1 is secreted by stromal cells and cells of the osteoclast lineage express CSF-1 receptors. Interleukin (IL)-1α and β are potent stimulators of osteoclasts that work at all stages of formation and activation whose effects are mediated through RANKL.141,153 IL-1 has been implicated in conditions of increased bone turnover, including osteoporosis, bone loss seen in

Liver

Osteoblast OPG

RANKL

M-CSF M-CSF RANK

Osteoblast RANKL

Monocyte/ macrophage

M-CSF

Osteoclast CFU-F

Bone

BMPs, TGFβs, IGFs, FGFs Fig. 38.2 Basic bone remodeling. Osteoclastogenesis depends on the association of macrophage colony-stimulating factor (M-CSF) and the receptor for activation of nuclear factor kappa B (RANK) ligand (RANKL), found on stromal cells and osteoblasts, with their receptors on monocytes/macrophage cells. This process is inhibited by osteoprotegerin (OPG). The differentiated osteoclast polarizes on the bone surface, forming a ruffled membrane that acidifies the extracellular microenvironment, mobilizes the mineral phase of bone and provides the milieu for organic matrix degradation. Bony dissolution releases various hormones and growth factors including members of the bone morphogenetic protein (BMP), transforming growth factor-β (TGF-β), insulin-like growth factor (IGF), and fibroblast growth factor (FGF) families. In a process that couples bone formation to resorption, these signaling molecules stimulate osteoblast differentiation and proliferation.

some malignancies, and in rheumatoid arthritis.154 Lymphotoxin and TNF-α are functionally related to IL-1 and their effects on bone are synergistic with IL-1.155 The list of other locally-acting factors is growing. Those that stimulate osteoclast formation and activity include IL-6, IL-15, IL17, vitamin A, and TGF-α. Inhibitors of osteoclast formation and activity include interferon-γ (IFN-γ), TGF-β, IL-18, inorganic phosphate, and high extracellular calcium. In humans, exogenous TGFβ inhibits proliferation and differentiation of osteoclast precursors and enhances osteoclast apoptosis, presumably by increasing OPG expression in osteoblasts and bone marrow stromal cells. However, endogenous TGF-β may actually stimulate osteoclastogenesis.156,157 The role of other factors such as prostaglandins and leukotrienes is less clear. The major systemic hormones that influence osteoclast activity are PTH, vitamin D3, calcitonin, glucocorticoids, and the sex hormones. PTH has dual effects on bone mediated through its regulation of Cbfa1, which is obligatory for bone formation and also influences RANKL expression on osteoblasts.158 Intermittent administration of PTH stimulates bone formation while continuous administration stimulates osteoclastic bone resorption. PTH-related protein has identical skeletal effects to those of PTH. The D vitamin 1,25 (OH)2D3 stimulates osteoclastic bone resorption by stimulating differentiation and fusion of osteoclast progenitors.159 These effects of 1,25 dihydroxyvitamin D are mediated indirectly by osteoblasts through RANKL signaling. Calcitonin, made by the parafollicular cells of the thyroid gland, is a potent inhibitor of osteoclastic bone resorption whose effects are transient owing to downregulation of its receptor.160 Glucocorticoids have inhibitory effects on formation of osteoclasts in vitro and on bone resorption in organ culture, but in vivo are associated with increased bone resorption. The latter effect may, in part, be due to glucocorticoid inhibition of calcium absorption from the gut and secondary hyperparathyroidism. For up to 10 years after the menopause, lack of estrogen is associated with enhanced osteoclastic bone resorption. Estrogens may have a direct effect on osteoclasts, but they may also suppress peripheral blood monocyte production of cytokines such as IL-1, TNF-α, and IL-6 that stimulate osteoclast formation.154,161–163

REMODELING IN THE SPINE Coupling of bone formation and resorption Remodeling of bone occurs in focal and discrete microscopic sites throughout the skeleton. Complete remodeling at each site takes 3–6 months, and is probably longer in cancellous than in cortical bone. Cancellous bone is more abundant in the vertebral column, comprising more than 66% of total bone in the lumbar spine. This is in contrast to the intertrochanteric portion of the femur, where bone is 50% cortical and 50% cancellous, and in the mid-radius where greater than 95% of bone is cortical bone. At sites of bone turnover an activation phase is followed by a resorption phase that is followed by a bone formation phase. Although anatomically different from each other, cortical and cancellous bone follow the same general remodeling sequence. However, turnover events in cancellous bone are probably influenced more by factors produced by adjacent bone marrow cells, whereas these events in cortical bone, distant from marrowderived cytokines, are likely influenced more by systemic hormones such as PTH and 1,25 dihydroxyvitamin D3.164 In the initial step of the remodeling sequence, osteoclasts are activated in focal sites by mechanisms that are not well understood and the rate of bone turnover is dependent on the activation frequency of osteoclasts. Interactions between integrins on the osteoclast cell membrane and bony matrix proteins may initiate the activation 427

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phase. After a resorptive phase lasting up to 10 days, repair of resulting defects proceeds by attraction of osteoblasts and subsequent bone formation. The mechanisms by which bone formation is coupled to previous osteoclastic resorption are still unclear, but several possibilities can be supported by existing evidence. Coupling may be mediated by local humoral factors acting on osteoblasts or osteoblast precursors (see Fig. 38.2). These mediators may serve as osteoblast-stimulating factors, such as IGF-I or TGBβ, that are released from the bone matrix with osteoclastic resorption.165–167 A factor that stimulates resorption may also stimulate osteoblasts, but at a much slower rate, so as to time the initiation of bone formation to occur after osteoclast activity has ceased.168 Coupling may instead involve transcription factors, such as Runx2/ Cbfa1, that are both obligatory for bone formation but also play a role in the regulation of osteoclast formation.169 Alternatively, systemic factors such as leptin may play a role in the regulation of the bone formation component of the coupling process by presumptive hypothalamus-mediated β2-adrenergic stimulation of osteoblasts and their precursors.170 Lastly, coupling may be a more simple process whereby osteoblasts or their precursors in proximity to resorption sites repopulate bony defects after osteoclasts leave or die after their last resorptive cycle.

Regulation of the resorption phase The resorption phase begins with osteoclast activation and is followed by osteoclast formation, polarization, ruffled membrane demarcation of future resorbing sites, resorption, and apoptosis. Osteoclast programmed cell death may be precipitated by resorption inhibitors such as estrogen and TGF-β and often occurs at reversal sites, locations where osteoclastic resorption has ceased and preosteoblastic migration and differentiation are soon to proceed. The regulation of the resorption phase is under complex control as described above under Regulation of Osteoclast Activity.

Regulation of the formation phase The formation phase of bone remodeling occurs through a series of events beginning with osteoblast precursor chemotaxis and proliferation. These events are followed by osteoblast differentiation, mineralized bone formation, and cessation of osteoblast activity. Chemotaxis of osteoblast precursors is likely mediated by soluble factors produced locally as well as factors released from the dissolution of bone by osteoclastic resorption. Likely candidates include TGF-β, PDGF, and digested fragments of type I collagen and osteocalcin.171–176 Proliferation of osteoblast precursors is also likely to be stimulated by local factors released during the resorptive process including IGFs, FGFs, TGF-βs, and PDGF. Differentiation of osteoblastic precursors into mature bone-forming cells is likely to be induced by bone-derived growth factors such as IGF-I and BMP2. The role of TGF-β may thus be to trigger the process of bone formation by first attracting and then expanding the pool of osteogenic precursors, after which its disappearance or inactivation allows these precursors to differentiate into osteoblasts. The cessation of osteoblast activity may also be mediated by TGF-β, since TGF-β decreases osteoblast activity and it is expressed by osteoblasts as they become terminally differentiated.177 Osteoblast life span and factors that regulate it (see below under Osteoblast Senescence) may be critically important to terminating the formation phase of bone turnover, particularly with aging.

Bone remodeling and disease In diseases which tend to increase osteoclast activation, such as primary hyperparathyroidism, hyperthyroidism, and Paget’s disease, 428

there is also a roughly balanced increase in the amount of new bone formation, although new bone is not necessarily architecturally equivalent to bone formed under normal physiologic conditions. In diseases that cause osteolytic lesions of bone, namely multiple myeloma and certain malignant solid tumors, osteoblasts do not completely repair defects made by osteoclastic resorption. In the former case there appears to be a defect(s) in osteoblast differentiation while in the later case malignant cells produce local factors that stimulate osteoclast activity.178,179 Osteoblastic lesions occur at sites where no previous bone resorption has occurred, and can be found with cancers of the prostate or breast, or with administration of pharmacologic doses of fluoride. With aging, there appears to be an uncoupling of bone resorption and formation that begins after about 35 years of age, depending on the skeletal site. There is a resulting decrease in trabecular wall thickness owing to the inability of osteoblasts to repair osteoclastic resorptive defects, presumably secondary to decreased osteoblast activity or a decrease in the number of osteoblasts available to initiate bone formation.180

THE AGING SPINE Age-related changes in biomechanical properties The strength of cancellous bone declines 8–10% per decade in comparison to cortical bone strength which declines only 2–5% per decade. This translates into a much higher risk of fracture in bones of the vertebral column. Inherent fragility of bone increases with age, allowing damage to accumulate more readily with repeated loading.181 Damaged bone is less able to sustain further deformation and less able to absorb energy with any impact, predisposing it to failure.182 Fracture risk in older adults is greater than predicted by loss of bone mass alone, suggesting that age-related changes in bone quality or architecture are important. Ultramicroscopic tears in bone or fatigue damage results in fracture whenever damage occurs faster than the remodeling apparatus can repair it (slower bone turnover) or when remodeling is defective (uncoupling of bone formation to resorption).183 Bones vertically loaded, such as the vertebral bodies, depend on horizontal, cross-hatching trabeculae, for support. Loss of trabecular connectivity is thought to be a major contributor to the female preponderance of vertebral bone loss and susceptibility to vertebral fractures. The decline in collagen content with age is associated with a reduction in bone strength and stiffness, two parameters generally used to define bone health. Fewer reducible collagen cross-links per unit of total collagen are associated with increase bone fragility in osteoporotic women.184,185 Periosteal apposition of bone with age serves as a compensatory mechanism for reduced bone volume in men, but not in women, at both the femoral neck and for the vertebral bodies.186–188

Bone loss: secondary hyperparathyroidism, menopause, and somatopause The uncoupling of bone formation to resorption leads to remodeling imbalances that ultimately result in age-related bone loss. With aging, bone formation is affected by the reduction of osteoblast differentiation, activity, and life span that is potentiated by secondary hyperparathyroidism and, in women, by estrogen deprivation and increased osteoclast activity with menopause.189 Secondary hyperparathyroidism is caused by decreased intestinal and renal calcium resorption, precipitated by vitamin D deficiency in the housebound (lack of sunlight) and undernourished older adult, and by age-onset

Section 2: Osseous Spinal Tumors

changes in renal function. Both processes are affected by estrogen deficiency. However, secondary hyperparathyroidism is ameliorated by a diet high in calcium. Impaired osteoblast function is thought to be a major contributing factor to remodeling imbalances that occur with age. Decline in growth hormone production, decrease in physical activity, and osteoblast senescence (see below) impart age-related deleterious effects on osteoblast function. Some of these effects may be mediated by low levels of circulating and/or local IGF-I. Changes in the levels of other locally acting growth factors and cytokines that also impair osteoblast function may be mediated by estrogen withdrawal. The consequences of impaired osteoblast function are a relative increase in osteoclast activity and uncompensated bone resorption made worse by the increase in activation frequency (of remodeling events) with estrogen loss. Random remodeling errors that accumulate over time may also play a role, albeit small, in the fidelity of aging bone.

Osteoblast senescence Telomeres shorten with age in most human tissues, including bone, and because telomere shortening is a cause of cellular replicative senescence in cultured cells, including osteoblasts and MSCs,190–192 it is hypothesized that telomere shortening contributes to the aging of bone. Conversely, after forced ectopic expression of telomerase in human MSCs, proliferative capacity is extended in vitro and the capacity for bone formation is enhanced in vivo.190–192 Telomerase not only extends the life span of osteogenic precursors, but accelerates the osteogenic differentiation of MSCs.193 These observations provide strong evidence that telomerase status in MSCs is likely a critical component of bone formation. Functional deficits in osteoblasts that occur with cellular senescence play a major role in the uncoupling of bone formation and resorption, resulting in a net loss of bone tissue.194 Thus, recruitment of osteoblast precursors (MSCs) and osteoblast differentiation become a critical component in maintaining the balance between these two opposing processes. If the number and activity of osteoblasts responsible for synthesizing new bone matrix are substantially reduced, then the diminished recruitment of osteogenic precursors to replace senescent osteoblasts may potentially explain many aspects of age-related bone loss. The osteogenic potential of murine MSCs have been reported to decline with increasing donor age.195 There are conflicting reports regarding the effects of age on human MSCs with the weight of evidence in favor of modest declines in several measures associated with osteogenic potential, particularly after the age of 40.196–203 However, there are at least two well-conceived studies that suggest no significant age-related differences.201,202 Thus, decrements in osteogenic stem cell potential with age may only partially account for changes in bone integrity associated with osteoporosis and poor fracture repair. It has also been suggested that reductions in bone density seen with age may be the result of osteoblast replicative senescence, either directly (decreased proliferation and apoptosis) or secondary to other changes that accompany replicative senescence (e.g. failure to express an osteoblast phenotype).204 It is unclear if these alterations are solely a consequence of decreased osteoblast responsiveness to extracellular signals, but reduced expression of osteoblast markers such as alkaline phosphatase, osteocalcin, and type I collagen has been shown in response to various hormones and growth factors including 1,25 (OH)2 vitamin D3 [1,25 (OH)2 D3], insulin-like growth factor-I (IGFI), parathyroid hormone (PTH), and prostaglandin E2 (PGE2).205–212 Many of these changes have been documented in primary osteoblast cultures from old donors as well as in osteoblasts aged in vitro by serial passage.

If the osteogenic potential of bone marrow stromal cells is sufficiently intact, but the number and activity of osteoblasts responsible for synthesizing new bone matrix are substantially reduced, then the diminished recruitment of osteogenic precursors to replace senescent osteoblasts may explain many aspects of age-related bone loss.

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129. Hock JM, Canalis E. Platelet-derived growth factor enhances bone cell replication, but not differentiated function of osteoblasts. Endocrinology 1994; 134(3): 1423–1428.

156. Chenu C, Pfeilschifter J, Mundy GR, et al. Transforming growth factor beta inhibits formation of osteoclast-like cells in long-term human marrow cultures. Proc Natl Acad Sci USA 1988; 85(15):5683–5687.

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157. Kaneda T, Nojima T, Nakagawa M, et al. Endogenous production of TGF-beta is essential for osteoclastogenesis induced by a combination of receptor activator of NF-kappa B ligand and macrophage-colony-stimulating factor. J Immunol 2000; 165(8):4254–4263.

131. Xu T, Bianco P, Fisher LW, et al. Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice. Nat Genet 1998; 20(1):78–82. 132. Gorski JP. Is all bone the same? Distinctive distributions and properties of noncollagenous matrix proteins in lamellar vs. woven bone imply the existence of different underlying osteogenic mechanisms. Crit Rev Oral Biol Med 1998; 9(2): 201–223. 133. Gokhale JA, Robey PG, Boskey AL. The biochemistry of bone. Osteoporosis. Vol. 1. San Diego, CA: Academic Press; 2001:107–188. 134. Ducy P, Desbois C, Boyce B, et al. Increased bone formation in osteocalcin-deficient mice. Nature 1996; 382(6590):448–452. 135. Glimcher M.J. The nature of the mineral phase in bone: biological and clinical implications. Metabolic bone disease and clinically related disorders. 3rd edn. San Diego, CA: Academic Press; 1998:23–51. 136. Eppell SJ, Tong W, Katz JL, et al. Shape and size of isolated bone mineralites measured using atomic force microscopy. J Orthop Res 2001; 19(6):1027–1034. 137. Termine JD, Belcourt AB, Conn KM, et al. Mineral and collagen-binding proteins of fetal calf bone. J Biol Chem 1981; 256(20):10403–10408. 138. Boyle WJ, Simonet WS, Lacey DL. Osteoclast differentiation and activation. Nature 2003; 423(6937):337–342. 139. Hofbauer LC, Heufelder AE. Role of receptor activator of nuclear factor-kappa B ligand and osteoprotegerin in bone cell biology. J Mol Med 2001; 79(5–6):243–253. 140. Theill LE, Boyle WJ, Penninger JM. RANK-L and RANK: T cells, bone loss, and mammalian evolution. Annu Rev Immunol 2002; 20:795–823. 141. Walsh MC, Choi Y. Biology of the TRANCE axis. Cytokine Growth Factor Rev 2003; 14(3–4):251–263. 142. Bucay N, Sarosi I, Dunstan CR, et al. Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification. Genes Dev 1998; 12(9):1260–1268. 143. Mizuno A, Amizuka N, Irie K, et al. Severe osteoporosis in mice lacking osteoclastogenesis inhibitory factor/osteoprotegerin. Biochem Biophys Res Commun 1998; 247(3):610–615. 144. Akatsu T, Murakami T, Ono K, et al. Osteoclastogenesis inhibitory factor exhibits hypocalcemic effects in normal mice and in hypercalcemic nude mice carrying tumors associated with humoral hypercalcemia of malignancy. Bone 1998; 23(6):495–498. 145. Khosla S, Arrighi HM, Melton LJ 3rd, et al. Correlates of osteoprotegerin levels in women and men. Osteoporos Int 2002; 13(5):394–399. 146. Sakata M, Shiba H, Komatsuzawa H, et al. Expression of osteoprotegerin (osteoclastogenesis inhibitory factor) in cultures of human dental mesenchymal cells and epithelial cells. J Bone Miner Res 1999; 14(9):1486–1492. 147. Atkins GJ, Kostakis P, Pan B, et al. RANKL expression is related to the differentiation state of human osteoblasts. J Bone Miner Res 2003; 18( 6):1088–1098. 148. Kong YY, Yoshida H, Sarosi I, et al. OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph node organogenesis. Nature 1999; 397(6717):315–323. 149. Hughes AE, Ralston SH, Marken J, et al. Mutations in TNFRSF11A, affecting the signal peptide of RANK, cause familial expansile osteolysis. Nat Genet 2000; 24(1):45–48. 150. Johnson-Pais TL, Singer FR, Bone HG, et al. Identification of a novel tandem duplication in exon 1 of the TNFRSF11A gene in two unrelated patients with familial expansile osteolysis. J Bone Miner Res 2003; 18(2):376–380. 151. Li J, Sarosi I, Yan XQ, et al. RANK is the intrinsic hematopoietic cell surface receptor that controls osteoclastogenesis and regulation of bone mass and calcium metabolism. Proc Natl Acad Sci USA 2000; 97(4):1566–1571.

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158. Krishnan V, Moore TL, Ma YL, et al. Parathyroid hormone bone anabolic action requires Cbfa1/Runx2-dependent signaling. Mol Endocrinol 2003; 17(3):423–435. 159. Roodman GD, Ibbotson KJ, MacDonald BR, et al. 1,25-Dihydroxyvitamin D3 causes formation of multinucleated cells with several osteoclast characteristics in cultures of primate marrow. Proc Natl Acad Sci USA 1985; 82(23):8213–8217. 160. Takahashi S, Goldring S, Katz M, et al. Downregulation of calcitonin receptor mRNA expression by calcitonin during human osteoclast-like cell differentiation. J Clin Invest 1995; 95(1):167–171. 161. Jilka RL, Hangoc G, Girasole G, et al. Increased osteoclast development after estrogen loss: mediation by interleukin-6. Science 1992; 257(5066):88–91. 162. Oursler MJ, Osdoby P, Pyfferoen J, et al. Avian osteoclasts as estrogen target cells. Proc Natl Acad Sci USA 1991; 88(15):6613–6617. 163. Girasole G, Jilka RL, Passeri G, et al. 17 beta-estradiol inhibits interleukin-6 production by bone marrow-derived stromal cells and osteoblasts in vitro: a potential mechanism for the antiosteoporotic effect of estrogens. J Clin Invest 1992; 89(3):883–891. 164. Mundy GR, Chen D, Oyajobi BO. Bone remodeling. Primer on the metabolic bone diseases and disorders of mineral metabolism. 5th edn. Washington, DC: American Society for Bone and Mineral Research; 2003:46–58. 165. Rodan GA, Martin TJ. Role of osteoblasts in hormonal control of bone resorption – a hypothesis. Calcif Tissue Int 1981; 33(4):349–351. 166. Howard GA, Bottemiller BL, Turner RT, et al. Parathyroid hormone stimulates bone formation and resorption in organ culture: evidence for a coupling mechanism. Proc Natl Acad Sci USA 1981; 78(5):3204–3208. 167. Locklin RM, Khosla S, Turner RT, et al. Mediators of the biphasic responses of bone to intermittent and continuously administered parathyroid hormone. J Cell Biochem 2003; 89(1):180–190. 168. Manolagas SC, Jilka RL. Bone marrow, cytokines, and bone remodeling. Emerging insights into the pathophysiology of osteoporosis. N Engl J Med 1995; 332(5): 305–311. 169. Enomoto H, Shiojiri S, Hoshi K, et al. Induction of osteoclast differentiation by Runx2 through receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin regulation and partial rescue of osteoclastogenesis in Runx2–/– mice by RANKL transgene. J Biol Chem 2003; 278(26):23971–23977. 170. Takeda S, Elefteriou F, Levasseur R, et al. Leptin regulates bone formation via the sympathetic nervous system. Cell 2002; 111(3):305–317. 171. Mundy GR, Rodan SB, Majeska RJ, et al. Unidirectional migration of osteosarcoma cells with osteoblast characteristics in response to products of bone resorption. Calcif Tissue Int 1982; 34(6):542–546. 172. Mundy GR, Poser JW. Chemotactic activity of the gamma-carboxyglutamic acid containing protein in bone. Calcif Tissue Int 1983; 35(2):164–168. 173. Dallas SL, Rosser JL, Mundy GR, et al. Proteolysis of latent transforming growth factor-beta (TGF-beta)-binding protein-1 by osteoclasts. A cellular mechanism for release of TGF-beta from bone matrix. J Biol Chem 2002; 277(24): 21352–21360. 174. Pfeilschifter J, Wolf O, Naumann A, et al. Chemotactic response of osteoblastlike cells to transforming growth factor beta. J Bone Miner Res 1990; 5(8):825–830. 175. Grotendorst GR, Seppa HE, Kleinman HK, et al. Attachment of smooth muscle cells to collagen and their migration toward platelet-derived growth factor. Proc Natl Acad Sci USA 1981; 78(6):3669–3672. 176. Seppa H, Grotendorst G, Seppa S, et al. Platelet-derived growth factor is chemotactic for fibroblasts. J Cell Biol 1982; 92(2):584–588.

152. Dougall WC, Glaccum M, Charrier K, et al. RANK is essential for osteoclast and lymph node development. Genes Dev 1999; 13(18):2412–2424.

177. Canalis E, Pash J, Varghese S. Skeletal growth factors. Crit Rev Eukaryot Gene Expr 1993; 3(3):155–166.

153. Boyce BF, Aufdemorte TB, Garrett IR, et al. Effects of interleukin-1 on bone turnover in normal mice. Endocrinology 1989; 125(3):1142–1150.

178. Valentin-Opran A, Charhon SA, Meunier PJ, et al. Quantitative histology of myeloma-induced bone changes. Br J Haematol 1982; 52(4):601–610.

154. Pacifici R, Rifas L, McCracken R, et al. Ovarian steroid treatment blocks a postmenopausal increase in blood monocyte interleukin 1 release. Proc Natl Acad Sci USA 1989; 86(7):2398–2402.

179. Stewart AF, Vignery A, Silverglate A, et al. Quantitative bone histomorphometry in humoral hypercalcemia of malignancy: uncoupling of bone cell activity. J Clin Endocrinol Metab 1982; 55(2):219–227.

Section 2: Osseous Spinal Tumors 180. Darby AJ, Meunier PJ. Mean wall thickness and formation periods of trabecular bone packets in idiopathic osteoporosis. Calcif Tissue Int 1981; 33(3):199–204. 181. Courtney AC, Hayes WC, Gibson LJ. Age-related differences in post-yield damage in human cortical bone. Experiment and model. J Biomech 1996; 29(11):1463– 1471. 182. McCalden RW, McGeough JA, Barker MB, et al. Age-related changes in the tensile properties of cortical bone. The relative importance of changes in porosity, mineralization, and microstructure. J Bone Joint Surg Am 1993; 75(8):1193–1205. 183. Seeman E. Pathogenesis of bone fragility in women and men. Lancet 2002; 359(9320):1841–1850. 184. Oxlund H, Mosekilde L, Ortoft G. Reduced concentration of collagen reducible cross links in human trabecular bone with respect to age and osteoporosis. Bone 1996; 19(5):479–484. 185. Bailey AJ, Wotton SF, Sims TJ, et al. Biochemical changes in the collagen of human osteoporotic bone matrix. Connect Tissue Res 1993; 29(2):119–132.

198. Mueller SM, Glowacki J. Age-related decline in the osteogenic potential of human bone marrow cells cultured in three-dimensional sponges. J Cell Biochem 2001; 82:583–590. 199. Muschler GF, Nitto H, Boehm CA, et al. Age- and gender-related changes in the cellularity of human bone marrow and the prevalence of osteoblastic progenitors. J Orthop Res 2001; 19:117–125. 200. Nishida S, Endo N, Yamagiwa H, et al. Number of osteoprogenitor cells in human bone marrow markedly decreases after skeletal maturation. J Bone Miner Metab 1999; 17:171–177. 201. Oreffo RO, Bord S, Triffitt JT. Skeletal progenitor cells and ageing human populations. Clin Sci (Lond) 1998; 94:549–555. 202. Stenderup K, Justesen J, Eriksen EF. Number and proliferative capacity of osteogenic stem cells are maintained during aging and in patients with osteoporosis. J Bone Miner Res 2001; 16:1120–1129.

186. Martin RB, Atkinson PJ. Age and sex-related changes in the structure and strength of the human femoral shaft. J Biomech 1977; 10(4):223–231.

203. D’Ippolito G, Schiller PC, Ricordi C, et al. Age-related osteogenic potential of mesenchymal stromal stem cells from human vertebral bone marrow. J Bone Miner Res 1999; 14:1115–1122.

187. Beck TJ, Oreskovic TL, Stone KL, et al. Structural adaptation to changing skeletal load in the progression toward hip fragility: the study of osteoporotic fractures. J Bone Miner Res 2001; 16(6):1108–1119.

204. Kassem M, Ankersen L, Eriksen EF, et al. Demonstration of cellular aging and senescence in serially passaged long-term cultures of human trabecular osteoblasts. Osteoporos Int 1997; 7(6):514–524.

188. Duan Y, Turner CH, Kim BT, et al. Sexual dimorphism in vertebral fragility is more the result of gender differences in age-related bone gain than bone loss. J Bone Miner Res 2001; 16(12):2267–2275.

205. Kveiborg M, Flyvbjerg A, Rattan SI, et al. Changes in the insulin-like growth factorsystem may contribute to in vitro age-related impaired osteoblast functions. Exp Gerontol 2000; 35(8):1061–1074.

189. Chan GK, Duque G. Age-related bone loss: old bone, new facts. Gerontology 2002; 48(2):62–71.

206. Fujieda M, Kiriu M, Mizuochi S, et al. Formation of mineralized bone nodules by rat calvarial osteoblasts decreases with donor age due to a reduction in signaling through EP(1) subtype of prostaglandin E(2) receptor. J Cell Biochem 1999; 75(2):215–225.

190. Shi S, Gronthos S, Chen S, et al. Bone formation by human postnatal bone marrow stromal stem cells is enhanced by telomerase expression. Nat Biotechnol 2002; 20:587–591. 191. Simonsen JL, Rosada C, Serakini N, et al. Telomerase expression extends the proliferative life-span and maintains the osteogenic potential of human bone marrow stromal cells. Nat Biotechnol 2002; 20:592–596. 192. Yudoh K, Matsuno H, Nakazawa F, et al. Reconstituting telomerase activity using the telomerase catalytic subunit prevents the telomere shortening and replicative senescence in human osteoblasts. J Bone Miner Res 2001; 16:1453–1464. 193. Gronthos S, Chen S, Wang C-Y, et al. Telomerase accelerates osteogenesis of bone marrow stromal stem cells by upregulation of cbfa1, Osterix, and osteocalcin. J Bone Miner Res 2003; 18(4):716–722. 194. Chan GK, Duque G. Age-related bone loss: old bone, new facts. Gerontology 2002; 48:62–71. 195. Bergman RJ, Gazit D, Kahn AJ, et al. Age-related changes in osteogenic stem cells in mice. J Bone Miner Res 1996; 11(5):568–577. 196. Erdmann J, Kogler C, Diel I, et al. Age-associated changes in the stimulatory effect of transforming growth factor beta on human osteogenic colony formation. Mechanisms Aging Devel 1999; 110:73–85.

207. Martinez ME, Medina S, Sanchez M, et al. Influence of skeletal site of origin and donor age on 1,25(OH)2D3-induced response of various osteoblastic markers in human osteoblastic cells. Bone 1999; 24(3):203–209. 208. Martinez ME, del Campo MT, Medina S, et al. Influence of skeletal site of origin and donor age on osteoblastic cell growth and differentiation. Calcif Tissue Int 1999; 64(4):280–286. 209. Long MW. Osteogenesis and bone-marrow-derived cells. Blood Cells Mol Dis 2001; 27(3):677–690. 210. Battmann A, Battmann A, Jundt G, et al. Endosteal human bone cells (EBC) show age-related activity in vitro. Exp Clin Endocrinol Diabetes 1997; 105(2):98–102. 211. Kveiborg M, Rattan SI, Clark BF, et al. Treatment with 1,25-dihydroxyvitamin D3 reduces impairment of human osteoblast functions during cellular aging in culture. J Cell Physiol 2001; 186(2):298–306. 212. Martinez P, Moreno I, De Miguel F, et al. Changes in osteocalcin response to 1,25dihydroxyvitamin D(3) stimulation and basal vitamin D receptor expression in human osteoblastic cells according to donor age and skeletal origin. Bone 2001; 29(1):35–41.

197. Long MW, Ashcraft EK, Normalle D, et al. Age-related phenotypic alterations in populations of purified human bone precursor cells. J Gerontol A Biol Sci Med Sci 1999; 54:B54–B62.

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SPECIFIC DISORDERS

Section 2

Osseous Spinal Tumors ■ i: Physiology and Assessment

CHAPTER

Osteoporosis

39

Christopher J. Mattern, Julie T. Lin and Joseph M. Lane

Osteoporosis is a systemic skeletal disease characterized by compromised bone strength that predisposes the skeleton to fracture. The strength of bone is related to the mass of the bone, the distribution of the mass, the microarchitectural alignment, the age of the bone, and the quality of the bone. The connectivity and microarchitectural alignment of the bone matrix play a critical role in providing strength to the bone. Niebur and colleagues have clearly demonstrated that loss of connectivity or the presence of sites of limited dimension increase the likelihood of local trabecular fracture.1 At the onset of bone formation, the initial bone that is deposited is undermineralized with respect to the final bone product and over time there is increased mineralization and saturation with crystal. The strength of bone increases with aging as a result of this maturation process. Highturnover bone states are associated with increased risk of fracture. Biochemically, bone is a composite material consisting of collagen and mineral. Collagen provides tensile strength, while mineral provides compressive strength. Collagen is biased in its orientation and bone is stronger along the primary axis of the collagen fibers and weaker in the transverse axis. In disease states of altered bone mineral content, such as osteomalacia, rickets, and osteogenesis imperfecta, the strength of bone can be seriously compromised. Consequently, both the quantity and quality of bone profoundly affect the overall strength of bone. Altered performance in either of these two areas can lead to an increased risk of low-energy fracture.

bone mass, men also lose bone gradually. During the period of greatest bone loss, trabecular bone is resorbed at least eight times greater than cortical bone due to the increased surface area of trabecular bone. Fortunately, in an effort to compensate for this loss of bone, the endosteal bone is preferentially lost, leaving the bulk of the bone at the greatest distance from the axial center which takes advantage of the moments of inertia to partially compensate for loss of bone. There is also a gradual increase in the dimensions of the cortical side of bone to partially compensate for this diminished mass. These findings are most evident in the diaphysis of long bones, and are less visible in the metaphyseal regions and in bones with a high proportion of trabecular bone. As bone is resorbed, the individual trabeculae begin to narrow and sites of prominent osteoclastic resorption begin to develop. These areas eventually lead to disconnectivity of the trabeculae. Since these areas of bone loss are not recognized as fractures, there is no effort on the part of the body to heal these trabeculae. As a result, the interconnectivity of the trabeculae declines in the trabecular bone, particularly during times of rapid resorption. The collagen in bone is continuously being turned over through osteoclastic bone resorption. This process is driven by the metabolic state or the presence of a site of imperfection. Osteoclasts work to carve out an area of Howship’s lacunae along the trabeculae or penetrating into the cortical bone. Following osteoclastic resorption, osteoblasts will begin to reestablish the skeleton. After the age of 40, this metabolic bone disease unit is incompletely reconstituted, leading to a net loss of bone through every cycle.

FRACTURE RISK

BONE TURNOVER

In the year 2002 an estimated 30 million women aged 50 or older had osteoporosis or were at risk of developing this condition (National Osteoporosis Foundation data). Fifty-five percent of people aged 55 and older have either osteoporosis or low bone mass. With the aging of the population this trend will increase. The lifetime risk of fracture of the hip, wrist, and spine approximates 40%.2–4

Calcium and vitamin D metabolism are intimately related and are both a part of the bone turnover cycle. Vitamin D is produced in the skin from 1 hour of sunlight or can be obtained by dietary supplementation. Vitamin D itself is made in the skin and is then transported to the liver where it is converted to 25-hydroxy vitamin D. This form of vitamin D has a half-life of 3 days. Alternatively, the liver can degrade vitamin D by activating the P-450 hydrolase system. Certain drugs that activate the P-450 system can lead to enhanced vitamin D catabolism and in some cases vitamin D deficiency. In particular, this has been well documented with the barbiturates and the seizure medications.5 In the face of low serum calcium levels, the human body activates parathyroid hormone, which travels to the kidney where it stimulates the conversion of 25-hydoxy vitamin D into the active vitamin D metabolite, 1,25 dihydroxy vitamin D. Activated vitamin D will then stimulate the kidney to retain calcium and excrete phosphate. The 1,25 dihydroxy vitamin D also travels to the intestine where it activates a cascade that ultimately leads to the increased absorption of calcium from the diet. Parathyroid hormone also travels to the bone where it activates bone resorption. Osteoblasts have receptors for parathyroid hormone and initiate the Rank-L system

INTRODUCTION

BONE BIOLOGY All individuals increase their bone mass after birth with a peak gain in bone mass occurring at the onset of rapid growth and during adolescence. Final peak bone mass is achieved between the ages of 25 and 30.4 Men can expect to achieve a higher peak bone mass than women. Certain ethnic groups such as African-Americans have greater bone mass than do Caucasian Americans. Once peak bone mass is achieved in women, there is a plateauing of bone mass followed by a very gradual decline in bone mass of approximately 0.3% per year until menopause. At menopause, the rate of bone loss will accelerate and women will lose 2% per year for a short period of time and then resume the gradual decline thereafter. After achieving peak

435

Part 3: Specific Disorders

that ultimately leads to the development of new osteoclasts via activation of preosteoclasts. Thus, calcium can be elevated by retaining calcium from the kidney, increasing calcium absorption from the gut, and releasing calcium by catabolizing the skeleton. Vitamin D has several other functions, most notably the physiological differentiation of osteoclasts. Vitamin D is also critical in calcium membrane transport in skeletal muscle. Disorders of the kidney such as renal osteodystrophy, which leads to destruction of the kidney, will lower the production of 1,25 dihydroxy vitamin D. Intestinal absorption is compromised in malabsorption syndromes, most notably celiac sprue, Crohn’s disease, and steroid overdose.6 In fact, serological evidence of celiac sprue is found in approximately 9% of osteoporotic patients.7 Calcium plays a critical role in bone homeostasis. As an intracellular signaler, calcium is tightly regulated by the body’s homeostatic mechanisms, and the body will maintain calcium levels at the expense of other tissues. The requirements of calcium vary with age and activity. Simple dairy products such as an 8-ounce glass of milk or a container of yogurt contain 280 mg of calcium. Certain foods rich in calcium, such as spinach, are unavailable for absorption. This results from the high oxalate content in spinach which binds the calcium and prevents its absorption. Calcium requirements for a growing child are 715 mg per day. From the ages of 10 to 25, 1300 mg of calcium are required per day. A healthy adult needs 800 mg per day. A pregnant woman requires 1500 mg of calcium per day, and this requirement increases to 2000 mg per day in lactating women. A postmenopausal woman needs 1500 mg per day, and any individual experiencing negative nitrogen balance or recovering from a major fracture requires 1500 mg per day.8,9 There are various forms of supplemental dietary calcium. The two major types are calcium carbonate and calcium citrate. Calcium carbonate has a higher content of calcium but requires a very low gastric pH to dissolve it. H2 blockers (e.g. cimetidine, famotidine) are often used in individuals with dyspepsia in order to obtain a more neutral pH, and this can preclude the ability to absorb calcium carbonate. Calcium citrate will dissolve at any pH. In addition, the citrate contained in calcium citrate will bind with the oxalate and prevent kidney stones. Consequently, calcium citrate is protective in individuals who have a history of kidney stones and can be absorbed in almost any pH environment. Calcium citrate is frequently the first choice of calcium supplementation, except in younger individuals or in instances where the clinician can document perfectly normal gastric function. There are a number of drugs that interfere with calcium retention, including cortical steroids, heparin, isoniazid, tetracycline, furosemide, and very large doses of caffeine. Vitamin D nutrition remains critical and studies have demonstrated the efficacy of calcium in the prevention of fractures. Calcium is typically supplemented in conjunction with Vitamin D. A recent review by Dawson-Hughes has indicated that the RDA of 400 units of vitamin D may in fact be insufficient.10 Eight hundred units, particularly in the older patient, may be more reasonable and appears to be the cutoff point at which improved muscle function and a subsequent decrease in falls and fractures were identified. Vitamin D in doses of up to 2000 units per day appear to be safe except in individuals with noted history of multiple kidney stones. Vitamin D can be given either as vitamin D2 or D3 or as final pathway products (1,25 dihydroxy vitamin D). The former will last for 2 months while the latter has a 4-hour half-life. Drugs with hydroxyl groups are degraded in the liver and often activate the P-450 hydrolase system leading to premature degradation of vitamin D. Most notable in this group are the antiepileptic seizure medications. In patients taking antiepileptics or any other drug that is degraded in the liver, vitamin D metabolism may be disrupted and higher dosages of vitamin D may be warranted.11 436

Peak bone mass is very closely associated with menstrual status. Women who have normal menstrual cycles of 10 episodes per year of approximately 4 days per episode are able to maintain their skeletal integrity and will lose bone at a maximal rate of 0.3% per year.12 This loss can be partially compensated with better nutrition and supplemental calcium. Women who are amenorrheic or who have irregular menstrual cycles may lose bone at a rate of up to 2% per year. In the young amenorrheic individual who has yet to achieve peak bone mass, there is a diminished ability to gain bone at precisely the time when one should be increasing her peak bone mass. Primary amenorrhea is defined as the absence of menses before the age of 16; however, women who have irregular or no periods after the age of 14 are susceptible to compromises of skeletal integrity. Common disorders that affect the menstrual cycle are low body weight, eating disorders, and excessive exercise. Young athletes who lack a normal menstrual cycle have an increased rate of stress fracture compared to women who have a normal menstrual cycle.13 Birth control pills, while reestablishing cycles, may not be totally successful in protecting the skeleton.14 Low body mass is frequently the common factor in most of these disorders and good nutrition is critical, particularly during skeleton growth and development. Mechanical factors affect bone mass. Bone responds to mechanical load by increasing bone mass and remodeling along lines of increased stress. Bone that lacks stress suffers a decline in bone mass. Normal load bearing will maintain the skeleton. Elevated loading will lead to changes in the skeleton as well. This is found primarily in bones of younger individuals with thick periosteum and decreases with aging and in those bones with limited periosteum. Very high loads overcome the ability of the body to adjust and can lead to stress fractures. In growing individuals up to the age of 30, exercise can lead to enhanced bone mass. High-impact programs have led to almost an 8% increase in bone mass compared to peers without similar programs.15 Once individuals reach a postmenopausal state, exercise rarely changes bone density. However, detailed studies have suggested that bone turnover is in fact decreased in such individuals. They have a lower rate of falling and, when corrected for the number of falls, the fracture rate is decreased. N-telopeptide, a measure of bone turnover, is similarly decreased in those individuals who exercise.16

BONE MASS Low bone mass is the single most accurate predictor of increased fracture risk. Bone mineral density is used to establish a diagnosis of postmenopausal osteoporosis and can predict future fracture risk. In the National Osteoporosis Risk Assessment (NORA) study, approximately 150 000 women were evaluated for 1 year in order to define a critical role for bone density in predicting fracture risk.17 Results from this study suggested a strong continuous relationship between lower bone mineral density and higher fracture rate as expressed by the number of women who experienced fractured vertebrae. Fracture rates were highest among women with the lowest T-scores. Bone density can be determined by dual-energy X-ray absorptiometry (DEXA scan), quantitative computed tomography (q-CT), peripheral measurements, and ultrasound. Of these modalities, DEXA (Fig. 39.1) is the most accurate and is considered to be the gold standard.18 Furthermore, DEXA is the most common form of bone density utilized in centers that measure the area of bone density of the spine and several parameters within the hip, most notably, the total femur, femoral neck, and intertrochanteric area. During DEXA scanning, an intervertebral assessment of the spine (Fig. 39.2) can be performed to assess the anatomic detail of the thoracic and lumbar spine and determine if vertebral compression is present. The area of mineral content is then compared with

Section 2: Osseous Spinal Tumors

DXA Results Summary: Region

Area (cm2)

BMC (g)

BMD (g/cm2)

T -Score

PR (%)

Z -Score

AM (%)

L1 L2 L3 L4 Total

9.38 10.49 12.07 13.15 45.08

6.66 7.73 10.16 10.65 35.20

0.711 0.737 0.842 0.810 0.781

−1.9 −2.6 −2.2 −2.8 -2.4

77 72 78 73 75

−1.9 −2.6 −2.2 −2.7 -2.4

77 72 78 73 75

B

1.6

Total

1.4

BMD

1.2 1.0 0.8 0.6 0.4 0.2 20 A

25

30

35

40

45

50 55 Age

60

65

70

75

80

85

C

Fig. 39.1 (A) Dual energy x-ray absorptiometry (DEXA) scan of the lumbar spine (L1–4) in a 29-year-old woman with suspected osteoporosis. (B) A summary of bone mineral density values and corresponding T- and Z-scores confirm the presence of osteoporosis (T-score <2.5 standard deviations). The Z-score of less than 1.5 standard deviations prompted a work-up for secondary causes of osteoporosis. (C) A graphical representation of the patient’s bone mineral density score as compared to age-matched controls.

age-corrected peers in order to obtain a Z-value and then with an ideal peak bone mass in a normal individual not corrected for age to obtain a T-value. The precision of DEXA is approximately 2% in the spine and a little over 3% in the hip. It is important to recognize that the presence of scoliosis or arthritis can artificially elevate DEXA scores in the spine. The precision of q-CT is less than that of DEXA and the radiation exposure is greater. Peripheral bone mass evaluations have only a 70% correlation with the hip and the spine. The World Health Organization has defined a normal bone density as a T-value of less than 1 standard deviation compared to normals.19 Osteopenia is defined as bone mass between 1 standard deviation and 2.4 standard deviations below normal. Osteoporosis is classified as a bone deficiency of 2.5 or more standard deviations. The risk of fracture is increased twofold in the spine and 2.5 times in the hip for each standard deviation below peak bone mass.20 In recent protocols, however, these values are used for epidemiological and demographic studies, and treatment protocols call for an earlier intervention with far less bone deficiency. The Z-value becomes critical in differentiating primary osteoporosis from secondary forms of osteoporosis. In particular, Z values of 1.5 or worse should be evaluated for secondary forms of osteoporosis. Strength of bone is also related to turnover and other aspects of bone quality. While the fracture rate is greatest in those individuals with the lowest bone mass, there are individuals

with apparently relatively normal levels of bone mass who in fact have vertebral and hip fractures. Patients with hip or vertebral fractures are more likely to experience future fractures than are patients with no fractures. The risk of vertebral fracture rises rapidly with age for both men and women. In the United States women are two to three times more likely to experience a vertebral fracture than men, but when corrected for age, this disparity disappears. Biochemical markers have been introduced to evaluate and differentiate between high- and low-turnover osteoporosis. Bone resorption markers include collagen breakdown products – most notably, the N-telopeptides and C-telopeptides in the pyridinoline collagen cross-link products. These components are not degraded by the body and can be detected in both the serum and the urine. Bone formation markers are more popularly directed toward bone-specific alkaline phosphatase and osteocalcin. Bone resorption markers appear to have better correlation with fracture risk. The bone formation markers are disease specific and often used to test the efficacy of treatment interventions. The overall risk for a low-energy fracture is related to high-turnover states and low bone mass. Additional independent risk factors include low body weight, recent loss of body weight, personal history of fragility fracture, a first-degree relative with a fragility fracture, and smoking.21 In individuals with low body weight (persons less than 127 lb for a 5' 5" individual), there is inadequate body fat 437

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Fig. 39.2 An intervertebral assessment of the spine can be obtained during DEXA scanning to provide additional anatomic detail of the thoracic and lumbar spine and allow for the identification of vertebral compression fractures. The film is from the same patient as in Figure 39.1.

to sustain extraovarian production of estrogen. Recent loss of body weight correlates with an increased number of bone resorption sites within the trabecular skeleton, and this weakens the trabecular microarchitecture and increases the risk of fracture. A personal history of fragility fracture or a family history might suggest genetic causes such as variations in collagen quality or quantity. Smoking is associated with inadequate nutrition and enhanced destruction of endogenous estrogen. Additional risk factors which have been identified include impaired vision, estrogen deficiency at an early age, dementia, poor health and fragility, recent falls, low calcium, lifetime history of low calcium intake, low physical activity, and alcohol intake in excess of two drinks per day. Lastly, individuals taking drugs that are known to cause osteoporosis (e.g. glucocorticoid steroids) and patients with diseases associated with osteoporosis (e.g. polio and various high bone turnover states) are also at high risk.

WORK-UP OF A PATIENT WITH OSTEOPOROSIS A patient who presents with a fracture should be queried as to whether it was a high-energy or low-energy event (Fig. 39.3). All lowenergy fractures should be considered pathologic, stemming either from a local disease or a deranged metabolic state. If the patient does not have evidence of decreased bone density then a careful examina438

tion of the fracture should include special imaging studies (CT scan or MRI) to rule out the possibility of a primary or metastatic tumor. To begin the work-up, a complete blood count with differential, a sedimentation rate, and immunoelectrophoresis of both urine and blood should be obtained as these studies can help to rule out marrow disorders. Bone marrow disorders can account for up to 1–2% of pathologic fractures. Multiple myeloma currently affects 400 000 patients in the United States, and this number dwarfs the prevalence of osteogenic sarcomas (600 people per year). Multiple myeloma can be diagnosed by serum blood studies in 80% of patients, while the remaining 20% will have mild abnormalities on serum analysis followed by confirmatory testing of urine. Anemia and an increased sedimentation rate demands a work-up for multiple myeloma. Among the endocrinopathies, the common forms aside from early menopause include hypoparathyroidism, hyperparathyroidism, type 1 diabetes, and Cushing’s disease. Primary hyperparathyroidism occurs in 1 in 200 women and is diagnosed with elevated calcium.22 Hyperthyroidism is often iatrogenic, typically arising in individuals who are being treated for low thyroid function who take excessive doses of thyroid replacement hormone, which shuts off TSH and increases bone turnover. High turnover is associated with loss of bone in each cycle. Type 2 diabetes is associated with high insulin, while Type 1 diabetes is associated with low insulin. Insulin is a growth factor necessary for bone health; therefore, type 1 diabetes, with low insulin and a loss of calcium in the urine, is frequently associated with osteoporosis. Excessive steroids used in the treatment of an array of diseases can lead to iatrogenic osteoporosis. Corticosteroids lead to decreased absorption of calcium across the gut, increased urinary calcium loss, decreased osteoblastic bone formation, and increased bone resorption and secondary hyperparathyroidism. Avenues of treatment include increased therapeutic doses of vitamin D, calciumretaining diuretics, and agents that decrease bone resorption such as bisphosphonates (see below). There may be a possible role for therapeutic PTH in this disorder but this claim is premature at this period in time. Work-up for this group of patients should include a T-3, T-4, TSH-Irma, Intact-PTH, fasting glucose levels, and an investigation of present or past steroid use. Osteomalacia, or failure of mineralization, is a common entity in the United States. Among the hip fracture patients, up to 40–50% of patients will demonstrate this disorder. Even in patients undergoing primary hip replacement without existing apparent mineral disorders, approximately 20% have evidence of osteomalacia.23 The causes of osteomalacia are nutritional, vitamin D deficiency, and disorders of intestinal absorption of vitamin D, such as celiac sprue. This latter entity occurs in 1 in 22 patients presenting with osteoporosis and at a much higher rate in those individuals with milk intolerance.24 Other diseases include renal osteodystrophy, renal tubal acidosis, and defects of vitamin D metabolism caused by drugs such as seizure medications. Laboratory tests that are diagnostic include an elevated intact PTH and a low 25-hydroxy vitamin D. An elevated bone alkaline phosphatase, decreased serum phosphate (except in renal disease), and low serum calcium also suggest abnormal vitamin D metabolism. In the setting of a fracture, alkaline phosphatase will rise and peak, usually within 5 days of the fracture. Therefore, in the setting of a new fracture, an elevated alkaline phosphatase becomes very meaningful if the evaluation is carried out 2–3 weeks after the fracture has occurred. It is important to recognize that alkaline phosphatase may be elevated simply because of the repair process itself and may not correlate with osteomalacia. Conversely, Intact-PTH and 25-hydroxy vitamin D are the markers of choice and are valid indicators of mineral metabolism. Confirmation of low vitamin D levels can be demonstrated by low urinary calcium, typically at a level of less than 100 mg per liter of urine.

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Low energy vertebral fracture

DEXA scan

Normal bone density

CT or MRI to rule out tumor

Low bone density

Rule out multiple myeloma • Hemoglobin • ESR • Serum/urine immunoelectrophoresis

Rule out endocrinopathy • Hyperthyroidism (T3, T4, TSH) • Hyperparathyroidism (PTH) • Cushing’s disease • Type I diabetes mellitus

Rule out osteomalacia • 25(OH)vitamin D • PTH • Bone alkaline phosphatase • Serum/urine calcium

Osteoporosis • N-telopeptide

Low turnover osteoporosis • N-telopeptide < 30

High turnover osteoporosis • N-telopeptide > 40

Thus, the work-up for metabolic bone disease should include eliciting a history of low-energy fragility fracture. A further work-up should include a complete blood count with differential, immunoelectrophoresis, and evaluation for an underlying endocrinopathy or osteomalacia. Once this has been performed attention should then be directed to differentiating between high or low turnover since the treatment modalities are different. Bone markers, most importantly collagen breakdown products, may be of assistance in this endeavor. For example, the normal range of urinary N-telopeptide is 5–65 nm BCE/mm CRT; however, in healthy individuals the N-telopeptide is usually 20–40 nm. Values over 40 but less than 65 may indicate a high-turnover bone loss state, and values over 65 represent a pathological bone resorption state. Individuals who present with low Ntelopeptide and osteoporosis suffer from a low-turnover state with the primary defect being inadequate bone formation rather than increased bone resorption.

Fig. 39.3 Algorithmic approach to vertebral compression fractures.

BIOMECHANICS AND FRACTURES Fractures are often related to injuries. Greenspan and colleagues demonstrated that the odds ratio is increased with falls to the side by 5.7 in the ambulatory patients,25 and by 2.7 for every standard deviation below peak bone mass. In a nursing home setting, however, a fall to the side is associated with a 21-fold increase risk of fracture.26 Aharonoff et al., in a series of hip fractures, found that 75% fell while standing, 3.5% fell down stairs, 7% fell out of a bed or a chair, 3% were involved in a car or a bike accident, 2.5% in assault, and 9% from other issues.27 Most falls occurred at home in the afternoon but there was no evidence of a seasonal variation. Myers and Wilson reviewed falls and injuries to the spine.28 They found that patients over the age of 60 with symptomatic vertebral fractures could recount a clear fall in 50% of cases and could report a controlled activity, such as reaching, bending or lifting, in 20% of cases. Only 30% could not identify an initiating event. 439

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The epidemiology of vertebral fractures is continuously under evolution, often because there is a lack of universal clinical definition. There are 1.5 million low-fragility fractures in the United States each year, of which 700 000 occur in the spine, and only one-third of which are symptomatic.29 Some patients may present with either no symptoms or such trivial symptomatology that they are unaware that a fracture has occurred. Drug trials have helped to redefine vertebral fractures, which can be defined as a new fracture in which there is a 20% collapse of the vertebral body or a 40% decrease in the total area of the vertebral body. When less dramatic changes were used, the diagnostic precision decreased dramatically. The FDA has now accepted the former definition. Clinically significant fractures have a very loose description, ranging from patients with mild back pain to those whose pain requires narcotics or interventions. The majority of patients with new vertebral fractures go undiagnosed. Quite often, the recognition of the fracture occurs due to the patient’s awareness of loss of height. Height loss of up to 2" can occur naturally from narrowing of the disc space and some physiological kyphosis. Changes of more than 2" suggest the presence of osteoporosis. Other diseases include kyphosis, scoliosis, and spondylolisthesis. Vertebral fractures occur more commonly from spontaneous minor trauma such as anterior loading secondary to gravitational forces during daily activities. Myers and Wilson identified a safety factor indicating that once the load surpasses the strength of the bone, the bone is at risk.28 There is a clear correlation between decreasing bone density and the ability to handle loads anterior to the body. Risk factors associated with vertebral fractures include postmenopausal women over the age of 55, low bone mass evaluations, diagnosis of osteoporosis, prominent thoracic kyphosis, loss of 2" of height, and glucocorticoid steroids. The most common locations for vertebral fractures are in the midthoracic range and at the thoracolumbar junction. These correspond to the most compromised regions of the spine. A history of prior vertebral fractures places a patient at risk for future vertebral fracture. Lindsay et al. showed that in those individuals who have had a fracture, a subsequent fracture within the next year occurred in 14–20%.30 Drug therapies have a profound ability to decrease the risk of vertebral fracture (see below). Fractures that occur proximal to T4 or fractures in men and women less than 50 years of age with little or no trauma should raise the clinician’s suspicion for an osteoporotic state. Similarly, fractures in a population at low risk such as men, blacks, and Latino women require special studies to rule out other etiologies, most notably tumorous conditions. There are three forms of low-energy vertebral fractures including wedge, biconcave, and crush. The European Prospective Osteoporosis Study trial evaluated vertebral deformity and future fracture risk in men and women.31 Over 1500 men and women were evaluated in Europe. The prevalence of all deformities were 12% in females and 12% in males, and the prevalence increased with age for both sexes, while the rate of increase was larger in the female population. The consequences of vertebral fractures can affect the physical well-being of the patient. Vertebral fractures may cause severe pain, kyphosis deformity, loss of height, impaired physical function, and decreased lung capacity. Leidig et al. studied 63 postmenopausal women with at least one vertebral fracture and showed that pain and disability was significantly greater in women with a relatively greater height loss and a high degree of kyphosis compared to less height loss and medium kyphosis.32 With respect to pulmonary compromise, Leech et al. found that both decreased lung capacity and reduced pulmonary function are serious complications of multiple vertebral fractures and resultant kyphosis.33 Studies suggest that there may be a relationship between vertebral height loss and decreased lung function. In the review of vertebral fractures, Kado et al. showed an increased risk of death following fracture, including 11 000 exces440

sive deaths per year for 5 years following fracture.34 Hip fracture patients have 33 000 excessive deaths in the first year, and vertebral compression fractures are associated with more deaths than hip fractures. Furthermore, the study showed that patients with a moderate fracture had a 23% increased death rate and patients with a severe fracture had a 37% increased risk of death compared to osteoporotic patients without vertebral compression fractures. The study found that the deaths were strongly associated with pulmonary disease. Other problems patients with vertebral fractures encounter include severe pain, deformity, gait alterations resulting in an increased risk of falls, social role alterations, clinical depression including discomfort, anxiety about the future, and compromise of a number of quality of life parameters. A final issue for these patients is the change in posture that accompanies vertebral wedge fractures. If the kyphosis is associated with a wedge fracture, it can be compensated by hyperlordosis. Often, these patients can function quite well in terms of gait parameters. However, if the patient has limited flexibility of the lumbar spine or preexisting spinal stenosis, the kyphosis cannot be compensated. In these instances, the head is thrust forward, the center of gravity is shifted in front of the ankle, and the patient has a decreased performance in the 6-minute walking test, the ‘get up and go’ test, and the single stance time test. In an effort to compensate for the progressive kyphosis, the patient can aggravate preexisting asymptomatic or controllable spinal stenosis due to his/her intent to acquire hyperlordosis. A relatively recent advancement in the treatment of vertebral compression fractures features minimally invasive kyphoplasty, which aims to reduce the fracture, restore vertebral height and alignment, and provide a solid foundation to maintain fracture reduction and prevent future compression fracture (Fig. 39.4).

AGENTS IN THE TREATMENT OF OSTEOPOROSIS Therapeutic agents for osteoporosis fall into two groups: those which are antiresorptive and those which stimulate bone anabolic (Table 39.1). Antiresorptive agents include the estrogens and the selective estrogen receptor modulators (SERMs), calcitonin, and the family of bisphosphonates, including alendronate and risedronate. Oral bisphosphonates include alendronate and risedronate, and intravenous agents include pamidronate and zolendronate. Bone stimulatory agents have in the past included largely the experimental fluorides and the PTH-rP analogs. The recent release by the FDA of the recombinant PTH now provides a strong anabolic agent. As might be expected, the antiresorptive agents work primarily in those patients with high resorptive rates as evidenced by increased collagen breakdown products, whereas the anabolic agents are most effective for those patients with low bone turnover states. The first line of therapy against osteoporosis remains dietary supplementation with calcium and vitamin D. These agents in combination can decrease bone resorption and can lead to a better quality of bone mineralization. Numerous studies have demonstrated that in combination these agents can decrease hip fractures on the order of 25% in nursing home populations.35 This occurs even in the situation where the bone density may not increase or could in fact decrease slightly. In the subpopulation that presents with osteomalacia, 20–40% will respond to these agents. In addition, calcium is critical for the efficacy of the antiresorptive agents, and the bisphosphonates will not work in the absence of calcium supplementation. The benefits of calcium carbonate versus calcium citrate have been discussed previously. The carbonates have the highest calcium content, but are associated with constipation and flatulence. As well, in the absence of normal gastric acidity, calcium carbonate is poorly absorbed. Consequently, patients on

Section 2: Osseous Spinal Tumors

B

A

C

D

Fig. 39.4 Kyphoplasty. (A) Preoperative standing lateral radiograph of a 71-year-old woman with osteoporosis, kyphotic spine deformity, and vertebral compression fractures at T7, T11, and T12. (B) Intraoperative fluoroscopic image demonstrates a guide needle crossing the pedicle of T7 prior to entering the vertebral body of T7. (C) A balloon catheter is inflated to reduce the fracture and restore vertebral height. Three to four milliliters of bone cement are then injected into the cavity produced by balloon inflation to obtain a stable reduction. (D) Postoperative standing radiograph reveals reduction of the T7 vertebral fracture.

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Table 39.1: Treatment of Osteoporosis CALCIUM SUPPLEMENTATION Calcium citrate (1200–1500 mg/day) Calcium carbonate (1200–1500 mg/day) VITAMIN D SUPPLEMENTATION Vitamin D (400–800 units/day) HIGH-TURNOVER OSTEOPOROSIS (N-TELOPEPTIDE >40) ANTIRESORPTIVE AGENTS Oral bisphosphonates Alendronate (10 mg/day or 70 mg/week) Risedronate (5 mg/day or 35 mg/week) Intravenous bisphosphonates Pamidronate (30 mg q 3 months)† Zolendronate (4 mg/year)† Selective estrogen receptor modulators (SERMs)‡ Raloxifene Calcitonin Nasal calcitonin (200 IU/day) LOW-TURNOVER OSTEOPOROSIS (N-TELOPEPTIDE <30) ANABOLIC AGENTS Recombinant parathyroid hormone (1–34) (20 μg/day sq) †

Off-label use in the United States. ‡ The reduction of osteoporotic fracture risk in postmenopausal women is no longer an FDA-supported indication for estrogen replacement.

H2 blockers are poor candidates for calcium carbonate. In contrast, calcium citrate dissolves in all ranges of gastric acidity and clearly decreases the risk of kidney stones. Target doses of vitamin D are 800 units per day in patients older than 60 and greater than 1000 units per day in patients taking drugs that increase vitamin D degradation (e.g. antiepileptic medications).

Hormone therapy Estrogen hormone therapy has been used for over 40 years. Based on numerous studies, including the Women’s Health Initiative, there is now very clear evidence that hormone therapy with or without progesterone can decrease all fractures by approximately 35%.36 However, it carries with it some inherent problems. Specifically, it may lead to an increased risk of stroke, heart attack, phlebitis, pulmonary emboli, and a significantly increased risk of breast cancer. The breast cancer risk is increased up to 40% after 10 years of therapy and even stopping estrogen still carries the risk. Recent data would suggest that even in the absence of progestin, estrogen is deleterious, and there is some suggestion that it may increase the risk of dementia. Thus, the FDA no longer accepts estrogen in the treatment of osteoporosis, and its use should only be for those conditions that require estrogen such as postmenopausal symptomatology. From the perspective of the bone cell, SERMS, such as tamoxifen, are estrogen agonists. Seventy percent of patients on tamoxifen will experience the beneficial effects of estrogen. Tamoxifen cannot be used in the treatment of osteoporosis because it has profound postmenopausal symptomatology and has a very high rate of secondary uterine cancer. The most commonly used SERM is raloxifene. This agent has been shown to increase the bone mass in the spine and decrease the fracture rate by 40%.37 There is no risk of uterine cancer and the risk of breast cancer is decreased, but there is an increased risk of thrombophlebitis and pulmonary embolism. In addition, there is no protection against hip fracture. Therefore, this agent only works in the spine and does not appear to function in the areas of nonvertebral fracture. 442

Calcitonin Calcitonin is an agent which can be delivered through a nasal administration. In a study of 100 versus 200 versus 400 international units per day, the 200-unit dose decreased spinal fractures by 33% but there was no statistical protection at the low or high dose, and at no dose was there protection against hip fractures.38 Calcitonin appears to have some role in the pain pathway and therefore is used often in those cases of painful osteoporosis but clearly its benefit is quite meager compared to the bisphosphonates and Intact-PTH. A major side effect is one of nasal irritation and occasional nosebleeds.

Bisphosphonates Bisphosphonates are a family of drugs which are analogs of pyrophosphate. The central oxygen between the two phosphates is substituted with a carbon and then a side chain of variable length, which may or may not contain a ring structure or nitrogen group, is added. Bisphosphonates are nondegradable. They bind the surface of bone beneath osteoclasts and prevent the resorption of bone by acting as a biochemical shield. If imbibed by the osteoclasts they either interfere with the lipid membrane production or with the cell cycle leading to premature death of the osteoclast via apoptosis. Thus, they are inhibitors of osteoclasts and lead to apoptosis of the osteoclasts. The second- and third-generation bisphosphonates seem to disassociate the inhibition of resorption from the inhibition of bone formation, with resorption being more markedly affected than formation. Bisphosphonates have been shown to decrease all fractures in all bones by about 50%.39–41 They are more effective in those individuals with previous vertebral fractures but they can decrease hip fractures by 50% within 6 months of therapy. They are acidic medications and must be taken on an empty stomach, and less than 1% of the medication is absorbed. Dyspepsia initially occurred at a rate of 30%, but this side effect can be decreased dramatically by switching the medications from a daily dose to a single weekly dose in the case of

Section 2: Osseous Spinal Tumors

risedronate and the alendronate. Bisphosphonates also have shown a benefit in the treatment of men with osteoporosis, children with osteogenesis imperfecta, osteonecrosis, prosthetic loosening, and steroid-induced osteoporosis. Alendronate has been used for the longest period of time. In a recent study, 3658 women with osteoporosis and an existing vertebral fracture or osteoporosis of the femoral neck without vertebral fracture were treated for 3–4 years with alendronate.42 The investigators found that the pooled group of patients treated with alendronate demonstrated a diminished relative risk of hip fracture (0.47 relative risk), radiographic vertebral fracture (0.52 relative risk), clinical vertebral fracture (0.55 relative risk), and all other clinical features (0.70 relative risk). Studies in animal models have suggested treatment with high doses of bisphosphonates results in the accumulation of microdamage.43 This microdamage can be measured, with loss of toughness as the only biomechanical parameter, and has given rise to concerns about the long-term benefit of these agents. Current recommendations under consideration include a rest after 5 years of therapy once the benefit to the patient has reached a plateau, with a resumption of the medication once the bone resorption markers begin to rise again. There have been no randomized, controlled studies from which to develop clear recommendations; however, there is a clear concern by the bone biologists about long-term continued use. A number of individuals cannot tolerate oral bisphosphonates due to poor physiology of the esophagus or clinically significant esophagitis. In those individuals, intravenous bisphosphonates, most notably pamidronate and zolendronate, appear to provide a comparable decline in resorption markers and increase in bone density to that of alendronate and risedronate. Of interest is that a 4 mg dose of the zolendronate may be given once a year leading to protection of the skeleton for at least 12 and perhaps 18 months.44 The efficacy of treatment with bisphosphonates should not be judged by increasing bone density. Studies have indicated that if one breaks down the bisphosphonate users into low-dose users who gained a low amount of bone mass and high-dose users who gained a high amount of bone, there is the same fracture potential in both groups. Therefore, only a small percentage of the protection against fractures is actually related to gains in bone density while the remainder is due to other changes in bone quality and turnover.

Parathyroid hormone Parathyroid hormone (PTH) is the only proven anabolic agent for the treatment of osteoporosis. In continuous doses, PTH is associated with high levels of bone resorption and a gradual loss of bone. However, when given in a pulsatile fashion lasting only 15–30 minutes, it will stimulate osteoblasts and will have very little effect on the osteoclast recruitment. A shortened version of PTH that includes the N-terminal 1–34 amino acids has been on trial and is now in active use. At a dose of 20 μg per day this can increase the bone mass up to 8% in the spine and about half that level in the hip.45 Hip fracture protection occurs from 10–12 months which is slightly longer than with the bisphosphonates. PTH is a daily subcutaneous injection, and its side effects include cramps, hypertension, and headaches. Clearly, bisphosphonates can prevent fractures and prevent disuse osteoporosis. Several studies have demonstrated that bisphosphonates do not adversely affect fracture healing in animals.46,47 However, in these studies, the data suggested that bisphosphonates have a profound effect on the fracture remodeling process. There is a delay in conversion of woven bone to lamellar bone and all markers of progression are prolonged. However, the callus is much larger, and when tested biomechanically, the fracture seems to be of equal strength to those of control subjects. These studies have been per-

formed in animals that always heal their fractures, and there are few data in the compromised patient or in the compromised animal. PTH, on the other hand, has been shown in many studies to enhance fracture healing so that the maturation is faster than in controls, and the biomechanics of every stage of healing are superior to those in the control population.48 Therefore, PTH may augment fracture healing. Bisphosphonates, in most circumstances, probably have such a small effect on the fracture healing process that they are of little consequence, particularly in those fractures which heal in a timely manner and are located in the metaphyseal/diaphyseal area. In the compromised patient or in those patients with fractures that have a track record of poor healing, bisphosphonates may be more deleterious. An alternative would be to hold off on bisphosphonates for 3–6 weeks in those fractures that heal regularly and hold off entirely in those fractures that are compromised. There are no data regarding the effect of bisphosphonates or PTH on spine fusion. As bone healing in spine fusion is much more difficult than long bone fractures, caution should be urged in the use of bisphosphonates until further data are available, particularly in cases of long spine fusions of compromised individuals.

CONCLUSIONS Osteoporosis is a common entity that is occurring with increased frequency due to the aging of the population, and affects women more than men, though both sexes are at risk. Osteoporosis is associated with increased fractures. The diagnosis of osteoporosis can be made with a bone density evaluation. Primary versus secondary osteoporosis should be established. Secondary causes include endocrinopathies, osteomalacia, and bone marrow alterations. Vertebral fractures do lead to significant mortality and morbidity and the mere presence of a fracture should raise the clinician’s suspicion of underlying osteoporosis, especially in the case of fractures out of proportion to the energy level of the trauma. In the absence of treatment, secondary fractures are inevitable and treatments that can decrease fracture risk by 50% should be strongly considered. All individuals should receive calcium and vitamin D supplementation. There is an array of medications for the prevention and treatment of osteoporosis. The most prominently used are the bisphosphonates for their antiresorptive effects and PTH for its anabolic effects. With an increased awareness of the effectiveness of these treatment modalities, coupled with the development of new therapies, the clinician can play an important role in decreasing the morbidity and mortality of osteoporosis.

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32. Leidig G, Minne HW, Sauer P, et al. A study of complaints and their relation to vertebral destruction in patients with osteoporosis. Bone Miner 1990; 8(3):217–229. 33. Leech JA, Dulberg C, Kellie S, et al. Relationship of lung function to severity of osteoporosis in women. Am Rev Respir Dis 1990; 141(1):68–71. 34. Kado DM, Browner WS, Palermo L, et al. Vertebral fractures and mortality in older women: a prospective study. Study of Osteoporotic Fractures Research Group. Arch Intern 1999; 159(11):1215–1220. 35. Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D3 and calcium to prevent hip fractures in the elderly women. N Engl J Med 1992; 327(23):1637–1642. 36. Anderson GL, Limacher M, Assaf AR, et al. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women’s Health Initiative randomized controlled trial. JAMA 2004; 29(14):1701–1712. 37. Maricic M, Adachi JD, Sarkar S, et al. Early effects of raloxifene on clinical vertebral fractures at 12 months in postmenopausal women with osteoporosis. Arch Intern Med 2002; 162(10):1140–1143. 38. Chestnut CH III, Silverman S, Andriano K, et al. A randomized trial of nasal spray calcitonin in postmenopausal women with established osteoporosis: The Prevent Recurrence of Osteoporotic Fractures Study. PROOF Study Group. Am J Med 2000; 109:267–276. 39. Lips P. Prevention of hip fractures: drug therapy. Bone 1996; 18(3 Suppl): 159S–163S. 40. Seeman E. Osteoporosis: trials and tribulations. Am J Med 1997; 103(2A):74S– 87S; discussion 87S–89S.

22. Bilezikian JP, Silverberg SJ. Clinical practice. Asymptomatic primary hyperparathyroidism. N Engl J Med 2004; 350(17):1746–1751.

41. Chrischilles EA, Dasbach EJ, Rubenstein LM, et al. The effect of alendronate on fracture-related healthcare utilization and costs: the fracture intervention trial. Osteoporos Int 2001; 12(8):654–660.

23. Arnala I, Kyrola K, Kroger H, et al. Analysis of 245 consecutive hip fracture patients with special reference to bone metabolism. Ann Chir Gynaecol 1997; 86(4): 343–347.

42. Black DM, Thompson DE, Bauer DC, et al. Fracture risk reduction with alendronate in women with osteoporosis: the Fracture Intervention Trial. FIT Research Group. J Clin Endocrinol Metab 2000; 85(11):4118–4124.

24. Green PH, Jabri B. Coeliac disease. Lancet 2003; 362(9381):383–391.

43. Komatsubara S, Mori S, Mashiba T, et al. Suppressed bone turnover by long-term bisphosphonate treatment accumulates microdamage but maintains intrinsic material properties in cortical bone of dog rib. J Bone Miner Res 2004; 19(6):999–1005.

25. Greenspan SL, Myers ER, Maitland LA, et al. Fall severity and bone mineral density as risk factors for hip fracture in ambulatory elderly. JAMA 1994; 271(2):128–133. 26. Greenspan SL, Myers ER, Kiel DP, et al. Fall direction, bone mineral density, and function: risk factors for hip fracture in frail nursing home elderly. Am J Med 1998; 104(6):539–545. 27. Aharonoff GB, Dennis MG, Elshinawy A, et al. Circumstances of falls causing hip fractures in the elderly, 1998. J Orthop Trauma 2003; 17(8 Suppl):S22–S26. 28. Myers ER, Wilson SE. Biomechanics of osteoporosis and vertebral fracture. Spine 1997; 22(24 Suppl):25S–31S. 29. Riggs BL, Melton LJ III. The worldwide problem of osteoporosis: Insights afforded by epidemiology. Bone 1995; 17:505S–511S. 30. Lindsay R, Silverman SL, Cooper C, et al. Risk of new vertebral fracture in the year following a fracture. JAMA 2001; 285(3):320–323.

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31. Reeve J, Lunt M, Felsenberg D, et al. Determinants of the size of incident vertebral deformities in European men and women in the sixth to ninth decades of age: the European Prospective Osteoporosis Study (EPOS). J Bone Miner Res 2003; 18(9):1664–1673.

44. Reid IR. Bisphosphonates: new indications and methods of administration. Curr Opin Rheumatol 2003; 15(4):458–463. 45. Neer RM, Arnaud CD, Zanchetta JR, et al. Effect of parathyroid hormone (1–34) on fractures and bone mineral density in postmenopausal women with osteoporosis. N Engl J Med 2001; 344(19):1434–1441. 46. Koivukangas A, Tuukkanen J, Kippo K, et al. Long-term administration of clodronate does not prevent fracture healing in rats. Clin Orthop 2003; 408:268–278. 47. Li J, Mori S, Kaji Y, et al. Effect of bisphosphonate (incadronate) on fracture healing of long bones in rats. Bone Miner Res 1999; 14(6):969–979. 48. Nakajima A, Shimoji N, Shiomi K, et al. Mechanisms for the enhancement of fracture healing in rats treated with intermittent low-dose human parathyroid hormone (1–34). J Bone Miner Res 2002; 17(11):2038–2047.

PART 3

SPECIFIC DISORDERS

Section 2

Osseous Spinal Tumors ■ i: Physiology and Assessment

CHAPTER

Paget’s Disease

40

Clifford R. Everett and Rajeev Patel

INTRODUCTION Osteitis deformans was initially described by Sir James Paget, an English surgeon, in 1877 as a chronic inflammation of bones.1 Paget’s disease is the second most common metabolic bone disease after osteoporosis, and frequently involves the spine. It is uncommon prior to middle age. In its milder form it can be quite common, with 2–4% of individuals older than 55 showing evidence of the disease. It is characterized by a slowly progressive deformation and enlargement of bone. This chapter will review pertinent information about this disorder that is relevant to spine care.

ETIOLOGY The etiology of Paget’s disease remains unclear. Possible viral, genetic, environmental, and neoplastic causes have all been proposed but are without agreement. An infectious cause of this disorder has some support through ultrastructural, immunologic, and molecular studies. Specifically, osteoclasts in patients with Paget’s disease have microfilaments in the nucleus and cytoplasm that are similar to the nucleocapsids of viruses of the paramyxovirus family. The paramyxovirus family includes the measles virus, canine distemper virus, and the respiratory syncytial virus.2 In a study of 53 English patients with known Paget’s disease the presence of measles virus of the paramyxovirus family was examined.3 Reverse-transcription polymerase chain reaction was performed on bone biopsy specimens, bone marrow, or peripheral blood mononuclear cells looking for evidence of paramyxovirus RNA. Other subsequent evaluation of the tissue was also performed. No evidence of paramyxovirus was found. None of the proposed viral causes of this disorder has shown consistent results. In up to 40% of patients there is a familial connection.4 A genetic cause that is autosomal dominant has been described within families particularly affected with the disorder.5–7 A genetic cause for the common form of the disorder has not been found. In a similar rare disorder, familial expansile osteolysis, a mutation on chromosome 18 associated with receptor activator of nuclear factor κB (RANK).8 No RANK mutations have been found in Paget’s disease. It is likely that a combination of genetic, environmental, and possibly infectious factors interact in the occurrence of disease.

EPIDEMIOLOGY The epidemiology of Paget’s disease of bone is difficult to study, as most individuals are diagnosed with Paget’s disease in an asymptomatic state through routine testing for other problems. It is found routinely in the United States, Australia, England, New Zealand, Canada, and France. A Mayo Clinic retrospective chart review study to determine some of the characteristics of patients with this dis-

ease was performed.9 Patients with the diagnosis of Paget’s disease diagnosed for the first time between 1950 to 1994 from Olmsted County, MN, were identified. Demographic information about this population was presented. The mean age of patients with this diagnosis was 69.6 years with a statistically greater number of men (n=129) than women (n=107) being diagnosed with the disease. The diagnosis of Paget’s disease became less frequent during the study period and the authors suggested that this may be due to changes in the routine chemistry panel early in the study producing an increase in incidence. To estimate the prevalence of Paget’s disease in the United States a secondary review of pelvis films obtained during the First National Health and Nutrition Examination Survey (NHANES-I) was performed.10 The NHANES-I study sampled a representative population of citizens and included, among other information, radiographs. Of this sample all men between the ages of 25 and 74 and women from 50 to 74 had pelvic radiographs. Of the 4897 radiographs of the pelvis 3936 were available for review. The radiographic criteria for Paget’s disease used in the study included the following: expansion of bone size, thickened disorganized trabeculae, thickened expanded cortex, osteosclerosis, and deformity. Pelvic Paget’s disease prevalence was estimated as 0.71%±0.18%. No racial difference was observed in this sample. Factors associated with the presence of disease were older people with a slightly higher male predominance and distribution in the northeast United States. Geographic variation in Paget’s disease has also been observed in the United Kingdom in a study performed through 1974 involving 14 towns.11 The overall prevalence rate was 5.4% for people older than 55 years. Within this study a focus of increased prevalence in three towns clustered in Lancashire was observed, with a prevalence of 8.3%. This was compared to a prevalence of 2.3% in Aberdeen, Scotland. This increased prevalence in Lancashire was confirmed in a follow-up in 1980 and has suggested the possibility of an environmental or infectious factor but this could not be confirmed.12 No other area in Europe had demonstrated as high a prevalence rate as the United Kingdom for this time period. Cooper et al.13 performed an interesting subsequent study with the same design and 10 of the original towns as performed in 1974 study by Barker et al. The goal was to determine if there had been a change in the prevalence since the original study. A record review was performed for the period 1993–1995. Any patient over 55 years of age with a pelvis, lumbar spine, sacrum and femoral head film was included in the study. The films were reviewed by two radiologists including a consultant radiologist who participated in the original 1974 study. For this period of time they were able to identify 9828 individuals (4625 men, 5203 women). The overall prevalence rate was 2%, with a male:female ratio of 1.6:1. As observed previously, there was an increase in prevalence with an increase in age. The prevalence in the 10 towns studied was 40% less than that observed in 445

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the initial study performed in 1974. This reduction in prevalence was greatest in the towns with the highest rates in the initial study. During an archeological survey of 2770 skeletons in the United Kingdom for Paget’s disease a prevalence of 2.1% was observed.14 The prevalence prior to AD 1500 was 1.7% and after this time increased to 3.1%. This difference was possibly due to the small sample size. The distribution of involvement was the same as within modern studies. In a French study, 770 patients were randomly selected from 7598 women being studied for fracture risk.15 The anteroposterior and lateral radiographs of the spine were reviewed by two rheumatologists and classified into categories with or without Paget’s disease. These radiographs were subsequently read by two masked reviewers for the presence of Paget’s disease. Spinal Paget’s disease was present in 0.54%, which provides an overall prevalence of disease in the 1.1–1.8% range. Paget’s disease is a less frequent diagnosis in Asian countries with most descriptions being case reports.16 The reason for this reduced frequency in Asian countries, like the etiology of Paget’s disease itself, remains unclear.

Anatomic distribution Paget’s disease affects one bone in 5% of patients with the average number of areas involved averaging 6.5 per patient.17 Cranial enlargement can be associated with change in hat size or prominence of superficial scalp veins. In a study designed to examine the anatomic distribution of Paget’s disease in patients older than 55 with films of the lumbar spine, pelvis, and proximal femur within the UK, the stored films of radiology practices of 31 different centers were examined.18,19 The diagnosis of Paget’s disease was made on radiographic criteria and further films examined for 1864 patients. Pelvic involvement was observed in 76% of patients. The lumbar spine was next in frequency with 34%, followed by the femur in 32%, shoulder 24%, thoracic spine 22%, sacrum 14%, skull in 12%, and cervical spine in 5%. Quality of life issues were addressed in a questionnaire mail survey of 958 patients with Paget’s disease. The most commonly affected areas within the sample were skull (34%), spine (35%), pelvis (49%), and leg (48%).20 Hearing loss was reported by 37% of patients. Problems of deformity associated with Paget’s disease were also a frequent complaint with bowed legs (31%), enlarged heads (17%), leg length discrepancies (25%). Of concern was that 47% reported depression associated with the disorder and this was found to have a greater impact on quality of life than the biomedical or self-care domains.

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HISTOPATHOLOGY Paget’s disease involves accelerated bone turnover and remodeling (Fig. 40.1) There is simultaneous excessive osteoclastic resorption and osteoblastic deposition. The involved bone is extremely vascular and may exhibit arteriovenous shunts. The initial active phase is predominantly osteolytic, creating weakened, deformed bone. Following this phase is an osteosclerotic phase which is primarily osteoblastic, resulting in deposition of bone and enlargement of the long bones with thick dense bone without the normal lamellar pattern. The resulting pattern is an irregular mosaic pattern of mature and immature bone. This creates the potential for fractures as well as the deformities observed in the long bones due to deposition.

PRESENTATION AND COMPLICATIONS Low back pain and osteoarthritis Low back pain is a complaint of approximately a third of patients with Paget’s disease.21 As in other areas of spine care, it is difficult to separate other potential causes of spinal pain from Paget’s disease. It has been suggested that the presence of osteoarthritis is greater in patients with Paget’s disease.22 Paget’s disease as a causative factor due to altered mechanics around the joint has been proposed a potential reason for this observation. A matched-control radiographic comparison study was performed to resolve the question if a greater occurrence of osteoarthritis exists in patients with Paget’s disease.23 Using 100 patients with Paget’s disease of the spine and a matched sample without disease, no difference in prevalence was observed. In a similar radiographic study to determine the prevalence of articular osteoarthritis associated with Paget’s disease 153 matched pairs of patients with and without Paget’s disease was selected. At the time of comparison 87 matched pairs with 248 films were available for review and there was no difference in articular osteoarthritis between the groups.24 In a well-designed descriptive study Hadjipavlou and Lander found 54% of patients complained of low back pain.25 It was felt that within this group of patients the symptoms could be attributed to a specific cause based on radiologic causes. In the majority of patients, 50%, complaints of low back were felt to be due to degenerative disease. In the remaining patients, the complaint was related in 26% to a combination of Paget’s disease and osteoarthritis, and in 24% of these patients the complaint of low back pain was attributed solely to Paget’s disease.

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Fig. 40.1 Histopathology of Paget’s disease. (From Kilpatrick: Diagnostic musculoskeletal surgical pathology. Philadelphia: WB Saunders; 2004:369) 446

Section 2: Osseous Spinal Tumors

In a retrospective study of 245 patients with complete spinal radiographs 14 were found to have Paget’s vertebral ankylosis (PVA).26 The presence of diffuse interstitial hyperostosis (DISH) within this study population was 80 out of 245. Out of the 11 patients with PVA, 8 had findings consistent with DISH. The authors suggest that the presence of DISH may allow Paget’s disease to spread to adjacent vertebrae. A separate study to determine if DISH is more prevalent in patients with Paget’s disease was performed. In a group of 50 patients with Paget’s disease compared to 50 age- and sex-matched controls a statistically significant higher prevalence of DISH was observed, 24% compared to 6% in the control group.27

Spinal stenosis Spinal stenosis due to Paget’s disease bony encroachment can occur. The mechanism by which this produces neurogenic claudication is likely related to the compressive nature of the bony ingrowth into the spinal canal. These bony ingrowths can produce either singly, or in combination, central, lateral recess, or foraminal stenosis. The symptom complaints are similar to those of patients without Paget’s disease.28 An alternative mechanism has been proposed that involves arteriovenous shunting from the cauda equina to the Pagetoid bone producing neurogenic ischemia.29,30

Radiographic study Paget’s disease is usually discovered incidentally on plain radiographs obtained for other reasons and is most commonly in a subclinical and asymptomatic state. The radiographic criteria for Paget’s disease include increased bone density and size. Also seen is a disorganization of the normal bone architecture with cortical thickening, enhancement of the trabecular pattern, and thickening of the iliopectineal line (Figs 40.2–40.3).31 MRI findings on T2 imaging reveals a mottled signal appearance of the vertebral body. On T1 imaging a mottled appearance is also noted. This low signal intermixed with marrow fat produces the abnormal appearance. Also seen is an increase in the trabecular markings, and cortical thickening can be helpful in making the diagnosis (Figs 40.4,A–D).32 Bone scan is very useful in the diagnosis and reveals increased activity in the involved bony structures effected by Paget’s disease. It is more sensitive than plain radiographs. Pagetoid bone demonstrates increased nuclide activity 3–5 times that of normal bone. It can also provide a measure of the effectiveness of antipagetic treatment agents. The appearance has been described as a ‘mouse face’ as the increased signal involves the vertebral body, posterior elements, and spinous process.33 This appearance can also be helpful in differentiating Paget’s disease from metastatic disease (Fig. 40.10).

Pathological fracture In spite of the increase in bone density pagetic bone has an increased risk of fracture. In the spine this is usually manifested by a compression fracture. Long bones are susceptible to transverse fractures. Long bones may also show evidence of chronic incomplete ‘stress’ fractures on the convex surface of affected bowed bones. Healing of these fractures can take longer than expected due to the abnormal mineralization in the area.

Sarcomatous degeneration There is an increased incidence of sarcoma in pagetoid bone. It is rare, occurring in less than 1% of patients. It is felt to occur in older patients with the disease for a longer period of time. Histologically, it appears that the sarcomas that are most common are of the mixed cell type. These are characterized by the most aggressive cell type, resulting in osteosarcoma being the most common. Giant cell tumors represent another rare type of transformation that has been found in pagetoid bone.

DIAGNOSIS Paget’s disease is usually found incidentally in the majority of patients, and they are asymptomatic.

Laboratory findings In Paget’s disease patients have an elevated serum alkaline phosphatase level due to the increased osteoblastic activity. The serum alkaline phosphatase level can be used to monitor treatment efficacy. There is usually no benefit of using fractionated alkaline phosphatase levels unless a person has a separate abnormality such as liver disease. To make sure this is the case, initial testing should include fractionated alkaline phosphatase, hematologic profiles, serum electrolytes, and renal and liver function tests. The elevated bone turnover also produces an increase in urinary hydroxyproline excretion to 20–30 times the normal value. This can be measured in a 24-hour urine measurement of 5-hydroxyproline (5-HP). Urinary N-telopeptide (NTX) is also a sensitive marker for bone resorption and is seeing increased use as a marker for improvement with therapy.

TREATMENT Prior to initiating treatment, a clear understanding of what the goals are must be determined. If the symptoms are clearly related to Paget’s disease then the response to treatment should be positive. If the symptoms are related to a combination of osteoarthritis and Paget’s, the patient needs to understand the limitations of antipagetic treatment. With the development of osteoclast inhibitor therapy for osteoporosis, treatment for active Paget’s disease has improved significantly. If the Paget’s disease is asymptomatic and inactive it is reasonable to follow the patient without intervention. Treatment should be initiated for patients with active disease as measured by bone metabolic factors and increased uptake on bone scan. If the symptoms are related to a combination of osteoarthritis and Paget’s disease treatment for the mechanical pain should be included. Calcitonin, the bisphosphonates, plicamycin, gallium nitrate, and ipriflavone have all been used in the treatment of Paget’s disease. With a reduction in the biochemical markers of disease a normalization of bone lamellar pattern is observed. Patients that will likely respond to treatment are patients with pain associated with Paget’s disease. It is also suggested that patients with asymptomatic disease at risk of progression and prior to surgical procedures be treated aggressively. Calcitonin is a hormone that inhibits osteoclast bone resorption. It seems most helpful for patients in a predominantly lytic phase of disease. The form available in the United States is a synthetic formulation of salmon calcitonin. It is initiated at 200–400 U intranasally per day and can be reduced after an effect is observed. Calcitonin is as effective as etidronate in the majority of patients with Paget’s disease, with two-thirds seeing a 50% reduction of metabolic markers.34 There appears to be a plateau in the effect to calcitonin that increased medication can not improve. Additionally, there is a rapid loss of effect once the medication is discontinued. Bisphosphonate therapy is efficacious in the treatment of Paget’s disease. It inhibits osteoclast resorption initially and osteoblast activity later in the treatment course. The rapid inhibition of osteoclast activity is helpful in a patient with Paget’s disease, hypoparathyroidism, and hypocalcemia.35

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B

Figs 40.2 A,B AP and lateral radiographs of the lumbar spine demonstrates disorganization of the normal bone architecture at the L5 vertebra. On the lateral view, note enhancement of the trabecular pattern. Also note ossification of the anterior longitudinal ligament related to DISH. The AP radiograph demonstrates the characteristic ‘picture frame’ appearance due to cortical thickening.

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Figs 40.3 A,B CT scan axial and 3-D reconstruction sagittal image. The CT scan with 3-D reconstruction gives greater detail to the L5 vertebral body affected by Paget’s disease. Again, the disorganization of the normal bone architecture and enhancement of the course trabecular pattern are observed. There is also a slight compression fracture/deformity of L5. On the CT scan the cortical thickening becomes easier to identify. 448

Section 2: Osseous Spinal Tumors

A

C

B

D

Figs 40.4 A–D MRI T2 sagittal, T1 sagittal, T1 fat saturated coronal image postgadolinium, axial T2. These MRI images demonstrate at the L5 vertebral body the characteristic mottled appearance with increased trabecular markings and cortical thickening.

Pamidronate is an i.v. regimen bisphosphonate. In a 2-year study, 71 patients stratified by Paget’s disease severity were randomized and treated with pamidronate disodium 30 mg or 60 mg infusions.36 They found a significant reduction in pagetic bone, joint, and musculoskeletal pain at 6 months and 2 years. The dosing regimen suggested by the researchers was two 60 mg infusions for mild disease and four 60 mg infusions for moderate or severe disease. Most patients did have a relapse during the 2 years and repeat dosing may be necessary.

Etidronate dosing for patients with Paget’s disease is 5 mg/kg per day for 6 months. As in calcitonin a reduction of biochemical markers by 50% is observed in two-thirds of patients. It is suggested that treatment for 6 months be alternated with 6 months off treatment to avoid any secondary metabolic effects that can have the appearance of osteomalacia and lead to pathologic fracture.37 This is one medication that may not be a good choice prior to surgical procedures such as spinal decompression with fusion due to the reduction in mineralization. It appears to be most helpful in the blastic or mixed phase of disease. 449

Part 3: Specific Disorders

Fig. 40.5 Bone scan demonstrating increased uptake within the L5 vertebral body, posterior elements, and spinous process.

Alendronate is an oral bisphosphonate that has received approval in the United States for the treatment of Paget’s disease. It does not appear to have the same effects on mineralization observed with etidronate and would be a good presurgery choice. The dose used in Paget’s disease is 40 mg per day for 6 months. Risedronate is an oral bisphosphonate that has also received approval in the United States for Paget’s disease.38 In an open label trial, 26 patients with Paget’s disease demonstrated an improvement in radiographic appearance in the majority of patients at 12 months.39 The dosing used in the study was 30 mg/day for 86 days followed by 112 days without medication. This regimen was repeated in patients without a response to the first treatment. No major side effects or complications were reported. Plicamycin (mithramicyn) is an antibiotic that can be effective in the treatment of Paget’s disease. It is of limited use currently, as the bisphosphonates have fewer serious side effects and are easier to administer. As in the newer agents described below, and the newer bisphosphonates, it is still a medication to consider if the patient fails to respond to initial treatment with etidronate or calcitonin. Plicamycin is given as an i.v. infusion over 4–8 hours every 2–3 days. The usual dose in Paget’s disease is 15–25 μg per kilogram of body weight.40 Gallium nitrate and ipriflavone are newer medications for Paget’s disease. Both are in initial experimental trials but show promise in the treatment of Paget’s disease.41

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4. Siris ES, Ottman R, Flaster E, et al. Familial aggregation of Paget’s disease of bone. J Epidemiol Community Health 1983; 37:226–231. 5. Hocking L, Slee F, Haslam SI, et al. Familial Paget’s disease of bone: patterns of inheritance and frequency of linkage to chromosome 18q. Bone 2000; 26(6):577–580. 6. Haslam SI, Van Hul W, Morales-Piga A, et al. Paget’s disease of bone: evidence for a susceptibility locus on chromosome 18q and for genetic heterogeneity. J Bone Miner Res 1998; 13(6):911–917. 7. Laurin N, Brown JP, Lemainque A, et al. Paget’s disease of bone: mapping of two loci at 5q35-qter and 5q31. Amer J Hum Genet 2001; 29(3):528–543. 8. Hughes AE, Ralston SH, Marken J, et al. Mutations in TNFRSF11A, affecting the signal peptide of RANK, cause familial expansile osteolysis. Nat Genet 2000; 24:45–48. 9. Tiegs RD, Lohse CM, Wollan PC, et al. Long-term trends in the incidence of Paget’s disease of bone. Bone 2000; 27(3):423–427. 10. Rosenkrantz JA, Wolfe J, Kaicher JJ. Paget’s disease (osteitis deformans). AMA Arch Intern Med 1952; 90:610. 11. Altman RD, Bloch DA, Hochberg MC, et al. Prevalence of pelvic Paget’s disease of bone in the United States. J Bone Miner Res 2000; 15(3):461–465. 12. Barker DJ, Cough PW, Guyer PB, et al. Paget’s disease of bone in 14 British twins. Br Med J 1977; 1:1181–1183. 13. Barker DJ, Bhamberlain AT, Guyer PB, et al. Paget’s disease of bone: the Lancashire focus. Br Med J 1980; 280:1105–1107. 14. Cooper C, Schafheutle K, Dennison E, et al. The epidemiology of Paget’s disease in Britain: is the prevalence decreasing? J Bone Miner Res 1999; 14(2):192–197. 15. Lecuyer N, Grados F, Dargent-Molina P, et al. Prevalence of Paget’s disease of bone and spinal hemangioma in French women older than 75 years: data from the EPIDOS study. Joint Bone Spine 2000; 67:315–318.

SUMMARY

16. Hsu LF, Rajasoorya C. A case series of Paget’s disease of bone: diagnosing a rather uncommon condition in Singapore. Ann Acad Med Singapore 1998; 27:289–293.

Paget’s disease is a relatively common disorder of bone affecting 2–4% of individuals older than 50 years. The spine is the second most common area of involvement. Patients can present with pain or neurological complications secondary to compression due to bone expansion. Treatment options are available, with the bisphosphonates showing great promise in reducing metabolic markers of disease and radiologic progression.

17. Kanis J. Pathophysiology and treatment of Paget’s disease of bone. In: Fogelman I, ed. London: Martin Dunitz Ltd; 1991.

References

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2. Singer FR. Update on the viral etiology of Paget’s disease of bone. J Bone Miner Res 1999; 14(Suppl 2):29–33.

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3. Helfrich MH, Hobson RP, Brabowski PS, et al. A negative search for a paramyxoviral etiology of Paget’s disease of bone: molecular, immunological and ultrastructural studies in UK patients. J Bone Miner Res 2000; 15(12):2315–2329.

24. Helliwell PS, Porther G. Controlled study of the prevalence of radiological osteoarthritis in clinically recognized juxta-articular Paget’s disease. Ann Rheum Dis 1999; 58:762–765.

Section 2: Osseous Spinal Tumors 25. Hadijipalou A, Lander P. Paget’s disease of the spine. J Bone Joint Surg [Am] 73:1376–1381. 26. Marcelli C, Yates AJ, Barjon MC, et al. Pagetic vertebral ankylosis and diffuse idiopathic skeletal hyperostosis. Spine 1995; 20(4):451–459. 27. Morales AA, Valdazo P, Corres J, et al. Coexistence of Paget’s bone disease and diffuse idiopathic skeletal hyperostosis in males. Clin Exp Rheum 199311:361–365. 28. Weisz GW. Lumbar canal stenosis in Paget’s disease. Clin Orthop 1986; 206:223–227. 29. Hartman JT, Dohn DF. Paget’s disease of the spine with cord or nerve root compression. J Bone Joint Surg [Am] 1966; 48A(6):1079–1084. 30. Poncelet A. The neurologic complications of Paget’s disease. J Bone Miner Res 1999;14 suppl 2:88–91. 31. Griffiths HJ. Radiology of Paget’s disease. Curr Opinion in Rad 1992; 4(6):124–128. 32. Whitten CR, Saifuddin A. MRI of Paget’s disease of bone. Clin Radiol 2003; 58(10):763–769. 33. Kim CK, Estrada WN, Lorberboym M, et al. The ‘mouse face’ appearance of the vertebrae in Paget’s disease. Clin Nucl Med 1997; 22(2):104–108.

35. Stuckey BG, Lim EM, Kent GN, et al. Bisphosphonate therapy for Paget’s disease in a patient with hypoparathyroidism: profound hypocalcemia, rapid response, and prolonged remission. J Bone Miner Res 2001; 16(9):1719–1723. 36. Gutteridge DH, Retallack RW, Ward LC, et al. Clinical, biochemical, hematologic, and radiographic responses in Paget’s disease following intravenous pamidronate disodium: a 2 year study. Bone 1996; 19(4):387–394. 37. MacGowan JR, Pringle J, Morris VH, et al. Gross vertebral collapse associated with long-term disodium etidronate treatment for pelvic Paget’s disease. Skeletal Radiol 2000; 29:279–282. 38. Dunn CJ, Goa KL. Risedronate. Drugs 2001; 61(5):685–712. 39. Brown JP, Chines AA, Myers WR, et al. Improvement of pagetic bone lesions with risedronate treatment: a radiologic study. Bone 2000; 26(3):263–267. 40. Tiegs RD. Paget’s disease of bone: indications for treatment and goals of therapy. Clin Ther 1997; 19(6):1309–1329. 41. Smidt WR, Hadjipavlou AG, Lander P, et al. An algorithmic approach to the treatment of Paget’s disease of the spine. Orthop Rev 1994; 23(9):715–724.

34. O’Donoghue DP, Hoskins DJ. Biochemical response to combination of disodium etidronate with calcitonin in Paget’s disease. Bone 1987; 8:219–225.

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Osseous Spinal Tumors ■ i: Physiology and Assessment

CHAPTER

Primary Tumors

41

Jesse T. Torbert, Harish S. Hosalkar, Kingsley R. Chin, Edward J. Fox, Carol A. Dolinskas, Richard Daniels and Richard D. Lackman

INTRODUCTION Primary tumors of the spine are uncommon, accounting for 5–10% of all primary skeletal tumors. At the Rizzoli Institute, 323 patients (adults and children) with primary spine neoplasms were seen over the past 50 years; 27% were malignant and 73% were benign.1 The most commonly encountered benign tumors of the mobile spine (the cervical, thoracic, and lumbar segments) include osteoblastomas, osteochondromas, giant cell tumors, hemangiomas, osteoid osteomas, and aneurysmal bone cysts. Common malignant primary tumors of the mobile spine include chordomas, chondrosarcomas, osteosarcomas, and Ewing’s sarcoma (Table 41.1). Less common malignant lesions of the mobile spine include solitary myeloma, solitary lymphoma, fibrosarcoma, and hemangioendothelioma.2 Chordomas and Ewing’s sarcomas are much more common in the sacrum. In fact, the incidences and clinical characteristics of many sacral tumors differ from those found in the mobile spine. Therefore, statistics and characteristics regarding sacral lesions are included in the discussion of these particular tumor types that are commonly found in the sacrum. There is a strong correlation between patient age and likelihood of malignancy in primary tumors of the spine.3,4,5 In children, nearly 70% of primary tumors of the spine are benign,6 and 70% of primary spine tumors in adults (>21 years old) are malignant.7 As in many tumors, certain tumors of the spine have a predilection for certain age groups. In patients younger than 10 years, neuroblastoma, eosinophilic granuloma, and Ewing’s sarcoma dominate. Aneurysmal bone cysts, giant cell tumors, osteoid osteomas, osteoblastomas, and eosinophilic granulomas are the most frequent primary spine tumors found in adults less than 30 years of age. Patients between 30 and 50 years of age more often have chondrosarcoma, chordoma, lymphoma, and hemangioma as well as metastatic lesions. Those over 50

Table 41.1: Most Common Primary Tumors of the Mobile Spine Common Benign Primary Common Malignant Primary Tumors of the Mobile Spine2,5 (%) Tumors of the Mobile Spine2 (%) Osteoblastoma (20–23)

Chordoma (33)

Osteochondroma (13–23)

Chondrosarcoma (25)

Giant cell tumors (16–22)

Osteosarcoma (19)

Hemangioma (10–20)

Ewing’s (8)

Osteoid osteoma (7–21) Aneurysmal bone cyst (13)

years of age mostly likely have metastatic disease, but may present with solitary myeloma or chondrosarcoma.8 The spine can be divided into anterior elements and posterior elements (Fig. 42.1). Anterior elements consist of the vertebral bodies, and the posterior elements include the remainder of the vertebra (pedicles, transverse processes, laminae, and the spinous process). Most malignant tumors, both primary and metastatic, occur in the anterior elements. Primary spine tumors located in the anterior elements have a 76% probability of being malignant. Those tumors located in the posterior elements are more likely benign (64%).6 Metastatic lesions of the spine are found in the anterior elements approximately 95% of the time. Common primary spine tumors involving the posterior elements are aneurysmal bone cysts, osteoblastomas, and osteoid osteomas. Primary spine tumors that have a predilection for the vertebral body include osteosarcomas, chordomas, solitary lymphomas, eosinophilic granulomas, giant cell tumors, and hemangiomas.8 An early diagnosis is critical in primary spinal tumors, for both local control and prevention of metastasis from malignant lesions. A high index of clinical suspicion and an awareness of symptoms related to the neoplastic conditions is therefore important to the practicing clinician. Significant improvements have aided diagnosis and treatment over the past several decades, and improved outcomes have resulted. Advances in imaging, such as magnetic resonance imaging (MRI) and computed tomography (CT), allow for detailed preoperative evaluation. This, along with improved instrumentation and surgical techniques, provides the means to achieve adequate surgical margins and reconstruction with less morbidity and mortality. Adjuvant therapy, such as radiation and chemotherapy, has also led to significant improvement in outcomes. Also, new minimally invasive techniques, such as radiofrequency ablation, selective arterial embolization, and vertebroplasty/kyphoplasty, have increased treatment options in some spine tumors. The primary goals in treatment of primary spine lesions are to preserve/improve neurologic function, prevent/correct spinal instability, provide a cure/prevent metastasis, and alleviate pain. Because of the various treatment options, which involve many specialties, the treatment of a patient with a spine tumor requires a multidisciplinary approach, which often includes a pain specialist, medical oncologist, interventional radiologist, spine surgeon, physical medicine/rehabilitation specialist, social worker, and hospice care.

CLINICAL PRESENTATION As mentioned previously, early diagnosis is critical in primary spinal tumors. Early detection can lead to optimal local control and prevention of distant spread. Therefore, a high index of clinical suspicion and an awareness of symptoms is vital. A careful history describing the characteristics and timeline of symptoms is important in diagnosis 453

Part 3: Specific Disorders Suspected spine tumor

Presence of severe/rapidly progressing neurologic symptoms ? Yes

No

Thorough ROS/PE emergent labs and X-ray/MRI

Thorough ROS/PE appropriate labs X–ray and subequent imaging (usually MRI)

Emergent spine surgery consult

Diagnosis apparent? Yes

Does appropriate treatment involve radiation/chemotherapy/surgery ?

Yes

No

No Percutaneous, CT-guided biopsy

Metastatic or malignant ? Yes

Percutaneous, CT-guided biopsy to avoid misdiagnosis and erroneous treatment

Proceed with appropriate treatment (observation/ conservative management)

Staging studies

and may direct the work-up and treatment. A proper history includes a summary of prior treatment and provides a baseline to evaluate the course of the disease and the effect of therapy.

Pain Back pain is the most common presenting symptom in both primary (84%)5 and secondary tumors (>90%)9,10 of the spine. Tumor pain is typically unrelenting, progressive, and often present during the night, although many types of pain can present. These include local, axial, radicular, and myelopathic pain, which are discussed in detail in the following chapter. Pain at night is particularly suggestive of tumors such as osteoid osteoma and sometimes more aggressive lesions. Tumor pain may be localized to a specific spinal segment or reproduced by pressure/percussion over the involved area. Tumor expansion may erode the cortical margins leading to pathologic fractures. Both pathologic fractures and tumor growth may involve the spinal canal and neural foramina, with compression of the cord and/or nerve roots resulting in neurologic deficits as well as pain. Ongoing destruction may also lead to development of spinal instability. A history of persistent back pain should be taken seriously and usually warrants further investigation. Patients with a history of irradiation or Paget’s disease of the spine warrant added vigilance due to their risk of secondary osteosarcoma.11 In general, pain from tumors commonly mimics the pain produced by nontumorous disorders. Thus, it is necessary for the clinician to have a high index of suspicion when dealing with back pain, even if the patient does not present with the characteristic types of pain associated with spinal tumors. 454

No Proceed with appropriate treatment

Fig. 41.1 Algorithmic approach to the work-up of suspected spine tumors.

Neurologic impairments Neurological presentation entirely depends on the level of the lesion and the degree of nerve or cord compression. Neurological manifestations, including radiculopathy and myelopathy, may present some time after the onset of pain. Forty-one percent of patients with primary spine tumors complained of a subjective sense of weakness on initial presentation.5 Malignant tumors are associated with a higher incidence of neurologic deficit than are benign lesions.12 Benign tumors of the spine can often present with a history of symptoms of long duration or may remain asymptomatic for some time.

Other symptoms Systemic or constitutional symptoms tend to be more common with malignant or metastatic disease than in benign lesions. As such, constitutional symptoms such as fatigue, fever, and unexpected weight loss must be included in a careful review of symptoms when a malignant or metastatic lesion is suspected. Red flags that suggest malignancy of the spine are presented in Table 41.2.

PHYSICAL EXAM A complete examination of the spine and neurologic function should be performed on any patient with a suspected tumor of the spine. Also, a search for signs of a primary malignancy responsible for metastatic lesions to spine is necessary if metastatic disease is in the differential. Careful examination of the neck, breasts, lungs, abdomen, and prostate as well as a search for lymphadenopathy can often reveal a potential source of metastatic spinal tumors.

Section 2: Osseous Spinal Tumors

Table 41.2: Elements of the Presentation that are Worrisome for Spinal Malignancy Red Flags History of prior malignancy Back pain worse at night/pain and wakes patient from sleep Consistent progression of pain Pain unchanged during rest or activity Acute neurologic deterioration Presence of a mass Presence of constitutional symptoms

Musculoskeletal inspection of the spine The patient should be inspected for any obvious deformities of the spine and abnormal posturing. A bony prominence, kyphotic deformity, or acute angular scoliosis can be observed after vertebral collapse.13 Scoliosis is often associated with osteoid osteoma and osteoblastoma located on the concave side of the apical portion of the deformity. Spine tumors are rarely palpable due to the amount of tissue and muscle layers superficial to the spine. However, the spinous processes of the spine should be palpated, while paying special attention to any tenderness, masses, vertebral defects, and spastic paraspinal musculature. Range of motion testing in flexion, extension, rotation, and lateral bending should be carefully performed.

Neurologic examination In evaluating neurologic function, motor, sensory, and reflex function must be assessed and recorded. Although weakness is rarely the first symptom of a spinal column tumor, it can be objectively identified in 55% of patients with malignant lesions and in 35% of patients with benign lesions.5 Sensory findings are less common than motor findings in patients with either radiculopathy or cord compression. However, testing with pinprick and light touch, particularly in the sacral dermatomes should be performed. Saddle sensory loss may be associated with tumors in the area of the cauda equina. Compression above the cauda equina often spares the sensation to these sacral dermatomes.14 Reflex testing is essential in evaluating a patient with spine complaints and should include deep tendon reflexes: biceps (C5), brachioradialis (C6), triceps (C7), patellar tendon (L4), and Achilles tendon (S1) reflexes. Any hypo- or hyperreflexia or asymmetry is worth noting. Clonus should be sought. Hoffman’s sign, a reflexive flexion of the thumb in response to flicking of the distal phalanx of the middle finger, would be indicative of myelopathy in the cervical region. A positive Babinski’s test is also indicative of a myelopathic process. Also, a rectal exam including sensory, motor, and reflex components should also be carried out. Occasionally, a very large chordoma can be felt posteriorly on rectal examination.

WORK-UP Laboratory studies The laboratory work-up in a patient with a suspected tumor of the spine can be involved. A complete blood count (CBC) with a differential is important when working up any suspected malignancy. Elevated erythrocyte sedimentation rates (ESR) and C-reactive protein (CRP) levels signal that an inflammatory process is involved, but cannot consistently differentiate an infectious process from a malignancy. Lactate dehydrogenase (LDH) levels can be elevated in

sarcomas, and LDH isoenzymes 2 and 3 can suggest a diagnosis of lymphoma.15 To evaluate for liver cancer, alpha fetoprotein (AFP) levels are often obtained in patients with hepatitis C or those who are heavy drinkers. Carcinoembryonic antigen (CEA) is a marker of adenocarcinomas such as colonic, rectal, pancreatic, gastric, and breast.16 Prostate specific antigen (PSA) levels can help diagnose prostate cancer. A thyroid panel can help eliminate the suspicion of a rare thyroid primary, and parathyroid hormone (PTH) can be ordered to look for hyperparathyroidism. An elevated PTH level may lead to diagnosis of a brown tumor of the spine. The diagnosis of myeloma can be confirmed by the identification of monoclonal proteins in the serum or urine via serum protein electrophoresis (SPEP) or urine protein electrophoresis (UPEP);17 however, monoclonal proteins are more often absent or undetectable in solitary myeloma compared to multiply myeloma.18 A chemistry panel can be used to assess kidney function and allows calcium and phosphate levels to be followed to detect and avoid the development of malignant hypercalcemia. An elevated alkaline phosphatase level can also suggest a neoplastic bone disease.

Imaging techniques X-ray The sensitivity of plain radiographs is low for detecting both primary and metastatic tumors of the spine. However, plain films should be initially obtained in the routine work-up of a suspected spine tumor. If the patient’s condition is rapidly deteriorating, and he or she is in need of urgent care, an X-ray and MRI (the most sensitive study) should be performed urgently. Plain films are inexpensive and often demonstrate characteristic changes and patterns that offer important information regarding the nature of the lesion. Collapse of the vertebral body with gibbus formation, winking owl sign of a destroyed pedicle, and jailhouse trabecular pattern found in hemangiomas of the vertebral body are some of the popular radiographic descriptions. Flexion and extension studies, performed with caution, may be warranted if instability is suspected. The presence of instability is demonstrated by 25% translation of vertebral elements or >50% collapse and is an indication for operative treatment.

Bone scan Bone scanning (skeletal scintigraphy) utilizes a disphosphonate compound, tagged with technetium 99m, which becomes incorporated into bone by osteoblastic activity after intravenous injection. Bone scans may be instrumental in detecting tumors of the spine, and images of the entire body can be obtained in a fairly short period of time. One weakness is low specificity. Bone scans are known to be highly sensitive in localizing osteoid osteomas.19 This provides an earlier diagnosis and accurate localization of the tumor. Bone scans are also useful in identifying multifocal lesions and for evaluating metastatic disease.

Computed tomography Computed tomography provides the best images of bone architecture and readily detects small areas of bone destruction or blastic change, although magnetic resonance imaging is more effective in detecting lesions before changes in bone structure can be demonstrated. In the past, CT was not considered a good screening tool for lesions in the spine, but with multidetector scanners, the entire spine can be scanned in great detail in under 5 minutes. Images can be reconstructed into any plane for the evaluation of bone alignment and extent of compression in a compression fracture. CT imaging can also provide the spine surgeon with an image of remaining bone in an abnormal vertebra, a factor in the feasibility of fixation. CT imaging is also valuable for planning and guiding percutaneous biopsies of 455

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vertebral lesions. CT imaging of the spine is especially useful in those patients who cannot undergo MRI (claustrophobic, cannot lie flat for long periods of time, or have implanted, metallic devices).

Myelography (conventional and CT-myelography) To perform a myelogram, iodinated contrast material is instilled into the dural sac in order to detect external compression of the sac or space-occupying lesions within the spinal cord. Therefore, it is an invasive procedure with inherent risks. Before MRI, conventional myelography was the gold standard for detection of cord compression and intrinsic cord lesions, but it has been largely replaced by MR scanning, and by CT-myelography when MRI is contraindicated. Myelography may fail to reveal secondary sites of epidural spinal cord compression and has been shown to be less sensitive in diagnosing spinal tumors than MRI.20 CT-myelography, like conventional myelography, involves the instillation of contrast into the dural sac, but the amount of contrast used is much less due to the enhanced ability of CT to depict subtle contrast differences. By employing various window settings for the images, details of the paraspinal structures, bone, and dural sac contents are well demonstrated. Both conventional and CT-myelography may be used when metallic fixation devices have been placed in and around the spine and MRI is unable to provide adequate images. This, however, is becoming less frequent with the increased use of titanium spinal hardware.

Magnetic resonance imaging MRI detects spinal and paraspinal pathology better than any other imaging technique. It reliably depicts changes in the water content of structures, and thus most pathology, before changes in gross architecture occur. Pathology is detected by employing imaging sequences that emphasize various components of tissues such as fat, fluid, and vascularity. MR images can be obtained in any plane without changing the patient’s position. It is the only noninvasive technique able to visualize pathology within the spinal cord, and clearly depicts the degree of cord compression, as well as the process causing the compression. MR imaging defines lesions in the vertebrae as well as disc pathology and is the best method to diagnose discitis and paraspinal infections. MRI is also more reliable than other techniques in separating benign compression fractures from pathologic fractures of the vertebral bodies. This distinction is made by analyzing signal intensity changes in the bone and paraspinal space as well as by evaluating the shape of the vertebrae and integrity of the cortical margins. The intrinsic contrast created by the tumor itself relative to the intensities of the normal vertebrae are usually sufficient to detect a primary or metastatic lesion in the spine. Contrast may be helpful to detect adjacent soft tissue invasion. It is also useful to know if a lesion enhances, as small foci of recurrent tumor may be more easily detected if they enhance, especially in a background of extensive postoperative change. Another purpose of contrast is in the detection of internal necrosis, a marker for the response of a tumor to chemotherapy. If a tumor enhances fairly solidly, with a response to chemotherapy, nonenhancing foci of necrosis appear within the lesion. Limitations of MRI include the relatively long time to acquire a complete imaging sequence (at least 1 hour to study the entire spine in detail), degradation of the images by patient motion and by implanted metal such as fixation devices, the need for the patient to be able to lie flat and supine for the study, and contraindications such as pacemakers, various other implanted electronic devices, brain aneurysm clips of uncertain composition, and claustrophobia. Magnetic resonance angiography (MRA) can help in defining the vascularity of the lesions and preoperative evaluation and may also play a role in defining the response to adjuvant therapy. 456

Positron emission tomography The most common radiotracer used in clinical positron emission tomography (PET) imaging is fluorine-18-fluoro-2-D-deoxyglucose (18F-FDG), which accumulates in areas of high glycolysis and membrane transport of glucose, both known to be increased in malignant tissue. Unlike the agent used in bone scanning, 18F-FDG may detect bone marrow-occupying lesions before cortical involvement occurs, thus detecting bone metastases before they can be found on bone scans. Sclerotic metastases, however, as found in some breast and prostate cancers, are less likely to be detected by PET as these lesions have lower glycolytic rates and are less cellular than lytic metastases.21 18F-FDG is not specific for tumors and may accumulate at sites of infection but is less likely to be detected at sites of degenerative change than technetium 99m, the agent used in bone scans. Therefore, it is somewhat more specific for tumors. PET also demonstrates metastases in soft tissue throughout the body, resulting in additional diagnostic value. In addition to detecting spine tumors, PET may also be useful in distinguishing malignant lesions from benign. One study of 29 patients with cancer and spine abnormalities showed that two nuclear medicine physicians were in agreement in calling abnormalities benign, equivocal, or metastasis in 90%.22 In addition, 100% of abnormalities interpreted as benign or malignant were correctly identified. The only discrepancies were in three abnormalities that were interpreted as equivocal and which turned out to be metastatic. CT and/or MRI were important in arriving at the final diagnosis in equivocal cases. The ability of PET to evaluate the response of bone tumors to chemotherapy has also been studied. In one study of patients who underwent preoperative chemotherapy for osteosarcoma, changes in tumor 18F-FDG uptake were correlated with percentage tumor necrosis on histopathology. Tumor necrosis was accurately predicted on PET scan in 15 out of 16 patients by visual assessment and in 14 out of 15 patients by final tumor to background ratio (TBR).23

Biopsy When a lesion is identified with the appropriate imaging, it is usually necessary to establish a histologic diagnosis for purposes of treatment, especially if treatment involves radiation, chemotherapy, or a surgical procedure. This helps to avoid misdiagnosis and erroneous treatment.

Types of biopsy There are two types of biopsy commonly used for biopsy of spinal lesions: percutaneous, guided and open, surgical biopsy. Both fluoroscopic-guided and CT-guided percutaneous biopsies can be utilized, and both are effective. The tip accuracy of CT makes it superior when dealing with small, deep-seated lesions especially in the cervical and thoracic regions.24 CT better allows selection of the optimal location to sample tissue. For lesions visible via fluoroscopic monitoring, fluoroscopic-guided biopsy offers real-time positioning of the needle. Open biopsy maximizes tissue retrieval and providing the highest diagnostic success rate; however, it is typically reserved for failed percutaneous biopsies due to the increased morbidity of the open procedure and greater risk of wound contamination with tumor. Regardless of which method is used, the goal is to obtain an adequate amount of tissue while minimizing complications.

Biopsy success rate Accurate diagnosis of tumorous and nontumorous lesions using CTguided biopsy is achieved more than 90% of the time.24–26 In lesions

Section 2: Osseous Spinal Tumors

with central necrosis, the ability to obtain the correct diagnosis may be enhanced by obtaining tissue from the periphery of the lesion. In paucicellular aspirates, a cell block can be prepared or additional tissue, such as a core biopsy, can be obtained. If histology yields only peripheral blood in an obviously destructive mass, biopsy can be repeated, by directing the needle/device at a slightly different area of the lesion.26 If indicated, corticosteroids should ideally be administered after biopsy due to their lytic effect on certain tumors, including leukemia; this lytic effect can lead to a nondiagnostic biopsy.

Percutaneous biopsy of solitary lesions The approach to the percutaneous biopsy of a solitary spinal lesion is fairly straightforward. Usually, the approach involves the shortest path to the lesion that does not place vital structures at risk. For biopsies of the spine, this typically involves a posterior approach; however, in the cervical spine anterolateral approaches are often used. A posterior transpedicular approach is often used to biopsy lesions in the vertebral body. The transpedicular approach helps to avoid vital structures while minimizing the amount of tissue susceptible to tumor contamination of the needle tract. Virtually any lesion within the vertebral body of cervical, thoracic, or lumbar vertebrae can by accessed via this approach.34 Lesions located in the posterior elements are typically easy to biopsy with a direct approach. Occasionally, primary lesions of the spine can locally metastasize to other vertebrae. In this instance, the decision of which lesion to biopsy is important and should be based on several factors including the size of the lesion, radiologic morphology, location along the spinal column, and location within the vertebra. These factors are discussed further in the next chapter.

Complications of biopsy Biopsies of potentially tumorous lesions should be well planned. It is well known that inadequate or inappropriate biopsies adversely affect outcome. Complications arising in these unsound biopsies include disability due to more complex resection, loss of function, local recurrence, and death.28 The surgeon that will be performing the definitive surgical procedure, if further surgery becomes necessary, should always perform the open biopsy. This ensures that the subsequent surgery can be performed using the optimal incision and approach, while excising the biopsy incision and tract. This can also help eliminate unnecessary and improperly performed open biopsies. Complications of percutaneous needle biopsy include bleeding, infection, neurologic compromise, fracture, biopsy tract contamination, and death, although serious complications are rare. Due to the risk of tumor contamination of the biopsy tract,29 the needle tract should be excised if a subsequent surgery is indicated, although this is somewhat controversial. Whenever possible, guided biopsies should be done at the same institution where definitive surgical treatment will occur. Typically, pathologists at the larger referral centers will be more experienced with uncommon primary and secondary malignant tissues obtained from the spine and will typically review specimens despite previous histologic diagnosis from outside institutions. Also, a team approach between the interventional radiologist and the treating surgeon is more likely to produce a favorable result.

Algorithmic approach to work-up When a spine tumor is suspected in a patient with severe or rapidly progressing neurologic symptoms, a thorough review of systems (ROS) and physical examination (PE) should be performed and laboratory tests and imaging, usually X-ray and MRI, should be

obtained promptly. In the absence of severe or rapidly deteriorating symptoms, a thorough ROS and PE are again necessary. Laboratory tests should be selected and performed based on the working differential diagnosis. Plain films should be obtained and are usually followed up with subsequent imaging. If the diagnosis is apparent at this point in time, appropriate treatment may be initiated. However, if treatment involves radiation, chemotherapy, or surgery, tissue diagnosis is typically required. If the diagnosis is in question, percutaneous CT-guided biopsy should be performed. Appropriate treatment may be initiated if the diagnosis is benign, but staging studies, such as CT of the chest, abdomen, and pelvis, may be appropriate before initiating treatment if the lesion is a metastatic or primary malignant lesion.

BENIGN TUMORS OF THE SPINE Eosinophilic granuloma Also known as Langerhans cell histiocytosis (LCH), eosinophilic granuloma is a benign and self-limiting process that can lead to focal destruction of bone. It is most prevalent in children, with half of patients under the age of 10 years. The etiology is unknown and the lesion is comprised of lipid-containing histiocytes from the reticuloendothelial system and eosinophils. Lesions are most common in the skull although virtually any bone may be affected, with vertebral involvement occurring in approximately 10–15% of cases. The most common appearance is a well-circumscribed, punched-out lesion with no periosteal reaction. Less common is the moth-eaten pattern with periosteal reaction. Both are demonstrated in Figure 41.2. Vertebral destruction with complete collapse of the vertebral body can occur and is classically referred to as ‘vertebra plana.’ Multiple vertebrae may occasionally be involved. Collapse can produce pain and spasm of the paraspinal muscles. Deformities in the form of gibbus or kyphus may develop in some cases. Diagnosis is confirmed by needle or open biopsy. Most lesions of eosinophilic granuloma regress without any treatment or with bracing alone. Local steroid injections have also been used.30,31 Chemotherapy is recommended in cases of LCH with disseminated lesions. When neurologic symptoms are present, with or without vertebral collapse, irradiation and immobilization is recommended.32 Neurologic recovery is usually excellent and partial reconstitution of vertebral height is often seen in young patients. In rare cases of cord compression, surgical decompression and stabilization are indicated.

Fig. 41.2 This axial CT of an eosinophilic granuloma demonstrates multiple lytic lesions and cortical destruction with increased density in the remaining bone. The lytic lesions located anteriorly have a punched-out appearance, and those located posteriorly on the left side of the vertebral body (white arrow) appear more moth-eaten. 457

Part 3: Specific Disorders

Osteochondroma Osteochondromas, also known as exostoses, are cartilage capped, and the cortex of the lesion is continuous with the cortex of the involved bone. An osteochondroma of the cervical vertebra is shown in Figure 41.3. Osteochondromas accounted for 35% of all benign bone tumors in one series.2 They can occur in any bone in which enchondral ossification occurs, but are usually found in the metaphyseal region of long bones in the limbs. These lesions involve the spine in 3–7% of cases2,33 and make up approximately 2% of all solitary spine tumors and 13–23% of all benign tumors of the spine.2 Osteochondromas typically occur in patients aged 20–30 years. They are often painless, and neurologic deficits with this type of spinal lesion are rare. The cartilage cap of osteochondromas should be less than 2 cm in adults. Lesions with a cap greater than 2 cm should be suspected of malignant transformation to chondrosarcoma. Solitary osteochondromas are reported to have a 3% chance of malignant transformation, which increases to 27% if the lesion is one of the many found in multiple hereditary exostoses (MHE).34 Patients with MHE typically develop lesions earlier in life and more frequently experience neurologic deficits. Neurologic deficit due to canal or foraminal encroachment and pain are the main indications for surgical intervention. Because these lesions progress slowly, surgical excision often results in neurologic recovery. No adjuvant treatment is usually required.

Osteoid osteoma/osteoblastoma Histologically, osteoid osteomas and osteoblastomas are alike; however, they have different clinical characteristics. Osteoid osteomas are smaller, by definition less than 2 cm in diameter, and tend to have thick sclerotic margins. Approximately 10% of osteoid osteomas are located within the spine. Osteoid osteomas have a distinct predilection for the posterior elements in the spine and typically present in patients 10–20 years of age. Scoliosis is often found in both osteoid osteoma and osteoblastoma, with 50–63% of patients with either condition having significant scoliosis.35,36 Osteoid osteoma lesions secrete prostaglandins, and patients often present with the classic history of night pain and pain relief with NSAIDs. In the spine, an

Fig. 41.3 This is a CT (soft tissue window) of an osteochondroma (black arrow) of the C2 vertebra. 458

osteoid osteoma can be difficult to identify on plain radiographs as the diameter of the lesion is less than 2 cm and is often obscured by overlapping shadows of the vertebral column. MRI may demonstrate surrounding bone and soft tissue edema creating the false impression of an aggressive lesion. The bone scan is the most sensitive test for locating osteoid osteomas, and the central nidus shows markedly increased uptake. Fine-cut (1 mm) CT scans show the lesion clearly and best differentiate it from other lesions. An osteoid osteoma of the spine is shown in Figure 41.4. The treatment of choice for spinal osteoid osteomas is surgical excision. The entire tumor nidus should be removed. Reliable pain relief is achieved, and the secondary spinal deformity resolves in most cases. Percutaneous CT-guided resection has also been shown to be useful.37,38 Radiofrequency (RF) ablation has also been utilized in the spine, but is associated with higher risks. Some authors feel that RF ablation may have a limited role in osteoid osteomas of the spine.39 Occasionally, long-term treatment with NSAIDSs may be a viable option especially when the lesion is in a difficult location, as spontaneous regression is known to occur over a period of time and malignant transformations are rare. In comparison to osteoid osteomas, osteoblastomas are larger than 2 cm, and antiinflammatory medications provide little or no symptom relief, as osteoblastomas are not known to secrete prostaglandin. The spinal column and sacrum are involved in approximately 42% of all lesions.2,35 Like osteoid osteomas, osteoblastomas tend to involve the posterior elements. Rarely is osteoblastoma confined to the vertebral body. Similar to osteoid osteomas, the population affected is young, 10–30 years of age. Osteoblastoma is a rare tumor with occasional malignant transformation and should not be labeled as just a large osteoid osteoma. Radiographically, they are usually characterized by a lytic lesion with expansile behavior and varying lesional ossification (Fig. 41.5). It is important to remember that an osteoblastoma is a benign, but often locally aggressive tumor, and must be treated as such. Marked radionucleotide uptake is exhibited on bone scans. MRI is non-specific, but is used to assess the effect of the tumor on surrounding tissues and the spinal cord if cord involvement is suspected. These lesions are radioresistant. Marginal resection is usually the best surgical option. When complete excision of the osteoblastoma is not feasible, curettage and bone grafting may provide an acceptable longterm result.35,40 Aggressive osteoblastomas have a recurrence rate of approximately 50% if negative margins are not obtained.

Fig. 41.4 This CT of an osteoid osteoma located in a pedicle demonstrates the lucent nidus (black arrow) and surrounding sclerosis that are characteristic of this lesion.

Section 2: Osseous Spinal Tumors

Asymptomatic hemangiomas rarely develop into symptomatic lesions. Symptomatic hemangiomas usually respond well to conservative surgical procedures. Selective arterial embolization may be a safer and more effective treatment than radiation. Hemangiomas respond to low-dose radiation, but radiation may not be an ideal treatment due to the risk of radiation-induced secondary sarcomas. Vertebroplasty has been used in Europe to treat these lesions and reinforce the vertebral body percutaneously.13 Anterior resection and fusion are reserved for pathologic collapse and neural compromise or refractory cases. Fig. 41.5 This axial CT of an osteoblastoma of the posterior elements demonstrates the expansile nature of these lesions while showing lesional calcification, which is often present.

Hemangioma Hemangiomas of the spine are common, occurring in approximately 10% of all adults and are typically in the anterior elements. These lesions are rarely symptomatic and are typically found incidentally, although they may occasionally exhibit extraosseous extension and neural compromise. Hemangiomas typically contain trabecular condensations surrounded by abnormal vascular channels which are more lucent on plain films and CT, giving the vertebral body vertical striations on plain films, which is popularly referred to as the ‘jailhouse’ vertebra (Fig. 41.6A). The appearance of these lesions on axial CT images resembles polka-dots.2 They may exhibit sclerotic margins. On MRI, hemangiomas are hyperintense on T1 (Fig. 41.6B), which may make them undistinguishable from normal fatty marrow, and are hyperintense on T2-weighted images.2,41 The trabecular condensations may appear on MRI as dark dots against a more hyperintense background, giving a ‘salt and pepper’ appearance. Hemangiomas demonstrate contrast enhancement on MRI.

A

Aneurysmal bone cyst Aneurysmal bone cysts (ABCs) are sometimes excluded from discussions of neoplasms because they have been known to regress after incomplete removal. The cause of these lesions is unknown, but approximately 28% of the time, they arise secondary to other lesions such as giant cell tumor, chondroblastoma, and osteosarcoma.42 The region around the knee, including distal femur and proximal tibia, are the most common locations for this lesion. ABCs involving the spine are not common, representing approximately 13% of benign spine tumors. They are most commonly found in the lumbar region. Presenting patients are most often younger than 20 years of age. Both the anterior and posterior elements may be involved (Fig. 41.7A) with the posterior elements being involved most of the time. These lesions can also involve adjacent vertebrae, sometimes spanning more than three vertebrae. Radiographs usually demonstrate an expansive osteolytic cavity (Fig. 41.7B) with a ‘soap-bubble’ appearance within the lesion. The cortex is often expanded and thinned. MRI is especially helpful in the evaluation of patients with suspected ABC of the spine. MRI characteristically shows a multiloculated expansile lesion with multiple characteristic (but not pathognomonic) fluid-fluid levels. The lesions are often extremely vascular. Selective arterial embolization has become a useful adjunct to surgical excision of spinal lesions to reduce intraoperative bleeding potential. Curettage usually eradicates the lesion, and recurrences, which do not tend to invade vital structures, may be successfully treated by repeated curettage or excision.33

B

Fig. 41.6 (A) The characteristic ‘jailhouse vertebra’ appearance of hemangioma is shown. (B) This T1-weighted MRI of a hemangioma demonstrates a diffusely hyperintense lesion within the vertebral body of L1.

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B

A

Giant cell tumor Giant cell tumors (GCTs) of the spine are most commonly found in the sacrum. These are usually benign, but locally aggressive, and may not present until the third or fourth decade of life. Cord compression has been noted in about 20% of cases. Even though the tumor is classified as benign, it metastasizes in approximately 3% of the cases.2 There is a 2% risk of lung metastasis associated with GCT and is unrelated to the extent of radiographic aggressiveness. GCTs usually involve the vertebral body, but may extend to the surrounding bone and soft tissues as the tumor enlarges (Fig. 41.8A, B). Plain films show an area of focal destruction of the vertebral body and lesions are lucent with marginal sclerosis. Giant cell tumors can be highly vascular. In the authors’ experience, embolization of sacral lesions has been a successful primary approach for management.43 It is reasonably noninvasive, has documented excellent functional outcomes and is not associated with neurologic complications. Marginal and, when appropriate, wide excision with adjuvant therapy may be indicated in some cases (espe-

A

460

B

Fig. 41.7 (A) This axial CT (bone window) shows destruction of the posterior elements as well as the vertebral body on the right. (B) This AP radiograph of an ABC reveals a ‘winking owl’ sign due to destruction of the right pedicle and demonstrates the expansile nature of the lesion (white arrows).

cially in those resistant to embolization). Because of the tendency of these lesions to recur, CT and MRI are important in planning an operation that will provide wide margins. In cases not amenable to surgical excision, low-dose radiation therapy (less than 30 Gy) with contemporary techniques carries a small rate of secondary malignancy. Bisphosphonates have been shown to induce apoptosis in giant cell tumors.44,45 Treatment of spine GCTs with bisphosphonates and radiotherapy has been reported to produce favorable results in three patients.46 The distinction between a benign vertebral body tumor such as a giant cell tumor and an aneurysmal bone cyst sometimes can be difficult. The distinction, nevertheless, may be important because of a giant cell tumor’s potentially more aggressive nature that demands more complete excision than an aneurysmal bone cyst. An aneurysmal bone cyst, while commonly involving the vertebral body, virtually always involves a pedicle or other posterior elements. Therefore, a lesion that only involves the vertebral body is more likely to be a giant cell tumor than an aneurysmal bone cyst, although metastatic lesions

Fig. 41.8 This figure demonstrates a sacral GCT on MRI. (A) On the T1-weighted image, there is a low-intensity mass with extraosseous extension into the spinal canal. (B) The mass is hyperintense on the T2-weighted image.

Section 2: Osseous Spinal Tumors

and myeloma are also in the differential of a lytic, expansile lesion in the vertebral body.

MALIGNANT TUMORS OF THE SPINE Solitary myeloma (solitary plasmacytoma) Solitary myeloma is one of many B-cell lymphoproliferative diseases, which include multiple myeloma. Multiple myeloma of the spine, which is discussed in the next chapter, is typically due to metastatic spread to the spine. True solitary myeloma is relatively rare, constituting only 3% of all plasma cell neoplasms.47 Of all solitary plasmacytomas, approximately 55% involve the vertebral column.48 Solitary plasmacytoma of the spine usually affects the vertebral body. As mentioned previously, monoclonal proteins are more often absent or undetectable in solitary myeloma compared to multiply myeloma.18 Solitary myeloma is an isolated lesion and treatment may result in cure. Treatment of choice in solitary plasmacytoma and multiple myeloma is radiation. The prognosis for patients with solitary plasmacytoma is much better than that for multiple myeloma. Disease-free survival for patients with solitary plasmacytoma of the spine is 60% at 5 years with a median survival of 92 months.49 Surgical intervention is typically reserved for decompression of neural structures and stabilization in cases of severe destruction. Postoperative adjuvant radiation is recommended. Surgery is the treatment of choice for recurrent lesions or those that do not respond to radiotherapy in which en bloc resection and prophylactic reconstruction with repeat radiotherapy may provide extended disease-free survival. Dissemination of myeloma can occur after years of disease-free survival, and patients should undergo regularly scheduled follow-up. MRI provides the earliest indication of local recurrence, and serum protein electrophoresis (SPEP) has proven to be the best indicator of dissemination. The treatment for disseminated myeloma is systemic chemotherapy.

Osteosarcoma Approximately 3% of all primary osteosarcomas arise in the spine,2 and this percentage increases with age.50 Spinal osteosarcoma arises in the vertebral body in approximately 95% of cases. Plain films will often reveal cortical disruption, soft tissue calcification, periosteal reactions, and in advanced cases, vertebral collapse. Paraspinal soft tissue involvement can involve vascular, neural, and other contiguous structures. Median survival of these patients typically ranges from 6 to 18 months.51–53 However, extensive anterior and posterior resection and adjuvant chemotherapy have improved local tumor control, neurologic function, and survival.53 When local control can be obtained with an appropriate surgical margin, survival is comparable to a similar lesion in an extremity. However, complete resection can be difficult and is not possible in the majority of spinal osteosarcomas.13,48

Secondary osteosarcomas Within osteosarcomas, there is a subgroup of secondary osteosarcomas which arise secondarily in Pagetoid or irradiated bone. This subgroup accounts for approximately 4% of all intramedullary osteosarcomas.50 However, of all osteosarcomas within the spine, secondary osteosarcomas represent almost 30%.51,52 The majority of patients with secondary osteosarcoma are over 60 years of age.50 Lesions that develop in pagetoid bone progress rapidly and produce extensive destruction of bone. Prognosis in these patients is poor, with less than 5% achieving long-term survival. The majority of patients with osteosarcoma secondary to radiation have received 50 Gy or more. Most patients were exposed to radiation for nonosseous disease including

Hodgkin’s lymphoma, breast cancer, and carcinoma of the cervix. The 5-year disease-free survival rate is approximately 17%, slightly better results than in those with pagetoid osteosarcoma. Both forms of secondary osteosarcoma can present long after exposure. One patient presented with osteosarcoma of the spine 31 years after being irradiated for Hodgkin’s lymphoma.54

Ewing’s sarcoma Ewing’s sarcoma presents as a primary, and rarely a secondary, tumor of the spine. Approximately 3% of all Ewing’s tumors arise in the mobile spine, and 6.4% are located in the sacrum.2 Most patients (88%) with primary Ewing’s of the spine are 20 years or younger. Sometimes difficult to detect on plain radiographs, these tumors have a permeative, destructive pattern. The first radiographic findings are usually vertebral collapse and vertebra plana (Fig. 41.9A), which may make it difficult to differentiate from eosinophilic granuloma. Frequently, due to the aggressive nature of this tumor, extraosseous involvement is present at initial diagnosis (Fig. 41.9B, C). Often neurologic symptoms due to intraspinal extension occur prior to radiographic detection, making MRI the imaging procedure of choice for evaluation of cord and nerve root involvement. Ewing’s sarcoma can be treated with radiation plus a combination of chemotherapeutics. Surgery is indicated when open biopsy is needed or when decompression of neural structures or stabilization of the spine is indicated. Prognosis of spinal Ewing’s sarcoma is worse than that for those of the extremities. The 5-year survival is approximately 50% with the combination of radiation and chemotherapy.

Chordoma Chordoma is a low-grade, relatively common malignancy of the spine typically found in patients in their fourth to sixth decade. It accounts for approximately 6% of all primary malignant bone tumors.2 An even higher percentage (8.4%) was found in the National Cancer Institute’s Surveillance Epidemiology and End Results (SEER) study. Chordomas, always localized to the midline, arise from primitive notochord remnants and are primarily found in the sacrococcygeal area (47%) and spheno-occipital region (38%) in the base of the skull.2 The rest of the time they are found in the cervical, thoracic, and lumbar areas. Approximately 5% of patients develop metastases; sites include the liver, lungs, lymph nodes, peritoneum, skin, and heart. Although metastasis is relatively rare, nearly 70% of patients die from these lesions, illustrating the severity of local tumor extension.55 Chordomas grow slowly and progressively, reaching considerable size before metastasizing, sometimes causing nerve root compression, constipation, and urinary frequency. Occasionally, an advanced, very large chordoma can be palpated posteriorly on rectal examination. Initial symptoms are typically mild in nature and progress as the tumor slowly enlarges. Chordomas on T1-weighted MRI are typically hypointense to isointense compared to the surrounding musculature (Fig. 41.10A). In T2-weighted images, they invariably show high signal and an inhomogeneous texture (Fig. 41.10B). Surgical resection with wide margins is the only curative procedure. Intralesional resection is associated with a high rate of recurrence and mortality.56 Appropriate staging studies should be done prior to biopsy. Biopsy should be performed through a direct posterior approach, and the biopsy incision should be excised en bloc with the tumor at the time of resection.11

Chondrosarcoma Chondrosarcoma is another low-grade, slow-growing malignancy. Chondrosarcomas are primarily a tumor of adulthood and old age. 461

Part 3: Specific Disorders

A

B

C

Fig. 41.9 (A) This radiograph demonstrates vertebral plana due to an Ewing’s lesion. (B) This axial CT demonstrates extraspinal soft tissue involvement (white arrows). (C) T1-weighted MRI shows extraosseous extension of the lesion producing cord compression.

Approximately 8% of chondrosarcomas are primary tumors of the spine.2 Advanced chondrosarcoma usually has a characteristic radiologic appearance. Lesions often appear with a large area of destruction containing flocculent calcifications and have an associated soft tissue mass. If there is no soft tissue mass, the vertebral lesion may be primarily lytic with sclerotic margins and without calcification. CT is useful in evaluating the extent of the lesion and amount of spinal canal compromise. On MRI, the signal intensity of chondrosarcoma is heterogeneous because of the mixture of soft tissue cartilage, cal-

A

cification, and hemorrhage. Associated soft tissue masses are defined well by MRI (Fig. 41.11A). High signal intensity on T2-weighted and STIR images (Fig. 41.11B) is typical. Areas of mineralization show low intensity in both sequences. These tumors are relatively resistant to radiation and chemotherapy. Like chordomas, chondrosarcomas tend to recur locally and require complete surgical resection with a wide margin of uninvolved tissue to achieve cure. They also have a poor prognosis. In cases where a clear margin is not obtained, adjuvant radiotherapy may improve local control.

B

Fig. 41.10 (A) T1-weighted MR imaging demonstrates a chordoma in the sacrum, which is slightly hypointense to the nearby musculature. (B) This image shows the same lesion, which is hyperintense and inhomogeneous on T2-weighted MRI.

462

Section 2: Osseous Spinal Tumors

A

B

Fig. 41.11 (A) Coronal T1-weighted MRI demonstrates a chondrosarcoma of the thoracic spine with intermediate signal intensity. (B) A sagittal STIR image of the same lesion shows high signal intensity.

Solitary lymphoma

Bisphosphonates

Lymphoma may present as an isolated tumor within bone, referred to in the past as reticulum cell sarcoma, or as a systemic disease. Primary lymphomas of the bone accounted for 3% of all malignant bone tumors in one review.44,45 Whether considered a primary or secondary lesion, lymphomas do account for a significant number of spinal tumors. In cases of solitary lymphoma, patients typically have none of the general constitutional complaints so commonly associated with systemic lymphoma, even when lesions are extensive. However, those lesions that involve the spine frequently have neurologic symptoms. Surgical intervention is typically reserved for decompression of neural structures and stabilization in cases of severe destruction and is used as an adjuvant to radiation and chemotherapy. Systemic lymphoma involving the spine is discussed in the next chapter as a secondary tumor.

Bisphosphonates are drugs that inhibit osteoclastic activity, suppressing bone resorption. The use of bisphosphonates in metastatic disease has been studied much more than primary tumors of bone. Studies have shown that bisphosphonates induce apoptosis in giant cell tumors,46 and giant cell tumors of the spine have been treated with radiotherapy and bisphosphonates alone with favorable results.57 There are orthopedic surgeons who are currently using bisphosphonate-soaked cancellous allograft when treating aneurysmal bone cysts, although this has not been published. Bisphosphonates have also been studied as a potential treatment for osteosarcoma. Bisphosphonates have been shown to induce apoptosis in osteosarcoma cells58 and inhibit canine osteosarcoma tumor growth.59 Further investigation into the efficacy of bisphosphonate treatment in these primary bone tumors is needed.

MANAGEMENT The management of spine tumors requires a multidisciplinary approach. Treatment modalities can be categorized into general medical treatment, tumor-specific medical treatment, minimally invasive procedures, and surgery. Unlike treatment of secondary tumors of the spine, which is often palliative, the treatment of primary tumors may result in a cure. The primary goals in treatment of primary spine lesions are the following: ● ● ● ●

Preserve/improve neurologic function; Prevent/correct spinal instability; Provide a cure/prevent metastasis; and Alleviate pain

General medical treatment Deep vein thrombosis prophylaxis Patients with cancer are often in a hypercoagulable state. Although sufficient data on patients with primary tumors of the spine are not available, prophylaxis against deep vein thrombosis (DVT) with appropriate medication or sequential compression devices (SCD) is recommended for patients who are nonambulatory and at risk.

Corticosteroids Corticosteroids, by reducing the vasogenic edema of acute spinal cord compression, stabilize or improve neurologic status and relieve pain in some patients. Due to the low mineralocorticoid activity, low cost, and use in clinical trials, dexamethasone is commonly used. The optimal dose used to treat acute spinal cord compression is controversial. One randomized, control trial showed that an initial 100 mg i.v. bolus of dexamethasone and subsequent doses of 96 mg/day (split into four daily doses) in patients with epidural spinal cord compression provided a significantly higher percentage of patients that were still ambulatory at long-term follow-up.60 One retrospective study comparing 16 and 96 mg/day doses demonstrated a significantly higher incidence of both serious and nonserious side effects with the higher dose.59 This study also showed no difference in efficacy between the two doses; therefore, the recommended dose for symptomatic patients is a 10 mg i.v. bolus followed by 16 mg/day, administered four times daily. The larger dose of 96 mg/day should only be administered to patients with rapidly progressing neurologic deficits.61 Steroids are recommended for neurologic compromise of acute onset. However, caution must be taken in a patient with an 463

Part 3: Specific Disorders

undiagnosed spinal mass with regards to corticosteroids treatment. One must not deliver steroids prior to biopsy because of the oncolytic effect for certain tumors, such as lymphoma.60 Other complications of corticosteroid treatment include metabolic abnormalities, GI bleeding/perforation, steroid withdrawal, osteoporosis, osteonecrosis, and psychosis. Postoperative infection and wound breakdown are also increased with corticosteroid use. Although steroids can be useful in acute neurologic compromise, the importance of surgical treatment in patients with primary malignant spine tumors cannot be overstated. Steroids should not replace or delay definitive treatment in patients with primary malignant tumors as it sometimes does in the more conservative management of metastatic tumors of the spine.

Pain management Management of pain in patients with tumors of the spine often begins with a trial of nonsteroidal antiinflammatory drugs (NSAIDs). NSAIDs work extremely well for some lesions including osteoid osteoma. NSAIDs should be discontinued prior to surgery to avoid the potential for excessive blood loss. Although nonsteroidal antiinflammatory agents may provide pain control, patients may require opiates. Surgical excision typically relieves pain. As mentioned previously, steroids may alleviate pain due to cord compression. If available, a pain management consultation may be helpful in patients with pain refractory to standard treatment.

Bracing Bracing is a palliative treatment and is more often used in treatment of spinal metastases. External spinal bracing performs two functions: alleviation of pain and prevention or halting vertebral collapse. By preventing or halting vertebral collapse, bracing can help prevent neurologic involvement in those patients with intact neurologic function while they receive more definitive treatment.

Tumor-specific medical treatment Chemotherapy The use of chemotherapy in the treatment of spine tumors depends on the chemosensitivity of the tumor in question. Chemotherapeutics have been useful in Ewing’s and osteosarcoma. Also, patients with myelomas and lymphomas that become disseminated can benefit from chemotherapy. Possible complications of chemotherapy vary depending on the chemotherapeutic agent used, but typically include immunosuppression, delayed wound healing, and perioperative wound infection. Interestingly, chemotherapy for bone sarcomas does not negatively affect fertility rates or childbirth; the authors showed that 15 of the 36 patients attempted conceptions, and all were successful.62

Radiation therapy Similar to chemotherapy, radiation therapy has a variable effect among tumor types. Radiation may be helpful in eosinophilic granulomas, Ewing’s sarcomas, and lymphomas either as a primary or adjuvant treatment. The appropriate use of radiation is included in the previous discussion of each tumor type.

Minimally invasive procedures Radiofrequency ablation Radiofrequency (RF) ablation has been used more commonly in metastatic spine lesions.63–65 However, one study of 263 patients that underwent RF ablation for osteoid osteoma included 3 patients 464

with osteoid osteoma of the spine.39 These authors suggest that the electrode should be at least 1 cm away from major nerves; therefore, most spinal osteoid osteomas should not be treated with this method.

Embolization Selective arterial embolization is not a curative treatment for spinal tumors, but it can reduce operative blood loss and reduce the size of tumors. Preoperative embolization of hypervascular vertebral tumors can make a previously unresectable tumor resectable. Embolization has become a useful preoperative adjunct to surgical excision of spinal ABCs, and it may be a safer and more effective option than radiation for the treatment of hemangiomas. As mentioned previously, the authors have found embolization of sacral lesions to be a successful approach for primary management.43 It is reasonably noninvasive, has documented excellent functional outcomes, and has not been associated with neurologic complications.

Vertebroplasty/Kyphoplasty Percutaneous vertebroplasty using polymethyl methacrylate (PMMA) has been used in the treatment of benign compression fractures since the late 1980s. Some authors have reported the use of vertebroplasty in treating local and axial pain due to vertebral metastases,66–68 although treatment of primary spine tumors has not been well described. Over the past decade vertebroplasty has been used in Europe to treat hemangiomas, reinforcing the vertebral body.13

Surgical treatment Surgery plays an important role in the management of primary tumors of the spine. For benign disease, surgery can be curative. For malignant disease, the outcome of adjuvant therapy may depend on the ability of surgery to achieve adequate removal of tumor, preferentially with negative margins. In one report, patients with malignant lesions that were completely excised had a 75% 5-year survival, while those with incompletely resected lesions had a 19% 5-year survival.6 The evolution of instrumentation and surgical techniques has provided the surgeon with a wide armamentarium with which to adequately excise or debulk tumors, decompress the neural structures, and stabilize the spine.

Indications The indications for surgery in patients with primary tumors include impingement of neural structures causing myelopathy or intractable pain, structural instability, presence of tumor type that is radioresistant, tumor recurrence in a patient who cannot receive further medical or radiotherapy, fractures or impending fractures, and the need for a diagnostic biopsy in a patient with an unknown primary (approximately 9% of patients).69 The objective of surgery should be to achieve a cure, extend life expectancy, or provide palliation but the decision should be carefully discussed with the oncology management team and the patient and family. Once the objective is established, desirable goals are early patient mobilization, relief of pain, spinal alignment, decompression to relieve neurologic deficits to permit return of useful ambulation and bowel function, and stabilization of the involved motion segments. Surgery is contraindicated in patients with quadriplegia and no reasonable chance to restore neurologic function, diffuse spinal involvement of the operative segment, and a life expectancy of less than 4 months.70–72 The decision to operate within this range should weigh the patient’s remaining quality of life against the pain, life disruption, hospitalization, and recovery necessary after an operation.

Section 2: Osseous Spinal Tumors

Preoperative assessment Thorough preoperative assessment is necessary to achieve a successful outcome and should include the patient’s overall nutritional and immune status, prognosis, surgical alternatives, rate of disease progression, prior radiation to the surgical site, and surgical and anesthetic expertise. Additionally, the ability of the bone stock to reasonably allow stabilization, the location of the tumor and the need for a thoracic, vascular, otolaryngology, plastic, or general surgeon for access, and the presence of significant cord compression with or without paralysis should guide the preoperative decision-making process, including the need for awake fiberoptic nasal or endotracheal intubation in cases of cervical instability or severe myelopathy. Myelopathic patients are monitored for neurologic changes using electrophysiologic monitoring such as motor and somatosensory evoked responses prior to positioning and during the operation to help prevent further cord injury during surgery. Preoperative spinal angiography may be used to identify the major arterial branches supplying the tumor, followed by selective angiography to reduce intraoperative blood loss such as in some aneurysmal bone cysts.

Surgical approaches The surgical approach should be determined by the tumor location and its behavioral characteristics. In general, primary tumors affecting the anterior spinal elements and causing anterior compression should be approached anteriorly and those located posteriorly affecting the pedicles, facets, lamina, and spinous processes should be approached posteriorly. In cases of benign tumors, a single approach is often enough to achieve the goals of surgery. However, if the goal is to remove as much tumor as possible or to achieve negative margins in the case of a malignant or locally aggressive benign tumor, a combined anteroposterior approach may be required to achieve en bloc resection and preserve stability. Alternatively, a posterolateral approach may provide wide or marginal resection of the tumor and simultaneous decompression of the neural structures with much less morbidity than a combined approach. Variations of the posterolateral approach such as the transpedicular, extrapleural, or costotransversectomy approach, may necessitate sacrifice of one or more nerve roots and risks a pneumothorax or vascular injury of the great vessels. In many cases, however, the tumor has already destroyed much of the posterior elements, making it easier to perform the dissection and remove the tumor. For patients with recurrent tumors of the spine who have already undergone surgery and radiation, it is advantageous to avoid the same approach if possible, especially after anterior thoracic approaches, since the revision surgery is often made more difficult by the radiation and risks substantial blood loss.

Cervical spine Tumors in this location are approached based on whether they are located anteriorly or posteriorly. Anterior corpectomies will adequately decompress the spinal cord for anterior tumors affecting the vertebral bodies while posterior laminectomies will address dorsal and lateral tumors of the posterior elements. Both approaches will need instrumented stabilization.

Thoracic spine Laminectomy effectively removes tumors confined to the posterior elements such as the pedicle, facets, lamina, and spinous process. Tumors located anteriorly or causing anterior compression are not effectively removed through a laminectomy without risking signifi-

cant neurologic deficits and paralysis. Wide laminectomies and facetectomies risk instability and kyphosis which results in further cord compression despite the support of the rib cage and thus require stabilization. If a posterior approach is deemed the most effective with the least morbidity, then a posterolateral, extrapleural, transpedicular, or costotransversectomy approach is safer for removal of anterior tumor. Tumors causing anterior compression or significant kyphosis are best approached anteriorly through a thoracotomy. Access is permitted to remove tumors as high as T2, especially via a right-sided approach.

Lumbar spine There is less risk of neurologic deficits associated with surgery in this region of the spine due to the absence of the spinal cord below the L1–2 interspace. The conus and cauda equina are much more tolerant of compression and manipulation than the spinal cord in the cervical and thoracic regions and neurologic recovery is more rapid. The majority of primary tumors affect the posterior elements in this region and can be safely removed with a laminectomy. Anterior extension of tumor can also be removed with gentle retraction of the dura. A retroperitoneal or transperitoneal approach may be required to approach the spine anteriorly for cases in which a circumferential tumor resection is required or for correction of a kyphotic deformity. The retroperitoneal approach is preferred over the transperitoneal approach due to a lower risk of bowel and ureter injury, retrograde ejaculation, and peritonitis. Stabilization is required after an anterior approach or if the facets or pedicles are involved and the spine is deemed unstable after tumor resection.

Sacrum Primary tumors of the sacrum such as Ewing’s sarcoma, giant cell tumor, chondrosarcoma, aneurysmal bone cysts, osteoblastoma, synovial sarcoma, and chordomas are often large at presentation. Benign tumors can be cured with intralesional curettage and adjuvant therapy in contrast to radio- and chemoresistant malignancies that require en bloc wide resection.73 It is often difficult to adequately resect malignant tumors without neurologic deficits and diminished bowel and bladder function. In order to achieve en bloc resection, a circumferential approach is needed and begins with an anterior transperitoneal approach. The L5–S1 disc is removed and the internal iliac vessels are ligated. A rectus abdominus pedicle flap may be placed in the pelvis and used to fill the defect that remains after a staged posterior sacrectomy and en bloc removal of the tumor. The thecal sac is ligated, which often requires sacrificing many of the sacral roots, and the L5 nerve roots are preserved during the posterior dissection. Bowel function can be assisted with laxatives and diet control, and self-catherization is needed for bladder control.74 Stabilization is achieved between the lumbar vertebras and the ilium.75

Operative stabilization Orthopedic spine surgeons are increasingly trained to apply recent, advanced techniques of instrumentation using pedicle and lateral mass screws, rods, plates, and vertebral body replacement devices such as titanium mesh cages. With these newer stabilization techniques and devices, orthopedic surgeons are more aggressively removing tumors and restoring adequate stability. Stabilization after corpectomy or vertebrectomies can be achieved with either humeral or fibula strut grafts, but metallic cages are more durable in cases of recurrence and are preferred if postoperative radiation will be used since there is a 50% nonunion rate with bone graft in the face of radiation.76 465

Part 3: Specific Disorders Primary spine tumor

Malignant vs. benign ? malignant Staging studies

benign Benign, aggressive lesion ? (GCT, osteoblastoma) Yes

Resection and stabilization as indicated ± radiation ± chemotherapy

No

Resection and stabilization as indicated

Symptomatic ? Yes

Proceed with appropriate treatment

Polymethyl methacrylate (PMMA) can be used to fill vertebral body defects without risk of cord damage from the heat generated from polymerization.77 Postoperative radiation should be postponed for 1 month to maximize wound healing.

ALGORITHMIC APPROACH TO TREATMENT The approach to treatment of primary spine tumors varies dramatically depending on the type of tumor. The treatment of each type is included in the discussion of each tumor type. However, there are general principles that guide the treatment of these tumors. First, malignant tumors are treated more aggressively than benign tumors. Staging studies should be performed to rule out metastatic spread of the malignant spine tumor, and the appropriate treatment should be provided, which often involves resection and stabilization with or without radiation or chemotherapy. In benign spine tumors, the question becomes one of aggressiveness. Typical benign, aggressive lesions are giant cell tumors and osteoblastomas. These are treated with marginal resection, and stabilization when need. If the benign tumor is not an aggressive type, it can often be observed or treated, depending on how symptomatic it is (Fig. 41.12).

Acknowledgments The authors would like to thank Christina Heathcock and Catherine Timby for their contributions to this chapter.

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Fig. 41.12 Algorithmic approach to the treatment of primary spine tumors.

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56. Boriani S, Chevalley F, Weinstein JN, et al. Chordoma of the spine above the sacrum. Treatment and outcome in 21 cases. Spine 1996; 2113:1569–1577. 57. Mackie PS, Fisher JL, Zhou H, et al. Bisphosphonates regulate cell growth and gene expression in the UMR 106-01 clonal rat osteosarcoma cell line. Br J Cancer 2001; 847:951–958. 58. Farese JP, Ashton J, Milner R, et al. The effect of the bisphosphonate alendronate on viability of canine osteosarcoma cells in vitro. In Vitro Cell Dev Biol Anim 2004; 403–404:113–117. 59. Heimdal K, Hirschberg H, Slettebo H, et al. High incidence of serious side effects of high-dose dexamethasone treatment in patients with epidural spinal cord compression. J Neurooncol 1992; 122:141–144. 60. Sorensen S, Helweg-Larsen S, Mouridsen H, et al. Effect of high-dose dexamethasone in carcinomatous metastatic spinal cord compression treated with radiotherapy: a randomised trial. Eur J Cancer 1994; 30A1:22–27. 61. Aebi M. Spinal metastasis in the elderly. Eur Spine J 2003; 12(Suppl 2): S202–S213. 62. Hosalkar HS, Weiss A. Chemotherapy for bone sarcoma does not affect fertility rates or childbirth. Clin Orthop 2004; 429:352.

38. Towbin R, Kaye R, Meza MP, et al. Osteoid osteoma: percutaneous excision using a CT-guided coaxial technique. Am J Roentgenol 1995; 1644:945–949.

63. Callstrom MR, et al. Painful metastases involving bone: feasibility of percutaneous CT- and US-guided radio-frequency ablation. Radiology 2002; 2241:87–97.

39. Rosenthal DI, Hornicek FJ, Torriani M, et al. Osteoid osteoma: percutaneous treatment with radiofrequency energy. Radiology 2003; 2291:171–175.

64. Nakatsuka A, Yamakado K, Maeda M, et al. Radiofrequency ablation combined with bone cement injection for the treatment of bone malignancies. J Vasc Interv Radiol 2004; 157:707–712.

40. Griffin JB. Benign osteoblastoma of the thoracic spine. Case report with fifteenyear follow-up. J Bone Joint Surg [Am] 1978; 606:833–835. 41. Ross JS, Masaryk TJ, Modic T, et al. Vertebral hemangiomas: MR imaging. Radiology 1987; 1651:165–169. 42. Martinez V, Sissons HA. Aneurysmal bone cyst. A review of 123 cases including primary lesions and those secondary to other bone pathology. Cancer 1988; 6111:2291–2304. 43. Lackman RD, Khoury LD, Esmail A, et al. The treatment of sacral giant-cell tumours by serial arterial embolisation. J Bone Joint Surg [Br] 2002; 846:873–877. 44. Chang SS, Suratwala SJ, Jung KM, et al.Bisphosphonates may reduce recurrence in giant cell tumor by inducing apoptosis. Clin Orthop 2004; 426:103–109. 45. Cheng YY, Huang L, Kumta SM, et al. Cytochemical and ultrastructural changes in the osteoclast-like giant cells of giant cell tumor of bone following bisphosphonate administration. Ultrastruct Pathol 2003; 276:385–391. 46. Fujimoto N, Nakagawa K, Seichi A, et al. A new bisphosphonate treatment option for giant cell tumors. Oncol Rep 2001; 83:643–647. 47. Corwin J. Solitary plasmacytoma of bone vs. extramedullary plasmacytoma and their relationship to multiple myeloma. Cancer 1979; 43:1007–1013. 48. Bielack SS, Wulff B, Delling G, et al. Osteosarcoma of the trunk treated by multimodal therapy: experience of the Cooperative Osteosarcoma Study Group (COSS). Med Pediatr Oncol 1995; 241:6–12. 49. McLain RF, Weinstein JN. Solitary plasmacytomas of the spine: a review of 84 cases. J Spinal Disord 1989; 22:69–74. 50. Huvos, AG. Osteogenic sarcoma of bones and soft tissues in older persons. A clinicopathologic analysis of 117 patients older than 60 years. Cancer 1986; 577: 1442–1449.

65. Poggi G, et al. Percutaneous ultrasound-guided radiofrequency thermal ablation of malignant osteolyses. Anticancer Res 2003; 236D:4977–4983. 66. Barr JD, Barr MS, Lemley TJ, et al. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine 2000; 258:923–928. 67. Deramond H, Depriester C, Toussaint P, et al. Percutaneous vertebroplasty. Semin Musculoskelet Radiol 1997; 12:285–296. 68. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful vertebral body fractures in cancer patients. J Neurosurg Spine 2003; 981:21–30. 69. Ratanatharathorn V, Powers WE. Epidural spinal cord compression from metastatic tumor: diagnosis and guidelines for management. Cancer Treat Rev 1991; 181: 55–71. 70. Bilsky MH, Lis E, Raizer J, et al. The diagnosis and treatment of metastatic spinal tumor. Oncologist 1999; 4:459–469. 71. Boriani S, De Lure F. Bone tumors of the spine and epidural cord compression: treatment options. Semin Spine Surg 1995; 7:317–322. 72. Vieweg U, Meyer B, Schramm, J. Tumour surgery of the upper cervical spine – a retrospective study of 13 cases. Acta Neurochir (Wien) 2001; 1433:217–225. 73. Sar C, Eralp L. Surgical treatment of primary tumors of the sacrum. Arch Orthop Trauma Surg 2002; 1223:148–155. 74. Gokaslan ZL, Romsdahl MM, Kroll SS, et al. Total sacrectomy and Galveston L-rod reconstruction for malignant neoplasms. Technical note. J Neurosurg 1997; 875:781–787. 75. Doita M, Harada T, Iguchi T, et al. Total sacrectomy and reconstruction for sacral tumors. Spine 2003; 2815:E296–E301.

51. Barwick KW, Huvos AG, Smith J. Primary osteogenic sarcoma of the vertebral column: a clinicopathologic correlation of ten patients. Cancer 1980; 463:595–604.

76. Rao S, Badani K, Schildhauer T, et al. Metastatic malignancy of the cervical spine. A nonoperative history. Spine 1992; 1710(Suppl):S407–S412.

52. Shives TC, Dahlin DC, Sim FH, et al. Osteosarcoma of the spine. J Bone Joint Surg [Am] 1986; 685:660–668.

77. Wang GJ, Reger SI, McLaughlin RE, et al. The safety of cement fixation in the cervical spine. Studies of a rabbit model. Clin Orthop 1979; 139:276–282.

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PART 3

SPECIFIC DISORDERS

Section 2

Osseous Spinal Tumors ■ i: Physiology and Assessment

CHAPTER

Secondary Bone Tumors

42

Jesse T. Torbert, Edward J. Fox, Harish S. Hosalkar, Kingsley R. Chin, Carol A. Dolinskas, Richard Daniels and Richard D. Lackman

INTRODUCTION Approximately 10% of all cancer patients develop clinically significant spinal metastases.1 Metastatic spine tumors are 40 times more frequent than all primary bone tumors combined.2 In autopsy series, vertebral body metastases were found in over one-third of patients dying of cancer.3 The most common cancers to metastasize to the spine are breast, lung, prostate, and renal carcinomas (Table 42.1). Lymphoid cancers, including lymphoma and myeloma, are systemic diseases and common sources of spinal involvement. However, many authors do not consider these lesions true spinal metastases, and they are not included in many clinical series. When lymphoma and myeloma are included, they represent 8% and 5% of secondary spine tumors, respectively.4 Although spinal metastases can occur in all age groups, the risk of metastatic spread to the spine coincides with the relatively high cancer risk period of 40–65 years of age.5 The average time between diagnosis of primary cancer and occurrence of spinal metastases varies widely (lung: 4 months; prostate: 22 months; breast: 86 months).6 Like most metastatic disease, metastatic spine tumors are rare in children. Exceptions to this are Ewing’s sarcoma and osteosarcoma (from other skeletal sites), neuroblastoma, and rhabdomyosarcoma.7 The spine can be divided into anterior elements and posterior elements (Fig. 42.1). Anterior elements consist of the vertebral body, and the posterior elements include the remainder of the vertebra (pedicles, transverse processes, laminae, and spinous process). Metastases involving the spine are located in the bony vertebral column 85% of the time,8 and the anterior elements of the spine are 20

Table 42.1: The Most Common Primary Cancers that Metastasize to the Spine4,11 Primary Malignancy

Percentage of all Metastatic Spine Lesions

Breast

21–30

Lung

13–19

Prostate

7–10

Renal

6–12

Gastrointestinal

4–7

Thyroid

5

Various other cancers

9

Cancers of unknown origin/primary

10–15

times more likely to be involved than the posterior elements.9 Other metastases involving the spine may be located in the paravertebral region and less often in the epidural space. The thoracic spine is most frequently invaded by metastases, followed by cervical, then lumbar segments.10 It has been suggested that the distribution of metastases to the spine is roughly proportional to the height of each segment, with the cervical spine hosting 24% of metastases, thoracic 48%, lumbar 26%, and sacral 2% (Fig. 42.2).11 Early diagnosis is critical in both primary and secondary tumors of the spine. Unlike primary tumors, the early diagnosis and treatment of secondary tumors will not prevent metastatic disease. However, much of the significant morbidity related to spinal metastases can be lessened with early intervention. For instance, the best predictor of neurologic outcome after radiotherapy is the neurologic function prior to treatment; patients with severe neurologic deficit before radiation are unlikely to improve.12 In addition, patients undergoing surgery for neurologic symptoms had much better outcomes if they were ambulatory prior to surgery.13 Neoplastic paraplegia not only reduces a patient’s quality of life, it results in decreased life expectancy and a large economic cost to society. The primary treatment goals in metastatic spine disease are to preserve/improve quality of life, alleviate pain, preserve/improve neurologic function, prevent/correct spinal instability, and optimize local tumor control as well as treatment of primary malignancy. Treatment options include various medications, external bracing, chemotherapy, radiation therapy, vertebroplasty/kyphoplasty, radiofrequency ablation, embolization, and surgery. Due to the many goals and modes of therapy, treatment of a patient with spinal metastatic disease requires a multidisciplinary approach, which often includes a pain specialist,

Spinous process Lamina Transverse process

Posterior elements

Pedicle Vertebral foramen Vertebral body

Anterior elements

Fig. 42.1 This axial view of a vertebra illustrates the anterior elements and posterior elements.

469

Part 3: Specific Disorders Posterior vein of internal vertebral plexus

24%

Anterior vein of internal vertebral plexus

Internal vertebral plexus

Intervertebral vein Basivertebral vein

48%

Fig. 42.3 This axial view of a vertebra (with the superior half of the vertebral body cut away) shows the relationship of the intervertebral, basivertebral, and the anterior, and posterior veins of the internal vertebral plexus. 26%

vertebral plexus, metastatic lesions occur at multiple noncontiguous levels in approximately 25% of cases.18 Some authors disagree with the Batson’s plexus theory and instead believe that arterial hematogenous spread to the marrow of the vertebral body results in the characteristic growth of tumors in the vertebral body, which eventually grow to directly or indirectly impinge the spinal cord (Fig. 42.3).19

2% Fig. 42.2 This view of the spinal column demonstrates the approximate distribution of metastases within the spine.

medical oncologist, interventional radiologist, spine surgeon, physical medicine/rehabilitation specialist, social worker, and hospice care.

EXPLANATION OF ANATOMIC LOCATION It is thought that the highly vascular, sinusoidal nature of the red marrow within vertebral bodies makes them particularly susceptible to seeding of metastatic cells. Moreover, retrograde venous flow into the internal vertebral plexus (Batson’s plexus)14 has historically been implicated in the spread of metastases to the spine. The internal vertebral plexus, a network of valveless veins in the vertebral canal, travels outside the dura from the foramen magnum to the coccyx. Due to the lack of valves, a rise in intrathoracic or intra-abdominal pressure can cause venous blood from the azygous system and the pelvic venous plexus to enter the internal vertebral plexus, allowing seeding of metastatic emboli from various organs. Drainage of the breast through the azygous vein and the prostate through the pelvic venous plexus predisposes the spine to metastatic processes from these areas. Drainage of the lung through the pulmonary vein, and colon through the portal system, tend to result in more diffuse embolic patterns.15 Oeppen et al. published a case report of a patient with renal vein involvement of renal cell carcinoma with spinal metastases that centered on the basivertebral veins at three contiguous levels in the low thoracic spine. Magnetic resonance imaging (MRI) demonstrated tumor in the intervertebral veins, which link the azygous system to the internal vertebral plexus.16 This case was highly suggestive of vertebral metastases due to retrograde venous spread through the internal vertebral plexus. Oge et al. described a case of a broken pacemaker lead tip migrating from the common iliac vein to a vein within the internal vertebral plexus at the level of L5.17 Due to the lack of valves and lengthy nature of the internal 470

CLINICAL PRESENTATION As mentioned previously, the early diagnosis of secondary spinal tumors is essential. Symptoms suggestive of spine involvement in a patient with a prior malignancy must be taken seriously. Also, a high index of suspicion is necessary in those patients without known malignancies. The clinician must be thoroughly familiar with the symptoms that are typically present in patients with metastatic spine tumors, which are often the same presenting symptoms as in primary tumors of the spine. A careful history characterizing the character and timeline of symptoms is important in the diagnosis and direction of their work-up. Likewise, elements of the history can dictate the treatment plan. A proper history provides a baseline to evaluate the course of the disease and the effect of therapy and includes a summary of prior treatment (chemotherapy, radiation, prior surgery).

Pain As in primary spinal tumors, the first indication of spinal metastases is most often due to the pain produced by these tumors. Back pain is so common, and is typically such an early symptom of spinal metastases, that it may lead to recognition of a previously undiagnosed primary malignancy, such as lung carcinoma or prostatic cancer. Back pain is the first symptom of a spinal metastasis in 90–97% of cases.11,13 The presence of back or neck pain in a child with a cancer is caused by metastatic disease in approximately half of patients, and of these patients with spinal metastatic disease, spinal cord compression is present in approximately one-third.20 Pain often precedes other neurologic symptoms by weeks or months. In 42 patients undergoing surgery for metastatic disease of the spine, the median time from onset of back pain to appearance of neurological signs was 7 months with a range of 0–72 months.21 In addition, back pain may be present before a radiographic lesion can be detected. Metastatic disease to the spine can manifest in back pain in various ways and is often multifactorial (Table 42.2). When possible, it is important to determine the mechanism of back pain because

Section 2: Osseous Spinal Tumors

Table 42.2: Types and Characteristics of Back Pain Found in Tumors of the Spine22,24,102 Type of pain

Mechanism

Exacerbated by

Alleviated by

Local

Intraosseous mass/periosteal disturbance/inflammatory mediators

Night time

Steroids/NSAIDs

Axial

Structural abnormality causing mechanical pain

Motion, especially axial loads of spine

Rest

Radicular

Compression of nerve root

Motion/positional

Rest/positional

Myelopathic

Pain directly from cord compression by tumor or bone

Recumbency

Corticosteroids

the treatment may vary depending on the mechanism. Local pain is produced by an intraosseous mass effect of the tumor or local stretching/distortion of the periosteum due to tumor destruction. In addition, this pain may be produced and exacerbated by inflammatory mediators. Local pain is persistent, often worse at night, and not typically affected by movement. Low-dose steroids (decadron 12 mg daily) often relieve the pain. In addition, local pain is often relieved by treatment of the underlying tumor with radiation or surgery.22 Axial pain, which is mechanical in nature, evolves from a structural abnormality of the spine and may indicate instability. Axial pain may be produced by axial loads on the spine; therefore, in such cases, it is exacerbated by motion and alleviated by rest. Radicular pain may develop from nerve root compression by tumor epidural extension and is worse with motion. It is often positional, alleviated by one position and exacerbated by another. Cauda equina syndrome, caused by compression of the nerve roots below the conus medularis, may exhibit lumbar and sacral radicular pain as well as paresthesias and weakness. Symptoms are often asymmetric. Some patients may develop a combination of radiculopathy and axial pain resulting from instability and neuroforaminal compression. Myelopathic pain is due to direct compression of the spinal cord either by tumor or bone. Recumbency often makes myelopathic pain worse; this is thought to be due to the distention of the internal venous plexus. Steroids often reduce myelopathic pain by reducing vasogenic edema. In general, pain from tumors commonly mimics the pain produced by nontumorous disorders. It is therefore necessary for the clinician to have a high index of suspicion when dealing with back pain, even if the patient does not present with the characteristic types of pain associated with spinal tumors. In a patient with known malignancy, back pain should be considered spinal metastases until proven otherwise.

Neurologic impairments Neurologic manifestations other than pain often begin with radiculopathy, followed later by myelopathy due to spinal cord compression.22 Progression of symptoms can be gradual, but acute deterioration may occur as a result of spinal instability. Acutely worsening symptoms in patients with spinal metastases requires emergent attention. Along with pain, radiculopathy in the cervical and lumbar regions causes weakness in the arms and legs, respectively. Radiculopathy due to lesions in the thoracic spine may cause pain in a band-like pattern in the corresponding dermatomes along the thorax and abdomen. Objective sensory loss is rare when a single nerve root is involved due to the overlap from neighboring roots. Cauda equina syndrome may present with loss of sensation in the buttocks and legs, unilateral or asymmetric leg weakness, hypotonia, decreased reflexes, early bladder and bowel incontinence, and lumbosacral radicular pain. Myelopathy, which occurs in 20% of adult patients with spinal metastases,23 often begins as hyperreflexia below the level of the

compression. This can progress to weakness, proprioceptive sensory loss, loss of pain and temperature sensation, urinary and fecal incontinence, impotence, and even paralysis. Eighty percent of patients with spinal cord compression will have weakness or paralysis.24 Impaired proprioception, sphincter function,24 and ability to ambulate25 indicate more serious neurologic damage when affected, and they are less likely to be recovered with treatment. In addition, patients tend to underestimate the loss of bladder and bowel control and sometimes discount them as symptoms of other medical problems, such as prostatic hypertrophy or side effects of chemotherapy.

Other symptoms As with any suspected malignancy, constitutional symptoms such as fatigue, fever, and unexpected weight loss must be included in a careful review of symptoms. If suspicious of a metastatic lesion in the spine, the physician should inquire about symptoms of possible primary cancers. A family history of cancer may also be helpful in elucidating the diagnosis of a patient with a suspected metastatic lesion. Red flags that suggest malignancy of the spine are presented in Table 42.3.

PHYSICAL EXAMINATION The examination in a patient with possible metastatic disease to the spine is similar to that in a patient with a suspected primary tumor (see previous chapter). A complete examination of the spine and its neurologic function should be performed on any patient with a suspected spine tumor. One may cautiously attempt to elicit Lhermitte’s sign. Lhermitte’s sign is defined as a subjective electric shock-like sensation traveling down the spinal column and through the upper and lower limbs that occurs with neck flexion. This finding was encountered in 15% of patients with symptomatic spinal metastases, and all lesions associated with this finding were in the thoracic spine.26 In addition, careful examination of the neck, breasts, lungs, abdomen, and prostate can often reveal a potential source for metastatic spinal tumors. Identification of lymphadenopathy in the cervical,

Table 42.3: Elements of the Presentation that are Worrisome for Spinal Malignancy Red Flags History of prior malignancy Back pain worse at night/pain that wakes patient from sleep Consistent progression of pain Pain unchanged during rest or activity Acute neurologic deterioration Presence of a mass Presence of constitutional symptoms

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Part 3: Specific Disorders

axillary, and inguinal lymph nodes can suggest leukemia, lymphoma, or other systemic malignancy. A rectal exam, including stool guaiac and assessment of sensory, motor, and reflex components, may be informative. Careful palpation of the extremities, rib cage, and iliac crests for painful areas can alert the examiner to other sites of bony metastatic disease.

vertebral body lesions typically spare the disc spaces, which can differentiate them from osteomyelitis. Flexion and extension studies, performed with caution, may be warranted if instability is suspected. The presence of instability is demonstrated by 25% translation of vertebral elements or >50% collapse, and is an indication for operative treatment.

WORK-UP

Bone scan

Laboratory studies

Bone scanning (skeletal scintigraphy) utilizes a disphosphonate compound, tagged with technetium 99m, which, after intravenous injection becomes incorporated into bone by osteoblastic activity. Bone scanning provides images of the entire body in a fairly short period of time. It is a fairly sensitive technique for the detection of bone metastases and can detect these lesions earlier than plain films; however, its one weakness is low specificity. Bone scans demonstrate areas of osteoblastic activity, and the radionuclide accumulates at sites of fracture, infection, degenerative disease, bone metastases, and benign tumors such as some hemangiomas and fibrous dysplasia. The pattern of uptake is frequently helpful in deciding if uptake is likely to represent metastatic disease. False-negative bone scans are often due to destructive activity that exceeds reactive or blastic activity, as in multiple myeloma, aggressive tumors, and in tumors which are confined to the medullary cavity and do not affect the cortex.30 Also, paraspinal tumors that invade the epidural space through the intervertebral foramen are often missed on bone scan.

The laboratory work-up in a patient with a suspected tumor of the spine can be involved, especially if an undiagnosed primary malignancy is suspected. A complete blood count (CBC) with a differential is important when working up any suspected malignancy. Elevated erythrocyte sedimentation rates (ESR) and C-reactive protein (CRP) levels signal that an inflammatory process is involved, but cannot consistently differentiate an infectious process from a malignancy. Lactate dehydrogenase (LDH) levels can be elevated in sarcomas, and LDH isoenzymes 2 and 3 can suggest a diagnosis of lymphoma.27 In order to check for liver cancer, alpha fetoprotein (AFP) levels are often obtained in patients with hepatitis C or those who are heavy drinkers. Carcinoembryonic antigen (CEA) is a marker of adenocarcinomas such as colonic, rectal, pancreatic, gastric, and breast.28 Prostate specific antigen (PSA) levels can help diagnose prostate cancer. A thyroid panel can help eliminate the suspicion of a rare thyroid primary, and parathyroid hormone (PTH) can be ordered to look for hyperparathyroidism. An elevated PTH level may lead to diagnosis of a brown tumor of the spine, which can be mistaken for metastatic disease. The diagnosis of multiple myeloma can be confirmed by the identification of monoclonal proteins in the serum or urine via serum protein electrophoresis (SPEP) or urine protein electrophoresis (UPEP); however, up to 3% of patients may have negative serum and urine electrophoresis.4 A chemistry panel can be used to assess kidney function and allows calcium and phosphate levels to be followed to detect and avoid the development of malignant hypercalcemia associated with metastatic lysis of bone. An elevated alkaline phosphatase level can also provide evidence for a neoplastic bone disease.

X-ray The sensitivity is low for early metastatic involvement of the spine; however, plain films should be obtained initially, as in the work-up of primary tumors of the spine. Of patients with spinal metastases that underwent autopsy, 48% had no visible lesions on plain films, and 26% had negative X-rays despite gross involvement by tumor.3 The high false-negative rate can be partly attributed to the amount of cancellous bone (50%)29 that must be destroyed before becoming radiographically evident. Paraspinal tumors invading through the neural foramen may produce no radiographic abnormality. Therefore, the work-up of a spinal tumor does not end with a negative plain film. Despite low sensitivity, plain films are inexpensive and can offer information not provided by MRI and other imaging modalities. Pedicle erosion is one of the more common X-ray findings in the thoracic and lumbar spine. The absence of one pedicle, which normally appears as an ovoid margin of dense cortical bone, gives the appearance of a ‘winking owl’ on the anteroposterior radiograph. This is a manifestation of pedicle erosion due either to a bony spine lesion or a lesion extrinsic to the vertebrae. Pedicle involvement is typically seen early because of the predominant cortical bone content. Pathological compression fractures may be seen, but may be distinguished from benign compression fractures unless pedicle erosion, other cortical erosion, or a soft tissue mass is associated with the fracture. Neoplastic 472

Computed tomography Computed tomography (CT) provides the best images of bone architecture and readily detects small areas of bone destruction or blastic change, although MRI is more effective in detection of lesions before changes in bone structure can be demonstrated. In the past it was not considered a good screening tool for lesions in the spine, but with multidetector scanners, the entire spine can be scanned in great detail in under 5 minutes. Using bone and soft tissue windows, both bone and paraspinal lesions are readily detected. The images can be reconstructed into any plane for the evaluation of bone alignment and extent of compression in a compression fracture. CT imaging can also provide the spine surgeon with an image of remaining bone in an abnormal vertebra, a factor in the feasibility of fixation. CT imaging is also valuable for planning and guiding percutaneous biopsies of vertebral lesions. CT imaging of the spine is especially useful in those patients who cannot undergo MRI (claustrophobic, cannot lie flat for long periods of time, or have implanted devices liable to be affected by magnetic field).

Myelography (conventional and CT-myelography) Myelography is an invasive procedure with inherent risks. Before MRI, conventional myelography was the gold standard for detection of cord compression and intrinsic cord lesions, but it has been largely replaced by MRI scanning, and by CT-myelography when MRI is contraindicated. Myelography may fail to reveal secondary sites of epidural spinal cord compression and has been shown to be less sensitive in diagnosing spinal tumors than MRI.31 CT-myelography, like conventional myelography, involves the instillation of contrast into the dural sac, but the amount of contrast used is much less due to the enhanced ability of CT to depict subtle contrast differences. By employing various window settings for the images, details of the paraspinal structures, bone, and dural sac contents are well demonstrated. Both conventional and CT-myelography may be used when metallic fixation devices have been placed in and around the spine and MRI

Section 2: Osseous Spinal Tumors

is unable to provide adequate images. This problem is becoming less frequent with the increased use of titanium spinal hardware.

Magnetic resonance imaging Magnetic resonance imaging detects spinal and paraspinal pathology better than any other imaging technique. It reliably depicts changes in the water content of structures, and thus most pathology, before changes in gross architecture occur. Pathology is detected by employing imaging sequences that emphasize various components of tissues such as fat, fluid, and vascularity. MRI is the only noninvasive technique able to visualize pathology within the spinal cord and clearly depicts the degree of cord compression, as well as the process causing the compression. MRI defines lesions in the vertebrae as well as disc pathology and is the best method to diagnose discitis and paraspinal infections. MRI is also more reliable than other techniques in separating benign compression fractures from pathologic fractures of the vertebral bodies. This distinction is made by analyzing signal intensity changes in the bone and paraspinal space as well as by evaluating the shape of the vertebrae and integrity of the cortical margins. MRI reveals bone metastases earlier than bone scintigraphy and depicts foci of osteolytic and osteoblastic activity equally. Most bone metastases are readily detected without the use of gadolinium-based intravenous contrast (most are easily demonstrated on T1-weighted and fat-suppressed T2-weighted images without contrast).32 Contrast actually may obscure metastases to bone as enhancement may cause the signal in the lesion to increase to that of normal bone marrow on T1-weighted scans.33 Limitations of MRI include the relatively long time needed to acquire a complete imaging sequence (at least 1 hour to study the entire spine in detail), degradation of the images by patient motion and by implanted metal such as fixation devices, the need for the patient to be able to lie flat and supine for the study, and contraindications such as pacemakers, various other implanted electronic devices, brain aneurysm clips of uncertain composition, and claustrophobia.

Positron emission tomography The most common radiotracer used in clinical positron emission tomography (PET) imaging is fluorine-18-fluoro-2-D-deoxyglucose (18F-FDG), which accumulates in areas of high glycolysis and membrane transport of glucose, both known to be increased in malignant tissue. Unlike the agent used in bone scanning, 18F-FDG may detect bone marrow-occupying lesions before cortical involvement occurs, thus detecting bone metastases before they can be found on bone scans. Sclerotic metastases, however, as found in some breast and prostate cancers, are less likely to be detected by PET as these lesions have lower glycolytic rates and are less cellular than lytic metastases.34 18F-FDG is not specific for tumors and may accumulate at sites of infection but is less likely to be detected at sites of degenerative change than technetium 99m, the agent used in bone scans. Therefore, it is somewhat more specific for tumors. PET also demonstrates metastases in soft tissue throughout the body, resulting in additional diagnostic value. In addition to detecting spine tumors, PET may also be useful in distinguishing malignant lesions from benign.

Biopsy When a lesion is identified by radiologic means, it is often necessary to establish a histologic diagnosis for purposes of treatment. Biopsy is vital when the patient without a known primary possesses a spinal lesion that is suspicious for malignancy. In a patient with a previously diagnosed malignancy who presents with a new, solitary spinal lesion, biopsy of the spinal lesion is always required to confirm diagnosis

before treatment with radiation, chemotherapy, or surgery. Benign spine lesions can develop in a patient with a known malignancy, and spine metastases may arise from a primary tumor unrelated to a previously diagnosed cancer. Therefore, the proper histological diagnosis of the spinal lesion helps avoid misdiagnosis and erroneous treatment.

Types of biopsy As discussed in the preceding chapter, there are two types of biopsy commonly used for spinal lesions: percutaneous, guided biopsy and open, surgical biopsy. Both fluoroscopic-guided and CT-guided percutaneous biopsies can be utilized, and both are effective. The accuracy of CT makes it superior when dealing with small, deep-seated lesions, especially in the cervical and thoracic regions.37 CT allows better selection of the optimal location to sample tissue. For lesions visible via fluoroscopic monitoring, fluoroscopic-guided biopsy offers real-time positioning of the needle. Open biopsy maximizes tissue retrieval, providing the highest diagnostic success rate; however, it is typically reserved for failed percutaneous biopsies due to the increased morbidity of the open procedure and greater risk of wound contamination with tumor. Regardless of which method is used, the goal is to obtain an adequate amount of tissue while minimizing complications.

Biopsy success rate Accurate diagnosis of tumorous and nontumorous lesions using CTguided biopsy is achieved greater than 90% of the time.37–39 In lesions with central necrosis, the ability to obtain the correct diagnosis may be enhanced by obtaining tissue from the periphery of the lesion. In paucicellular aspirates, a cell block can be prepared or additional tissue, such as a core biopsy, can be obtained. If histology yields only peripheral blood in an obviously destructive mass, biopsy can be repeated, by directing the needle/device at a slightly different area of the lesion.39 If indicated, corticosteroids should only be administered after biopsy due to their lytic effect on certain tumors, including leukemia. This lytic effect can lead to a nondiagnostic biopsy.

Percutaneous biopsy of solitary lesions The approach to the percutaneous biopsy of a solitary spinal lesion is fairly straightforward. Usually, the approach involves the shortest path to the lesion that does not place vital structures at risk. For biopsies of the spine, this typically involves a posterior approach; however, in the cervical spine, anterolateral approaches are often used. Since most metastatic lesions are found in the vertebral body, a posterior transpedicular approach is often used. The transpedicular approach, shown in Figure 42.4, helps to avoid vital structures while minimizing the amount of tissue susceptible to tumor contamination of the needle tract. Virtually any lesion within the vertebral body of cervical, thoracic, or lumbar vertebrae can by accessed via this approach.40 Lesions located in the posterior elements are typically biopsied with a direct approach.

Percutaneous biopsy when multiple lesions are present When multiple lesions are present in the spine, biopsy of one lesion may be satisfactory if the lesions appear to be from the same malignancy. Several factors play a role in choosing which lesion to biopsy: size of the lesion, radiologic morphology, location along the spinal column, and location within the vertebra. Often, the largest lesion is easier to biopsy and more tissue is available to aid in the histologic diagnosis. The biopsy of the most aggressive lesion may demonstrate 473

Part 3: Specific Disorders

Fig. 42.4 This is a percutaneous, CT-guided biopsy performed through a transpedicular approach. (Image provided by Dr. Neil Roach.)

malignant cells that may be less abundant or not present in more benign-appearing lesions. Lumbar lesions are often easier to biopsy with the transpedicular approach because of the large size of lumbar pedicles when compared to those in the thoracic and cervical levels. Also, it is often desirable to biopsy a lesion that requires the least amount of bone disruption in order to cause the least amount of structural damage to the vertebra, which may already be compromised by tumor destruction. As mentioned before, biopsies of presumed spinal metastases are typically required before definitive treatment, even in a patient with a known primary malignancy. In a patient with metastatic involvement of multiple organs, biopsy of each lesion is often not feasible. Instead, biopsy of the single most representative, accessible lesion is common practice. In this case, the physician must weigh the risks and morbidity associated with biopsy of the spine lesion against the possibility of misdiagnosis and incorrect treatment of the spinal lesion.

Complications of biopsy Biopsies of potentially tumorous lesions should be well planned. It is well known that inadequate or inappropriate open biopsies adversely affect outcome. Complications arising in these unsound biopsies include disability due to more complex resection, loss of function, local recurrence, and death.41 The surgeon who performs the definitive surgical procedures, if further surgery becomes necessary, should ideally perform the open biopsy. This ensures that the subsequent surgery can be performed using the optimal incision and approach, while excising the biopsy incision and tract. This also helps to eliminate unnecessary and improperly performed open biopsies. Complications of percutaneous needle biopsy include bleeding, infection, neurologic compromise, fracture, biopsy tract contamination, and death, although serious complications are rare. There may be risk of tumor contamination of the biopsy tract.42 The needle tract may be excised if a subsequent surgery is indicated, although this procedure is somewhat controversial. Whenever possible, guided biopsies should be done at the same institution where definitive surgical treatment will occur. Typically, pathologists at the larger referral centers will be more experienced with uncommon primary and secondary malignant tissues obtained from the spine and will typically review specimens despite previous histologic diagnosis from outside institutions. Also, a team approach between the interventional radiologist and the treating surgeon is more likely to produce a favorable result.

Algorithmic approach to work-up When a spine tumor is suspected in a patient with severe or rapidly progressing neurologic symptoms, a thorough review of systems (ROS) and physical examination (PE) should be performed and laboratory tests and imaging, usually MRI and radiographs, should 474

be obtained promptly (Fig. 42.5). A spine surgeon should be consulted as soon as possible. In the absence of severe or rapidly deteriorating symptoms, a thorough ROS and PE are again necessary. Laboratory tests should be selected and performed based on the working differential diagnosis. Plain films should be obtained and are usually followed up with more sophisticated imaging. If the diagnosis is apparent at this point in time, appropriate treatment may be initiated. However, if treatment involves radiation, chemotherapy, or surgery, tissue diagnosis is typically required. If the diagnosis is in question, percutaneous CT-guided biopsy should be performed. Appropriate treatment may be initiated if the diagnosis is benign, but staging studies, such as CT of the chest, abdomen, and pelvis, may be appropriate before initiating treatment if the lesion is a metastatic or primary malignant lesion.

PRIMARY MALIGNANCIES THAT METASTASIZE TO THE SPINE Breast Breast cancer has a high propensity for bone. Typical skeletal sites include vertebral bodies, pelvis, proximal femur, and humerus. One autopsy study demonstrated that approximately 75% of breast cancer patients developed metastases to spine.3 A portion of the venous drainage from the breast empties into the thoracic portion of the azygous system, which accounts for thoracic location of most spine metastases. Lumbar involvement is not uncommon in breast cancer. One study found the L2 vertebra most commonly involved, followed closely by T9.43 Breast metastases are often osteolytic; however, some can be of mixed type, and less frequently purely sclerotic.44,45 Breast tumors that metastasize to bone are more frequently estrogen receptorpositive and well differentiated than those that metastasize to the lungs or liver.4 In general, breast metastases are relatively sensitive to radiation therapy. However, radiotherapy may be more effective on poorly differentiated, rapidly growing lesions when compared to well-differentiated, slower growing lesions of bone.

Lung Lung carcinoma commonly metastasizes to liver, skeleton, bone marrow, and brain.46,47 In one autopsy study approximately 45% of patients dying of lung cancer developed metastases to spine.3 The most common location for spine metastatic disease was the lower thoracic region, with T12 involved in 10 of 15 cases examined in one study.43 Metastatic spine lesions due to lung cancer most often result in lytic lesions. Small cell lung carcinoma has the best prognosis and longest survival. Lung carcinomas are generally considered to be intermediately responsive to radiation. Small cell carcinoma is more responsive than other forms to radiation, as well as to chemotherapy. Given the limited survival of most patients with lung cancer, and the responsiveness of small cell carcinoma to radiation and chemotherapy, most are not candidates for operative treatment.4

Prostate Prostate cancer and metastases of prostate cancer to the spine are common. In autopsy studies prostate cancer is found in 24–46% of men over the age of 50 years.48 One autopsy study demonstrated that approximately 90% of prostate cancer patients dying of their disease developed metastases to spine.3 Prostatic spinal metastases are most often located in the lumbar spine. Skeletal prostate metastases are typically osteoblastic, and sclerotic lesions in the vertebral bodies and pelvis are most common.

Section 2: Osseous Spinal Tumors Suspected spine tumor

Presence of severe/rapidly progressing neurologic symptoms ? Yes

No

Thorough ROS/PE emergent labs and X-ray MR imaging

Thorough ROS/PE, appropriate labs X–ray, and subsequent imaging (usually MRI)

Emergent spine surgery consult

Diagnosis apparent ? Yes

Does appropriate treatment involve radiation/chemotherapy/surgery ?

Yes

No Percutaneous, CT-guided biopsy

No

Metastatic or malignant ? Yes

Percutaneous, CT-guided biopsy to avoid misdiagnosis and erroneous treatment

Proceed with appropriate treatment

Staging studies

Although skeletal metastases are typically osteoblastic (80%), a mixed osteoblastic/osteolytic pattern is not uncommon (12%.)49 An osteolytic pattern represents 4% of these skeletal metastases49 and is typically found in poorly differentiated tumors (combined Gleason’s score of 9 to 10).50 Expression of prostate-specific antigen and prostate-specific acid phosphatase, which can be identified immunohistochemically, is a helpful feature in diagnosis, although some poorly differentiated prostate carcinomas may be negative for both. Treated prostate carcinoma can be very inconspicuous, mimicking non-neoplastic cells such as histiocytes, in which case epithelial markers such as keratin can aid in diagnosis.50 Because prostate metastatic lesions in the spine are usually blastic, pathologic fractures and neurologic involvement are relatively rare.51 The prognosis for life expectancy when cord compression occurs is better than that of most metastatic diseases. Treatment of prostate cancer includes hormonal therapy, radiation, chemotherapy, and surgery. The need for surgical intervention for spinal metastases is not as common as for tumors of other origins.

Renal Renal cell carcinoma is the fourth most common type of metastatic spinal tumor. By the time renal carcinoma is diagnosed, it has often reached advanced stages. These carcinomas are known to metastasize to unusual sites such as the eye, skin, tongue, heart, and breast. Eighty percent of patients with renal cell carcinoma will eventually develop metastases.52 In one autopsy study, approximately 30% of patients dying of renal cancer had developed metastases to spine.3 Renal cell carcinoma most often produces lytic lesions.53 The margins are generally indistinct and aggressive lesions expand into the surrounding soft tissues (Fig. 42.6).4 A small proportion of renal cell carcinomas dedifferentiate into pleomorphic sarcomatoid carcinoma

No Proceed with appropriate treatment

Fig. 42.5 Algorithmic approach to the work-up of suspected spine tumors.

and the sarcomatoid elements may be the only components present in spine metastases. These lesions may have features like fibrosarcoma and malignant fibrous histiocytoma and can be misdiagnosed as primary bone lesions. Gross pathologic examination shows the majority of renal cell carcinomas to be very hypervascular. To date, chemotherapy has been shown to be ineffective in the treatment of renal metastases to the spine. Although radiation treatment is often used, the tumor is relatively radioresistant. While median survival times are short (generally 6–9 months),54 the clinical course of metastatic renal carcinoma is variable. Survival of patients with renal cell carcinoma and spinal metastases is most dependent on the pathologic characteristics of the primary tumor, followed by severity of neurologic deficit and presence of other metastases.52 Those with predominantly osseous metastases fare better than those with other organ involvement. Renal cell carcinoma more commonly causes neurologic deficiencies than other spinal metastases,52 and surgery is relatively common for these spinal lesions. Preoperative arterial embolization is often necessary to diminish intraoperative blood loss, which can be extensive.52,55 In a study by Sundaresan et al., 90% of patients with cord compression causing neurologic compromise showed neurologic improvement after surgery.55 In another study, 88% of patients had partial or complete relief of pain, with 64% of the bedridden patients able to walk after surgery.52

Gastrointestinal Most carcinomas of the gastrointestinal tract are highly aggressive lesions with a high propensity for metastasis.56 The skeletal sites most frequently involved are the spine, ribs, pelvis, and femur. Patients dying of gastrointestinal tract tumors, including those of the pancreas and liver, have histological evidence of spine metastases 25% of the time.3 Gastric carcinomas are more prone to develop metastases to 475

Part 3: Specific Disorders

A

B

Fig. 42.6 (A) This CT (bone window) demonstrates the lytic, aggressive nature of renal cell metastases. (B) This CT (soft tissue settings) shows the expansion of the lesion into the surrounding soft tissues.

the spine than carcinomas of the colon. Colorectal cancers, which are unusual sources of spinal metastases, favor the lumbar spine.57 Spine metastases are often late findings in colorectal cancer and often generate lytic lesions.53

Thyroid The behavior of thyroid carcinomas varies widely from indolent, welldifferentiated tumors to highly malignant, poorly differentiated carcinomas. Well-differentiated carcinomas, especially follicular, have a unique propensity to metastasize to bone. After metastases to the neck lymph nodes, the skeleton is the next most frequent metastatic location.50 In one autopsy study, approximately 40% of patients dying of thyroid cancer had metastases to spine.3 Radiographically, thyroid carcinomas typically appear as destructive, lytic lesions in bone. The lesions are usually poorly demarcated, and it is unusual for these tumors to demonstrate a periosteal reaction.4 Histologically, thyroid carcinoma is usually easily recognized in bone; however, immunohistochemical staining for thyroglobulin in follicular and papillary carcinomas and calcitonin in medullary carcinomas may be helpful.50

Lymphoma In one study, 29% of patients that died of lymphoma had evidence of spinal metastases.3 The typical route of metastasis for lymphoma is by direct, contiguous spread from the retroperitoneum to the paraspinous and epidural spaces via the neural foramina. Neurologic symptoms are usually due to spinal cord compression; however, direct infiltration of the spinal cord and nerve roots may also occur. On MRI, metastases to the spine usually show vertebral body involvement accompanying the paraspinous soft tissue mass. This can also be seen in CT with soft tissue settings (Fig. 42.7). The vertebral body lesion usually has lower signal intensity than marrow on T1-weighted images. This low signal abnormality may be subtle in children; it may be difficult to detect in older patients with heterogeneous marrow signal. On T2-weighted MRI, these tumors exhibit high signal intensities.58 For a patient with confirmed systemic lymphoma and newly diagnosed epidural metastases, local radiation therapy using 30–40 Gy is the treatment of choice.

Multiple myeloma Multiple myeloma and solitary myeloma are often considered separate entities due to their significant differences. Solitary myeloma, 476

Fig. 42.7 This CT (soft tissue settings) of systemic lymphoma shows a sclerotic (sclerotic being somewhat atypical) lesion in an intact vertebral body with soft tissue extension that is not associated with cortical bone destruction.

which is addressed in the previous chapter, is a rare disease that occasionally occurs in the spine. Multiple myeloma is more common, with an incidence of approximately 35 per million and is found most commonly in patients over 40 years of age. Multiple myeloma involves the uncontrolled proliferation of malignant plasma cells and their products. An elevated level of IgG monoclonal light chains is most frequently found followed by IgA and IgD monoclonal light chains. Multiple myeloma is most commonly found in bones that contain hematopoietic marrow with the majority of lesions found in the axial skeleton. Fifty-five percent of patients that died of myeloma in one study had evidence of spinal involvement.3 Regarding location within the spinal column, no one vertebral level seemed to be preferentially involved.43 The majority of multiple myeloma lesions in the skeleton are lytic, and sporadic areas of sclerosis may be present. As mentioned previously, bone scans may be negative. The typical appearance of untreated multiple myeloma on MRI is similar to that of other metastatic lesions that replace fatty bone marrow. These lesions have relatively low T1-weighted signal intensity and high T2-weighted signal intensity when compared to normal bone marrow. The usual pattern

Section 2: Osseous Spinal Tumors

of involvement is diffuse marrow replacement in multiple vertebral bodies, often with multiple well-circumscribed lesions.58 Patients with multiple myeloma fare poorly, with a median survival of 28 months. In cases with spinal metastases the prognosis is worse, with 76% of patients deceased within 1 year.59 In the case of disseminated myeloma, chemotherapy should be initiated. The treatment of choice in multiple myeloma is radiation, bisphosphonate therapy, and if necessary, bracing. Because of the sensitivity of this cancer to radiation and the poor survival rate, surgery is not often indicated. If indicated, surgery is often difficult to perform due to multilevel involvement and severe osteopenia seen in these patients.4

MANAGEMENT The management of spinal metastases is complex and requires a multidisciplinary approach. Not only does management include spinal lesions, but primary tumors and other metastatic sites as well. Treatment modalities can be categorized into general medical treatment, tumor-specific medical treatment, minimally invasive procedures, and surgery. The treatment of spinal metastases must be carried out with the patient’s anticipated length of survival in mind. The primary goals in treatment of metastatic spine lesions are the following: ● ● ● ● ●

Preserve/improve quality of life Alleviate pain Preserve/improve neurologic function Prevent/correct spinal instability Optimize local metastatic tumor control and treatment of primary.

General medical treatment Deep vein thrombosis prophylaxis Patients with cancer are often in a hypercoagulable state. Although sufficient data on patients with spinal metastases are not available, prophylaxis against deep vein thrombosis (DVT) with heparin or sequential compression devices (SCD) is often provided for patients who are nonambulatory and at risk.

Bisphosphonates Bisphosphonates are drugs that inhibit osteoclastic activity, suppressing bone resorption. The most common bisphosphonate used in cancer patients is pamidronate. Used in conjunction with systemic chemotherapy, pamidronate has been shown to decrease or delay pathologic fractures due to bone metastases in breast cancer60 and multiple myeloma61 patients.

Corticosteroids The use of corticosteroids in the treatment of spinal cord compression in secondary tumors of the spine is similar to their use in primary tumors, discussed in the previous chapter. Corticosteroids, by reducing the vasogenic edema of acute spinal cord compression, stabilize or improve neurologic status and relieve pain in some patients. Due to the low mineralocorticoid activity, low cost, and use in clinical trials, dexamethasone is commonly used. The optimal dose used to treat acute spinal cord compression is controversial. One randomized, controlled trial showed that 96 mg/day of dexamethasone in patients with epidural spinal cord compression provided a significantly higher percentage of patients who were still ambulatory at long-term follow-up.62 One retrospective study comparing 16 and 96 mg/day doses demonstrated a significantly higher incidence of both serious and nonserious side effects with the higher dose.63 This study also

showed no difference in efficacy between the two doses; therefore, the recommended dose for symptomatic patients is a 10 mg i.v. bolus followed by 16 mg/day administered four times daily. The larger dose of 96 mg/day should only be administered to patients with rapidly progressing neurologic deficits.1 Steroids are recommended for neurologic compromise of acute onset. However, caution must be taken in a patient with an undiagnosed spinal mass with regards to corticosteroid treatment. One must not deliver steroids prior to biopsy because of the oncolytic effect for certain tumors, such as lymphoma.62 Other complications of corticosteroid treatment include metabolic abnormalities, GI bleeding/perforation, iatrogenic adrenal insufficiency after discontinuation of steroids, osteoporosis, osteonecrosis, and psychosis. Postoperative infection and wound breakdown are also increased with corticosteroid use.

Pain management Management of pain in patients with spinal metastases often begins with a trial of nonsteroidal antiinflammatory drugs (NSAIDs). NSAIDS should be discontinued prior to surgery to avoid the potential for excessive blood loss. Although nonsteroidal antiinflammatory agents may provide pain control, patients with cord compression usually require opiates for adequate pain relief. Opiates, along with autonomic dysfunction and limited mobility, can cause constipation. Therefore, patients may need an aggressive bowel treatment regimen to prevent constipation and resulting pain during straining.65 As mentioned previously, steroids may alleviate pain due to cord compression. A pain management consultation may be helpful in patients with spinal metastases.

Bracing External spinal bracing performs two functions: alleviating pain and preventing or halting vertebral collapse. In so doing, bracing can help prevent neurologic involvement in those patients with intact neurologic function while they receive medical treatment. Patients can be treated with radiation and bracing alone if there is no neurologic deficit, minimal compression fracture, no significant kyphosis, and no bony retropulsion compromising the canal. Moreover, the patient who has a short life expectancy can be treated in this fashion. The Halo vest was studied in patients with metastatic prostate cancer to the cervical spine. Good maintenance of neurologic function was achieved; however, the average patient wore the vest for approximately one-third of his or her remaining life.66 Some recommend the use of an antiflexion device, such as the Jewitt brace, for lesions between T7 and L2, or a molded lumbosacral orthosis corset for lesions of the lower lumbar spine.4 Spinal bracing in patients with neurologic deficits has not been carefully studied and should be considered only in patients with pain who cannot receive standard management or those with pain refractory to the standard management. Bracing is not for every nonoperative patient. Bracing should only be used in those who will likely benefit from them due to their ability to decrease quality of life.

Tumor-specific medical treatment Chemotherapy The use of chemotherapy as the primary treatment for some vertebral metastases from systemic diseases such as myeloma and lymphoma can be successful. Chemotherapy can reduce the size of spinal lesions in these cancers and may eliminate the need for surgery. Adjuvant chemotherapy in preoperative and postoperative settings has an 477

Part 3: Specific Disorders

important role in the treatment of chemosensitive tumors such as Ewing’s sarcoma, osteosarcoma, and lymphoma.22 Chemotherapy is more effective for certain tumor types, whereas others remain without significant response. For those tumors that are sensitive, the issue becomes one of responsiveness rather than sensitivity alone. The most important variables in cases of neural compression secondary to spinal metastases are the time required for a measurable response to drug therapy and the duration of that response. Possible complications of chemotherapy vary depending on the chemotherapeutic agent used, but typically include immunosuppression, delayed wound healing, and perioperative wound infections.13

Radiation therapy Radiation is the mainstay of spinal metastatic treatment unless the tumor is radioresistant and progressive, causes instability of the spine or bony compression of the cord/cauda equina, or causes significant spinal cord or cauda equina dysfunction. Similar to chemotherapy, radiation has a variable effect among tumor types. Prostate, lymphoid, and breast are the most sensitive to radiation therapy. Lung and thyroid are intermediately responsive; GI, melanoma, and renal are typically radioresistant lesions.13,54 Response of tumors is often difficult to predict. An aggressive tumor type with low curability may respond rapidly to radiation, whereas a less aggressive tumor type may take a relatively long time to respond locally to the radiation therapy, even though treatment is more likely to result in a cure. This is particularly pertinent when neural compression is due to tumor because if the tumor responds rapidly to radiation, surgical intervention may be avoided. Radiation therapy leads to resolution of back pain in most patients. Pretreatment neurologic function is the strongest predictor of posttreatment neurologic function.65 In one study, a significant difference was found in the duration of response between patients with radiosensitive malignancies and those with radioresistant malignancies (11 months versus 3 months).67 This study also showed median survival varied significantly between patients with radiosensitive malignancies and those with radioresponsive malignancies. The standard radiotherapy treatment for palliation of spinal metastases is daily 3 Gy fractions with a total dose of 30 Gy.65 Spinal cord and cauda equina tolerance to radiotherapy is the limiting factor in significantly raising the dose to greater levels to achieve higher rates of local control.22 Advances in radiotherapy, including intraoperative radiation therapy (IORT), three-dimensional conformal radiation therapy (3D-CRT), and intensity-modulated radiation therapy (IMRT) are being developed and studied.22 Such approaches may permit the delivery of higher doses of radiation to target tissue, while allowing the dose delivered to the spinal cord to remain within acceptable limits.

Minimally invasive procedures Radiofrequency ablation Radiofrequency (RF) ablation has received increasing attention as a promising technique in the treatment of malignant tumors.68,69,70 One study of patients with unresectable spine metastases demonstrated significant pain relief and reduction of disability with RF ablation guided with CT and fluoroscopy.71 Neurologic function was preserved or stabilized in the vast majority of these patients. However, RF treatment is not advisable for most spinal lesions because of the proximity to nerves within the spinal canal, lateral recesses, and neural foramina. For safety, the electrode should be at least 1 cm away from major nerves.72 The use of RF ablation for treating osteoid 478

osteomas of the spine has been documented and is discussed in the previous chapter.

Embolization Embolization is often performed preoperatively for hypervascular tumors, including renal cell and thyroid carcinomas. Preoperative embolization is safe and effective and can make complete resection possible in a previously unresectable tumor by reducing tumor size and reducing intraoperative blood loss.73 The average intraoperative blood loss in 51 patients with hypervascular metastatic spinal neoplasms (30 patients with renal cell carcinoma) treated with preoperative embolization was 2586 mL. Intraoperative blood loss for tumors with near-total or total embolization was largely related to unembolized epidural veins.74 Embolization has also been used for palliation of pain and reduction of tumor volume in renal metastases to the skeleton75 and spine.76 Chemoembolization, the administration of selective arterial chemotherapy at the time of embolization, has been shown to significantly reduce pain in bony pelvic and spinal metastases.77 Embolization has been successfully used as a primary treatment for sacral giant cell tumors78,79 as well as an effective preoperative surgical adjuvant in the treatment of aneurysmal bone cysts of the spine. Treatment of these primary tumors is discussed in the previous chapter.

Vertebroplasty and kyphoplasty Percutaneous vertebroplasty using polymethyl methacrylate (PMMA) has been used in the treatment of benign compression fractures since the late 1980s. Although this does not expand collapsed vertebrae, it has demonstrated utility in restoring mechanical stability and decreasing pain in patients with collapsed vertebrae. Some authors have reported the use of vertebroplasty in treating local and axial pain due to vertebral body metastases.80–82 The relief of pain in vertebral metastases is less likely to be successful compared to benign compression fractures.80 This may be due in part to the multifactorial nature of metastatic spine pain. However, one study demonstrated that seven out of eight patients with metastatic disease had no further vertebral compression, and spinal canal compromise was prevented.80 Epidural extension of PMMA more often complicates cases of vertebral metastases when compared to benign compression fractures.81 This may produce or dramatically worsen neurologic impairments. Complications due to extravasation of PMMA can be significantly reduced when caution is observed and excellent imaging conditions are maintained in key steps of the procedure. The use of high-viscosity cement, relatively small injection volumes, and use of kyphoplasty in selected cases can reduce cement leakage-related complications even further.82 Other complications of vertebroplasty include pulmonary embolism due to injection of PMMA into the venous system of the vertebral body, infection, cement toxicity, and adjacent vertebral compression. Although vertebroplasty alleviates pain and restores mechanical stability, the inability to restore vertebral body height is a limitation. Kyphoplasty uses an inflatable bone tamp, which is placed in the vertebral body and inflated to restore vertebral height, although the extent of height restoration is debatable. PMMA is then injected similarly to vertebroplasty. The use of kyphoplasty for vertebral metastases has not been extensively studied, but one study of 32 kyphoplasties and 65 vertebroplasties (56 patients) revealed complete pain relief in 84% of procedures and no instances of worsening of pain.82 Asymptomatic cement leakage occurred during vertebroplasty 9.2% of the time, and no cement extravasation occurred during kyphoplasty. Precise indications for the use of vertebroplasty and

Section 2: Osseous Spinal Tumors

kyphoplasty in the treatment of metastatic spine tumors are evolving; however, vertebroplasty and kyphoplasty are safe and feasible in well-selected patients with pain refractory to standard treatment.82 In the case of cortical disruption, especially in the posterior wall, or vertebral height loss below one-third of the original, vertebroplasty and kyphoplasty are technically difficult. Contraindications to vertebroplasty and kyphoplasty include neural compression, infection, elevated WBC count of uncertain etiology, known allergic reactions to PMMA, and pregnancy.83 Significant coagulopathy and severe cardiopulmonary disease are relative contraindications.

Surgery The role for surgery in the treatment of spinal metastases has changed significantly over the last 30 years. Because metastatic lesions usually involve vertebral bodies, neural elements are more often compressed from the ventral side. Laminectomy alone, however, is a posterior decompressive procedure. Early on, several comparative studies showed no difference in outcomes between external photon beam radiation therapy and laminectomy53,84 and numerous investigators found a high incidence of neurologic worsening after laminectomy;85,86 therefore, radiation therapy became the first-line therapy. The evolution of instrumentation allowing rigid segmental spine stabilization and the development of more aggressive surgical approaches have made more appropriate surgical options available. In addition, the life expectancy of patients with cancer is increasing, with many living longer with their disease due to more aggressive medical therapy and fewer side effects. As these patients survive longer, there is an increasing probability that they will develop metastases to the spine that will become symptomatic, negatively affect quality of life, and lead to death. Improved surgical options and a better understanding of patient life expectancy, coupled with the desire of patients to seek all available interventions for survival, are allowing surgery to play an increasing role in the treatment of spine metastases. The spine surgeon should consider these factors in deciding when to intervene and should do so within the framework of the overall management provided by the oncology team.

Surgical indications The indications for surgery include impingement of neural structures causing myelopathy or intractable pain, structural instability, presence of tumor type that is radioresistant, tumor recurrence in a patient who cannot receive further medical therapy or radiotherapy, progressive pain or neurologic dysfunction unresponsive to radiation, fractures or impending fractures, and the need for a diagnostic biopsy.

Surgical contraindications Contraindications to surgery include quadriplegia without a reasonable chance to restore neurologic function, short life expectancy less than 4 months, diffuse involvement of the spine with multiple sites of cord compression, absolute neutrophil count <1500, platelet count <50 000, abnormal coagulation, and poor pulmonary function tests (PFTs). The subject of life expectancy is controversial and varies from 4 weeks to 4 months.87,88,89 Therefore, the decision to operate in this range should be carefully considered, and the spine surgeon should be reasonably certain the patient’s quality of life would be improved enough to justify the pain, life disruption, hospitalization, and recovery.

Additional surgical considerations The objective of surgical treatment for spinal metastases in most instances is palliative, but can significantly extend life expectancy. The goals should be relief of pain, spinal alignment, decompression of

neural elements, stabilization when necessary, and local control of the tumor if possible. Thorough preoperative assessment is a prerequisite to good outcome in this often-fragile patient population. The quality of the bone stock, location of the tumor, presence of significant cord compression (with or without paralysis), and medical condition of the patients should guide the preoperative decision-making process, including the need for awake fiberoptic nasal or endotracheal intubation in cases of cervical instability or severe myelopathy. Myelopathic patients are monitored for neurologic changes using somatosensory evoked potentials (SSEP) prior to positioning and during the operation to help prevent further cord injury.

Surgical approaches The surgical approach should be determined by the underlying pathology along with its location and behavioral characteristics. The majority of metastases will involve the vertebral body and pedicles and as such most will present with epidural extension posteromedially from the junction of the pedicle and vertebral body to cause primarily anterior compression of the neural structures. The most effective approach to decompress the neural structures is an anterior approach. In general, tumors located anteriorly causing anterior compression should be approached anteriorly, and those located posteriorly should be approached posteriorly. However, if the goal of surgery is to remove as much tumor as possible or to achieve negative margins, a combined anteroposterior approach may be required to achieve en bloc resection and stability. In cases where there is involvement of the anterior and posterior elements of the thoracic and lumbar spine, a posterolateral approach may provide wide or marginal resection of the tumor and simultaneous decompression of the neural structures with much less morbidity than a combined approach, especially in the thoracic spine. The combined approach increases the risk of pneumothorax and vascular injury of the great vessels, and at times necessitates the sacrifice of one or more nerve roots.

Operative stabilization Historically, the vast majority of surgical patients underwent laminectomy for tumor removal and subsequently had worsening pain, neurologic deterioration, and progressive deformity. It is now more universally accepted to perform anterior approaches, and spine surgeons are increasingly trained to apply recent advanced techniques of instrumentation using pedicle and lateral mass screws, rods, plates, and vertebral body replacement devices such as cages. Bone graft stabilization should be augmented with a plate or rod construct, but a metallic cage device is preferred if postoperative radiation will be used since there is a 50% nonunion rate with bone graft with the use of postoperative radiation.90 However, there are times when metallic cages are not long enough to achieve stabilization and bone graft or PMMA will have to suffice. Although PMMA generates substantial heat with polymerization, there is no risk of cord damage from the heat.91 Postoperative radiation should be postponed for 1 month to maximize wound healing.

OUTCOMES In a review of the recent literature, an average of 60% of patients regained ambulatory function after surgical treatment.92 Surgical decompression and stabilization has been shown to improve pain and overall well-being.93 Patients with spinal metastases who were treated with anterior, posterior, or combined decompression and stabilization demonstrated a mean survival time of 16 months after surgery. Seventy-five percent of patients maintained neural function, while 20% improved.94 479

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With newer stabilization techniques and devices, spine surgeons are more confident in aggressively removing the metastatic tumors and restoring stability while limiting the extension over multiple segments. As such, surgical outcomes are much better and patients are living longer and more enjoyable lives. The information listed in Table 42.4 is helpful when consulting a spine surgeon; however, one should not delay consultation to obtain test results if the patient has significant or rapidly deteriorating symptoms.

Table 42.4: Information that may be Helpful when Consulting a Spine Surgeon

ALGORITHMIC APPROACH TO TREATMENT In regards to treatment of patients with histologically identified spine metastases (Fig. 42.8), one should first consider if the patient has spinal instability. If the patient has instability of the spine, surgical stabilization is necessary. If neural symptoms, in addition to instability, are present due to compression of the cord, cauda equina, or nerve roots, decompression or en bloc resection should be performed in addition to the stabilization procedure. In a solitary spine lesion, resection may be considered even in the absence of neural symptoms,

Location of lesion within spine

Pain evaluation

Solitary or multiple spinal levels

Approximate life expectancy

Thought to be primary or secondary

Presence of any contraindications for surgery

Presence of instability

Patient comorbidities

Neurologic status

History of prior treatment

if resection is feasible and if the patient has a chance of cure. If surgical intervention is contraindicated, bracing and chemotherapy or radiation therapy along with palliative measures may be the best treatment. In the absence of neurologic compression, which is a contraindication, vertebroplasty or kyphoplasty may be a treatment option for instability when more invasive surgery is contraindicated.

Metastatic spine lesion

Presence of instability ? Yes

No

Presence of neural symptoms ? Yes

No

Contraindications to surgery ? Yes

Yes

Contraindications to surgery ?

No

Bracing chemotherapy, radiation, palliative measures

Presence of neural symptoms ?

Yes

No

Vertebro/ kyphoplasty or bracing chemotherapy, radiation

Surgical resection or decompression and stabilization

Surgical stabilization and resection if solitary lesion and chance at cure

No

Bony impingment ? Yes

Radiation/ chemotherapy

No

Surgical decompression

Cauda equina ?

Yes

No

Surgical decompression

Tumor type radiation chemoresistant ?

Yes

No

Surgical decompression Yes Surgical decompression and steroids

Acute deterioration of neural syptoms ? No Radiation/ chemotherapy Failed ? Surgical decompression

480

Fig. 42.8 Algorithmic approach to treatment of metastatic spine lesions.

Section 2: Osseous Spinal Tumors

Beyond the treatment of instability, the role of surgery is not well defined. Considerable differences of opinion exist. However, the recommendations presented here are based on the literature and the experiences of physicians at the authors’ institution. Ultimately, the medical oncologist and surgeon must weigh the morbidity and risks of surgery against the patient’s life expectancy and quality of life. If the patient has a stable spine and no bony impingement, the presence and characteristics of neural symptoms should dictate treatment. A patient with neurologic compromise in the absence of instability or bony impingement typically responds to radiotherapy alone.95 If the patient experiences acute deterioration, some authors suggest that radiation and/or chemotherapy treatment can be augmented by systemic corticosteroids.12,96,97 However, we recommend surgical decompression for acute deterioration if the patient’s condition permits. In the absence of acute deterioration, surgery is indicated for patients who have persistent pain or neurologic symptoms despite appropriate treatment with radiation and/or chemotherapy, keeping in mind that radiation, chemotherapy, and steroids contribute significantly to subsequent surgical morbidity.98,99 Due to the increased complications of surgery after radiation and chemotherapy, surgery should be considered as a primary treatment option in patients with tumor types that are characteristically radiation and chemotherapy resistant. This is particularly true in patients with rapidly progressive neurologic symptoms. Surgical treatment is also indicated for cauda equina syndrome, a surgical emergency. Generally, in patients without neurologic symptoms, radiation and/or chemotherapy are the primary treatment modalities. Vertebroplasty may be performed if a compression fracture is causing significant pain. Whenever there is doubt about the origin of a metastasis, a biopsy should be performed. This can typically be done without surgical intervention via CT- or MRI-guided biopsy. However, if a surgical biopsy is required and the patient is at risk of fracture, vertebral collapse, or neurologic compromise, surgical stabilization with or without decompression may be performed at the time of surgical biopsy.100 Patients in whom instability is likely to develop despite radiotherapy may undergo surgical stabilization before starting radiotherapy to maintain spinal alignment and to minimize wound complications.100 For patients who present with complete paraplegia, it is recommended that surgical decompression and fusion be considered with caution, although, surgical decompression and fusion may be appropriate if a surgical procedure is required for diagnostic purposes.101

8. Byrne TN. Spinal cord compression from epidural metastases. N Engl J Med 1992; 327(9):614–619. 9. Brihaye J, Ectors P, Lemort M, et al. The management of spinal epidural metastases. Adv Tech Stand Neurosurg. 1988; 122:166. 10. Gokaslan ZL, York JE, Walsh GL, et al. Transthoracic vertebrectomy for metastatic spinal tumors. J Neurosurg 1998; 89(4):599–609. 11. Nazarian S. Place de la chirurgie dans le traitement des metastases du rachis. Rev Chir Orthop suppl III 1997; 83:109–174. 12. Gilbert RW, Kim JH, Posner JB. Epidural spinal cord compression from metastatic tumor: diagnosis and treatment. Ann Neurol 1978; 3(1):40–51. 13. Nazzaro JM. Metstatic spinal lesions. In: Benzel E, ed. Spine surgery: techniques, complication avoidance, and management. New York: Churchill Livingstone; 1999:679–695. 14. Batson O. The role of vertebral veins in metastatic processes. Ann Intern Med 1942; 16:38–45. 15. Wetzel FT. Spine. In: Simon MA, Springfield D, eds. Surgery for bone and softtissue tumors. Philadelphia: Lippincott-Raven; 1998:649–670. 16. Oeppen RS, Tung K. Retrograde venous invasion causing vertebral metastases in renal cell carcinoma. Br J Radiol 2001; 74(884):759–761. 17. Oge HK, Aydin S, Cagavi F, et al. Migration of pacemaker lead into the spinal venous plexus: case report with special reference to Batson’s theory of spinal metastasis. Acta Neurochir (Wien) 2001; 143(4):413–416. 18. O’Rourke T, George CB, Redmond J 3rd, et al. Spinal computed tomography and computed tomographic metrizamide myelography in the early diagnosis of metastatic disease. J Clin Oncol 1986; 4(4):576–583. 19. Arguello F, Baggs RB, Duerst RE, et al. Pathogenesis of vertebral metastasis and epidural spinal cord compression. Cancer 1990; 65(1):98–106. 20. Antunes NL. Back and neck pain in children with cancer. Pediatr Neurol 2002; 27(1):46–48. 21. Hatrick NC, Lucas JD, Timothy AR, et al. The surgical treatment of metastatic disease of the spine. Radiother Oncol 2000; 56(3):335–339. 22. Bilsky MH, Lis E, Raizer J, et al. The diagnosis and treatment of metastatic spinal tumor. Oncologist 1999; 4:459–469. 23. Schaberg J, Gainor BJ. A profile of metastatic carcinoma of the spine. Spine 1985; 10(1):19–20. 24. Healey JH, Brown HK. Complications of bone metastases: surgical management. Cancer 2000; 88(12 Suppl):2940–2951. 25. Sorensen S, Borgesen SE, Rohde K, et al. Metastatic epidural spinal cord compression. Results of treatment and survival. Cancer 1990; 65(7):1502–1508. 26. Perrin R. Metastatic tumors of the axial spine. Curr Opin Oncol 1992; 4:525–532. 27. Dumontet C, Drai J, Bienvenu J, et al. Profiles and prognostic values of LDH isoenzymes in patients with non-Hodgkin’s lymphoma. Leukemia 1999; 13(5):811–817. 28. Sarobe P, Huarte E, Lasarte JJ, et al. Carcinoembryonic antigen as a target to induce anti-tumor immune responses. Curr Cancer Drug Targets 2004; 4(5):443–454.

Acknowledgments

29. Schiff D. Clinical features and diagnosis of epidural spinal cord compression, including cauda equina syndrome. UpToDate Online 2003.

The authors would like to thank Christina Heathcock and Catherine Timby for their contributions to this chapter.

30. Duncker CM, Carrio I, Berna L, et al. Radioimmune imaging of bone marrow in patients with suspected bone metastases from primary breast cancer. J Nucl Med 1990; 31(9):1450–1455.

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69. Nakatsuka A, Yamakado K, Maeda M, et al. Radiofrequency ablation combined with bone cement injection for the treatment of bone malignancies. J Vasc Interv Radiol 2004; 15(7):707–712. 70. Poggi G, Gatti C, Melazzini M, et al. Percutaneous ultrasound-guided radiofrequency thermal ablation of malignant osteolyses. Anticancer Res 2003; 23(6D): 4977–4983. 71. Gronemeyer DH, Schirp S, Gevargez A. Image-guided radiofrequency ablation of spinal tumors: preliminary experience with an expandable array electrode. Cancer J 2002; 8(1):33–39. 72. Rosenthal DI, Hornicek FJ, Torriani M, et al. Osteoid osteoma: percutaneous treatment with radiofrequency energy. Radiology 2003; 229(1):171–175. 73. Shi H, Jin Z, Suh DC, et al. Preoperative transarterial embolization of hypervascular vertebral tumor with permanent particles. Chin Med J (Engl) 2002; 115(11):1683–1686. 74. Prabhu VC, Bilsky MH, Jambhekar K, et al. Results of preoperative embolization for metastatic spinal neoplasms. J Neurosurg Spine 2003; 98(2):156–164. 75. Treves R, Legoff JJ, Doyon D, et al. [Therapeutic or palliative embolization aimed at analgesia for bone metastases of renal origin]. Rev Rhum Mal Osteoartic 1984; 51(1):1–5. 76. O’Reilly GV, Kleefield J, Klein LA, et al. Embolization of solitary spinal metastases from renal cell carcinoma: alternative therapy for spinal cord or nerve root compression. Surg Neurol 1989; 31(4):268–271. 77. Chiras J, Adem C, Vallee JN, et al. Selective intra-arterial chemoembolization of pelvic and spine bone metastases. Eur Radiol 2004; 14(10):1774–1780. 78. Lackman R, Hosalkar HS, Khoury LD, et al. Podium presentation: Serial arterial embolization for sacral giant cell tumors. MSTS annual meeting, Long Beach, CA; 2004. 79. Lackman RD, Khoury LD, Esmail A, et al. The treatment of sacral giant-cell tumours by serial arterial embolisation. J Bone Joint Surg [Br] 2002; 84(6):873–877. 80. Barr JD, Barr MS, Lemley TJ, et al. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine 2000; 25(8):923–928. 81. Deramond H, Depriester C, Toussaint P, et al. Percutaneous vertebroplasty. Sem Musculoskelet Radiol 1997; 1(2):285–296. 82. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful vertebral body fractures in cancer patients. J Neurosurg Spine 2003; 98(1):21–30. 83. Wenger M. Vertebroplasty for metastasis. Med Oncol 2003; 20(3):203–209.

58. Enzmann D, De La Paz, RL. Tumor. In: Achenbach F, ed. Magnetic resonance of the spine. St. Louis: CV Mosby; 1990:301–422.

84. Hall AJ, Mackay NN. The results of laminectomy for compression of the cord or cauda equina by extradural malignant tumour. J Bone Joint Surg [Br] 1973; 55(3):497–505.

59. Valderrama J, Bullough PG. Solitary myeloma of the spine. J Bone Joint Surg [Br] 1988; 50B:82–90.

85. Cobb CA. Indications for nonoperative treatment of spinal cord compression due to breast cancer. J Neurosurg 1977; 47(5):653–658.

60. Hortobagyi GN, Theriault RL, Lipton A, et al. Long-term prevention of skeletal complications of metastatic breast cancer with pamidronate. Protocol 19 Aredia Breast Cancer Study Group. J Clin Oncol 1998; 16(6):2038–2044.

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61. Berenson JR, Lichtenstein A, Porter L, et al. Efficacy of pamidronate in reducing skeletal events in patients with advanced multiple myeloma. Myeloma Aredia Study Group. N Engl J Med 1996; 334(8):488–493. 62. Sorensen S, Helweg-Larsen S, Mouridsen H, et al. Effect of high-dose dexamethasone in carcinomatous metastatic spinal cord compression treated with radiotherapy: a randomised trial. Eur J Cancer 1994; 30A(1):22–27. 63. Heimdal K, Hirschberg H, Slettebo H, et al. High incidence of serious side effects of high-dose dexamethasone treatment in patients with epidural spinal cord compression. J Neurooncol 1992; 12(2):141–144.

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87. Bilsky MH, Shannon FJ, Sheppard S, et al. Diagnosis and management of a metastatic tumor in the atlantoaxial spine. Spine 2002; 27(10):1062–1069. 88. Boriani S, De Lure F. Bone tumors of the spine and epidural cord compression: treatment options. Sem Spine Surg 1995; 7:317–322. 89. Vieweg U, Meyer B, Schramm J. Tumour surgery of the upper cervical spine – a retrospective study of 13 cases. Acta Neurochir (Wien) 2001; 143(3):217–225. 90. Rao S, Badani K, Schildhauer T, et al. Metastatic malignancy of the cervical spine. A nonoperative history. Spine 1992; 17(10 Suppl):S407–S412.

64. Aebi M. Spinal metastasis in the elderly. Eur Spine J 2003; 12(Suppl 2): S202–S213.

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Section 2: Osseous Spinal Tumors 95. Harrington KD. Anterior decompression and stabilization of the spine as a treatment for vertebral collapse and spinal cord compression from metastatic malignancy. Clin Orthop 1988; (233):177–197. 96. Boland PJ, Lane JM, Sundaresan N. Metastatic disease of the spine. Clin Orthop 1982; (169):95–102. 97. Sundaresan N, Galicich JH, Lane JM. Harrington rod stabilization for pathological fractures of the spine. J Neurosurg 1984; 60(2):282–286. 98. Martenson JA Jr, Evans RG, Lie MR, et al. Treatment outcome and complications in patients treated for malignant epidural spinal cord compression (SCC). J Neurooncol 1985; 3(1):77–84.

99. Sundaresan N, Bains M, McCormack P. Surgical treatment of spinal cord compression in patients with lung cancer. Neurosurgery 1985; 16(3):350–356. 100. McLain RF, Bell GR. Newer management options in patients with spinal metastasis. Cleve Clin J Med 1998; 65(7):356–359. 101. Ryken TC, Eichholz KM, Gerszten PC, et al. Evidence-based review of the surgical management of vertebral column metastatic disease. Neurosurg Focus 2003; 15(5):E11. 102. Ratliff JK, Cooper PR. Metastatic spine tumors. South Med J 2004; 97(3): 246–253.

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SPECIFIC DISORDERS

Section 2

Osseous Spinal Tumors ■ ii: Treatment

CHAPTER

Spinal Orthoses

43

Thomas N. Bryce, Parag Sheth, Bojun Chen and Kristjan T. Ragnarsson

INTRODUCTION Spinal orthoses are external devices which are typically applied circumferentially about the body with the intent of altering spinal motion. Lumbar supports fashioned from tree bark have been found in pre-Columbian cliff dwellings, and the use of orthoses was described both by Hippocrates and Galen.1 Centuries later, in the United States alone, some 1.8 million people use a spinal orthosis in any given year.2 Orthoses have several potential functions, including prevention of deformity, correction of deformity, enhancement of function, limitation of motion to allow healing, relief of pain, and spinal support. Orthoses can be designed to restrict gross spinal motion, restrict individual segmental motion, reduce the loading force on the spine, correct a spinal deformity, and to prevent the progression of an existing deformity. In this chapter, the use of cervical and thoracolumbar spinal orthoses will be discussed primarily in relation to treatment of pain and providing spinal support.

CLASSIFICATION OF ORTHOSES In 1973, the Task Force on the Standardization of ProstheticOrthotic Terminology Committee proposed a systematic nomenclature in which spinal orthoses are named by the segments that are immobized by the device.3 An orthosis spanning the cervical spine is a cervical orthosis (CO). An orthosis spanning the thoracic, lumbar, and sacral spine is a thoracolumbosacral orthosis (TLSO), while an orthosis spanning the lumbar and sacral spine is a lumbosacral orthosis (LSO). This terminology is accepted by all the major professional organizations which commonly deal with the devices, including the American Academy of Orthotics and Prosthetics, the American Academy of Physical Medicine and Rehabilitation, and the American Academy of Orthopedic Surgeons. The Center for Medicare and Medicaid Services (CMS), which is the most common payer for such devices, utilizes a procedural coding system which is based upon this terminology. A more complete description of an orthosis may include not only the regions of the spine covered by the orthosis but also the direction of motion control of the orthosis. For example, a LS ELO is a lumbosacral extension lateral control orthosis, which spans the lumbar and sacral spine allowing flexion, but limiting extension and lateral bending. In addition to the terminology noted above, in order to distinguish between different devices of the same basic segmental immobilization, but of different design or manufacture, orthoses have often been named after their inventor, such as Knight-Taylor or Jewitt; after the city near which the orthosis was designed, such as Philadelphia, Miami, Boston, or Malibu; or for its appearance, such as four-poster, two-poster, hard collar, soft collar, or sternal-occipital-mandibular

immobilizer (SOMI). The above-noted LS ELO is also called a Williams flexion orthosis. The term ‘profile’ is often used to describe the relative height that an orthosis extends rostrally on the body. The original scoliosis correction orthoses had cervical extensions which caused the orthoses to be noticeable when worn and not particularly cosmetic. Subsequently, these have been designated as high-profile orthoses. Later orthoses, which only extended to the clavicles and were less noticeable under clothing, have been designated, in contrast, as low-profile orthoses.

BIOMECHANICS Flexion, extension, lateral bending, and rotation are motions which occur in the sagittal, coronal, and axial planes. In general, since the cervical spine is the most mobile and the thoracic spine is the most rigid, most orthoses have traditionally been used to immobilize the cervical or lumbar spine. Since biomechanical stresses are often concentrated at the junctions between the mobile and rigid portions of the spine, the most stabilizing spinal orthoses usually encompass one or more of these junctions. From an orthotics viewpoint several clinically relevant points about segmental spinal motion are worth emphasizing. The orientation of the facet joints plays an important role in regional spinal mobility. In theory, if a facet acts as the center of rotation, a facet oriented within a given plane will allow unrestricted motion in that plane. Conversely, a facet oriented at 90° to a plane will restrict any motion in that plane. In the upper cervical spine, the occipitoatlantal joint accounts for 20% of the total available cervical flexion and extension. The atlantoaxial joint or C1–2 accounts for 14% of the total available cervical flexion and extension and 54% of the total available cervical rotation. Motion at these joints, however, accounts for only 10% of lateral bending. The greatest cervical flexion and extension takes place at C5–6 and C6–7, whereas the greatest side bending occurs at C2–3 and C3–4 with relatively less motion occurring at the lowest cervical levels.4 The thoracic facets are angled on average only 20° from the coronal plane and are positioned obliquely to the transverse and sagittal planes. Thus, lateral bending is most freely allowed at these segments. This mechanical feature is counterbalanced in the upper thoracic spine by the presence of the rib cage. The thoracic spine has been shown to be 27% stiffer in flexion, 45% stiffer in lateral bending, and 132% stiffer in extension due to the stabilizing effect of the rib cage.5 Upper thoracic segments are most mobile in axial rotation, while lower thoracic regions, less restricted by the ribs, allow the most lateral bending, flexion, and extension.4 The lumbar facet joints, which lay nearly parallel to the sagittal plane and at a nearly transverse angle to the transverse and coronal planes, will allow full flexion and extension, but limit rotation and 485

Part 3: Specific Disorders

Fig. 43.1 Jewitt flexion control TLSO. The orthosis provides posteriorly directed forces originating from the sternal and suprapubic pads (small arrows) and an anteriorly directed force originating from the thoracolumbar pad (large arrow) to create a three-point pressure system which encourages hyperextension of the spine.

side bending. Due to the true axis of rotation, obliquity, and contour of joint surfaces, there is some gliding of facet surfaces and some motion in the transverse and coronal planes; however, normal lumbar motion for flexion and extension is by far greater than normal lumbar axial rotation and lateral bending.4,6 Motion control by spinal orthoses is based on the principle of a three-point pressure system. This is illustrated most readily with the flexion control TLSO Jewitt orthosis seen in Figure 43.1. The orthosis provides posteriorly directed forces originating from the sternal and suprapubic pads and an anteriorly directed force originating from the thoracolumbar pad. This configuration encourages hyperextension of the spine. Thus, a simple anterior wedge compression fracture located at the midpoint of the thoracolumbar pad would be ideally treated with this type of brace. Care must be taken when prescribing an orthoses to ensure that the site of intended action is located near the central fulcrum of the three-point system. Poorly prescribed devices can create destabilizing forces and worsen injuries. With more complex fractures or disease, rotatory control may be required. Depending on the site of injury, the orthosis will be extended and incorporate more body surface contact area, typically in the form of a body jacket. For a T7–L3 level injury a full skin contact TLSO with a high-profile trim line extending to just below the clavicles can control rotation by acting against the opposite anterior superior iliac crest. Rotational control at L5–S1 is best achieved with a low-profile TLSO with a hip spica.7 If motion control is desired above the T7 level some authors recommend a cervical extension be added.8–10 When doubt exists about the effectiveness of a brace, flexion and extension radiographs can be taken while the patient is wearing the orthosis, keeping in mind special beam angulations may be required to avoid artifact due to the superimposition of the image of the orthosis on the image of the desired spinal segments. An awareness of these spinal mechanics combined with an understanding of a given patient’s pathologic process facilitates a logical orthosis prescription.

CERVICAL ORTHOSES The term ‘soft collar’ refers to a broad strip of open-cell foam, plastic, or foam rubber encased in cotton stockinet with a Velcro closure (Fig. 43.2). It is the least restrictive and most common cervical orthosis. Soft cervical collars generally provide minimal restriction in range of 486

Fig. 43.2 Soft collar.

motion.11–13 A collar which is too large tends to force the neck into extension, potentially decreasing the size of the neural foramina. A soft collar which positions the neck into approximately 10° of flexion maximizes the size of the foramina and minimizes the potential for nerve root irritation. A soft collar with the Velcro closure placed in the front may provide increased resistance to flexion, whereas a collar with the Velcro closure placed in the back may provide increased resistance to extension.13 A soft collar can provide warmth and comfort which may reduce pain and muscle spasm. Moreover, it often acts as a reminder for a person to avoid an active range of motion which may be painful. Another CO, the Thomas collar, initially developed by Hugh Owen Thomas, a physician in the nineteenth century, is a rigid collar, originally made of sheet metal and now typically made from rigid polyethylene, which mainly acts to restrict flexion and extension up to about 75% from neutral.14 It offers little control of lateral bending or rotation due to its lack of head and thorax contact. The Philadelphia, Miami J, Aspen, Malibu, NecLoc, and Stiffneck collars are also hard collars made of different materials with different types of linings. However, unlike the COs described above, these orthoses incorporate the mandible and the occiput in their design and can be classified as head cervical orthoses or HCOs. They provide head support and partially restrict motion of cervical spine in all planes, especially in the sagittal plane (Table 43.1). The Philadelphia HCO, which consists of two pieces of closed-cell polyethylene foam attached with Velcro closures (Fig. 43.3), is prototypical of the wide variety of HCOs which are produced in a multitude of sizes and shapes by different manufacturers. The Philadelphia HCO, like other prefabricated HCOs, is available in multiple configurations to accommodate a variety of clinical needs and neck shapes, including a snugly fitting version which can be used to control hypertrophic scarring.22 The Miami J and the Aspen HCOs consist of a two-piece semirigid plastic supporting structure with removable open cell foam liners. This design is often better tolerated than the solid orthoses made of closed-cell foam. In many instances, persons who require a HCO for an extended period of time will have a solid closed-cell foam orthosis, such as the Philadelphia collar, for showering and a HCO constructed like the Miami J or Aspen for everyday use. With regards to effectiveness in restriction of motion, numerous studies have been

Section 2: Osseous Spinal Tumors

Table 43.1: Restriction of Motion by Spinal Orthoses15–21 Restriction of motion (%) Type of orthosis

Flexion/extension

Lateral bending

Rotation

Soft collar

26/26

8

17

Philadelphia HCO 42–74/47–59

25–33

29–56

Aspen HCO

31

38

59/64

Miami J HCO

48–85/38–75

48–63

65–76

Malibu HCO

53–57/40–67

41

61

NecLoc HCO

83/77

43–60

62–73

SOMI

93/42

34–66

66

Minerva HCTO

86/86

84

100

Halo HCTO

88–96/88–96

92–96

98–100 Fig. 43.4 Four-post HCTO.

Fig. 43.3 Philadelphia HCO.

performed comparing the different types of HCOs. The results vary by study methodology, often with conflicting results.23,24 Cervical orthoses that include rigid vertical posts are cooler than hard collars, due to the lack of total skin contact, and are more stabilizing as they incorporate an additional inferior portion which is supported on the upper thorax. They are classified as head cervical thoracic orthoses or HCTOs. These orthoses may include two, three or four posts (Fig. 43.4). A prototypical HCTO is the threeposted sternal occipital mandibular immobilizer (SOMI) (Fig. 43.5). Because of its points of attachment, as described in its name, the SOMI greatly restricts cervical flexion, particularly lower cervical segments; however, because of a swivel-type occipital pad, it allows some extension.11 Lateral bending is also less restricted than flexion. Maximal cervical immobilization is achieved with either a halo vest orthosis (Fig. 43.6) or a Minerva orthosis (Fig. 43.7). Both devices are HCTOs. A halo vest consists of a metal ring which is fixed to the outer table of the skull by four screws, a plastic chest jacket, and superstructure of bars and connectors which connect the ring to the jacket. The jacket is usually lined with sheepskin to improve pressure distribution and comfort. Due to the fixation

Fig. 43.5 SOMI threepost HCTO.

Fig. 43.6 Halo vest HCTO. 487

Part 3: Specific Disorders

Fig. 43.7 Minerva HCTO.

of the halo ring to the skull, a halo vest has optimal rotational motion control. As a result, it is commonly used to immobilize the upper cervical segments, which, as described earlier, are the segments responsible for the majority of rotation of the cervical spine. However, because of its lack of total contact over the neck, intersegmental snaking of vertebral segments has been reported to occur.25,26 A Minerva HCTO, which has greater skin contact, may provide better control of this intersegmental motion and this may be a better option if this is a major concern.27 The Minerva orthoses may be prefabricated or custom made. The posterior section has a padded band that extends forward to encircle both the mandible and the forehead, thus creating a longer lever arm for cervical control.28 Its name derives from the mythological daughter of Zeus, a warrior who radiated thunderbolts from her forehead. One disadvantage of the halo device as compared to the Minerva orthosis is that it significantly changes the center of gravity of the wearer, potentially leading to balance difficulties and falls.29 Another disadvantage is the requirement of the halo to have pins seated into the skull which presents a risk for both infection and slippage.

Although increased intra-abdominal pressure is associated with increased lumbar spinal stability and decreased spinal load, the effect of a TLSO on abdominal muscle activity and abdominal pressure is controversial.32–36 Nevertheless, the available evidence seems to support that intra-abdominal pressure plays a role in the stabilization of the lumbar spine by a TLSO. The effect of a TLSO or LSO on intradiscal pressure is also uncertain. Nachemson showed intradiscal pressure decreased by about 25% when subjects wore an inflatable lumbar corset.37 However, when he studied several other lumbar orthoses, an inconsistent effect on intradiscal pressure was found.38 Rohlmann studied several different lumbar orthoses regarding the effect on the load on an internal spinal fixation device, and did not find any reduction of the load by any of the orthoses.39 Since intradiscal pressure is increased with spinal flexion and decreased with the extension, a TLSO may indirectly reduce intradiscal pressures by restricting flexion. If the principal objective of a prescribed orthosis is to limit flexion and extension of the thoracic spine, and there is not a strong need for rotational control, a simple flexion control orthosis is a good option. There are two principal types of flexion control TLSOs: the cruciform anterior spinal hyperextension (CASH) brace and the Jewitt orthosis (see Fig. 43.1 and 43.8). The basic biomechanical principles underlying these orthoses is a three-point fixation.. Such orthoses are commonly made of flat aluminum bars with a vinyl-covered foam pad attached posteriorly over the midspine and two other vinylcovered foam pads attached anteriorly over the sternum and pubis. The Jewitt orthosis is most effective for simple compression fractures or thoracic sprains between T7 and L1. It should be avoided for fractures or thoracic sprains above T6 as the sternal pad can act as fulcrum and actually worsen the condition. The chairback orthosis is a traditional, partially open orthosis for the lower spine that can be classified as a lumbosacral flexion extension control orthosis (LS FEO). This orthosis restricts trunk flexion through a posteriorly directed force across the superior and inferior aspects of the anterior abdominal corset and an anteriorly directed force from the center of the two posterior uprights. Extension is limited by anteriorly directed forces from the thoracic and pelvic bands, and posteriorly from the midsection of the abdominal corset.40 Currently, this orthosis is primarily used to treat low back pain in a stable spine rather than for fracture immobilization since other orthoses offer greater restriction of motion.41 The chairback orthosis can be seen as basic building block to

THORACOLUMBOSACRAL ORTHOSES The effects of a TLSO on the restriction of spinal motion, intraabdominal pressure, intradiscal pressure, and muscle activity have all been studied, with conflicting results.30–32 No study has yet shown even near complete elimination of either segmental or gross spinal mobility by any orthosis. In one study of subjects without spinal abnormalities, who were custom fitted with a lumbosacral corset, chairback orthosis, or molded plastic TLSO, it was found that all three restricted gross body motion.31 Approximately two-thirds to one-half of orthotic free gross body motion was observed.31 When a mean percentage of restriction of all directional movement was calculated, the TLSO was found to be twice as effective as the corset, while the chairback brace was of intermediate effectiveness. The spinal motion controlled by wearing a TLSO is greatest at the upper and midlumbar segments. In contrast, motion controlled at the L4–S1 levels by wearing a TLSO is only minimal: an 8–12% reduction, or even an increase, as compared to spinal motion without a TLSO in place.30,33 488

Fig. 43.8 Jewitt flexion control TLSO.

Section 2: Osseous Spinal Tumors

which additional supports can be added to increase support and restriction of motion. By adding lateral supports, the chairback becomes a Knight spinal orthosis or a lumbosacral flexion extension lateral control orthosis (LS FELO) (Figs 43.9, 43.10). This orthosis is also mainly used for low back pain in a stable spine and sometimes for immobilization of stable lumbar fractures which have maintained their vertebral body height.41 By extending the chairback orthosis superiorly to include the thoracic spine through posterior uprights that terminate above the scapula, the orthosis becomes a Taylor orthosis or a thoracolumbosacral flexion extension control orthosis (TLS FEO). Biomechanically, the interscapular band and the axillary straps in the Taylor orthosis resist extension and flexion, respectively. When a Knight LS FELO design extends superiorly to encompass the thoracic spine similar to a Taylor TLS FEO, a Knight-Taylor orthosis or a thoracolumbosacral flexion extension lateral control orthosis (TLS FELO) is created (Fig. 43.11). This orthosis provides increased resistance to lateral bending, in addition to flexion and extension, by the addition of long vertical lateral supports to which the thoracic and pelvic bands attach.

The Williams flexion orthosis, a lumbosacral extension lateral control orthosis (LS ELO), is another traditional, partially open orthosis. It was originally designed for treatment of spondylolisthesis and is still used for that purpose today.42,43 Extension is limited by posterior oblique bars and a pelvic band, but some flexion is allowed due to a mobile anterior thoracic band. Lateral bending is restricted by lateral bars attached to the thoracic and pelvic bands. All of the aforementioned orthoses with an open design will allow some rotatory movement of the spine. A thermoplastic version of the Williams flexion orthosis is available which is called the Raney flexion LSO. This orthosis has semirigid anterior and posterior shells, which immobilize the lumbosacral spine in a flexed position, not allowing further flexion as is possible with the Williams flexion orthosis. The Raney flexion LSO is an LS FELO. When rotatory control is necessary, a more restrictive TLSO which encases the trunk, such as the commonly prescribed plastic body jacket, is required (Fig. 43.12). These TLSOs are known as thoracolumbosacral flexion extension lateral rotatory control

Fig. 43.9 Knight LS FELO (anterior view). Fig. 43.11 KnightTaylor TLS FELO.

Fig. 43.10 Knight LS FELO (posterior view).

Fig. 43.12 Molded plastic TLSO. 489

Part 3: Specific Disorders

orthoses (TLS FELROs). Some body jacket models have a posterior inflatable pillow intended to adjust the snugness of fit. When a high trim line with subclavian pads is employed these orthoses are known colloquially as cowhorn braces. A shorter version of the body jacket, an LS FELRO, which ends below the xiphoid process and scapula, is designed to restrict motion in the lower trunk to L3 (Fig. 43.13). A rigid TLS FELRO or LS FELRO depending on the level of abnormality is the orthosis of choice for postsurgical immobilization or external stabilization of lumbar fracture. However, it should be noted that a rigid TLS FELRO or LS FELRO may actually increase motion of L5–S1 level as mentioned earlier.30 If it is necessary to immobilize this level, then a hip spica extension should to be attached to the orthosis. The most frequently prescribed orthosis for low back pain is an LS corset (Fig. 43.14). Typically, these are flexible orthoses, less restrictive than those mentioned above, made of fabric that is woven with synthetic elastic material. The upper extent of the orthoses, which encircle the torso, is the xiphoid process anteriorly and a point just

Fig. 43.15 Sacroiliac belt.

Fig. 43.13 Molded plastic LSO.

below the lower margin of scapula posteriorly, while the lower extent is the pubic symphysis and apices of the buttocks. Laces or Velcro straps allow for control of fit. Many are reinforced with either metal or plastic removable stays that can be inserted into an incorporated posterior pocket. Due to the elastic nature of the LS corsets, if worn snugly, intra-abdominal cavity pressures may increase thereby reducing the loading force on the spine. LS corsets provide a moderate degree of lumbosacral motion control.44 In addition, LS corsets may provide warmth to lumbar area, improve trunk proprioception, and act as a reminder for avoiding lumbosacral motion which may cause pain.45 Highly elastic corsets designed without laces or straps are also available. They are often called abdominal binders and are prescribed to support weakened abdominal muscles postpartum, after extensive abdominal surgery, or for pendulous abdomens. Persons with highlevel spinal cord injuries may use them to counteract postural hypotension or to facilitate diaphragmatic breathing. Sacroiliac orthoses (Fig. 43.15), also referred to as sacroiliac belts because of their narrow width and low positioning over the pelvis between the iliac crests and the inguinal ligaments, have been prescribed to reduce postpartum sacroiliac diastases or pubic symphysis separation. To prevent superior migration of the orthosis, groin or garter straps are often added. These are most frequently used by manual laborers. The United States National Institute for Occupational Safety and Health does not support the use of back belts as a preventive measure.46 In contrast, the United States Occupational Safety and Health Administration’s recent ergonomics regulation classified lumbar supports as personal protective equipment and suggested that they may prevent back injuries in certain settings.47 In summary, the literature in this area is inconclusive.48

MATERIALS, MANUFACTURING, AND FIT OF SPINAL ORTHOSES Fig. 43.14 LS corset. 490

Most spinal orthoses today are made principally from plastic polymers such as polyethylene and polypropylene. These polymers offer the advantages of being relatively lightweight, strong, and easy to

Section 2: Osseous Spinal Tumors

maintain. They resist corrosion, mildew, and fatigue and have great durability. When heated, they become malleable and can be shaped. Many of the more durable and rigid thermoplastics require heating to high temperatures and therefore must be custom fitted on molds rather than directly on the patient. In these cases the orthotist will first cover the area of the body to be immobilized with plaster to create a negative mold. The next step involves building a positive mold by filling the initial negative mold with plaster. This positive mold is in turn modified to accommodate pressure-sensitive areas. The thermoplastic is then molded to the positive plaster mold. Some thermosetting plastics, such as polyester, once set, cannot be reshaped and must be altered by grinding or cutting. Orthoses are often uncomfortable to wear at the beginning and many adjustments and alterations may need to be made by the orthotist before the patient is comfortable. Fitting, both of custom and off-the-shelf orthoses, optimally should be performed in sitting, supine, and standing positions. As one would expect, custom fitting often improves compliance and results.49 Of note, computer-aided design and computer-aided manufacture (CAD-CAM), although not widely used today, may facilitate correct fit and comfort in the future by allowing more precise body contour measurements and orthotic manufacturing. Relative contraindications to the prescription of spinal orthoses include insensate or sensory-impaired skin and an inability to tolerate increased intra-abdominal pressure, i.e. pregnancy or the presence of an abdominal aortic aneurysm or organomegaly. If a person is cognitively impaired and at high risk for removing an easily removable orthosis, a more difficult to remove orthosis, such as a body cast or a plaster-reinforced prefabricated orthosis may be a better option. Compliance with wearing an orthosis is dependent on the ease of donning and doffing the orthosis, cosmesis, comfort, and the knowledge of the risk of untoward consequences if an orthosis is not worn as prescribed. Therefore, all these things should be taken into consideration, along with the primary consideration of the known effectiveness of a particular orthosis, when a prescription is developed by the healthcare provider.

COMPLICATIONS OF ORTHOSIS USE Pressure sores develop at areas of orthosis and skin contact. The greater the orthosis and skin contact surface area, the lower the unit pressure per area, and the lower the risk for skin breakdown. Unfortunately, due to the limited skin surface area available for contact by any particular cervical orthosis, mandibular and occipital sores are especially frequent.50 Marginal mandibular nerve palsy in which a branch of the facial nerve is compressed by a hard collar and manifested by the drooping of the lower lip with drooling has been described.51 Dysphagia and aspiration can develop due to the limitation of the normal cervical flexion which occurs during a normal swallow. In the case of total skin contact type of orthoses, heat dissipation may become a problem and users should be instructed to wear absorptive cotton garments under the orthoses, so that perspiration does not lead to skin maceration. Excessive use of moisturizing lotions should also be avoided. Some manufactures will perforate portions of the orthoses to allow for air circulation and cooling. Fit should be snug but not tight. A cervical orthosis adjusted to provide a skin–orthosis interface pressure greater than 25 mmHg does not provide any greater immobilization of the cervical spine than a cervical orthosis adjusted to provide a skin–orthosis interface pressure of 25 mmHg. Moreover, higher interface pressures are often not tolerated, causing individuals to loosen their orthoses.52 Polyethylene foam or its equivalent may need to be added to or removed from

parts of the orthosis to improve fit, and thus comfort, by eliminating pressure points and increasing skin surface contact. Additional complications of prolonged immobilization include the development of muscle atrophy, weakness, and contractures in the immobilized spinal segments. Hypermobility may be seen in areas of the spine adjacent to the immobilized segments. Finally, psychological dependence on an orthosis and issues of secondary gain from orthosis use must be considered when it is difficult to wean a patient from an orthosis.

SPECIFIC INDICATIONS FOR SPINAL ORTHOSES Neck pain Although soft collars are commonly proscribed after ‘whiplash’ injuries, there is no strong evidence in the literature that they are beneficial for this condition. In a 3-year prospective trial of 97 subjects exposed to whiplash trauma in motor vehicle collisions who were prescribed either an active intervention, which consisted of active exercises, including cervical rotation, without use of a cervical orthosis, or a standard intervention, which consisted of initial rest, soft collar use, and gradual self-mobilization, it was found that pain intensity and sick leave were significantly reduced in the group who received the active intervention.53,54 In another prospective study, 197 subjects with neck pain following motor vehicle collisions who did not have fractures, subluxations, or focal deficits were randomly assigned to use either a soft collar or no collar. No difference was found between the groups with regards to complete recovery, deterioration, or improvement in symptoms.55 If a cervical orthosis is prescribed to treat pain not due to instability, it should be chosen to unload a specific pain generator, e.g. a soft collar with the Velcro closure in the front may be an adjunct in the treatment of acute radicular pain due to a focal disc protrusion or spondylotic foraminal narrowing. A soft collar worn in this fashion promotes cervical flexion and foraminal widening with presumed decreased pressure on an inflamed nerve root, the presumed pain generator in this situation. The use for use of a soft collar may be particularly beneficial when the person is trying to go to sleep. It bears re-emphasis that cervical orthoses prescribed for pain not due to instability should only be used for a limited duration of time in order to minimize disuse atrophy.

Low back pain Biomechanical studies have demonstrated that the disc is the major anterior load-bearing structure while the facet joints are the major posterior load-bearing structures.56 When in an upright standing position, facets carry 10–20% of the compressive load and more than 50% of the anterior shear load on the spine. When the spine is extended, the compressive load is transmitted through the pedicles, lamina, and articular facets. This load transmission in extension can relieve some of the load on the anterior column of the spine, including the vertebral body and intravertebral disc. Rotation combined with axial compression and flexion also appears to load the facets. In contrast, when the spine is fixed in a flexed position, the compressive load will be significantly decreased on the facets and increased on intervertebral discs, the latter leading to increased intradiscal pressures. Clinically, lumbar positioning into either flexion or extension by an orthosis has the potential to decrease low back pain depending on the condition treated, as demonstrated in the studies described below. Gavin reported the results of a prospective study of 36 persons, who had back or leg pain for greater than 6 months, who were fitted with the test instrument of Willner, a rigid aluminum TLSO with a sagittal 491

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492

lumbar pad that is adjustable into lumbar flexion or extension, for a 5-day trial. For subjects with discogenic pain, including disc herniation, multiple-level disc bulging, and degenerative disc disease, the geometry of the orthosis was set in maximum extension, whereas, for subjects with spondylolisthesis, lumbar stenosis, or the pain thought to originate from the facet joints, the geometry of the orthosis was set in maximum lumbar flexion. Twenty-nine of the subjects were fitted after an acceptable trial into a TLSO in a degree of flexion or extension deemed optimal for comfort. Six of 25 subjects had recurrence of pain and underwent surgery, the remainder did not undergo surgery by 3–12 months.57 For young athletes with discogenic back pain, Micheli reported that treatment with a modified Boston brace, a TLSO which uses prefabricated thermoplastic pelvic modules designed to provide antilordotic straightening of the lumbar spine, was effective in reducing pain in only 50% of subjects. However, for 31 young athletes with spondylolysis, he reported good to excellent results in 90% using the same orthosis.58 In 1985, Willner reported on the orthotic treatment with a rigid TLSO, set in lumbar flexion, of adults with pain due to spinal stenosis with claudication, isthmic spondylolisthesis with documented slippage of 25–50% of L5–S1, or low back pain of unknown etiology with a negative myelogram and X-rays showing only spondylosis. Evaluation occurred on average after 1 year of brace use. For the subjects with spondylolisthesis, similar to the results reported by Micheli five years earlier, 13/15 had pain relief and 2/15 had pain improvement. For the subjects with stenosis, the majority, 6/7, had pain improvement or relief. For the subjects with low back pain of unknown etiology, the majority, 17/26, had no improvement.59 In 1981, Million studied 19 subjects with back pain present for greater than 6 months who also did not have any other abnormality other than lumbar spondylosis. Subjects were randomly assigned a lumbar corset with or without a spinal support. The spinal support was a heat-molded plastic insert, molded to the subjects back in the upright position, that was placed into a pocket in the back of the corset. At both 4 and 8 weeks, there was a significant relief of symptoms in only those who wore the lumbar corset with the lumbar support.60 In summary, a brace, if prescribed appropriately, can be a useful adjunct or an effective treatment for some types of back pain. The appropriate brace should be chosen to unload a specific pain generator, e.g. a posterior spinal element pain generator relieved by spinal flexion should be treated with a brace which promotes spinal flexion. Conversely, an anterior spinal element pain generator relieved by spinal extension should be treated with a brace which promotes spinal extension. As was true in the cervical region, an orthosis should only be prescribed for a limited period of time in order to minimize disuse atrophy.

CONCLUSION

Osteoporosis

14. Kamenetz HL. Eponymic orthoses. In: Redford JB, ed. Orthotics etcetera, 3rd edn. Baltimore: Williams and Wilkins; 1986:803.

Spinal orthoses are commonly used to treat osteoporotic compression fractures, using the biomechanical principles outlined previously, with few outcome studies available to recommend their use. However, in 2004, Pfeifer reported on a partial crossover prospective study of 62 subjects with at least one vertebral fracture and an angle of kyphosis greater than 60° resulting from osteoporosis who wore a specific orthosis for 6 months. This orthosis consisted of an abdominal pad and lightweight metal splint which was fitted along the spine and attached with Velcro straps. After 6 months of use, the subjects were found to have a 73% increase in back extensor strength, an 11% decrease in angle of kyphosis, and a 38% decrease in average pain. There was only a 3% reported drop-out rate, possibly indicating good compliance with orthosis use.61

15. Lunsford TR, Davidson M, Lunsford BR. The effectiveness of four contemporary cervical orthoses in restricting cervical motion. J Prosthet Orthop 1994; 6:93–99.

The use of a spinal orthosis is an effective treatment for many selected spinal conditions. However, in prescribing a particular orthosis, one must keep in mind the pathologic process which is being treated, the biomechanical principles and orthotic designs needed to correct the problem, and the available evidence that a particular orthosis has been effective in treating similar problems in others in the past. One must also be cognizant of both potential complications and issues related to compliance with the use of prescribed orthoses.

Acknowledgments We would like to thank Juvy Villanueva, P.T. for serving as our model and Edna Mieles, C.O. and Richard Conceircao C.P.O. from TMR Prosthetic and Orthotics for providing and fitting the orthotics in the figures.

References 1. Gavin TM, Patwardhan AG, Bunch WH, et al. Principles and components of spinal orthoses. In: Goldberg B, Hsu JD, eds. Atlas of orthoses and assistive devices, 3rd edn. St. Louis: Mosby; 1997:155–194. 2. Russell JN, Hendershot GE, LeClere F, et al. Trends and differential use of assistive technology devices: United States, 1994. Adv Data 1997 13(292):1–9. 3. Harris EE. A new orthotics terminology – guide to its use for prescription and fee schedules. Orthotics Prosthetics 1973; 27:6–19. 4. White AA, Panjabe MM. Clinical biomechanics of the spine. Philadelphia: JB Lippincott; 1990. 5. Andriacchi T, et al. A model for studies of the mechanical interaction between the human spine and the ribcage. J Biomech 1974; 7:497. 6. Fielding JW. Normal and selected abnormal motion of the cervical spine from the second cervical vertebra to the seventh cervical vertebra based on cineradiography. J Bone Joint Surg 1964; 46A:1779. 7. Jones RF, Snowdon E, Coan J, et al. Bracing of thoracic and lumbar spine fractures. Paraplegia 1987; 25:386–393. 8. Harlow ML, Russ JC, Nolinske TL, et al. Orthotic management of the spine. In: Meyer PR Jr, ed. Surgery of spine trauma. New York: Churchill Livingston; 1989:279–304. 9. Meyer PR. Fractures of the thoracic spine: T1–T10. In: Meyer PR Jr, ed. Surgery of spine trauma. New York: Churchill Livingston; 1989:525–571. 10. Nachemson AL. Orthotic treatment for injuries and diseases of the spinal column. Phys Med Rehabil: State Art Rev 1987; 1:11–24. 11. Johnson RM, Hart DL, Simmons EF, et al. Cervical orthosis: a study comparing their effectiveness in restricting cervical motion in normal subjects. J Bone Joint Surg [Am] 1977; 59:332–339. 12. Colachis SC, Strohm BR, Ganter, EL. Cervical spine motion in normal women. Arch Phys Med Rehabil 1973; 5:161–169. 13. Carter VM, Fasen JM, Roman J, et al. The effect of a soft collar, used normally recommended or reversed, on three planes of cervical range of motion. J Orthop Sports Phys Ther 1996; 23:209–215.

16. Lysell E. Motion of the cervical spine [Thesis]. An experimental study on autopsy specimans. Acta Orthop Scand Suppl 1969; 123:1. 17. Maiman D, Millington P, Novack S, et al. The effect of the thermoplastic Minerva body jacket on cervical spine motion. Neurosurgery 1989; 25:363–368. 18. Ducker TB. Restriction of cervical spine motion by cervical collars [abstract]. Proceedings of 58th Annual Meeting of the American Association of Neurological Surgery, Park Ridge, IL, 1990. 19. Johnson RM, Owen JR, Callahan RA. Cervical orthoses: a guide to their selection and use. Clinical Orthop Rel Res 1981; 154:34–45. 20. Flanagan P, Gavin TM, Gavin DQ, et al. Spinal orthoses. In: Lusardi MM, Nielsen CC, eds. Orthotics and prosthetics in rehabilitation. Boston: Butterworth-Heinemann; 2000.

Section 2: Osseous Spinal Tumors 21. Anderson DG, Vaccaro AR, Gavin KF, et al. Spinal orthoses. In: Vaccaro AR, Betz RR, Zeidman SM, eds. Principles and practice of spine surgery. St. Louis: Mosby; 2003. 22. Edelstein JE, Bruckner J. Trunk and cervical orthoses. In: Orthotics: a comprehensive clinical approach, Thorofare: SLACK Inc.; 2002:113. 23. Askins V, Eismont FJ. Efficacy of five cervical orthoses in restricting cervical motion. A comparison study. Spine 1997; 22(11):1193–1198. 24. Gavin TM, Carandang G, Havey R, et al. Biomechanical analysis of cervical orthoses in flexion and extension: a comparison of cervical collars and cervical thoracic orthoses. J Rehabil Res Dev 2003; 40(6):527–537. 25. Koch RA, Nickel VL. The halo vest: an evaluation of motion and forces across the neck. Spine 1978; 3:103–107. 26. Lind B, Sihlbom H, Nordwell A. forces and motions across the neck in patients treated with halo-vest. Spine 1988; 13:162–167.

42. Williams PC. Lesions of the lumbosacral spine–lordosis brace. J Bone Joint Surg 1937; 19:702. 43. Kim SS, Denis F, Lonstein JE, et al. Factors affecting fusion rate in adult spondylolisthesis. Spine 1990; 15:979–984. 44. Vogt L, Pfeifer K, Portscher M, et al. Lumbar corsets: their effect on three-dimensional kinematics of the pelvis. J Rehabil Res Dev 2000; 37:495–499. 45. McNair PJ, Heine PJ. Trunk proprioception: enhancement through lumbar brace. Arch Phy Med Rehabil 1999; 80:96–99. 46. National Institute for Occupational Safety and Health. Workplace use of back belts. Centers for Disease Control and Prevention. Washington: US Department of Health and Hyman Services; 1992 Pub. No. 94–122. 47. Occupational Safety and Health Administration. Ergonomic program: final rule. In: Federal Register 2000; 65(220)68261–870. Washington.

27. Benzel E. A comparison of the Minerva and Halo jackets for stabilization of the cervical spine. J Neurosurg 1989; 70:411–414.

48. Ammendolia C, Kerr MS, Bombadier C, et al. Canadian Task Force on Preventive Health Care. Use of back belts to prevent occupational low-back pain. Recommendation statement. CMAJ 2003; 169(3):213–218.

28. Sharpe KP, Rao S, Ziogas A. Evaluation of the effectiveness of the Minerva cervicothoracic orthosis. Spine 1995; 81:255–257.

49. Bernardoni G. Are off-the-shelf TLSOs helpful or harmful? Newsletter and Articles Ballert Orthopedics of Chicago www.ballert-op/newsletter

29. Richardson JK, Ross AM, Riley B, et al. Halos vest effects on balance. Arch Phys Med Rehabil 2000; 81:255–257.

50. Davis J, Parks S, Detlef C, et al. Clearing the cervical spine in obtunded patients: The use of dynamic fluoroscopy. J Trauma 1995; 39(3):435–438.

30. Norton PL, Brown T. The immobilizing efficiency of back braces the effect on the posture and motion of the lumbosacral spine. Bone Joint Surg 1957; 39A:111–139.

51. Rogers J, Rogers W. Marginal mandibular nerve palsy due to compression by a cervical hard collar. J Ortho Trauma 1994; 9(2):177–179.

31. Lantz SA, Schultz AB. Lumbar orthosis wearing. I. Restriction of gross body motions. Spine 1986; 11:834–837.

52. Fisher SV. Proper fitting of the cervical orthosis. Arch Phys Med Rehabil 1978; 59(11):505–507.

32. Cholewicki J, Juluru K, Radecold A, et al. Lumbar spine stability can be augmented with an abdominal belt and/or increased intra-abdominal pressure. Eur Spine J 1999; 8:388–395.

53. Rosenfeld M, Seferiadis A, Carlsson J, et al. Active intervention in patients with whiplash-associated disorders improves long-term prognosis: a randomized controlled clinical trial. Spine 2003; 28(22):2491–2498.

33. Fidler MW, Plasmans CMT. The effect of four types of support on the segmental mobility of the lumbosacral spine. J Bone Joint Surg 1983; 65A:943–947.

54. Rosenfeld M, Gunnarsson R, Borenstein P. Early intervention in whiplash-associated disorders: a comparison of two treatment protocols. Spine 2000; 25(14):1782– 1787.

34. Morris JM, Lucas DB, Bressler MS. Role of the trunk in stability of the spine. J Bone Joint Surg 1961; 43A:327–351. 35. Waters RL, Morris JM. Effect of spinal supports on the electrical activity of muscles of the trunk. J Bone Joint Surg Am 1970; 52:51–60. 36. Lantz SA, Schultz AB. Lumbar spine orthosis wearing. II. Effect on trunk muscle myoelectric activity. Spine 1986; 11:838–842. 37. Nachemson A, Morris JM. In vivo measurements of intradiscal pressure. J Bone Joint Surg Am 1964; 46:1077–1092. 38. Nachemson A, Schultz A, Andersson G. Mechanical effectiveness studies of lumbar spine orthoses. Scand J Rehabil Med Suppl 1983; 9:139–149. 39. Rohlmann A, Bergmann G, Graichen F, et al. Braces do not reduce loads on internal spinal fixation devices. Clin Biomechanics 1999; 14:97–102. 40. Spratt KF, Weinstien JN, Lehmann TR, et al. Efficacy of flexion and extension treatments incorporating braces for low-back pain patients with retrodisplacement, spondylolisthesis, or normal sagittal translation. Spine 1993; 18:1839–1849. 41. Nachemson AL. Orthotic treatment for injuries and diseases of the spinal column. Phys Med Rehabil 1987; 1:22–24.

55. Gennis P, Miller L, Gallagher EJ, et al. The effect of soft cervical collars on persistent neck pain in patients with whiplash injury. Acad Emerg Med 1996; 3(6):568–573. 56. Schultz AB, Ashton-Miller JA. Biomechanics of the human spine. In: Mow VC, Hayes WC, eds. Basic orthopaedic biomechanics. New York: Raven Press; 1991. 57. Gavin TM, Boscardin JB, Patwardhan AG, et al. Preliminary results of orthotic treatment for chronic low back pain. JPO 1993; 5(1):5–9. 58. Micheli LJ, Hall JE, Miller ME. Use of modified Boston brace for back injuries in athletes. Am J Sports Med 1980; 8(5):351–356. 59. Willner S. Effect of a rigid brace on back pain. Acta Orthop Scand 1985; 56(1): 40–42. 60. Million R, Nilsen KH, Jayson MI, et al. Evaluation of low back pain and assessment of lumbar corsets with and without back supports. Ann Rheum Dis 1981; 40(5):449–454. 61. Pfeifer M, Begerow B, Minne HW. Effects of a new spinal orthosis on posture, trunk strength, and quality of life in women with postmenopausal osteoporosis: a randomized trial. Am J Phys Med Rehabil 2004; 83(3):177–186.

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SPECIFIC DISORDERS

Section 2

Osseous Spinal Tumors ■ ii: Treatment

CHAPTER

Vertebroplasty

44

Michael J. DePalma and Curtis W. Slipman

OVERVIEW Fracture of the intervertebral body represents structural failure of its osseous components, causing compression deformity.1 Although compression fractures can be quite painful and incapacitating, many are asymptomatic and heal undetected.2 Uncovering a vertebral body compression fracture must alert the treating clinician to properly diagnose the responsible etiology. Vertebral fracture is the most common complication of osteoporosis.3 The lifetime risk of a clinically relevant vertebral fracture due to osteoporosis is approximately 16% in white women, and this proportion varies depending on the radiographic definition utilized in the study.4 Age, history of fracture and osteoporosis, and decreased height and physical activity have all been associated with vertebral fractures in both genders.5 Less common etiologies of vertebral compression fractures include multiple myeloma, lymphoma, metastatic disease, and benign vascular lesions. Malignant compression fractures account for approximately 25% of nontraumatic vertebral compression fractures.6 Hemangiomas are even less common, occurring with an incidence of 10–12%, many of which are asymptomatic and discovered incidentally.7 Vertebral body compression fractures typically manifest as episodes of acute and frequently explosive axial pain precipitated by routine activities of daily living. Movement is limited by pain, and flexion is restricted more than extension. This spinal pain is exacerbated by axial loading during sitting or standing, and alleviated by recumbent positioning. The process of changing position is particularly uncomfortable, leaving the afflicted patient with the desire to remain in a position of comfort; particularly resting supine in bed. Thoracic fractures can result in thoracic kyphosis (dowager’s hump) (Fig. 44.1) leading to a discrepancy between standing height and arm span, and pulmonary dysfunction. Involvement of the lumbar spine may lead to progressive loss of normal lumbar lordosis, leading to early satiety and abdominal bloating. Neurologic involvement is rare in osteoporotic compression fractures because the posterior cortical wall is rarely breached.8 When involvement of the spinal cord or cauda equina occur, it should suggest other conditions that can lead to a compression fracture such as infection, metastatic or primary bone tumors, myeloma, Paget’s disease, or lymphoma.9 Pain and disability consequent to osteoporotic vertebral fractures tax the health care, industrial, and societal systems. Approximately 750 000 new osteoporotic vertebral fractures occur in the United States each year,3 and over one-third of these become chronically painful.10 Vertebral fractures in patients aged 65 years or older account for 150 000 hospital admissions per year11 with an estimated total cost of 1.5 billion dollars.3 Patients aged 45 years or older account for 161 000 physician office visits and more than 5 million restricted-activity days per year.12 Hence, osteoporotic vertebral compression fractures are a leading cause of disability and morbidity

in the elderly.13 Such outcomes are due to chronic pain, progressive vertebral collapse, and spinal kyphosis.14 Osteoporotic compression fractures have been shown to adversely affect quality of life, physical functioning, mental health, and survival.15

TRADITIONAL TREATMENT APPROACH Traditional treatment pursuits strive to achieve pain relief, reduction of the sequelae of deconditioning, and maximal function. These objectives are largely achieved by conservative measures including relative rest, narcotic analgesics, antiosteoporotic medications, spinal orthotics, and gradual extension-biased exercises.3,16 Rarely, these fractures are associated with neurologic compromise or spinal instability necessitating surgical repair. Bed rest is prescribed in the acute

Fig. 44.1 Lateral photograph of an 87-year-old female with thoracic pain following a minor fall. Notice that her fingertips reach the distal third of her thigh.

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phase, but must be minimized to 2 days to reduce the occurrence of contractures,17 worsening osteoporosis,18 muscle weakness and atrophy,19 and thromboembolic complications.20 Each of these entities will increase the morbidity and mortality resulting from a compression fracture. In the majority of cases, the pain will abate within 2–4 weeks to as many as 8–12 weeks. However, a significant number will remain painful,15 possibly due to incomplete healing with progressive bony collapse, altered spinal kinematics resulting from deformity, or development of a pseudoarthrosis at the involved segment.14 Analgesic medications are poorly tolerated by elderly patients due to confusion, increased fall risk, and constipation. Bracing may not be well tolerated due to decreased diaphragmatic excursion, and restriction of abdominal movement. Overall, these treatment interventions aim to ameliorate the symptoms associated with osteoporotic compression fractures, while not addressing underlying tissue injury.

Historical overview of vertebroplasty Over the past two decades, vertebroplasty, the percutaneous injection of polymethyl methacrylate (PMMA) directly into the fractured vertebral body, has been increasingly utilized to stabilize vertebral body compression fractures. This technique was invented in 1984 by two French physicians, Galibert and Deramond, to treat symptomatic vertebral angiomas, and their findings were subsequently published in 1987.21 Nine years later, Cotton et al.22 and Weill et al.,23 in two independent studies, established the efficacy of vertebroplasty in patients suffering from metastatic spine disease or multiple myeloma. Jensen et al. published the first American trial in 1997 of applying vertebroplasty to treat osteoporotic vertebral compression fractures.24 Hence, European physicians have served the pioneering role in establishing the utility of vertebroplasty, acquiring greater experience with this new technology in pursuit of primarily treating painful spinal tumors. In contrast, North American physicians have witnessed a growth in deploying this procedure to treat painful osteoporotic patients who themselves served as the impetus for exploring this treatment option.25 Consequently, vertebroplasty has been promoted as a viable option to treat painful vertebral compression fractures in the absence of sound methodologic prospective trials supporting this contention. Although conclusive evidence is lacking, diligent studies have been and are being performed to explain vertebroplasty’s therapeutic benefit, substantiate its safety, demonstrate the durability of its efficacy, and refine its technique.

apparent density squared. Thus, a decrease in the later will cause a disproportionate reduction in trabecular bone strength.1 Vertebral trabeculae are arranged in vertical and horizontal columns, and the vertical columns outnumber the horizontal ones at any given density.1 Compressive loads are initially borne by the vertical trabecular struts, and when these struts begin to bow their horizontal counterparts act as cross-beams to restrain this displacement (Fig. 44.2).26 Consequently, an axial load is sustained by a combination of vertical pressure and transverse tension within the trabeculae. The ability to transfer load from vertical pressure to transverse tension confers resilience to the vertebral body.26 As the number of trabeculae decrease with aging, osteoporosis, or space-occupying lesion, the altered architecture reduces the vertebral body’s resiliency, thus lowering its threshold for fracture under load.1 A strong, positive correlation between lumbar spine bone mineral density (BMD) and failure force required to fracture a lumbar vertebra has been unequivocally established.27 Hence, BMD can be used as a convenient and specific predictor of the risk of vertebral body failure under compressive loads. This correlation appears to be a continuum without a single fracture threshold value for BMD at which a vertebral body will fail.1 A given vertebra will fatigue with repetitive loading, allowing it to fail at a lower load force than would be required during a single load application.28 The phenomenon of vertebral fatigue may be due to intraosseous crack initiation, crack growth, and final failure.29 Indeed, such bony deficits have been observed in human vertebral bone, irrespective of age, lending credence to the presence of such microdamage reducing vertebral fracture resistance.30

Extrinsic factors Extrinsic factors such as loading conditions are as integral to vertebral body fracture as the already discussed intrinsic factors. Fractures occur at a point when external loads result in internal stresses that exceed the strength of the bone. Clinical recognition of the features of osteoporotic vertebral compression fractures can be difficult. Cooper et al. reviewed charts from 341 fracture patients over a 5-year period and found that 16% of patients were diagnosed incidentally, 33% after a fall, and 9% after routine lifting.2 Within this study cohort, approximately 50% of the vertebral fractures were

PATHOPHYSIOLOGY OF VERTEBRAL BODY COMPRESSION FRACTURE Mechanical failure of the vertebral body represents disrupted structural integrity. The vertebral body’s ability to function properly to bear and transmit loads is a function of the health of its trabecular bone; its structural design as dictated by shape, size, and organization; and the loading conditions involving the energy it absorbs.1

A

B

C

D

E

F

Intrinsic factors The strength of the trabecular bone is a key attribute in determining a vertebral body’s risk of fracture. Trabecular bone functions to carry the axial load transmitted to the vertebral body from the adjacent intervertebral discs. Trabecular bone will fail if its strength is less than the working stresses experienced within the vertebral body during physiologic or traumatic loads. Whole bone fractures are the consequence of such failures. Trabecular bone strength is determined by apparent density and its architecture. Reductions in apparent density occur with aging, osteoporosis, and tumor infiltration. The compressive mechanical strength of trabecular bone is proportional to the

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Fig. 44.2 Reconstruction of the internal architecture of the vertebral body. (A) With just a shell of cortical bone, a vertebral body is like a box, and collapses when a load is applied (B). (C) Internal vertical struts brace the box (D). (E) Transverse connections prevent the vertical struts from bowing, and increase the load-bearing capacity of the box. Loads are resisted by tension in the transverse connections (F). (Adapted from Bogduk N. The lumbar vertebrae. In: Clinical anatomy of the lumbar spine and sacrum, 3rd edn. Churchill Livingstone, London, 2002.

Section 2: Osseous Spinal Tumors

reported as spontaneous or incidental,2 perhaps a result of vertebral fatigue.1 In a smaller study, Myers et al. recorded a history of a fall in 50% of osteoporotic acute fracture patients over 60 years old, a history of acute fracture in 20% of patients with routine activities of daily living, with the remainder of patients not able to recall a specific event at the time of injury.31 The apparent disparity among the causes of osteoporotic vertebral compression fractures might be explained by a combination of intrinsic and extrinsic factors. A single traumatic event leading to a load sufficient to fracture a weak vertebra might explain a fracture due to osteoporosis or a tumor. A fracture associated with routine activity or no apparent cause may represent structural fatigue due to age, osteoporosis, or tumor-related vertebral changes. A ‘factor of risk’ has been established incorporating an individual patient’s BMD to forecast the risk of vertebral fracture consequential to some routine activities of daily living.32 Factors of risk are the ratio of the estimated forces applied to the spine to the vertebral failure threshold based on lumbar BMD. A ratio equal to or greater than 1 represents a strong likelihood of fracture.1,32 Individuals with low BMD routinely operate near a ratio of 1, and women with below average BMD who lift a toddler experience a factor of risk near 1.1 For women with very low BMD, innocuous activities such as tying one’s shoes increases the risk of fracture.1 Implicit in the dynamic relationship between routine activities and fracture risk is a role for posture and neuromuscular conditioning, and degenerative disc disease. Evidence has recently been published substantiating this contention.33,34 An involutional loss of functional muscle motor units occurs with aging and predisposes an individual to poor postural control.35 A 2-year structured back extension exercise program has been shown to reduce the incidence of vertebral compression fractures and increase bone mineral density in healthy, postmenopausal women, up to 8 years after cessation of the program.33 Thus, extension-based exercise helps maintain bone mineral density and prevent vertebral compression fractures, perhaps due to improved posture and spinal stabilization. Pollitine et al., in an elegant study, defined the relative loads experienced by the three columns of the spine in patients with degenerative discs.34 Twice as much load is assumed by the posterior column than by the anterior vertebral body in the erect standing position in patients with degenerative intervertebral discs. In contrast, the anterior vertebral body’s axial load increases almost three times during forward bending in the presence of degenerative discs. A relative ‘off-loading’ of the anterior vertebral body during upright posture will result in bone loss due to a lack of routine dynamic strain.36,37 Ultimately, the weakened anterior vertebral body is abnormally loaded above its counterpart in spines containing healthy, nondegenerate discs. The findings of Pollitine et al. suggest that in a person with severely degenerated intervertebral discs, the load placed on the anterior vertebral body increases by greater than 300% in flexion as compared to standing erect.34 Sinaki et al.’s reduction in compression fractures may be due to their patients’ increased spinal extensor conditioning as well as an independent increase in BMD. Their treatment arm utilized extension exercises without specific land-based weightbearing exercises.33 The increased extensor conditioning may have decreased the load incurred by the anterior vertebral body during flexion activities, and may have inadvertently increased the anterior vertebral body’s resilience to fracture. However, Sinaki et al. did not remark about the presence or absence of disc degeneration. An accurate comprehension of the pain generating mechanisms of vertebral compression fractures is indispensable if successful treatment is to be effectuated. Traditional treatment interventions assume adequate tissue healing with time, which seems to be logical given the natural history of gradual resolution of pain within 2–12 weeks. However, chronic pain may develop due to microfracture nonunion,14,38

pseudoarthrosis,3 sensitization of the basivertebral nerve,39 or spinal deformity14 leading to painful paraspinal muscle spasm. The first three of these probable pathophysiologic mechanisms can be addressed with the percutaneous injection of PMMA. Although kyphotic deformity is not maximally corrected by vertebroplasty, reduction in pain allowing extension-based spinal stabilization may reduce painful myofascial dysfunction, thus reducing kyphosis.

MECHANISM OF ACTION OF VERTEBROPLASTY The pain relief afforded to patients having undergone vertebroplasty has not yet been successfully attributed to a primary mechanism. Thermal,40–43 chemical,44,45 and mechanical46 effects have all been reported as possible mechanisms. However, the mechanical effects of vertebroplasty have been regarded as the critical factor leading to symptom reduction.46–48 Tohmeh et al., in 1999, demonstrated increased strength and stiffness in osteoporotic cadaveric compression fractures utilizing either a unipedicular or bipedicular approach.46 However, the authors did not investigate the distribution or volume of PMMA injected relative to these mechanical parameters. Liebschner et al. subsequently established that symmetric deposition of PMMA is ideal to prevent single-sided load transfer, and that overall a small amount is needed to restore stiffness and strength.49 Belkoff et al. provided preliminary guidance for the amount of injected PMMA necessary to restore stiffness and strength;47 however, Molloy et al. later established the approximate percentage of vertebral body volume required to be filled to restore adequate strength and stiffness.48 A weak correlation has been noted between percentage of fill and restored strength and stiffness,48 which echoes previous clinical observations of minimal correlation between pain relief and the amount of PMMA injected.22 If an intravertebral cleft is present, there is a trend toward greater pain relief if these clefts are opacified during vertebroplasty.50 These findings suggest that either the singular factor of achieving a minimum threshold of stabilization is needed to abate micromotion or malunion induced pain, or that an alternate painreducing mechanism is yet to be demonstrated. The polymerization process of PMMA is exothermic and its effects have been studied utilizing cadaveric vertebral bodies.42,51 Deramond et al. observed sufficiently elevated and sustained intraosseous temperatures in the central and anterior vertebral bodies during PMMA injection, and lack thereof at the anterior wall of the spinal canal, to cause thermal damage to intraosseous neural structures.42 Belkoff and Molloy subsequently observed higher temperature elevation in vertebral specimens during intraosseous injection of PMMA, perhaps due to a different temperature recording technique, but these higher temperatures did not occur at the spinal canal.51 The authors were led to believe that the risk of thermal necrosis may have been underappreciated. Yet histologic examination of four vertebral bodies, previously treated with percutaneous injection of PMMA, retrieved from human spines during spinal surgery, identified rare foci of necrosis.52 Unfortunately, histologic assessment was not performed on the intraosseous neural structures of these four samples. Further, a vast network of substance-P containing nerves has been documented within the vertebral body.39 Consequently, thermal and/or chemical denervation may contribute to the pain-relieving effect of vertebroplasty.

INDICATIONS AND CONTRAINDICATIONS Vertebroplasty was first developed to treat symptomatic vertebral body hemangiomas.21 Since 1984, the conditions for which percutaneous injection of PMMA has been undertaken have been expanded to include primary and metastatic spinal fractures (Fig. 44.3),22,23 497

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Fig. 44.3 Lateral sagittal T1-weighted MR image of an upper lumbar malignant compression fracture. Notice the obscure cortical margins of the superior endplate (white arrowhead).

osteoporotic compression fractures (Fig. 44.4),24 vertebral fractures due to osteogenesis imperfecta,53 recurrent fracture or pain at a previously treated segment,54 and pseudoarthroses associated with noninfected avascular necrosis of the vertebral body.55 The universally accepted indications for performing percutaneous vertebroplasty (PVP) are severe, focal, intractable spinal pain,

Fig. 44.4 Lateral T2-weighted MR image of an acute T11 osteoporotic compression fracture (white arrow), and a remote L2 fracture (white arrowhead). Notice the increased T2 signal intensity in the T11 vertebral body indicating a more acute injury in contrast to the relative lack of increased signal in the L2 body. 498

in the absence of radicular pain, recalcitrant to traditional treatment measures due to acute compression fractures.3,14,22,25,24,56–72 An acute fracture is substantiated by a typical history and evidence of new or progressive fracture by magnetic resonance imaging (MRI) (Fig. 44.5). Alternatively, persistent pain, despite appropriate conservative care, greater than 3 months due to an imaging confirmed compression fracture is a relative indication.73 In a retrospective observational investigation, Kaufmann et al.73 found that fracture age at the time of PVP was not independently associated with postprocedural pain or activity. In subsequent retrospective study, Brown et al.74 found that 80% of 41 osteoporotic fracture patients with symptom duration of greater than 12–24 months had post-PVP pain improvement; in comparison, 92% of 49 control patients, those with symptoms less than 1 year, experienced pain relief. Although the number of patients achieving partial or complete pain relief was not statistically different between groups, complete pain relief was more frequent in the control group. The ideal time frame during which to intervene with PVP to treat painful vertebral compression fractures has yet to be determined in well-controlled prospective studies. However, some contend that the likelihood of improvement probably decreases over time and appears to be low for remote, 6 months or older, fractures.3 Contraindications to PVP include a fracture that breaches the posterior vertebral wall, retropulsed bone fragments, gross spinal instability, clinical evidence of myelopathy or radiculopathy, osteoblastic metastatic lesions, uncorrectable coagulopathy, systemic or spinal infection, or medical conditions that preclude safe emergent surgical decompression.3 A loss of vertebral body height of greater than 75%, has been cited as a relative contraindication to PVP (Fig. 44.6).23,56 However, Peh et al. evaluated 37 patients who underwent PVP to treat vertebra plana, defined as a collapsed vertebra to less than onethird of its original height.57 Ninety-four percent of these patients experienced pain reduction, with 51% of the 37 patients reporting complete pain relief.57 No major complications were reported, and

Fig. 44.5 Fat suppression sagittal MR images depict an acute L2 compression exhibited by the increased signal intensity. These findings suggest an acute or subacute fracture or fracture progression.

Section 2: Osseous Spinal Tumors

Fig. 44.6 A severe compression fracture involving T12 and L1 with greater than 75% loss of the L1 vertebral body height (white arrow).

the authors concluded that PVP of severe osteoporotic vertebral body compression fractures should not be withheld from this category of patient.57 At this point, it seems most prudent to regard severe vertebral compression fractures as relative indications in the absence of myelopathy, instability, or disruption of the posterior vertebral body wall.

EFFICACY OF PERCUTANEOUS VERTEBROPLASTY Successful clinical outcomes have been reported since the inception of PVP in 1984.21 A plethora of studies have been published documenting the therapeutic benefit of PVP in treating painful vertebral body compression fractures.3,14,21–25,53–58–65,75 The excitement generated by a treatment intervention that achieves complete or near complete pain relief has fueled many investigations attesting to its efficacy. Many of these reports have evaluated pain reduction, and less commonly quality of life or patient satisfaction. Only one study included a control group, and no studies to date have employed a prospective, randomized trial incorporating a control group. Hence, the natural history of a certain vertebral compression fracture has not been concurrently compared to the clinical course of this condition after treatment with PVP. Rather, several investigations have seemingly established PVP’s safety and efficacy at reducing disruptive pain symptoms due to vertebral body compression fractures.

Osteoporotic compression fractures Vertebral compression fracture is a common clinical manifestation of osteoporosis, but rarely leads to neurologic compromise.9 However, osteoporotic vertebral compression fractures are invariably associated with significant impairment in functional, physical, and psychosocial indices.76 Quality of life suffers after the first osteoporotic compression fracture and decreases further with subsequent fractures.77 Afflicted individuals experience pain, disability, loss of activity, fear of falling, and embarrassment over their appearance.78 Increased mortality has been observed after an initial osteoporotic compression fracture, and progressively increases with advancing time after the initial injury.79 As our society continues to age, refining the appropriate role of PVP

in treating osteoporotic vertebral compression fractures has emerged as the multifaceted impetus for a variety of investigations. Jensen et al. first addressed the efficacy of PVP to treat osteoporotic vertebral compression fractures in the late 1990s.24,75 Ninety percent of 29 patients treated with PVP reported significant reduction in pain within 24 hours after the procedure.24 At a mean follow-up of 281 days, 23 of these 26 patients who initially experienced significant improvement reported sustained pain reduction and increased mobility.75 In a larger study of 245 osteoporotic patients, Evans et al.58 reported significant reduction in pain, and improved ambulatory status and activities of daily living at a median follow-up interval of 7 months. Yet the 245 cases were reviewed retrospectively and represented the only cases out of 488 available for follow-up. The authors did not use a validated disability assessment tool, and it was administered at varying times after treatment intervention. Long-term observations were conducted by Grados et al.59 who documented a statistically significant reduction in visual analog scale (VAS) pain scores in 96% of osteoporotic compression fracture patients treated with PVP. The mean duration of follow-up was 48 months with a range of 12–84 months. The authors concluded that the results obtained by PVP are durable over time, as their findings did not deteriorate from 1 month to a mean of 48 months after treatment intervention. However, 15 of the original cohort of 40 were not available at follow-up, the methodology was retrospective, and clinical significance, such as quality of life or disability, of the reduced VAS ratings was not assessed. These findings have been corroborated by those of other retrospective studies incorporating smaller subgroups of osteoporotic patients with significant pain relief occurring in 75–95% of treated patients.56,60–63 Peters et al.64 prospectively observed a statistically significant decrease in VAS ratings in 84% of 42 osteoporotic compression fracture patients treated with PVP at 56 levels, and 7 patients reported no change in their pain level. All 42 patients were available at followup at 6 weeks, and had failed to improve despite a 6-week course of undefined medical management. The authors employed a bipedicular approach to inject PMMA into each fractured vertebrae except for six that were treated with a unipedicular technique. No relationship was disclosed between unipedicular technique and failure of pain reduction, and follow-up occurred at 6 weeks. Focusing on the efficacy of PVP in treating severe (>70% vertebral body collapse) osteoporotic compression fractures, Peh et al.57 prospectively found complete or partial pain relief in 97% of 38 patients undergoing 48 PVPs. Just 30 of the initial 38 patients were available for follow-up at a mean of 11 months (range 3–24 months). Pre-intervention symptoms ranged from 2 weeks to over 1 year. Bipedicular injection was competed in 20 levels, and 28 underwent unipedicular injection. McGraw et al.65 prospectively followed 100 patients undergoing 156 PVPs for osteoporotic (n=92), neoplastic (n=5), concomitant spinal stenosis (n=2), and osteogenesis imperfecta (n=1) related fractures. Ninety-nine patients were available for follow-up at a mean interval of 21.5 months (range 6–44 months), and 93% of patients reported improvement in their back pain with a statistically significant reduction in VAS ratings. However, the authors did not report the pre-PVP symptom interval, stratify results according to diagnostic category or how many levels were treated using a bipedicular technique. All three investigations used similar inclusion criteria including painful osteoporotic compression fractures refractory to medical management, proven by imaging and history and physical examination. The severity of collapse varied among the studies, and all three inquiries used pain reduction and mobility as the outcomes measures without incorporating a valid disability tool. Cortet et al.66 prospectively evaluated the efficacy of PVP in treating 20 osteoporotic vertebral compression fractures in 16 patients suffering from intractable pain despite 3 months of medical management. A statistically significant improvement was noted in VAS ratings, 499

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McGill-Melzack scoring system, and five out of six dimensions of the Nottingham Health Profile at 1, 3, and 6 months after PVP. Zoarski et al.67 prospectively followed 30 patients utilizing verbal pain scores and the Musculoskeletal Outcomes Data Evaluation and Management Scale (MODEMS) spinal intervention questionnaire. All patients demonstrated a lack of improvement after a minimum of 4 weeks of conservative care prior to PVP. Twenty-nine patients reported pain relief within hours of the procedure, and at 2 weeks 80% reported feeling better and 90% reported they would undergo the procedure again. All four modules of the MODEMS data (treatment score, pain and disability, physical function, and mental function) improved with statistical significance at 2 weeks. Ninety-six percent of 23 available patients at follow-up at 15–18 months reported continued pain relief and satisfaction with their outcome. All 30 patients underwent bipedicular injection of PMMA. Findings in a long-term, prospective study by Perez-Higueras et al.68 seem to support the durability of the results afforded to patients by PVP. Thirteen out of 17 original patients treated for 39 osteoporotic vertebral compression fractures were available at a mean follow-up of 65 months (range 60–71). All patients had failed to improve after a minimum of 3 months of conservative care. Outcomes were measured by VAS ratings and the short McGill questionnaire and all 13 demonstrated significant improvement at 3 months which increased slightly at the 5-year follow-up. These prospective studies have helped to provide greater insight regarding the efficacy of PVP in treating osteoporotic vertebral compression fractures. However, none incorporated a control group for comparison to the treatment arm. Implicit in this methodology is that a regression toward the mean has already occurred during the period of conservative care. Hence, any treatment intervention after this time frame would be attributed to the intervention itself. However, none of these studies recorded such statistical analysis. To date, one prospective study has incorporated a control group of patients treated with conventional therapy.69 In a nonrandomized fashion, Diamond et al.69 compared the clinical outcomes of 55 osteoporotic patients who underwent PVP with 24 patients who refused PVP and were conservatively managed. Inclusion criteria were acute severe vertebral compression pain unrelieved by 1–6 weeks of oral analgesics, densitometric evidence of osteoporosis, and acute fracture activity as indicated by MRI or technetium-99 m bone scan. No differences existed between the two groups regarding smoking history, alcohol intake, corticosteroid use, thyroxine therapy, vitamin D and parathyroid hormone levels, bone density, or degree of vertebral collapse. More importantly, both groups had statistically similar baseline levels of pain and disability. Fifty-three patients in the PVP group and 21 of the conservative group were available at a mean follow-up of 215 days (range 57–399), and outcomes were measured by VAS ratings and the Barthel index level of function. Statistically significant improvement in pain and physical functioning was noted at 24 hours in the PVP compared to the conservatively treated group. No differences were observed at 6 weeks or 6–12 months. A 40% reduction in the mean length of hospitalization was observed in the PVP group. These findings suggest, but do not prove, that PVP provides effective pain relief in the short term. The absence of a clinical separation between the two groups at longer follow-up may be due to the natural history of most compression fracture symptoms abating over 6–12 weeks. Hence, these cases may have been destined to clinically improve within 6 weeks after initiation of the study due to the natural history of the condition itself.

Neoplastic compression fractures The first series limited to patients with malignant disease was published in 1989 when Kaemmerlen et al.70 briefly described their experience in treating 20 patients with 33 neoplastic vertebral body 500

fractures. At an average follow-up of 2.8 months, 85% of patients noted substantial pain relief requiring either no analgesic medication or a reduced dose. Two patients did not respond and one patient developed spinal cord compression. In 1996, Weill et al.23 treated 37 patients for 48 metastatic lesions. At 6 months, 73% of treated patients reported marked or complete pain relief, and 21% reported moderate pain relief. The 94% reporting significant pain relief at 6 months dwindled to 65% at 1 year. Recurrent pain was attributed to the development of adjacent metastatic vertebral lesions or meningitis as identified by MRI. Later in the same year, Cotten et al.22 prospectively evaluated 37 patients treated for 40 metastatic or multiple myelomatous lesions in a controlled trial. The enrolled patients had experienced severe spinal pain not amendable to surgical intervention. Patients were evaluated using the McGill-Melzack questionnaire at 48 hours, 3 months, and 6 months after intervention with a mean follow-up at 4.2 months. All patients received concurrent radiation therapy between 12 to 22 days after PVP. Within the first 48 hours, 13.5% were pain free, 55% reported substantial improvement, and 30% were moderately improved. These results were sustained in 89% at 3 months, and 75% at 6 months. Twelve patients were not available at long-term follow-up. In a larger study, Deramond et al.71 evaluated 101 patients treated for spinal malignancies. Over 80% of patients experienced moderate to complete pain relief, and injection of PMMA may have had an antitumoral effect as local tumor recurrence was rare during the follow-up course.71 Only one investigation has been reported in the North American literature,60 which assessed a small number of patients treated for 13 primary or metastatic lesions. Significant pain relief was observed in just 50% of eight patients at a mean follow-up of 12 months. Due to the small number of neoplastic induced compression fractures studied by Barr et al,60 conclusive statements may be erroneous. However, it appears as if neoplastic vertebral compression fractures treated with PVP may have a less durable effect compared to their osteoporotic counterparts. Yet one must consider differences between these two patient populations. A significant proportion of patients fall out of the study cohort due to death or morbidity that precludes follow-up evaluation.72 Furthermore, one must not lose sight of the existence of a concomitant variable unique to patients with a compression fracture due to a malignancy; radiation therapy may skew the outcomes after treatment with PVP. Immediate pain relief is likely due to the percutaneous intervention itself. However, benefit months later may be partially attributable to radiation therapy.72 However, others propose that spinal segment involvement distant to the treated level may result in less durable effects.60 Percutaneous vertebroplasty appears to offer significant pain relief in a safe manner to patients suffering from neoplastic or osteoporotic spinal fractures that are not managed by conservative care or radiation therapy alone.60,72

Benign vascular lesions Benign vascular lesions can be treated by PVP, achieving results similar those regarding osteoporotic compression fractures. Galibert et al.’s initial series of seven patients experienced immediate and sustained relief at 2-year follow-up after PVP.21 Several studies, mostly case series, have upheld the observation of significant pain relief in up to 90% of patients.56,62,71,80–83 Clinical and radiological characteristics can classify vertebral hemangiomas (VH) with treatment implications.25 Asymptomatic VH without radiologic signs of aggressiveness do not require treatment. Radiologic aggressiveness is typified by predominantly soft tissue stroma (exhibited by low signal intensity on T1-weighted MR images),84 involvement of the entire vertebral body, irregular, honeycomb vertical striations, and a poorly defined

Section 2: Osseous Spinal Tumors

cortex.85 Vertebral hemangiomas producing severe spinal pain without radiologic signs of aggressiveness can be successfully treated with PVP.25,71,80,81 Asymptomatic patients in which aggressive VH are incidentally discovered may be monitored clinically.25 Symptomatic VH with aggressive features causing acute myelopathy or cauda equina injury can be successfully treated by preoperative PVP and subsequent surgical decompression.25,56, 81–83 Progressive neurologic compromise due to a symptomatic, aggressive VH can be successfully treated with PVP.25 Spinal VHs are rarely symptomatic and occur in the spine with an incidence of less than 12%. Hence, a symptomatic lesion would be expected to respond well to a treatment that effectively embolizes the vasculature and solidifies the vertebral segment.

Specific osseous parameters Solidifying a fracture nonunion seems to be the primary means by which PVP achieves symptom reduction in a subset of vertebral compression fractures.50,55,86 Lane et al.50 retrospectively examined pain relief in compression fracture patients with fractures demonstrated intraosseous clefts and those without clefts. Although a statistically significant difference was not found, the authors found a trend toward greater improvement in patients with intraosseous clefts versus those without. However, the calculated p-value was 0.18; thus, statistical support for a meaningful trend was not established. Regardless, this study did lend credence to the utility of PVP in treating patients with vertebral compression fractures with intraosseous clefts. Eighteen patients reported a mean VAS rating reduction of 66% at 12-months follow-up. However, 45 patients were initially enrolled, and at the time of publication only 18 were 12 months post-PVP. Perhaps this VAS reduction is an underestimation. This conjecture seems to be upheld by Peh et al.’s work86 in which 18 patients were prospectively evaluated after undergoing PVP for treatment of vertebral compression fractures with intraosseous vacuum phenomena. Post-PVP radiographic evaluation confirmed the invariable filling of the clefts with PMMA in all cases. Forty-four percent of patients enjoyed complete pain relief and 33.3% reported partial pain reduction, while 22.2% did not benefit from PVP. Again, the power of this study suffers from a small cohort, and 7 of the 18 patients were not available for follow-up beyond a mean of 4 months due to death. The 11 surviving patients were followed up at a mean of 13.6 months. Seventy-seven percent of patients reporting complete or partial pain relief at a mean followup of 4–13.6 months suggests that PVP can effectively reduce pain in compression fractures containing intraosseous clefts or vacuum phenomena. Larger trials will need to confirm these preliminary findings, especially in comparison to fractures without such clefts, if we are to accept the notion that such clefts represent a painful nonunion. An interesting complication of these intraosseous clefts is dynamic instability. Jang et al.55 evaluated the efficacy of PVP in the treatment of intravertebral pseudoarthrosis caused by vertebral body avascular necrosis as demonstrated by intravertebral vacuum phenomena or fluid collection. Thirteen of 16 total cases involved the thoracolumbar junction or one segment adjacent to the T12–L1 level. It is not surprising that the preponderance of such cases occurred at the transition between the rigid thoracic spine and relatively mobile lumbar spine. As well, the flexion–extension motion is most pronounced at the thoracolumbar junction as a consequence of the changeover from relative spinal axial rotation to relatively greater spinal sagittal motion. Repetitive stress and strain at these spinal segments would likely interfere with adequate healing of vertebral insufficiency fractures occurring at these levels in contrast to other segments which are less mobile.55 Intravertebral pseudoarthrosis was confirmed by changes in anterior vertebral body height on dynamic lateral flexion and extension

X-rays. Intraosseous vacuum phenomena were confirmed by plain radiography and computed tomography. Marked to complete pain relief occurred in 50% of patients, and moderate relief in 38% patients at a final follow-up interval of 11 months. Two patients experienced neither improvement nor worsening of their pain level. Significant correction simultaneously occurred in kyphosis and anterior vertebral body height; post-PVP imaging did not demonstrate instability. For spinal instability pain that is associated with avascular necrosis of a compressed vertebral body, percutaneous vertebroplasty is an effective means of relief. Symptom reduction appears to be related to a reduction in instability, and lends support to the notion that PVP solidifies fracture nonunion-induced micromotion. Excellent outcomes may also be achieved with repeat PVP preformed at prior treated levels.54 Gaughen et al.54 retrospectively observed excellent pain relief in 83% of 6 subjects treated at the same level as prior PVP, a mean of 41 days after initial PVP. Recurrent symptoms correlated with increased radiotracer uptake at that level on bone scan in three subjects, increased radiographic compression in one, stable fracture with diffuse edema on MR images in one, and no evidence of new fracture by CT in another patient. The initial PVPs were performed via unilateral pedicular approach in five patients with four of these demonstrating bilateral hemivertebral body spread of PMMA. The authors did not report at what follow-up interval their findings were recorded. They proposed that recurrent symptoms might be due to new fractures around the PMMA cement, or poor fracture healing from insufficient filling. Although it appears that PVP may be successfully repeated at a previously treated segment for a recurrent or new pathologic condition, PVP may not have needed to be repeated if bipedicular injection was performed initially, thus preventing a unilateral toggle effect. Other conditions in which osseous fragility manifests as fractures may result in vertebral body compression fractures. Osteogenesis imperfecta (OI) is such a condition in which defective collagen production results in weakened osseous structures. Painful spinal compression fractures due to OI may be effectively treated by PVP.53 Rami et al.53 reported a case of T10 compression fracture successfully treated with PVP. At 1 week the patient was pain free, and at a 17-month follow-up the patient still enjoyed a marked improvement in quality of life and pain relief. Ultimately, large, prospective trials are needed to confirm this preliminary finding. However, PVP should be offered as an effective treatment for persistent pain due to OI-related vertebral compression fracture.

SIDE EFFECTS AND COMPLICATIONS Justification of an invasive treatment intervention, regardless of how minimal this intervention may be, requires an accurate risk:benefit ratio calculation. A natural consequence of the excitement for performing PVP for painful vertebral compression fractures is a blurring of the appropriate indications and neglecting to adhere to proposed exclusion criteria. Despite numerous clinical trials and investigations,14,22,24,25,58–72 most retrospective, PVP has not been adequately studied using a randomized, prospective methodology. The lack of such evidence should not serve as dissuasion to pursuing original research. Rather, such a void ought to serve as the impetus for future projects that strive to answer the questions raised by the current foundation of investigations. Reported clinical complications related to PVP using PMMA include transitory fever, transient worsening of pain, radicular pain, rib fractures, cement pulmonary embolism, infection, spinal cord compression, and predisposition toward adjacent segmental injury.24, 56,59,60,63,70,87–91 Most complications are non-neurologic, transitory, and 501

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subclinical; however, the rate of complications varies considerably with the indication. The frequency of complications is 1.3% in osteoporosis, 2.5% in spinal hemangiomas, and 10% neoplastic disease.90 Detailed analysis of most literature regarding complication rates in clinical trials reveals rates reported per patient rather than per procedure. It is more telling to cite complication rates per procedure as risk certainly inflates with increasing levels treated.

Paravertebral leakage of cement occurs more commonly with spinal metastatic disease (56%) than with myeloma (15%).22 Eighty-seven percent of epidural leaks occurred in the presence of pre-PVP posterior cortical destruction, and 87% of these leaks were asymptomatic.22 Intradiscal extension due to cortical fracture or osteolysis of the vertebral endplate occurs invariably in neoplastic fractures with no immediately overt symptoms.22

Complications in osteoporotic patients

Cardiovascular side effects and complications

The complication rate for osteoporotic vertebral compression fractures is relatively low, reportedly 0–4.3% per level treated.57,60,64,65,69 Among the reported complications are transient radicular pain responding to oral steroid therapy,60,63,65 subcutaneous extravasation of cement requiring surgical removal,64 fractured transverse process and psoas muscle hemorrhage in a patient on heparin therapy.69 More commonly, subclinical extravasation of cement occurred in up to 65% of treated levels.66 Follow-up CT after treatment of 20 vertebral bodies demonstrated cement deposition in the paravertebral soft tissue in 30% of cases, peridural space in 15% of cases, intradiscally in 15% of cases, and the lumbar venous plexus in 5%.66 Intradiscal leakage of PMMA has been observed in 35% of treated levels in osteoporotic fractures.57 Catastrophic neurological complications by report are much more rare. Three cases have been published of spinal cord injury due to cement encroachment into the spinal canal (Fig. 44.7).87–89 At this juncture, it appears the benefits afforded by PVP in treating osteoporotic vertebral body compression fractures outweighs the calculated risks. Extravasation of bone cement outside of the vertebral body may have few clinical ramifications in most instances. Escape of the cement into the venous system has the chance of fatal outcome if it reaches the pulmonary vasculature.90 This seems to occur more frequently in neoplastic fractures due to their vascularity.22,91

A fatal outcome of venous leakage of PMMA is an embolus that travels to the inferior vena cava, eventually reaching the pulmonary vasculature, resulting in pulmonary infarction.91,93 Instances of pulmonary embolism (PE) have been reported,23,91,93 one of which did not demonstrate radiographic evidence of pulmonary PMMA.23 Padovani et al.91 suspected that insufficient polymerization allowed a less viscous mixture of PMMA to be injected into a Langerhans cell histiocytosis-related vertebral fracture resulting in venous leakage. The patient in this case report responded favorably to anticoagulant therapy. More recently, Jang et al.93 reported a case series of three patients developing a PE after PVP. The authors had treated 72 vertebrae for malignant osteolytic spinal tumors. Each of the 3 patients had multiple myeloma-related vertebral compression fractures at numerous levels, and underwent PVP at four to six segments. The authors concluded that appropriate cement viscosity should be obtained prior to injection, high-resolution real-time imaging and mixing the PMMA with barium or tungsten for opacification should be undertaken, and greater caution exercised during multilevel procedures. These are prudent points of concern when performing PVP regardless of the underlying condition. However, they are particularly important when approaching fractures due to highly vascularized tumors such as renal cell carcinoma, thyroid tumor, hemangioma, hepatoma, or an extensive osteolytic tumor such as multiple myeloma.22,91 Cardiovascular instability has been observed in orthopedic procedures employing acrylic bone cement,94 and some have proposed this to be a lesser risk in PVP.62 Aebli et al.95 utilized a sheep model to study the effects of bone cement injected into healthy vertebrae. The authors observed a transient, immediate drop in heart rate and mean arterial pressure by 1 to 7 seconds after cement injection and a second hypotensive episode occurring approximately 18 seconds after injection. These hemodynamic changes returned to baseline in less than 3 minutes. The second drop in heart rate and blood pressure occurred concomitantly with the appearance of echogenic particles within the pulmonary artery. The authors concluded that the first drop in the cardiovascular parameters occurred by cardiac reflex inhibition due to intraosseous pressurization. The second drop may have been related to the systemic extravasation of bone cement. Yet the PVPs were performed in healthy bone and not monitored by real-time imaging. Thus, extravasation may very well have occurred due to a relatively high intraosseous pressure and the interventionalist not terminating injection once the cement had breached the posterior portion of the vertebra. Aebli et al.’s follow up study evaluated the value of placing a vent hole in the contralateral pedicle when performing multilevel unipedicular PVP in healthy sheep.96 Placement of the vent hole reduced the amplitude of deterioration in heart rate and mean arterial pressure, and the amount of pulmonary intravascular fat. The fall in blood pressure appears to be due to peripheral vasodilatation resulting from the methylmethacrylate monomer, vasoactive substances released from the bony cavity or fat–platelet aggregations, or a reduction in sympathetic tone.96 Similar decrements in blood pressure and heart rate, and increased fat emboli, occur when wax is injected rather than PMMA during PVP.97 It appears that pressurization of multiple vertebral bodies leads to decreased sympathetic tone and the release of bone marrow contents into the bloodstream, resulting in transient

Complications in neoplastic patients The complication rate increases in patients with malignant compression fractures consequential to the cortical destruction from the neoplastic process. Transient radiculopathy occurs in 3–6% of patients treated with PVP that responds to oral steroids or nonsteroidal antiinflammatory medications.22,71,90 Yet a minority of these patients experience persistent symptoms requiring surgical extraction of foraminal cement.22,23 Infection was reported in just one case of an immunocompromised patient.90 Spinal cord injury due to cement extravasation into the central canal has been reported71,92 but is rare.

Fig. 44.7 Extravasation of acrylic bone cement into the central canal causing central stenosis and cord injury. 502

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hemodynamic abnormalities.96,97 What remains to be determined is the clinical relevance of these findings. Will injecting PMMA into a weakened vertebra lead to similar hemodynamic alterations? In a retrospective review of 142 PVPs performed in 78 patients, no such cardiovascular abnormalities were detected.98 However, one case of transient hypotension during monosegmental PVP has been reported.99 Prudence would call for stringent monitoring of cardiovascular parameters during PVP, especially when performing multiple levels.

Increased incidence of future fractures Augmentation of weakened and fractured vertebrae alters spinal biomechanics. It has been well established that injection of PMMA into osteoporotic vertebral bodies increases their stiffness by 174%, and this effect becomes more pronounced the lower the pre-PVP bone mineral density of the treated vertebra.100 In an osteoporotic cadaveric model, Berlemann et al.101 demonstrated an increase in new vertebral body fractures in the vicinity of a PVP-treated segment compared to fracture occurring in the vicinity of an untreated level. The adjacent cranial segment was invariably injured after PVP, whereas both the cranial and caudal segments were involved adjacent to untreated levels. Lower failure thresholds correlated with increased vertebral filling with cement. The reduced ultimate failure load of a functional spinal unit containing a cemented vertebra may be due to a ‘stress-riser’ effect101 as greater load is transmitted to an adjacent weakened vertebral body via a stiffer vertebral body and an intervening degenerate intervertebral disc. Indeed, clinical studies lend support to an increased risk of a new osteoporotic vertebral compression fracture near a level treated by PVP.59,63,67,102,103 Recently, in 38 patients treated with PVP, Lin et al.102 retrospectively observed new fractures in 58% of vertebral bodies adjacent to an intervertebral disc containing extruded bone cement in contrast to 12% of vertebra adjacent to a disc without cement leakage. Grados et al.59 observed a slight but significantly increased risk of vertebral fracture in the vicinity of a cemented vertebra (odds ratio 2.27, 95% CI 1.1–4.56) compared to a new fracture in the vicinity of an uncemented vertebra (odds ratio 1.44, CI 0.82–2.55). Although these results might be impressive, the methodology was not stellar. It was a retrospective investigation of 40 patients with just 25 available at follow-up. In a larger study, Uppin et al.103 documented 36 new fractures in 177 previously treated osteoporotic patients, 67% of which involved vertebrae adjacent to a previously treated level, and 67% of the new fractures occurred within 30 days after PVP treatment of the initial fracture. Although association does not imply causality, the findings of these studies seem to be logical in that they demonstrate what may occur when increased load is transferred to the anterior vertebral body. Neither article commented whether the patients were prescribed physical therapy for extension-biased spinal stabilization and conditioning. Strong back-extensor muscles reduce vertebral fractures in estrogen-deficient women.33 It is intuitive that such a therapy program would help reduce the incidence of new compression fractures adjacent to PVP-treated fractures. However, prospective, controlled trials must confirm this intuition. Biomechanical models have been constructed to provide confirmatory evidence of altered load bearing in augmented vertebrae.104–106 Geometrically accurate, specimen-specific, three-dimensional computer-simulated finite element models of human vertebrae have been generated from quantitative CT data. By using nonuniform bone density and nonlinear, anistropic trabecular bone material properties, Sun and Liebschner were able to create a computational vertebral body model with realistic stress and strain distributions.104 After calibrating the model for characteristics of osteoporotic vertebrae, the authors applied axial loads to the model before and after treatment with 20% volume fill of PMMA bipedicularly. Regions of high

strains were identified in local areas above and below the virtually implanted PMMA, and these peaks were absent for the untreated model at the same locations. Thus, the load was centered along the longitudinal axes of the injected PMMA, confirming that the rigid PMMA cement acts as an ‘upright pillar’ ‘which amplified the stress applied in their locale.’104 Increased intradiscal pressure ensues due to this stress concentration, causing a significant inward deflection of the adjacent vertebra’s endplate.105 It appears that the shift in load distribution consequent to the PMMA injectate ultimately results in adjacent vertebral fractures.104 The key to minimizing recurrent fractures at adjacent levels may lie in choosing softer bone cement materials without sacrificing strength104 as adjusting the volume or placement of injected cement does not affect load transfer.106

CLINICAL UTILITY AND FUTURE DIRECTIONS OF PERCUTANEOUS VERTEBROPLASTY Almost 330 clinical and basic science studies have been published on the subject of percutaneous vertebroplasty. A large proportion of these studies is retrospective, with unclear indications and nonuniform outcomes, or are editorials and review articles.107 The prospective studies are largely case series with only one including a comparison control group in a nonrandomized fashion. More discussion about this procedure seems to permeate the literature rather than rigorous and sound clinical research methodology.107 Although animal and cadaveric studies can be valuable, extrapolating findings from these studies to those of humans is a calculated leap of faith. Such investigations provide the foundation on which meaningful clinical trials ought to be constructed for determining clinical efficacy.108 The value of descriptive studies such as case series lies in provoking original and clinically relevant thought. Analytic study design, such as a case-control study, cohort study, or randomized trial with an appropriate control group, is necessary to adequately determine the utility of therapeutic interventions, and thoroughly test these hypotheses.108 The evidence underpinning the use of percutaneous vertebroplasty as a definitive treatment for a painful vertebral compression fractures is strongly suggestive, but is not definitive. Progress is underway toward producing investigations that will provide categorical evidence. The utility of computational biomedical models such as outlined by Sun and Liebschner may currently be underappreciated. Such virtual models allow the evaluation of consequences of injecting bone cement into a sophisticatedly calculated vertebral body model, allowing the study of an array of scenarios. Thus, vast knowledge can be gathered about how an intervention will probably behave, and what effects it will have on the physiology of the model’s living counterpart. Once such knowledge is honed, more educated and definitive guidance may be provided regarding technique, complications, bone cement materials such as biodegradable materials, and the role of prophylactic vertebroplasty.104

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49. Liebschner MAK, Rosenberg WS, Keaveny TM. Effects of bone cement volume and distribution on vertebral stiffness after vertebroplasty. Spine 2001; 26(14):1547–1554. 50. Lane JI, Maus TP, Wald JT, et al. Intravertebral clefts opacified during vertebroplasty: pathogenesis, technical implications, and prognostic significance. AJNR 2002; 23:1642–1646. 51. Belkoff SM, Molloy S. Temperature measurement during polymerization of polymethacrylate cement used for vertebroplasty. Spine 2003; 28(14):1555–1559. 52. Togawa D, Bauer TW, Lieberman IH, et al. Histologic evaluation of human vertebral bodies after vertebral augmentation with polymethyl methacrylate. Spine 2003; 28(14):1521–1527. 53. Rami PM, McGraw JK, Heatwole EV, et al. Percutaneous vertebroplasty in the treatment of vertebral body compression fracture secondary to osteogenesis imperfecta. Skeletal Radiol 2002; 31:162–165. 54. Gaughen JR, Jensen ME, Schweickert PA, et al. The therapeutic benefit of repeat percutaneous vertebroplasty at previously treated vertebral levels. AJNR 2002; 23:1657–1661. 55. Jang JS, Kim DY, Lee SH. Efficacy of percutaneous vertebroplasty in the treatment of intravertebral pseudoarthrosis associated with noninfected avascular necrosis of the vertebral body. Spine 2003; 28(14):1588–1592. 56. Deramond H, Derpriester C, Galibert P, et al. Percutaneous vertebroplasty with polymethylmethacrylate: technique, indications, and results. Radiol Clin North Am 1998; 36:533–546. 57. Peh WCG, Gilula LA, Peck DD. Percutaneous vertebroplasty for severe osteoporotic vertebral body compression fractures. Radiology 2002; 223:121–126. 58. Evans AJ, Jensen ME, Kip KE, et al. Vertebral compression fractures: pain reduction and improvement in functional mobility after percutaneous polymethylmethacrylate vertebroplasty. A retrospective report of 245 cases. Radiology 2003; 226(2): 366–372.

Section 2: Osseous Spinal Tumors 59. Grados F, Depriester C, Cayrolle G, et al. Long-term observations of vertebral osteoporotic fractures treated by percutaneous vertebroplasty. Rheumatology 2000; 39(12):1410–1414. 60. Barr JD, Barr MS, Lemley TJ, et al. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine 2000; 25(8):923–928. 61. Martin JB, Jean B, Sugiu K, et al. Vertebroplasty: clinical experience and follow-up results. Bone 1999; 25(2):11S–15S. 62. Gangi A, Kastler BA, Dietman JL. Percutaneous vertebroplasty guided by a combination of CT and fluoroscopy. Am J Neuroradiol 1994; 15:83–86. 63. Cyteval C, Sarrabere MP, Roux JO, et al. Acute osteoporotic vertebral collapse: open study on percutaneous injection of acrylic surgical cement in 20 patients. Am J Roetgenol 1999; 173:1685–1690. 64. Peters KR, Guiot BH, Martin PA, et al. Vertebroplasty for osteoporotic compression fractures: current practice and evolving techniques. Neurosurgery 2002; 51(5)Suppl 2:S2096–S2103. 65. McGraw JK, Lippert JA, Minkus KD, et al. Prospective evaluation of pain relief in 100 patients undergoing percutaneous vertebroplasty: results and follow-up. J Vasc Interv Radiol 2002; 13(9):883–886. 66. Cortet B, Cotton A, Boutry N, et al. Percutaneous vertebroplasty in the treatment of osteoporotic vertebral compression fractures: an open prospective study. J Rheumatol 1999; 26:2222–2228. 67. Zoarski GH, Snow P, Olan WJ, et al. Percutaneous vertebroplasty for osteoporotic compression fractures: quantitative prospective evaluation of long-term outcomes. J Vasc Interv Radiol 2002; 13:139–148. 68. Perez-Higueras A, Alvarez L, Rossi RE, et al. Percutaneous vertebroplasty: long-term clinical and radiological outcome. Neuroradiology 2002; 44:950–954. 69. Diamond TH, Champion B, Clark WA. Management of acute osteoporotic vertebral fractures: a nonrandomized trial comparing percutaneous vertebroplasty with conservative therapy. Am J Med 2003; 114(4):257–265. 70. Kaemmerlen P, Thiesse P, Jonas P, et al. Percutaneous injection of orthopaedic cement in metastatic vertebral lesion [letter]. N Engl J Med 1989; 321:121. 71. Deramond H, Depriester C, Galibert P, et al. Percutaneous vertebroplasty with polymethylmethacrylate: technique, indications and results. Radiol Clin North Am 1998; 36:533–546. 72. Jensen M, Kallmes D. Percutaneous vertebroplasty in the treatment of malignant spine disease. Cancer J 2002; 8(2):194–206. 73. Kaufmann TJ, Jensen ME, Schweickert PA, et al. Age of fracture and clinical outcomes of percutaneous vertebroplasty. Am J Neuroradiol 2001; 22:1860–1863. 74. Brown DB, Gilula LA, Sehgal M, et al. Treatment of chronic symptomatic vertebral compression fractures with percutaneous vertebroplasty. Am J Roentgenol 2004; 182:319–322.

84. Laredo JD, Assouline E, Gelbert F, et al. Vertebral hemangiomas: fat content as a sign of aggressiveness. Radiology 1990; 177:467–472. 85. Laredo JD, Reizine D, Bard M, et al. Vertebral hemangiomas: radiologic evaluation. Radiology 1986; 161:183–189. 86. Peh WCG, Gelbart MS, Gilula LA, et al. Percutaneous vertebroplasty: treatment of painful vertebral compression fractures with intraosseous vacuum phenomena. Am J Roentgenol 2003; 180:1411–1417. 87. Harrington KD. Major neurological complications following percutaneous vertebroplasty with polymethylmethacrylate: a case report. J Bone Joint Surg [Am] 2001; 83:1070–1073. 88. Wenger M, Markwalder TM. Surgically controlled, transpedicular methylmethacrylate vertebroplasty with fluoroscopic guidance. Acta Neurochir 1999; 141:625–631. 89. Lee BJ, Lee SR, Yoo TY. Paraplegia as a complication of percutaneous vertebroplasty with polymethylmethacrylate: a case report. Spine 2002; 27(19):E419–E422. 90. Chiras J, Depriester C, Weill A, et al. Vertebroplasties percutanees: technique et indications. J Neuroradiol 1997; 24;45–59. 91. Padovani B, Kasriel O, Brunner P, et al. Pulmonary embolism caused by acrylic cement: a rare complication of percutaneous vertebroplasty. Am J Neuroradiol 1999; 20:375–377. 92. Ratliff J, Nguyen T, Heiss J. Root and spinal cord compression from methylmethacrylate vertebroplasty. Spine 2001; 26(13):E300–E302. 93. Jang JS, Lee SH, Jung SK. Pulmonary embolism of polymethylmethacrylate after percutaneous vertebroplasty. A report of three cases. Spine 2002; 27(19): E416–E418. 94. Philips H, Cole PV, Lettin AWF. Cardiovascular effects of implanted acrylic cement. Br Med J 1971; 3:460–461. 95. Aebli N, Krebs J, Davis G, et al. Fat embolism and acute hypotension during vertebroplasty. An experimental study in sheep. Spine 2002; 27(5):460–466. 96. Aebli N, Krebs J, Schwenke D, et al. Cardiovascular changes during multiple vertebroplasty with and without vent-hole. An experimental study in sheep. Spine 2003; 28(14):1504–1512. 97. Aebli N, Krebs J, Schwenke D, et al. Pressurization of vertebral bodies during vertebroplasty causes cardiovascular complications. An experimental study in sheep. Spine 2003; 28(14):1513–1520. 98. Kaufmann TJ, Jensen ME, Ford G, et al. Cardiovascular effects of polymethylmethacrylate use in percutaneous vertebroplasty. Am J Neuroradiol 2002; 23:601–604. 99. Vasconcelos C, Philippe G, Martin JB, et al. Transient hypotension induced by polymethylmethacrylate injection during percutaneous vertebroplasty [letter]. J Vasc Rad 2001; 12(8):1001–1002.

75. Jensen ME, Dion JE. Vertebroplasty relieves osteoporosis pain. Diagn Imaging 1997; 19:68,71–72.

100. Heini PF, Berlemann U, Kaufmann M, et al. Augmentation of mechanical properties in osteoporotic vertebral bones – a biomechanical investigation of vertebroplasty efficacy with different bone cements. Eur Spine J 2001; 10(2):164–171.

76. Lyles KW, Gold DT, Shipp KM, et al. Association of osteoporotic vertebral compression fractures with impaired functional status. Am J Med 1993; 94:595–601.

101. Berlemann U, Ferguson SJ, Nolte LP, et al. Adjacent vertebral failure after vertebroplasty. A biomechanical investigation. J Bone Joint Surg [Br] 2002; 84:748–752.

77. Kanis JA, Johnell O. The burden of osteoporosis. J Endocrinol Invest 1999; 22:583–588.

102. Lin EP, Ekholm S, Hiwatashi A, et al. Vertebroplasty: cement leakage into the disc increases the risk of new fracture of adjacent vertebral body. Am J Neuroradiol 2004; 25:175–180.

78. Ross PD, Ettinger B, Davis JW, et al. Evaluation of adverse health outcomes associated with vertebral fractures. Osteoporosis Int 1991; 1:134–140. 79. Cooper C, Atkinson EJ, Jacobsen SJ, et al. Population-based study of survival after osteoporotic fractures. Am J Epidemiol 1993; 137:1001–1005. 80. Feydy A, Cognard C, Miaux Y, et al. Acrylic vertebroplasty in symptomatic cervical vertebral haemangiomas: report of 2 cases. Neuroradiology 1996; 38: 389–391. 81. Cotten A, Deramond H, Cortet B, et al. Preoperative percutaneous injection of methyl methacrylate and n-butyl cyanoacrylate in vertebral hemangiomas. Am J Neuroradiol 1996; 17:137–142. 82. Ide C, Gangi A, Rimmelin A, et al. Vertebral haemangiomas with spinal cord compression: the place of preoperative percutaneous vertebroplasty with methyl methacrylate. Neuroradiology 1996; 38:585–589. 83. Cortet B, Cotton A, Deprez X, et al. Vertebroplasty with surgical decompression for the treatment of aggressive vertebral hemangiomas. A report of three cases. Rev Rhum Ed Fr 1994; 61(1):14–20.

103. Uppin AA, Hirsch JA, Centenera LV, et al. Occurrence of new vertebral body fracture after percutaneous vertebroplasty in patients with osteoporosis. Radiology 2003; 226:119–124. 104. Sun K, Liebschner AK. Evolution of vertebroplasty: a biomechanical perspective. Ann Biomed Eng 2004; 32(1):77–91. 105. Baroud GJ, Nemes J, Heini P, et al. Load shift of the intervertebral disc after vertebroplasty: a finite-element study. Eur Spine J 2003; 12(4):421–426. 106. Polikeit A, Nolte LP, Ferguson SJ. The effect of cement augmentation on the load transfer in an osteoporotic functional spinal unit. Finite-element analysis. Spine 2003; 28(10):991–996. 107. Mirza SK. Point of view. Cardiovascular changes during multiple vertebroplasty with and without vent-hole. An experimental study in sheep. Spine 2003; 28(14):1521–1522. 108. Jarvik JG, Kallmes DF, Mirza SK. Vertebroplasty – learning more, but not enough. Spine 2003; 28(14):1487–1489.

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SPECIFIC DISORDERS

Section 2

Osseous Spinal Tumors ■ ii: Treatment

CHAPTER

Kyphoplasty

45

Daisuke Togawa and Isador H. Lieberman

INTRODUCTION The National Osteoporosis Foundation estimates that over 100 million people worldwide, and nearly 30 million in the United States, are at risk to develop fragility fractures secondly to osteoporosis. In the United States there are an estimated 700 000 pathological vertebral body compression fractures each year, of which over one-third become chronically painful (Fig. 45.1).1,2 Although the standard of care for most other fragility fractures including hip and wrist fractures is immediate reduction and stabilization, vertebral body compression fractures are traditionally treated with medical modalities and only rarely treated with surgical modalities (Fig. 45.2). This benign neglect arose because open surgical repair of these fractures was too invasive, with poor outcomes. Unfortunately, the medical management of painful fractures (bed rest, hospitalization, narcotic analgesics, and bracing) does nothing to restore spinal alignment and may compound the problem. Just as unfortunate and due to its

inherent risks, invasive nature, and the poor quality of osteoporotic bone, surgical treatment of vertebral body compression fractures has traditionally been limited to cases where there is concurrent spinal instability or neurologic deficit. In response to the limited results of medical and surgical modalities, to stabilize and strengthen the collapsed vertebral bodies, interventional neuroradiologists, first in France and now the US, initiated percutaneous bone cement injections.3,4 Direct cement injection or ‘vertebroplasty’ has been shown to reduce fracture pain. Vertebroplasty, however, does not address the spinal deformity. Also, this technique requires a forced cement injection using low-viscosity, slow-curing cement, thus increasing the risk of cement leaks through the fracture clefts or the venous sinuses. ‘Kyphoplasty’ is a minimally invasive technique for the treatment of osteoporotic or osteolytic painful progressive vertebral wedge compression fractures (VCFs). This technique has a number of ben-

Vertebral compression fracture (wedge or biconcave configuration) • painful • progressive Diagnostic work-up 1 X-ray 2 MRI 3 DEXA

DEXA score <– 2 SD *1

Primary osteoporosis

Myeloma

Secondary osteoporosis

Kyphoplasty of index levels *2

Kyphoplasty of index and risk levels *3

DEXA score > – 1 SD *1 Infection Burst configuration Posterior wall deficient Bleeding diathesis Neurological

Metastases

Osteolytic

Osteosclerotic and collapse

Kyphoplasty

To rule out infection, malignancy, or other metabolic bone diseases

Matrix producing tumor

Appropriate treatment for pathology

Possible kyphoplasty later

*1 cases with DEXA between –1 and –2 should be evaluated on individual basis *2 index level: clinically painful and verified acute or subacute fracture on MRI or chronic pseudarthrosis with cleft on X-ray and MRI *3at risk level: thoracolumbar junction (T11, T12, L1, L2) or thoracic apex (T6, T7, T8)

Fig. 45.1 Flow chart for treatment of vertebral compression fractures. 507

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A

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Fig. 45.2 Patient (A) and operating room (B) set-up.

efits and potential advantages over traditional medical and surgical treatment modalities for VCFs. It involves the introduction of a cannula into the vertebral body, followed by insertion of an inflatable bone tamp (IBT) designed to elevate the endplates and reduce the vertebral body back towards its original height, while creating a cavity to be filled with bone cement (Fig. 45.3). By reducing the vertebral body back towards its native height the sagittal alignment of the spine is restored, providing patients with cosmetic and functional improvement.5–7 This also acts to potentially protect other levels from collapse by alleviating the force transmission associated with a kyphotic posture.8,9 By creating a cavity the cement augmentation is performed with more control by depositing into the preformed cavity partially cured cement, thereby reducing the risk of cement extravasation. By stabilizing the vertebral body, pain from the progressive fracture collapse or altered biomechanics can be minimized or even eliminated. The first kyphoplasty was performed in August, 1998, and up to January, 2004, over 30 000 patients in the United States have had kyphoplasty procedures for over 40 000 fractures.

A

In preliminary reports well over 90% of patients attained significant pain relief. The data from the recent published reports also indicate that kyphoplasty has a significant positive effect on spinal malalignment and patient quality of life.5–7

INDICATIONS Kyphoplasty is currently indicated for progressive, painful osteoporotic or osteolytic vertebral body wedge compression fractures. Similar to any other fragility fracture the goals are to restore stability, anatomical alignment, and function as soon as safely possible. Even though the quoted natural history of vertebral compression fractures is for two-thirds of the patients to eventually become pain free, one must appreciate that not one of those vertebral bodies ever regains its normal height, and that the presence of a vertebral collapse predicts both increased mortality and a fivefold increase in further fractures at adjacent or remote levels within 1 year.10–12 If one subscribes to the philosophies of spinal biomechanics and appreciates that ‘kyphosis

B

Fig. 45.3 Fracture reduction using the inflatable bone tamp and cement deposition.

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Section 2: Osseous Spinal Tumors

begets kyphosis,’ especially in the face of low bone density, then it only makes sense to intervene before the deformity progresses significantly, in order to minimize the effects of sagittal imbalance on the spine. Pain relief then becomes the secondary indication and protection of sagittal spinal alignment becomes the primary indication. The results of vertebral augmentation seem most predictable with immediate intervention.

CONTRAINDICATIONS The contraindications to kyphoplasty include locally active osteomyelitis or any systemic pathology such as sepsis, prolonged bleeding times, or other cardiopulmonary pathology, which would preclude the safe completion of the procedure under either conscious sedation or general anesthesia. Osteoblastic or matrix-producing vertebral metastases are also contraindications to kyphoplasty. Other relative contraindications include nonosteolytic infiltrative spinal metastases, vertebral bodies with deficient posterior cortices, burst fracture configurations, or patients presenting with neurological signs or symptoms. The use of inflatable bone tamp to create a cavity in physiologically normal bone has not yet been documented, and normal bone should be considered a contraindication. Vertebra plana fracture configurations may be technically difficult, and fracture geometries limiting vertebral body access are also contraindications. The feasibility of using an inflatable bone tamp under these circumstances should be assessed on a case by case basis. The sagittal and axial CT and MRI scans are particularly important to plan the trajectory for the percutaneous procedure. Suboptimal intraoperative radiographic visualization of the fracture is undesirable and kyphoplasty should not be performed in such an environment.

CONTROVERSIES There exists a certain level of debate regarding the number of levels to augment and the indication for prophylaxis in the setting of vertebral compression fractures. Vertebroplasty proponents are more liberal in recommending multiple levels at any one time. One must, however, consider the volume of cement and the potential for monomer toxicity. It is well established that cement monomer is arrythmogenic and cardiotoxic at the volumes used for a total hip or knee replacement. The risk appears to be somewhere in the neighborhood of 1 in 3000 to 1 in 5000.13,14 Taking into account the volume of cement (6 cc per level) and the direct access to the cardiovascular system, and then assuming one is willing to accept the same degree of risk, then it seems most appropriate to limit vertebroplasty or kyphoplasty to one or two levels at any surgical setting. Kyphoplasty does have a built-in advantage to vertebroplasty in that the technique dictates a thicker partially cured cement be poured into the cavity in a controlled fashion rather than a highly liquid cement forced into the closed space of the collapsed vertebral body. The liquid cement of vertebroplasty has more free monomer available to enter the circulation and the liquid cement will obey the laws of fluid dynamics seeking out the path of least resistance, thus readily entering the venous sinuses or exiting through the vertebral body fissures and cracks, resulting in more cement leaks.

COST Many patients who have osteoporotic fractures have concomitant medical comorbidities common to an older age group. Thus, it is difficult to assess the economic impact of these fractures separately from that of other problems. Vertebroplasty has the advantage of being a relatively less expensive procedure because no inflatable bone tamps are used. Kyphoplasty is associated with increased cost but offers the potential to improve spinal alignment that may provide

better pulmonary mechanics and reduce the risk of adjacent-level collapse. The cost should be considered through a long-term followup study, analyzing economic and clinical risk to benefit ratios.

EVIDENCE-BASED OUTCOMES In the authors’ ongoing Institutional Review Board approved study,5–7 over 900 consecutive kyphoplasty procedures were performed in over 300 patients between April, 1999, and February, 2004. The mean age was 69 years (range 35–89). The mean duration of symptoms was 7 months. Outcome data were obtained by administering the Short Form-36 health survey (SF-36) and visual analog scale (VAS) for pain rating; additionally, the patients underwent detailed neurological and radiographical examinations pre- and postoperatively (Fig. 45.4). Perioperative and clinical follow-up revealed that the procedure was well tolerated with improvement in pain and early mobilization. The levels treated ranged from T3 to L5 with 47% of the vertebrae at thoracolumbar junction. Length of stay ranged from 0.5 day to 9 days (mean 1.1 day). In the experience of the authors there were no clinically significant cement leaks and no perioperative complications attributable to the inflatable bone tamp or tools. Pre- and postoperative SF-36 data are available on over 230 patients (72%) with follow-up ranging from 1 week to 59 months (mean 14 months). SF-36 scores improved in every category, statistically significant in all but the general health modality. Physical function improved from 22.0 to 36.0 ( p=0.0001). Role physical improved from 9.3 to 27.3 ( p=0.0001). Bodily pain improved from 22.4 to 41.9 ( p=0.0001). Vitality improved from 31.4 to 40.7 ( p=0.0001). Social function improved from 37.7 to 61.2 ( p=0.0001). Role emotional improved from 54.8 to 65.5 ( p=0.030). Mental health improved from 63.1 to 68.0 ( p<0.001). General health was unchanged from 51.3 to 49.2 ( p=0.067). The VAS scores improved from a preoperative level of 7.0 to an initial postoperative level of 3.2 ( p<0.0001). At last followup examination, the value remained unchanged at 3.4 ( p<0.0001). With regard to height restoration, a mean vertebral body height restoration of 46.8% (midline measurement) in 70% of 70 treated levels was reported in the initial study.7 Garfin et al. reported in a prospective multicenter series that the average anterior and midline height were 83±14% and 76±14% before treatment, respectively, that were increased to 99±13% and

90

Preoperation Latest follow-up SF-36 agematched control

80 70 60 50 40 30 20 10 0

VAS Osw PF

RP

BP GH

V

SF

RE MH

SF-36 Fig. 45.4 Short Form-36 health survey (SF-36) and visual analog scale (VAS) for pain rating (VAS, visual analogue pain score; Osw, Oswestry disability index; PF, physical function; RP, role physical; BP, bodily pain; GH, general health; V, vitality; SF, social function; RE, role emotional; MH, mental health). 509

Part 3: Specific Disorders

92±11% after the treatment, respectively. In vertebral bodies with 15% or more of the estimated height lost, the average anterior and midline height were 68±12% and 64±13% before treatment, respectively, that improved to 84±14% and 90±12% after the treatment, respectively.15 Ledlie et al. reported functional and radiographic outcomes in their first 96 kyphoplasty patients with 133 fractures.16 Their followup period was a minimum of 12 months and the mean patient age at the time of surgery was 76 years (range 51–93). With regard to pain as rated by the patient using a 10-point VAS, the mean score was decreased to 1.4 at the 1-year follow-up, while the mean preoperative VAS score was 8.6. Ambulatory status was also improved postoperatively. Over 90% of the patients (27/29, with 1-year follow-up) were ambulatory at 1 year, while only 35% of the patients (28/79) were ambulatory preoperatively. In this study vertebral body height restoration was reported from radiographic measures of anterior and midline points of the fractured vertebrae using the two nearest normal vertebrae as reference points. At 1 year, the anterior vertebral height was 85% of the predicted height and midline height was 89%, while their preoperative heights were 66% and 65%, respectively.16 Phillips et al. also recently reported their early radiographic and clinical results of kyphoplasty17 In this study, 29 patients with 61 fractures between T6 to L5 were evaluated. The mean age of these 29 patients was 70 years. Their clinical information including pain relief, improvement in activity, and satisfaction with the surgical procedure as well as their sagittal spinal alignment on the standing radiographs were assessed and followed up to 1 year. Average pain scores were significantly decreased to 2.6 and 0.6, at 1 week and 1 year, respectively, while average pain score was 8.6 preoperatively. Local kyphosis was improved by a mean of 14 degrees in patients with reducible fractures.17

COMPLICATIONS In the authors’ series of patients,5,7 cement extravasation was seen in less than 10% of cases. No problems were identified clinically immediately after surgery or at final follow-up as a result of these extravasations. In one patient a myocardial infarction occurred as a result of fluid overload during the procedure. In a separate prospective multicenter series reported by Garfin and Reilley, there were six major complications out of 600 cases associated with the kyphoplasty procedure. Four of these were neurologic complications (0.75%).18 These were directly attributable to surgeon error and breach of technique. To date, no reports of primary or secondary infection of the cement mantle have been published. In the authors’ series of over 300 patients there were no primary infections. There was, however, one hematogenous infections 2 years after the kyphoplasty in a patient receiving multiple blood and platelet transfusions for Waldenström’s macroglobulinemia. Ledlie et al. reported that asymptomatic cement leaks were noted in 9% of vertebral bodies treated, but no device- or procedure-related complications were reported.16 Phillips et al. reported that asymptomatic cement leaks were observed in 6 of 61 vertebral fractures (9.8%).17 In this series as well there were no clinical consequences attributable to the bone tamp or cement deposition.

BIOPSY RESULTS A diagnostic bone biopsy can be easily performed during a kyphoplasty procedure and does not affect the safety of the procedure if done appropriately (Fig. 45.5). The authors histologically evaluated 178 biopsies obtained from 142 patients during 246 kyphoplasty procedures. These

A

B

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D

E

F

Fig. 45.5 Biopsy performed during kyphoplasty. (A) Anteroposterior X-ray. (B) Biopsy trephine (lateral X-ray). (C) Pituitary Rongeur (lareral X-ray). (D) Biopsy specimen. (E) Low-magnification photomicrograph of the biopsy specimen (hematoxylin and eosin stain). (F) Common histologic appearance of the biopsy. Most of the biopsy shows partially necrotic bone (NB) as well as hematopoietic spaces (H). Most of bone in this area is viable (× 100, hematoxylin and eosin stain). 510

Section 2: Osseous Spinal Tumors

showed partially necrotic fragments of bone as well as areas of fibrosis and variable stages of woven bone, suggesting ongoing fracture healing.19 The specimens obtained from 30 patients (21%) showed marked increased osteoid in undecalcified sections. These thickened osteoid seams may suggest possible mineralization defect (osteomalacia). Osteoid can be increased either because of increased bone remodeling activity or because of a mineralization defect. Tetracycline labeling is the method of choice to distinguish between these two diagnoses. Careful administration of tetracycline labels may help identify any correlation between vertebral fracture and osteomalacia. Also in this series, the biopsies of 4 patients provided a definite diagnosis of plasma cell dyscrasia in otherwise unsuspected or unknown spinal lesions. These findings suggest that a biopsy is useful for all initial vertebral augmentation cases to rule out any occult lesions.

HISTOLOGY OF HUMAN RETRIEVED SPECIMENS In spite of reported good clinical results, several aspects of the kyphoplasty procedure are controversial, including the optimum methods of mixing and depositing the cement, the potential importance of a foreign body reaction at the cement–bone interface, efficacy of bone tamp usage, the use of relatively high concentrations of radiopaque agents and antibiotics in the cement, and the clinical indications for the procedure. The authors were able to document histologically four vertebral bodies from two cases 1 month and 2 years after cement augmentation, after a surgical corpectomy and at an autopsy (Fig. 45.6).20 In this study the histology of vertebrae treated using the kyphoplasty technique revealed a dense cancellous shell around the cement mantle. This suggests that the tamping had displaced bone, essentially autografting the space around the cement. Bone immediately around the cement did not show extensive necrosis. However, foreign body giant cells contained material consistent with cement particles and/or

A

C

barium sulfate. Particles were also identified within vascular spaces. Further histologic evaluation may help clarify the safety and efficacy of kyphoplasty.

INCIDENCE OF ADJACENT AND REMOTE FRACTURES One issue continuously raised by spine practitioners regards the incidence of remote and adjacent-level vertebral compression fractures after an index vertebral compression fracture has been augmented by either vertebroplasty or kyphoplasty. Keller et al. investigated the biomechanics of age-related spinal deformity using a sagittal plane finite element analysis model and showed that postural forces were responsible for initiation and propagation of osteoporotic spinal deformity in the elderly.21 Kayanja et al. reported their results of biomechanical tests for cadaveric thoracic wedge compression fractures and showed that anterior cortical strain was concentrated at the apex of a thoracic kyphotic curve and the vertebral body immediately above it had the next highest strain with an increased risk of secondary fracture.22 Moreover, Hasserius et al. reported a Swedish cohort, in a 10-year population based study of 598 individuals, and suggested a prevalent vertebral deformity could predict both increased mortality and increased fracture incidence during the following decade in both men and women.12 Left untreated, the incidence of subsequent vertebral fracture after an index fracture is reported in other studies as approximately 20%.10,11 From the vertebroplasty literature, only one study reported a 52% rate of remote or adjacent level fractures after vertebroplasty.23 From the kyphoplasty literature, Harrop et al. reported that the incidence of postkyphoplasty vertebral compression fracture in the primary osteoporotic patients was 11.25% (9 fractures/80 patients), while the incidence in the steroid-induced osteoporotic patients was 48.6 % (17 fractures/35 patients).9

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D

Fig. 45.6 Histology of human retrieval after kyphoplasty. (A) L2 specimen from surgical excision. (B) T8 specimen from autopsy. (C) Phagocytosis by macrophages (CP, cement particles, × 400, hematoxylin and eosin stain) (D) Cement particles within vascular spaces (CP, cement particles, × 200, hematoxylin and eosin stain). 511

Part 3: Specific Disorders

The above results imply that the intervention, kyphoplasty, in primary osteoporotic patients may not increase the rate of remote or adjacent level fractures compared to the published natural history reports. These results also imply that the secondary osteoporotic patients are in fact at increased risk compared to primary osteoporotic patients for subsequent vertebral compression fractures although there is no natural history benchmark to which this rate can be compared.

KYPHOPLASTY FOR MULTIPLE MYELOMA Multiple myeloma is a monoclonal proliferation of malignant plasma cells that usually affects the bone marrow. Excessive bone resorption due to an increase of proinflammatory cytokines is a characteristic feature of the disease.24 Grossly, this tumor is a very soft vascular tumor, as evidenced by the backflow of blood from the working cannulae during kyphoplasty. The near-fluid consistency of the tumor and the lytic nature of the bone make it easy for the inflatable bone tamp to displace tissue in the act of reducing the fracture and creating the cavity. This then results in impressive cement filling of the vertebra. Dudeney et al. reported satisfying results in the treatment of osteolytic vertebral compression fractures due to multiple myeloma.6 As of February, 2004, the authors treated 80 myeloma patients using the kyphoplasty method. The mean age of patients was 60.6 (range 35–82) years. There were no major complications related directly to use of this technique. Pre- and postoperative SF-36 data were available on 61 patients (75.3%) with follow-up ranging from 6 weeks to 59 months (mean 15.6 months). Significant improvement in SF-36 scores occurred for bodily pain: 23.0 to 44.4 (p<0.0001) and physical function: 25.5 to 36.6 (p=0.034), vitality: 30.3 to 38.1 (p=0.039), and social function: 35.4 to 67.5 (p=0.0002). Mental health improved from 60.3 to 66.2 (p=0.0009). Role emotional was unchanged from 54.6 to 63.0 (p=0.086). General health was unchanged from 51.2 to 49.0 (p=0.084). These results suggest that the kyphoplasty technique is efficacious in the treatment of osteolytic vertebral compression fractures due to multiple myeloma, and associated with early clinical improvement of pain and function as well as some restoration of vertebral body height in these patients. The effects of potential tumor dissemination, in what is already widespread disease, is not known. Significant systemic effects are not suspected and have not been noted by the authors in this initial group.6,25

KYPHOPLASTY FOR SPINAL METASTASES In an ongoing evaluation of kyphoplasty for spinal metastases, the results have remained very favorable.25 From April, 1999, to February, 2004, the authors treated 21 patients of spinal metastases (9 breast, 4 leukemia/lymphoma, 3 lung, 5 unknown origin). All patients had painful compression fractures secondary to a metastatic lesion to the spine. The kyphoplasty procedure was successfully performed in all 21 patients. The perioperative and clinical follow-up revealed that the procedure was well tolerated with improvement in pain and early mobilization. Pre- and postoperative SF-36 data were available on 14 patients (66.7 %) with follow-up ranging from 3 weeks to 206 weeks (mean 44.9 weeks). Physical function improved from 20.9 to 33.5 ( p=0.036). Vitality improved from 31.2 to 42.9 ( p=0.012). Social function improved from 37.5 to 66.1 ( p=0.011). Role physical improved from 12.5 to 19.6 ( p=0.59). Bodily pain improved from 31.6 to 39.0 ( p=0.24). Mental health improved from 60.0 to 62.0 ( p=0.69). Role emotional decreased from 55.6 to 51.3 ( p=0.77). General health decreased from 52.1 to 46.0 ( p=0.73). The VAS improved from 6.5 to 3.9 ( p=0.15).

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Barr et al. reported their results with osteolytic metastatic vertebral collapse in eight patients and revealed that only four patients experienced any pain relief. In this group of patients there was a 6% complication rate.26 Fourney et al. reported their results of vertebroplasty and/or kyphoplasty for painful vertebral body fractures in cancer patients.27 Asymptomatic cement leakage occurred during vertebroplasty at 6 (9.2%) of 65 levels, while no cement extravasation was seen during kyphoplasty in this study. The mean percentage of restored vertebral body height by kyphoplasty was 42±21%. Other solid organ or matrix-producing tumors and previously irradiated tumors may not be as compliant to the inflatable bone tamp while reducing the fracture or creating a cavity. In this situation some form of tumor evacuation or ablation may need to be performed prior to the vertebral augmentation. Further investigation into various modalities of treatment need to be completed before a definitive recommendation on indications in other tumor types can be made.

CONCLUSIONS Vertebral augmentations by kyphoplasty, according to the early studies, are an effective treatment for painful, progressive osteoporotic compression fractures. By creating a cavity and realigning the sagittal contour of the vertebral body, kyphoplasty has significant advantages over vertebroplasty. Kyphoplasty also minimizes the risk of cement leakage by compacting the cancellous bone to the periphery and sealing off the fracture clefts, and by creating a cavity into which cement is poured as opposed to injected under pressure. This technique may prevent propagation of further fractures by reducing the collapsed vertebral bodies toward its native height and thus normalizing force transmission and sagittal spinal alignment. This technique has proven to be valuable and, with future developments, other techniques may also evolve.

References 1. Cooper C, Atkinson EJ, O’Fallon WM. et al. Incidence of clinically diagnosed vertebral fractures: a population-based study in Rochester, Minnesota, 1985–1989. J Bone Miner Res 1992; 7:221–227. 2. Riggs BL, Melton LJ 3rd. The worldwide problem of osteoporosis: insights afforded by epidemiology. Bone 1995; 17:505S–511S. 3. Galibert P, Deramond H, Rosat P, et al. [Preliminary note on the treatment of vertebral angioma by percutaneous acrylic vertebroplasty]. Neurochirurgie 1987; 33:166–168. 4. Jensen ME, Evans AJ, Mathis JM, et al. Percutaneous polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral body compression fractures: technical aspects. Am J Neuroradiol 1997; 18:1897–1904. 5. Coumans JV, Reinhardt MK, Lieberman IH. Kyphoplasty for vertebral compression fractures: 1-year clinical outcomes from a prospective study. J Neurosurg 2003; 99:44–50. 6. Dudeney S, Lieberman IH, Reinhardt MK, et al. Kyphoplasty in the treatment of osteolytic vertebral compression fractures as a result of multiple myeloma. J Clin Oncol 2002; 20:2382–2387. 7. Lieberman IH, Dudeney S, Reinhardt MK, et al. Initial outcome and efficacy of ‘kyphoplasty’ in the treatment of painful osteoporotic vertebral compression fractures. Spine 2001; 26:1631–1638. 8. Kayanja MM, Ferrara LA, Lieberman IH. Distribution of anterior cortical shear strain after a thoracic wedge compression fracture. Spine J 2004; 4:76–87. 9. Harrop JS, Prpa B, Reinhardt MK, et al. Primary and secondary osteoporosis’s incidence of subsequent vertebral compression fractures after kyphoplasty. Spine 2004; 29:2102–2105. 10. Lindsay R, Silverman SL, Cooper C, et al. Risk of new vertebral fracture in the year following a fracture. JAMA 2001; 285:320–323. 11. Silverman SL. The clinical consequences of vertebral compression fracture. Bone 1992; 13(Suppl 2):S27–S31. 12. Hasserius R, Karlsson MK, Nilsson BE, et al. Prevalent vertebral deformities predict increased mortality and increased fracture rate in both men and women: a 10-year

Section 2: Osseous Spinal Tumors population-based study of 598 individuals from the Swedish cohort in the European Vertebral Osteoporosis Study. Osteoporos Int 2003; 14:61–68. 13. Charnley J. Systemic effects of monomer. In: Acrylic cement in orthopaedic surgery. London: E. & S. Livingstone; 1970:72–78. 14. Coventry MB, BeckenBaugh RD, Nolan DR, et al. 2,012 total hip arthroplasties: A study of postoperative course and early complications. J Bone Joint Surg Am 1974; 56:273–284.

20. Togawa D, Bauer TW, Lieberman IH, et al. Histological evaluation of human vertebral bodies after vertebral augmentation with polymethyl methacrylate. Spine 2003; 28:1521–1527. 21. Keller TS, Harrison DE, Colloca CJ, et al. Prediction of osteoporotic spinal deformity. Spine 2003; 28:455–462. 22. Kayanja MM, Ferrara LA, Lieberman IH. Distribution of anterior cortical shear strain after a thoracic wedge compression fracture. Spine J 2004; 4:76–87.

15. Garfin SR, Yuan HA, Reiley MA. New technologies in spine: kyphoplasty and vertebroplasty for the treatment of painful osteoporotic compression fractures. Spine 2001; 26:1511–1515.

23. Grados F, Depriester C, Cayrolle G, et al. Long-term observations of vertebral osteoporotic fractures treated by percutaneous vertebroplasty. Rheumatology (Oxford) 2000; 39:1410–1414.

16. Ledlie JT, Renfro M. Balloon kyphoplasty: one-year outcomes in vertebral body height restoration, chronic pain, and activity levels. J Neurosurg 2003; 98: 36–42.

24. Lecouvet FE, Vande Berg BC, Maldague BE, et al. Vertebral compression fractures in multiple myeloma. Part I. Distribution and appearance at MR imaging. Radiology 1997; 204:195–199.

17. Phillips FM, Ho E, Campbell-Hupp M, et al. Early radiographic and clinical results of balloon kyphoplasty for the treatment of osteoporotic vertebral compression fractures. Spine 2003; 28:2260–2265.

25. Lieberman I, Reinhardt MK. Vertebroplasty and kyphoplasty for osteolytic vertebral collapse. Clin Orthop 2003; Supplement 415:S176–186.

18. Garfin SR, Reilley MA. Minimally invasive treatment of osteoporotic vertebral body compression fractures. Spine J 2002; 2:76–80. 19. Togawa D, Bauer TW, Lieberman IH, et al. Occult osteomalacia and myeloma in patients with osteoporotic compression fractures. Eur Spine J 2003; 12:S3.

26. Barr JD, Barr MS, Lemley TJ, et al. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine 2000; 25:923–928. 27. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful vertebral body fractures in cancer patients. J Neurosurg 2003; 98:21–30.

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PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ i: Anatomy and Assessment

CHAPTER

Developmental and Functional Anatomy of the Cervical Spine

46

Russell V. Gilchrist

INTRODUCTION A thorough knowledge of human anatomy continues to be the cornerstone for all diagnosis and treatment planning. This awareness allows spine physicians to rise above mediocrity and arm themselves for the complex issues involved in spine care. Unlike peripheral joints, spinal anatomy involves multiple joints interacting in conjunction to bring about complex, multiplanar motions. This motion has physiologic restrictions and weaknesses based upon anatomy. These weaknesses allow for the unfortunate consequences resulting in axial and radicular pain syndromes that spine physicians know so well. This chapter will provide the reader with a basic understanding of both the developmental and functional anatomy of the cervical spine.1

DEVELOPMENTAL ANATOMY Embryologic development In order to give a temporal flow to the embryologic development of the cervical spine we will use the general staging scale devised originally by Streeter.2 This scale consists of 23 stages of growth that starts with fertilization and runs to the 60th day of growth.3 Each stage typically has a duration of 2–3 days in length.4 Growth and differentiation of the neurospinal axis begins in embryonic stage 6. These cells typically originate from the primitive streak and node at the 13th–15th day from fertilization. In the following stage the cells that will form the notochord travel rostrally from the primitive node. The notochordal cells’ growth causes abutment to the overlying ectoderm which thickens and becomes the neural plate.5,6 This neural plate serves as the primordium for all nervous system evolution.7 This stage occurs at the 17th–19th day (stage 8) and marks the first stage of nervous system development. The superior notochord promulgates growth of neuroectodermal structures, while the inferior notochord stimulates growth of mesodermal structures.8 In stage 9 the neural plate molds itself into a neural fold/groove.6 This stage is also notable as the first three somites are formed during this period of the 19th to 21st day. The somites represent paired, blocklike masses of mesoderm lying alongside the neural tube. The human embryo develops 42–44 paired somites; 4 occipital, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 8–10 coccygeal somites. They consist of two cell collections: the ventromedially placed sclerotomal cells and dorsolaterally situated dermomyotomes.9 The sclerotomal structures are responsible for the formation of the vertebral column, and the dermomyotomal cells form the segmental skin and musculature.10 It is postulated that early vertebral segmentation occurs during this stage; most notable is the formation of the first two cervical vertebrae and cranial–vertebral junction.6 These bony structures are formed by the first eight occipital somites. Spinal cord primordium

is also present during this stage with continuing growth occurring through stage 12. In this stage the inferior neuropore closes and 21 to 29 somite pairs have formed. At this point, vertebral differentiation has occurred through the lumbar segments. Stage 13 (days 28–32) marks completion of pontine and cervical flexures of the spine and continuing neurulation caudal to closure of the posterior neuropore.11 Contouring of the caudal neural tube and adjacent vertebrae begins in this stage and progresses through gestation and into early infancy.6,11 Structures such as the conus medullaris, ventricular terminalis, and filum terminale originate from this caudal neural tube.12 Specific vertebral development occurs through three stages: membrane, cartilage, and bone formation.13 Membrane formation occurs as the notochord encounters the neural tube dorsally and the foregut ventrally. As growth progresses, cavities are formed between the notochord and neural tube/foregut interface. Sclerotomic cells then infiltrate these cavities. Dorsal migration of sclerotomic cells also occurs during this period. These migrating cells settle in regions that ultimately will become the neural arches.13 This occurs in stages 10 through 12 of embryologic growth. Anterolateral movement of sclerotomal cells occurs in stage 13. These pockets provide primordium for future growth of the ribs. Stages 15 and 16 are characterized by fissuring and flexures of the notochord alongside vertebral body and intervertebral disc primordium.6 The period of cartilage formation in vertebral development takes place during embryonic stages 17 through 23. This chondrification begins in the vertebral bodies and subsequently migrates dorsally into the neural arches.6 During the latter part of stage 23 the dorsal aspect of the neural arches begins to deviate medially. Bone formation starts in the early fetal stage of growth with ossification of the cervical and thoracic regions followed by lumbar and sacral vertebral segments. This final period continues on into infancy and adolescence.14 Growth of spinal nerves begins with formation of the spinal cord. This initial differentiation involves clumping of neural crest cells in embryologic stage 12.15 Over the next three stages of development the neural crest cells form spinal ganglia that expand and move ventrally. The first ventral root fibers occur during stage 13. The primordium of the cervical and brachial plexuses also forms during this stage. Stage 14 is marked by complete development of all motor roots from C1 to S2 and growth of intersegmental anastomoses between these motor roots.16 Shortly after this stage the motor nerve roots move away from the spinal ganglia and toward their respective intervertebral foramen. Formation of the spinal nerve by mingling of motor and sensory root fibers occurs in stage 15. The roots enter the medial aspect of the foramen during stage 18, and progress completely into the foramen by stage 23. Other motor nerve development worth noting are the following: at the end of stage 14 the motor nerve fibers from the L2–4 segments moving a short distance into the leg.17 515

Part 3: Specific Disorders

Creation of the brachial plexus begins in stage 16 and progresses through stage 23. At this point the major motor subdivisions of the brachial plexus resemble those of the adult.15 Stage 16 also heralds formation of the lumbar plexus and the individual femoral, obturator, tibial, and peroneal nerves, and stage 17 marks development of the hypogastric, pudendal, genitofemoral, and ilioinguinal nerves.15 The sensory nerves develop in a similar manner as their neighboring motor fiber counterparts. As discussed above, the formation of sensory spinal ganglia anlage begins in stage 12 of embryologic development.18 Sensory root fibers grow out first centrally from the ganglia to make connections with the spinal cord in stage 14. In the following stage the fibers move peripherally to blend with the motor root fibers to form the spinal nerve. Entrance to the intervertebral foramen is gained by the end of embryologic stage 16, and complete access to the foramen by all sensory nerve roots is gained by stage 23.19 The autonomic system also begins its formation during the middle embryologic stages of development. Unlike the motor and sensory nerve roots, the autonomic nerve differentiation begins with primordium formation in the lower thoracic, esophageal, and upper abdominal regions rather than in the cephalocaudal growth of the vertebra and nerve roots.20 This occurs at embryologic stage 13. This primordium continues differentiation in the lower cervical to sacral region in stage 14. The first white communicantes fibers can be identified in the T2–9 level at this stage.15 Anlage of the autonomic pelvic plexus begins in stage 15.21 Stage 16 is marked by continued growth of the white rami communicantes through the L3 spinal level. The sympathetic chain also has a cephalad movement from the thoracic to upper cervical segments during this stage. The first gray rami communicantes begin to appear at the C8–T1 level around this time (days 37–42).22 Auerbach’s plexus begins differentiation in embryologic stage 17. Continued growth of gray rami communicantes occurs through stage 23 with formation of autonomic nerve fibers to the S5 spinal level.16 The development of the meninges originates from a thin cellular network that exists between the somites, notochord, and neural tube.6 Its early formation is termed the ‘meninx primitiva.’ It serves as a host site for the migration of cells and eventual development of the meninges. This meninx primitiva generation occurs in embryologic stage 15, and grows to surround the complete neural tube in stage 16. In the following stage, the denticulate ligaments begin to form. By stage 18 the spinal canal has started to take shape with cavitation of the meninx primitiva quickly following in embryologic stage 19. Evidence of pia mater structure formation also occurs during this time. It consists primarily of meninx primitiva cells with a small contribution from neural crest cells. Formation of the dura mater in the cervical and thoracic regions follows pia mater growth in stage 20. It consists of mesodermal cells from sclerotomal and meninx primitiva origins. It initiates growth anterior to the spinal cord with progression longitudinally and circumferentially around the cord. Dura mater growth reaches the lumbar region by stage 22, and completely surrounds the spinal cord end to end at stage 23. Construction of the epidural space also begin during this last stage. Arachnoid mater development continues to be poorly understood at this time. It is believed to be the last of the meninges to form. This occurs after completion of the embryologic stages, i.e. post 60 days fertilization.

Fetal development All major structures of the spine are clearly distinguishable by the end of the embryologic period of spinal growth. The next stage of development occurs during the fetal period. Its temporal boundaries include the termination of stage 23 of the embryologic period to birth. As discussed above, chondrification of the vertebra begins in the embryological period. It can be identified in the pedicles, lamina, and transverse processes of vertebrae prior to the fetal period. Early 516

into the fetal period these chondrification centers enlarge and migrate into the posterior arches and vertebral bodies. Fusion of the posterior vertebral structures and dorsal growth of the spinous processes occur at the end of the first trimester (12th week).23 This period is also marked by the onset of ossification anteriorly in the body and posteriorly in the lamina of the vertebra. These two bony growth centers progress in a dissimilar manner. Ossification of the vertebral body first occurs in the thoracic region and spreads bi-directionally towards the cervical and lumbar segments. The laminar bony growth takes place in a more typical cephalocaudal pattern from cervical to coccygeal segments.24 In addition, we see a longitudinal growth of the spinal structures during this fetal period. This growth is demonstrated by measurement of the vertex-coccyx segment over this period. At 3 months, this segment measures about 10 cm long, and reaches to roughly 34 cm at birth.25 The intervertebral disc undergoes changes during this fetal period. The end of the embryologic stage and beginning of the fetal period see the notochord expand into the center of the disc. This cell in-growth to the disc forms a strandlike appearance that is implanted into an amorphous mucoid substance called chorda reticulum.26 The embryologic cartilage surrounding the expanding notochordal cells begins to have collagen fibers formed within it around the 10th week of gestation.27 Interestingly, their growth patterns are identical to those in the adult.28 Their formation is well established by the 6th month of fetal growth. In addition, the neighboring anterior and posterior longitudinal ligaments begin to develop around the same time as the annular fibers. They grow from perivertebral mesenchymal cells.29 As the fetal period continues, the chorda reticulum enlarges and radially expands. During the terminal stage of this period the chorda reticulum cells bordering the annular cartilage themselves begin a transition to fibrocartilage cells. These cells arrange themselves into patterns similar to those seen in the collagen fibers of the adult anulus fibrosus.26,30

Postnatal development This final stage of development takes place from birth to adulthood. It is by far the longest of the three stages in duration. In contrast, this stage involves minimal plastic changes in the spinal tissues. This period primarily involves tissue maturation and longitudinal growth of the spine.25 The spinal maturation process involves continued ossification of the vertebrae. This is a continuation from its onset in the fetal period. As discussed above, the vertebrae typically have three centers of ossification, one in the ventral vertebral body and one in each of the lamina. At birth, approximately 30% of the spine is ossified, primarily from these ossification centers. The articular processes, transverse processes, spinous processes, and the last few sacral and coccygeal segments still demonstrate a cartilaginous pattern at birth.31 Hyaline cartilage also still persists in the superior, inferior, and peripheral portions of the vertebral body. A striking feature at birth is that all pars interarticularis of the cervical, thoracic, and lumbar spine are ossified at birth. Failure of this pars ossification at birth has clinical implications for development of spondylolysis and spondylolisthesis in adulthood.32 Except for the first two cervical vertebrae, the growth and development of the cervical spine is fairly uniform.33 The atlas, like other cervical vertebrae, has three centers of ossification. Unlike other cervical vertebrae, the atlas does not possess a body or centrum. In this case, the anterior ossification center forms in the anterior arch of the atlas. This anterior ossification center is visible on radiography in about 20% of neonates.34 By the end of the first year the anterior center is readily apparent on radiography. The neural arches ossify at 6–12 months of age.35,36 The posterior arches typically fuse around 3 years of age. Prior to this fusion, a secondary ossification center may be seen in the

Section 3: Cervical Spine

posterior tubercle.33 Other potential secondary ossification centers include the anterior tubercle and at the tip of the transverse processes. The posterior arches may fail to fuse, leaving a bifid process in place. This bifid process does not hold any potential pathologic consequences to the spine. It should typically be regarded as a normal variant similar to spina bifida occulta of the S1 posterior arches. The axis has five primary and two secondary centers of ossification. Three of the primary centers are typical placed in the centrum and the bilateral posterior arches. These posterior arches normally fuse together between 2 and 3 years of age.31 The remaining two primary ossification centers appear during the 20th–24th weeks of gestation. They appear at the base of the cartilaginous rostral projection at the anterosuperior aspect of the axis. A secondary ossification center occurs in the apical portion of the dens around the end of the second year of life. This apical ossification center is phyletically derived from the centrum of the first cervical vertebra. The secondary center in combination with the two primary centers at the base of the odontoid result in a persistent cartilaginous region in the central area of the odontoid. This area is homologous for the intervertebral disc between the atlas and axis.35 The last secondary ossification center forms in this cartilaginous area in the late teens and usually completes union of the apex and base of the odontoid in the mid twenties. Absence of this last ossification step results in failure of fusion of the apical portion of the odontoid to the base of the axis. This results in a condition called os odontoideum. The presence of this condition can be easily confirmed by magnetic resonance imaging. The stability of the atlantoaxial joint then falls directly on the atlantoaxial ligaments and the degree of fibrous union between the dens and the body of the axis.35 Partial ossification of this site can occur, which can create the appearance of a fracture through the middle to inferior aspect of the dens. The rate of bony growth can also be very slow at this site, causing the area to fuse late in life. The remaining cervical segments all develop in a more traditional pattern to the thoracic and lumbar segments. As noted above, they have three primary ossification centers: one located in the vertebral body, and one in each lamina. The vertebral body is almost entirely ossified by 6 years of age, and the neural arches approximate posteriorly at around 2–3 years of age.31 The epiphyseal plates of the vertebral bodies do not undergo ossification until completion of growth. This occurs around the twentieth year of life. This bony growth progresses in a radial pattern in a peripheral to central direction. However, this inward growth is arrested to leave a central cartilaginous portion that becomes the endplate zone in the adult. The pedicles remain cartilaginous until the sixth year of life when their ossification process is complete and they fuse with their respective vertebral bodies.37 Secondary ossification sites occur at the transverse processes and spinous processes around the fifteenth to sixteenth year of life. These areas usually fuse in the second to third decade of life. An accessory secondary ossification site may occur in the transverse process of the seventh cervical vertebrae.32 If this accessory center fails to fuse with the main secondary center in the transverse process, the accessory site may progress to formation of a cervical rib.33 The intervertebral disc also undergoes changes during the postnatal period. There is a progressive decline in the notochordal mesenchymal cells at birth. This is accompanied by a steady increase in the mucoid substance of the nucleus pulposus. A fibrocartilage capsule surrounds these diminishing notochordal cells and increasing mucoid substance. This change is typically evident by the 5th month of growth.38 By 4 years of age there are no active notochordal cells within the nucleus.39 After this point, the nucleus pulposus halts any further growth. Future growth of the disc thereafter occurs through the anulus fibrosus. This growth primarily involves production of fibrous elements. As years advance there is in-growth of fibrous tissue into the nucleus pulposus with resultant

progressive loss of its liquid content.40 The intervertebral disc in the newborn has a relatively wedge-shaped appearance with the nucleus located posteriorly in the disc.41 The nucleus reverses position and is primarily anteriorly placed by 2 years of age.41 As the child assumes a more upright posture and gait, the nucleus takes on a more central position in the disc. This occurs around the fourth to the eighth year of life.30,41 A significant horizontal and longitudinal growth phase occurs in the disc after birth. This growth progresses late into adolescence. A more generalized discussion on growth after birth and to adulthood will be summarized to demonstrate the developmental requirements of the spine. It is marked by two main growth spurts: one occurring after birth and the second during puberty.42 The early growth spurt takes place from birth through the age of five. Almost half of this initial growth occurs during the first year of life.41 As mentioned above, at birth the sitting height measures around 35 cm. After the first year of growth this sitting height increases to about 47 cm.25 In the following four years of growth, the sitting height increases from 47 cm to 62 cm, so that by the time the normal infant reaches 5 years age it has increased its height 27 cm. Over the next 5 years the truncal growth slows dramatically in comparison to the prior 5 years. It increases about 10 cm over this period. The pubertal, or adolescent, phase marks the last stage of linear spinal growth. This commonly occurs in the tenth through eighteenth years of life. During this final stage the second growth spurt occurs. Its onset is slightly different for each gender. In females it usually begins slightly earlier than in males. Most commonly, it occurs around the age of 11. There is an initial period of rapid growth over the first 2 years that is followed by a slower growth phase over the remainder of the pubertal stage. The early phase increases sitting height approximately 7 cm, while the slower second stage increases height by another 5 cm. In males, the pubertal stage usually has its onset around age 13. The male growth pattern is similar to that of the females. However, there is a slight increase in height versus the female growth during the first phase of this growth spurt.41 By the time we progress from birth to adulthood the spine has nearly tripled in size. This longitudinal growth is accomplished primarily through growth of the vertebral bodies. As discussed earlier, this growth occurs at the superior and inferior surfaces of the bodies.42 These regions persist as cartilaginous zones for continued growth and ossification of the vertebral body.43 The cartilage cells in these regions are arranged in a perpendicular-like pattern to the body. Thus, the longitudinal growth of the vertebral body is much the same as the growth of the metaphyses of long bones in the human body.25,44 Whereas cells closest to the vertebral body undergo ossification and unite with the vertebral body, other cartilaginous cells move toward the vertebral body and replace these ossifying cells.45 Hence, the vertebral body continues its longitudinal growth through this ossifying process.44 This growth terminates between the ages of 18 and 25.46 The growth plate then thins and calcifies. However, there remains a fibro-cartilaginous region neighboring the disc. This area becomes the adult vertebral endplate. Each level (i.e. cervical, thoracic, lumbar, and sacral) increases its vertebral height to different degrees. The average cervical and thoracic vertebral body height triples from birth to adulthood.23 The lumbar vertebral segments quadruple their longitudinal size by adulthood.23 At birth, the vertical length of the cervical spine measures about 3.7 cm. It doubles in length by 6 years of growth, during the first growth spurt, and nearly doubles its length again at the pubertal growth spurt. By the end of the pubertal growth spurt the cervical spine constitutes about 22% of the total spine length, and 15–16% of sitting height.23 In addition to vertical growth, the vertebral body also expands in a radial pattern.45 Periosteal ossification is primarily responsible for this horizontal growth. Most expansion, similar to vertical growth, occurs during the two main growth spurts.47 517

Part 3: Specific Disorders

FUNCTIONAL ANATOMY Bony structures The bony structures of the cervical spine consist of seven vertebrae connected together by a system of complex articulations that primarily serves four main functions: (1) to support the head, (2) to allow for an extensive, precisely controlled range of motion for the head, (3) to provide a protective covering for the spinal cord and nerve roots, and (4) to supply an entrance and exit zone for neurovascular structures. The cervical spine is unique, as the morphology of the two cephalad segments is markedly different from the rest of the cervical spine.35 We will first discuss the bony anatomy of the atlas and axis, followed by the third through seventh cervical segments. The atlas is the first cervical vertebrae. Along with the axis, it serves to connect the cranium to the spine. Metaphorically speaking, it acts as the ‘cradle’ for the occiput. It is unique to the other cervical segments because it lacks a vertebral body. In place of the body the atlas develops an anterior arch that runs almost perpendicular to the connecting lateral masses. A small tubercle forms in the midline on the anterior aspect of the arch. This tubercle serves as the insertion point of the longus colli muscle.48 A rounded cavity can be seen on the posterior surface of the anterior arch. This depression marks the synovial articulation of the odontoid process. The paired, cylindrical lateral masses contribute their articular processes, or zygapophyseal joint, to the atlanto-occipital and atlantoaxial articular joints. The underside of the lateral masses are slightly concave, directed medially and posteriorly to articulate with the superior articular process of the axis. The cephalad portion of the lateral mass is oriented superiorly and medially to interdigitate with the articulation of the occipital condyles. Small tubercles can be noted on the ventromedial aspect of the pillars. These tubercles serve as the attachment sites of the transverse atlantal ligaments.35 These ligaments hold the odontoid against its anterior synovial membrane. The ring-shaped atlas is closed dorsally by the formation of a posterior arch connecting to each lateral mass. At the juncture of the lateral masses to the posterior arch there is a small groove that marks the passing of the vertebral arteries towards the foramen magnum.49 The transverse processes of the atlas are short and compact structures. Within each transverse process exists a small rounded transverse foramen for passage of the vertebral artery.49 Unlike other cervical segments, the atlas does not have a spinous process. There exists a small tubercle lying in the midline on the dorsal aspect of the posterior arch.33 This tubercle serves as the attachment site of the ligamentum nuchae.35 As mentioned above, the lateral masses of the atlas combine with the occiput to form the occipital– atlantal (OA) and the axis to form the atlantal–axial (AA) articulations (Fig. 46.1).50 The primary motion of the OA joint is flexion–extension

moments.51 There is minimal appreciable axial rotation of the OA joint. The reason for this limitation is secondary to the concavity of the superior portion of the lateral masses. The concavity essentially encloses the condyles within its bony walls, preventing the required anterior and posterior translation for rotation to occur.52 However, the cupping nature of the superior lateral masses does allow for a sagittal rotation (i.e. rolling) movement to occur through the OA joint. This nodding motion is achieved through multiple actions occurring through the OA joint. As the head nods forward the condyles roll forward in the sockets of the atlas. Concomitantly, the condyle slides up the concave anterior wall of each socket. Posteriorly and inferiorly directed forces by the flexor muscles, weight of the head, and tension of the OA capsule prevent anterior dislocation of the condyles and maintain them snugly within the lateral mass sockets.52 The reverse process occurs in extension. Normal flexion and extension of the AO joint has a range of 14–35 degrees.53–55 The second cervical vertebra is commonly referred to as the axis (Figs 46.2. 46.3). This name is very proper for this cervical segment as its main function is to allow the atlas to rotate upon it.48 Like the atlas, it also serves to transmit the load of the head to the remainder of the cervical spine. It is regarded as the strongest of all the cervical vertebrae. Its body and posterior arch are similar to those of the lower cervical segments. The uniqueness of the axis is the presence of the odontoid process. It is a vertical cylindrical bony growth that emanates from the superoventral aspect of the axis’s body. The tip of the dens (odontoid) typically terminates at the superior border of the anterior arch where it forms an articulation. A small, smooth, oval indentation is present on the base of the dorsal aspect of the dens. This area is occupied by a synovial joint that serves to protect the transverse ligament from contact with the bony dens.33 A synovial articular process is also present on the ventrosuperior aspect of the dens. It is commonly referred to as the median atlantoaxial joint.52 The dens acts as a pivot for the atlas directly above to spin and glide around to achieve axial rotation. It forms an articulation with the dorsal aspect of the atlas’s anterior arch. A large bifid spinous process is usually present at Dens Pedicle

Superior articular facet

Transverse process Transverse foramen Flaring inferior articular process

Lamina Anterior tubercle (attachment site for longus colli) Synovial articulation dens

Anterior arch Transverse foramen

Bifid spinous process Fig. 46.2 Superior view, axis.

Dens Anterior synovial joint (articulation with atlas) Superior articular facet Groove for vertebral arteries Posterior arch

Fig. 46.1 Superior view, atlas. 518

Tubercles for transverse ligaments Posterior tubercle (attachment site for ligamentum nuchae)

Superior articular facet Transverse foramen Fig. 46.3 Lateral view, axis.

Synovial joint (protect transverse ligaments)

Spinous process

Section 3: Cervical Spine

this level. This spinous process is the first one to be palpated in the superoposterior groove of the neck.48 The inferior articular process of the lateral masses is directed caudally. It forms a facet joint with the superior articulating process of the third cervical vertebrae. A convex and medial-to-lateral orientation is present in the superior articulating process of the lateral masses. This orientation guarantees that the downward force of the atlas is transmitted directly through the central portions of the lateral masses of the axis.35 The primary motion of the atlantoaxial (AA) joint is axial rotation. This requires anterior displacement of one lateral mass with concomitant posterior translation of the opposite lateral mass.52 The alar ligaments are the primary structures to restrain axial rotation. The lateral AA joint capsules are thought to play a minor role in limiting rotation.56,57 The normal range of axial rotation is 0–45 degrees in each direction.58 It accounts for 50% of the total rotation of the neck, and gives almost all rotation over the first 45 degrees. Flexion and extension also occur at the AA joint. Flexion occurs by anterior translation of the atlas on the axis. This causes separation of the anterior arch of the atlas from the dens. Anterior translation is limited by increased tension of the transverse and alar ligaments.56,59 Extension occurs as a result of a slight posterior bend in the dens. This allows the anterior arch of the atlas to move dorsally and superiorly on the dens. Extension is limited by the anterior arch contacting the odontoid. The total range of motion of the flexion–extension moment is approximately 10 degrees.60 The remaining cervical segments all demonstrate a similar bony appearance (Figs. 46.4, 46.5). In general, these vertebrae are required to bear less weight than the thoracic and lumbar segments so they are smaller and thinner than their caudal counterparts. The conventional cervical vertebrae consist of two main parts: the cylindrical, blocklike ventral vertebral body, and the dorsal vertebral arch. This posterior arch is formed by a number of bony components: the pedicles, lamina, spinous process, transverse process, and superior/inferior articulating processes. Their fusion creates vertebral foramens at each cervical segment that serve to create a longitudinal spinal canal for housing of the spinal cord and nerve roots. The pedicles are short, cylindrical bony structures projecting from the superior and dorsolateral aspect of the vertebral bodies. Connecting to each pedicle is a thin, flat, platelike bone called the lamina. These bony plates project dorsomedially until they fuse together in the sagittal plane of the body. At the dorsal juncture of the lamina projects a small, flat, rectangular bone called the spinous process. This bone typically has a bifid appearance at the second

Transverse process

Body

Pedicle

Intertubercular groove (exit of spinal nerve)

Anterior tubercle Transverse foramen

Superior vertebral notch

Spinous process

Body

Transverse process

Fig. 46.5 Lateral view of vertebra.

through sixth cervical segments. The seventh cervical spinous process tends to be very long. Hence, it has been termed the vertebra prominens, and is the most palpable of the cervical vertebrae. The transverse processes project laterally from the junction of the pedicle and lamina.32 The cervical spine transverse processes are rather short in comparison to those of the thoracic and lumbar regions. In addition, these processes also have a transverse foramen just lateral to the pedicle–transverse process junction. Through these foramens pass the vertebral artery on its way toward the foramen magnum. The exception to this rule is the C7 transverse foramen, which only transmits veins.49 A more concise description of this artery will be discussed later. There are two tubercles located on the lateral edge of the transverse process. One is positioned anteriorly and posteriorly. Each tubercle serves as insertion points for the ventral and dorsal cervical musculature. An intertubercular groove exists proximally on the transverse process. This groove has important clinical implications, as this is where the spinal nerves exit the foramen. At this position, the nerves pass just dorsal to the vertebral artery as it passes through the neighboring transverse foramen.49 The superior and inferior articular processes project vertically at the juncture of the pedicle and lamina. In general, the superior articular processes face dorsally and cephalad at about a 45 degree angle to the transverse plane.51 This superior position permits the articular process to bear the weight of the pillar above.52 The height of the superior articular process increases in a cephalocaudal direction. It plays a major role in controlling cervical spine segmental motion in the sagittal plane. As a general rule, the smaller the superior articular process, the greater the segmental flexion.51 In other words, there is a much greater range of sagittal motion seen through the upper cervical segments compared to the lower segments due to this phenomenon. The inferior articular processes mirror the superior articular process position by facing ventrally and caudally. The approximation of a superior articular process from a vertebra with an inferior articular process to the vertebrae above results in the formation of a facet, or zygapophyseal, joint.50 The uncinate processes are paired bony protuberances that project superiorly from the posterolateral aspect of the superior endplate of the C3 through C7 vertebral bodies (Fig. 46.6). It is believed they

Posterior tubercle Superior articular facet

Lamina

Uncovertebral joint (uncinate process)

Zygopophyseal joint

Lateral masses Spinous process

Body Fig. 46.4 Superior view of vertebra.

Fig. 46.6 Anterior view of vertebrae. 519

Part 3: Specific Disorders

represent phylogenetic remnants of ancient costovertebral joints in birds and reptiles. These processes are absent in infants and toddlers. They develop in late childhood and early adolescence. Their function is unknown. However, some investigators believe that they function to bolster the cervical disc laterally to prevent herniation.61 Other studies suggest these uncinate processes act as guide rails for the translation which occurs in the cervical discs during flexion and extension.62 A cleft formed between this uncinate process and the medially located cervical disc creates the uncovertebral joint, or joint of Luschka.63 As these clefts do not contain articular cartilage, synovium, or a capsule they should not be referred to as a joint. These clefts allow for a large degree of movement between the vertebral bodies and the intervertebral disc,64,65 particularly in axial rotation.66

Ligaments The unique configuration of the axis (i.e. dens) to allow for rotation of the head creates a situation for potential instability and cord injury. This potential for damage is counteracted by the presence of four atlantoaxial ligaments (Fig. 46.7). The transverse ligament is a strong band extending between the anterior tubercles on the medial aspect of the lateral masses of the atlas. It crosses over the dens, which lies anterior to the ligament. This ligament serves to hold the odontoid process into the notch located posteriorly in the center of the anterior arch of the atlas.63 A small synovial joint sits between the transverse ligament and dens. It serves to prevent friction wear on the ligament against the odontoid process. The main function of this ligament is to prevent posterior translation of the dens, thereby maintaining the integrity of the spinal canal. The cross, or cruciform, ligament is a thick, wide band crossing the OA joint. It consists of vertically oriented superior and inferior fibers from the transverse ligament to the occipital bone superiorly and to the posterior arch of the axis inferiorly. Its function is to limit anterior– posterior shear and some lateral motion of the OA and AA joints.63 The paired alar ligaments attach inferiorly to the anterolateral aspects of the dens. Superiorly, they insert into the lateral margins of the foramen magnum. Their function is to restrict rotation and prevent posterior translation of the odontoid.48

Superior longitudinal fibers cruciform ligament Alar ligaments Base of skull

Base of skull

Accessory ligament

Accessory ligament

Transverse ligament Transverse ligament of cruciform ligament

Cut lamina of axis Body of axis

Dens (underlying ligament) Inferior longitudinal ligament

Fig. 46.7 Axial ligaments. Posterior view, anterior spinal canal. 520

The accessory ligaments are thick, broad bands that attach superiorly to the lateral masses of the atlas, and insert inferiorly into the dorsosuperior aspect of the axis body. These ligaments’ primary function is restriction of rotation of atlas on axis. Severance of one ligament will allow excessive rotation in one direction while maintaining normal restriction of motion in the opposite direction.63 The tectorial ligament is a continuation of the posterior longitudinal ligament. This ligament begins inferiorly at the dorsal aspect of the axis body and spreads superiorly in a fanlike pattern to insert into the internal surface of the occiput.48 Its function is to maintain patency of the spinal canal and restrict cervical flexion. The ligamentum nuchae is a large continuous ligament that runs from the external occipital protuberance inferiorly to the C7 level. It is homologous to the interspinous and supraspinous ligaments of the thoracic and lumbar spine. Elastic fibers compose a majority of this ligament. The primary function of the ligamentum nuchae is reinforcement of the posterior cervical spine,63 and acting as a strong truss that supports the cantilevered position of the head.35 It also serves as a median septum for the posterior neck muscles. The intertransverse ligaments connect successive transverse processes together. They are not well developed in the cervical spine and on dissection they can occasionally be found as a few thin, tough fibers. They are much more developed in the thoracic and lumbar spine where they exist as individual structures.35 In general, the anterior longitudinal ligament (ALL) is one of the longest and most important ligaments of the spine. It lies on the anterior surface of the vertebral bodies and runs from the sacrum superiorly to insert into the base of the skull. The ligament is relatively narrow and cordlike in the cervical spine. In the lumbar spine the ALL significantly widens to cover the anterolateral aspects of the vertebrae.35 The cervical portion of the ALL is composed of four layers.67 The superficial (first) layer contains vertically running fibers crossing several segments. These fibers were primarily attached to the central regions of the anterior surface of the vertebral bodies. Superiorly, they insert into the anterior tubercle of the atlas. In the proximal region of the cervical spine the fibers are densely packed together. As the fibers move caudally they become more loosely packed. This diffusion of the superficial fibers is due to the natural widening of the ALL as it travels caudally. The second layer of fibers is also vertically oriented. In contrast to the superficial layer, these fibers insert into adjacent vertebral bodies and intervening discs.67 The fibers of the third layer span only one intervertebral disc segment, with insertion into the superior and inferior borders of the vertebral bodies. The fourth, or deepest, layer of the ALL also has very short-running fibers. Like the third layer, they pass across individual intervertebral discs and insert into the superior and inferior margins of the intervening vertebral bodies. The function of the ALL is to resist vertical excursion and hyperextension of the cervical spine. The posterior longitudinal ligament (PLL) is located on the dorsal aspect of the vertebral bodies. Like the ALL, the PLL extends from the axis to the sacrum. Above the level of the axis, this ligament is referred to as the tectorial membrane. It has three main layers: superficial, intermediate, and deep.67 The superficial layer has both verticalyl and laterally directed fibers. The vertical fibers span a variable number of segments. Lateral fibers are seen exiting from the vertical fibers. These lateral extensions cross one disc level and attach to the base of the pedicle one to two segments below.67 These fibers attach themselves to tubercles on the posterocentral aspect of the vertebral bodies. Much shorter longitudinal fibers are found in the intermediate layer. They span no more than one intervertebral disc. Their attachment sites, like the superficial fibers, are located in the midline of the vertebrae. In contrast to the superficial fibers, the intermediate fibers attach just cephalad and caudal to the tubercles on the dorsal

Section 3: Cervical Spine

vertebral bodies. The deep layer consists of both vertical and lateral fibers. These fibers span only one intervertebral disc. The vertical fiber attachment sites are just above and below their respective superior and inferior border margins. The lateral fibers insert on the median aspect just above the superior margin of the vertebrae above. They then spread in an anterolateral direction to insert into the posterior end of the base of the uncinate process. In the cervical spine, the PLL is 3–5 times thicker than in the thoracic and lumbar spine. Due to the laterally directed fibers in the superficial and deep layers, the PLL in the cervical spine has a much wider coverage of the posterolateral discs. It is broadest at the tectorial membrane. Its primary function is to resist vertical separation of the posterior aspect of the vertebral bodies and prevent hyperflexion moments to the cervical spine. Ligamentum flavum are paired ligaments that are present from the axis to the sacrum (Fig. 46.8). They serve to connect the lamina of neighboring vertebrae.68 They insert superiorly into the inferior half of the anterior surface of the lamina and caudal portion of the pedicle. Its inferior insertion site has two main areas of attachment: medial and lateral. Laterally, it inserts into the anterior aspects of the inferior and superior articulating processes. Medially, the fibers insert into the posterior–superior surface of the next lamina below. These latter fibers serve a dual role as they contribute to the capsule of the intervening facet joint between the laminas.69 The primary function of the ligamentum flavum is to resist posterior column distraction forces, and to prevent hyperflexion moments to the cervical spine.70 Like the lumbar spine, the cervical ligamentum flavum fibers are primarily made of elastic fibers. These fibers allow the ligament to undergo stretching and deforming forces without causing buckling of the ligament into the spinal canal.71 In contrast to the lumbar spine, buckling of the ligamentum flavum is rarely seen in the cervical spine. This is due to a number of contributing factors, namely the lack of progressive loss of disc height as seen in the lumbar spine.

Vascular supply The vascular supply of the cervical spine has been sparsely investigated. Most of the descriptions available are from the works of H.V.

Laternal mass Zygopophyseal joint capsule

Body

Intervertebral disc Ligamentum flavum Spinous process A Posterior atlanto-occipital membrane Occipital portion of skull Atlanto-occipital joint Atlas Atlanto-axial joint

Ligamentum nuchae

Axis B Fig. 46.8 Cervical spine: (A) lateral view; (B) posterior view.

Crock, H. Yoshizawa, W.W. Parke, and D.C.M Schiff. We will use their works to briefly review the vasculature to this region. For a more detailed account, the reader is referred to their more comprehensive publications.35,72,73 The vertebral arteries give the majority of blood supply to the cervical region. They arise from the first part of the subclavian artery and travel cranially between the longus colli and anterior scalene muscles. As the artery enters the cervicothoracic junction it passes anterior to the C7 and C8 ventral rami and transverse process of the C7 segment.74 The artery then enters the C6 transverse foramen and moves superior through the successive cephalad transverse foramens to the level of C1. It does not pass, however, through the C7 transverse foramen. After passing through the transverse foramen of the atlas it turns sharply in a dorsomedial direction to wind around the posterior aspect of the lateral mass of C1 and pass directly over the posterior arch of the atlas. The artery then pierces the posterior atlanto-occipital membrane, dura, and the arachnoid as it enters the skull through the anterior portion of the foramen magnum. At this point the artery is resting in the subarachnoid space of the cerebellomedullary cistern. It then moves forward on the ventrolateral aspect of the medulla and unites with its counterpart of the opposite side at the caudal border of the pons to form the basilar artery.75 Just prior to their union they each give off small branches that combine with each other to form the anterior spinal artery.76,77 As the vertebral artery crosses each cervical segment, it gives off anterior vertebral body branches. These anterior vertebral body branches emerge from beneath the longus colli muscles and are applied to the front and sides of the vertebrae. At the vertebral body border they are connected longitudinally by thin, fine ascending and descending branches which form an arterial plexus on the anterolateral surface of the cervical vertebrae. This arterial plexus is primarily present from the C2 to the C6 levels. Other arteries also support this plexus with their branches. Most notable is the inferior thyroid artery, a branch of the thyrocervical trunk, which gives rise to welldelineated vertebral branches which travel superiorly and inferiorly, creating discrete longitudinal chains along the dorsal aspect of the longus colli muscles. These chains commonly extend from the third or fourth thoracic level and end superiorly near the anterior arch of the atlas. This plexus, through small penetrating arteries, gives arterial supply to the anterior vertebral body.72 The anterior spinal canal and posterior aspect of the vertebral body gain their vascular supply by way of an arcuate system of arteries lying on the dorsal surface of the vertebral bodies. The anterior spinal canal branches of the vertebral artery form this arcuate plexus. They occur at every segmental level of the cervical spine beginning at the C2 level. These arteries are single, fine branches that extend from the vertebral arteries at the level of the intervertebral foramen. As the arteries move toward the foramen they cling to the pedicle. Once in the canal, they separate into superior- and inferiorrunning branches that help to form the arcuate system mentioned above. Transverse anastomoses connecting the right and left arcuate complexes occur by small, linking arteries underneath the posterior longitudinal ligament.72 The deep cervical artery, a branch of the subclavian artery or costocervical trunk, also may give off branches in the lower cervical region.72 These branches travel along the same route as the anterior spinal canal branches to help form the arcuate system along the posterior vertebral bodies. The posterior spinal canal of the cervical spine receives its vascular supply primarily from posterior spinal canal branches of the vertebral artery. Like the anterior spinal branches, they emanate from the vertebral artery and pass through the intervertebral foramens. They branch into ascending and posterior vessels that form a posterior arcuate system on the ventral surface of the lamina and 521

Part 3: Specific Disorders

ligamentum flavum.72 A number of branches arise from the posterior arterial arcuate system. The most notable of these are the laminar branches. They arise from the lateral arterial arcade just medial to the intervertebral foramen. They enter the lamina at its junction with the pedicle. Upon entering the lamina, the artery divides to form short ascending and long descending branches.72 Both branches course through the lamina, providing its vascular supply. The short ascending branch terminates in the superior articular process, which it supplies. Concomitantly, the long descending branch courses into the inferior articular process where it terminates to give this structure its vascular supply.72 Small anterior branches from the posterior plexus pass ventrally to communicate to an arterial plexus located on the dorsal surface of the dura mater. Similar to the lumbar spine, the radicular arteries give vascular supply to the nerve roots (Fig. 46.9). Their origin is commonly from the vertebral arteries; however, in the lower cervical spine they may emanate from the thyrocervical trunk arteries (i.e. the ascending cervical artery).72 Two radicular arteries are present. They are named anterior and posterior according to the nerve root they supply. As they branch from the vertebral artery, the radicular vessels take a cephalad course to make contact with the superior edge of the adjacent nerve root. Upon making contact with the nerve root sleeve it will run along the external dural lining a short distance prior to entering it.78 They continue to travel rostrally along the nerve root, providing a vascular supply. They terminate by merging with the vascular trunks of the spinal cord. The anterior radicular artery feeds into the anterior longitudinal arterial trunk while the posterior radicular artery inserts into the posterolateral longitudinal arterial trunks.72 The spinal cord receives its arterial supply from three main sources: the anterior median longitudinal and two posterolateral longitudinal Ventral root

Spinal cord

Dorsal root C1 Dorsal root ganglion

C2

C3

C4

Dorsal root

arterial trunks. Three main arteries, the anterior spinal artery and two posterior spinal arteries, form these longitudinal trunks. The anterior spinal artery is formed by merging branches of the right and left vertebral arteries at the level of the medulla oblongata.72 It then courses inferiorly the length of the spinal cord within the anterior median fissure of the cord. As mentioned earlier, this artery also receives segmental feeder vessels from the anterior radicular artery. This anterior longitudinal arterial network gives blood supply to the anterior two-thirds of the spinal cord. The two posterior spinal arteries emanate from branches of the vertebral or inferior cerebellar arteries (Fig. 46.10).79 They course caudally in the posterolateral sulcus of the spinal cord. The additions of feeder arteries occur segmentally from the vertebral, ascending cervical, and deep cervical arteries. This combination of feeder vessels creates a plexiform plexus on the posterior aspect of the spinal cord. This posterior longitudinal arterial plexus gives vascular supply to the dorsal one-third of the spinal cord.79

Veins of the cervical spine For the most part, the venous supply of the cervical spine follows a pattern similar to the arterial supply. Venous supply of the spinal cord consists of three longitudinally running veins on the anterior and posterior aspects of the spinal cord. These anterior and posterior spinal veins subsequently drain into segmental radicular veins. These radicular veins move laterally toward the intervertebral foramens where they drain into intervertebral veins.72,80 Two main plexuses of veins exist in the spine (Fig. 46.11). They are the external vertebral and internal vertebral plexuses. The external vertebral plexus is a collection of large veins located on the dorsolateral aspect of the spinous processes and lamina of the spine. This plexus segmentally blends to form connections anteriorly with the intervertebral veins. In the cervical region the intervertebral vein subsequently drains into the deep cervical veins. Anteriorly, circumferential veins wrap around each vertebral body to give venous drainage to the vertebral body wall. These segmental, anterior, and external veins drain into the vertebral veins at the level of each intervertebral foramen. The deep cervical and vertebral veins both drain into the brachiocephalic veins adjacent to the internal jugular entry points.72 The internal vertebral venous plexus is composed of two divisions: the anterior and the posterior. These internal plexuses run the length of the spinal canal. They begin superiorly in the region of the sphenoidal clivus and connect with the prostatic venous plexus in the sacral region.72,81 The anterior internal plexus lies just dorsal to the anterior epidural arterial arcade. It is a complex grouping of veins that drains the anterior elements of the spinal canal, including the vertebral body. The basivertebral vein serves to connect the vertebral body to the anterior internal venous plexus. The vertebral body

Posterior branch radicular artery Posterior spinal artery (supplies 1/3 of spinal cord) Radicular artery

Spinal cord

Dorsal root ganglion

Anterior branch radicular artery Ventral root Fig. 46.9 Posterior view, spinal canal. 522

Anterior spinal artery Fig. 46.10 Cranial view (supplies 2/3 of spinal cord) of cervical spinal cord.

Section 3: Cervical Spine

venous flow through the basivertebral vein is not limited to posterior flow only. It also has a small ventral vein connecting it with the anterior external vertebral veins.72 The posterior internal plexus lies just ventral to the posterior arterial arcade. It serves to drain the dura and posterior spinal canal. Connecting venous anastomoses between the posterior internal venous plexus are made with the anterior internal plexus and posterior external venous plexus. The internal venous plexuses both segmentally drain into the intervertebral veins through the foramens. Paralleling radicular veins to their respective arteries give venous supply to the nerve roots.72

Muscles of the cervical spine The muscles of the cervical spine can be divided into superficial and deep muscles. The superficial muscles primarily are responsible for gross movements of the cervical spine while the deep muscles give more segmental control to the upper and lower regions of the cervical spine. The superficial and deep muscles can further be subdivided into primary flexors and extensors of the spine. Rotation and side bending of the neck is brought about by co-contraction of multiple cervical muscles. There are no primary muscles responsible for these motions.

Anterolateral muscles The primary flexors of the cervical spine are located in the anterolateral compartments of the neck.75 They include the sternocleidomastoid, longus colli, longus capitis, and rectus capitis anterior.82 The sternocleidomastoid muscle inserts superiorly into the mastoid process of the skull. It has two inferior attachment sites: a tendinous portion inserts into the sternum, and a thinner muscular portion attaches to the clavicle.82 Bilateral contraction of this muscle’s anterior fibers result in forward flexion of the spine. Unilateral contraction of this muscle results in a lateral sidebending to the same side with concomitant contralateral rotation of the head and neck.83 It receives motor innervation from the spinal accessory nerve and sensory innervation from the second, and possibly the third, cervical spinal nerves.82 The sternocleidomastoid muscle serves as key landmark in the neck.83 It divides the neck into anterior and posterior triangles, which aides in description for both surgical and interventional procedures. The longus colli muscles lie on the ventral surface of the cervical vertebrae. They are the longest and most medial of the prevertebral muscles, which include the longus capitis, rectus capitis anterior, and rectus capitis lateralis.83 They consist of basically three subdivisions: lower lateral, superior lateral, and vertical-medial fibers.82 The lower lateral fibers insert inferiorly into the first through third vertebral bodies of the thoracic spine. They attach superiorly to the fifth and sixth transverse processes of the cervical spine. The superior lateral fibers insert inferiorly into the third through fifth transverse processes of the cervical spine, and attach superiorly into the ventral aspect of the atlas.82 The vertical medial fibers attach distally into the ventral aspect of the lower three cervical vertebrae and first through third thoracic vertebrae. They insert superiorly into the ventral aspect of the second through fourth cervical vertebrae. It receives its nervous innervation from the second through sixth cervical ventral rami.83 Contraction of this muscle results in a flexion moment to the cervical spine. The longus capitis is a broad and thick muscle that lies just lateral to the longus colli muscle.84 It inserts caudally into the transverse processes of the third through sixth cervical vertebrae. Superior attachment occurs at the occipital bone. Like the longus colli, the longus capitis is innervated by the first through third ventral rami. Its primary motor action is flexion of the head and upper cervical spine (Fig. 46.12).82 The rectus capitis anterior is a short and wide muscle that lies deep to the longus capitus muscle. It inserts distally into the lateral

Anterior external venous complex

Vertebral body

Anterior internal venous complex

Basivertebral vein Circumferential vein

Intervertebral vein

Anterior spinal vein Posterior spinal vein

Spinal cord

Posterior external venous complex

Posterior internal venous complex

Fig. 46.11 Axial view, cervical spine. Venous plexuses.

Occipital bone C1 Longus colli (superior lateral fibers)

C2

Longus capitis

C3 Longus colli (vertical medial fibers)

C4 C5 C6

Longus colli (lower lateral fibers)

C7 T1 T2

Fig. 46.12 Ventral view of cervical spine.

mass of the atlas. Superiorly, the rectus capitis anterior attaches to the base of the skull, just ventral to the occipital bone. Innervation to this muscle is from the ventral rami of the first two cervical nerves. Contraction of this muscle results in flexion of the head and upper cervical spine. A secondary function of this muscle is to stabilize the atlanto-occipital joint.82 The rectus capitis lateralis is a short and flat muscle that also lies deep and just lateral to the longus capitis muscle.84 It attaches inferiorly to the transverse process of the atlas and inserts superiorly into the jugular process of the occipital bone. It also receives innervation from the ventral rami of the first two cervical nerves. Contraction of this muscle results in flexion of the head and upper cervical segments. It also serves to stabilize the atlanto-occipital joint and cause a lateral flexion moment the spine (Fig. 46.13). 523

Part 3: Specific Disorders

Occipital bone

Rectus capitis lateralis Rectus capitis anterior

C1 C2 C3 C4 C5 C6

Anterior scalene muscle

C7

Clavicle

T1

Middle scalene muscle Posterior scalene Clavicle

T2

Fig. 46.13 Anterior view of cervical spine.

There are three scalene muscles located in the anterolateral aspect of the neck. They lie just deep to the sternocleidomastoid and superficial to the longus colli and capitis muscles. The anterior scalene inserts superiorly into the anterior tubercles of the transverse processes of the third through sixth cervical vertebrae. Caudally, it attaches to the medial portion of the clavicle in close proximity to the sternoclavicular joint. It receives innervation from the cervical ventral rami corresponding to its attachment levels. Contraction of this muscle results in forward and lateral flexion of the cervical spine. It also aids in elevation of the first rib during forced inhalation. On the ventral belly of this muscle lie the phrenic nerve and internal jugular and subclavian veins.82,84 The middle scalene muscle attaches superiorly to the anterior tubercles of the transverse processes of the lower three to four cervical vertebrae. It inserts inferiorly into the first rib, just posterior to the groove for the subclavian artery. It is the longest and largest of the scalene muscles. Innervation of the middle scalene occurs from the third through eighth ventral rami cervical nerves. Its primary motor action is similar to that of the anterior scalene. Important neighboring structures include the dorsal scapular nerve and the fourth and fifth nerve roots of the long thoracic nerve. These nerves traverse the midbody of the muscle. In addition, the ventral rami of the brachial plexus travel in between the anterior and middle scalene muscles.82,83 The posterior scalene muscle is the deepest and smallest of the three. It maintains a muscular connection with the middle scalene muscle. It attaches superiorly to the anterior tubercles of the transverse processes of the fifth and sixth cervical vertebrae. Distally, it inserts into the second rib. This muscle receives innervation from the ventral rami of the seventh and eighth cervical nerves. Primary motor actions of the posterior scalene muscle include lateral and forward flexion of the head and neck. It also aids in elevation of the second rib during forced inhalation (see Fig. 46.13).82,84

Posterior muscles The posterior muscles of the cervical spine are commonly divided into a superficial and deep set. The superficial muscles of the 524

posterior neck include the larger muscles which cross over multiple segments of the cervical spine. They are involved in more gross movements of the head and neck. They serve as the power movers of the cervical spine. The deep muscles of the neck include those muscles that commonly cross less than three to four cervical segments. These muscles can also be subdivided into suboccipital and deep cervical muscles. The trapezius muscle lies on the most dorsal aspect of the neck region. It has multiple superior attachment sites that include external occipital protuberance, ligamentum nuchae, lower cervical spinous processes, and all thoracic spinous processes. Distally, it inserts into the lateral third of the clavicle, acromion, and spine of the scapula. The motor innervation to the trapezius is from the spinal accessory nerve, which runs just underneath this muscle. Sensory innervation to the trapezius is believed to originate from the dorsal rami of the third and fourth cervical nerves.82,84 Bilateral contraction of the trapezius muscles results in an extension moment through the cervical spine. Unilateral contraction of the trapezius muscle results in a lateral flexion moment to the head and neck, with concomitant rotation of the head to the contralateral side. This muscle also gives control of the scapula through multiple planes of motion, which include elevation, retraction, and depression.82 Just deep to the trapezius muscle lay the splenius muscles. They consist of the splenius capitis and splenius cervicis. They are described as bandage-like muscles based upon their ‘wrapping’ configuration around the cervical spine. The splenius cervicis inserts inferiorly into the lower half of the ligamentum nuchae and the first six spinous processes of the thoracic spine. It attaches superiorly into the posterior tubercles of the transverse processes of the first through fourth cervical vertebrae. Innervation of the splenius cervicis occurs through the middle and lower dorsal rami cervical nerves. Bilateral contraction results in extension of the head and neck. Unilateral contraction causes a lateral flexion moment to the head and neck with ipsilateral rotation of the head and neck.84,85 The splenius capitis muscle inserts distally into the lower half of the ligmentum nuchae and the first six spinous processes of the thoracic spine. It attaches cranially into the lateral third of the superior nuchal line of the occipital bone and the lateral aspect of the mastoid process. Innervation of the splenius capitis occurs through the dorsal rami of the upper, middle, and lower cervical nerves. Bilateral contraction results in extension of the head and neck. Unilateral contraction causes a lateral flexion moment to the head and neck with ipsilateral rotation of the head and neck.84 Just below the splenius muscles are a group of muscles known as the erector spinae. From lateral to medial, the erector spinae group consists of the iliocostalis, longissimus, and spinalis muscles. They all receive regional innervation from the dorsal rami of the cervical and upper lumbar spine. Bilateral contraction of these muscles results in extension of the cervical and upper lumbar spine. Bilateral contraction of these muscles results in extension of the cervical spine. Unilateral contraction causes a lateral flexion moment to the side of contraction. The iliocostalis cervicis attaches inferiorly to the angles of the upper six ribs. It inserts superiorly into the posterior tubercles of the transverse processes of the fourth and sixth cervical vertebrae. The longissimus muscle is divided into a cervicis and capitis group. The longissimus cervicis muscle inserts distally into the transverse processes of the first through sixth thoracic vertebrae. It attaches superiorly into the transverse processes of the second through sixth cervical vertebrae. The longissimus capitis muscle inserts inferiorly into the tendons of the longissimus cervicis and articular processes of the fourth through seventh cervical vertebrae. Cranially, it attaches to the mastoid process.84

Section 3: Cervical Spine

Similar to the longissimus muscle, the spinalis muscle is also divided into a cervicis and capitis group. The spinalis cervicis muscle inserts caudally into the ligamentum nuchae and spinous processes of the lower two cervical and first through third thoracic vertebrae. It inserts cranially into the spinous process of the axis. The spinalis capitis is intimately connected with the medial half of the semispinalis capitis, and therefore will be discussed as part of the semispinalis muscle.82,84 Deep to the erector spinae muscle group lays the semispinalis muscles. The cervical portion of this muscle is divided into a cervicis and a capitis group. In gross dissection, this muscle can be differentiated from the erector spinae group by the oblique plane of its muscle fibers. The erector spinae muscle fibers travel in a more inferior to superior direction, paralleling the plane of the spinous processes. The semispinalis cervicis arises inferiorly from the transverse processes of the first through sixth thoracic vertebrae. It inserts superiorly into the spinous processes of the second through fifth cervical vertebrae.82 The semispinalis capitis attaches caudally to the transverse processes of the first six cervical vertebrae. It inserts cranially into the medial edge in between the superior and inferior nuchal lines. Both of these muscles are innervated by the dorsal rami of the corresponding cervical and thoracic levels. Bilateral contraction of these muscles results in extension of the head and neck. Unilateral contraction of these muscles results in a lateral flexion moment with rotation of the head and neck to the contralateral side.84 Just beneath the semispinalis muscle lays the multifidi muscles. They are differentiated from the semispinalis in that they are shorter in length, resulting in them taking a slightly more oblique plane than the semispinalis muscles. They attach inferiorly into the transverse processes of the second through seventh cervical vertebrae. The superior insertion of each of these muscle fiber bundles is into the spinous process two to four segments above their inferior insertion site (Fig. 46.14). Innervation of the multifidi originates from the dorsal rami of the cervical spinal nerves. Bilateral contraction of the multifidi muscles results in an extension moment to the cervical spine. Unilateral contraction causes lateral flexion to the ipsilateral side with concomitant rotation of the spine to the opposite side.82,84 The deepest and most medial muscles of the cervical spine are the rotator muscles. They are less developed in the cervical spine as compared to the thoracic region. They insert inferiorly into the transverse processes of the second through seventh cervical vertebrae. Cephalad attachment occurs at the spinous processes one to two segments above their inferior insertion site (see Fig. 46.14). These muscles

Rectus capitis minor

Obliquus capitis superior

Rectus capitis major Obliquus capitis inferior

Intertransversarii muscles Interspinales muscles Multifidi Rotator muscles

Fig. 46.14 Posterior view of cervical spine/deep cervical muscles.

are innervated by the dorsal rami of the cervical nerves. Bilateral contraction of the rotators results in extension of the cervical spine. Unilateral contraction results in rotation of the corresponding segmental vertebrae to the opposite side.84 The interspinales are small muscles that connect neighboring spinous processes. They are innervated by the dorsal rami of the cervical spinal nerves. Their main action is to extend the cervical spine. The intertransversarii muscles are segmental muscles in the cervical and lumbar spine. They are absent from the thoracic spine. Their attachments are neighboring transverse processes. In the cervical spine there commonly exist two of these muscles at each segment, one posterior and one anterior. They are innervated by both dorsal and ventral rami fibers of the cervical spine.82,84 The suboccipital region refers to that area between the axis and the occipital bone. This region consists of four sets of muscles: the rectus capitis posterior major, rectus capitis posterior minor, obliquus capitis inferior, and obliquus capitis superior. They are all innervated by the dorsal rami of the first cervical spinal nerve. The rectus capitis posterior major is a triangular muscle that has its inferior attachment site at the posterior edge of the spinous process of the axis. It inserts superiorly into the occipital bone just inferior to the inferior nuchal line. Bilateral contraction results in extension of the head. Unilateral contraction causes weak rotation of the head to the ipsilateral side (see Fig. 46.14). The rectus capitis posterior minor inserts inferiorly into the posterior tubercle on the posterior arch of the atlas. Similar to the rectus capitis major, the rectus capitis posterior minor also inserts superiorly into the occipital bone just inferior to the inferior nuchal line. Its motor action is the same as the rectus capitis major (see Fig. 46.14). The obliquus capitis inferior attaches caudally to the lateral surface of the axis, and inserts superiorly into the inferior surface of the transverse process of the atlas. Unilateral contraction results in ipsilateral rotation of the head. The obliquus capitis superior inserts caudally into the superior surface of the transverse process of the atlas and inserts cranially into a small lateral impression between the superior and inferior nuchal lines on the posterior aspect of the occipital bone (see Fig. 46.14). Bilateral contraction of this muscle results in extension of the head. Unilateral contraction causes lateral flexion of the head.84

Innervation of the cervical spine The cervical spine contains a host of structures capable of producing nociceptive responses. A thorough knowledge of these structures and their innervation is critical in determining the origin of a patient’s spinal pain. In general, the dorsal and ventral rootlets of the cervical spine exit the spinal cord. At each level there can be between 5 and 16 dorsal rootlets and approximately 20 ventral rootlets exiting the spinal cord.86 These rootlets coalesce into respective dorsal and ventral roots just prior to entering the intervertebral foramen. Just prior to entrance into the intervertebral foramen, a small oblong enlargement is seen in the dorsal root. This entity is known as the dorsal root ganglion. The dorsal root ganglion contains the sensory neuron cell bodies for the majority of the peripheral nervous system. Upon entering the spinal canal the dorsal and ventral roots combine to form the spinal nerve (Fig. 46.15). Once in the foramen, the nerve roots and spinal nerve inhabit the inferior aspect of the foramen. The cephalad portion of the foramen is commonly occupied by veins and adipose tissue.87 As the spinal nerve exits the intervertebral foramen it separates into ventral and dorsal rami (Fig. 46.16).85 The dorsal rami turn posteriorly away from the intervertebral foramen as they exit. At this point they maintain intimate contact with the ventrolateral portion of the articular pillars.88 Sometimes, 525

Part 3: Specific Disorders Intervertebral disc Spinal cord Ventral rami Dorsal root ganglion Ventral rootlets Dorsal rootlets Lamina

Transverse foramen Spinal nerve Intervertebral foramen Dorsal rami Superior articular facet

Fig. 46.15 Axial view of Spinous process cervical spinal canal.

Intervertebral foramen

Veins Artery Spinal nerve Fig. 46.16 Saggital view, foramen.

the angulation around the articular pillar is so acute that a groove is actually produced in the articular pillars. This phenomenon is most notable at the C4 and C5 dorsal rami.85 As the dorsal rami enter the posterolateral portion of the articular pillars they divide into medial and lateral branches. The lateral branches travel dorsally away from the articular pillars to innervate the erector spinae, splenius capitis, and cervicis muscles.89 These lateral branches finally terminate in the skin of the dorsal neck where they give sensory innervation. Of note, the C6, C7, and C8 dorsal rami typically do not have cutaneous branches.89 The medial branches of the dorsal rami stay close to the posterolateral bony elements so they may give sensory innervation to the multifidis and interspinales muscles. The innervation of the multifidis muscles by the medial branches follows a rigid pattern of nervous supply. In short, each medial branch gives innervation to the multifidi muscle that inserts into the spinous process of a vertebral segment numbered one less than the nerve. For example, the medial branch of C6 gives nervous supply to the multifidi muscles inserting into the spinous process of C5.85,88 Each medial branch also imparts sensory innervation to the corresponding facet joints above and below it.88 This pattern of innervation discussed above holds true for the dorsal rami of the C4 through C8 spinal nerves. The C1 through C3 dorsal rami represent a more novel course and distribution that we will briefly discuss below. The C1 spinal nerve exits the spinal canal by passing over the posterior arch of the atlas. As it crosses the posterior arch it separates into ventral and dorsal rami branches. The dorsal branch travels between the posterior arch of the atlas and the vertebral artery. At this point, the C1 dorsal ramus is known as the suboccipital nerve. It then traverses in a cephalad direction approximately 1 cm where it enters the suboccipital triangle. Upon entering the suboccipital triangle, it gives innervation to the surrounding musculature, and gives a connecting branch to the dorsal ramus of C2. There is currently conflicting evidence regarding the presence of a C1 cutaneous branch that supplies the posterior scalp region.85,88 The C2 spinal nerve exits the vertebral canal by passing between the posterior arch of the atlas and the lamina of the axis at its most ventral end. It branches into dorsal and ventral rami as it passes the lateral atlantoaxial joint. The dorsal rami turns in a cephalad direction and subsequently branches into a medial, lateral, superior communicating, inferior communicating branches, and a branch to the obliquus capitis 526

inferior.88 The medial branch of the dorsal rami travels in a horizontal plane across the lamina of the axis. It then takes a cranial direction to enter the scalp with the occipital artery in an aponeurotic sling between insertion of the sternocleidomastoid and trapezius muscles.88 This sling serves as a protective mechanism to prevent compression of the medial branch during contraction of these muscles. After passing through the sling, the medial branch continues cephalad underneath the scalp, giving cutaneous branches to a broad coverage area ranging from the occipital, parietal, and temporal regions of the scalp. The medial branch of C2 is more commonly known as the greater occipital nerve. The lateral branch of the C2 dorsal ramus gives motor innervation to the semispinalis capitis, splenius capitis, and longissimus capitis muscles.88 The C2 dorsal ramus has the distinction of being the largest of all the cervical dorsal rami. The C3 spinal nerve exits through the most cephalad of the cervical intervertebral foramen. It divides into ventral and dorsal rami just prior to leaving the C2–3 intervertebral foramen. The dorsal ramus then turns posterior to pass between the transverse processes of the axis and C3 vertebrae. At this point it separates into deep and superficial branches, a lateral branch, and a connecting branch with the C2 dorsal ramus.85,88 The superficial branch, also known as the third occipital nerve, is the largest division of the C3 dorsal rami. It takes a posterior and medial course around the superior articular process of the C3 vertebra.88 It continues in a medial direction across the posterior aspect of the C2–3 facet joint, giving innervation to it. After crossing the C2–3 facet joint the superficial branch turns in a cephalad direction to pass through and give innervation to the semispinalis capitis, splenius capitis, and trapezius muscles. It terminates by giving cutaneous sensory innervation to the suboccipital region.88,90 The lateral branch of the C3 dorsal rami gives innervation to the semispinalis capitis, splenius capitis, and longissimus capitis muscles. The deep medial branch of the C3 dorsal rami gives nervous supply to the most proximal multifidis muscles.88 The ventral rami of the cervical nerves combine into two distinct plexuses, a cervical and brachial plexus, respectively. The cervical plexus involves the C1 through C4 anterior rami while the C5 through T1 ventral rami form the brachial plexus. Prior to joining their respective plexus, each ventral rami exits in the dorsal aspect of the intervertebral foramen. It then traverses just posterior to the vertebral artery and bisects the anterior and posterior intertransversarii muscles.88 Just prior to merging into their respective plexus formations, the ventral rami give motor branches to the rectus capitis anterior and lateralis, longus colli, and longus capitis muscles. The cervical plexus lies deep to the internal jugular vein and the sternocleidomastoid muscle.84 It forms a series of looping connections with each other from which its peripheral branches originate (see Fig. 46.17).83 Cutaneous sensory innervation from this plexus occurs in the region between the ear and the external occipital protuberance. These nerves commonly surface near the midpoint of the dorsal border of the sternocleidomastoid muscle.84 They are derived primarily from the C2 through C4 ventral rami and include the following: lesser occipital nerve, great auricular nerve, transverse cervical nerve, and the supraclavicular nerves. The motor portion of the cervical plexus is contained within the superior and inferior roots of the ansa cervicalis. The superior root contains motor fibers from both the C1 and C2 ventral rami. The inferior root of the ansa cervicalis is composed of motor fibers of the C2 and C3 ventral rami. Branches from the ansa cervicalis give innervation to all of the infrahyoid muscles excluding the thyrohyoid muscle, which derives its innervation from the ventral ramus of C1.84 The phrenic nerve also branches from the cervical plexus. It is composed of motor fibers from the ventral rami of the C3, C4, and C5 cervical nerves. Its primary contribution is from the C4 ventral rami. The phrenic nerve travels caudally from

Section 3: Cervical Spine

its origin until it reaches the anterior scalene muscle, at which point it curves around ventrally to this muscle. It continues to descend in an oblique direction across the ventral aspect of this muscle. The nerve enters the thorax by crossing the beginning of the internal thoracic artery, between the subclavian vein and artery.84 Finally, it descends to the diaphragm where it gives both motor and sensory innervation.84 In some cases, an accessory phrenic nerve may also be present. This nerve primarily derives its nerve fibers from the C5 ventral ramus. It typically takes a similar, but slightly more lateral, route as the phrenic nerve. Communication of the accessory phrenic nerve to the phrenic nerve commonly occurs either at the root of the neck near the first rib or just within the thorax. The C5 through T1 ventral rami combine to form three trunks of the brachial plexus (Fig. 46.18). The upper trunk is composed of the C5 and C6 ventral rami, while the middle trunk comprises solely the C7 ventral rami. The lower trunk comprises the remaining C8 and T1 ventral rami. These trunks are located in the posterior cervical triangle, cephalad to the clavicle.84,85 The ventral rami produce two peripheral nerves just prior to formation of the trunks. They include the dorsal scapular and long thoracic nerves. The dorsal scapular nerve is composed primarily of the C5 ventral rami fibers and innervates the levator scapulae and major and minor rhomboid muscles. Small branches from the posterior aspect of the C5, C6, and C7 ventral rami combine to form the long thoracic nerve. It passes distally through the apex of the axilla dorsal to other components of the brachial plexus to give innervation to the serratus anterior muscle. Branches of the upper trunk include the nerve to the subclavius and suprascapular nerves. The suprascapular nerve branches from the distal end of the upper trunk. It travels through the scapular notch to supply the supraspinatus and infraspinatus muscles. A small nerve to the subclavius muscle also branches off the upper trunk. This nerve innervates the subclavius muscle, which underlies the clavicle. There are no peripheral nerve branches from the middle and inferior trunks. As the trunks dive underneath the clavicle they each divide into anterior and posterior divisions. The anterior divisions of the upper and middle trunk coalesce to form the lateral cord. The anterior division of the lower trunk does not merge with any of the remaining

divisions. It travels onward solely to become the medial cord. The posterior divisions of all three trunks unite to become the posterior cord. These cords go on to form specific peripheral branches to give sensory and motor innervation to the upper extremity. The reader is referred to Clinically Oriented Anatomy for a more detailed description of the brachial plexus.84 The sympathetic trunks in the cervical spine are positioned anterolateral to the vertebral column, lying on top of the longus capitis muscle (Fig. 46.19). This sympathetic chain consists of three ganglia: the superior, middle, and inferior. These ganglia contain the cell bodies of the postganglionic axons. They also serve as the synapse sites of the preganglionic sympathetic axons with the postganglionic axons, via the postganglionic cell body.91,92 The preganglionic fibers originate from their cell bodies within the intermediate gray matter of the thoracic spinal cord. These sympathetic fibers exit the spinal cord and travel within the ventral roots along with the motor fibers. When the spinal nerve divides, these preganglionic autonomic fibers branch off and feed into the sympathetic trunk. These feeding branches are also known as the white rami communicans nerves. The name is derived secondary to these preganglionic fibers being myelinated. The thoracic spinal nerves feeding the cervical sympathetic chain typically include levels T1 through T6.92 The superior ganglia are the largest of the cervical sympathetic ganglia. They measure approximately 2–3 cm in length, and are located at the level of the C1 through C3 vertebral bodies.84 They lie just anterior to the longus capitis muscle and dorsal to the internal carotid artery. Postganglionic fibers from these ganglia develop an intimate relationship with the internal carotid artery and travel with it into the cranial cavity. These internal carotid fibers of the superior cervical ganglia have autonomic effects in the head and upper neck region. Other postganglionic branches of the superior cervical ganglia include a laryngopharyngeal and cardiac branches, branches to the common and external carotid arteries, and branches to the first four cervical spinal nerves. These branches are commonly referred to as the gray rami communicans secondary to them being unmyelinated postganglionic fibers.91,92 The middle cervical ganglia are typically the smallest of the three ganglia. They lie on the ventral aspect of the inferior thyroid artery at the level of cricoid cartilage and transverse process of the C6 vertebrae, just ventral to the vertebral artery.84 Sometimes, these ganglia

C1

Ventral ramus Trunks Divisions Cords Peripheral nerves

Ventral rami Hypoglossal nerve

C5 Superior trunk Middle trunk Inferior trunk

C6 C2

C7 Lesser occipital nerve

C3

Great auricular nerve

Clavicle

C8 T1 First rib

C4

C5

Superior root ansa cerviculis Inferior root ansa cerviculis Supraclavicular nerve

Anterior Posterior

Musculocutaneous Axillary Ulnar Radial Median

Lateral Posterior Sternum Medial

Phrenic nerve Fig. 46.17 Cervical plexus.

Fig. 46.18 Brachial plexus. 527

Part 3: Specific Disorders

may be absent. Postganglionic fibers from the middle ganglia send branches to the thyroid gland and the heart. They also sends branches to the C5 and C6 cervical spinal nerves. These branches, as in the superior cervical ganglia, are called the gray rami communicans. Occasionally, they may also send branches to the fourth and seventh cervical spinal nerves.91,92 The inferior cervical ganglia is a collection of autonomic nerve fibers that lie between the superior border of the neck of the first rib and the inferomedial aspect of the transverse process of the C7 vertebra, where it wraps around the posterior aspect of the vertebral artery.84,91 This ganglia is commonly fused with the first, and sometimes the second, thoracic ganglia. When this occurs the structure is known as the cervicothoracic, or stellate, ganglion. Fibers from this ganglion send branches to the heart, the subclavian artery, and the vertebral artery. It also sends branches to the C7, C8, and T1 spinal nerves.92 The recurrent meningeal nerve is a branch of the ventral ramus. It occurs at all levels of the cervical spine. As it branches from the ventral ramus it receives a small branch from the gray rami communicans and autonomic fibers from the cervical sympathetic chain surrounding the vertebral artery.84,93 After the sympathetic nerves merge with the recurrent meningeal nerve, it curves medially and enters the intervertebral foramen at the same level as the ventral rami it originated from. It passes through the cephalad portion of the foramen, typically between the posterolateral surface of the vertebral body and the spinal nerve.94,95 Sliding around the inferior aspect of the pedicle, it divides into superior and inferior branches. These branches subsequently give both sensory and autonomic innervation to the structures that exist within the spinal canal and those that form the anterior boundaries of the canal.93 A more detailed discussion regarding this innervation can be read in the lumbar anatomy chapter of this text. The medial branches of the dorsal rami supply the posterior canal structures, i.e. facet joints, from C3–4 through C8–T1.96 The C2–3 facet joint is supplied solely by the third occipital nerve as it passes dorsally across this joint.97 The atlantoaxial joint, tectorial membrane, components of the cruciate ligament, and the alar ligaments all receive nervous supply from the recurrent meningeal nerves of C1, C2, and C3 ventral rami.97 The atlanto-occipital joint receives innervation from the ventral rami of the C1 and C2 spinal nerves.97

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C2

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Spinous process

Fig. 46.19 Lateral view, cervical spine.

Hopefully, this chapter has given the reader a basic understanding of the developmental and functional anatomy of the cervical spine. Knowledge of this anatomy is essential to understanding the mechanical basis for injury in the cervical spine, and aiding in designing an appropriate treatment plan.

C1

Superior ganglion (C1–C3)

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CONCLUSION

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37. Schmorl G, Junghanns H. The human spine in health and disease. New York: Grune and Stratton; 1971:1–18. 38. Joplin RJ. The intervertebral disc: embryology, anatomy, physiology, and pathology. Surg Gynecol Obstet 1935; 61:591–560. 39. Coventry MB. Anatomy of the intervertebral disc. Clin Orthop 1969; 67:9–15. 40. Meachim G, Cornah MS. Fine structure of juvenile human nucleus pulposus. J Anat 1970; 107:337–350. 41. Taylor JR. Growth of the human intervertebral discs and vertebral bodies. J Anat 1975; 120:49–68. 42. Blick EM, Copel JW. Longitudinal growth of the human vertebrae. J Bone Joint Surg [Am] 1950; 32:803–814. 43. Donisch EW, Trapp W. The cartilage endplate of the human vertebral column. Anat Rec 1971; 169:705–716.

70. Yung-Hing K, Reilly J, Kirkaldy-Willis WH. The ligamentum flavum. Spine 1976; 1:226–234. 71. Yahia LH, Garzon S, Strykowski H. Ultrastructure of the human interspinous ligament and ligamentum flavum. Spine 1990; 15:262–268. 72. Crock HV, Yoshizawa H. Origins of arteries supplying the vertebral column. In: Crock HV, Yoshizawa H, eds. The blood supply of the vertebral column and spinal cord in man. New York: Springer-Verlag; 1977:1–21. 73. Schiff DC, Parke WW. The arterial supply of the odontoid process. Anat Rec 1972; 172:399–400. 74. Ebraheim N, Lu J, Brown J. Vulnerability of vertebral artery in anterolateral decompression for cervical spondylosis. Clin Orthop 1996; 322:146–151. 75. Sato K, Watanabe T. MRI of C2 segmental type of vertebral artery. Surg Neurol 1994; 41:45–51.

44. Gooding CA, Neuhauser EBD. Growth and development of the vertebral body in the presence and absence of normal stress. Am J Roentgenol 1965; 93:388–394.

76. Vaccaro R, Ring D, Scuderi G. Vertebral artery location in relation to the vertebral body as determined by two-dimensional computed tomography evaluation. Spine 1994; 19:2637–2641.

45. Knuttson F. Growth and differentiation of the post-natal vertebrae. Acta Radiol 1961; 55:401–408.

77. Moore KL. The head. In: Moore KL. Clinically oriented anatomy. Baltimore: Williams and Wilkins; 1992:637–782.

46. Carpenter EB. Normal and abnormal growth of the spine. Clin Orthop 1961; 21: 49–55.

78. Dommisse GF, Grobler L. Arteries and veins of the lumbar nerve roots and cauda equina. Clin Orthop 1976; 115:22–29.

47. Brandner MF. Normal values of the vertebral body and intervertebral disc index during growth. Am J Roentgenol 1970; 110:618–627.

79. Dommisse GF. The blood supply of the spinal cord. J Bone Joint Surg [Br] 1974; 56:225.

48. Moore KL. The back. In: Moore KL. Clinically oriented anatomy. Baltimore: Williams and Wilkins; 1992:323–372.

80. Kubo Y, Waga S, Kojima T. Microsurgical anatomy of the lower cervical spine and cord. Neurosurgery 1994; 34:895–902.

49. Parke WW. The vascular relations of the upper cervical vertebrae. Orthop Clin North Am 1978; 9:879–889.

81. Batson OV. The function of the vertebral veins and their role in the spread of metastases. Ann Surg 1940; 112:138–149.

50. Pratt NE. Back, Chapter 2. In: Pratt NE. Clinical musculoskeletal anatomy. Philadelphia: JB Lippincott; 1991:21–50.

82. Jenkins DB. The back. In: Jenkins DB, ed. Hollinshead’s functional anatomy of the limbs and back. Philadelphia: WB Saunders; 1998:199–231.

51. Nowitzke A, Westway M, Bokduk N. Cervical zygapophyseal joints; geometrical parameters and relationship to cervical kinematics. Clin Biomech 1994; 9:342–348.

83. Heller JG, Pedlow FX, Gill SS. Anatomy of the cervical spine. In: Clark CR, ed. The cervical spine. Philadelphia: Lippincott Williams & Wilkins; 2005:3–36.

52. Mercer SR, Bogduk N. Joints of the cervical vertebral column. J Orthopaed Sports Phys Ther 2001; 31(4):174–182.

84. Moore KL. The neck. In: Moore KL, ed. Clinically oriented anatomy. Baltimore: Williams and Wilkins; 1992:783–852.

53. Fielding JW. Cineroentgenography of the normal cervical spine. J Bone Joint Surg [Am] 1957; 39:1280–1288.

85. Kramer GD. The cervical region. In: Cramer GD, Darby SA, eds. Basic and clinical anatomy of the spine, spinal cord, and ANS. St. Louis: Mosby; 1995:109–155.

54. Kottke FJ, Mundale MO. Range of mobility of the cervical spine. Arch Phys Med Rehabil 1959; 40:379–382.

86. Kubo Y, Waga S, Kojima T. Microsurgical anatomy of the lower cervical spine and cord. Neurosurgery 1994; 34:895–902.

55. Lind B, Silhlbom H, Nordwall A, et al. Normal range of motion of the cervical spine. Arch Phys Med Rehabil 1989; 70:692–695.

87. Tanaka N, Fujimoto Y, An HS. The anatomic relation among the nerve roots, intervertebral foramina, and intervertebral discs of the cervical spine. Spine 2000; 25:286–291.

56. Dvorak J, Schneider E, Saldinger P, et al. Biomechanics of the craniocervical region: the alar and transverse ligaments. J Orthop Res 1988; 6:452–461. 57. Crisco JJ, Oda T, Panjabi MM, et al. Transections of the C1–C2 joint capsular ligaments in the cadaveric spine. Spine 1991; 16:S474–S479.

88. Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine 1982; 7: 319–330.

58. Dvorak J, Panjabi MM. Functional anatomy of the alar ligaments. Spine 1987; 12:183–189.

89. Kasai T. Cutaneous branches from the dorsal rami of the cervical nerves, with emphasis on their positional relations to the semispinalis cervicis. Okajimas Folia Anat Jpn 1989; 66:153–160.

59. Fielding JW, Cochran GVB, Lawsing JF, et al. Tears of the transverse ligament of the atlas. J Bone Joint Surg [Am] 1974; 56:1683–1691.

90. Bogduk N, Marsland A. On the concept of third occipital headache. J Neurol Neurosurg Psychiatry 1986; 49:775–780.

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Part 3: Specific Disorders 91. Darby SA, Daley DL. Neuroanatomy of the spinal cord. In: Cramer GD, Darby SA, eds. Basic and clinical anatomy of the spine, spinal cord, and ANS. St. Louis: Mosby; 1995:251–354. 92. Cabot JB. Sympathetic preganglionic neurons: cytoarchictecture, ultrastructure, and biophysical properties. In: Loewy AD, Spyer KM, eds. Central regulation of autonomic functions. New York: Oxford University Press; 1990:125–140. 93. Groen G, Baljet B, Drukker J. Nerves and verve plexuses of the human vertebral column. Am J Anat 1990; 188:282–296.

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94. Wiberg G. Back pain in relation to nerve supply of the intervertebral disc. Acta Orthop Scand 1949; 19:211–221. 95. Roofe PG. Innervation of anulus fibrosus and posterior longitudinal ligament. Arch Neuro Psych 1940; 44:100–103. 96. Groen G, Baljet B, Drukker J. The innervation of the spinal dura mater: anatomy and clinical implications. Acta Neurochir 1988; 92:39–46. 97. Bogduk N, Marsaland A. The cervical zygapophyseal joints as a source of neck pain. Spine 1988; 13:610–617.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ i: Anatomy and Assessment

CHAPTER

Medical Causes of Neck Pain

47

Paul Cooke, Alvin Antony and Ramnik Singh

Primary benign tumors of the cervical spine

INTRODUCTION 1

Neck pain is a frequent complaint to doctors in Western societies. Valkenburg et al.2 demonstrated in a large epidemiological study in the Netherlands that the lifetime prevalence of neck pain was 30% in males and 43% in females. By definition, neck pain is pain perceived in a region bounded superiorly by the superior nuchal line, laterally by the lateral margins of the neck, and inferiorly by an imaginary transverse line through the T1 spinous process.3 Pain in the neck may arise from any of the structures in the neck, which include the ligaments, osseous structures, intervertebral discs, muscles, zygapophyseal joints, dura, and nerve roots. For the purposes of this chapter, the discussion of the potential causes of neck pain will be limited to nonmechanical or medical causes of neck pain. Other chapters within this text will further elaborate on mechanical etiologies of neck pain. Potential medical causes of neck pain include tumor, infection, inflammatory and inflammatory-like conditions (e.g. spondyloarthropathies, rheumatoid arthritis, fibromyalgia), metabolic disorders (e.g. Paget’s disease), and cardiovascular disease (e.g. myocardial infarctions, carotid dissection).

TUMORS The initial clinical presentation of a patient with tumor involvement of the cervical spine varies considerably. Evaluating and diagnosing cervical tumors early is clinically challenging because the initial symptom of neck pain is a common complaint. Most patients tend to be observed for some time before full evaluation or radiographic investigation is done. For this reason, clinicians must pay special attention to certain ‘red flags’ that may suggest a non-benign origin of the symptoms. Clinical presentation may range from mild pain, stiffness, or palpable mass to significant neurologic compromise. Night pain, weight loss, and anorexia are classic hallmarks of neoplasm. A history of malignancy should raise the suspicion of possible recurrence or a new primary tumor. Evaluating the patient with suspected neoplasm begins with a complete history and physical examination. Appropriate diagnostic imaging studies should begin with plain radiographs and consideration of cervical computed tomographic (CT) scan, magnetic resonance imaging (MRI), and bone scan, when indicated. Primary cervical spine bone tumors are rare, accounting for only 0.4% of all tumors4 and for only 4.2% of the primary bone tumors that occur in the spine above the sacrum.5 Cervical spine primary bone tumors occur disproportionately less frequently than those in the thoracic and lumbar spine. Dreghorn et al.6 found that five of 55 primary spinal bone tumors were cervical. Boriani and colleagues5 noted 63 cervical tumors out of 366 primary bone tumors of the spine. In another series, Weinstein and McLain7 reported only six of 82 primary spinal bone tumors involved the cervical spine.

Primary benign bone tumors of the cervical spine occur most commonly in the first 20 years of life, with the incidence of malignant tumors increasing significantly with age. In a series of 41 benign tumors of the cervical spine (patient ages 4–50 years old) treated at the Istituto Ortopedico Rizzoli between 1952 and 1988, Levine and colleagues8 noted that 32 patients were younger than 20 years old. Another study, by Bohlman et al.,9 noted that nine out of nine patients under 21 years old had benign cervical tumors, but 10 of 12 patients over 23 years old had a primary malignant tumor. Neurologic findings may be common on initial presentation. The most common initial symptom is neck pain that is often worse at night, with continued pain at rest that is not typically relieved with analgesics.9 The duration of symptoms may be prolonged, averaging 19 months in some series.10 Benign primary bone tumors are generally distributed to all levels of the cervical spine. The most common vertebral levels are C2, C4, and C7; C1 is the least frequent site.11 Radicular symptoms can be a common complaint but neurologic abnormalities may be absent. In a series by Levin et al.10 of 41 patients, most of the benign tumors were located in the posterior elements. Osteoid osteomas and osteoblastomas were found in the pedicles and facet joints. Giant cell tumors, eosinophilic granulomas, and aneurysmal bone cysts were most common in the vertebral body, although aneurysmal bone cysts commonly occur in the posterior elements as well.10

Hemangiomas Hemangiomas are the most common benign spinal tumor and occur in about 10% of the population. While they are usually asymptomatic, pathological fractures or expansion of the bony architecture into neural structures may create symptoms.12 These tumors demonstrate a slight female predominance. Hemangiomas of the cervical spine are much less common than in the thoracic and lumbar spines. In a review of literature, Nguyen and colleagues found 10 of 148 reported cases of hemangiomas were located in the cervical spine. Radiographically, hemangiomas have a striated or honeycomb texture, which is the expression of hamartomatous growth of the vascular tissue within the vertebral body. The posterior spinal elements are rarely involved.10

Aneurysmal bone cyst Aneurysmal bone cysts typically occur in the first two decades of life without male or female predilection.13 Isolated disease commonly occurs in the posterior arch, but patients may have circumferential involvement.14 Aneurysmal bone cyst is a pseudotumoral, hyperplastic, and hemorrhagic lesion whose pathogenesis is unknown. These cysts

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frequently occur in the spine, most commonly in the thoracic or lumbar spine.15 Twenty-five percent of aneurysmal bone cysts of the spine observed at the Rizzoli Institute presented in the cervical spine.16

Fibrous dysplasia Fibrous dysplasia is a hamartomatous condition rarely occurring in the vertebrae. When it does occur, it is usually asymptomatic and generally found incidentally. It can, however, cause weakening of trabecular structures and vertebral collapse, thus causing neck pain, muscle spasm, and associated torticollis. Typical radiographs may show an expanded vertebral outline with faded radiolucency of the vertebral body. No treatment is necessary for latent lesions, but stability is indicated when mechanical failure occurs or is impending.17 Radiotherapy should be avoided in active lesions as it is ineffective and can induce sarcoma. Rarely, bone grafting and curettage may be advised.18

Osteoid osteoma The most common benign primary tumor in the cervical spine is osteoid osteoma, which is frequently found in the posterior arch.8 The male to female ratio of occurrence is 2:1 with most cases presenting before the age of 25. One-tenth of all osteoid osteomas occur in the spine and 30% of those in the cervical region. One should consider this diagnosis among adolescents or young adults complaining of persistent neck pain frequently associated with nondermatomal radiation to the upper limb. The pain often interferes with sleep, sometimes causing muscle spasm or torticollis. Patients may respond favorably to aspirin. On imaging, this tumor appears as a small radiolucent area which is more commonly identified by the zone of reactive sclerosis around it. Bone scans are often helpful to focus the examinations on standard radiographs and localize the CT/MRI scan to the suspected lesion. Although there have been some cases of spontaneous regression, curettage of the nidus is usually necessary. In addition, one potential developing technology is percutaneous radiofrequency denervation, which has shown effectiveness in nonspinal lesions and may be useful for the cervical spine.

Osteoblastoma Osteoblastomas are similar to osteoid osteomas but are larger (>2 cm) and less common. Forty percent of reported osteoblastoma cases were found in the spine19 with 25% of those occurring in the cervical region. There is a male predominance and they generally occur before the age of 25. They most commonly arise from the posterior elements, sometimes invading the vertebral body. Symptoms range from nocturnal pain to severe neck pain with muscle spasm.20 Plain radiographs can usually identify osteoblastomas. Patterns vary from that of a giant osteoid osteoma, a rounded radiolucent mass larger than 2 cm with variable amount of scanty ossifications, to that of a highly aggressive purely lytic lesion, which is distinguished from low-grade osteosarcoma.19 The ‘active’ lesions are positive on bone scan and present on CT scan with well-marginated sclerotic borders and a thin reactive shell that thickens the cortical outline.21 These lesions can be treated with curettage with low recurrence rates (5–10%). More aggressive lesions can also be treated with curettage but have higher recurrence rates (20%). If feasible, selective arterial embolization is mandatory to reduce bleeding before curettage and may serve as a treatment option or adjuvant. Cryotherapy or postoperative radiotherapy may also be indicated.

Giant cell tumors Giant cell tumors are ironically considered ‘benign’ by some despite the fact that they have a high recurrence rate and sometimes metastasize into the pulmonary region. Their prevalence in the spine is 532

low (2–10%). Giant cell tumors are more common in females, with a peak incidence in the third decade. On plain radiographs, they often manifest as purely lytic lesions. Staging utilizes a combination of plain films, bone scan, CT scan, MRI, and biopsy. Surgical treatment depends on the staging of the tumor and the degree of involvement of critical vascular and neural structures. Stage 2 lesions may be treated with curettage plus adjuvant therapy (phenol, liquid nitrogen, or methylmethacrylate), whereas stage 3 lesions may require marginal en bloc resection. If the tumor demonstrates malignant transformation, then radiation therapy may be initiated. Preoperative embolization should be considered to reduce blood loss and morbidity. Giant cell tumors have a high recurrence rate and re-resection is often not an option. Therefore, repeated embolization may be necessary to control or perhaps even cure a very large lesion.22 In addition, cryosurgery,23 bisphophonates,24 and interferon and radiotherapy may hold some potential for control of the lesion.

Osteochondroma Osteochondromas are the second most common tumor of the bone but occur infrequently in the spine (1–3% of all osteochondromas). They are often asymptomatic but may become painful if an exostosis grows into the spinal canal or if it develops a large subcutaneous protuberance. In most cases, a palpable painless mass arising from the anterior or anterolateral surface of the vertebral body is found by the patient during skeletal maturation. The tumor forms dense conglomerate masses containing radiolucent areas with clusters of calcifications; typically, the cortex of the host is evaginated, with the cancellous bone continuing directly into the vertebral cancellous bone.25

Primary malignant tumors of the cervical spine Due to their rarity as well as proximity to vital structures, diagnosis and treatment of primary malignant tumors of the cervical spine can be challenging. Accurate diagnosis is often delayed due to their slow evolution and non-specific symptoms. They are frequently discovered only after imaging has been ordered to evaluate intractable pain, or neurologic or anatomical abnormalities. Some of the highergrade malignancies (osteosarcoma, malignant fibrous histiocytoma) that have a more rapidly evolving clinical picture may be found earlier but again are difficult to treat given their anatomic locations adjacent to other critical structures. Definitive treatment decisions are individualized, and there is no clear evidence-based algorithmic approach. The clinical onset is usually non-specific. Patients will often present with cervical pain mostly occurring at night accompanied by muscular spasm. Larger lesions extending anteriorly from C2 might cause dysphagia. Pathologic fracture may occur from neoplastic destruction and erosion. Finally, major neurologic deficits from cord compression or the development of incomplete quadriplegia can also occur. While plain radiographs remain the first imaging study, MRI of the cervical spine is essential in making a definitive diagnosis and should be performed after negative plain radiographs are obtained if the following symptoms persist: dysphagia, persistent night pain, sudden occurrence of neurologic symptoms, and extremity pain which may or may not fit a dermatomal distribution. CT scan and bone scan may also be helpful. Vertebral body tissue biopsy is also important to differentiate between primary and secondary malignancies and to determine individual treatment options. Oncologic staging is based on the histology and local aggressiveness of the tumor and is a key determinant of treatment. Depending on the stage, type of tumor, and resectability, treatment options for malignant tumors may involve surgery, chemotherapy, and/or radiation.

Section 3: Cervical Spine

Chondrosarcoma Chondrosarcoma is a malignant bone tumor whose cells tend to differentiate into cartilage. Its prevalence in the spine is greater than 6%26 but shows no specific prevalence in the cervical, thoracic, or lumbar segments. Patients may present with a slow-growing mass or neurological symptoms if the tumor compresses nearby neural or vascular structures. Plain radiographs may show an extraosseous mass found arising from the posterior elements of the involved vertebra. This may appear irregularly ossified, lobulated, or cauliflower-like, with irregular limits extending out toward the soft tissues. On CT scan, a cartilaginous cap may be appreciated. Treatment is surgical excision, as radiation and chemotherapy are not effective.

Chordoma Chordomas are malignant tumors that transform from ectopic notochordal remnants and are typically seen in the spheno-occipital region (including the first cervical vertebra) and sacrum. They are slow-growing tumors which generally manifest clinically after the fifth decade of life. Fewer than 5% occur before age 20. Chordomas of the cervical spine occur almost exclusively in the vertebral body. The most common complaint is a long history of mild neck pain together with symptoms related to an anterior slow-growing mass: dysphagia, upper respiratory obstruction, and Claude-Bernard-Horner syndrome, or slow cord and nerve root compression from expansile chordomas within the spinal canal.9,22 In rare cases, a palpable mass may be appreciated. Cranial nerve compression can be provoked by craniocervical chordomas.28 On plain radiographs, chordomas generally appear completely radiolucent, although calcifications may occasionally be present within the tumor mass.29 Treatment options include surgery and radiation therapy. Metastases are rare and late; however, local progression of the disease is the most frequent cause of death.

Malignant fibrous histiocytoma Malignant fibrous histiocytoma is a sarcoma of histiocytic origin that consists generally of histiocytes and fibroblasts and is quite rare in the cervical spine.18 In the cervical region, pathologic fracture and neurological symptoms may occur at onset as a result of the rapid collapse of bone. Cases of malignant fibrous histiocytoma can be confused with eosinophilic granulomas. However, because of their rapid progression, one should suspect malignancy in these rapidly growing, large, soft tissue masses that occurs during the second and third decade of life. Treatment of fibrous histiocytomas in the cervical region consists of palliative curettage combined with radiation and chemotherapy. Prognosis is poor.

Osteosarcoma Osteosarcoma is the most common malignant bone tumor but is extremely rare in the spine. Some reported cases of osteosarcoma of the spine are secondary, arising from Paget’s disease, or after radiation therapy.30 If osteosarcoma does occur in the spine, it arises from the vertebral body31 or from the posterior elements, but frequently involves the whole vertebra at the time of diagnosis.32 Varied patterns may appear on plain radiographs, ranging from total radiolucent vertebra with collapse and kyphosis to so-called ‘ivory’ vertebra with variable amounts of surrounding neoplastic tissue. The course of the disease is rapid, with early lung metastases. Treatment considerations include intralesional excision combined with chemotherapy and radiation therapy.

Ewing sarcoma Ewing sarcoma is a high-grade tumor that is rarely found in the spine and is exceptionally rare in the cervical spine. The course of symp-

toms is very rapid in the cervical region and cord compression may be the initial and only presentation. Radiographically, Ewing sarcomas show a totally lytic process collapsing the vertebra and expanding into proximal soft tissues. Treatment includes combined radiation, chemotherapy, and palliative surgery.

Solitary plasmacytoma Plasmacytomas are primary systemic malignant neoplasms of the bone marrow. The most common presenting symptoms include neck pain and muscle spasm. The typical radiograph will show a radiolucent area, central in the vertebral body with early collapse, without ossifications, and with fuzzy limits, mostly evolving toward a complete disappearance of the vertebral outline. This picture in an individual older than 60 years suggests the diagnosis of plasmacytoma and the need to perform appropriate laboratory tests: serum protein electrophoresis, urine analysis for Bence-Jones proteins, complete blood count (anemia), and bone marrow smear, to rule out multiple myeloma. If biochemical tests are positive and no neurologic injury or instability is present, the treatment of choice is radiotherapy combined with chemotherapy. However, surgery maybe necessary if one finds neurologic compromise or instability.

METABOLIC CAUSES OF NECK PAIN Paget’s disease Paget’s disease of the bone (osteitis deformans) is a chronic skeletal disorder, which may result in enlarged or deformed bones in one or more regions of the skeleton. Paget’s disease has a predilection for the axial skeleton and may be widespread at the time of diagnosis. It can present as chronic neck pain and stiffness when the cervical spine is involved. The condition commonly affects the pelvis and spine, particularly the lumbar spine, with a frequency of 30–75%. The sacrum is involved in 30–60% of cases and the skull in 25–65% of cases.33 The proximal long bones, especially the femur, also are affected in 25–35% of cases.34 Paget’s disease causes a malfunction in the normal process of bone remodeling. Excessive bone breakdown and formation can result in bone that is soft and porous. The bone affected by Paget’s disease tends to be more vascular, resulting in an increase in the blood supply and warmth to the involved area. In many cases, Paget’s disease is asymptomatic. Often, the disease is so mild that it is not diagnosed or symptoms may be mistaken with arthritis or other disorders. In other cases, the diagnosis is made only after complications have developed. The excessive bony remodeling associated with Paget’s disease may result in pain, fractures, limb bowing, and hearing loss if the auditory ossicles are affected. Complications associated with fractures, such as articular and neurologic problems, increase mortality in these patients. Sarcomatous degeneration also may occur but is less prevalent. The prognosis is extremely unfavorable if the patient has any type of sarcomatous degeneration, especially those with multicentricity. The 5-year survival rate for a patient with Paget’s disease and sarcoma is 5–7.5% but increases to 50% for those who undergo operative tumor ablation and chemotherapy before metastases. The 5-year survival rate for elderly patients with primary nonpagetic sarcoma is 37%. A more axial lesion carries a less favorable prognosis since higher doses of radiation can be delivered to the appendicular skeleton.35 Laboratory and radiographic studies are beneficial in arriving at the diagnosis. Biochemical indices reveal elevated alkaline phosphatase levels of bone origin, due to increased osteoblastic activity and bone formation. Analysis of alkaline phosphatase isoenzymes helps to identify the hepatic contribution to total levels of alkaline phosphatase. 533

Part 3: Specific Disorders

Radiographs reveal a typical expanding lytic lesion, transverse lucent areas or osteoporosis circumscripta, thickened cortices, sclerotic changes, and bone expansion with coarse disorganized trabecular patterns. Bone scanning is the most sensitive test for evaluating the extent of lesions in Paget’s disease. Bone scintigraphic abnormalities are observed earlier than radiographic changes during the active stage of Paget’s disease.36 The causes of Paget’s disease are still not clearly defined. Research suggests that Paget’s disease may be caused by a ‘slow virus’ infection of bone, a condition that is present for many years before symptoms appear. There is also a hereditary factor, which may be the reason that family members with Paget’s disease are susceptible to the suspected virus. Paget’s disease is the second most common bone disease in the United States, after osteoporosis. Paget’s disease is rarely diagnosed in people under 40. Men and women are affected almost equally. Prevalence in the population ranges 1.5–8% in older adults, depending on the patient’s age and where he or she lives. Several effective therapies for Paget’s disease have recently been approved in the United States.37

INFECTIOUS CAUSES OF NECK PAIN Neck pain is present in over 90% of patients with a cervical spinal infection.38 While cervical spine infections are less frequent than infections in the lumbar or thoracic spine, they deserve important consideration because they have the highest risk for neurologic compromise and disability.39 In this section, infections are classified by anatomic location for easier diagnosis.

Discitis and vertebral osteomyelitis Discitis and vertebral osteomyelitis most often are present together and share much of the same pathophysiology, symptoms, and treatment. Discitis is an inflammatory disorder of the intervertebral disc space often related to infection. Osteomyelitis is an acute or chronic inflammatory process of the bone secondary to infection with pyogenic organisms. Together, these are termed spondylodiscitis. Spondylodiscitis can develop from open spinal trauma, infections in adjacent structures, hematogenous spread of bacteria to a vertebra, or it can occur postoperatively. The cervical spine is only involved in 6% of cases of spondylodiscitis.40,41 Older and immunocompromised patients, including those with diabetes, organ transplantation, malnutrition, cancer, and HIV, are particularly susceptible to developing spondylodiscitis.39,42 Of note, the incidence of spondylodiscitis among intravenous drug users is in the cervical spine.38 Typically, the organism most involved in spinal infection is Staphylococcus aureus. Gram-negative organisms such as Escherichia coli, Pseudomonas, and Proteus species are also commonly found. Pseudomonas infections are prevalent in IV drug users. Nonpyogenic osteomyelitis can be caused by tuberculosis, fungus, yeast, or parasitic organisms. Patients may present acutely, subacutely, or with chronic symptoms. Intravenous drug users generally present most acutely.38 Fifty percent of patients have symptoms for over 3 months before presentation.41 Pain over the infected intervertebral segment is the first and most common clinical symptom, with over 90% of patients with cervical spondylodiscitis presenting with pain.38 The pain commonly radiates to the upper trapezius region or the shoulder but may present with a true radicular component if it is complicated by contiguous spread to an epidural abscess. Approximately only 50% of patients are febrile at the time of diagnosis.41 Neurologic compromise occurs in 17% of all patients with spondylodiscitis, but 50–82% of cervical patients have neurological involvement.43 The most common physical examination

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findings are bony tenderness, paravertebral muscle spasm, and range of motion limitations.44,45 White blood cell count may be elevated in patients with acute cervical infection, but is often normal in patients with chronic infections. However, the erythrocyte sedimentation rate (ESR), though non-specific, is elevated in over 90% of patients and may be a useful indicator of treatment response.41 C-reactive protein (CRP), which has a shorter half-life, is also valuable in monitoring disease response. Blood cultures are positive in 24% of patients.41 Plain radiographic abnormalities are usually not evident until 2–4 weeks after infection. Early findings include disc-space narrowing and abnormal prevertebral soft tissue contours. This is followed by destructive changes in the vertebral endplates and the anterior aspect of the vertebral body which may lead to fracture, collapse, and kyphosis.40,41 Computed tomography may be helpful, as may gallium radionuclide studies and single-photon emission CT (SPECT). However, MRI with gadolinium is considered the diagnostic test of choice, with 96% sensitivity, 93% specificity, and 94% accuracy in detecting spondylodiscitis.46 Decreased signal intensity on T1-weighted imaging, increased signal intensity on T2-weighted imaging, and enhancement on T1-weighted fat suppression imaging are noted47,48 Paravertebral infection, collections under the posterior longitudinal ligament, and epidural abscesses can also be best delineated on T1-weighted fat suppression images.48 However, absolute diagnosis must be based on bacteriologic or histologic examination.39 Percutaneous needle biopsies and open biopsies can safely be performed, with open biopsies yielding a greater percentage of definitive histologic findings. The choice of an antibiotic agent should be based on culture and sensitivity results. If no neurologic compromise is noted, antibiotic treatment should be withheld until culture results become available. In septic or neurologically compromised patients, however, immediate broad-spectrum antibiotics should be started as soon as cultures are obtained. Once cultures become available, these should be changed to the most specific and least toxic agent. In consultation with an infectious disease specialist, patients usually receive 6 weeks of intravenous antibiotics, which may be followed by an oral regimen.39 The clinical picture and ESR should be used as a guide to successful treatment.49 In addition, the patient should be afebrile, have painless cervical spine range of motion, and have a nonfocal neurologic examination. Immobilization may limit pain and prevent deformity. In general, upper cervical spinal infections may require a halo vest and lesions in the lower cervical spine can be managed in a hard collar or cervicothoracic orthosis.39 Surgical treatment is indicated in cases requiring decompression for neural compromise, persistent pain, or elevated ESR despite treatment or to obtain bacteriologic diagnosis if needle biopsy has been equivocal.50 After debridement of the focus of infection, bone grafting or posterior instrumentation are performed to maintain stability. The mortality is less than 5%, but is much higher in elderly patients and those with diabetes or rheumatoid arthritis.47 Fewer than 7% of all patients have residual neurologic deficits.47

Epidural abscess The incidence of pyogenic infections in the epidural space is seen in approximately 2/10 000 hospital admissions but appears to be increasing.51 Most studies place the incidence of cervical epidural abscess at 6–18% of all epidural abscesses.52,53 The lower incidence is likely due to the epidural space in the cervical region being smaller than the thoracic or lumbar spine. Most cervical abscesses are located

Section 3: Cervical Spine

anteriorly in the epidural space where thoracic and lumbar epidural abscesses are commonly seen posteriorly.54,63 Infection is most often spread hematogenously, by direct extension from spondylodiscitis, or direct inoculation from surgery or epidural injection. S. aureus is the most common organism (60%), followed by Gram-negative organisms (18%). This distribution does not change for intravenous drug users. Clinical presentation is quite variable, resulting in a 50% incidence of initial misdiagnosis. Patients generally appear sicker than they do with spondylodiscitis and may present with fever, axial pain, spinal tenderness, and nuchal rigidity in acute cases. All the above symptoms/signs may be absent in chronic cases.53,54 In general, the disease can progress from local spinal pain to radicular pain, followed by weakness and potential paralysis.39 The ESR is generally increased in acute cases, as is the white blood cell count. Definitive diagnosis is, however, based on culture results, which are positive in 90% of cases if taken from the abscess directly, 60% if blood cultures are taken, and as low as 11% if taken from the cerebrospinal fluid (CSF).52,53 Plain radiographs are not useful in diagnosis and CT imaging has a high false-negative rate. MRI has replaced myelography as the standard imaging modality as it is safer and can visualize other pathology as well. A focus of infection would appear as a high-intensity area on a T2-weighted image. If MRI is nondiagnostic, myelography followed by CT may be helpful. An epidural abscess, especially one in the cervical region, is a true emergency and surgical decompression and intravenous antibiotic treatment need to be considered immediately.52,54 Broad-spectrum antibiotics should be started after cultures are obtained and should be changed based on culture results. Most authors recommend 3–4 weeks of intravenous therapy if an epidural abscess is the only lesion, and 6 weeks if spondylodiscitis is also present.52 Since most cervical epidural abscesses occur anteriorly, an anterior approach is often utilized for decompression and debridement. Instrumentation and fusion may be necessary if the decompression jeopardizes the stability of the spine. The prognosis for patients with cervical disease is worse than for those with thoracic or lumbar infections. With aggressive treatment, a majority of patients recover with either minimal or no weakness,51 though prognosis for neurologic recovery depends on the duration and severity of the neurologic deficit. If paralysis persists for longer than 36–48 hours, the likelihood of recovering adequate neurologic function is very poor.54 Prognosis is also worse in diabetics, patients with HIV infection, and those who have concomitant spondylodiscitis. The mortality rate is as high as 38%, even with aggressive treatment.52

Subdural and intramedullary abscesses Though subdural and intramedullary abscesses are rare, they present with spinal pain in one-third of all cases.55 They can also present with weakness, fever, and radicular pain. There are no stages of progression for either, as opposed to the four stages noted for epidural disease. As in all infections discussed thus far, the cervical spine is the least often affected region of the spine and infection is most commonly spread by the same mechanisms as epidural abscesses. Most infections are caused by S. aureus, though Streptococcus, E. coli, and Pseudomonas species have also been cultured.55 The white blood cell count and ESR are generally increased. CSF findings include a non-specific increase in protein. MRI is an effective diagnostic imaging modality. Of note, findings of spondylodiscitis on MRI make the presence of a subdural or intramedullary abscess less likely. Appropriate treatment includes intravenous antibiotic treatment and surgical decompression/drainage. The number of reported cases

of subdural and intramedullary abscesses is much smaller than that for epidural disease, and exact percentages in terms of prognosis are not known.

Deep neck infections Peritonsillar infections are the most common deep neck infections (49%), followed by retropharyngeal infections (22%), submandibular infections (14%), and buccal infections (11%).56 Deep neck infections are usually secondary to contiguous spread from local sites due to pharyngitis, tonsillitis, otitis media, or after dental procedures.57 The microbiology of deep neck infections usually reveals mixed aerobic and anaerobic organisms in approximately 90% of patients, often with a predominance of oral flora. Both Gram-positive and Gramnegative organisms may be cultured.58 Most patients present with generalized symptoms, including fever, chills, and malaise. Localizing symptoms include odynophagia, dysphagia, sore throat, neck stiffness, neck pain, trismus, and voice changes. Physical examination findings include neck swelling, elevation of the floor of mouth, drooling, diaphoresis, fever, and bulging or asymmetry of the pharyngeal wall.58 Tachypnea or shortness of breath may indicate emergent airway collapse.59 The work-up should include white blood cell count with differential, blood cultures, and plain radiographs of the cervical spine. On lateral radiographic view, prevertebral soft tissue thickening greater than 7 mm anterior to the C2 vertebral body or 22 mm anterior to the C6 vertebral body indicates a space-occupying lesion which would most likely be a retropharyngeal abscess.60 In clinical studies, CT with contrast combined with physical examination findings resulted in a sensitivity of 95% and a specificity of 80% for diagnosing deep neck infections. Abscesses are seen as lowdensity lesions with rim enhancement, occasional air fluid levels, and loculations.61 CT scanning of the chest may be helpful if extension into the mediastinum is suggested. The use of MRI for diagnosis of deep neck infections has not been studied in detail, though MRIs can give excellent soft tissue resolution to help localize the region of involvement. Depending on respiratory symptoms, the airway must be secured prior to any further treatment. Addressing the airway may involve observation, endotracheal or nasotracheal intubation, tracheostomy, or cricothyroidotomy for emergent situations. Subsequently, broadspectrum antibiotics should be initiated. In patients with small fluid collections and no respiratory compromise, 50% of deep neck infections can be managed nonsurgically.62 In patients who do not improve within 48–72 hours of antibiotic therapy, or if respiratory compromise is imminent, surgical or CT-guided drainage should be undertaken. Patients treated for deep neck infections can be expected to recover fully as long as the infection is treated properly and in a timely manner.

Meningitis Meningitis is inflammation of the meninges of the spine and is usually divided into bacterial, aseptic, and noninfectious etiologies. Aseptic etiologies include viruses (enterovirus, herpes simplex virus), mycobacterial, and fungal agents; noninfectious causes include carcinomatosis and medications. Bacterial meningitis is historically considered a pediatric illness. However, since the 1990 licensure of conjugate Haemophilus influenzae type b vaccines for use in infancy, the majority of cases of bacterial meningitis now occur in adults.63 In order of frequency, the five most common organisms implicated in bacterial meningitis are Streptococcus pneumoniae, Neisseria meningitidis, Streptococcus agalactiae, Listeria monocytogenes, and Haemophilus influenzae.64 535

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The classic presentation of meningitis includes fever, headache, neck stiffness, photophobia, nausea, vomiting, and signs of cerebral dysfunction (e.g. lethargy, seizure, confusion, or coma). However, the classic triad of fever, nuchal rigidity, and mental status change is found in only two-thirds of patients.65,66 On examination, cranial nerve palsies or other focal neurologic signs may be noted. In general, whenever the diagnosis of meningitis is strongly considered, a lumbar puncture should be performed promptly. The cornerstone in the diagnosis of meningitis is examination of the CSF. Opening pressure is measured and fluid sent for cell count (and differential count), chemistry (i.e. CSF, glucose and protein), and microbiology (i.e. Gram stain and cultures). CSF Gram stain permits rapid identification of the bacterial cause in 60–90% of patients with bacterial meningitis, and CSF bacterial cultures yield the bacterial cause in 70–85% of cases.67 Also, white blood cell count with differential and peripheral blood cultures are required as part of the evaluation. There is minimal role for imaging of the neck in meningitis other than to rule out other etiologies. Treatment is started with empiric intravenous antimicrobial therapy (i.e. antibacterial treatment or antivirals and antifungal therapy in selected cases) as soon as the lumbar puncture and blood cultures have been drawn.68 Once culture results are available, the antibiotic can be changed, though most cases of bacterial meningitis are treated with broad-spectrum cephalosporins for 14–21 days.65,68

Tuberculosis Tuberculosis deserves special mention as it may lead to neck pain secondary to: tuberculous spondylitis, paraspinal or retropharyngeal abscesses, vertebral collapse, atlantoaxial subluxation and epidural, subdural, or intramedullary granulomas.39 In addition to spinal pain, patients generally present with malaise, weight loss, and intermittent fevers. The ESR is generally elevated and the tuberculin purified protein derivative skin test is usually positive.69 Sputum culture may be helpful in patients with pulmonary disease. While radiographs may demonstrate scalloping of the anterior aspect of the vertebrae and bone rarefaction, MRI is the imaging modality of choice. Since intervertebral discs are generally resistant to tuberculosis, disc signal will likely remain preserved. Signal changes on MRI are similar to those seen in pyogenic etiologies. However, with gadolinium, granulomas can be easily differentiated from abscesses since they enhance globally, while abscesses generally enhance in the periphery.70 First-line medications currently include isoniazid, rifampin, pyrazinamide, streptomycin, and ethambutol. Multiple drugs should be used after consultation with an infectious diseases specialist to counteract resistance. Treatment may be continued on an outpatient basis, maintaining the oral regimen for 6–9 months.71 Surgery is indicated if neurologic compromise occurs, medical therapy is failing, or deformity is present. Before surgery, patients with pathologic fractures, kyphosis, or spinal instability should be immobilized in skeletal traction.39 Prognosis for patients with tuberculosis of the spine has improved since chemotherapeutic regimens have diversified. Currently, mortality rates are below 5%.69 In general, early surgery results in a better prognosis. In one study, all patients were relieved of their neck pain within a few days of surgery and kyphosis was corrected from 25.5 to 5.4 degrees.72

References 1. Andersson GBJ. The epidemiology of spinal disorders. In: Frymoyer JW, eds. The adult spine: principles and practice. Philadelphia: Lippincott Raven; 1997:130–141 2. Valkenburg HA, Laar A, Van Hofman A, et al. Nek-en lage rugklachten. In: Instituut epidemiologie. Jaarverslag instituut epidemiologie en zesde voortgangsverslag van het epidemiololgisch preventief onderzoek Zoetermeer. 1980:99–109.

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55. Levy ML, Wieder BH, Schneider J, et al. Subdural empyema of the cervical spine: clinicopathological correlates and magnetic resonance imaging. Report of three cases. J Neurosurg 1994; 81(1):160.

37. Meunier PJ, Vignot E. Therapeutic strategy in Paget’s disease of bone. Bone 1995; 17(5 Suppl):489S–491S.

56. Ungkanont K, Yellon RF, Weissman JL, et al. Head and neck space infections in infants and children. Otolaryngol Head Neck Surg 1995; 112(3):375–382.

38. Sapico FL, Montgomerie JZ. Vertebral osteomyelitis. Infect Dis Clin N Am 1990; 4(3):539–550.

57. Brook I. Microbiology and management of peritonsillar, retropharyngeal, and parapharyngeal abscesses. J Oral Maxillofac Surg 2004; 62(12):1545–1550.

39. Currier BL, Kim CW, Heller JG, et al. Cervical spinal infections. In: Clark CR, ed. The cervical spine, 4th edn. New York; Lipincott, Williams and Wilkins; 2004: 858–889.

58. Asmar BI. Bacteriology of retropharyngeal abscess in children. Pediatr Infect Dis J 1990; 9(8):595–597.

40. Malawski SK, Lukawski S. Pyogenic infection of the spine. Clin Orthopaed Rel Res 1991; 272:58–66.

60. Tannebaum RD. Adult retropharyngeal abscess: a case report and review of the literature. J Emerg Med 1996; 14(2):147–158.

41. Sapico FL, Montgomerie JZ. Pyogenic vertebral osteomyelitis: report of nine cases and review of the literature. Rev Infect Dis 1979; 1(5):754–776.

61. Miller WD, Furst IM, Sandor GK, et al. A prospective, blinded comparison of clinical examination and computed tomography in deep neck infections. Laryngoscope 1999; 109(11):1873–1879.

42. Sapico FL, Montgomerie JZ. Vertebral osteomyelitis in intravenous drug abusers: report of three cases and review of the literature. Rev Infect Dis 1980; 2(2): 196–206. 43. Stone JL, Cybulski GR, Rodriguez J, et al. Anterior cervical debridement and strutgrafting for osteomyelitis of the cervical spine. J Neurosurg 1989; 70(6):879–883. 44. Visudhiphan P, Chiemchanya S, Somburanasin R, et al. Torticollis as the presenting sign in cervical spine infection and tumor. Clin Pediatr 1982; 21(2):71–76. 45. Zigler JE, Bohlman HH, Robinson RA, et al. Pyogenic osteomyelitis of the occiput, the atlas, and the axis. A report of five cases. J Bone Joint Surg [A] 1987; 69(7):1069–1073. 46. Modic MT, Feiglin DH, Piraino DW, et al. Vertebral osteomyelitis: assessment using MR. Radiology 1985; 157(1):157–166.

59. Silvio M, Andrew JH. Deep neck infections. Am J Otolaryngol 1996;17(5):287.

62. Broughton RA. Nonsurgical management of deep neck infections in children. Pediatr Infect Dis J 1992; 11(1):14–18. 63. Peltola H. Worldwide Haemophilus influenzae type b disease at the beginning of the 21st century: global analysis of the disease burden 25 years after the use of the polysaccharide vaccine and a decade after the advent of conjugates. Clin Microbiol Rev 2000; 13(2):302–317. 64. Hussein AS, Shafran SD. Acute bacterial meningitis in adults. A 12-year review. Medicine 2000; 79(6):360–368. 65. El Bashir H, Laundy M, Booy R. Diagnosis and treatment of bacterial meningitis. Arch Dis Child 2003; 88(7):615–620.

47. Tali ET. Spinal infections. Eur J Radiol 2004; 50(2):120–133.

66. Goossens H, Sprenger MJ. Community acquired infections and bacterial resistance. Br Med J 1998; 317(7159): 654–657.

48. Longo M, Granata F, Ricciardi G, et al. Contrast-enhanced MR imaging with fat suppression in adult-onset septic spondylodiscitis. Eur J Radiol 2003;13(3):626–637.

67. Durand ML, Calderwood SB, Weber DJ, et al. Acute bacterial meningitis in adults: a review of 493 episodes. N Engl J Med 1993; 328:21–28.

49. Kemp HB, Jackson JW Jeremiah JD, et al. Pyogenic infections occurring primarily in intervertebral discs. J Bone Joint Surg [Br] 1973; 55(4):698–714.

68. Quagliarello VJ, Scheld WM. Treatment of bacterial meningitis. N Engl J Med 1997; 336(10):708–716.

50. Emery SE, Chan DP, Woodward HR. Treatment of hematogenous pyogenic vertebral osteomyelitis with anterior debridement and primary bone grafting. Spine 1989; 14(3):284–291.

69. Lifeso RM, Weaver P, Harder EH. Tuberculous spondylitis in adults. J Bone Joint Surg [Am] 1985; 67(9):1405–1413.

51. Hlavin ML, Kaminski HJ, Ross JS, et al. Spinal epidural abscess: a ten-year perspective. Neurosurgery 1990; 27(2):177–184. 52. Baker AS, Ojemann RG, Swartz MN, et al. Spinal epidural abscess. N Engl J Med 1975; 293(10):463–468. 53. Hancock DO. A study of 49 patients with acute spinal extradural abscess. Paraplegia 1973; 10(4):285–288. 54. Redekop GJ, Del Maestro RF. Diagnosis and management of spinal epidural abscess. Can J Neurolog Sci 1992; 19(2):180–187.

70. Kim NH, Lee HM, Suh JS. Magnetic resonance imaging for the diagnosis of tuberculous spondylitis. Spine 1994; 19(21):2451–2455. 71. Working Party on Tuberculosis of the Spine. A 15-year assessment of controlled trials of the management of tuberculosis of the spine in Korea and Hong Kong. Thirteenth Report of the Medical Research Council Working Party on Tuberculosis of the Spine. J Bone Joint Surg [Br] 1998; 80(3):456–462. 72. Hsu LC, Leong JC. Tuberculosis of the lower cervical spine (C2 to C7). A report on 40 cases. J Bone Joint Surg [Br] 1984; 66(1):1–5.

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PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ i: Anatomy and Assessment

CHAPTER

Examination of the Cervical Spine

48

Hillel M. Sommer, Brinda S. Kantha and Larry H. Chou

SCOPE AND LIMITATIONS Perhaps there is no better example of the ‘art’ of medicine than in a review of the various physical examination techniques used in clinical diagnosis. More than any other organ system, the musculoskeletal system is the purview of a diverse group of medical specialists and subspecialists who care for persons with spinal and spine-related pain. In the field of medicine alone, the responsibility for physical diagnosis is undertaken by many disciplines including neurology, neurosurgery, occupational medicine, orthopedic surgery, physical medicine and rehabilitation, sports medicine, etc. Beyond allopathic medicine there are osteopathic physicians, chiropractors, and physical therapists among others who examine the spine. While there are some elements common to all groups, each craft presents its own unique nomenclature and terms of reference and stakes a claim to the role of gatekeeper for musculoskeletal pathology. This diversity leads to a heterogeneous approach to the physical diagnosis of spinal pain. Examination techniques vary widely both across and within disciplines. The algorithm used to make a diagnosis by examination is derived primarily from a particular practitioner’s own experience and education and promulgated via authoritative opinion. These techniques are passed down from generation to generation as one clinician incorporates it as part of his own routine, or copies it from other sources. Not surprisingly, then, the evidence base supporting the diagnostic utility of any particular clinical maneuver varies widely. The cervical spinal examination is no exception to this dilemma. For example, cervical spinal range of motion is perhaps the most commonly performed assessment, common to most if not all practitioners, in the assessment of the patient presenting with neck pain. Notwithstanding the popularity of this examination component, there is a wide range of intra-subject variability depending upon the time of day it is measured. In addition, within a given individual, motion in a particular plane differs according to where the starting point of the motion is measured. Accordingly, establishing normal ranges for spinal motion is challenging.1,2 This has led to the development of various devices and technologies that can measure spinal range of motion more precisely.3–7 While certain devices have shown improved reliability as compared to manual physical examination techniques, the use of such devices is not commonplace in clinical practice, leaving the practitioner to rely upon manual techniques to guide clinical decision-making. Compounding these reliability issues is the notion that impaired spinal range of motion correlates with impaired spinal function. In spite of evidence demonstrating a lack of correlation between loss of range of spinal motion and spinal dysfunction,8,9 the use of range of motion as a diagnostic tool remains well engrained in medical culture. Accordingly, range of motion models are regularly used as the basis upon which spinal impairment is rated.

Even more problematic is the attempt to establish whether a particular spinal motion segment, within the multiarticulated spine, has an abnormally restricted or lax range of motion. Despite numerous descriptions of techniques for the palpation of spinal structures, the inter-rater reliability and validity for motion palpation are both lacking in literature support.10–13 Consequently, there is no evidence-based normative database that represents a gold standard against which any single range of motion data set can be compared to determine whether it is ‘normal’ or not. Moreover, there is no hard and fast rule to determine whether a particular patient’s range of motion values are likely to be clinically relevant, even if they do fall outside the range of ‘normal.’ This example will be discussed in more detail later in this chapter. The quest for sources of anatomic pain generators has led examiners to teach provocative maneuvers that are designed to provoke local or referred pain.14 As a result, many syndromic diagnoses have included reproduction of a patient’s habitual pain as an essential diagnostic element. Nevertheless, the combination of the subjectivity of the pain response to palpation and the inherent biases of both examiner and examinee, have limited the predictive value of this aspect of the examination.15,16

WHY EXAMINE THE SPINE AT ALL? The goal of the spinal physical examination is to provide the clinician with clues that support or refute the possible origin of spinal pain and dysfunction. This information is used in conjunction with the history to direct diagnostic testing and treatment to form a clinical report card. When the results of each of these components are concordant, the clinician can be more confident about the certainty of the clinical diagnosis. In addition, cervical spinal pain can be broadly classified into one of three descriptive diagnostic categories: ominous, neurogenic, and non-specific. Ominous spinal pain implies a diagnosis with potentially severe adverse health consequences including spinal tumors, infections, fractures, etc. Physical examination often detects focal abnormalities, but is generally insufficient to render a tissue-specific clinical diagnosis. Neurogenic spinal pain implies a referral from the neural elements including the spinal nerves or spinal cord. In general, these presentations are associated with objective findings more readily and reliably demonstrable on physical examination, including altered spinal reflexes, diminished sensation, weakness on manual muscle testing, and possibly adverse dural tension. Finally, non-specific spinal pain implies pain of non-ominous and non-neurogenic origin. In general, this diagnostic category is consistent with a more benign prognosis than the other two categories. The anatomic origin, if detectable by alternate means, may be discrete 539

Part 3: Specific Disorders

or diffuse. The spinal examination is often non-specific and exhibits wide variability among patients in this descriptive category. Using this diagnostic frame of reference, the anatomic sources in both ominous and neurogenic spinal pain conditions are readily diagnosed using the clinical report card. In these two categories (neurogenic spinal pain in particular), the physical examination is a very powerful tool in the development of management decisions and in the determination of clinical progress. However, the same cannot be said for non-specific pain disorders. Here, the physical examination is often insufficiently specific to render an anatomic diagnosis. The reader is referred elsewhere in this text for the specific techniques used to diagnose anatomic pain generators (disc, zygapophyseal joints, etc.). Nevertheless, there is a role for physical examination, even in this category. Even in the absence of a discrete anatomic diagnosis, function can be assessed either quantitatively or qualitatively by physical examination. In this way the clinician has a measuring stick to use to gauge clinical progress, including response to treatment. Therefore, the utility of the physical examination of the cervical spine is to provide the clinician with an overall impression of the patient. While individual physical examination maneuvers may be lacking in either sensitivity or specificity, the combination of clinical tests used, in the context of the clinical report card, is meaningful in providing the clinician with evidence to generate clinical hypotheses and working diagnosis upon which to base initial treatments. Spinal examination is a dynamic process where findings may change over time, either by chance, as a response to intervention (sometimes even despite intervention) or as a reflection of the condition’s natural history. Repeated examinations over time, in the context of the clinical report card, may prove to be the best way to compensate for the deficiencies inherent in the examination process. In the end, the clinician using physical examination techniques still has to rely somewhat on the art of medicine. The following physical examination protocol is but one of many approaches to clinical examination, and is a synthesis of techniques derived from many sources in the context of the authors’ collective clinical experiences.

PHYSICAL EXAMINATION Since there is often an overlap in the symptoms associated with upper limb conditions and neck conditions referring to the upper limb, evaluation of the cervical spine should not only include a detailed neurological evaluation of the upper limbs, but also an examination of the upper limb joints that could potentially be the source of the presenting symptoms. Symptoms referable to the shoulder often mirror presenting complaints frequently seen in the cervical spine. The examination of the upper limb joints is outside the scope of the present chapter, so the focus will be on the remaining elements of the cervical spinal evaluation. For further information on the shoulder, please refer to Chapter 49. The examination of the cervical spine is tailored to the clinical impression presented by the patient’s history. The presence of local or referred pain, motion restriction, guarding, posturing, etc. will influence the emphasis placed by the examiner on various examination techniques. The various components of the examination should include inspection of posture and musculoskeletal symmetry, evaluation of range of motion in both sitting and supine positions, palpation of the bony and soft tissue structures, and special neural tests. In addition, a detailed neurological examination of the upper limbs must be performed.

540

Inspection Inspection should be performed with the patient both standing and sitting. This provides the examiner with the opportunity to evaluate the patient’s habitual posture to look for signs of asymmetry and potential sources of soft tissue overload. The skin should be inspected for scars, subcutaneous masses, and for lesions that may be consistent with herpes zoster (shingles). Since the thoracic spine is the base of support for the cervical spine, it too should be assessed for scoliosis, kyphosis, and scapular winging. Lastly, station and gait should be screened, specifically looking for signs of spasticity or altered motor tone. Any gait or balance abnormalities may direct further investigation of the central nervous system. Poor posture, in particular, poor sitting posture, is considered to be a significant contributor in back and neck pain.17 When sitting in a slumped or unsupported position, there is a loss of lumbar lordosis, which results in a compensatory thoracic kyphosis. Consequently, there is a resultant compensatory forward inclination of the head with flexion of the lower cervical spine and hyperextension of the upper cervical pole to level the head horizontally. Postural imbalances such as these may impart significant mechanical stress to the cervical spine during sitting. Therefore, it is important to evaluate the patient in both the seated and standing position for compensatory changes in cervical lordosis based on the posture of the lumbar spine. The head-forward posture is typically associated with ‘rounded shoulders,’ with protracted scapulae and internally rotated shoulders. This is often associated with scapulothoracic muscle imbalance with weakness of the mid and lower trapezius, rhomboids, and serratus anterior, and tightness of the anterior shoulder girdle muscles (pectoralis and latissimus dorsi), upper trapezius, and levator scapulae. Since many of these muscles have spinal attachments or are innervated by cervical nerves, abnormal scapulothoracic muscle mechanics can alter the mechanics of cervical paraspinal muscles. Over time, substitution patterns develop to compensate for these pathomechanical features, resulting in a vicious cycle of tissue overload often present in local or referred pain. Diminished cervical lordosis is often the result of paravertebral muscle guarding. This is often a ‘reflex’ response to a variety of possible conditions including muscle overload or a structural abnormality. Altered cervical lordosis should be investigated with a detailed clinical examination and diagnostic imaging, if indicated. Changes in cervical lordosis may also result from compensation for thoracic or lumbar spine posture. Thoracic kyphosis may arise from weak posterior and tight anterior shoulder and chest wall musculature. However, underlying congenital or developmental structural abnormalities must be excluded. These include Scheuermann’s kyphosis, a hemivertebrae, and scoliosis. Acquired thoracic kyphosis may be a result of fractures, both pathologic and traumatic, as well as infections such as tuberculosis. In addition, the examiner should look for signs of muscle atrophy and side-to-side asymmetry that may provide clues of the underlying clinical diagnosis. Normal asymmetry such as depressed dominant shoulder needs to be recognized, and, unless extreme in nature, need not raise concern. Muscle wasting is generally not seen in the neck itself, but rather in the upper limbs, periscapular region, or shoulder girdle. In particular, neurogenic cervical conditions may reveal a myotomal pattern of wasting that provides valuable clues as to the source of anatomic dysfunction. Muscle atrophy, however, is not always indicative of a neurogenic source. Pain is a powerful inhibitor of function, and therefore disuse atrophy should also be considered when muscle asymmetry is noted.

Section 3: Cervical Spine

Range of motion The spine specialist must be able to assess active and passive ranges of motion (ROM) of the cervical spine and understand the potential clinical implications of ‘abnormal’ findings. With the patient seated, the examiner should stand behind the patient in order to assess spinal range of motion. From behind, the examiner can best control motion and optimally view the response of the trunk muscles and adjacent spinal regions to motion. The patient should be given simple commands such as, ‘Touch your chin to your chest,’ ‘Look up to the sky,’ etc. By placing one hand on the head or chest, the examiner can also provide proprioceptive cues to guide the patient through his active motion (Fig. 48.1). In this way the unrehearsed patient is easily able to perform the requested active range of motion with confidence, and without the need for the examiner to demonstrate the required maneuver. Notwithstanding the controversies regarding quantitative spinal range of motion mentioned previously, there is a wide range of published values that are considered ‘normal’ for cervical range of motion. The valid quantification of cervical range of motion demands that the examiner be able to isolate cervical motion from that occurring below. In addition, since the aggregate motion observed is as a result of the sum of spinal segmental motion, it is difficult to determine, especially by manual techniques, whether a particular segment or segments are the source of the limitation. With this in mind, certain parameters can be applied to the evaluation of cervical range of motion to depict the normal population. Cervical flexion is limited by contact of the chin upon the chest. Generally, up to two finger-widths between the chin and chest with a closed mouth is considered full. This may also be envisioned by the arc formed by a point at the vertex with a maximum range of 90°. Extension is limited by the approximation of the posterior zygapophyseal joints. A point on the vertex may pass approximately 70° in extension. Guidelines for cervical side-bending are more difficult to establish since the range of motion is dependent of position (sitting versus supine), neck muscle bulk and tone. All of these factors may affect the particular observed range of motion in a particular individual. In sitting, the passage of a point on the vertex through an arc of approximately 20–45° in either direction is often considered as normal. This is often equivalent to approximately 2–4 finger-breadths between the ear and the shoulder tip. Lateral rotation may also be subject to the variation affecting sidebending. In sitting, the arc passed by a point of the subject’s nose is generally 70–90° in either direction. At the end of the patient’s active range, gentle over-pressure can be applied to determine the end-feel and the extent of the passive range

Fig. 48.1 The examiner places a hand on the chest to provide a target for the end of range of motion and block any forward motion of the trunk. The other hand is positioned on the occiput to provide gentle proprioceptive cues to guide the patient through the active motion without any passive assistance.

Fig. 48.2 Note the examiner’s forearms are used to block trunk rotation while the hands provide tactile cues to guide motion without assisting. At terminal active range of motion, over-pressure can be gently applied to evaluate for a bony or soft end-feel.

(Fig. 48.2). This overpressure also allows the examiner to differentiate between the anatomical versus physiological end range. Palpation will be discussed below. In general, passive ROM (PROM) is greater than the active (AROM), and PROM is increased in the supine versus sitting position. This positional ROM increase is due to the relaxation of resting muscular tone that normally holds the head against gravity. A primary example is the relative ease with which the patient is able to approximate his ear to his shoulder with side-bending when supine as compared to sitting (Fig. 48.3). In the supine examination, cervical extension may be evaluated with the head and cervical spine off the end of the table. Cervical extension can then be performed with passive assistance with one of the examiner’s hands guiding motion and the other blocking motion at the lower, mid and upper cervical spine (Fig. 48.4). Evaluation of flexion is then assessed by resting the examinee’s head against the examiner’s crossed arms and trunk (Fig. 48.5). Cervical range of motion is the summation of movements of the entire cervical spine. Nevertheless, cervical spinal ROM is often reported as ‘flexion is 90 degrees’ leaving the reader the impression that the observed motion occurred at ‘the neck joint.’ To some extent overall ROM also takes into account disc flexibility, inclination of the articular processes, and laxity of the supporting ligaments.

Fig. 48.3 Note the ease at which the patient is able to approximate the ear to the shoulder in supine (below) as compared to sitting (above). This may be attributed to the relative relaxation of axial muscles in supine as compared to sitting positions. 541

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Fig. 48.4 Cervical extension is evaluated with both the head and cervical spine off the head of the table. Cervical extension can then be performed with passive assistance with one of the examiner’s hands guiding motion and the other blocking motion at the lower, mid, and upper cervical spine. In this figure, motion of the upper cervical spine is blocked with the examiner’s left hand.

With the aforementioned wide variability in cervical ROM, and the many associated factors that influence an examiner’s ability to validly measure range of motion, it is perhaps even more important to assess and document range of motion qualitatively. In this regard, it is essential to understand that the different regions of cervical spine serve different functions. For example, the upper cervical segments, C0–C1–C2 function quite differently than the lower segments C3–7. The primary observed upper cervical spine motions are nodding (C0–C1) and rotation (C1–2). The latter motion contributes approximately 50% of rotation with the lower cervical segments contributing the balance. In general, the upper cervical segments function to orient the head on the neck, while the lower segments orient the neck on the trunk. For example, consider the execution of two qualitatively different motions: right rotation and right side-bending. In both cases, the motion at C3–7 is qualitatively similar with ipsilateral coupled sidebend/rotation occurring at each segment. However, the upper cervical motion differs markedly between the two. In the first instance, there is ipsilateral C1–2 rotation, whereas contralateral C1–2 rotation occurs in the latter instance. It is frequently helpful, when AROM restriction is suspected, to assess the motion separately, thus determining to what degree the blockage is due to the upper and lower segments, respectively. For example, when observing sagittal plane motion (flexion–extension), it is helpful to note whether the subject is primarily nodding (indicating lower c-spine restriction) or chin thrusting (indicating upper c-spine restriction). Rotational restrictions can be evaluated by comparing the degree of rotation achievable with the cervical spine in neutral flexion–extension as compared to full flexion. In the latter position, almost all the rotation observed is occurring at the C1–2 joint. By relatively limiting lower cervical spine rotation through

Fig. 48.5 Cervical flexion is performed passively with the patient’s head resting against the examiner’s crossed arms. 542

flexion, the examiner can estimate the degree to which the restriction is arising from the upper or the lower cervical segments. The examiner should be mindful that both age and possibly gender affect cervical ROM. Chen and colleagues performed a meta-analysis of 13 reports looking at these correlations. The majority of these studies found that ROM generally decreases with age. Most found that women had greater range of motion than men, although the gender differences were not statistically significant.1 As discussed previously, spine ROM is a major determinant of impairment in many disability rating schedules. A study by Lowery et al. suggests that impairment ratings based solely on decreased ROM produces less than accurate results.8 In this study, 81 healthy subjects were evaluated using a double inclinometer method. They concluded the current method of impairment determination, based on spinal motion criteria, overestimates impairment by up to 38%. Accordingly, impairment guides have moved away from a range of motion model of assessment of spinal impairment to one based on diagnosis-related estimates. Range of motion evaluation, however, should not be dismissed entirely in correlating pathology. Dall’Alba et al. demonstrated that ROM alone allowed blinded evaluators the ability to discriminate between asymptomatic persons and those with persistent whiplashassociated disorders in 90% of their subjects, with a sensitivity of 86.2% and specificity of 95.3%.18 Perhaps other methods for impairment evaluation should be developed and incorporated that are more specific for individuals with true functional impairment and that account for age-related differences in spinal motion.

Palpation In palpating the soft tissues, the examiner should be cognizant of the three-dimensional anatomy of the underlying tissues. In this way the examiner may better appreciate superficial from deep structures and may direct palpation intentionally either parallel or tangential to the structure’s orientation. While both tenderness to palpation and tissue texture are frequently used tests, they are both lacking in reliability and validity. Nevertheless, these techniques may be useful clinical adjuncts when interpreted in the context of the examination as a whole as part of the clinical report card. Focal tenderness or perceived alteration of tissue texture may be more meaningfully interpreted if accompanied by other focal signs of anatomic dysfunction (e.g. myotomal weakness, crepitus, etc.). Where possible, bony palpation should be performed on each spinal segment. While this may be non-specific as to anatomic cause (and occasionally falsely positive) it may provide the examiner with clues as to the region of the cervical spine (e.g. upper, mid or lower) that is dysfunctional. In general, bony or segmental palpation of the spine is best performed with the patient supine since the postural muscles are better relaxed in this position, providing better access to bony landmarks. In this position, longitudinal friction can be applied to the posterior articular pillars at almost each cervical segment. Pressure can be applied along the groove located between the paraspinal muscles and the trapezius. This can occasionally be facilitated by slightly rotating the examinee’s neck away from the side of palpation (Fig. 48.6). The examiner should also assess the cervical soft tissues including skin texture and muscle tone about the neck. Although non-specific, alterations is texture and tone are often a result of an underlying condition. There must be a familiarity with bony landmarks, including the external occipital protuberance, the spinous processes of each cervical vertebrae, and regions overlying the Z-joints. The occipital protuberance is found at the posterior skull in the midline. The

Section 3: Cervical Spine Fig. 48.6 Longitudinal friction is applied to the posterior articular pillars with the examiner’s middle finger along the groove located between the paraspinal muscles and the trapezius. This is facilitated by slightly rotating the examinee’s neck away from the side of palpation.

spinous processes of C2, C6, and C7 are most obvious. The first prominence palpated caudal to the occiput is C2. The next most obvious spinous processes distally are C6 and C7. Vertebra prominens, also known as the nuchal tubercle, is the most prominent spinous process in the cervicothoracic region. It is the spinous process of the seventh cervical vertebra in 70% of the cases, sixth in 20%, and the first thoracic vertebra in 10%. When the examiner is uncertain which vertebra is the most prominent, flexing and extending the patient’s neck can typically discriminate between the C6 and C7 prominences. Whereas C7 remains fairly stationary with this maneuver, C6 will translate anteriorly on extension and then posteriorly on flexion. In the lateral aspect of the cervical spine, the transverse processes can be palpated. The C1 transverse process is located slightly inferior and anterior to the mastoid process. Moving caudally, the subsequent transverse processes follow the lordotic path of the cervical vertebrae under the sternocleidomastoid muscle. Lymph nodes, carotid pulse, and parotid glands are also palpated in the lateral aspect of the cervical spine. Lymph nodes are readily palpable if swollen. They are located along the anterior border of the sternocleidomastoid muscles. The carotid pulse should be examined at the midportion of the lateral neck to assess whether the pulse is normal and symmetric bilaterally. The parotid gland lies superior to the angle of the mandible and may feel boggy if swollen. Other anterior structures important to identify are the trachea, thyroid cartilage, and thyroid gland. The trachea must be in midline, and any deviation is cause for concern. The thyroid cartilage lies anterior to the C4 and C5 vertebrae. Superficial to the cartilage is the thyroid gland. The gland should be palpated for tenderness or enlargement, which also mandates further investigation.

Special neural tests After completing an evaluation of motion in the cardinal planes, the examiner can evaluate the effect of complex motions by combining

Fig. 48.7 The modified Spurling’s compression test (also known as the maximal compression test) is performed by applying axial pressure with the spine in extension, ipsilateral rotation, and ipsilateral side bending. A positive response occurs when this maneuver reproduces ipsilateral upper limb pain.

various degrees of sagittal, frontal, and transverse planar motion. In 1944, Spurling and Scoville, first described the ‘neck compression test’ stating that it is almost pathognomonic of a cervical intraspinal lesion.19 They performed the test by side-bending the neck towards the painful side and applying axial pressure on the top of the head to reproduce the patient’s characteristic pain and radicular symptoms. They did not indicate how long this position was to be held or with how much axial loading. Side-bending the neck away from the lesion usually provides relief. Tong et al. performed a cross-sectional study to determine the sensitivity and specificity of Spurling’s maneuver for cervical radiculopathy.20 The test was performed as in Spurling’s original description, and was considered positive if it reproduced pain or paresthesias that began in the shoulder and radiated distally to the elbow. They concluded that Spurling’s maneuver is not very sensitive (30%) but is specific (93%) for cervical radiculopathy diagnosed by electromyography. Therefore, it appears not as useful as a screening test, but more clinically useful in confirming a cervical radiculopathy. Bradley and colleagues suggested a three-stage protocol to the test.21 If symptoms are reproduced, subsequent stages need not be performed. The first stage consists of axial compression with the cervical spine in neutral position. The second stage involves compression with the neck in extension, and the third stage places the neck in extension and lateral rotation to the unaffected side first and then to the symptomatic side, both with axial compression. Radicular pain into the arm is considered a positive test and indicates irritability of a nerve root. The dermatomal distribution of the symptoms suggests involvement of a specific nerve root. The neck positions of each stage of the test progressively narrows the intervertebral foramen, which may be seen in conjunction with uncovertebral and zygapophyseal hypertrophy and disc herniations. A similar test, called the maximal compression test, incorporates side-bending and rotation towards the symptomatic side, along with extension and axial compression (Fig. 48.7). This combination of positions causes maximal neuroforaminal compression and is positive if pain radiates into the arm. Most clinicians perform the maximal compression test but erroneously refer to it as the Spurling’s maneuver, when in fact it is a ‘modified’ Spurling’s compression test. Another provocative maneuver used in patients with cervical radiculopathy is the application of lateral pressure against the vertebrae. This maneuver, also known as the doorbell sign, is considered positive when pressure to the anterolateral cervical spine reproduces referral of pain into the ipsilateral upper limb (Fig. 48.8). A positive sign is considered to be consistent with spinal nerve irritability or other unspecified spinal segmental dysfunction. The distraction test is used to diagnoses spinal nerve irritation by alleviating radicular symptoms. The examiner places one hand on the patient’s chin and the other hand around the occiput and slowly

Fig. 48.8 Lateral pressure is applied to the cervical spine against the various cervical segments. This maneuver is considered positive when pressure to the anterolateral cervical spine reproduces referral of pain into the ipsilateral upper limb. 543

Part 3: Specific Disorders

applies upward traction to the patient’s head. The test is positive if the patient reports a decrease in radicular symptoms. The shoulder abduction relief sign, also called Bakody’s sign, is observed when the patient abducts the arm and places the hand or forearm on the top of the head. This arm placement, which may be performed subconsciously by the patient for symptomatic relief, is also indicative of presence of cervical nerve root traction that is being alleviated as a result of this maneuver. Thoracic outlet syndrome (TOS) should be tested as part of the comprehensive cervical examination. Classic, or neurogenic, TOS occurs when the lower trunk of the brachial plexus becomes compressed within the scalene triangle by a cervical rib, fibrous band of tissue, or from an elongated C7 transverse process. In TOS, neck pain is rarely a prominent symptom.22 The patient may complain of deep, aching pain in the ulnar side of the forearm, occasionally involving the hand. Subjective hand weakness and clumsiness may be present. Muscle wasting may be seen in the thenar eminence, particularly involving the abductor pollicis brevis. This is also referred to as the Gilliatt-Sumner hand.23 There is sometimes decreased sensation on the ulnar side of the hand. Roos describes several methods to reproduce symptoms of classic TOS.24 The more well known of the tests, also referred to as Roos’ test, involves a 3-minute elevated arm stress test. The shoulder is abducted to 90° and externally rotated, and the elbow is flexed at 90°. Additional stress is incorporated by asking the patient to open and close the hands for the duration of the test. The test is considered positive if typical upper limb symptoms are reproduced. Another less-known TOS test was also described by Roos. Percussion or light pressure held for 30 seconds over the supraclavicular fossa may reproduce pain, thereby distinguishing these symptoms from those emanating from the cervical spine. Compression of the subclavian vessels has been termed vascular TOS. Adson’s maneuver evaluates for obliteration of the radial pulse when the arm is placed at the side in a slightly extended and externally rotated position with the head laterally rotated to the contralateral side. However, the false-positive rate is high.25 Furthermore, Wright’s test is positive when the radial pulse is diminished when the arm is placed in a horizontally abducted position with the head turned to either side. This indicates only positional compression of the subclavian artery, and is not necessarily indicative of vascular TOS. In Wright’s series of 150 asymptomatic normal subjects, 92.6% had reduction of the radial pulse in this position, calling into question the clinical utility of this test.26 Upper limb neural tension tests, also known as dural tension tests, place stress on the neural elements of the upper limb. They are analogous to the straight leg raise test performed in the lower extremities for reproduction of lumbar radicular pain. The upper limb neural tension tests may be performed in ulnar, median, and radial bias positions. In all testing positions, it is important to keep the ipsilateral shoulder depressed. For upper limb neural tension testing with median nerve bias, the shoulder is first abducted to 90°. The arm is externally rotated, the forearm is supinated and the elbow, wrist, and fingers are extended. For ulnar nerve bias testing, the arm is abducted to 90°, the elbow is flexed to 90°, the forearm is maximally pronated, the wrist is extended and radially deviated, and the fingers are extended. The radial nerve bias dural tension is performed with the shoulder abducted to approximately 10°, the elbow extended, the forearm fully pronated, the wrist flexed with ulnar deviation, and the fingers held in flexion. With all of the above neural tension tests, the neck may be positioned in contralateral side-bending to further increase tension on the nerves analogous to slumping or neck flexion in the straight leg raise. 544

Upper limb neural tension tests are considered positive only if the patient’s typical symptoms are reproduced, and if there is a side-toside difference, assuming the contralateral side is asymptomatic. Coppieters et al. tested the reliability of neural provocation tests in both the laboratory and clinical setting.27 Their study, focusing on median bias dural tension, demonstrated that pain provocation during neurodynamic testing is a stable phenomenon with good inter-tester and intra-tester reliability with intra-class correlation coefficient of 0.98.

The neurologic examination Neurogenic neck pain should be suspected when a patient presents with a complaint of neck and upper limb pain. Shoulder girdle pain, while often interpreted to be of thoracic origin, is most commonly a sign of either intrinsic shoulder pathology or referred pain from the cervical spine. The regional neurological examination should screen for special neural tests, altered reflexes (either augmented or diminished), weakness in a myotomal pattern, and sensory loss in a dermatomal pattern. Key reflexes to be evaluated include: ● ● ●

C5 – biceps and brachioradialis, C6 – pronator teres, C7 – triceps.

Key muscle groups to be evaluated include: ● ● ● ● ● ●

C4 – shoulder elevators, C5 – shoulder abductors, C6 – elbow flexors, wrist extensors, C7 – elbow extensors, wrist flexors, C8 – thumb and finger extensors, T1 – hand intrinsic muscles.

Key sensory areas to be evaluated correspond to regions of minimal dermatomal overlap including: ● ● ● ● ● ● ●

C4 – base of neck and shoulder, C5 – lateral epicondyle, C6 – thumb, C7 – long finger, C8 – small finger, T1 – medial epicondyle, T2 – axilla.

The regional neurological evaluation may be performed in either sitting or supine position, provided that the patient is relaxed. Once in position, it is desirable not to move the patient’s limbs too much in order to avoid altering tone or guarding. The biceps reflex is performed with the forearm in neutral pronation/supination. Firm pressure is applied with the thumb over the biceps tendon at the elbow. The reflex hammer is applied directly to the examiner’s thumb, and the muscle contraction is either observed or palpated. If the reflex is not evoked, the forearm may be supinated to increase tension and facilitate the reflex. The brachioradialis reflex is applied directly to the tendon at the distal forearm. Augmentation can be induced with slight stretch applied as ulnar wrist deviation. The pronator reflex is performed with the patient’s wrist in supination. The examiner’s thumb is firmly applied to the distal radius. The reflex hammer strikes the thumb in an effort to induce further supination, thus stretching the pronator. The response is forearm pronation or elbow flexion. The reflex may be augmented by applying more supination or slightly decreased elbow flexion.

Section 3: Cervical Spine Fig. 48.9 Here, the examiner positions the upper limb in a position to test the elbow flexors. The patient is told, ‘Don’t let me move it.’ Prior to resisting, the examiner can apply a few brief jerks in the direction of the resistance in order to give proprioceptive cues to guide the patient through the resisted motion.

The triceps reflex is performed with patient’s forearm supported comfortably by the examiner. The reflex may be augmented by slightly increasing the elbow flexion, or by asking the patient to very gently push away to activate the triceps. Manual muscle testing requires that the examiner be in a position where mechanical advantage is obtained. In this way a mismatch between a small examiner and large patient is minimized and the interpretation of weakness is more sensitive. Simple commands should be given to the patient in order to evoke the desired patient response. Generally, the examiner should position the limb in the position to be tested (Fig. 48.9). The patient should be told, ‘Don’t let me move it.’ Prior to resisting, the examiner can apply a few brief jerks in the direction of the resistance in order to give proprioceptive cues to guide the patient through their resisted motion. Manual muscle testing should always be performed bilaterally, one muscle at a time. This allows for a more valid side-to-side comparison. The unaffected side should be tested first in order to maximize the learning effect prior to assessing the side where weakness is suspected. This helps ensure better effort on the affected side, since the process has been learned by the patient. Sensory function may be best screened with a single modality such as pinprick. The key sensory areas noted previously from C4 to T2 should be screened bilaterally one level at a time. The patient should be asked to report any side-to-side differences. A positive response may include hypoesthesia or hyperesthesia. Tests for upper motor neuron (UMN) signs can direct the physician to consider abnormalities occurring at the level of the spinal cord or above. A widely practiced UMN response is the Babinski reflex, or plantar response. This reflex is elicited by stroking the undersurface of the foot from the heel to the great toe. Extension and fanning of the toes is considered a positive, abnormal response. The Hoffman reflex is the UMN sign analog in the hand. It is elicited by quick flexion of the distal interphalangeal joint of the long finger. Abnormal reflex is noted if there is immediate interphalangeal joint flexion of the ipsilateral thumb. This reflex can be indicative of an upper motor neuron lesion. However, the reflex is normal in some, especially young female individuals, and may be seen in the overly anxious patient. Lhermitte’s sign is elicited by briskly flexing the patient’s neck. Shock-like sensations radiating down the patient’s thoracic spine often indicate spinal cord pathology, although this can also occur in some patients with herniated cervical discs. Other findings on inspection warranting further work-up include muscle fasciculations, which may be benign in nature or can indicate underlying UMN pathology. Gait dysfunction, such as spastic or circumducted gait, raises clinical suspicion for cervical myelopathy.

NECK OR SHOULDER DYSFUNCTION? Due to the often-overlapping clinical presentations, it is essential to always examine both the shoulder girdle and the cervical spine in a patient presenting with either neck or upper limb pain. The similarity in presentations is due to several reasons: ● ● ● ●

Neck pathology frequently refers to the shoulder by either somatic or spinal nerve referral patterns. C5–6 is the most commonly affected cervical segment, with a somatic referral pattern that mimics intrinsic shoulder pathology. In C5 and C6 radiculopathy, shoulder weakness may lead to the development of mechanical shoulder girdle dysfunction. Finally, the incidence of cervical radiculopathy and rotator cuff disease both peak in the fourth and fifth decades.

SUMMARY Despite the numerous flaws associated with individual physical examination maneuvers with respect to sensitivity, specificity, reliability, and validity, the spinal examination remains a critical part of the evaluation of the patient presenting with neck pain and dysfunction. The physical examination, taken as a whole, still has a role to play in providing the examiner with an overall impression of the patient’s condition. In the context of a clinical report card comprised of a history, physical examination, diagnostic testing, and response to treatment, the examiner has at his disposal a powerful tool to guide clinical management decisions.

Acknowledgments The authors would like to thank Ai Mukai MD, Department of Medicine, Hershey Medical Center, Pennsylvania State College of Medicine, for her assistance in the literature search and retrieval of original publications.

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PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ i: Anatomy and Assessment

CHAPTER

Biomechanics and Assessment of the Painful Shoulder

49

Mark I. Ellen and Faisel M. Zaman

INTRODUCTION During the routine assessment and treatment of ‘neck pain’ the physician treating spinal disorders will be presented with extrinsic pathology that generates pain in similar patterns to that of cervical spine disorders. Therefore, the history, physical examination, and diagnostic work-up should all point to the same etiologic agent of the patient’s chief complaint. As clinicians, our best treatment rationale is based upon an accurate diagnosis. The more understanding that other factors may contribute to, or cause pain about the cervical region, the better it should be for patient care. Spinal pain itself is complex in nature. To add another dimension to the diagnostic dilemma, the shoulder itself is among the most complex of all the body’s joints (Fig. 49.1). The shoulder is composed of four joints: the glenohumeral (GH), the acromioclavicular (AC), the sternoclavicular (SC), and the scapulothoracic (ST). It entails anywhere from 22 to 26 individual muscles and/or muscle slips, which are utilized for a combination of stability, power, and control of elevation and rotation. The shoulder is unique in that it is highly mobile, with an estimated 16 to 17 thousand positions in which the upper extremity may be placed, while necessarily exhibiting a concurrent

Acromion

lack of bony stability. The arm can move through approximately 180 degrees in elevation, 150 degrees of internal and external rotation, and flexion and extension or anterior and posterior rotation in the horizontal plane of approximately 170 degrees.1 The very interaction of the musculature both as agonist and antagonist must be coordinated for even the simplest motions in order for there to be an effective movement. An understanding of the anatomy and biomechanics of the shoulder is essential for clinicians who treat spinal disorders, as well as for other orthopedic practitioners.

ANATOMY The shoulder joint is unique, as multiplanar mobility of the joint is dominant over static stability. This generous amount of mobility can lead to a multitude of intrinsic ailments about the shoulder and, in fact, a majority of shoulder problems stem from this relative lack of bony stability. All of the 26 or so muscles about the shoulder play a role in ensuring appropriate motion of the joint complex but, as a nonweight-bearing joint, there is tolerance of some loss of individual muscle and/or tendon function that still allows for adequate usage in activities of daily life.

Clavicle Trapezoid part, conoid part of coracoclavicular ligament

Coracoacromial ligament Capsular ligaments Supraspinatus tendon (cut)

Superior transverse scapular ligament and scapular notch

Coracohumeral ligament

Coracoid process

Greater tubercle, lesser tubercle of humerus

Supraspinatus tendon Capsular ligament Synovial membrane Subdeltoid bursa

Acromion Glenoid labrum

Deltoid muscle

Openings of subscapular bursa to shoulder joint

Intertubercular synovial sheath (communicates with articular synovial cavity) Subscapularis tendon (cut)

Biceps brachii tendon (long head) A

Outline of subscapular bursa Capsular ligaments

B

Axillary recess Glenoid fossa of scapula

Fig. 49.1 (A and B) The shoulder is composed of four joints: the glenohumeral (GH), the acromioclavicular (AC), the sternoclavicular (SC), and the scapulothoracic (ST). 547

Part 3: Specific Disorders

Sternoclavicular joint Four ligaments and an intra-articular disc stabilize the sternoclavicular joint, which is mobile about all three axes (x, y, and z planes). The interclavicular ligament provides restraint to medial clavicular motion superiorly. It interconnects one medial clavicle to the other medial clavicle via its attachment to the sternum. However, this ligament may be absent or nonpalbable in 22% of individuals.2 The interclavicular ligament is taut when the arm is brought to the side. There are anterior and posterior capsular structures that prevent motion in the anterior and posterior planes; of the two, the anterior is the stronger restraint. The costoclavicular ligaments, which run obliquely and laterally from the first rib to the clavicle, provide for stabilization inferiorly. The posterior capsular structure is the strongest stabilizing force that resists downward motion, and the anterior structure resists superior motion of the medial clavicle.

Acromioclavicular joint The acromioclavicular joint also has mobility about all three axes, but it is generally less mobile than the sternoclavicular joint. It is the sole articulation of the scapula to the clavicle, and thus, the only bony connection the upper limb has with the axial skeleton. The acromioclavicular joint is a plane-shaped, diarthrodial joint that is found between the lateral end of the clavicle and the medial side of the acromion. Within the joint is a perforated cartilaginous disc that is thought to decrease the bony stressors placed upon the joint during elevation and rotation of the upper extremity. The coracoclavicular ligament provides stabilization to superior migration of the distal clavicle. It actually consists of two distinct bands, the medial conoid and lateral trapezoid ligaments. Encompassing the distal end of the clavicle and the medial aspect of the acromion is the acromioclavicular ligament, which acts as the primary restraint to motion in the anteroposterior plane.

Glenohumeral joint The glenohumeral joint is what the layman and many in the healthcare field think of as the ‘shoulder joint.’ Although this joint is considered a ball (humerus) and socket (glenoid) joint, the socket covers only onequarter of the humeral head.3–5 This ratio was initially calculated by the following simple formula, known as the glenohumeral index:

in appearance. There are wide variations in labral anatomy among individuals, and there is no correlation between labral depth and glenoid size. Two aspects of labral anatomy that are fairly consistent are that the most stable, largest portion is the anterior and inferior area, and that the labrum itself acts to physically double the depth of the socket for the humeral head. The glenohumeral joint allows for three distinctly different types of motion: spinning, sliding, and rolling. Spinning is when the contact point on the glenoid remains the same, but the contact point of the humeral head is changing. Sliding occurs when the contact point on the glenoid is changing, but that of the humerus remains the same. This generally occurs in unstable joints, and in extremes of motion in normal joints. The third type of motion, rolling, is when the contact points on both the glenoid and humeral head change.12 Anatomically, the proximal humerus is separated into four parts: the articular surface, the greater tuberosity, the lesser tuberosity, and the diaphyseal shaft. In relation to the shaft, there is a 45-degree medial angulation to the humeral head, and a 30-degree retroversion relative to the transcondylar axis of the distal humerus. The intertubercular groove lies between the greater and lesser tuberosities, and it is here that the tendon of the long head of the biceps lays.13 This tendon is held in place not only by the coracohumeral ligament, but also by the transverse humeral ligament. During shoulder abduction, the humeral head slides on this tendon. If the biceps tendon should rupture, anterior translation of the humeral head is subsequently increased.14 Utilizing an elegant approach, Johnson noted in 1937 that in order for the upper limb to maximally elevate, the humerus must externally rotate.15 Initially, research pointed to a physical obstruction caused by the coracoacromial arch to the greater tuberosity of the humeral head. By 1976, it was realized that this movement provides for loosening of the inferior ligaments of the glenohumeral joint while simultaneously allowing for optimal articulation with the glenoid.16 Thus, full arm elevation combined with external rotation is a position of greater stability than full elevation alone. This is due to a combination of relative laxity and stability of the three glenohumeral ligaments, intrinsic muscular forces, and negative intracapsular pressure.17 The ligamentous restraints of the glenohumeral joint are the inferior glenohumeral ligament (IGHL), the middle glenohumeral ligament (MGHL), and the superior glenohumeral ligament (SGHL) (Fig. 49.2). These glenohumeral ligaments, which insert onto the

Maximum diameter of the glenoid:maximum diameter of humeral head Saha recalculated the ratio to 0.6 in the transverse plane and 0.75 in the sagittal plane.6 Maki and Gruen further refined the ratio to 0.58 and 0.86 in a presentation to the Orthopedic Research Council in 1976. Three different types of glenohumeral articulations have been identified, and in each case the humeral head is classified as being smaller, equal to, or larger than the radius of curvature of the glenoid.6,7 This difference is believed to impact a variety of shoulder instability patterns. A smaller glenoid surface diameter is necessarily a smaller effective contact surface for the humeral head and is thus a more unstable configuration.6,8,9 In the coronal plane, the articular surface of the glenoid comprises an arc of approximately 75 degrees, whereas the articular surface of the humeral head is roughly 120 degrees, or one-third of a sphere. The glenoid labrum increases coverage about the humeral head by nearly 100%, and doubles the depth.10 The glenoid labrum is composed of dense fibrous connective tissue, and serves not only to increase the surface area and depth of the glenoid, but also to increase the structure’s load-bearing ability.11 The labrum is a structure which appears to be fibrocartilagenous in structure when examined superiorly but, as one approaches the inferior surface, is almost capsular 548

Acromion Supraspinatus tendon Glenoid fossa (cartilage) Subdeltoid bursa Infraspinatus tendon Openings of subscapular bursa

Teres minor tendon Cut edge of synovial membrane

Coracoacromial ligament Coracoid process Coracohumeral ligament Biceps brachii tendon (long head) Superior glenohumeral ligament Subscapularis tendon Middle glenohumeral ligament

Inferior glenohumeral ligament Fig. 49.2 The ligamentous restraints of the glenohumeral joint are the inferior glenohumeral ligament (IGHL), the middle glenohumeral ligament (MGHL), and the superior glenohumeral ligament (SGHL).

Section 3: Cervical Spine

glenoid labrum and humeral neck, have often been described as ‘capsular thickenings.’15 This ‘capsular-ligamentous’ complex is the major static stabilizer of the shoulder, and although all of the ligaments are necessary for proper function, the IGHL is the most essential component of this complex. Studies have shown that the shoulder joint capsule possesses greater elasticity and twice the strength of that of similar structures within the elbow.19 The superior, middle, and inferior glenohumeral ligaments are considered the anterior glenohumeral ligaments. The coracohumeral ligament, which runs laterally from the coracoid process to insert upon the superior–anterior aspect of the humeral head, is the most consistent of the ligaments of the shoulder capsule.20 In addition to providing an anterior stabilizing force to the biceps tendon, it also renders stability to the shoulder, particularly when the arm is in the dependent position.21 The superior glenohumeral ligament lies beneath the coracohumeral ligament, and has been found to contribute little to the stability of the glenohumeral joint. It also is a relatively constant structure, and arises from the tubercle of the glenoid, inserting upon the lesser tuberosity of the proximal humerus. The long head of the biceps tendon originates posteriorly to the SGHL. In concert with the superior tilt of the glenoid, the SGHL provides passive resistance to inferior subluxation and dislocation of the humerus.22 The middle glenohumeral ligament exists underneath the subscapularis muscle, and its presence is the most variable of the glenohumeral ligaments.20 Its origin is at the supraglenoid tubercle at the superior glenoid and anterior superior labrum, and inserts with the subscapularis muscle at the lesser tuberosity of the humerus. This ligament provides the majority of resistance to anterior humeral head displacement.20,23 It may measure up to 2 cm wide, and as much as 4 mm in thickness.24 The thickest of the glenohumeral ligaments is the inferior glenohumeral, which originates from most of the anterior glenoid labrum, and inserts on the inferior margin of the humeral head articular surface. The IGHL is the main static stabilizer in the abducted arm, and it reinforces the inferior capsule.25,26 A fundamental knowledge of the anatomy of the IGHL is instrumental in understanding the pathophysiology behind recurrent anterior humeral dislocation. When the humeral head dislocates in an anterior direction, the associated detached bone–labral complex essentially renders the IGHL an incompetent structure. The IGHL is composed of an anterior and posterior band with an axillary pouch in between.27 The anterior band serves as the major stabilizer of the glenohumeral joint when the arm is in abduction and external rotation.25 In this position, the anterior band appears to fan out, while the posterior band becomes cordlike. With the arm in internal rotation, the anterior band becomes cordlike, while the posterior band spreads into a fan shape to support the joint.

Codman’s paradox As noted earlier in this chapter, the capsular–ligamentous complex is the major static stabilizer of the shoulder. This soft tissue envelope has made studying and hence understanding the complex movements about the shoulder quite difficult, as it hampers observation of skeletal motion in the natural state. For as long as there have been observations reported on shoulder biomechanics, there has been much discussion of these complex motions such as reported in ‘Codman’s paradox.’ This has been demonstrated as follows: While seated or standing, have the arm resting at the side with the medial epicondyle of a flexed elbow facing the midline of the trunk; take the arm to a position flexed forward to 90 degrees. Next, abduct the arm 90 degrees so that the epicondyle is then pointing perpendicular to the coronal plane. Then, bring the arm back to the side to

its initial position. After performing these motions, the medial epicondyle is no longer facing medially towards the trunk, but is rather rotated away from the body in an ‘anterior’ position all without the humerus ever being actively axially rotated.15 Discussions have abounded surrounding this concept. It has been noted that the angular rotations involved with this movement do not add up to the concluding position, and that they are thus sequence dependent. The sequence of these complex rotations is what allows this phenomenon to occur. In aerospace terminology, these rotations are called the ‘Eulerian angles’ of yaw, pitch, and roll.10

Scapulothoracic joint The scapulothoracic joint can be thought of as the base that stabilizes the shoulder girdle. Jobe and Pink28 have likened it to a seal balancing a ball on its nose. If that seal is able to stand still it can balance a ball for a lengthy time; however, if the seal is unable to obtain a stable position the ball will fall. This basic premise of strength at the base of the shoulder or core stabilization as referred to in spine rehabilitation is quite similar and will be discussed later. As noted above, the only bony attachment site of the scapula to the axial skeleton is at the acromioclavicular joint. Therefore, it is the muscular attachments, the scapulothoracic muscles, that are referred to as the scapular stabilizers. It is these muscles that act to position the scapula to the proper orientation on the thoracic cage for a given shoulder motion. These muscles include the trapezius, levator scapulae, serratus anterior, pectoralis minor, and rhomboids (major and minor). Shoulder abnormalities can stem from weakness or tears of one or all of these muscles. Disorders may also result from neuropathic abnormalities such as entrapment of the suprascapular nerve or compression of the dorsal scapular or long thoracic nerve, resulting in neuropraxia, neurotmesis, or axonotmesis. Space-occupying masses such as cysts or tumors as well as arthritic spurs and bony deformity in the glenohumeral joint can also result in abnormalities of function of the scapular stabilizers and hence the scapulothoracic joint.

BIOMECHANICS The relative motion between the scapulothoracic articulation and the glenohumeral joint during shoulder abduction is termed the scapulothoracic rhythm.17,29–31 Over the entire arc of abduction, the glenohumeral joint moves more than the scapulothoracic joint; however, this difference is large at the beginning of abduction, and minimal at the end range of motion. Glenohumeral motion is much greater than scapulothoracic motion for the first 30 degrees of abduction; this ratio has been reported as ranging from 4:1 to 7:1.16,32 Over the subsequent 30–180 degrees of shoulder abduction there is less asymmetry between glenohumeral motion and scapulothoracic motion, and the ratio is then closer to 5:4. The arc of full arm elevation involves anterior rotation of the scapula by about 6 degrees, with subsequent posterior rotation of the scapula on the order of 16 degrees until the arm is at its final resting position. That is, 10 degrees posterior to it’s starting position.33 In addition to these movements, there is also a simultaneous forward tilt of the scapula by 20 degrees.10,34 Passive stability about the shoulder girdle is afforded by a united structure consisting of the joint articulation itself, the capsuloligamentous restraints, glenoid labrum, and resting muscle tension, as well as negative intra-articular pressure within the shoulder joint. The articulation of the humeral head with the glenoid portion of the scapula was found by Saha6 to be posteriorly oriented by an average of 7 degrees in relation to the body of the scapula. This apparently minor retroversion is thought to be an important element of the static restraint system. It has been clinically correlated that those 549

Part 3: Specific Disorders

individuals with less retroversion have a greater tendency towards recurrent anterior dislocation at the glenohumeral joint. While there is agreement that there is a wide array of the amount of retroversion within individuals, there is still no consensus with regards to the clinical relevance, or in research with regards to these variations and their part in instability of the joint. Within the glenohumeral joint there is a small but measurable amount of negative pressure, on the order of −4 mmHg. This also is thought to be a small but important contributor to static stability of the joint. It is believed that any compromise of the capsule or even some fraying of the undersurface of the supraspinatus may result in the loss of this stabilizer. While this work has relied on cadaver examination, it is still not known the extent of loss that may occur in living tissue, as the entire human body is believed to be under negative pressure. Resting muscle tension appears to account for much of the stability about the shoulder girdle. The base of the shoulder girdle is the scapula, and three groups of muscles concordantly maintain its stability: the posterior, intrinsic, and extrinsic groups.35 The scapulohumeral stabilizers comprise the posterior group of muscles, consisting of the trapezius, levator scapulae, rhomboids, and serratus muscles. This group helps to provide a stable base of rotation for glenohumeral motion, and maintains the glenoid in a position of maximal congruency with the humeral head, thus maintaining the proper length–tension relationship of the glenohumeral musculature.36,37 The intrinsic groups of muscles are the glenohumeral stabilizers and include the rotator cuff musculature: the supraspinatus, infraspinatus, teres minor, and subscapularis. Dynamic stability about the shoulder is dependent upon muscular forces generated by these muscles and those surrounding the scapulothoracic joint.38 The deltoid is the primary muscle of the extrinsic group, with biceps and triceps being secondary extrinsic muscles. These muscles comprise the primary positioners of the humerus and forearm.38 Pink and Perry have made an excellent point to acknowledge that while these restraints are static in nature, they are also plastic. They have the ability to deform by stretching from different sources, whether intrinsic or extrinsic. Once deformation has occurred there may be further clinical sequelae that need to be addressed. Inman and associates first described the concept of a ‘force couple’ in 1944.13 They described the dynamics of multiple forces passing across and through the shoulder during active motion to allow for any desired arm position. For example, their theory noted that if the deltoid were to pull the humerus superiorly, then the subscapularis, infraspinatus, and teres minor would act as a single functional unit to counteract any shearing forces that the deltoid placed upon the glenohumeral joint. This would then allow the humeral head to maintain itself in a congruent alignment to the glenoid by simultaneously depressing the humeral head and allowing the head to rotate about the glenoid. In addition to causing direct joint compression, the rotator cuff musculature provides dynamic stability in another manner. It allows finely tuned asymmetric contractions to maintain the humeral head in the glenoid during active motions that may otherwise cause subluxation or shoulder instability.

STRENGTH Up to 26 muscles have been described as encompassing the shoulder girdle. However, as the cross-sectional area, overall length, and bony attachment sights of each muscle vary, strength about the shoulder is not symmetrical. Rather, there are contrasting relative strength differences dependent upon the particular plane of motion within which movement takes place. These relative strengths in descend-

550

ing order are as follows: adduction, extension, flexion, abduction, internal rotation, and external rotation. The maximal force a muscle can produce is proportional to the number and size of muscle fibers it contains. This is indirectly measured by the muscle’s cross-sectional mass. Lever length, or muscle–joint orientation, is composed of both the actual length of the muscle as well as how distant its attachment sites are from the joint proper. This determinant is variable, as it is dependent on joint position. The greater the perpendicular distance between a muscle’s line of pull and the fulcrum of motion, the more effective is the muscle’s force. This is related to Inman’s ‘force-couple’ concept previously discussed. Muscle activity level as measured by electromyogram (EMG) is a concept related to muscle endurance. This is usually expressed as a percentage of maximum muscle test (MMT) by generally accepted muscle strength testing positions. Some authors prefer to use the terms percentage of maximum muscle activity (MMA), or percentage of maximal voluntary contraction (MVC), also determined by manual strength testing. In general, when a muscle is firing at less than an MMT (MMA or MVC) of 25–40% it can be used for an extended period of time without fatiguing. Conversely, when a muscle is utilized at an MMT of greater than 50% it will fatigue relatively quickly. For discussion, we can think in terms of a general arrangement of the shoulder musculature. Muscles that link the axial skeleton to the scapula, such as the rhomboids major and minor, levator scapulae, serratus anterior, and trapezius, are muscles which act as stabilizers, of the shoulder. The muscles that serve to link the axial skeleton to the humerus, namely the pectoralis major and latissimus dorsi, yield power to the extremity in internal rotation, adduction, and extension. The four muscles of the rotator cuff along with the teres major and deltoid, control elevation and rotation, as well as serve to link the scapula with the humerus. The muscles that provide the power of elevation, the upper pectorals and middle trapezius, link the scapula and clavicle to the humerus. To effectively elevate the upper extremity, four muscles need to act in a coordinated fashion. The deltoid and supraspinatus muscles act to elevate the humerus while the trapezius and serratus anterior muscles act to stabilize the scapula. If there is a deficiency of any two of these muscles, functional elevation of the upper extremity becomes impossible. Precise control of shoulder motion is allowed by the muscle action as described by Inman’s concept of the ‘force-couple.’ This coupling of forces about a joint is based on the theory that with greater generation of compressive force there tends to be less shear and, therefore, less nonrotational motion about a joint. It is easier to understand if we think of those forces directed toward the center of the joint as compression forces, and those that run parallel to the joint surface as shear forces. At the glenohumeral joint, maximum shear forces are generated when the extremity is held at 60 degrees of abduction, and maximum compression forces are with the extremity at 90 degrees of abduction. Pure compression allows the joint to support approximately 10 times the weight of the arm, or approximately the weight of the entire body. Thus, the primary role of the rotator cuff is to minimize glenohumeral shearing force, as rotational control is secondary.

NERVE SUPPLY Innervation of the shoulder complex (Fig. 49.3) is mainly via the C5 through C7 nerve roots, via the brachial plexus. Because of its proximity to many bony structures, the great mobility about the shoulder and neck, and superficial location, the brachial plexus is particularly

Section 3: Cervical Spine Dorsal scapular nerve Rhomoideus major muscle Rhomoideus minor muscle Levator scapulae muscle (supplied also by branches from C5 and C6) Supraspinatus muscle Suprascapular nerve Deltoid muscle Teres minor muscle Axillary nerve

Superior lateral brachial cutaneous nerve

Radial nerve

Inferior lateral brachial cutaneous nerve

Infraspinatus muscle Teres major muscle Lower subscapular nerve

Posterior antebrachial cutaneous nerve

Posterior brachial cutaneous nerve (branch of radial nerve in axilla) Lateral intermuscular septum Brachialis muscle (lateral part) Triceps brachii muscle

Long head Lateral head Medial head Brachioradialis muscle Triceps brachii tendon Extensor carpi radialis longus muscle Medial epicondyle Olecranon Anconeus muscle

Extensor digitorum muscle Extensor carpi ulnaris muscle

susceptible to traumatic injury.39 The branches that come off of the lateral cord of the brachial plexus, the lateral pectoral nerve and musculocutaneous nerve, are those that are most essential to shoulder function. The musculocutaneous nerve passes through the coracobrachialis muscle, several centimeters below its insertion when leaving the axilla.40 The upper and lower subscapular nerves are also important branches off the posterior cord of the brachial plexus with regards to innervation of the subscapularis muscle. Also from the posterior cord arises the thoracodorsal nerve (also known as the middle subscapular nerve), which supplies the latissimus dorsi, and travels along the lateral border of the scapula.40 The axillary nerve, after obtaining its contributions from the C5 and C6 nerve roots, travels along the inferior portion of the subscapularis

Extensor carpi radialis brevis muscle

Fig. 49.3 Innervation of the shoulder complex is mainly via the C5 through C7 nerve roots, via the brachial plexus.

muscle, and is a large terminal branch of the posterior cord of the brachial plexus. It winds around the surgical neck of the humerus to supply the teres minor and deltoid muscles, and terminates as the upper lateral brachial cutaneous nerve and supplies skin sensation over the inferior half of the deltoid and adjacent areas of the arm.38 This intimate association with the humeral neck places the axillary nerve in a potentially compromising position, as it is susceptible to injury from trauma to the area or from surgical procedures about the shoulder.41 The long thoracic nerve is made up of contributions from the ventral branches of the C5, C6, and C7 nerve roots. It then travels along the medial wall of the axilla and supplies the serratus anterior. The suprascapular nerve, after receiving its innervation from the C5 and C6 nerve roots from the upper trunk of the brachial plexus, 551

Part 3: Specific Disorders

travels along the superior border of the scapula in the suprascapular notch, eventually supplying the supraspinatus and infraspinatus muscles. The transverse scapular ligament is a potential entrapment site and may compress the suprascapular nerve as it crosses through the scapular notch.40 The innervation of the glenohumeral joint is mainly from the axillary nerve, suprascapular nerve, and the lateral pectoral nerves.42

VASCULAR SUPPLY The arterial supply of the entire upper limb comes from the subclavian artery, which becomes the axillary artery after crossing the first rib, and continues into the arm as the brachial artery (Fig. 49.4).43 The axillary artery extends between the first rib and the lower border of the teres major muscle, and gives off branches to the thoracic wall and its covering muscles, as well as to the shoulder and upper part of the arm. There are six named branches off of the axillary artery.43

Coracoid process Deltoid muscle Anterior circumflex humeral artery

Venous drainage is mainly by the axillary vein, which is joined by the cephalic vein, lying between the deltoid and pectoralis major muscles, and two brachial veins. The upper end of the cephalic vein is the only superficial vessel of any size in the shoulder region.43 Many anatomic variations may be found at the cervicothoracic junction, some which can compress neurovascular structures to generate a variety of thoracic outlet syndromes (TOSs).39 There are three distinctly different pathophysiologic types of thoracic outlet syndrome.44 The most common type of TOS may also be referred to as costoclavicular syndrome, and presents without neurologic or vascular anomalies, but with symptoms of pain and/or paresthesias in the arms. The symptomatology is felt to be a direct result of brachial plexus compression between the clavicle and a normal first rib.39 A second type of TOS is neurologic TOS, in which weakness and sensory deficits stem from stretch and/or compression of the lower trunk of the brachial plexus. Some anatomic variations that may be responsible for the neurologic TOS are an accessory cervical rib with

Axillary artery Pectoralis minor muscle head

Humerus

Lateral cord, medial cord of brachial plexus

Pectoralis major muscle and tendon

Musculocutaneous nerve

Long head, short head of biceps brachii muscle

Subscapularis muscle Anterior and posterior circumflex humeral arteries

Coracobrachialis muscle

Teres major muscle

Brachial artery

Latissimus dorsi muscle

Muscular branch

Deep brachial artery Medial brachial cutaneous nerve Median nerve

Ulnar nerve

Muscular branch Biceps brachii muscle Brachialis muscle

Medial antebrachial cutaneous nerve Long head Medial head

Triceps brachii muscle

Superior ulnar collateral artery Radial recurrent artery Biceps brachii tendon

Medial intermuscular septum Inferior ulnar collateral artery

Ulnar artery

Medial epicondyle of humerus

Radial artery

Pronator teres muscle

Brachioradialis muscle

Bicipital aponeurosis Flexor carpi radialis muscle

552

Fig. 49.4 The arterial supply of the entire upper limb comes from the subclavian artery, which becomes the axillary artery after crossing the first rib, and continues into the arm as the brachial artery.

Section 3: Cervical Spine

or without an associated fibrous band, an enlarged cervical transverse process, an abnormal first rib, hypertrophy of the anterior scalene muscle (termed scalenus anticus syndrome), and hyperabduction syndrome.4 The third type of TOS is vascular, and consists of narrowing of the subclavian artery as it angles over the first rib in patients with a well-developed cervical rib. In this case there are often signs of vascular compromise such as intermittent blanching of the fingers or entire hand, and rarely, frank ischemia, and gangrene. Neurologic symptoms should be absent in this purely vascular type of TOS.39 Rarely, Doppler ultrasound and duplex scanning can indicate that subclavian artery compression by the scalene muscles is the etiology of early fatigue, arm heaviness, and hand coldness in the upper extremity of well-conditioned athletes.45,46 When the shoulder is positioned in abduction and external rotation, these findings can be elicited in many asymptomatic individuals, as well as overhead athletes; therefore, this test is not considered specific. This is the basis behind ‘Adson’s maneuver,’ in which the examiner externally rotates and extends the patient’s test arm while palpating the radial pulse. The patient then extends and rotates the neck towards the test arm and takes a deep breath. Absence or diminishing radial pulse is felt to indicate vascular TOS caused by compression of the subclavian artery by the scalene muscles. As mentioned above, this test is nonspecific and is thought to have a greater than 50% incidence of false positivity.47–49 Occasionally, symptoms may result from a subclavian artery aneurysm with thrombosis. In this case, embolization to the hand with severe ischemia may result.46 Compression of the axillary, posterior humeral circumflex, suprascapular, or subscapular arteries may all result in similar, localized symptoms.46

ASSESSMENT As difficult as it is to master the biomechanics of the shoulder, to perform and understand the findings of the examination may be only slightly easier. Even some of the most accomplished leaders in the field have confided that, at times, they still have diagnostic difficulty based upon history and physical examination of the shoulder alone. The physical complexity of the joints under what can be a vast soft tissue covering, coupled with the wide ranges of motion that may be achieved, make both the sensitivity and specificity of any single examination finding somewhat questionable. Even with a relatively lengthy examination, many of the previously accepted assumptions have come under more scrutiny. The improvement in diagnostic imaging as used as an adjuvant for shoulder maladies, along with the ability of enhanced surgical techniques, have led many authors and clinicians to question previously accepted standards. The assessment should include an adequate history to evaluate for an underlying etiologic agent such as trauma, repetitive motion, metabolic illness, rheumatoid history (familial and personal), nicotine or other pharmaceuticals, change in or additions to a workout regimen, overall intensity of shoulder usage, and older versus younger populations. In athletes, sports-specific questions such as sport, position, training techniques, dominant versus nondominant side, and expectations of future usage are all pertinent areas to query. A detailed history of the pain complaint should also be elicited including: relative intensity, positional differences (including the effect of direct weight bearing), radiation, aggravating and alleviating factors, associated symptoms, and of course, the location of the pain. Not all patients have the ability to see a physician in a timely fashion, so the presentation may be either acute or chronic. In the senior author’s practice he has noted that the more acute the process, the more closely the above descriptors correlate with the origin of the pain.

With acute injuries, pain is usually associated with a decrement in range of motion. In addition, to avoid pain, the patient will position the affected arm in a dependent posture at the side. Motion of the glenohumeral joint can be affected within a few days or less and, especially in the older population, a secondary adhesive capsulitis may develop relatively easily. Some patients may present with a visible or palpable deformity or, more rarely, localized edema or an effusion may be present. These are typically the residua from a traumatic event such as a fall or other direct trauma. The correlation of history and physical findings in this instance is typically quite high. Treatment rationale can therefore follow established protocols with expected success rates dependent upon extent of injury, provider skill, medication delivery, other underlying medical processes, and patient commitment. It is the patient that presents with a chronic history of shoulder pain of more than a few months that typically represents the greater diagnostic challenge. As the pain persists, other areas in continuity with or near the shoulder may become symptomatic areas. Chronic shoulder symptoms may include pain, instability, stiffness, weakness, a sense of ‘catching,’ crepitus, deformity, paresthesias or dysethesias, or any combination of the above. This multitude of symptoms may or may not be reported in combination with neck, elbow, or arm pain, which may confuse the diagnosis, as the work-up is no longer as simple as that of the acutely involved patient. The classic teaching of mid-deltoid pain for conditions such as inflammation or tears of the rotator cuff, degenerative arthritis, calcific tendinitis, labral tearing, avascular necrosis of the humeral head, localized bursitis, or adhesive capsulitis usually allows for a direct approach to treatment. Making the correct diagnosis becomes more challenging, however, when the pain is either within this region or described beyond the local area without the above ‘classic’ findings on examination, plain radiographs, or magnetic resonance imaging (MRI) scans. Several authors have reported an approximately 5% incidence of pain referable to the cervical spine in patients presenting with shoulder pain.50–54 Slipman et al. reported of a case of extrinsically induced pain that included symptoms that all pointed to an intrinsic cause of pain. Despite diagnostic work-up for both shoulder and cervical spine etiologies, all signs pointed to an intrinsic pathology, but arthroscopic findings were minimal and postoperatively there was no change in symptoms. Repeat diagnostic studies of the cervical spine were performed and there was no change from the initial findings. A diagnostic selective nerve root block was then performed, providing complete relief of pain and immediate return of full range of motion.55 This case helps to illustrate that even though the entire work-up may point toward one etiology, when evaluating nonacute presentations of pain, perseverance may be needed to correctly diagnose and adequately treat the condition, and a referal for ‘chronic pain management’ may be premature. In those patients with chronic shoulder symptoms, the history may be less helpful for several reasons. The duration of symptoms may lead to some forgetfulness on the part of the patient, blurring memory of some of the initial symptoms and treatment as well as other associated medical maladies at the onset. As noted above, loss of range of motion of the shoulder girdle, primarily at the glenohumeral joint, typically happens since the arm tends to be held in a pain-free, dependent position, mainly at one’s side. This lack of glenohumeral mobility demands an alteration of the basic biomechanics of the shoulder. The patient will have to substitute another aspect of the shoulder complex to allow overhead or other reaching motions. Typically, a greater contribution from the scapulothoracic joint is needed to achieve the elevation required to perform even simple activities of daily living.56 553

Part 3: Specific Disorders

This alteration in the pattern of movement of the shoulder will therefore require an increase in contribution from the joints adjacent to the shoulder girdle proper. Whether there is a substitution pattern of the adjacent musculature, or if greater motion of the elbow is required to place the upper limb in a desired position, an increase in stress to these regions will lead to associated symptoms such as an epicondylitis of the elbow as the problem progresses. Most of us were taught that pain radiating to or from the paracervical region or below the elbow is not consistent with primary shoulder pathology. While this is typical in acute conditions, the senior author has not found this to be true after just a few months, if symptoms are left untreated. In his practice, many patients with ongoing symptoms of at least a few months report both upper limb paresthesias, primarily in an ulnar nerve distribution, as well as radiating pain either across the scapula or about the upper trapezius to the paraspinal musculature. Some patients report concomitant headaches with, more rarely, photophobia. The history is taken in the same way, with attention to onset, and previous treatments and studies, with a particular interest with regards to changes in the pattern or severity of the pain. We are always interested in not only which particular treatments have been rendered, but also how well they seem to have worked. In particular, we find it necessary to ask where about the shoulder an injection may have been given and not simply if one has been performed. Was the injection to the subacromial space, acromioclavicular joint, or to the glenohumeral joint? The patient may have undergone a trigger point injection or an injection to the long head of the biceps sheath. Dependent upon the previous injection site, one might consider another injection. This would depend upon further physical examination findings in combination with recent radiological tests. Abnormalities seen on radiographic evaluation, as well as bone or soft tissue masses found clinically, need to be evaluated in a methodical and well-organized fashion.57 Both benign and malignant tumors may be found in and about the shoulder complex. The goals in treatment of malignant tumors are, in order of priority, preservation of life, limb, and function.57 Benign tumors found about the shoulder include osteoid osteoma, osteoblastoma, osteochondroma, enchondroma, giant cell tumors, chondroblastoma, eosinophilic granuloma, and synovial osteochondromatosis57. Malignant tumors include osteosarcoma, chondrosarcoma, Ewing’s sarcoma, and myeloma.57 In addition to malignant and benign tumors, there may also be various tumor-like conditions associated with the shoulder, such as aneurysmal bone cyst, simple bone cyst, fibrous dysplasia, and Paget’s disease of the bone.57 We always ask not just if physical therapy has been advised or how long they may have been in therapy but what precisely was the composition of that therapy. We find it helpful to go over all of the therapeutic exercises since, even in the most restricted cases, the ability to place the arm in a multitude of positions can lead to enhanced pain. This pain most often appears to be caused by repeated tensile forces about the long head of the biceps tendon. This tendon can act to function as a humeral head depressor, creating increased anterior shoulder pain with motion. Typically, we prefer to protect the anterior structures of the shoulder by only stretching those of the posterior cuff and capsule. Resistive exercises are performed in planes that also are protective of these anterior structures, principally by limiting the ranges of motion of the involved limb. All motions should be pain-free during the workout and none need to be performed with the involved hand above shoulder height in a non-thrower. Typically, a simple program consisting of just four to six exercises is initiated with progression determined by amount of pain, overall range of motion, strength, and patient requirements.

554

The assessment itself then turns to the physical examination. While no human is perfectly symmetrical, we do look for side-to-side differences in muscle mass, height and angulation of the shoulder, and motion of the scapula and arm during both passive and active range of motion. Watching the scapula itself is a superb way to evaluate for subtle pathologic findings. We observe not only the rotation of the scapula (rhythm) but its positional changes on the torso, such as how much it may move laterally, and its stability upon the torso.58 Glenohumeral impingement testing as well as compression testing of the acromioclavicular joint is performed. Manual muscle testing of all shoulder related and upper extremity musculature is performed bilaterally as well. Resistive testing to enhance subtle scapular instability may also be performed. Assessment of distal pulses, sensation, muscle stretch reflexes, and distal extremity muscle bulk is performed. Palpation of not only the bony prominences but also of the bicipital groove, posterior cuff structures, trapezius, latissimus dorsi, and parascapular muscles is also performed to assess for tender spots or myofascial trigger points to conclude the initial examination. Assessment for other etiologies may need to be performed either at the end of the shoulder evaluation or on an ensuing visit to ascertain for extrinsic causes of pain including spinal, peripheral nerve, or vascular etiologies. Many times, radiating pain that has a dysesthetic quality emanates from a non-neurogenic cause. When assessing the scapula, weakness of the supporting musculature will allow the scapula to wing away from the thoracic cage, thus creating scapular instability. The rhomboids, upper trapezius, any of the four rotator cuff muscles, or paraspinal muscles may have been weakened from the initial injury. As noted earlier, when a muscle is chronically firing at 40% or more of MMT, fatigue will become a factor. Myofascial trigger points have been described in the literature since the mid-1800s.59 Trigger points presumably appear in these fatigued muscles and on cursory look may mimic either cervical or thoracic radicular symptoms. These symptoms may include, but are not limited to, paracervical radiating pain, radiating pain through the scapular body, and radiating pain about the thorax either anteriorly or posteriorly. As described by Simmons et al., both observation and hands-on experience are needed to help delineate these etiologies.60 Symptoms may be exacerbated by manual muscle testing as well. Observation of the scapula during resistive testing such as infraspinatus strength testing or a wall push-up may help in making the diagnosis. Observing both active and passive range of motion of the shoulder contributes to the determination of intrinsic or extrinsic etiologies as well. Patients may be able to have near-symmetrical active range of motion by utilizing muscular substitution patterns. However, they are rarely able to reproduce such a full range when the arm is passively moved as the scapula is stabilized. Most patients do have either a decrement in abduction–internal rotation or abduction–external rotation and many may have positive impingement signs. It is rare that extrinsic causes of pain would yield any significant difference in side-to-side comparison. Motor strength testing of the shoulder girdle and rotator cuff is very useful in the overall examination of the shoulder, but not in differentiating the etiology of symptoms. Typically, intrinsic shoulder pathology will lead to weakness in one or more of the muscles of the cuff, such as the supraspinatus or infraspinatus. When the parascapular musculature is weakened, there may be good to excellent strength within the rotator cuff itself, but there may be early fatigue or enhancement of scapular instability during resistive maneuvers. Direct palpation may yield areas over the rhomboids consistent with myofascial trigger points as well. In cases of chronic cervical spine disease, especially at the C5 and C6 levels, a similar result may be

Section 3: Cervical Spine

noted due to the effects of neurogenic damage affecting the shoulder girdle musculature, with resultant weakness. Evaluation of muscle stretch reflexes may help indicate a neurogenic cause of pain. However, while a Tinel’s sign may reveal irritation of a peripheral nerve, it has not helped in our practice in the differential diagnosis of shoulder pathology. As noted earlier, a more extensive neurovascular examination may be warranted if the initial examination does not point to a defined etiologic agent or previous work-up has failed. Diagnostic imaging is beneficial to evaluate for both intrinsic agents of pain such as arthritic causes, calcific and degenerative tendinopathies, tumors, fractures, dislocations, separations, avascular necrosis, soft tissue injuries such as cuff tears or labral injuries, as well as to assess for foreign and loose bodies. Plain radiographs may be obtained in three orthogonal planes with views dependent upon the type and extent of injury, patient mobility, and physician preference. If further imaging is sought, the MRI is the test of choice and may be performed with an intra-articular contrast agent to better evaluate the integrity of the labral lining or postoperative changes that would be difficult to differentiate by MRI alone. Electrodiagnostic studies play an important role in evaluation of the painful shoulder. It has been shown that sensory loss, such as an axillary patch for axillary nerve injuries, is unreliable in the diagno-

sis of axillary nerve injury.61 Electrodiagnostic testing can delineate neuromuscular involvement, including severity, and help with prognostication. Appropriately timed studies are important in defining the degree of nerve compromise.62 Electrodiagnostic testing usually is not performed until wallerian degeneration has taken place, approximately 3 weeks after injury, unless there is suspicion of nerve transection, which can be identified within 1 day of the event. The most common nerve injury associated with shoulder pathology is axillary nerve injury. Axillary nerve injury is most commonly associated with traumatic anterior shoulder dislocation, resulting in a neuropraxia or axonotmesis caused by traction.61,63 Spontaneous recovery of axillary nerve function has been documented up to 7 months after injury.64 The shoulder examination may not be straightforward, even when performed by the most experienced of clinicians (Fig. 49.5) One must always be aware of extrinsic etiologies of pain in this region. The cervical spine is a primary extrinsic cause of pain and not all patients will present with ‘classic’ symptoms. A solid fund of knowledge in combination with an appropriately detailed diagnostic workup is crucial to completely address a patient’s need for treatment and future prevention of both clinical symptoms and recurrence of pathology.

References 1. Steindler A. Kinesiology of the human body under normal and pathological conditions. Springfield, IL: Charles C. Thomas; 1955. 2. Bearn JG. Direct observations on the function of the capsule of the sternoclavicular joint in clavicular support. J Anat 1967; 101:159–170.

History

3. Codman EA. The shoulder. Boston: Thomas Todd; 1934.

–

Injury acute/chronic

No injury

4. Bost FC, Inman VTG. The pathologic changes in recurrent dislocation of the shoulder. J Bone Joint Surg 1942; 24:595. 5. Steindler A. Kinesiology of the human body under normal and pathological conditions. Springfield, IL: Charles C. Thomas; 1955.

Diabetes, smoking, vasculitis

6. Saha AK. Dynamic stability of the glenohumeral joint. Acta Orthop Scand 1971; 42: 491.

Exam

7. Sarrafian SK. Gross and functional anatomy of the shoulder. Clin Orthop 1983; 173:11.

– Deformity

Unlimited

Limited and pain in entire ROM

Range of motion

Impingement testing –

8. Cyprien JM, et al. Humeral retrotorsion and glenohumeral relationship in the normal shoulder and in recurrent anterior dislocation (scapulometry). Clin Orthop 1983; 175:8.

X-ray

+

9. Randelli M Gambrioli PL. Glenohumeral osteometry by computed tomography in normal and unstable shoulders. Clin Orthop 1986; 208:151.

Shoulder specialist

Winging, lateral offset, obvious dysrhythm

Isolated weakness with or without pain Global weakness with pain

No pain

Positive exam

Neurovascular

13. Inman V, Saunders M, Abbot L. Observations on the function of the shoulder joint. J Bone Joint Surg 1944; 27:1–30. 14. Warner JP, McMahon PJ. The role of the long head of the biceps brachii in superior stability of the glenohumeral joint. J Bone Joint Surg [Am] 1995; 77:366–372. 15. Johnston TB. The movements of the shoulder joint: A plea for the use of ‘plane of the scapula’ as the plane of reference for movements occurring at the humeroscapular joint. Br J Surg 1937; 25:252.

Motor strengths Intact

11. Soslowsky LJ, Flatow EL, Bigliani LU, et al. Articular geometry of the glenohumeral joint. Clin Orthop Rel Res 1992; 19:26–34. 12. An K-N, Chao CYS. Kinematic analysis of human movement. Ann Biomed Eng 1984b; 12:585.

Scapular stabilizers Intact

10. Morrey B, An K-N. Biomechanics of the shoulder. In: Rockwood CJ, Matsen F, eds. The shoulder. Philadelphia: WB Saunders; 1990:208–245.

Negative exam

Fig. 49.5 Algorithmic approach to patient presenting with shoulder injury.

16. Poppen N, Walker PS. Normal and abnormal motion of the shoulder. J Bone Joint Surg [Am] 1976; 58:195–201. 17. Dvir Z, Berme N. The shoulder complex in the elevation of the arm: a mechanism approach. J Biomech 1978; 11:219. 18. Warwick R. Williams PL, eds. Gray’s anatomy, 35th edn (British Edition). Philadelphia: WB Saunders; 1973. 19. Kaltsas DS. Comparative study of the properties of the shoulder joint capsule with those of other joint capsules. Clin Orthop 1983; 173:20. 20. De Palma AF, Callery G, Bennet GA. Variational anatomy and degenerative lesions of the shoulder joint. Am Acad Orthop Surg Instr Course Lect Ser 1949; 6:225– 281.

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Part 3: Specific Disorders 21. Basmajian JV, Bazant FJ. Factors preventing downward dislocation of the adducted shoulder joint. J Bone Joint Surg [Am] 1959; 41:1182.

43. Hollinshead WH. The upper limb. In: Jenkins DB, ed. Hollinshead’s functional anatomy of the limbs and back, 8th edn. Philadelphia: WB. Saunders; 2002:63–219.

22. Terry GC, Hammon D, France P. Stabilizing function of passive shoulder restraints. Unpublished data from the Hughston Orthopaedic Clinic, Columbus, GA, 1988.

44. Steward JD. Focal peripheral neuropathies, 2nd ed. New York: Elsevier; 1993.

23. Moseley HE, Overgaard B. The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. J Bone Joint Surg [Br] 1962; 44;913. 24. De Lorme D. die Hemmungs bander des Schultergelenks and ibrc Deductung fur die Schulter Luxationen. Arch fur Klin Chirurg 1910; 92:79. 25. Turkel SJ, et al. Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg [Am] 1981; 63:1208. 26. Ouesen J, Nielsen S. Stability of the shoulder joint. Acta Orthop Scand 1985; 56:149. 27. O’Brien SJ, Arnoczsky SP, Warren RF, et al. The anatomy of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 1990; 18:449. 28. Jobe FW, Pink M. Shoulder injuries in the athlete: The stability continuum and treatment. J Hand Therapy Ar 1991; June:69–72.

46. Nuber GW, McCarthy WJ, Yao JST, et al. Arterial abnormalities of the shoulder in athletes. Am J Sports Med 1990; 18:514–519. 47. Baker CL, Liu SH. Neurovascular injuries to the shoulder. J Orthop Sports Phys Ther 1993; 18:360–364. 48. Jensen C, Rayan GM. Thoracic outlet syndrome: provocative examination maneuvers in a typical population. J Shoulder Elbow Surg 1995; 4:113–117. 49. Konin JG, Wiksten DL, Isear JA Jr, et al. Special tests for orthopedic examination, 2nd edn. New Jersey: Slack; 2002. 50. Vecchio PR, Kavanagh BL, Hazelman RH, et al. Shoulder pain in a community-based rheumatology clinic. Br J Rheumotol 1995; 34:440–442.

29. Cleland J. Notes on raising the arm. J Anat Physiol 1884; 18:275.

51. Smith DL, Campbell SM. Painful shoulder syndromes: Diagnosis and management. J Gen Int Med 1992; 7:328–339.

30. Goss TP. The scapula: coracoid, acromial and avulsion fractures. Am J Orthop 1996; 25:106–115.

52. Symonds MB. Accurate diagnosis and treatment in painful shoulder conditions. J Int Med Res 1975; 3:261–266.

31. Nobuhara K. The shoulder: its function and clinical aspects. Tokyo: Igasu-Shoin; 1987.

53. Kessel L, Watson M. The painful arc syndrome. Clinical classification as a guide to management. J Bone Joint Surg 1977; 59:166–172.

32. Doody SG, Freedman L, Waterland JC. Shoulder movements during abduction in the scapular plane. Arch Phys Med Rehabil 1970; 51:595–604.

54. Chard M, Hazelman B. Shoulder disorders in the elderly (a hospital study). Ann Rheum Dis 1987; 46:684–687.

33. Perry J. Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics and tennis. Symposium on injuries to the shoulder in the athlete. Clin Sports Med 1987; 2:247.

55. Slipman CW, Shin CH, Ellen MI, et al. An unusual case of shoulder pain. Pain Phys 2000; 3(4):352–356.

34. Matsen FA, Craig TA. Subacromial impingement. In: Matsen F, Rockwood C, eds. The shoulder. Philadelphia: WB Saunders; 1990:623–647.

56. Cuomo F. Diagnosis, classification, and management of the stiff shoulder. In: Iannotti JP, Williams GR Jr, eds. Disorders of the shoulder: diagnosis and management. Philadelphia: Lippincott Williams & Wilkins; 1999:397–417.

35. Speer KE, Garret WE. Muscular control of motion and stability about the pectoral girdle. In: Matsen FA, Fu F, Hawkins RJ, eds. The shoulder: a balance of mobility and stability. Rosemont, IL: AAOS; 1994:159–173.

57. Wirganowicz PZ, Eckardt JJ. Neoplasms of the shoulder girdle. In: Iannotti JP, Williams GR Jr, eds. Disorders of the shoulder: diagnosis and management. Philadelphia: Lippincott Williams & Wilkins; 1999:929–947.

36. Ellen MI, Gilhool JJ, Rogers DP. Scapular instability. The scapulothoracic joint. Phys Med Rehabil Clin N Am 2000; 11(4):755–770.

58. Kibler WB. The role of the scapula in the overhead throwing motion. Contemp Orthop 1991; 22:525–532.

37. Dines DM, Lenison M. The conservative management of the unstable shoulder including rehabilitation. Clin Sports Med 1995; 14:707–816.

59. Froreip. Ein Beitrag zur pathologie und therapie des rheumatismus. Weimar. 1843.

38. Moore KL. Clinically oriented anatomy, 3rd edn. Baltimore: Williams and Wilkins; 1992:522. 39. Ferrante MF. Medical management of chronic shoulder pain. In: Iannotti JP, Williams GR Jr, eds. Disorders of the shoulder. Philadelphia: Lippincott Williams & Wilkins; 1999:1043–1073. 40 Hurley JA. Anatomy of the shoulder. In: Nicholas JA, Hershman EB, eds. The upper extremity in sports medicine. St. Louis: Mosby; 1995:23–38. 41. Bryan WJ, Schauder K, Tullos H. The axillary nerve and its relationship to common sports medicine shoulder procedures. Am J Sports Med 1986; 14:114. 42. Gardener E. The innervation of the shoulder joint. Anat Rec 1949; 102:1.

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45. McCarthy WJ, Yao JS, Schafer MF. Upper extremity arterial injury in athletes. J Vasc surg 1989; 9:317–326.

60. Simmons DG, et al. Myofascial pain and dysfunction. The trigger point manual, 2nd edn. Baltimore: Williams and Wilkins; 1999:21–45. 61. Blom S, Dahlback LO. Nerve injuries in dislocations of the shoulder joint and fractures of the neck of the humerus. Acta Chir Scand 1970; 136:461–466. 62. Dowdy PA, Ernlund LS, Warner JJP. Contracture and other complications. In: Warren RF, Craig EV, Altchek DW, eds. The unstable shoulder. Philadelphia: Lippincott-Raven; 1999:403–428. 63. Brown JT. Nerve injuries complicating dislocation of the shoulder. J Bone Joint Surg [Br] 1952; 34:526. 64. Hirsch S. Paralysis of the axillary (circumflex) nerve with spontaneous recovery after 7 months. JAMA 1936; 106:705.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ i: Anatomy and Assessment

CHAPTER

Cervical Myelopathy

50

Yoshiharu Kawaguchi and Björn Rydevik

Cervical myelopathy implies spinal cord dysfunction in the cervical spine. The etiologies are numerous and these are divided into extrinsic and intrinsic neurogenic conditions (Table 50.1). Extrinsic neurogenic conditions entail spinal cord compression. Structural abnormalities surrounding the spinal cord contribute to encroachment on the available space in the spinal canal, resulting in spinal cord compression. The spinal cord compression entities are some of the most common conditions in myelopathic patients older than 55 years of age, because these abnormalities are generally due to degeneration of the cervical spine. Intrinsic neurogenic conditions are based on the primary pathology in the spinal cord. These intrinsic pathologies are important as differential diagnoses of compressive myelopathy. This chapter reviews the pathology, diagnosis, and differential diagnosis of compressive myelopathy in the cervical spine.

PATHOLOGY OF COMPRESSIVE MYELOPATHY IN THE CERVICAL SPINE Causes of spinal cord compression Various pathologies have the potential for encroachment in the spinal canal.1–4 Although these conditions do not always result in compressive myelopathy, there is a risk of spinal cord involvement.

Table 50.1: The Causes of Cervical Myelopathy

Cervical spondylosis Cervical spondylotic myelopathy (CSM) (Fig. 50.1) is the most common cause of spinal cord dysfunction in patients with compressive myelopathy. Cervical spondylosis initially occurs due to degeneration of the intervertebral disc. Disc degeneration increases mechanical stress at the endplate and this condition results in subperiosteal bone formation. By such a mechanism, osteophytes develop at the upper or lower edge of the vertebral body. Osteophytes at the posterior margin of the vertebral body, which are also called ‘posterior bony spurs,’ have the potential to encroach on the spinal cord. These spondylotic changes are often observed at many levels in the cervical spine. However, the presence of cervical spondylosis alone does not usually lead to myelopathy. The pathology of cervical myelopathy is multifactorial. It is important to consider the context of static and dynamic mechanical factors as well as ischemic factors.5,6

Static mechanical factors The size of the spinal canal plays an important role in the development of cervical myelopathy.7,8 Spinal canal size is the distance between the posterior margin of the vertebral body and the anterior edge of the spinous process (Fig. 50.2). The normal canal diameter from C3 to C7 is 17–18 mm in Caucasian and 15–17 mm in Japanese.9,10 The canal size in patients with cervical myelopathy is smaller than in those without it (Fig. 50.3).10 It is believed that a sagittal diameter of

EXTRINSIC NEURAL CONDITIONS Cervical spondylosis Ossification of the posterior longitudinal ligament Cervical disc herniation Calcification of the ligamentum flavum Rheumatoid arthritis Spinal tumors Epidural abscess Destructive spondyloarthropathy INTRINSIC NEURAL CONDITIONS Viral infections Neoplasms Vascular diseases Motor neuron disease Amyotrophic lateral sclerosis (ALS) Multiple sclerosis (MS) Others Radiation myelopathy Nutritional myelopathy Syringomyelia

Fig. 50.1 Typical radiological findings of cervical spondylosis. A 73-year-old female with anterolisthesis of C3 and disc space narrowing at C4–5 and C5–6 levels. 557

Part 3: Specific Disorders Without myelopathy (n = 100) With myelopathy (n = 20) Static

Fig. 50.2 Measurement of the spinal canal. Arrows indicate size of spinal canal.

5,6,11

4,12,13

12 mm (or 13 mm in some reports ) or less is a critical factor in the development of cervical spondylotic myelopathy. The Pavlov ratio is also used in the judgment of cervical spinal stenosis.14 This is the ratio of the anteroposterior (AP) diameter of the spinal canal to the anteroposterior diameter of the vertebral body at the same level as measured on a lateral radiograph (Fig. 50.4). The merit of this measurement is that the ratio is not affected by variations in radiologic magnification. A normal ratio is 1.0 and a ratio of less than 0.82 indicates cervical spinal stenosis. The Torg ratio is the same as the Pavlov ratio. Torg stated that a ratio of less than 0.8 indicates cervical stenosis.15

Dynamic mechanical factors In cervical spondylosis, movement of the cervical spine could have an impact on spinal cord compression. During extension of the cervical spine, the ligamentum flavum buckles and it narrows the spinal canal. The spinal cord is compressed between the posterior margin of one vertebral body and the lamina or ligamentum flavum of the next caudal level. In flexion, spinal cord compression occurs by the posterior margin of the caudal vertebral body and the lamina or ligamentum flavum of the cranial level. This condition has been well explained as ‘the pincer effect’ of spinal cord compression (Fig. 50.5).16 As for the pathomechanism of cervical myelopathy in elderly patients, retrolisthesis of C4 occurs as a result of intervertebral disc degeneration and is one cause of spinal cord compression.17,18 In flexion of the cervical spine, the spinal cord must lengthen or move in an anterior direction in the spinal canal, resulting in axial tension. A bulging

Fig. 50.4 The Pavlov ratio is measured by A/B. 558

Dynamic

(mm) 20

(mm) 20

15

15

10

10

C2 C3 C4 C5 C8 C7

C2/3 C3/4 C4/5 C5/6 C6/7

Fig. 50.3 The comparison of the canal size between patients with cervical myelopathy and those without it. (Hayashi H, Okada K, Hamada M, et al. Etiologic factors of myelopathy. A radiographic evaluation of the aging changes in the cervical spine. Clin Othop 1987; 214:200–209 with permission.)

disc or anterior osteophytes can stretch the spinal cord in flexion. Anterolisthesis of the vertebral body can be a cause of spinal cord compression. These local conditions lead to the onset of myelopathy. The forward displacement of the spinal cord during flexion can bring about spinal cord dysfunction, even when cervical spondylosis is not present. Juvenile muscular atrophy of the distal upper extremity, which is called Hirayama disease,19 is considered to be a type of cervical myelopathy. In this disorder, findings of forward displacement of the dural sac and flattening of the lower cervical cord in a fully flexed neck have been shown on MRI.20 It has been reported that some patients with athetoid cerebral palsy show cervical myelopathy at an early age (30–40 years of age).21 This is due to the excessive movement of the cervical spine. These exemplify the importance of dynamic factors in cervical cord dysfunction.

Ischemic factors Spinal cord compression leads to ischemia in the spinal cord.22 Histopathological examination reveals the occurrence of ischemic

Flexion

Extension

Fig. 50.5 Pincer effect of the spinal cord. (Bernhardt M, Hynes RA, Blume HW, et al. Current concepts review. Cervical spondylotic myelopathy. J Bone Joint Surg 1993; 75A:119–128 with permission.)

Section 3: Cervical Spine

injury in the gray matter and white matter in patients with myelopathy.9 In addition, several animal models have shown that disturbance in the vascular supply to the spinal cord plays an important role in the pathophysiology of spinal cord dysfunction.5

Ossification of the posterior longitudinal ligament Ossification of the posterior longitudinal ligament (OPLL) (Fig. 50.6) often causes narrowing of the spinal canal due to the replacement of spinal ligamentous tissue by ectopic new bone formation.23 This disease is more common among Japanese and other Asians compared to Caucasians.24 The etiology of OPLL remains obscure; however, it has been reported that genetic background is a contributory factor. Recent studies using molecular biology have revealed that the collagen 11a2 gene (COL11A2),25,26 retinoic X receptor β gene (RXRβ)27 and nucleotide pyrophosphatase (NPPS) gene28 might be responsible for OPLL. It has been widely recognized that OPLL may cause severe myelopathy and radiculopathy. Ossification types of OPLL are classified into continuous type, segmental type, mixed type, and other types, according to the criteria proposed by the Investigation Committee on the Ossification of the Spinal Ligaments of the Japanese Ministry of Public Health and Welfare (Fig. 50.7)29 Among these types, myelopathy is frequently developed in the continuous or mixed types. OPLL progression is often observed in long-term follow-up after cervical laminoplasty and it can be a cause for the recurrence of myelopathy.30

Cervical disc herniation Cervical disc herniation (CDH) (Fig. 50.8) is one of the compressive lesions which might cause cervical myelopathy. It has been proposed that nuclear herniation or anulus protrusion compresses the spinal cord, but precise histopathological examinations have revealed that a disc herniation associated with the cartilaginous endplate is the predominant type of herniation in the cervical spine.31 The symptoms in patients with cervical disc herniation depend on the location of the herniated mass. A centrally located herniation mass, which is large enough to compress the spinal cord, produces cervical myelopathy, whereas laterally displaced herniation often leads to cervical radiculopathy. Patients with myelopathy due to disc herniation are relatively young, compared to those with cervical spondylotic myelopathy. The

Fig. 50.6 Ossification of the posterior longitudinal ligament (OPLL). Mixed type OPLL from C3 to C5 and C6 levels.

Continuous type

Segmental type

Mixed type

Other type

Fig. 50.7 Classification of OPLL by the Investigation Committee on the Ossification of the Spinal Ligaments, Japanese Ministry of Public Health and Welfare. (A) continuous type, (B) segmental type, (C) mixed type, and (D) other type.

spinal canal is narrower in patients with myelopathy due to herniation than those with an asymptomatic central herniation. A history of cervical spinal trauma appears to be a predisposing factor for disc herniation.32 In some patients with the median and/or diffuse type of disc herniation, spontaneous regression of the herniated mass is observed on MRI.33 The symptoms often recover during such regression and therefore conservative treatment can be an option for mild myelopathy caused by cervical disc herniation.34

Adjacent disc disease after anterior cervical fusion Although anterior cervical decompression and fusion is an established surgical procedure in the management of cervical lesions, numerous studies using long-term follow-up have revealed that adjacent disc disease could occur after fusion surgery (Fig. 50.9).35–38 In some cases, the adjacent disc disease leads to myelopathy in the long-term follow-up after anterior cervical fusion. Regarding the cause of the adjacent disc disease after anterior cervical fusion, it is believed that

Fig. 50.8 Cervical disc herniation. Centrally located disc herniation (arrows) compresses the spinal cord. 559

Part 3: Specific Disorders

Fig. 50.9 Adjacent disc disease after anterior cervical fusion. A 70-year-old female suffering from cervical myelopathy 10 years after anterior spinal fusion from C4 to C6. Spinal cord compression at the levels of C3–4 and C6–7 is obvious.

mechanical stress contributes to the disc degeneration at adjacent levels. A biomechanical study conducted by Matsunaga et al. demonstrated that shear strain of the adjacent segments had increased by on average 20% 1 year after surgery in the cases of double- or triple-level fusion.38

Calcification of the ligamentum flavum There have been a few cases reported in which calcification of the ligamentum flavum (CLF) (Fig. 50.10) narrows the spinal canal in the cervical spine, resulting in myelopathy. In the literature, most cases are Japanese,39 but one case was reported from the US.40 Kokubun et al. reported that 4% (11 patients) of 306 patients with cervical myelopathy in northern Japan had calcification of the ligamentum flavum.39 CT is the most useful diagnostic tool to detect this disease. Although the etiology is unknown, calcium phosphate deposition is observed in the pathology.

A

Fig. 50.11 Atlantoaxial subluxation in rheumatoid arthritis.

Rheumatoid arthritis Involvement of the cervical spine in rheumatoid arthritis (RA) has been well studied.41–47 Compression of the spinal cord may result from direct compression by synovial pannnus or indirect compression due to cervical subluxation. Upper cervical lesions, identified as atlantoaxial subluxation (Fig. 50.11) and vertical subluxation (Fig. 50.12), can be causes of cervical myelopathy.47 The atlas dental interval (ADI) is a useful marker for the analysis of atlantoaxial subluxation. In patients with an ADI exceeding 5 mm, the space available for the spinal cord (SAC) is narrowed and they have an increased risk of cervical myelopathy if the space available for the cord is less than 14 mm (Fig. 50.13). As for the analysis of vertical subluxation (Fig. 50.14), several methods have been reported. McGregor’s line connects the posterior margin of the hard palate to the most caudal point of the occiput. The tip of the odontoid should not project more than 4.5 mm above this line. Ranawat baseline measurement is another

B

Fig. 50.10 Calcification of the ligamentum flavum. (A) CT image obtained at C6. (B) T2-weighted axial MRI. 560

Section 3: Cervical Spine

Hard palate

Chamberline

McRae

Occiput

Ranawat’s line McGregor

Fig. 50.14 Judgment of vertical subluxation. (Reprinted with permission from The Cervical Spine. 3rd edn. by the Cervical Spine Research Society Editorial Committee. Philadelphia: Lippincott-Raven; 1998.) Fig. 50.12 Vertical subluxation in rheumatoid arthritis.

method. Ranawat’s line is from the center of the sclerotic ring of C2 to the line between the center of the anterior and posterior arches of C1. A distance of less than 13 mm is abnormal. Lower cervical lesions, such as subaxial subluxation (Fig. 50.15) and swan neck or goose neck deformity, also are causes of myelopathy. Although the cervical spine is affected in 36–86% of patients with RA, the incidence of myelopathy is reported to be 4.9–32%.47 Regarding the neurological evaluation in patients with RA, Ranawat’s four-grade criteria are often used (Table 50.2).48

spine is another entity which might cause compression myelopathy, although such lesions are rare in the cervical spine (Fig. 50.17).51,52 The most likely primary tumors to metastasize to the cervical spine are from breast, prostate, and lung cancer. The primary site for metastasis is the vertebral body in the cervical spine. The symptoms of myelopathy are sometimes acute and gradually progressive.

Spinal tumors Intradural extramedullary (IDEM) tumors might cause compressive myelopathy. Meningioma, neurofibroma, neurilemmoma, and schwannoma are common examples of IDEM tumors.49,50 Meningioma grows from the cells in the arachnoid (Fig. 50.16). Neurofibroma, neurilemmoma, and schwannoma usually arise from the dorsal sensory roots. Neurofibroma is accompanied by von Recklinghausen’s disease and sometimes follows the nerve root out of the spinal canal, resulting in a dumbbell-shaped tumor. IDEM tumors are typically eccentric and lead to Brown-Sequard type myelopathy. Gd-enhanced MRI is very useful to detect IDEM tumors. Metastasis to the cervical

SAC not < 13 mm Fig. 50.15 Subaxial subluxation in rheumatoid arthritis. A 54 year-oldfemale with anterior subluxation of C2 , C4, and C6.

Table 50.2: Ranawat’s Four-grade Criteria for the Neurological Evaluation in Patients with Rheumatoid Arthritis ADI not > 4 mm Fig. 50.13 Atlas dental interval (ADI) and space available for the spinal cord (SAC). (Reprinted with permission from The Cervical Spine. 3rd edn. by the Cervical Spine Research Society Editorial Committee. Philadelphia: Lippincott-Raven; 1998.)

Class I

Pain, no neurological deficit

Class II

Subjective weakness, hyperreflexia, dysesthesias

Class III

Objective weakness, long-tract signs

Class IIIa

Ambulatory

Class IIIb

Nonambulatory

561

Part 3: Specific Disorders

A

B

A

Kyphotic deformity due to vertebral collapse, direct tumor invasion in the epidural space, and insufficiency of the anterior spinal artery system might produce cervical myelopathy.

Epidural abscess Spinal epidural abscess (Fig. 50.18) can cause a mass to develop in the spinal canal, leading to acute myelopathy.53,54 In patients with epidural abscess, fever and neck pain are usually observed. Staphylococcus aureus is the etiologic agent in over 50% of cases with acute epidural abscess. Spondylodiscitis may be accompanied as a local pathology, whereas epidural infection may occur hematogenously from a distant site.

Anomaly in the cervical spine Anomalies in the cervical spine are frequently seen at the craniovertebral junction or at the upper cervical spine. In most patients, the anomalies are usually found in childhood as a congenital malformation; however, abnormal cervical structures in the cervical spine are 562

Fig. 50.16 Intradural extramedullary (IDEM) tumor. (A) T2-weighted sagittal MRI. IDEM tumor is extended from C5 to T1. Pathological examination reveals meningioma. (B) T2weighted axial MRI. Spinal cord shifts posterolaterally due to the tumor.

B

Fig. 50.17 Metastasis to the cervical spine (renal cell cartinoma). (A) T2-weighted axial MRI at the level of C3. Left side lamina is destroyed by the metastatic lesion. (B) T2-weighted frontal MRI. Spinal cord is compressed by the metastasis.

sometimes found in adulthood. Among the anomalies in the cervical spine, myelopathy can be developed in the basilar impression, Arnold-Chiari malformation, and atlantoaxial instability associated with Down’s syndrome.55 Os odontoideum with instability also might cause myelopathy.56

Destructive spondyloarthropathy Destructive change (Fig. 50.19) in the cervical spine is often seen in patients receiving long-term hemodialysis. The disease entity was first reported by Kunz et al. in 1984.57 Radiological features in this disease are disc space narrowing and irregularity of the cartilaginous endplate without osteophyte formation. The C5–6 level is involved in more than half of patients, but involvement of many levels is common. The prevalence of destructive spondyloarthropathy (DSA) is 4–20% in patients receiving hemodialysis and it increases in those who have long-term hemodialysis, longer than 10 years.58 The causes of myelopathy are cord compression due to spinal instability, intervertebral subluxation,

Section 3: Cervical Spine

Fig. 50.18 Spinal epidural abscess. A 55 year-old-female with acute onset of cervical myelopathy. T2-weighted sagittal MRI showing epidural abscess from C6–7 discitis.

Fig. 50.19 Destructive spondyloarthropathy. A 54 year-old-female having hemodialysis for 10 years. C4–5 disc is collapsed and retrolisthesis of C4 is observed.

intracanal amyloid deposition, and/or hypertrophy of the ligamentum flavum.59,60 Although the pathology of DSA has not been clearly elucidated, it has been reported that hyperparathyroidism and amyloidosis play an important role in the progression of DSA.59

Pathological findings in the spinal cord under compressive conditions In the macroscopic findings, the spinal cord with myelopathy shows anteroposterior flatness and it becomes atrophic due to compression. According to morphological studies using CT myelogram, the spinal cord sometimes reveals a boomerang shape or a triangular shape. Histopathological studies have shown that the damage of the neuronal

A

Mild compression case

B

Moderate compression case

Intrasegmental destruction of the gray and/or white matter such as rarefaction and cavitation Demyelination and spongy degeneration Ascending and descending degeneration Neuronal loss of the anterior horn

C

components is mild in the spinal cord with a boomerang shape, while such damage is marked in cases with a triangular shape spinal cord.9 In addition, it has been reported that two parameters, anteroposterior compression ratio and the transverse area, are well correlated with spinal cord destruction and the recovery after decompressive surgery.61–63 The pathological change of the spinal cord is quite different depending on age, and extent and duration of compression. Ogino et al.64 reported the precise pathology of the spinal cord in patients with compressive myelopathy. Their study showed that in mild compression, limited demyelination and spongy degeneration are seen in the posterolateral white column, whereas in severe compression, extensive degeneration and infarction of the gray matter with diffuse degeneration of the lateral white columns are observed (Fig. 50.20).

Severe compression case

Fig. 50.20 Histopathology of the spinal cord in cervical spondylotic myeloathy. (Ogino H, Tada K, Okada K, et al. Canal diameter, anteroposterior compression ratio, and spondylotic myelopathy of the cervical spine. Spine 1983; 8:1–15 with permission.) 563

Part 3: Specific Disorders

Further, severe cases always have accompanying developmental spinal stenosis. These pathological changes are not only localized at the most compressed site, but also at the craniocaudal regions in addition to the compression. Ascending degenerative demyelination is consistently seen in the cuneate and gracilis fasciculi of the posterior white columns in the spinal cord cranial to the compression site. Distinct descending demyelination of the lateral corticospinal tract is generally observed in the spinal cord caudal site.

DIAGNOSIS The diagnostic process is outlined in algorithmic form in Figure 50.21. The interview and physical examination are very important for the first step of diagnosis. Radiological examination is useful to detect the pathology and the level of the lesions which cause myelopathy.

Clinical presentation Clinical symptoms in cervical myelopathy vary from patient to patient. The symptoms are dependent on the stage of myelopathy and impaired pattern of the spinal cord. In the upper extremities, numbness, paresthesia, and clumsiness are often observed. The typical manifestation of numbness and paresthesia is a global and nondermatomal pattern in the upper extremities. Patients often complain of clumsiness. Their symptoms include difficulties in handwriting, manipulating buttons or zippers, and using a knife and fork and/or chopsticks. So-called ‘myelopathy hand,’65,66 which is defined as ‘loss of power of adduction and extension of the ulnar two or three fingers

Table 50.3: Classification of Cervical Myelopathy by Crandall and Batzdorf

Diagnostic plan Medical examination by interview

1

Transverse lesion syndrome

2

The motor system syndrome

3

Central cord syndrome

Physical examination

4

Brown-sequard syndrome

(myelopathy)

5

Brachialgia and cord syndrome

Yes

No

X-P

X-P

(ossified lesion)

(persistent or worsening symptoms) No Yes

Yes

(Fig. 50.22) and an inability to grip and release rapidly with these fingers,’ is one of the characteristic findings in patients with cervical myelopathy. In the lower extremities, subtle changes in gait and balance occasionally progress to spastic gait. Patients with cervical myelopathy have difficulties in going down stairs smoothly. They are often frightened using steps without a handrail. There are disparate opinions regarding the presenting symptoms of cervical myelopathy. Gorter reported that cervical myelopathy usually presents a subtle gait disturbance.67 On the other hand, Kokubun et al.39 stated that the most common initial symptom is numbness or tingling in the upper extremities, especially in the hand. It has been believed the symptoms gradually deteriorate. However, a recent study suggests that most patients with mild myelopathy show a stable condition which remains unchanged for a lengthy duration.34 When the myelopathic symptoms progress toward end stages, the symptom manifestation complex includes an inability to ambulate with a cane even on a flat surfaces. In addition, bowel or bladder dysfunction occurs in patients with severe myelopathy. There have been several attempts to classify the symptoms of spinal cord dysfunction in patients with cervical myelopathy. In 1966, Crandall and Batzdorf68 devised a classification system based on the differential susceptibility of various spinal cord tracts (Table 50.3). In 1975, Hattori and Kawai69 categorized spinal cord symptoms into three types based on clinical experience (Fig. 50.23). Ferguson and Caplan70 categorized spondylosis with nerve involvement into four distinct but overlapping syndromes (lateral or radicular syndrome, medial or spinal syndrome, combined medial and lateral syndrome, and vascular syndrome) in 1985.

No

Laboratory examination

CT, CTM

MRI

MRI

T 1 T2 (tumor suspected-enhanced)

T1 T2 (tumor suspected-enhanced)

Diagnosis Fig. 50.21 Algorithm of the diagnostic process. 564

Fig. 50.22 A 59-year-old male presenting with a typical myelopathy hand.

Section 3: Cervical Spine

pathological reflexes, such as Hoffmann’s reflex, Trömner’s reflex, Wartenberg’s reflex, and inverted radial reflex in the upper extremity and Babinski reflex, Chadock reflex and Oppenheim reflex, etc. in the lower extremity, also indicate abnormal long tract signs consistent with spinal cord compression (Fig. 50.24). The scapulohumeral reflex (SHR)74 is useful to detect lesions cranial to the C3 vertebral body level. The reflex is hyperactive when elevation of the scapula and/or abduction of the humerus are found in tapping at the spine of the scapula or at the acromion in a caudal direction. More than 95% of patients with high cervical cord compression have hyperactive SHR.

Type I: central cord type

Type II: Type I + posterolateral type

Motor weakness

Type III: Type II + anterolateral type

Fig. 50.23 A classification of myelopathy by Hattori.

Generalized weakness and extremity weakness are found in some patients with cervical myelopathy. Muscle atrophy, muscle wasting, and fasciculation can be observed in the upper extremity of patients with cervical myelopathy. This is caused by lower motor neuron dysfunction and is regarded as a segmental sign of a compressive lesion. On the other hand, it is speculated that the weakness in the lower extremity is caused by dysfunction of the corticospinal tract.

Sensory disturbance

Physical examination Neurological findings vary, depending on the level and nature of compression. Lower motor findings occur at the level of the compressive lesion and upper motor findings are observed below the lesion. This indicates that upper motor neuron findings are observed in the lower extremities, whereas in the upper extremities, lower motor findings occur at the level of the lesion and upper motor findings occur below the lesion. Careful physical examination should be carried out to detect whether cervical myelopathy exists or not.71,72 If myelopathy exists, it is necessary to detect the precise lesion of myelopathy.73 The finding of ‘myelopathy hand’65,66 strongly suggests the existence of cervical myelopathy. The diagnosis of myelopathy hand is made by two simple tests, the finger escape sign and the rapid grip and release test. The finger escape sign is positive when the patient is asked to hold all digits of the hand in an adducted and extended position and the two ulnar digits fall into flexion and abduction within 30 seconds. In the rapid grip and release test, a normal person can make a fist and rapidly release it 20 times in 10 seconds, but patients with cervical myelopathy are unable to do this test within the allotted time. L’Hermitte’s sign is positive in approximately 25% of the patients. This test is positive when neck flexion causes a generalized electric shock or paresthesia sensation to the upper and lower extremities. The gait becomes wide-based and jerky. Patients have difficulty in toe walking and heel walking These provocative tests are useful to detect subtle gait disturbance due to cervical myelopathy. A full neurologic examination is performed by careful evaluation of reflex change, motor weakness, and sensory disturbance.

Reflex change Reflex changes are of extreme importance in making a diagnosis of cervical myelopathy. Hyperreflexia is found as a long tract sign in the upper and lower extremities below the lesion. However, it must be taken into account that hyporeflexia in the upper extremity might be due to a segmental sign of the cord compression. Further, hyporeflexia in the lower extremity might be accompanied by lumbar spinal stenosis. Not many patients have clonus in their lower extremity, which is the classic indicator of hyperreflexia. The presence of

It is important to assess any alterations in the perception of pain, touch and vibration, and proprioception because they are carried through different tracts within the spinal cord. In cervical myelopathy, sensory change is global and ill-defined, compared to radiculopathy. A ‘cervical line’ is typical for cervical myelopathy. This is the sensory change around the clavicle. Patients have sensory disturbance below the level of the clavicle and normal sensation above the level. It is speculated that the phenomenon of ‘cervical line’ occurs by the distinct change of sensory lamination shown by Keegan’s dermatome. Loss of vibration and proprioception signifies involvement of the posterior columns and is an indicator of poor prognosis of cervical myelopathy.

Radiologic evaluation When patients are suspected to have cervical lesions, plain X-ray films should be taken first. Plain X-ray films include AP view, lateral views with neutral flexion and extension positions, and oblique views.75 On AP view, the findings, such as scoliotic deformity, tilting of cervical vertebrae, spondylotic change of uncovertebral joints (Luschka joints), and cervical ribs, are examined. Lateral views usually give the most useful information in patients with cervical myelopathy. Sagittal alignment, straight, lordotic, or kyphotic, is checked. Swan neck deformity and/or goose neck deformity can be observed in patients with RA. Destruction of the vertebral body might be caused by DSA or by metastasis of a malignant tumor. In the analysis of degenerative findings in the cervical spine, it is reasonable to categorize the findings regarding the spinal canal into static factors and dynamic factors (see above). The static factors include the degree of disc space narrowing, the size of endplate osteophyte, sagittal alignment, the size of spinal canal and ossified lesions, such as OPLL and CLF. The dynamic factors can be shown by lateral views with flexion and extension positions. Instability and retro- or anterolisthesis of cervical vertebrae are checked by flexion and extension views. Foraminal stenosis is shown by oblique views. In contrast, the finding of a wide foramen might indicate the existence of a dumbbell tumor. Further, the open-mouth AP view is applied to detect lesions of the upper cervical spine and may show C1–2 arthritis. In the 1970s and 1980s, myelography was the most useful and reliable tool to detect the lesions involving the spinal canal. However, 565

Part 3: Specific Disorders

A

B

D

C

E

2

5

1

4

3

F Fig. 50.24 (A) Hoffmann’s reflex. When the examiner clicks the nail of the patient’s middle finger in the position of wrist extension, the abduction movement of the patient’s thumb is observed. This is positive and pathological. (B) Trömner’s reflex. When the examiner clicks the palm side of the patient’s middle finger in the position of wrist extension, the abduction movement of the patient’s thumb is observed. This is positive and pathological. (C) Wartenberg’s reflex. When the examiner taps the palm side of the patient’s fingers with a hammer, the abduction movement of the patient’s thumb is observed. This is positive and pathological. (D) Babinski reflex. When the examiner rubs the sole of the patient’s foot, the extensor plantar response of the great toe and/or fanning sign of the toes are observed. This is positive and pathological. (E) Chadock reflex. When the examiner rubs the patient’s lateral calf, the extensor plantar response of the great toe is observed. This is positive and pathological. (F) Pathological reflexes in the lower leg. (Reprinted with permission from Physical examination of the nervous system. 16th edn. Tazaki Y, Saito Y, Sakai F, Suzuki N, Iizuka T. Tokyo: Nanzando Co. Ltd; 2003.)

myelography has less clinical utility since the widespread use of MRI. In myelography of the cervical spine, a C1–2 lateral puncture is carried out and the existence of spinal cord compression can be judged by the configuration of contrast medium. Total block of contrast medium indicates severe compression of the spinal cord. Under the 566

condition that contrast medium fills the spinal canal, anterior indentation suggests the existence of disc herniation, osteophytes, or OPLL, while posterior indentation might be due to buckling of the ligamentum flavum or CLF. CT after myelography (CTM) is beneficial to show clearly atrophy of the spinal cord (Fig. 50.25). Essentially, CT

Section 3: Cervical Spine

Fig. 50.25 Spinal cord atrophy shown by CT-M, OPLL is observed.

provides better information of bony lesions, such as bony spur and ossified ligament. Recently, 3D-CT has been developed and it has a clinical usefulness not only for the diagnosis of myelopathy, but also for the decision process and safety of surgical procedures in patients with myelopathy. MRI has become the most important tool to detect the characteristics of the lesion in patients with cervical myelopathy.76 However, MRI is not indicated for everyone who is suspected to have a cervical lesion. This examination is recommended to be applied for patients who have obvious neurological findings and persistent or worsening symptoms. The standard screening cervical spine MRI includes sagittal and axial sequences with T1- and T2-weighted images. The T1-weighted examination provides superior spatial resolution and a survey of bone marrow signal intensity, whereas the T2-weighted examination has the advantage of evaluating the central canal and thecal sac. As the cerebrospinal fluid (CSF) and spinal cord are shown to be white and black, respectively, on the T2 image, cord compression is easily identified by the disappearance of cerebrospinal fluid. MRI can detect the extent of pathologic changes of the soft tissues, such as disc herniation, and hypertrophy of the ligamentum flavum and posterior longitudinal ligament. Further, MRI is useful to visualize various aspects of the spinal cord. The size and shape of the spinal cord are evident on both sagittal and transverse images. Long-lasting severe compression leads to spinal cord atrophy. It is speculated that the size of the spinal cord is related to postoperative prognosis. Further, MRI can show the intramedullary pathology of the spinal cord. The presence of high intensity on the T2 image is considered to reflect a wide spectrum of pathologic changes of the spinal cord including reversible changes, such as edema, or irreversible changes, such as gliosis, myelomalacia, cystic necrosis, and syrinx formation (Fig. 50.26). Matsumoto et al.77 reported that increased signal intensity is not related to a poor prognosis or the severity of myelopathy. In contrast, Mizuno et al.78 examined the pathology of snake-eye appearance (a unique finding characterized as nearly symmetrical round, high signal intensity of the spinal parenchyma resembling the face of a snake) (Fig. 50.27) and found that it revealed a cystic necrosis of the spinal cord leading to poor recovery of upper extremity motor weakness. Therefore, the precise pathology of high intensity on a T2 image should be carefully analyzed.

Fig. 50.26 High intensity in the spinal cord at C5–6 level on T2-weighted MRI.

Clinical evaluation of cervical myelopathy Various systems have been proposed to evaluate the severity of cervical myelopathy. Originally, these systems were used for the analysis of the treatment results in patients with cervical myelopathy. In 1958, Odom and Finney79 first developed the criteria to evaluate cervical myelopathy due to cervical disc lesions (Table 50.4). Since 1972, the Nurick score80 has been widely used (Table 50.5). Rao81 modified this score in 2003. However, these scores lack an evaluating item for upper extremity function. The Japanese Orthopaedic Association (JOA) proposed a scoring system for cervical myelopathy as a basis for discussing treatment of cervical myelopathy in 1975.82 In 1990, the JOA proposed the new score which has a 17-2 point system (Table 50.6). This JOA system is reliable, because the inter- and intraobserver reliabilities of the scoring system are high.83 Therefore, this score is used not only in Japan, but also in other countries. Since the JOA score includes an evaluation system based on the use of chopsticks for upper extremity function, several

Fig. 50.27 Snake-eye appearance in the spinal cord. 567

Part 3: Specific Disorders

Table 50.4: Odom Criteria

Table 50.5: Nurick Score

Excellent

No complaints referable to cervical disease and patient able to carry on daily occupation without impairment

Grade 0

Signs or symptoms of root involvement but without evidence of spinal cord disease

Good

Intermittent discomfort which was related to cervical disease but which did not significantly interfere with patient’s work

Grade 1

Signs of spinal cord disease but no difficulty in walking

Satisfactory

Subjective improvement but patient’s activities were significantly limited

Grade 2

Slightly difficulty in walking which did not prevent fulltime employment

Poor

No improvement or worsen as compared with patient’s condition before operation

Grade 3

Difficulty in walking which prevented full-time employment or the ability to do all housework, but which was not so severe as to require someone else’s help to walk

Grade 4

Able to walk only with someone else’s help or with the aid of a frame

Grade 5

Chairbound or bedridden

Table 50.6: Modified Japanese Orthopaedic Association (JOA) Score for Evaluation of Cervical Myelopathy MOTOR FUNCTION Fingers 0

Unable to feed oneself with any tableware including chopsticks, spoon, or fork, &/or unable to fasten buttons of any size

1

Can manage to feed oneself with spoon &/or fork but not with chopsticks

2

Either chopstick feeding or writing is possible but not practical, &/or large buttons can be fastened

3

Either chopstick feeding or writing is clumsy but practical, &/or cuff buttons can be fastened

4

Normal

Shoulder & elbow Evaluated by MMT score of the deltoid or biceps muscles, whichever is weaker –2

MMT2 or below

–1

MMT3

–0.5

MMT4

0

MMT5

Lower extremity 0

Unable to stand and walk by any means

0.5

Able to stand but unable to walk

1

Unable to walk without a cane or other support on a level surface

1.5

Able to walk without support but with a clumsy gait

2

Walks independently on a level surface but needs support on stairs

2.5

Walks independently when going upstairs, but needs support when going downstairs

3

Capable of fast but clumsy walking

4

Normal

SENSORY FUNCTION Upper extremity

568

0

Complete loss of touch and pain sensation

0.5

≤50% normal sensation and/or severe pain or numbness

1

>60% normal sensation and/or moderate pain or numbness

1.5

Subjective numbness of slight degree without any objective sensory deficit

2

Normal

Section 3: Cervical Spine

Table 50.6: —Cont’d SENSORY FUNCTION Trunk 0

Complete loss of touch and pain sensation

0.5

≤50% normal sensation and/or severe pain or numbness

1

>60% normal sensation and/or moderate pain or numbness

1.5

Subjective numbness of slight degree without any objective sensory deficit

2

Normal

Lower extremity 0

Complete loss of touch and pain sensation

0.5

≤50% normal sensation and/or severe pain or numbness

1

>60% normal sensation and/or moderate pain or numbness

1.5

Subjective numbness of slight degree without any objective sensory deficit

2

Normal

Bladder function 0

Urinary retention and/or incontinence

1

Sense of retention and/or dribbling and/or thin stream and/or incomplete continence

2

Urinary retardation and/ or pollakiuria

3

Normal

MMT, manual muscle test. Total score for a healthy patient = 17.

modifications for the non-Asian population have been reported.84,85 In addition to the functional evaluation using these systems, recently much interest has centered on the evaluation system of quality of life, such as Short-Form 36-item health survey, in patients with cervical myelopathy. In an era requiring evidence-based medicine, easy and reliable systems should be used for evaluating cervical myelopathy.

DIFFERENTIAL DIAGNOSIS OF COMPRESSIVE MYELOPATHY In some patients with cervical myelopathy, spinal cord dysfunction is caused by problems of the nerve tissue itself. These pathological conditions are important for the differential diagnosis of compressive myelopathy.86 Many diseases are included in these entities and they are classified into (1) viral infections, (2) neoplasms, (3) vascular diseases, (4) motor neuron diseases, and (5) others.

Neoplasms Spinal cord dysfunction due to intramedullary tumor is severe in most cases. Intramedullary tumors cause swelling of the spinal cord, which is evident on MRI. Gd-enhanced MRI is very useful to detect intramedullary tumors. Both primary tumors, such as astrocytoma, ependymoma, and hemangioblastoma, and intraspinal metastasis develop in the cervical region, resulting in severe myelopathy.

Vascular diseases Vascular diseases include spinal infarction and hematomyelia. Both diseases cause acute myelopathy. Unless emergent treatment is carried out, these conditions have a poor prognosis. Spinal infarction can be caused by aortic diseases, such as thrombosis, arteriosclerosis, and dissecting aneurysm. Arteriovenous malformation in the spinal cord is suspected to be one of the causes of hematomyelia.

Viral infections

Motor neuron disease

Viral infection causes cervical myelopathy. HIV, human T-cell lymphotrophic virus type-I (HTLV-I) and polio virus are known to damage the spinal cord. The myelopathy due to HIV is characterized by spongiform myelin changes predominantly in the dorsal and lateral columns of the spinal cord. The spinal cord dysfunction caused by HTLV-I is known as HTLV-associated myelopathy or tropical spastic paraparesis (HAM/TSP). Pyramidal tract dysfunction affecting the lower extremities is a characteristic finding in HTLV-I infection. In contrast, poliomyelitis damage of the anterior horn cells in the spinal cord is a well-known phenomenon.

Amyotrophic lateral sclerosis (ALS) is the most important motor neuron disease which requires the differential diagnosis of compressive myelopathy. In patients with ALS, both lower motor neuron disease (weakness, wasting, fasciculation) and upper motor neuron disease (hyperactive deep tendon reflex, pathological reflex) are seen. ALS usually presents progressive muscular atrophy without sensory deficit. Bulbar or pseudobulbar involvement, with dysarthria, dysphagia, dysphonia, and tongue wasting is found. The disease is universally progressive and often fatal in 2–5 years.

Amyotrophic lateral sclerosis

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Fig. 50.28 Multiple sclerosis. A 31-yearold male showing multilevel high intensity (C5 and T2–3 levels) on T2-weighted MRI.

Multiple sclerosis

CONCLUSIONS

Multiple sclerosis (MS) (Fig. 50.28) is a chronic disease that begins most commonly in young adults. The initial onset is typically in the ages between 20 and 30. The lesions are multiple in space and in time. This indicates that the multiple lesions are found in the central nervous system. In addition, most patients have a relapsing and remitting illness. In the spinal cord lesion, the symptoms are similar to those of transverse myelitis. Therefore, it is sometimes difficult to distinguish MS from compressive myelopathy. Pathologically, multiple areas of white matter inflammation, demyelination, and glial scar are found. MRI is useful to detect the lesions. In laboratory data, the presence of oligiclonal IgG bands on electrophoretic analysis of CSF is the most frequent abnormality.

Cervical myelopathy is caused by extrinsic and intrinsic neurogenic conditions. The extrinsic neurogenic conditions cause encroachment of the spinal cord and spinal cord compression and include CSM, OPLL, CDH, CLF, RA, spinal tumors, epidural abscess, anomaly, and DSA. In the diagnostic process of compressive myelopathy, the history and physical examination provide important clues. Radiological examination is useful to detect the pathology and the level of the lesions which cause myelopathy. The intrinsic neurogenic conditions include those that cause primary pathology in the spinal cord. These conditions include entities such as (1) viral infections, (2) neoplasms, (3) vascular diseases, (4) motor neuron diseases, and (5) others. The intrinsic pathologies should be considered in the differential diagnoses of compressive myelopathy.

Others Radiation myelopathy Myelopathy is sometimes found after radiation therapy. Symptoms begin with numbness and paresthesia, and progress to transverse myelopathy 12–15 months after radiation. Direct damage to the spinal cord and damage to the vascular supply of the spinal cord are proposed as a pathologic mechanism for radiation myelopathy.

Nutritional myelopathy Long-term vitamin B12 deficiency due to inability of absorption or inadequate dietary intake results in demyelination in posterior and lateral columns of the spinal cord. Typical neurological findings begin with weakness and easy fatigability of the lower extremities, accompanied by paresthesia. A spastic-ataxic gait and loss of vibration and position sense are found with the progression of the disease.

Syringomeyelia Syringomyelia (Fig. 50.29) is defined as a ‘dilatation of the central canal of the spinal cord or formation of abnormal tubular cavities in its substance.’87 Arnold-Chiari malformation, tumor, trauma, arachnoiditis, vascular anomalies, and infective diseases have been reported in association with syrinx formation. MRI is the imaging modality of choice to make the diagnosis. 570

Fig. 50.29 A 9-year-old female with syringomyelia in the cervical spine due to Arnold-Chiari malformation.

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Section 3: Cervical Spine 10. Hayashi H, Okada K, Hamada M, et al. Etiologic factors of myelopathy. A radiographic evaluation of the aging changes in the cervical spine. Clin Othop 1987; 214:200–209. 11. Emery SE. Cervical spondylotic myelopathy: Diagnosis and treatment. J Am Acad Orthop Surg 2001; 9:376–388. 12. Montgomery DM, Brower RS. Cervical spondylotic myelopathy. Clinical syndrome and natural history. Orthop Clin North Am 1992; 23:487–493. 13. McCormack BM, Weinstein PR. Conferences and reviews. West J Med 1996; 165:43–51. 14. Pavlov H, Torg JS, Robie B, et al. Cervical spinal stenosis: Determination with vertebral body ratio method. Radiology 1987; 164:771–775. 15. Torg JS, Pavlov H. Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Clin Sports Med 1987; 6:115–133. 16. Penning L, Wilmink JT, van Woerden HH, et al. CT myelographic findings in degenerative disorders of the cervical spine: Clinical significance. Am J Roentgenol 1986; 146:793–801.

38. Matsunaga S, Kabayama S, Yamamoto T, et al. Strain on intervertebral discs after anterior cervical decompression and fusion. Spine 1999; 24:670–675. 39. Kokubun S, Sato T, Ishii Y. Cervical myelopathy in the Japanese. Clin Orthop 1996; 323:129–138. 40. Ellman MH, Vazquez T, Ferguson L. Calcium pyrophosphate deposition in ligamentum flavum. Arthritis Rheum 1978; 21:611–613 41. Lipson SJ. Rheumatoid arthritis in the cervical spine. Clin Orthop 1989; 239: 121–127. 42. Boden SD, Dodge LD, Bohlman HH, et al. Rheumatoid arthritis of the cervical spine: a twenty year analysis with predictors of paralysis and recovery. J Bone Joint Surg 1993; 75A:1282–1297. 43. Gordon DA, Hastings D. Rheumatoid arthritis. Clinical features of early, progressive and late disease. In: Klippel JH and Dieppe PA, eds. Rheumatology. London: Mosby; 1998:5.3.1–5.3.14. 44. Linquist PR, McDonnell DE. Rheumatoid cyst causing extradural compression. A case report. J Bone Joint Surg 1970; 52A:1235–1240.

17. Mihara H, Ohnari K, Hachiya M, et al. Cervical myelopathy caused by C3–C4 spondylosis in elderly patients. Spine 2000; 25:796–800.

45. Paimela L, Laasonen L, Kankaanpaa E, et al. Progression of cervical spine changes in patients with early rheumatoid arthritis. J Rheumatol 1997; 24:1280–1284.

18. Kawaguchi Y, Kanamori M, Ishihara H, et al. Pathomechanism of myelopathy and surgical results of laminoplasty in elderly patients with cervical spondylosis. Spine 2003; 28:2209–2214.

46. Yonezawa T, Tsuji H, Matsui H, et al. Subaxial lesions in rheumatoid arthritis: radiological factors suggestive of lower cervical myelopathy. Spine 1995; 20: 208–215.

19. Hirayama K, Tokumaru Y. Cervical dural sac and spinal cord in juvenile muscular atrophy of distal upper extremity. Neurology 2000; 54:1922–1926.

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20. Restuccia D, Rubino M, Valeriani M, et al. Cervical cord dysfunction during neck flexion in Hirayama’s disease. Neurology 2003; 60:1980–1983. 21. Fuji T, Yonenobu K, Fujiwara K, et al. Cervical radiculopathy or myelopathy secondary to athetoid cerebral palsy. J Bone Joint Surg 1987; 69A:815–821.

48. Ranawat CS, O’Leary, Pellicci P, et al. Cervical fusion in rheumatoid arthritis. J Bone Joint Surg 1979; 61A:1003–1010.

22. Hoff J, Nishimura M, Pitts L, et al. The role of ischemia in the pathogenesis of cervical spondylotic myelopathy. Spine 1977; 2:100–108.

49. Zeidman SM, Ellenbogen RG, Ducker TB. Intradural tumors. In: The Cervical Spine Research Society Editorial Committee, ed. The cervical spine. 3rd edn. Philadelphia: Lippincott-Raven Publishers; 1998:587–601.

23. Satomi K, Hirabayashi K. Ossification of the posterior longitudinal ligament. In: Herkowitz HN, Eismont FJ, Garfin SR, et al., eds. Rothman-Simeone, The spine, 4th edn. Philadelphia: WB Saunders; 1999:565–580.

50. Simeone FA. Intradural tumors. In: Herkowitz HN, Eismont FJ, Garfin SR, et al., eds. Rothman-Simeone, The spine. 4th edn. Philadelphia: WB Saunders Co; 1999:1359–1371.

24. Matsunaga S, Sakou T. Epidemiology of ossification of the posterior longitudinal ligament. In: Yonenobu K, Sakou T, Ono K, eds. Ossification of the posterior longitudinal ligament. Tokyo, Berlin, Heidelberg, New York: Springer; 1997:11–17.

51. Rao S, Davis RF. Cervical spine metastases. In: The Cervical Spine Research Society Editorial Committee, ed. The cervical spine. 3rd edn. Philadelphia: LippincottRaven Publishers; 1998:603–619.

25. Koga H, Sakou T, Taketomi E, et al. Genetic mapping of ossification of the posterior longitudinal ligament of the spine. Am J Hum Genet 1998; 62:1460–1467.

52. Jenis LG, Dunn EJ, An HS. Metastatic disease of the cervical spine. Clin Orthop 1999; 359:89–103.

26. Maeda S, Koga H, Matsunaga S, et al. Gender-specific haplotype association of collagen alpha2 (XI) gene in ossification of the posterior longitudinal ligament of the spine. J Hum Genet 2001; 46:1–4.

53. Currier BL, Heller JG, Eismont FJ. Cervical spine infections. In: The Cervical Spine Research Society Editorial Committee, ed. The cervical spine. 3rd edn. Philadelphia: Lippincott-Raven Publishers; 1998:659–690.

27. Numasawa T, Koga H, Ueyama K, et al. Human retinoic X receptor beta: complete genomic sequence and mutation search for ossification of posterior longitudinal ligament of the spine. J Bone Miner Res 1999; 14:500–508.

54. Flannery AM, Allen MB. Intradural infections. In: Herkowitz HN, Eismont FJ, Garfin SR, et al., eds. Rothman-Simeone. The spine. 4th edn. Philadelphia; WB Saunders; 1999:1373–1379.

28. Nakamura I, Ikegawa S, Okawa A, et al. Association of the human NPPS gene with ossification of the posterior longitudinal ligament of the spine (OPLL). Hum Genet 1999; 104:492–497.

55. Hensinger RN. Congenital anomalies of the cervical spine. In: Herkowitz HN, Eismont FJ, Garfin SR, et al., eds. Rothman-Simeone. The spine. 4th edn. Philadelphia; WB Saunders; 1999:221–265.

29. Tsuyama N, Terayama K, Ohtani K, et al. The ossification of the posterior longitudinal ligament (OPLL). The Investigation Committee on OPLL of the Japanese Ministry of Public Health and Welfare. J Jpn Orthop Assoc 1981; 55:425–440.

56. Matsui H, Imada K, Tsuji H. Radiographic classification of os odontoideum and its clinical significance. Spine 1997; 22:1706–1709.

30. Kawaguchi Y, Kanamori M, Ishihara H, et al. Progression of ossification of the posterior longitudinal ligament following en bloc laminoplasty. J Bone Joint Surg 2001; 83A:1798–1802.

57. Kuntz D, Naveau B, Bardin T, et al. Destructive spondylarthropathy in hemodialyzed patients. Arthritis Rheum 1984; 27:369–375. 58. Bindi P, Chanard J. Destructive spondyloarthropathy in dialysis patients: An overview. Nephron 1990; 55:104–109.

31. Kokubun S, Sakurai M, Tanaka Y. Cartilageous endplate in cervical disc herniation. Spine 1996; 21:190–195.

59. Ito M, Abumi K, Takeda N, et al. Pathologic features of spinal disorders in patients treated with long-term hemodialysis. Spine 1998; 23:2127–2133.

32.O’Laoire SA, Thomas DGT. Spinal cord compression due to prolapse of cervical intervertebral disc (herniation of nucleus pulposus). J Neurosurg 1983; 59:847–853.

60. Shiota E, Naito M, Tsuchiya K. Surgical therapy for dialysis-related spondyloarthropathy: Review of 30 cases. J Spinal Disord 2001; 14:165–171.

33. Mochida K, Komori H, Okawa A et al. Regression of cervical disc herniation observed on magnetic resonance images. Spine 1998; 23:990–997.

61. Ono K, Ota H, Tada K, et al. Cervical myelopathy secondary to multiple spondylotic protrusions. A clinicopathologic study. Spine 1977; 2:109–125.

34. Matsumoto M, Chiba K, Ishikawa M, et al. Relationship between outcomes of conservative treatment and magnetic resonance imaging findings in patients with mild cervical myelopathy caused by soft disc herniation. Spine 2001; 14:1592–1598.

62. Fujiwara K, Yonenobu K, Hiroshima K, et al. Morphometry of the cervical spinal cord and its relation to pathology in cases with compression myelopathy. Spine 1988; 13:1212–1216.

35. Hunter LY, Braunstein EM, Bailey RW. Radiographic changes following anterior cervical fusion. Spine 1980; 5:399–401.

63. Fujiwara K, Yonenobu K, Ebara S, et al. The prognosis of surgery for cervical compression myelopathy. An analysis of the factors involved. J Bone Joint Surg 1989; 71B:393–398.

36. Brunton FJ, Wilkinson JA, Wise KSH, et al. Cine radiography in cervical spondylosis as a means of determining the level for anterior fusion. J Bone Joint Surg 1982; 64B:399–404. 37. Baba H, Furusawa N, Imura S, et al. Late radiographic findings after anterior cervical fusion for spondylotic myeloradiculopathy. Spine 1993; 18:2167–2173.

64. Ogino H, Tada K, Okada K, et al. Canal diameter, anteroposterior compression ratio, and spondylotic myelopathy of the cervical spine. Spine 1983; 8:1–15. 65. Ono K, Ebara S, Fuji T, et al. Myelopathy hand. New clinical signs of cervical cord damage. J Bone Joint Surg 1987; 69B:215–219.

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78. Mizuno J, Nakagawa H, Inoue T, et al. Clinicopathological study of ‘snake-eye appearance’ in compressive myelopathy of the cervical spinal cord. J Neurosurg 2003; 99:162–168.

67. Gorter K. Influence of laminectomy on the course of cervical myelopathy. Acta Neurochir 1976; 33:265–281.

79. Odom GL, Finney W. Cervical disk lesions. JAMA 1958; 166:23–28.

68. Crandall PH, Batzdorf U. Cervical spondylotic myelopathy. J Neurosurg 1966; 25:57–66. 69. Hattori S, Kawai S. Diagnosis of cervical spondylosis. (In Japanese.) Orthopaedic Mook 1979; 6:13–40. 70. Fergason RJL, Caplan LR. Cervical spondylotic myelopathy. Neurol Clin 1985; 3:373–382. 71. An HS. Clinical presentation of discogenic neck pain, radiculopathy, and myelopathy. In: The Cervical Spine Research Society Editorial Committee, ed. The cervical spine. 3rd edn. Philadelphia: Lippincott-Raven; 1998:755–764. 72. Zeidman SM, Ducker TB. Evaluation of patients with cervical spine lesions. In: The Cervical Spine Research Society Editorial Committee, ed. The cervical spine 3rd edn. Philadelphia: Lippincott-Raven; 1998:143–161. 73. Dvorak J, Janssen B, Grob D. The neurologic workup in patients with cervical spine disorders. Spine 1990; 15:1017–1022. 74. Shimizu T, Shimada H, Shirakura K. Scapulohumeral reflex (Shimizu). Its clinical significance and testing maneuver. Spine 1993; 18:2182–2190. 75. Gore DR. Radiological evaluation of the degenerative cervical spine. In: The Cervical Spine Research Society Editorial Committee, ed. The cervical spine. 3rd edn. Philadelphia: Lippincott-Raven; 1998:765–778. 76. Kaiser JA, Holland BA. Imaging of the cervical spine. Spine 1998; 23:2207–2212. 77. Matsumoto M, Toyama Y, Ishikawa M, et al. Increased signal intensity of the spinal cord on magnetic resonance images in cervical compressive myelopathy. Spine 2000; 25:677–682.

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80. Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain 1972; 95:87–100. 81. Rao R. Neck pain, cervical radiculopathy, and cervical myelopathy: pathophysiology, natural history, and clinical evaluation. AAOS Instructional Course Lectures 2003; 52:479–488. 82. Hirabayashi K, Miyakawa J, Satomi K, et al. Operative results and postoperative progression of ossification of the posterior longitudinal ligament. Spine 1981; 6:354–364. 83. Yonenobu K, Abumi K, Nagata K, et al. Interobserver and intraobserver reliability of the Japanese Orthopaedic Association scoring system for evaluation of cervical compression myelopathy. Spine 2001; 26:1890–1895. 84. Hamburger C, Butter A, Uhl E. The cross-sectional area of the cervical spinal canal in patients with cervical spondylotic myelopathy. Correlation of preoperative and postoperative area with clinical symptoms. Spine 1977; 22:1990–1995. 85. Houten JK, Cooper PR. Laminectomy and posterior cervical plating for multilevel cervical spondylotic myelopathy and ossification croforaminotomy for treatment of cervical radiculopathy: part 1 – Disc-preserving ‘functional cervical disc surgery.’ Neurosurgery 2002; 51(5 Suppl):46–53. 86. Zeidman SM, Moses H, Ling GS, et al. Differential diagnosis of cervical myelopathy. In: The Cervical Spine Research Society Editorial Committee, ed. The cervical spine. 3rd edn. Philadelphia: Lippincott-Raven; 1998:163–178. 87. Stoodley MA, Jones NR. Syringomyelia. In: The Cervical Spine Research Society Editorial Committee, ed. The cervical spine. 3rd edn. Philadelphia: LippincottRaven; 1998:565–583.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ i: Anatomy and Assessment

CHAPTER

Cervical Instability

51

W. W. Lu, C. Y. Wen, G. X. Qiu and K. D. K. Luk

INTRODUCTION The definition of spinal instability has been a subject of considerable debate for decades, even among experts. According to White and Panjabi, ‘the loss of the ability of the spine under physiologic loads to maintain relationships between vertebrae in such a way that there is neither initial nor subsequent damage to the spinal cord or nerve root, and in addition, there is neither development of incapacitating deformity or severe pain.’1 In this definition, physiologic loads refer to those incurred during normal activity of the patients being examined. They preferred to emphasize the relationship between the mechanical derangement and pain or neurologic deficit. They also preferred a checklist to standardize the evaluation of cervical instability and show a systematic approach. Earlier, Allen et al.2 presented a mechanistic classification system of injuries to the lower cervical spine. In their opinion the skeletal injury, the neurologic injury, associated injuries, medical disorders, and unique individual factors should be analyzed in each case to determine acute injury and risk for late instability. Instability has been defined in anatomical, biomechanical, and clinical terms, but the variability of clinical presentations and the inability of sequential laboratory lesions to replicate clinical experiences indicate that instability should be defined in anatomical terms. Larson has emphasized that the stable spinal column is symmetrical in movement and configuration, whether normal or abnormal, and does not change with time.3,4 In considering spinal instability, it is necessary to generally review the column theory of vertebral stability. The two-column or three-column concepts of Holdsworth, White, Denis, and Louis are frequently used to conceptualize the mechanical integrity of the spinal column.1,5–7 The definition of the extent of injury to the soft tissues and bony components of the spinal column will assist the clinician in determining the risk to neural structures from alterations in stability or alignment. Although inclusion of a middle column has a theoretical advantage in thoracic and lumbar injuries, these considerations are not as anatomically important in the cervical spine and it is reasonable to use the two-column model in the cervical region (Fig. 51.1). As previously noted, laboratory studies of cervical instability determined through a sequential pattern of component section of a specific column are not usually representative of clinical injury which may include only selective elements of each column.8 The degree and character of a column compromise, however, are important indicators alerting the clinician to the potential risk of instability. Additionally, this information, especially the potential role of ligamentous injury, will assist in recognizing the possible development of delayed instability (subacute or chronic) which may be difficult to establish in the early post-trauma period. The degree of instability, irrespective of temporal occurrence, will be

an important influence upon the threat or occurrence of neurologic injury. Therefore, clarification of the degree of injury and a more precise measurement of displacement will assist in determining the threat to neurologic integrity. Clarification of these potentially important clinical elements will both assist in designing preventive measures and treatment options. This latter consideration has special importance in helping the treating physician to avoid exacerbating causative injury forces by reapplication of the predominant injury vector with potential accentuation of instability and risk of neurologic compromise. The type and degree of cervical column instability may be influenced by clinical factors which are deduced from a variety of historic and radiologic evidence. One should attend that the methodology of the clinical studies differs in comparison to laboratory investigations which are controlled and carefully observed, whereas the clinical situation is uncontrolled and frequently unobserved. This chapter provides insight into both clinical and laboratory investigations delineating the several biomechanical aspects of cervical instability. The anatomic and biomechanical characteristics of the occipitoatlantal (C0–C1–C2) joint are complex and its specific patterns of instability are very different from those of the subaxial cervical spine. To facilitate the discussion on this topic, the cervical spine will be divided into two parts herein: the upper parts consisting of occiput, atlas, and axis; and the subaxial or lower cervical spine, consisting of C3–7.

Fig. 51.1 Based on anatomy of cervical spine, the two-column model has been used in this chapter. Anterior column consists of vertebral bodies, intervertebral discs, and anterior and posterior longitudinal ligaments, whereas the posterior column consists of zygapophyseal joints, capsular ligaments, spinous processes, lamina, and interspinous and paraspinous ligaments. 573

Part 3: Specific Disorders

UPPER CERVICAL SPINE Anatomic and biomechanical considerations In the upper cervical spine instability is quite well understood and defined both clinically and biomechanically. The advancement of relationships between anatomy and function will be presented. The anatomic stability of occipito-atlanto-axial joint complex is gained mainly by the ligament, capsule, and structural membrane (Fig. 51.2). The stability of occiput–C1 joint is provided by their capsule, along with the anterior and posterior atlanto-occipital membrane, enhanced by the additional structures such as the alar ligament, apical ligament, and the tectorial membrane. The transverse, dentate, and apical ligaments play an important role in structural stability of the atlantoaxial joint. The injury or dysfunction of the transverse ligament leads to the translation of C1 on C2 and widening of the atlantodens interval (ADI), which can be detected by lateral X-ray of the cervical spine. Functional loss of the alar ligaments indicates a potential for rotatory instability, which, however, must be determined in conjunction with other clinical findings, such as neurological dysfunction, pain, and deformity.9 Knowledge of the normal movements of the occipito-atlanto-axial joint complex is important for evaluating clinical cases that may be potentially unstable. The occiput and axis are sometimes described as two rotating squares with the atlas as a bearing between them. The joints between the atlas and axis are almost horizontal and therefore allow for a wide range of motion in rotation, whereas rotation between the occiput and atlas is completely prevented by the geocentric anatomy of the articulation. The investigations of measurement of range of motion of C0–C1–C2 are shown in Tables 51.1 and 51.2. Both joints, C0–C1 and C1–2, participate in flexion and extension. Extension at occiput–C1 is one of the largest single motions in the spine. Lateral bending occurs at occiput–C1, but is almost negligible at C1–2. The greatest intervertebral motion in the spine is axial rotation at the C1–2 joint.10,11 Analysis of lateral neutral, flexion, and extension radiographs was performed using two measurements: occipitocervical angle (OCA), and occipitocervical distance (OCD). The OCA was defined by the junction of McRae’s line (a line intersecting the basion and the opisthion) and a line drawn parallel to the superior endplate of C3. The superior endplate of C3 was used for the caudal landmark because it was found to parallel the inferior endplate of C2 and was more

Anterior atlanto-occipital membrane Anterior atlanto-dental ligament Atlantal portion of alar ligament Occipital portion of alar ligament Apical ligament

Table 51.1: Average Rotation in Degrees at the Atlantooccipital Joint of C0–1 According to Different Investigators Reference

Flexion/ Extension

Side Bending

Axial Rotation

Penning (1978)

35

10

0

Goel et al. (1988)

23.0

3.4

2.4

Panjabi (1988)

24.5

5.5

7.2

readily visualized on all radiographs. The OCD was obtained by measuring the shortest distance from the superior-most aspect of the C2 spinous process to the occipital protuberance, found directly behind the mastoid process. The mean occipitocervical angles were 24.2°, 44.0°, and 57.2° in flexion, neutral, and extension, respectively. The mean occipitocervical distances were 21.5 mm in neutral, 28.0 mm in flexion, and 14.8 mm in extension.10 These are simple to determine on routine lateral radiographs. The differences in the occipitocervical angle and occipitocervical distance in neutral, flexion, and extension are significant. These measurements should be a valuable intraoperative tool for achieving occipitocervical fusion in appropriate alignment. The term coupled motion denotes that motion about one axis consistently occurs simultaneously with motion about another axis (rotation or translation).12 It is most dramatic in the cervical spine. Two kinds of coupled motion are especially well known in the cervical spine: axial rotation in the same direction as applied lateral bending, and lateral bending in the same direction as applied axial rotation. Posture affects motion coupling patterns of the upper cervical spine. The most dramatic change due to modification in posture is found in coupled sagittal plane rotation, which changes from extension at extended posture to flexion at flexed posture at both levels and in response to both load types. For the axial torque, the main axial rotation and coupled lateral bending changes little with posture.

Diagnosis In daily clinical practice, one often deals with patients with neck pain or stiffness resulting from injury or the ongoing degenerative changes rather than those with no relevant complaint. Active motion in patients with complaints of neck pain or stiffness is usually restricted by the motion-induced pain. Due to the closely related trigeminus nuclei, segmental functional disorders in the suboccipital area cause, in addition to local neck pain, frontoparietal and retro-orbital pain that can also irradiate to the upper and lower jaw. In addition, tendomyoses with trigger points and difficulties in swallowing may occur in the anterior part of the neck.13 The historical information collected

Table 51.2: Average Rotation in Degrees at the Atlantooccipital Joint of C1–2 According to Different Investigators

Transverse ligament

Reference

Flexion/ Extension

Side Bending

Axial Rotation

Goel et al. (1988)

10.1

42

23.3

Panjabi (1988)

22.4

6.7

38.9

Atlantooccipital membrane Ligamentum nuchae Fig. 51.2 Axial schematic of the major ligaments involved in the clinical stability of the upper cervical spine. 574

Penning (1987)

40.5

Section 3: Cervical Spine

from the patient is important in making the diagnosis, even given the aid of radiologic technology. In order to differentiate between hypomobility, hypermobility, or instability, clinical diagnosis requires specific examination of each particular segment in accordance with its biomechanics. Once the nature of the functional disorder is defined, the whole repertoire of therapeutic measures can be applied, with segment-oriented manual techniques being the most efficient. In cases of persistent and recurrent disturbances, rehabilitation must be completed by regular back exercises and optimal ergonomics. A few recognized criteria of radiology for C0–C1–C2 instability have been established. For instance, when the ADI value, which may describe the range of C1–2 translation, is larger than 3 mm in lateral flexion and extension view, the atlantoaxis is considered unstable.14 Asymmetry of the odontoid lateral mass interspace on open-mouth view is also an important clue for diagnosis. One should also assess whether vertical migration of the odontoid process exists, especially in rheumatoid patients. For evaluation of the function of the upper cervical spine, especially assessment of the range of motion, functional X-rays films are useful in addition to the clinical examination (Fig. 51.3). For the diagnosis of segmental instability, passive motion should be induced in order to obtain the full range. If anterior instability of the upper cervical spine is suspected, flexion–extension X-rays in the lateral view are appropriate. If a lesion of the alar ligaments is suspected, then lateral flexion X-ray films should be taken. In the normal situation, the atlas glides in the direction of bending, coupled by forced rotation of the axis. In cases with rotatory instability of the upper cervical spine, functional computed tomography should be performed. Atlantoaxial rotation of more than 52° should be considered pathological as a result of a lesion of the alar ligaments. For examination of the relationship between the spinal cord and bony structures or inflammatory tissue in patients with rheumatoid arthritis, functional MRIs are helpful.

Functional magnetic resonance tomography is an important diagnostic method for assessing the cervical spine in patients with rheumatoid arthritis. In particular, fusion and instabilities as well as compressions of the spinal cord or medulla often can only be detected with the help of functional MRI. Compared with static MRI examinations in patients with rheumatoid arthritis, functional magnetic resonance imaging identifies the extension of pannus tissue cranial, ventral, and dorsal to the dens with possible displacing and impinging effects on the spinal cord during flexion and extension. In addition, it is suitable for demonstration of the degree of instability in the atlanto-occipital and atlantoaxial planes. In contrast to conventional X-rays, CT, and static MRI, basilary impression as well as compressions and angulations of the spinal cord are better visualized by cinematic magnetic resonance tomography.15 Cineradiography is a valuable continuous recording tool and has been used in motion analysis of the musculoskeletal system (Fig. 51.4).16 Cineradiography has advantages over other techniques for analyzing the details of cervical spinal motion and diagnosis of spinal instability.17–20 The outcome from the cineradiographic motion analysis of the cervical spine can be taken into account to determine the level of spinal fusion for cervical spondylosis. An instantaneous center of rotation deduced from cineradiographic films has also been used to clarify the quality of motion and to justify therapy for the neck region. Hino et al. investigated the kinematics of the normal and pathologic atlantoaxial joints by cineradiography to determine the in vivo kinematic parameters for the quantification of atlantoaxial instability.21 The kinematics of the atlantoaxial joints were evaluated by cineradiography in healthy volunteers and in patients with atlantoaxial subluxation. The results revealed the different onset points of a rapid increase in motion between flexion-from-E and extension-from-F in atlantoaxial motion. They were defined, respectively, as points A and B (Fig. 51.5). The discrepancy between these points (i.e. zone A–B) was significantly more remarkable in patients with atlantoaxial

Fig. 51.3 Lateral view of the cervical spine at flexion, neutral position, and extension. 575

Part 3: Specific Disorders Sagittal rotation (deg.) 10 Flexion 5

6.8⬚ 1.8⬚

0 –5

Point B

–10 Extension –15

Extension-from-F 0

1

2

3

4

5 (Sec.) Zone A-B ROM

Flexion

10 Flexion-from-E

5 0

Point A

–5

–7.5⬚

–10 Extension –15

–14.2⬚ 0

1

2

3

4

5 (Sec.)

Fig. 51.5 The format of cineradiography outcome. Regarding the angulation of sagittal rotation, 0° means lines A1–P1 and A2–P2 (i.e. the x-axis is horizontal). Point A exists in a more extended position and point B in a more flexed position in the atlantoaxial range of motion.

Fig. 51.4 Radiographic examples and equipment setup. Cineradiographic images were projected onto a digitization table at 3.5-fold magnification. The template was superimposed onto every four frames (time interval, 0.13 seconds), and four vertebral landmarks were digitized.

subluxation than in the volunteers. Furthermore, in most of the cases with atlantoaxial instability, subluxation occurred when the cervical spine was in a more extended position, and it was reduced in a more flexed position.

Surgical indication and principle of internal fixation Although occipito-atlanto-axial region instability can occur suddenly from violent traumatic forces, it can also develop in a slow, progressive fashion as occurs with congenital abnormalities, infections, neoplasms, or rheumatoid arthritis. In certain instances, spinal elements may fail along a continuum; anatomic changes can appear long before pathologic motion develops. Neurological dysfunction due to spinal instability is the most urgent indication for arthrodesis. Mechanical compression of neural structures can present with occipital radicular pain, myelopathy, cranial nerve deficits, nystagmus, and bulbar dysfunction. Sudden death has been reported with occiput, C1, and C2 subluxations. Subluxations of the craniovertebral junction may also present with vertebral artery compression. In the absence of neurologic deficits, specific pathological and clinical features become crucial to consider in determining the need for internal fixation. Patients who are at high risk for nonunion of fractures, those at risk of developing neurological deficits from compression or progressive subluxations, or those with predominantly ligamentous injuries may be considered for arthrodesis. However, the decision for internal fixation must be individualized, based upon the patient’s neurological status, age, and medical condition and upon the extent of subluxations, the type of pathology, and the levels of instability. 576

The conclusion of the analysis of the in vitro biomechanical properties of one-, two-, and three-point fixations at the atlantoaxial segment is that one-point fixation results in high stiffness in flexion– extension, whereas the stiffness in axial rotation and lateral bending is lower, using new nonbone graft-dependent fixation devices. Twopoint fixation results in high stiffness in all motion directions except in flexion–extension. The reasons probably being that the screws are located close to the axis of rotation. Three-point fixation results in a high stiffness level in all degrees of freedom. The combination of transarticular screws with the C1-claw device results in stiffness equivalent to the traditional 3-point fixation technique, but without the need of structural bone graft and the use of cerclage wire in the spinal canal. From a biomechanical viewpoint the 3-point fixation technique is the method of choice for C1–2 fusion. Is fusion the right choice for the instability? Adjacent level motion has been found to increase as a result of one level cervical spine fusion. These findings were more prominent in the level below the fused segment. As the range of motion decreased stepwise in the fused segment, due to more rigid reconstruction techniques, no additional increase of motion was detected in the adjacent segments, as the segments presumably were loaded to their physiological limits. The additional load, shifted over from the fixed segment to adjacent levels, but not contributing to increased motion, may, however, contribute to increased intradiscal pressure, leading to accelerated degeneration in adjacent levels.

Upper cervical instability in congenital diseases Atlantoaxial instability occurs in 10–20% of patients with Down syndrome who are at risk for atlantoaxial subluxation and subsequent complications during anesthetic induction and during positioning and manipulation associated with surgery. To identify patients who are at risk for atlantoaxial subluxation, guidelines have been adapted from the recommendations of the American Academy of Pediatrics and the Special Olympics Inc, which include preoperative neurologic assessments and cervical roentgenograms in the neutral, flexion, and extension positions. Children with an atlantodental

Section 3: Cervical Spine

interval of greater than 4.5 mm or with peripheral neurologic findings should have further evaluation.22 All patients with Down syndrome should have a preoperative neurologic assessment screening by the operating surgeon and/or a cervical roentgenogram in the lateral, extension, and flexion positions. Any abnormality should be investigated before surgery. For children with Goldenhar’s syndrome, a high incidence of congenital malformations of the cervical spine, including odontoid hypoplasia, put them at particular risk during general anesthesia. Unfortunately, children with Goldenhar’s syndrome have many other malformations that would necessitate surgery under general anesthesia. Once diagnosed, children with C1–2 instability can be monitored by flexion–extension views at 6-month interval, and activity can be modified to minimize the risk of a catastrophic event. If the C1 displacement exceeds 6 mm, C1–2 fusion should be considered. The anteroposterior (AP) and lateral views of the c-spine, flexion–extension views of C1–2 and CT scan of C1–2 are recommended to assess and monitor such cervical instability.23 The similar situation also occurs in children and adolescents with cervical spine congenital synostosis as in Klippel-Feil syndrome (KFS). The more numerous the occipito-C1 abnormalities the more significant the neurologic risk.24 Careful clinical and radiologic observation of the cervical spine is necessary in children or adolescents with congenital disease. MRI with lateral views in flexion and extension seem to be the best method for detecting impingement of the spinal cord. Frequent imaging is also mandated.

LOWER CERVICAL SPINE Anatomic and biomechanical considerations Stability and kinematics in the cervical spine depend on the integrity and configuration of several anatomic structures including the intervertebral disc, uncovertebral joints, and posterior longitudinal ligament (PLL) (Fig. 51.6). The biomechanical effects of discectomy and uncovertebral joint resection have been studied.25–28 The relative biomechanical contributions of the anterior column elements also have been explored. A clear understanding of each element’s bio-

Posterior longitudinal ligament

mechanical contribution is necessary in order to predict how surgery will affect spinal movement and stability, and to determine whether an internal fixation device is needed. Motions in the subaxial cervical spine occurs at all levels and in all six degrees of freedom. However, most of the flexion–extension motion occurs in the central region with C5–6 considered to have the greatest range. The loss of motion due to degeneration or post-traumatic change has been observed to result in compensatory increase of motion in adjacent segments. The range of motion in axial rotation and lateral bending tend to be less in the more caudal segment.29

Intervertebral disc With discectomy, the increase in flexion–extension ROM (10.5°) was much larger than during lateral bending (2°) or axial rotation (1.8°).30 Therefore, the disc serves more as a stabilizer against flexion and extension than as a stabilizer against lateral bending or axial rotation. During torque to induce axial rotation, disc resection doubled the coupled flexion and significantly increased the coupled lateral bending. Disc resection also shifted the instantaneous axis of rotation (IAR) significantly in a posterior direction during extension. Therefore, the disc helps guide normal spinal motions. Without the disc, adjacent vertebral bodies collapse together, forcing the facets to support more load and dictating the motion pattern.

Uncovertebral joints When the unilateral and then the contralateral uncovertebral joint was resected, the increase in flexion–extension ROM was about twice that of lateral bending or axial rotation. Thus, the uncovertebral joints also stabilize more against flexion and extension than against lateral bending or axial rotation. Flexion and extension increased more than axial rotation or lateral bending after resection of the uncovertebral joints.27,31,32 However, the uncovertebral joints contributed more to preventing lateral bending than in the other study,28 a difference perhaps attributable to different loading methods and magnitudes. In all, the effect differs because of anatomic variations in uncovertebral joints. The major biomechanical function of uncovertebral joints includes the regulation of extension and lateral bending motion, followed by torsion, which is mainly provided by the posterior uncovertebral joints. The uncovertebral joint is also considered a primary source of cervical coupling, as are the facet joints.27 During torque to induce primarily axial rotation, uncovertebral joint resection doubled the coupled flexion and moderately increased the coupled lateral bending. The intact uncovertebral joints may therefore maintain normal spinal kinematics after discectomy.

Posterior longitudinal ligament

Uncinate process

Uncovertebral joint

With the PLL resected, ROM increased significantly during flexion–extension, lateral bending, and axial rotation, all by about the same magnitude.28 The PLL therefore contributes to stability during all three motions. The slight changes in coupling with PLL resection indicate that the PLL plays no major role in spinal kinematics (Table 51.3). However, the 4 mm posterior shift in the extension IAR after PLL resection indicates that the PLL helps to maintain normal joint rotation during extension.

Intervertebral joint

Clinical considerations Fig. 51.6 Anatomic structures studied. The intervertebral disc, uncovertebral joints/uncinate processes, and posterior longitudinal ligament were sequentially resected. (Reprinted with permission from Barrow Neurological Institute.)

Extensive cervical discectomy altered the cervical motion segment’s kinematics. Whether the substantial instability observed in vitro corresponds to clinical instability is uncertain. However, these results support the use of fusion with a bone graft or graft plus anterior plate after extensive cervical discectomy. 577

Part 3: Specific Disorders

Table 51.3: The Effect on the Motion of Cervical Spine After Surgical Intervention Surgical Site

Flexion/ Extension

Side Bending

Axial Rotation

Disc

++++

+

+

Uncovertebral joints

+++

+

+

PLL

++

++

++

Note: the grade of effect is determined by the relative comparison among the above three tissues: ++++, significant; +++, great; ++, moderate; +, slight.

The intervertebral disc helps to maintain posture, as indicated by significant increases in NZ and ROM during flexion–extension after discectomy. Between tests, the destabilized spine sagged noticeably in a flexed posture with loss of lordosis. Clinically, the intervertebral space usually collapses slightly after discectomy, but the preoperative lordosis can be maintained without fusion. The strong paraspinal muscles therefore may be significant for maintaining posture and stability after surgery.33–35 After extensive discectomy without fusion, a rigid cervical orthosis can apply dorsally and rostrally directed forces to help support the paraspinal musculature in extension, thereby reducing the chance of muscle overexertion and spasm. After each decompressive step, x-axis torque to induce flexion or extension showed the largest increase in primary angular motion. Furthermore, during y-axis torque to induce axial rotation, coupled flexion increased most dramatically. Therefore, if surgeons apply a fixation device to limit motion and promote bony fusion, its main function should be to limit flexion and extension. The uncovertebral joints appear to contribute substantially to cervical stability and kinematics, but may require resection during foraminotomy to decompress cervical nerve roots. If radiculopathic signs or symptoms are absent, surgeons should consider preserving these structures, especially during discectomy without fusion. The extent of disease will dictate the extent of decompression.36,37 However, resection of uncovertebral joints may be necessary to access osteophytes or other pathology.

Diagnosis Spinal instability should be precisely defined to evaluate pathologic spines and to determine the indication of spinal fusion. Usually, spinal motions in the sagittal plane (translation and angulation) are the most common parameters used to diagnose spinal instability. In a clinical setting, these parameters are usually measured by functional radiography, which provides only information on static spinal alignments in the maximum flexion or extension position. For better understanding of spinal instability, spinal motion should be evaluated qualitatively and quantitatively. White and Panjabi38 developed a checklist for the diagnosis of clinical instability of the lower cervical spine based on the radiological finding and the neurological status. This systematic checklist approach is recommended as a useful method for evaluating clinical instability, given the currently available knowledge. This methodology and current knowledge about the complex problem of spinal instability have limitations. Progress will come with more biomechanical experimental studies and controlled prospective clinical studies. Radiographic evaluation of the cervical spine begins with AP, lateral, and odontoid views. Unless the junction of C7–T1 can be adequately visualized on the cross-table lateral view, a swimmer’s 578

view is often performed. However, in cases of trauma, a CT scan is the best method to evaluate the C7–T1 junction. After fractures and subluxations have been excluded, spinal stability may be evaluated with stressed-view radiographs such as a flexion–extension series. However, there is currently no protocol for evaluating the distal spinal stability in patients in whom traditional flexion–extension radiographs fail to visualize the important distal C7–T1 juncture. Further study of this technique as a supplement to the conventional flexion and extension views in the stressed assessment of the entire cervical spine is recommended.39 Over 3000 cases of soft tissue injuries of the cervical spine are reported annually to SUVA (Swiss accident insurance).40 Although the majority of the patients are pain free within 4 weeks, it appears that approximately one-quarter of those injured still experience neck pain even years after the accident. The initial radiological assessment should include an AP and a lateral plain X-ray of the cervical spine, and in the case of radicular symptomatology oblique views are also recommended. Should the symptoms persist for more than 6–8 weeks after the accident, functional X-rays in flexion–extension and lateral flexion should also be performed. If no instability can be demonstrated by plain X-rays and symptoms are still present and severe enough to limit the patient’s working capacity after 3–6 months despite conservative therapy, further neuroradiological investigations, including functional CTs, are indicated. The decision to perform these investigations should lie with an interdisciplinary spinal team. Close cooperation between the clinicians and the radiologists is of utmost importance to ensure that the optimal radiological investigation can be performed on the basis of the clinical findings. The study by Kanayama et al.41 serves as the first investigation to quantify cervical motion patterns in normal and pathologic spines using cineradiography technique. Different cervical motion patterns were observed in spines of normal subjects and those of patients with cervical instability. The normal cervical motion pattern consisted of well-regulated stepwise motions that initiated at the C1–2 segment and transmitted to the lower cervical segments. These results were similar to the dynamic motion data in the lumbar and lumbosacral regions. Kanayama et al.41 have recently reported in their cineradiographic study that lumbar segmental motions occur not simultaneously but stepwise from the upper level, with motion lags during flexion. In pathologic cervical spines, however, cervical motion initiated at the unstable levels. In rheumatoid arthritis patients with atlantoaxial subluxation, motion in the unstable C1–2 segment initiate significantly earlier than that in the C2–3 segment. In spines with subaxial instability, motion in the unstable segments preceded that in the upper intact segments. Ogon et al.42 recently performed an in vitro dynamic motion analysis using human lumbar spine specimens. They observed discontinuous acceleration and deceleration during intersegmental motion, termed a ‘jerk.’ In the intact functional spinal unit, this dynamic motion parameter is located at the neutral position. However, the jerk shifts from the neutral position toward the beginning of the motion in increasing instability. They concluded this jerk shift is a sign of spinal instability. The current results in pathologic cervical spines are consistent with the jerk shift occurring toward the beginning of motion. In a clinical setting, functional radiographs are commonly used to evaluate spinal instability and treatment results such as solidity of spinal fusion. However, Woesner and Mitts43 documented that some cervical abnormalities are not visible on conventional radiographs but are detected by cineradiography. Brunton et al.44 also reported that cineradiography is the more accurate diagnostic technique for determining the level indicated for anterior fusion. Although further investigations are required, the cineradiographic method provides the

Section 3: Cervical Spine

capability of diagnosing and evaluating spinal instability that cannot be identified by conventional radiographic examination. In summary, patients with rheumatoid arthritis who had atlantoaxial subluxation, C1–2 motion initiated significantly earlier than C2–3 motion. In patients with segmental instability below C2, motions at the unstable segments preceded those of the upper intact segments. Cineradiographic motion analysis is a valuable adjunctive technique, especially in diagnosis of conditions that cannot be identified by conventional radiographic examination.

Surgical indications and principle of internal fixation The purpose of surgical intervention of the cervical spine in general is to decompress neurological structures if necessary, realign the cervical spine, and to stabilize a possible unstable motion segment. These purposes may be obtained in more than one way, using an anterior, posterior, or combined approach to the cervical spine. These considerations along with individual physiologic demands must be weighed against each other before a decision can be made on how to treat the patient. Numerous fixation techniques and devices have been developed over the years for stabilizing the lower cervical spine. The first techniques introduced were for posterior fixation. The wire technique introduced by Gallie for the upper cervical spine was also applicable in a modified way for use in the lower cervical spine. The posterior wire technique has been developed over the years, introducing different types of cables secured to the posterior lamina and spinous process,45–48 and is still the operative method of choice in many spine centers. However, these techniques provide for one-point fixation and depend on a structural bone graft. Posterior wiring provided significantly better flexion stability in two- rather than three-column disruptions.49 Posterior wiring reduced posterior displacement in two-column partial disruptions to 25% of control. In three-column dissociations, posterior wiring only reduced posterior displacement to 50% of control. In extension, posterior wiring was ineffective in preventing displacement. Anterior plating, used alone, tolerated only 37% of the maximum flexion moment before early failure. On the other hand, combined anterior plating and posterior Roger’s wiring reduced posterior displacement in flexion to 20% of control, while reducing anterior displacement in extension to 50% of control. After the insertion of the bone graft, a significant decrease in motion was seen in the effected segment in extension (±45.9%), with similar reductions in lateral bending and axial rotation and a smaller reduction in flexion. The application of an anterior metal plate in addition to the bone graft at the injured level provided significant reduction in motion (±70%) in all load modalities. These data may have clinical relevance regarding the role of internal fixation in cases of severe spine instability26 The stiffness of the simulated bone graft construct decreased progressively during flexion and lateral bending after each foraminotomy (p<0.05). Increased bone graft height of 79% returned stability to the preforaminotomy level.28 To avoid this, various plates were developed for posterior fixation of the cervical spine. Some general aspects of the two approaches may be stated initially. There are several advantages with the anterior as opposed to the posterior approach in trauma patients. The patient is positioned supine for the anterior approach. The potentially dangerous maneuver of turning a patient with an unstable cervical spine injury over to a prone position is thus avoided. Anterior approach allows for direct removal of an extruded disc. The anterior approach is less traumatic to muscles than the posterior approach, and complications are rare. The anterior approach has also proven to expose patients to less neck pain and risk of kyphosis compared to posterior surgery.

GUIDELINES OF THE DIAGNOSIS FOR CERVICAL INSTABILITY The following recommendations are a series of evidence-based guidelines for the safest and most effective means for identifying significant injuries of the cervical spine following trauma. Injuries which are most likely to lead to neurologic damage by causing or exacerbating trauma to the spinal cord are a particular focus, including bony, ligamentous, and other soft tissue abnormalities. Trauma patients at risk can be categorized according to their clinical presentation into four categories that are at special risk for various types of injuries, or at minimal or no risk for injury. The following guidelines present category of patients and recommendations specific to those categories.50–53 See also Figure 51.7. Radiologic clearance of the cervical spine should occur only after the patient is medically and surgically stable. Until such time, the cervical spine should be kept immobilized in a rigid cervical spine collar.

1. Alert, awake, not intoxicated, neurologically normal, no midline neck pain or tenderness even with full range of motion of neck and palpation of cervical spine54,55 Guidelines – general 1.1. Cervical spine X-rays are not necessary. 1.2. Attending level physician makes the determination, documents this in the medical record, and removes the cervical spine collar. 1.3. Appropriate specialties: Emergency medicine; Trauma surgery; Orthopedic spine surgery. Neurosurgery. 1.4. Optimal timing: within 2 hours after admission to the emergency ward.

Guideline – prehospital Spine immobilization is indicated in the prehospital trauma patient who sustained an injury with a mechanism having the potential for causing a spine injury and who has at least one of the following: 1. 2. 3. 4. 5.

2.

Altered mental status; Evidence of intoxication; A distracting painful injury (e.g. long bone extremity fracture); Neurologic deficits; Spinal pain or palpation tenderness.

Alert, awake, complaints of neck pain

Guidelines 2.1 Three-view cervical spine X-rays are obtained. 2.2 Axial CT images at 3 mm intervals obtained through suspicious areas identified on three-view cervical spine X-rays. 2.3 If lower cervical spine is not adequately visualized on lateral cervical spine X-ray: Swimmers view – if inadequate, then Axial CT images at 3 mm intervals through lower cervical spine with sagittal reconstruction. 2.4 If 2.1–2.3 are normal, the cervical collar is removed and flexion–extension lateral cervical spine X-rays are obtained with the patient sitting and voluntarily flexing and extending the neck.

579

Part 3: Specific Disorders Cervical instability?

Acute injury

A. What is the essence and essential issue in taking history from the patient suspected with cervical instability? • Understand the injury mechanism which can help you to analyze and assess the category or severity of cervical instability, while anticipating the occurrence of loads that could be dangerous. • Emphasize the chief complaint of the patient, especially the presence of pain and numbness in the upper extremities. Be cautious to differentiate and exclude the patient with evidence of intoxication.

Chronic injury or unknown Refer to A Yes

Alert and awake

No

Neck pain or tenderness

Neurologic deficit Yes

No

Yes

A&E doctors neurosurgeon

No

Standard 3-view X-ray for cervical spine

Normal

Abnormal

Cervical X-ray unnecessary

Not sure Remove cervical spine collar and follow-up

Axial CT scan and 3-D reconstruction

Functional X-ray

B. Radiographic criteria, • Standard lateral-view X-ray: 1. sagittal plane displacement > 3.5 mm or 20% (2 points) 2. relative sagittal plane angulation > 11⬚ (2 points) • Functional (flexion-extension) X-ray, sagittal plane displacement > 3.5 mm or 20% (2 points) • Computerized tomography, 1. sagittal diameter < 13 mm 2. Pavlov ratio < 0.8 • Magnetic resonance image, 1. spinal cord damage or nerve root involved 2. disc protrusion and canal narrowing (Pavlov ratio < 0.8) • Lateral cervical spine fluoroscope The range of motion more or less than normal

Swimmers view

Refer to B Lateral cervical spine fluoroscope Abnormal

Nothing special MRI

Cervical immobilization and follow-up (2 weeks)

Abnormal

If determine the anterior or posterior element destroyed or dysfunction

Determine anterior or posterior approach or combination and internal fixation Fig. 51.7 Standardized flowchart for diagnosis of cervical instability. (A) What is the essence and essential issue in taking history from the patient suspected with cervical instability? • Understanding the injury mechanism, which helps to analyze and access the category of the patient or severity of cervical instability, while anticipating the occurrence of loads that could be dangerous. • Appreciating the chief complaint of the patient, especially the presence of pain and numbness in upper extremities. Care must be taken to differentiate and exclude the patient with evidence of intoxication. (B) Radiographic criteria: • Standard lateral X-ray 1. Sagittal plane displacement >3.5 mm or 20% (2 points) 2. Relative sagittal plane angulation >11° (2 points) • Functional (flexion–extension X-ray 1. Sagittal plane displacement >3.5 mm or 20% (2 points) • Computerized tomography 1. Sagittal diameter <13 mm 2. Pavlov ratio <0.8 • Magnetic resonance imaging 1. Spinal cord damage or nerve root involved 2. Disc protrusion and canal narrowing (Pavlov ratio <0.8) • Lateral cervical spine fluoroscope Is the range of motion more or less than normal?

580

Section 3: Cervical Spine

Voluntary and painless excursion must exceed 30°. Flexion– extension X-rays are done by the radiology technician under the supervision of the radiologist. No other physician or nurse is required to be present when they are obtained. 2.5 If voluntary, painless excursion during flexion–extension does not exceed 30°, the cervical spine collar should be replaced and flexion–extension lateral cervical spine X-rays repeated in 2 weeks. 2.6 Optimal timing: within 4 hours of admission to the emergency ward.

3. Neurologic deficits referable to a spine injury Guidelines 3.1 Plain films and CT images as described in 2.1–2.3. 3.2 MRI of the cervical spine 3.3 Optimal timing: within 2 hours of admission to the emergency ward.

4. Altered mental status and return of normal mental status not anticipated for 2 days or more (e.g. severe traumatic or hypoxic, ischemic brain injury) Guidelines 4.1 Plain films and CT images as described in 2.1–2.3. 4.2 Axial CT images at 3 mm intervals with sagittal reconstruction from the base of the occiput through C2. 4.3 If 4.1 and 4.2 are normal, flexion–extension lateral cervical spine fluoroscopy with static images obtained at extremes of flexion and extension. Excursion of the neck is done by housestaff or attendings of: Trauma surgery Neurosurgery Orthopedic spine surgery 4.4 Optimal timing: within 48 hours of admission.

Addendum A.1 Three-view cervical spine X-rays are defined as follows: Lateral cervical spine radiograph: must be of good quality and adequately visualize from the base of the occiput to the upper part of the first thoracic vertebrae. Anteroposterior cervical spine radiograph: must reveal the spinous processes of C2 to C7. Open-mouth odontoid radiograph: must visualize the entire dens and the lateral masses of C1. A.2 For patients with neurologic deficits referable to a cervical spine injury (Category 3), and particularly those with normal plain films, it is extremely important to obtain an MRI scan as soon as possible after admission to the emergency ward. High-dose methylprednisolone therapy started within, but not after, 8 hours of injury may have a benefit but this is controversial and the associated risks should be weighed against potential benefits. Early decompression of mass lesions, such as traumatic herniated discs or epidural hematomas, is also likely to improve neurologic outcome. A.3 The ultimate evaluation of all radiographic studies will be the responsibility of attending radiologists. However, attendinglevel trauma surgeons, emergency medicine physicians, spine surgeons, and orthopedic spine surgeons are considered qualified to properly interpret cervical spine radiographs, and after proper documentation in the patient’s medical record, they may ‘clear’ the cervical spine and remove the cervical spine collar.

References 1. White AA, Panjabi MM. Biomechanics of spine. 2nd edn. Philadelphia: JB Lippincott; 1990. 2. Allen BL, Ferguson RL, Lehmann TR, et al. A mechanistic classification of closed, indirect fractures and dislocations of lower cervical spine. Spine 1982; 7(1):1–27. 3. Larson SL. Vertebral injury and instability. In: Holtzman RNN, Ed. Spinal instability. New York: Springer; 1993:101–137. 4. Larson SJ, Maiman DJ. In: Surgery of the lumbar spine. New York: Thieme; 1999:334. 5. Holdsworth H. Fractures, dislocations and fractures–dislocations of the spine. J Bone Joint Surg [Br] 1963; B45:6–20. 6. Denis F. Three-column spine and its significance in classification of acute thoracolumbar spinal injuries. Spine 1983; 8:817–831. 7. Louis R. Spinal stability as defined by three-column spine concept. Anat Clin 1985; 7:33–42. 8. White A III, Johnson R, Panjabi M, et al. Biomedical analysis of clinical stability in cervical spine. Clin Orthop 1975; 109:85–95. 9. Panjabi M, Dvorak J, Crisco JJ 3rd, et al. Effects of alar ligament transection on upper cervical spine rotation. J Orthop Res. 1991; 9(4):584–593. 10. Phillips FM, Phillips CS, Wetzel FT, et al. Occipitocervical neutral position. Possible surgical implications. Spine 1999; 24(8):775–778. 11. Panjabi M, Dvorak J, Duranceau J, et al. Three-dimensional movements of the upper cervical spine. Spine 1988; 13(7):726–730. 12. Panjabi MM, Oda T, Crisco JJ 3rd, et al. Posture affects motion coupling patterns of the upper cervical spine. J Orthop Res 1993; 11(4):525–536. 13. Baumgartner H. The upper cervical spine. Symptomatology, clinical diagnosis and therapy of functional disorder. Orthopade 1991; 20(2):127–132. 14. Dvorak J. Functional roentgen diagnosis of the upper cervical spine. Orthopade 1991; 20(2):121–126. 15. Allmann KH, Schafer O, Uhl M, et al. Kinematic versus static MRI study of the cervical spine in patients with rheumatoid arthritis. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1999; 170(1):22–27. 16. Neer CS, Foster CR. Inferior capsular shift for involuntary inferior and multi-directional instability of the shoulder. J Bone Joint Surg [Am] 1980; 62:897–907. 17. Fielding JM. Cineradiography of the normal cervical spine. J Bone Joint Surg [Am] 1957; 39:1280–1288. 18. Brunton FJ, Wilkinson JA, Wise KSH, et al. Cineradiography in cervical spondylosis as a mean of determining the level for anterior fusion. J Bone Joint Surg [Br] 1982; 64:399–404. 19. van Mameren H, Drukker J, Sanches H, et al. Cervical spine motion in the sagittal plane (I). Range of motion of actually performed movements, an X-ray cineradiographic study. Eur J Morphol 1990; 28:47–68. 20. Hino H, Abumi K, Kanayama M, et al. Dynamic motion analysis of normal and unstable cervical spine using cineradiography: an in vivo study. Spine 1999; 24: 163–168. 21. Hino H, Abumi K, Kanayama M, et al. Dynamic motion analysis of normal and unstable cervical spines using cineradiography: an in vivo study. Spine 24(2):163–168. 22. Harley EH, Collins MD. Neurologic sequelae secondary to atlantoaxial instability in Down syndrome. Implications in otolaryngologic surgery. Arch Otolaryngol Head Neck Surg 1994; 120(2):159–165. 23. Healey D, Letts M, Jarvis JG. Cervical spine instability in children with Goldenhar’s syndrome. Can J Surg 2002; 45(5):341–344. 24. Rouvreau P, Glorion C, Langlais J, et al. Assessment and neurologic involvement of patients with cervical spine congenital synostosis as in Klippel-Feil syndrome: study of 19 cases. J Pediatr Orthop B 1998; 7(3):179–185. 25. Richter M, Wilke HJ, Kluger P, et al. Load-displacement properties of the normal and injured lower cervical spine in vitro. Eur Spine J 2000; 9(2):104–108. 26. Ng HW, Teo EC, Lee KK, et al. Finite element analysis of cervical spinal instability under physiologic loading. J Spinal Disord Tech 2003; 16(1):55–65. 27. Penning L, Wilmink JT. Rotation of the cervical spine: A CT study in normal subjects. Spine 1987; 12:732–738. 28. Panjabi MM, Vasavada A, White AA III. Cervical spine biomechanics. Semin Spine Surg 1993; 5:10–16. 29. Dai L. Disc degeneration and cervical instability. Zhonghua Wai Ke Za Zhi. 1999; 37(3):180–182. 30. Schulte K, Clark CR, Goel VK. Kinematics of the cervical spine following discectomy and stabilization. Spine 1989; 14(10):1116–1121.

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44. Brunton FJ, Wilkinson JA, Wise KSH, et al. Cineradiography in cervical spondylosis as a means of determining the level for anterior fusion. J Bone Joint Surg [B] 1982; 64:399–404.

32. Clausen JD, Goel VK, Traynelis VC, et al. Uncinate processes and Luschka joints influence the biomechanics of the cervical spine: Quantification using a finite element model of the C5–C6 segment. J Orthop Res 1997; 15:342–347.

45. Bohlman HH. The management of cervical spine fractures and dislocation. In: American Academy of Orthopedic Surgeons. Instruction Course Lecture vol 34. St. Louis: CV Mosby; 1985:163–187.

33. Sonntag VKH, Klara P. Controversy in spine care: Is fusion necessary after anterior cervical discectomy? Spine 1996; 21:1111–1113.

46. Davey JR, Rorabeck CH, Bailey SI, et al. A technique of posterior cervical fusion for instability of cervical spine. Spine 1985; 10:722–728.

34. Nolan JP Jr, Sherk HH. Biomechanical evaluation of the extensor musculature of the cervical spine. Spine 1988; 13:9–11.

47. Stathoulis B, Govender S. The triple wire technique for bifacet dislocation of the cervical spine. Injury 1997; 28(2):123–125.

35. Schulte K, Clark CR, Goel VK. Kinematics of the cervical spine following discectomy and stabilization. Spine 1989; 14:1116–1121.

48. Weis JC, Cunningham BW, Kanayama M, et al. In vitro biomechanical comparison of multistrand cables with conventional cervical stabilization. Spine 1996; 21(18):2108–2114.

36. Hadley MN, Sonntag VKH. Cervical disc herniations: The anterior approach to symptomatic interspace pathology. Neurosurg Clin North Am 1993; 4:45–52. 37. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine 1983 8:817–831. 38. White AA 3rd, Panjabi MM. Update on the evaluation of instability of the lower cervical spine. Instr Course Lect 1987; 36:513–520.

50. Ajani AE, Cooper DJ, Scheinkestel CD, et al. Optimal assessment of cervical spine trauma in critically ill patients: a prospective evaluation. Anaesth Intensive Care 1998; 26:487–491.

39. Davidorf J, Hoyt D, Rosen P. Distal cervical spine evaluation using swimmer’s flexion–extension radiographs. J Emerg Med. 1993;11(1):55–59.

51. Beirne JC, Butler PE, Brady FA. Cervical spine injuries in patients with facial fractures: a 1-year prospective study. Int J Oral Maxillofac Surg 1995; 24:26–29.

40. Dvorak J. Radiological assessment protocol in injuries of the cervical vertebrae. Schweiz Med Wochenschr. 1990;120(51–52):1989–1998.

52. Blacksin MF, Lee HJ. Frequency and significance of fractures of the upper cervical spine detected by CT in patients with severe neck trauma. Am J Roentgenol 1995; 165:1201–1204.

41. Kanayama M, Abumi K, Kaneda K, et al. Phase lag of the intersegmental motion in flexion–extension of the lumbar and lumbosacral spine. An in vivo study. Spine 1996; 21:1416–1422.

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49. McLain RF, Aretakis A, Moseley TA, et al. Sub-axial cervical dissociation. Anatomic and biomechanical principles of stabilization. Spine 1994; 19(6):653–659.

53. Davis JW, Parks SN, Detlefs CL, et al. Clearing the cervical spine in obtunded patients: the use of dynamic fluoroscopy. J Trauma 1995; 39:435–438.

42. Ogon M, Bender BR, Hooper DM, et al. A dynamic approach to spinal instability. Part II: Hesitation and giving-way during interspinal motion. Spine 1997; 22: 2859–2866.

54. Feldborg Nielsen C, Annertz M, Persson L, et al. Fusion or stabilization alone for acute distractive flexion injuries in the mid to lower cervical spine? Eur Spine J 199; 6(3):197–202.

43. Woesner ME, Mitts MG. The evaluation of cervical spine motion below C2: A comparison of cineroentgenographic and conventional roentgenographic methods. Am J Roentgenol 1972; 115:148–154.

55. Jonsson H Jr, Cesarine K, Petren-Mallmin M, et al. Locking screw-plate fixation of cervical spine fractures with and without ancillary posterior plating. Arch Orthop Trauma Surg 1991; 111(1):1–12.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ ii: Whiplash

CHAPTER

The Biomechanics of the Cervical Spine during Whiplash Injury

52

Gerard A. Malanga and Luke Rigilosi

INTRODUCTION Understanding the true biomechanics of whiplash injury is important in that it can help the clinician in focusing on areas that are most likely to be injured (and painful) after these injuries. In addition, it can aid researchers in the development of head and neck restraints that can help to prevent or minimize the severity of injuries. The early, and still prevalent, understanding of whiplash injuries was that the neck was ‘whipped’ into hyperextension and then flexion. This led to the erroneous belief that chronic pain in these patients occurred due to the ‘overstretching’ of muscles, tendons, and ligaments. Recent research findings have elucidated a more precise and accurate understanding of what does occur following whiplash injury, i.e. compressive injuries and deformation of the normal cervical lordosis after rear-end motor vehicle accidents. In this chapter we will review the current scientific evidence of the biomechanics following rear-end motor vehicle accidents. The injury mechanism associated with ‘whiplash-associated disorder’1 has been studied for over 40 years. Cervical spine injury associated with rear-end collision was first described in 1867 with railroad workers, the so-called ‘railroad spine.’ In 1928, Crowe described the cervical spine injury associated with rear-end automobile collisions.2

The theories hypothesizing the biomechanical injuries have evolved from early years when the mechanism of injury was thought to be simple cervical hyperextension.3–6 Cadaveric, anthropomorphic, and animal (including human) studies as well as mathematical models have all been used to further investigate the biomechanical events that occur during whiplash injuries. The majority of these studies focus on the association between motion and injury to the cervical spine that occurs during rear-end impact, simulating motor vehicle collisions. Factors that affect energy transfer are the basis for injury to the cervical spine in these collisions. It has become more apparent through these studies that the mechanism of injury to the cervical spine is not, in fact, simply cervical hyperextension or hyperflexion as was once thought.3–6 Investigators have shown through studies of segmental cervical spine motion that an ‘S-shaped’ cervical spine deformation occurs in the sagittal plane at approximately 50–75 ms after impact (Fig. 52.1), which includes abnormal lower cervical spine extension coupled with upper cervical spine flexion, as well as axial cervical spine compression.7–11 It is now felt that this abnormal curvature and compression of the cervical spine is the etiology of the injuries that occur during rear-end collision. The Quebec Task Force defines whiplash as an ‘acceleration– deceleration mechanism of energy transfer to the neck. It may result

Axis

S-shape 44ms

110 ms

Fig. 52.1 The ‘S-shaped‘ cervical spine deformation occurs at approximately 50–75 ms after impact which includes abnormal lower cervical spine extension coupled with upper cervical spine flexion, as well as axial cervical spine compression. 583

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from rear-end or side-impact motor vehicle collisions, but can occur during diving or other mishaps.’6 As the majority of published studies that investigate whiplash simulate rear-end collision motor vehicle accidents, this chapter focuses on the biomechanical forces and energy transfer that is associated with rear-end collision.

ANATOMIC CERVICAL SPINE First, it is important to define the anatomic cervical spine. The cervical spine is the most mobile of any spinal section with the most physiologic lordosis.12 It is generally considered as two functional regions, the upper cervical spine, C0–2, and the lower cervical spine, C3–7 (Fig. 52.2). As a functional unit, the upper cervical region can be broken down into two adjacent segments of motion: C0–1 and C1–2. Physiologic motion at the C0–1 level generally accommodates 25° of flexion– extension and 5° of lateral flexion. There are 3–8° of rotation that occurs about the instantaneous axis of rotation.12 Paradoxical extension at C0–1 is observed at end-range cervical spine flexion.13 The C1–2 level accommodates 20° of flexion–extension and 5° of lateral flexion. There is significantly more rotation about the instantaneous axis of rotation, approximately 40° to each side, which accounts for approximately half of the total rotation of the cervical spine.12 The middle and lower cervical spine encompasses the cervical levels C3–7. Physiologic anterior–posterior translation can be up to 2–2.7 mm from the anterior-inferior corner of the moving vertebral body.14 On flexion and extension plain films of the cervical spine, a maximum of 3.5 mm of anterior–posterior translation is accepted as normal (Fig. 52.3). This takes into account approximately 25% magnification due to radiographic technique.9 There is also physiologic coupling in the lower cervical spine between lateral flexion and rotation. Coupling occurs when motion about one axis is accompanied by simultaneous motion around another axis. In the cervical spine, lateral flexion of a vertebra is accompanied by rotation so that the spinous process moves toward the convexity of the developing curve. This coupling pattern changes from the C2 to C7 level, with the more cephalad segments having a higher ratio of rotation to lateral flexion and the more caudal segments having a lower ratio of rotation to lateral flexion.14

C1 C2 C3 C4 C5 C6 C7 Fig. 52.2 Normal cervical lordosis. 584

Fig. 52.3 Normal cervical spine extension.

BIOMECHANICS OF THE REAR-END COLLISION Whiplash can be considered an acceleration–deceleration mechanism of energy transfer to the cervical spine. The events that lead to this energy transfer include, but are not limited to, diving injuries, collisions in sporting events, side collisions and rear-end motor vehicle accidents. The majority of studies investigating this process have looked at whiplash in a rear-end collision. As this is the case, this review will consider cervical spine biomechanics in terms of rear-end impact collisions. Researchers debated for many years as to the pathologic mechanism that leads to whiplash-associated disorder. The prevalent theories revolved around early stage hyperextension and late stage hyperflexion.3–6 These earlier studies investigated cervical spine motion as a whole during rear-end collision. As researchers began to look at individual segmental motion in the cervical spine, the abnormal posturing that occurs throughout the event was found. Grauer first described the abnormal S-shaped cervical spine curvature that occurs during rear-end collisions, with lower cervical spine flexion and upper cervical spine extension.15 The abnormal posture that occurs during this S-shaped curve is now implicated as the most likely etiology of injury in whiplash-associated disorder.9–12,16,17 The sequence of events that occur in rear-end collisions begins with the impact of the bullet vehicle, and ends with complete cervical spine flexion (Table 52.1). The energy transfer that occurs through this process causes the abnormal cervical spine curvature and compression which leads to the cervical spine injury. Immediately following the collision of the vehicles the first contact with the individual is the seat-back against the lumbar spine and pelvis. The base of the car seat forces the lumbar spine forward inducing lumbar straightening and cephalad axial compression of the spine (Fig. 52.4A). Contact between the individual and the seat-back induces a counterforce from the individual’s lumbar spine to the seat-back, causing a ramping effect of the seat. The forward movement of the caudal spine induces relative cervical flexion as inertia of the head resists motion initially and maintains its position in space. There is vertical displacement of the torso from this cephalad compression, as well as downward displacement of the seat-back from this ramping effect. The ramping effect of the seat-back will bring the head restraint down in

Section 3: Cervical Spine

Table 52.1: Typical sequence of events in rear-end collisions 1. Impact of bullet vehicle into rear of target vehicle. 2. Sudden acceleration of target vehicle. 3. Seat-back contact with torso of occupant. 4. Simultaneous forward and upward acceleration of torso. 5. Extension/compression of lower cervical spine and flexion– compression of upper cervical spine causing an ‘S’ curve. 6. Head contact with head restraint. 7. Cervical spine extension and rearward head rotation. 8. Forward acceleration of head past shoulders. 9. Flexion of complete cervical spine.

relation to the cervical spine and head. Thoracic contact with the seat at this point has also been considered as a mechanism for spinal compression, as the kyphotic thoracic spine is forced forward into a flattened posture.8 The clinician should be aware that much of this information comes from crash dummies which are rigid and do not replicate the normal flexible curves of the spine in human beings. In humans, these curves are able to absorb energy, which is not the case in these more rigid hybrid dummies. Matsushita et al.18 were the first to observe thoracic spine straightening during rear-end impact. It is reasonable that the thoracic spine would suffer the greatest kinematic change initially that would transfer compressive forces to the cervical and lumbar spines. The cervical spine would receive compressive forces from both the thoracic spine below and the cranium above. The normal thoracic kyphosis is lost as the seat back transmits forces to the thoracic spine. This results in thoracic straightening and longitudinal transmission of force to both the cervical and thoracic spines. This can result in injury of various structures including the intervertebral discs and the zygapophyseal joints of the cervical, thoracic, and lumbar spines. As energy is initially transmitted to the cervical spine, the sequence most often implicated in whiplash-associated disorder is initiated. At this point, the upper cervical spine is in relative flexion due to the forward displacement of the thoracic spine. Studies differ on which levels experience peak rotations, but all agree that forward acceleration and compression from the ascending energy transfer cause lower cervical extension and compression. As the head remains stationary, this induces upper cervical spine flexion. There is significant posterior element stress at the C5–7 region during this phase.7,8,11,12 There is no evidence demonstrating that the upper cervical spine flexion during the S-shaped curve exceeds physiologic flexion (Fig. 52.4B).11 As the torso continues in a forward direction and the relatively large head lags behind, the so called C-shaped curve of complete cervical extension occurs. This phase has been implicated in injury, as the amount of lower cervical hyperextension that occurs exceeds physiologic measures.11 Upper cervical spine extension does not exceed physiologic extension during either the C-shaped curve or the previous S-shaped curve.11 Contact with the head restraint will occur at this point if the head restraint system is positioned properly. Peak horizontal backward acceleration of the head occurs just prior to contact with the head restraint. This peak acceleration may cause the shearing forces associated with any axonal damage that is implicated in rear-end collisions. In addition, following these injuries there is an alteration of the instantaneous axis of rotation (Fig. 52.4C).

A

B

C

Fig. 52.4 (A–C) Changes of the cervical spine following rear-end collision with initial straightening of cervical lordosis, then S-shaped deformation, then head and neck flexion. 585

Part 3: Specific Disorders

The final event that occurs in the sequence follows as the head accelerates forward. Both the upper and lower cervical spine go into complete flexion (Fig. 52.5). Studies investigating segmental motion of the cervical spine have not demonstrated the cervical spine to reach levels of flexion that exceed physiologic cervical flexion.11 Depending on the individual’s restraint system, this stage may end with contact of the head against the steering wheel or windshield.

EFFECT OF MUSCULAR TENSION There has been significant debate as to the protective effect of the cervical spine’s dynamic stabilizers, including the cervical paraspinals, trapezius, and sternocleidomastoid, in rear-end collision. Preparation for a collision would include contraction of the cervical spine musculature, creating a dynamic splint that minimizes abnormal cervical spine curvature. Hence, knowledge of an impending collision could potentially minimize the injuries in rear-end collisions. Unfortunately, most rear-end impact collisions do not occur under the setting of preparation. Electrodiagnostic studies investigating the reaction time of the cervical spine musculature demonstrate that full contraction occurs at approximately 115–200 milliseconds. The S-shaped cervical spine as well as full hyperextension occur at up to 75 milliseconds.2,18 This suggests that muscular tension in unexpected rear-end collisions will not occur in time to stabilize the cervical spine, and therefore minimize whiplash-associated injuries. Dynamic stabilization via cervical muscular contraction may minimize the abnormal curvature of the cervical spine in rear-end collisions when the individual in the target vehicle is prepared for the impending collision.

will affect the amount of energy transferred to the cervical spine. Factors that decrease the amount of energy transfer will decrease the likelihood or severity of injury. These vehicle characteristics include the frame of the automobiles involved in the collision, the rigidity of the seats, the energy absorbing capacity of the bumpers on the vehicle involved, and the mass and velocity of the vehicles. Cars that are ‘compressible’ and absorb the energy in a collision will minimize the transfer of energy. The rigidity of the seat-back will also play a role, as more rigid seat-backs will increase the forward acceleration of the torso after the seat-back contacts the lumbar spine. There has been significant debate regarding the standards of the head restraint systems currently being used. Maximum protection for the cervical spine includes a head and neck restraint system that maintains the physiologic lordotic posture of the cervical spine following rear-end impact. Current head restraint systems tend not to protect the lordosis of the cervical spine on rear-end impact, as these restraints are often flat and not positioned correctly (Fig. 52.6). Newer head and neck bolstering systems may minimize injuries to the cervical spine following rear-end impact by maintaining the neck’s physiologic contour (Fig. 52.7).19

Human factors An individual’s mass and posture potentially change the injury suffered in a rear-end collision. Heavier individuals will have less

COLLISION FACTORS ASSOCIATED WITH WHIPLASH There are many factors that influence the amount of force an individual will experience in rear-end collisions. These factors include vehicle factors and human factors. These factors can assist in minimizing the amount of damage incurred by the individuals involved.

Vehicle factors Vehicle parameters, including speed, relative size of the involved vehicles, braking action, and the compressibility of the vehicles involved

Axis

586

Fig. 52.5 Finite element representation of the cervical spine following a rear-end collision demonstrating alteration of the instantaneous axis of rotation.

Fig. 52.6 New head and neck cervical support design for preventing whiplash injuries.

Fig. 52.7 Current head restraint system during Hybrid III dummy testing.

Section 3: Cervical Spine

acceleration for the same amount of force applied, as the energy of a collision is transferred from the seat-back to the lumbar spine. Pre-impact kyphotic postures of the cervical spine will exaggerate the S-shaped curve. Chronic kyphotic posturing may be associated with anterior contractures, which are particularly vulnerable to highvelocity movements. In addition, if the individual head is turned to one direction or another, there are questions regarding how this may influence injury of the underlying soft tissues. It is clear that the loss of cervical lordosis with the development of an S-shaped cervical spine will occur; however, with the cervical spine rotated, this may lead to greater injuries of the intervertebral discs due to torsion and to cervical nerve roots damage due to foraminal narrowing. In addition, cadaveric studies have shown that pre-torque of the capsular ligaments by rotation increases capsular strain when loaded, which may result in increased injury risk of the zygapophyseal joint.12 Females seem to have a predisposition for whiplash-associated disorder. The exact mechanism of this gender-based discrepancy is unclear.20 This may be due primarily to the size of most females compared to males and their body position in the car seat and head position relative to the headrest during driving. A smaller driver would tend to have relatively exaggerated thoracic kyphosis and a head positioned lower down on the headrest, which may actually predispose the driver to cervical spine injuries rather than preventing them. This would suggest that head and neck restraints that can conform to the individual driver would be an important development in the prevention of cervical spine injuries.

INJURY PATTERNS BASED ON WHIPLASH BIOMECHANICS Understanding the biomechanics of what occurs following a rearend automobile collision offers at least one clue as to potential injury patterns which may occur. There are several theoretical ‘pain generators’ following these injuries which include the bones, ligaments, muscles, discs, and joints (zygapophyseal). Given the current understanding of what occurs to the spine following a rear-end collision, the most likely structures to be injured are: the zygapophyseal joints, the intervertebral discs, and the upper cervical spine ligaments.

SUMMARY The biomechanics of whiplash injury have been elucidated by recent research using cineradiographs, cryomicrotomy techniques, and finite element model techniques. These studies have shown that after rearend impact there is alteration of the normal cervical lordosis that results in flexion at the lower cervical spine and extension in the upper cervical spine, resulting in an S-shaped deformation of the cervical spine. Along with deformation, there is vertical displacement of the torso separately, as forces are transmitted from the thoracic spine, resulting in compressive forces particularly on the posterior elements of the cervical spine. This would particularly affect the cervical zygapophyseal joints, especially from C5 to C7, which have been shown to be a prominent pain generator in patients with chronic neck pain following whiplash injury. Understanding the biomechanics of whiplash injury is quite helpful to the clinician treating patients with neck pain after these injuries as well as researchers and automobile engineers developing head and neck restraints that will greatly decrease or eliminate the deformation of the cervical spine causing these injuries.

References 1. Seletz E. Trauma and the cervical portion of the spine. J Int Coll Surg 1963; 40: 47–62. 2. Crowe HE. Injuries to the cervical spine. Presented at the Meeting of the Western Orthopedic Association, San Francisco, 1928. 3. Brault JR, Wheeler JB, Gunter P, et al. Clinical response of human subjects to rearend automobile collisions. Arch Phys Med Rehab 1998; 79:72–80. 4. Luan F, Yang KH, Deng B, et al. Qualitative analysis of neck kinematics during lowspeed rear-end impact. Clin Biomech 2000; 15(9):649–657. 5. Scifert J, Totoribe K, Goel V, et al. Spinal cord mechanics during flexion and extension of the cervical spine: a finite element study. Pain Phys 2002; 5(4):394–400. 6. Spitzer WO, Skovron MI, Salmi LR, et al. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: Redefining ‘whiplash’ and its management. Spine 1995; 10(Suppl 8):1S–73S. 7. Geigl BC, Steffan H, Leinzinger P, et al. The movement of head and cervical spine during rearend impact. Proceedings of the 1994 International Ircobi Conference on the Biomechanics of Impacts, pp 127–137. Lyons, 1994. 8. Kumar S, Narayan Y, Amell T. Analysis of low velocity frontal impacts. Clin Biomech 2003; 18(8):694–703. 9. Macnab I. Acceleration injuries of the cervical spine. J Bone Joint Surg 1964; 46A:1797–1799. 10. Gay R, Levine R. Biomechanics of whiplash. In: Malanga GA, Nadler SF, eds. Whiplash. Philadellphia: Hanley & Belfus; 2002. 11. Panjabi MM, Cholewicki J, Nibu K, et al. Simulation of whiplash trauma using whole cervical spine specimens. Spine 1998; 23(1):17–24. 12. White AA, Johnson RM, Panjabi MM, et al. Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop 1975; 109:85–96. 13. Panjabi MM, Pearson AM, Ito S, et al. Cervical spine curvature during simulated whiplash. Clin Biomech 2004; 19(1):1–9. 14. Versteegen GJ, Kingma J, Meijler WJ, et al. Neck sprain after motor vehicle accidents in drivers and passengers. Eur Spine J 2000; 9:547–552. 15. Grauer JN, Panjabi MM, Cholewicki J, et al. Whiplash produces an S-shaped curvature of the neck with hyperextension at lower levels. Spine 1997; 22(21): 2489–2494. 16. Harrison DD, Janik TJ, Troyanovich SJ, et al. Comparisons of lordotic cervical spine curvatures to a theoretical ideal model of the static sagittal cervical spine. Spine 1996; 21(6):667–675. 17. Kaneoka K, Ono K, Inami S, et al. Motion analysis of cervical vertebrae during whiplash loading. Spine 1999; 24(8):763–769. 18. Matsushita T, Sato TB, Hirabayashi K, et al. X-ray study of the human neck motion due to head inertia loading. 19. Foust DR, Chaffin DB, Snyder RG, et al. Cervical range of motion and dynamic response and strength of cervical muscles. In: Backaiatis SH, ed. Biomechanics of impact injury tolerances of the head-neck complex. Warrendale, PA: Society of Automotive Engineers; 1993:1023–1035. 20. Barnsley L, Lord S, Bogduk N. Pathophysiology of whiplash. In: Malanga G, Nadler S, eds. Whiplash. Philadelphia: Hanley and Belfus; 2002.

Further Reading 1. Clemens HJ, Burow K. Experimental investigation on injury mechanisms of the cervical spine at frontal and rear-frontal vehicle impacts. Proceedings of the 16th STAPP Car Crash Conference. Warrendale, PA: Society of Automotive Engineers; 1972:76–104. 2. Penning L. Normal kinematics of the cervical spine. Clinical anatomy and management of cervical spine pain. Vol 3. Oxford: Butterworth-Heinemann; 1998:51–55. 3. States JD, Korn MW, Maengill JB. The enigma of whiplash injuries. AAAM 1969; 84:12. 4. White AA, Panjabi MM. Clinical biomechanics of the spine. 2nd edn. Philadelphia: JB Lippincott; 1990. 5. Winkelstein BA, Nightingale RW, Richardson WJ, et al. The cervical facet capsule and its role in whiplash injury. Spine 2000; 25:1238–1246. 6. Yoganandan N, Pintar FA, Stemper BD, et al. Single rear impact produces lower cervical spine soft tissue injuries.

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SPECIFIC DISORDERS

Section 3

Cervical Spine ■ ii: Whiplash

CHAPTER

Pathophysiologic Evidence of Injury

53

Nikolai Bogduk

Imaging is the conventional approach to finding evidence of injury. When major trauma to the neck results in fractures or dislocations, these are typically evident on plain radiographs of the neck.1 Computed tomography (CT) can provide more detailed reconstructions of the injury. Magnetic resonance imaging (MRI) can reveal soft tissue components or consequences of the injury. Minor injuries to the neck do not result in major fractures or dislocations. Therefore, such injuries are not evident on imaging.2 Indeed, conventional imaging is typically normal. This lack of evidence of injury on imaging is used by some commentators to infer that there is no injury. That is false. The lack of evidence only reflects the limited resolution on conventional imaging. Plain radiographs or CT demonstrate only lesions in bone; they do not show soft tissue injuries. MRI demonstrates soft tissues, but it will not necessarily reveal small lesions. Normal imaging, therefore, does not exclude the presence of lesions that are beyond the resolution of the imaging technique used. Meanwhile, two lines of evidence have shown that lesions can and do occur, after minor injuries to the neck. Postmortem studies have shown the types of lesions that can and might occur. Clinical studies have shown the sites at which these lesions must be present.

POSTMORTEM STUDIES Independent studies, in countries as respectively remote as Sweden3 and Australia,4–6 have provided similar conclusions, which have now been systematically reviewed.7 Both sets of studies harvested the cervical spines of victims of fatal motor vehicle accidents. The Australian studies included victims who survived for various periods after the accident. The pathology of major head injury and suboccipital injuries was ignored. Instead, the studies focused on other lesions, which were not the cause of death, but which indicated what could happen to the cervical spine, in a motor vehicle accident. The same spectrum of injuries was consistently observed (Fig. 53.1). They included tears of the anterior anulus fibrosus, avulsion of the anterior anulus, contusions of the posterior anulus, tears or avulsions of the capsules of the zygapophyseal joints, contusions of the meniscoids of these joints, intra-articular hemorrhage, fractures of the articular cartilage, and subchondral or greater fractures of the articular pillars. Conspicuously, virtually none of these lesions was evident on plain radiographs of the cervical spine, taken postmortem, even when read retrospectively with the knowledge that a lesion was present.3–6 These lesions are consistent with the known biomechanics of whiplash injury.2 Anterior separation of the vertebral bodies could cause tears or avulsions of the anterior anulus fibrosus. Posterior impaction of the zygapophyseal joints could cause articular and subarticular fractures, or contusions of the intra-articular meniscoids. Excessive separation of the zygapophyseal joints, in extension or in flexion,8 could cause tears of the joint capsules.

The nature of these lesions is such that they should not be evident on conventional imaging. Injuries to fibrous connective tissues will not be seen on plain radiographs or CT. They cannot be seen on conventional MRI. In the future, perhaps high-resolution MRI or spectroscopic MRI might be able to resolve them, but studies in this regard have not yet been completed.

PATHOPHYSIOLOGY The nature of connective tissue injuries is that they are likely to be painful. Capsular tears, small fractures, and intra-articular hemorrhage are all causes of pain elsewhere in the musculoskeletal system. There is no reason why they should not be sources of pain if and when they occur in the neck. For these lesions to be symptomatic the structures in which they occur have to be innervated. In the cervical spine, the anuli fibrosi of the intervertebral discs are innervated, and the zygapophyseal joints are innervated. The discs receive their innervation from the vertebral nerve, the sympathetic trunks, and the sinuvertebral nerves.9 The zygapophyseal joints are innervated by the medial branches of the cervical dorsal rami.10 Because they are innervated, these structures can become sources of pain, even though the lesions that cause that pain are effectively invisible. It is the pain that implies the presence of the injury; and the site of injury can be determined by pinpointing the source of pain.

Fracture, articular cartilage Tear capsule Contusion, mesincoid

Tear, anterior anulus

Fracture araticular process

Fig. 53.1 The possible lesions after minor injuries to the cervical spine. 589

Part 3: Specific Disorders

CLINICAL STUDIES Pinpointing a source of pain requires a diagnostic test that can be applied in patients, who cooperate by reporting if their accustomed pain is uniquely provoked by the test or is relieved by it. The available procedures differ according to the target structure. Intervertebral discs can be tested by discography. Zygapophyseal joints can be tested with medial branch blocks.

Discography Cervical discography is a procedure designed to determine if a particular intervertebral disc is painful or not.11 It involves introducing into the nucleus of the disc a needle, which is used to stress the disc with an injection of contrast medium. The test is deemed to be positive if the patient’s pain is reproduced, but provided also that stressing adjacent discs does not reproduce the pain. Furthermore, in order to be valid, cervical discography must reproduce the patient’s pain to a clinically significant extent. The operational criteria require an intensity of evoked pain of 7 or more on a 10-point scale.12 Cervical discography has been described extensively in the surgical literature as a means of determining at which segments arthrodesis should be carried out for the treatment of neck pain.13–16 Other information, however, is scarce. No studies have shown what the prevalence is of discogenic neck pain, as diagnosed by discography. No studies have shown that cervical fusion for neck pain is particularly successful. None has shown that discography leads to better outcomes. Meanwhile, two studies have warned of the capricious validity of cervical discography. It is uncommon for a single cervical disc to be painful alone. More often, two, three, or more discs appear symptomatic.17 Indeed, the more segments that are investigated, the more discs emerge as painful. Consequently, cervical discography is not complete unless every cervical disc is studied. Cervical discography can be false-positive. The movement that discography induces can stress the zygapophyseal joints of the same segment. If these, rather than the disc, are the source of pain, the discography appears to reproduce the patient’s pain, but falsely so.18 The disc is not the source of pain; the zygapophyseal joints are. For this reason, some 25% of positive discograms are false-positive (Table 53.1). At present, cervical discography is the only means by which discogenic pain can be tested. For this reason, it is attractive to some practitioners. However, because of the limitations to its validity, and the lack of any prevalence data, cervical discography has not yet evolved to be a validated means of providing inferential evidence of injury to the neck. Furthermore, if the injury is a partial tear of the anterior anulus, discography will not necessarily reveal it. The physical basis of cervical discography is to stress it by raising its intranuclear pressure. However, cervical discs typically decompress as contrast medium escapes through uncovertebral clefts. Under this condition, the induced stresses achieved, before decompression, may not be great enough to stress significantly a tear in the outer, anterior anulus. To diagnose anterior annular tears requires a different procedure.

Anulus blocks No-one has yet developed a technique whereby symptomatic tears of the anterior anulus of a cervical disc might be diagnosed. In principle, such a procedure could involve accessing the tear with a needle, which could be used either or both to visualize the tear with an injection of contrast medium, and to anesthetize it selectively with a tiny volume of local anesthetic. Were such a procedure to 590

Table 53.1: A correlation table between responses to provocation discography and zygapophyseal joint blocks in patients who had both procedures at the segments indicated Disc Positive

Negative

C3–4: 2

C3–4: 1

C4–5: 5

C4–5: 5

C5–6: 4

C5–6: 4

Total 11

C6–7: 2

ZYGAPOPHYSEAL JOINT Positive

C5–6, 6–7: 1 Total 13 Negative

C3–4: 6

C3–4: 1

C4–5: 3

C4–5: 4

C5–6: 14

C5–6: 1

Total 23

C4–5, 5–6: 1 C5–6, 6–7: 2 Total 9

18

Based on Bogduk and Aprill.

be developed it would provide obtainable evidence of a symptomatic tear of the anulus. The procedure could be used in individual patients, to establish a diagnosis not possible by other means; it could be used to test if tears that might be apparent on high-resolution MRI are symptomatic or not. But until such a test, or a better one, is developed, evidence of symptomatic anterior tears will remain elusive.

Medial branch blocks In contrast to cervical discography, the science of cervical medial branch blocks is highly developed, and has been extensively tested for validity and utility. These blocks test if a particular zygapophyseal joint is painful or not. They are based on the principle that if the joint is painful then anesthetizing the medial branches that innervate it should relieve that pain (Fig. 53.2). The face validity of cervical medial branch blocks has been established.19 When small volumes of local anesthetic are used (0.3 mL) to anesthetize a given nerve, the injectate does not spread to adjacent structures that might be alternative sources of pain. It does not spread to adjacent medial branches; it does not spread to the spinal nerve; it does not indiscriminately anesthetize the posterior neck muscles. The injectate pools around the target nerve, and spreads only in a planar fashion along the cleavage plane between multifidus and semispinalis capitis. The construct validity of cervical medial branch blocks has been established in several ways. Single diagnostic blocks are not valid. They can be associated with a false-positive rate of up to 27%.20 To be valid, blocks must be controlled in each and every case that they are used. These controls can be placebo controls or comparative blocks. Comparative blocks have been validated using statistical methods,21 and by comparing them with placebo-controlled blocks.22 Furthermore, their diagnostic validity has been confirmed

Section 3: Cervical Spine

Fig. 53.2 A lateral radiograph of the cervical spine showing a needle in position for a C5 medial branch block.

by successful subsequent treatment. Denervating the painful joint by radiofrequency neurotomy provides complete and lasting relief of the pain.23–25

Implications When positive, controlled medial branch blocks implicate a genuine source of pain in the joint targeted. The criterion for a positive block is complete relief of pain. It is not partial relief or 50% relief. The pain must be completely relieved. Cervical medial branch blocks, performed under controlled conditions, have provided the strongest available pathophysiologic evidence of injury to the neck. Multiple and independent studies have established how often the zygapophyseal joints are the source of chronic neck pain. Among patients with neck pain after whiplash, two separate studies from the same unit have established the prevalence of cervical zygapophyseal joint pain to be 54%26 and 60%.27 A third study from the same unit established the prevalence of zygapophyseal joint pain in drivers injured in high-speed motor vehicle accidents to be 75%.28 An unrelated study, from a pain clinic serving a general population, found the prevalence of zygapophyseal joint pain to be at least 36%.29 This figure constituted a worst-case analysis. Patients who did not return for control blocks were not treated as positive. Another study from a pain clinic reported a prevalence of 60%.30 The confidence intervals of these various studies overlap (Table 53.2). Collectively, they paint a consistent picture. Zygapophyseal joint pain accounts for some 60% of patients with chronic neck pain after injury. The pattern of involvement is diverse. Single joints may

be painful, or both joints of a particular segment may be painful. Joints at other, adjacent or remote segments may be painful. The more common patterns are one or both joints painful at C5–6, or C2–3; and joints painful at C5–6 and C2–3. Less often, consecutive joints, at C5–6 and C6–7, are painful. The prevalence and distribution of cervical zygapophyseal joint pain correlate with two other, and independent, lines of evidence. The postmortem data point to injuries of the zygapophyseal joints that should be painful.3–6 The biomechanics data reveal that the mechanism of whiplash could cause injury to the zygapophyseal joints, of the nature found at postmortem.2 Furthermore, the biomechanics data implicate C5–6 and C2–3 as the most likely segments to be involved. Consequently, the postmortem data, the biomechanics data, and the clinical data, all point to the same conclusion. This constitutes convergent validity for the concept that cervical zygapophyseal joints can be injured and do became painful.31

CONCLUSION Notwithstanding this convergent validity of the concept of cervical zygapophyseal joint pain, for clinical practice the evidence for injury remains entirely physiological. The joints can be tested physiologically, using controlled diagnostic blocks, to determine if they are painful. The next step in the evolution of the concept requires direct demonstration of the injury. This could come in either or both of two ways. A traditional and laborious approach would be to register patients, with proven zygapophyseal joint pain, for postmortem study. The structure and biochemistry of the painful joint could be compared with those of adjacent joints known not to be painful. Such a study, however, is unlikely to be undertaken, for it requires not only the combined resources of diagnostic facility and a postmortem but also the perseverance to wait for the natural passing of the patients who might care to participate in such a study. A more expedient approach requires a new age of imaging. Techniques are required by which the detailed structure of the zygapophyseal joints might be resolved. Those techniques should be able to show small fractures or contusions in vivo. Joints shown to be painful by controlled diagnostic blocks could then be studied and compared with those in the same patient that are known not to be painful. Carefully applied, 3-Tesla MRI might be that technique. Otherwise, the concept requires further technological advances.

References 1. Cusick JF, Yoganandan N. Biomechanics of the cervical spine 4: major injuries. Clin Biomech 2002; 17:1–20. 2. Bogduk N, Yoganandan N. Biomechanics of the cervical spine. Part 3: minor injuries. Clin Biomech 2001; 16:267–275. 3. Jónsson H Jr, Bring G, Rauschning W, et al. Hidden cervical spine injuries in traffic accident victims with skull fractures. J Spinal Disord 1991; 4:251–263.

Table 53.2: The prevalence and 95% confidence intervals of cervical zygapophyseal joint pain amongst patients with chronic neck pain Study

Prevalence

Barnsley 26

54%

95% Confidence Intervals

0 10 20 30 40 50 60 70 80 90 100 Lord 27 Speldewinde Manchikanti Gibson 28

60% 29 30

36%

4. Taylor JR, Twomey LT, Corker M. Bone and soft tissue injuries in post-mortem lumbar spines. Paraplegia 1990; 28:119–129. 5. Taylor JR, Twomey LT. Acute injuries to cervical joints: An autopsy study of neck sprain. Spine 1993; 9:1115–1122. 6. Taylor JR, Taylor MM. Cervical spinal injuries: an autopsy study of 109 blunt injuries. J Musculoskeletal Pain 1996; 4:61–79. 7. Uhrenholt L, Grunnet-Nilsson N, Hartvigsen J. Cervical spine lesions after road traffic accidents. A systematic review. Spine 2002; 27:1934–1941. 8. Pearson AM, Ivancic PC, Ito S, et al. Facet joint kinematics and injury mechanisms during simulated whiplash. Spine 2004; 29:390–397.

60%

9. Bogduk N, Windsor M, Inglis A. The innervation of the cervical intervertebral discs. Spine 1988; 13:2–8.

75%

10. Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine 1982; 7: 319–330.

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Part 3: Specific Disorders 11. Bogduk N, Aprill C, Derby R. Discography. In: White AH, ed. Spine care, volume one: diagnosis and conservative treatment. St Louis: Mosby; 1995:219–238. 12. Schellhas KP, Smith MD, Gundry CR, et al. Cervical discogenic pain: prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers. Spine 1996; 21:300–312. 13. Cloward RB. Cervical diskography. A contribution to the aetiology and mechanism of neck, shoulder and arm pain. Ann Surg 1959; 130:1052–1064. 14. Kikuchi S, Macnab I, Moreau P. Localisation of the level of symptomatic cervical disc degeneration. J Bone Joint Surg 1981; 63B:272–277. 15. Whitecloud TS, Seago RA. Cervical discogenic syndrome. Results of operative intervention in patients with positive discography. Spine 1987; 12:313–316. 16. Garvey TA, Transfeldt EE, Malcolm JR, et al. Outcome of anterior cervical diskectomy and fusion as perceived by patients treated for dominant axial–mechanical cervical spine pain. Spine 2002; 27:1887–1894. 17. Grubb SA, Kelly CK. Cervical discography: clinical implications from 12 years of experience. Spine 2000; 25:1382–1389. 18. Bogduk N, Aprill C. On the nature of neck pain, discography and cervical zygapophyseal joint blocks. Pain 1993; 54:213–217. 19. Barnsley L, Bogduk N. Medial branch blocks are specific for the diagnosis of cervical zygapophyseal joint pain. Reg Anesth 1993; 18:343–350. 20. Barnsley L, Lord S, Wallis B, et al. False-positive rates of cervical zygapophyseal joint blocks. Clin J Pain 1993; 9:124–130. 21. Barnsley L, Lord S, Bogduk N. Comparative local anaesthetic blocks in the diagnosis of cervical zygapophyseal joints pain. Pain 1993; 55:99–106.

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22. Lord SM, Barnsley L, Bogduk N. The utility of comparative local anaesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophyseal joint pain. Clin J Pain 1995; 11:208–213. 23. Lord SM, Barnsley L, Wallis BJ, et al. Percutaneous radiofrequency neurotomy for chronic cervical zygapophyseal joint pain. N Engl J Med 1996; 335:1721–1726. 24. Lord SM, McDonald GJ, Bogduk N. Percutaneous radiofrequency neurotomy of the cervical medial branches: a validated treatment for cervical zygapophyseal joint pain. Neurosurg Quart 1998; 8:288–308. 25. McDonald G, Lord SM, Bogduk N. Long-term follow-up of patients treated with cervical radiofrequency neurotomy for chronic neck pain. Neurosurgery 1999; 45:61–68. 26. Barnsley L, Lord SM, Wallis BJ, et al. The prevalence of chronic cervical zygapophyseal joint pain after whiplash. Spine 1995; 20:20–26. 27. Lord S, Barnsley L, Wallis BJ, et al. Chronic cervical zygapophyseal joint pain after whiplash: a placebo-controlled prevalence study. Spine 1996; 21:1737–1745. 28. Gibson T, Bogduk N, Macpherson J, et al. Crash characteristics of whiplash associated chronic neck pain. J Musculoskeletal Pain 2000; 8:87–95. 29. Speldewinde GC, Bashford GM, Davidson IR. Diagnostic cervical zygapophyseal joint blocks for chronic cervical pain. Med J Aust 2001; 174:174–176. 30. Manchikanti L, Singh V, Rivera J, et al. Prevalence of cervical facet joint pain in chronic neck pain. Pain Physician 2002; 5:243–249. 31. Bogduk N. Point of view. Spine 2002; 27:1940–1941.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ ii: Whiplash

CHAPTER

Sociocultural Evidence and Whiplash

54

Robert Ferrari and Anthony S. Russell

INTRODUCTION Approximately one million diagnoses of whiplash-associated disorders (WAD) are made each year in the United States alone. The health and economic burden to society is substantial and made worse by our inability in most cases to identify a specific structural cause of ongoing complaints of pain and disability. In 1995, the Quebec Task Force (QTF) on Whiplash-Associated Disorders (WAD) did, however, make an important contribution by providing a grade 0 to grade 4 classification protocol based on the available literature.1 This classification system has been widely used both by clinicians and in research studies.2,3 The classification system is convenient because grades are primarily based on physical signs and symptoms. A patient with no symptoms is classified as grade 0. The more severe cases are grade 3, in which patient symptoms associated with neurological signs caused by a specific structural diagnosis, e.g. disc herniation causing nerve root compression, and grade 4, in which patients have symptoms caused by cervical fracture and/or dislocation. Ninety percent of ‘whiplash injury claims’ are, however, classified as grade 1 and grade 2.4 Grade 1 WAD classifies a patient who reports neck pain, stiffness, or tenderness with no other physical signs. Grade 2 WAD defines a patient who reports neck pain, stiffness, or tenderness and signs including reduced range of motion and point tenderness. The QTF classification of WAD is shown in Table 54.1. Although a structural diagnosis is often conjectural or unknown, up to 50% of whiplash victims with WAD 1 or 2 report persistent pain for more than 6 months after their collision.5–7 Despite the availability of modern imaging techniques and despite the increasing use of interventional diagnostic and therapeutic procedures, the incidence of chronic pain following whiplash injuries continues to rise. In this chapter, we de-emphasize the structural approach and instead discuss the cultural disparities of chronic whiplash, and review literature that suggests chronic whiplash pain can be better explained by patients expectations and by symptom amplification. We will argue that research efforts should be focused on reversal or prevention of the psychocultural phenomena that contribute to chronic pain following whiplash injuries. We emphasize diagnosis and treatment based on evidence and not ever-increasing use of unproven invasive interventions.

THE EVIDENCE ON CULTURAL DISPARITIES IN WHIPLASH Some cultures are Petri dishes for chronic whiplash and some are not. Every study reported from Canada,5,6 Sweden,4,8 the United States,9 England,10,11 Ireland,12 and Norway13 on the outcome of patients classified into WAD grade 1 or 2 indicate a high prevalence

of chronic pain. In these studies WAD 3 and 4 are either excluded or represent only a small minority of subjects and the vast majority of chronic whiplash complaints are classified as WAD 1 or 2. Even though patient samples were captured as ‘acute cases’ using different methods, such as insurance claims databases, advertising to primary care clinics, or from emergency departments, the reported prevalence of chronic pain are similar. No matter the source or whether questionnaires were or were not used, all studies from these Western countries confirm the high incidence of chronic pain after acute whiplash. On the other hand, using similar methodologies on the same WAD 1 and 2 classified patients, researchers conducting studies in Lithuania, Germany, and Greece report a very different incidence of chronic pain following whiplash injuries.

Lithuania Lithuania is a country in which there is no or little awareness or experience among the general population that a whiplash injury is a reason for chronic pain and disability. Collision victims do not often seek extended medical attention, and the possibilities for secondary gains are minimal. In a controlled, historical inception cohort study published in 1996,14 none of the 202 subjects involved in a rear-end car collision 1–3 years earlier had persistent and disabling complaints that could conceivably be linked to the collision. Both collision victims and controls had the same statistical occurrence of symptoms including neck pain, headache, and subjective cognitive dysfunction. In a later prospective, controlled inception cohort study,15 47% of 210 victims of rear-end car collisions consecutively identified from the daily records of the traffic police had initial pain. The symptoms disappeared in most cases after a few days. No subject reported collision-induced pain later than 3 weeks, compared to Canada where a mere 50% were symptom free by 6 months.5 After 1 year, there were no significant differences between the collision victim group and the control group in frequency or intensity of neck pain and headache. In a historical cohort study,14 31 collision victims recalled having had acute or subacute neck pain. In most cases symptoms lasted less than 1 week and only two subjects had neck pain for more than 1 month. Due to recall problems, the true incidence of collision victims with acute symptoms such as neck pain and/or headache was unknown. However, the prospective inception study provides a 95% confidence limit for the true prevalence of acute, post-collision symptoms as 40–54%.15 Because none of the 180 subjects in both Lithuanian studies was reported to have persistent and disabling symptoms due to the collision, the possibility of chronic pain was less than one in 60 (p<0.05). Thus, these studies evaluated either alone or together have sufficient power to reject the approximately 50% estimates5 of the development of the so-called chronic whiplash syndrome in other countries.

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Table 54.1: Clinical Interpretation of the Quebec Task Force Whiplash-Associated Disorders (WAD) Classification Scheme Grade

Injury (example) and Symptoms

Signs

1

Possible muscle sprain

Normal range of motion

Spinal symptoms included neck stiffness, pain, or tenderness only

Normal reflexes and muscle strength in the limbs X-ray not necessary

2

Possible muscle and/or ligament sprain Neck or back pain

Paraspinal tenderness AND restricted spine range of motion Normal reflexes and muscle strength in the limbs X-ray shows no fracture/dislocation

3

Possible disc protrusion with nerve root impingement, or spinal cord contusion without bony fracture/dislocation Neck or back pain, often arm or leg pain or numbness.

Absent or reduced reflexes and/or muscle weakness, and/or sensory changes in a dermatomal pattern suggesting nerve root or spinal level compression. X-ray shows no fracture/dislocation CT or MRI should show site of nerve involvement

4

Cervical fracture and/or dislocation Neck pain, possibly neurologic symptoms in limbs, urinary incontinence due to spinal cord involvement.

Possible hyperreflexia, positive Babinski’s sign, motor weakness and sensory changes if spinal cord injury present X-ray reveals fracture and/or dislocation CT or MRI may also show spinal cord injury.

Notes: 1. Symptoms and disorders that can be manifest in all grades include hearing disturbance, dizziness, headache, memory loss, dysphagia and jaw pain. 2. Back pain was not specified as part of the scheme, but clinically it is frequent in whiplash patients. 3. Within the QTF scheme, neck pain could radiate into the face, head, and shoulder region. 4. Symptoms of arm pain or numbness without objective neurologic signs is insufficient criteria for WAD 3. Symptoms of arm pain or numbness may exist in all grades, so WAD 3 is identified by objective neurologic signs.

Greece Chronic whiplash syndrome may also be rare in Greece. In 130 consecutive collision victims suffering acute whiplash symptoms, 91% recovered in 4 weeks. The remainder had substantial improvement and recovered within 3 months.16 Extending their series to 180 patients confirmed this results, not only for recovery from neck pain, but from the other symptoms commonly reported as part of the acute injury syndrome.17

Germany Germany also may have a low incidence of chronic whiplash pain. In a study of physical therapy treatment, by 6 weeks the active treatment group and control (healthy) groups were equal in their symptom reporting. Even the group given only a collar for 3 weeks and no other therapy recovered by 12 weeks. In this study the acute whiplash injury patient had no greater risk of reporting chronic symptoms than found in the general, uninjured population.18 A prospective outcome study by Keidel et al. of 103 subjects in another locale in Germany found the same good prognosis: recovery often within 3 weeks, and virtually all within 6 weeks.19 Similar, rapid recoveries have been found in other parts of Germany.20

Symptom expectation The differences between outcomes in these three countries cannot be ascribed to methodological issues, since methodological issues do not prevent researchers in countries such as Canada or Sweden from showing the existence of a high frequency of chronic pain. The diagnosis of a WAD case is the same in Sweden, Canada, or Lithuania – those who report symptoms after a collision are labeled as WAD – and the diagnosis of WAD 1 or 2 has no supporting objective manifestations or it would be classified as grade 3 or 4. The vast differences in outcomes cannot be simply ascribed to different medical systems, since Germany, Greece, 594

and Lithuania also have different systems, but show similar outcomes. There is no evidence for the existence of cultural stoicism. Patients with rheumatoid arthritis in Lithuania or Germany report the same symptoms and disabilities as those in North America.21,22 If cultural stoicism caused Lithuanians and Germans to underreport chronic pain, it should do so for chronic pain from rheumatoid arthritis. There must instead be a common factor amongst Lithuanians, Germans, and Greeks that differs from, say, Canadian or those from the United States. One such factor may be symptom expectation. Ferrari et al. have examined levels of expectation for outcomes after acute neck sprain in Canadians, Lithuanians, Greeks, and Germans.23–25 The studies showed that the responses of the Canadian, Lithuanian, German, and Greek subjects in their expectation of chronic disability due to rheumatoid arthritis were remarkably similar. The acute ‘whiplash’ symptoms anticipated by all these groups are also very similar, but there is a markedly different expectation of the duration of these common ‘whiplash’ symptoms. Canadians commonly expect certain symptoms to be chronic, while Lithuanians, Greeks, and Germans do not. This data is consistent with the hypothesis that the chronic whiplash syndrome is in many cases culturally conditioned illness, and that symptom expectation may be an important factor that accounts for some of the variance between the ‘Whiplash Cultures,’ where the chronic whiplash syndrome is epidemic in proportion (e.g. North America, Scandinavia), and ‘non-Whiplash Cultures’ such as Lithuania, Greece, and Germany, where the acute whiplash injury is common, but the outcome benign, recovery being measured in days to weeks. Even in ‘Whiplash Cultures,’ not all subjects develop chronic pain. It is also true that not all subjects anticipate chronic pain, and even among those who do, symptom expectation of the patient may be only one factor affecting outcome. Prospective studies evaluating multiple factors concomitantly will be able to separate out the variance due to each. When such data are available, one could at least begin to conceptualize how to intervene in each of the factors responsible for that variance in outcome.

Section 3: Cervical Spine

Thus, we should be focusing on why a particular whiplash patient has brought themselves for treatment and what factors may be making their pain more severe, and their coping less effective, before we immediately assume that the answer lies in biomechanical explanations. Besides symptom expectation, research suggests we need to consider many other factors, including what we as clinicians do or fail to do in the assessment and management of acute whiplash patients.

THE EVIDENCE ON PATIENT ASSESSMENT In the initial assessment, acute whiplash patients are classified into grade 0 through grade 4. Those with neurologic signs may require immediate imaging diagnostics and emergency management, but most will present with few objective findings. Although the history, including collision events, seat belt use, preexisting symptoms, and physical examination including spine range of motion, and tenderness are recorded, the usefulness of the routine history and physical examination for the purpose of predicting future outcome is controversial. There are no studies showing that the format for gathering historical and physical examination information ultimately alters the patient’s long-term prognosis. Intuitively, most physicians believe the whiplash patient requires the Art of Medicine as a necessary part of the effective therapeutic relationship. Collision victims are often anxious, angry, and resentful. One must be careful to not underestimate the patient’s perception of the seriousness of the injury. A thoughtful musculoskeletal examination and neurologic examination will help classify the patient but, more importantly, will reassure the patient that the injury is being taken seriously and is being properly assessed.

The literature on history-taking and physical examination of the whiplash patient usually focuses on the prognostic factors for WAD grades 1 and 2. Because of small patient samples done in a single geographical location, individual studies may not be helpful for identifying reliable prognostic factors and may not apply to other patient populations. In fact, as reviewed by Quebec Task Force1 there are only a few studies focusing on prognosis and outcome in WAD 1 and 2. The largest study with less selection bias, and greater breadth and detail of data concerning collision parameters, demographics, and symptoms as predictors of outcome is the Saskatchewan-based cohort by Cassidy et al.26–28 While the study by Cassidy et al.26 is controversial because the influence of the tort or no-fault system in Saskatchewan, there can be little doubt that the size of the population studied, and the extensive data gathering concerning individual subjects, makes this the most powerful study of whiplash prognosis. The study by Cassidy and all other pre-2001 outcome studies were analyzed by Cote et al. specifically to identify prognostic factors.28 The analyzed studies consistently showed the following postinjury factors were associated with poor outcome: age greater than 40; female gender; more intense baseline neck or back pain; more intense baseline headache; the presence of baseline radicular signs and symptoms; and the presence of depressive or other significant emotional distress symptoms within the early weeks after injury. These factors were prognostic in both the tort and no-fault system as opposed to the effect the tort system had on prognosis.26 More important were the factors that did not predict outcome. (See Table 54.2 for a summary.) Though pre-1995 studies had suggested that factors such as head position at time of collision, initial X-ray findings, the direction of

Table 54.2: Prognostic Factors for Grade 1 and 2 WAD FACTORS REPEATEDLY SHOWN TO BE ASSOCIATED WITH A WORSE OUTCOME Age greater than 40 Female gender More intense baseline neck or back pain More intense baseline headache The presence of baseline radicular signs and symptoms The presence of depressive or other significant emotional distress symptoms within the early weeks NOT ASSOCIATED WITH A WORSE OUTCOME IN POWERFUL STUDIES Direction of collision (rear, frontal or side) Seat belt or head restraint use Position of head restraint General health before the collision Previous whiplash injury Previous symptoms before collision LACK OF SUFFICIENT EVIDENCE TO CONFIRM OR DENY ROLE Marital status Socioeconomic status Level of education Number of dependants Level of income Initial X-ray findings of osteoarthritis (disc degeneration)

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impact, and amount of vehicle damage were prognostic, subsequent, larger, and better designed studies have not affirmed these findings, and have even contradicted them. Furthermore, in the Saskatchewan study the location of impact, seat belt or head restraint use or position of head restraint, the general health before the collision, previous whiplash injury, or symptoms before collision were of no prognostic value. In fact, the value of various prognostic factors are based on pre-1995 studies that were both small groups of highly selected subjects with inadequate data collection. Using a best-evidence approach, beside the obvious factors age and gender, the most relevant prognostic factors are the intensity initial symptoms and emotional distress. Merely noting how intensely the patient describes their symptoms and their level of distress will best identify the highest risk for delayed recovery. Although the physical examination obviously assists in ruling out other injuries, and classifying the WAD grade, there is little evidence that examination itself will identify factors that affect prognosis. Similar to the chronic low back pain patient, ‘nonorganic’ pain behaviors may predict failure to respond to almost any medical therapy, including medications, exercise, and surgery, if they are considering these therapies in patients with ‘pain behaviors.’29 These ‘behavioral’ signs are otherwise labeled as ‘nonorganic’ or Waddell’s signs and although these signs were described in low back patients, one might assume that the same signs would be important in pain in other areas. Waddell’s signs include grimacing, leaping when touched, inability to sit through the interview, marked superficial tenderness, back pain with axial skull loading, back pain with mild hip rotation, significant differences in straight leg raise when distracted, nondermatomal sensory loss, and jerky, give-way weakness. One can appreciate comparable findings in neck pain, including a neck that becomes rigid when the patient is specifically told they are having their neck range tested (versus their apparent range of motion when ‘unawares’), superficial tenderness, nondermatomal sensory loss, neck pain with minor movements of the shoulder joint, and jerky, give-way weakness of the arm.30 The presence of least three of these ‘behavioral’ signs has been found in studies to be a significant predictor of a poor response to medical or surgical therapy, and to correlate well with psychological distress.29 These signs are relevant: to dismiss or ignore them is to miss an opportunity for early intervention. Identifying Waddell’s signs may allow the physician to prescribe more effective therapy leading to improved outcome in chronic low back pain.31 When a patient has these signs, if behavioral (or cognitive) psychotherapy is the mainstay of treatment, the presence of Waddell’s signs are no longer predictive of a poor outcome.31 Since about 50% of whiplash patients have low back pain, the relevance seems likely, but has not been specifically studied in whiplash patients. There is no reason, however, why whiplash patients with pain behaviors should have any better prognosis, and the best

evidence from the chronic pain literature suggests physicians should identify these patients early in the course of their disorder. There are, however, important caveats. First, while they may obviously suggest a malingerer, who wrongly thinks to be making a more convincing impression on the physician, these signs are found even in individuals with known structural pathology. Their presence reflects not the absence of an organic cause (thus, ‘behavioral’ signs is a better term than ‘nonorganic’), but rather that the severity of symptoms, disability, and behavior cannot be explained on structural pathology alone. Thus, anxiety, depression, and a tendency to focus on symptoms will affect the behavior during examination in ways that physical pathology will not. Furthermore, their significance has not been formally evaluated in non-English cultures. Table 54.3 summarizes the ‘red flags’ that can be gathered from the history and physical examination.

Radiological Assessment Many physicians order a cervical spine X-ray to reassure the patient and themselves that the rare possibility of fracture in an apparently otherwise ‘typical’ soft tissue injury has been ruled out. This is a step in WAD grading. The Quebec Task Force suggested that an X-ray was not required for WAD grade 1. Even though most X-rays will be negative, if physical findings are present an X-ray is recommended to exclude fracture. Hoffman et al.32 studied over 30 000 cases of blunt nonpenetrating trauma to the neck caused mostly by motor vehicle collisions. They developed a decision instrument which requires patients to meet the following five criteria for a low probability of significant structural injury: no midline cervical tenderness; no focal neurologic deficit; normal alertness; no intoxication; and other painful injury that would distract the patient from noticing the severity of their neck tenderness. With this decision rule, eight of 818 patients with bony injury were missed, and only two of these eight were considered to have clinically significant injuries that might have a potential for complications. Another prospective study by Stiell et al.33 in nine Canadian emergency departments evaluated decision rules for X-rays in patients with trauma. None of 1812 patients in simple rearend collisions were found to have evidence on X-ray of cervical spine injury. But despite the apparent usefulness of criteria rules, concerns have been raised that to miss even two cases of relevant injury in 800 is unacceptable in our current medicolegal environment. Thus, many physicians will order neck X-rays. Besides the increased cost, there is perhaps a bigger problem of wrongfully elevating benign degenerative X-ray finding to pathological significance. Many physicians continue to attribute chronic neck pain syndrome secondary to degenerative disc disease, although once studies are controlled for age, there is no independent correlation between symptoms and disc findings, regardless whether the findings are detected with X-ray, discography, CT scan, or MRI.34 Even disc protrusions

Table 54.3: The ‘Red Flags’ that Indicate a Poor Prognosis in Patients with WAD 1 or 2 Age greater than 40 High initial intensity of headache, neck or back pain High emotional distress Presence of depressive symptoms Presence of radicular symptoms Pain behaviors and other behavioral (Waddell’s) signs present The presence of these flags suggests the physician may wish to have closer follow-up and/or involve specialist referral at an early stage.

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without nerve root or spinal cord compression, spinal stenosis, and small degrees of vertebral subluxation had no predictive value for the presence of neck pain, and are just as frequently found in asymptomatic subjects. On the other hand, where there is a good clinical reason to suspect a specific root lesion based on the neurological examination, a CT or MRI may provide necessary preoperative anatomical confirmation. Telling patients that their pain arises from degenerative change or osteoarthritis of the spine is not evidence based and may give the patient the impression that they have a chronic, unrelenting, and likely untreatable cause of pain. Furthermore, this belief could lead to withdrawing from activities, developing anxiety, and seeking many different forms of ‘cure.’ In the patient with neurologic physical signs, an MRI or CT scan should be obtained to help confirm or refute a WAD grade 3 and to identify which neurologic structures are involved. However, the MRI or other imaging studies are only important in identifying fractures, dislocations, or neurologic compromise and there is no evidence that other ‘degenerative’ findings will identify a cause of pain or physical findings. Minor degrees of forward angulation of the cervical spine or kyphosis, ‘straightening of the lordosis’ or ‘disc disease,’ or ‘osteoarthritis’ are found in asymptomatic controls as frequently as in acute whiplash injury patients.33 There is little evidence that having an abnormal X-ray at the time of the acute injury affects the outcome.34 Patients are often told that their X-ray shows many ‘abnormalities’ without the explanation that these findings are either normal or agerelated findings.34 Thus, in the vast majority of whiplash claimants, the various, commonly identified radiological abnormalities do not correlate with symptoms and merely represent the background prevalence of such findings in the general population. Patients with WAD 1 or 2 should, from an evidence-based approach, be reassured that they would have their neck pain regardless of osteoarthritis on their X-rays, and that they would (and did) have degenerative changes (‘arthritis of the spine’), even without pain.

THE EVIDENCE ON TREATMENT OF ACUTE WAD Although there are few studies allowing scientific evaluation of treatment of whiplash patients, there are several published literature reviews. These studies include Quebec Task Force 1995,1 Kjellman et al. 1996,35 and Peeters et al. 2001.36 The survey by Kjellman et al. includes non-English language scientific publications, and combines studies of therapy for both traumatic and nontraumatic neck pain. In addition, although the surveys by the Quebec Task Force and Peeters et al. were designed to study ‘whiplash therapy’ both included reviews of studies with mixed populations of neck pain patients. From available data, it is clear that therapy prescriptions including an active exercise are superior to those which rely on passive therapy modalities such as ultrasound, manual therapy, massage, heat, TENS, and laser. Controlled studies have not validated electromagnetic therapy, traction, collars, TENS, ultrasound, spray and stretch, local corticosteroid injections, trigger point injections, and laser therapy.1 The Quebec Task Force found the effectiveness of manipulation/chiropractic therapy in acute neck pain to be equivocal and noted that the study design either reflected significantly different baseline characteristics in cohorts, or some studies failed to find a therapeutic effect. Because of the mixed prescriptions of multiple passive modalities versus various exercises in some studies, it is not clear whether exercise is better because it is effective, or because passive therapy is harmful, or both. It is also not clear what aspect or type of exercise therapy is more effective. Peeters et al.36 recently summarized the few acute neck treatment studies published since 1995. These studies again indicate that exer-

cise therapies are superior to passive modalities and that ‘rest makes rusty.’ One of the most impressive studies in acute whiplash patients was by Borchgrevink et al.13 in Norway. The authors compared giving or not giving the therapeutic advice to ‘act as usual’ in a randomized group of 241 neck pain patients whose onset of pain was within 24 hours of a motor vehicle collision, and who had no signs or radiological findings to suggest neurological injury or fracture. All patients received instructions for self-training of the neck and a 5-day prescription for a nonsteroidal antiinflammatory drug. One group was instructed to act as usual and received no sick leave or collar. Patients in the immobilization group received 14 days of sick leave and a soft collar. At 6 months after the collision, the ‘act as usual’ group had a better outcome in several variables including pain, concentration, and memory. The study is impressive because the difference between the two groups was simply advice coupled with no sick leave and no collar, versus both sick leave and a collar. Although the beneficial effect of advice versus the adverse effect of wearing a collar could not be determined, the outcome in the ‘act as usual’ group was better than is typically reported in most studies, suggesting some definite benefit to that advice. Such an effect illustrates the importance of modifying patient behavior as a method to preventing the transition from acute to chronic neck pain. While there is a confirmed relationship between various measures of postural changes and chronic spinal pain, the exact role of postural changes in the transition from acute to chronic pain is unknown. McKinney et al. found a beneficial effect of postural exercises and the use of a lumbar roll. The comparison group was, however, using passive physical therapy modalities only and it is therefore not clear whether the treatment was beneficial or the control group had a deleterious outcome as a result of passive therapy. Nevertheless, the head-forward posture has been shown to be corrected by neck retractions,37 and lumbar rolls have been tested and found effective for low back pain,38 and were included in the active therapy studied by McKinney et al.12 Studies have shown collar use will delay recovery even in subjects with an otherwise expected good outcome.18,20 Thus, the advice to maintain usual activity, to exercise, and to use a lumbar roll is superior to the myriad of other therapies that are otherwise passive and may in fact be detrimental.

THE EVIDENCE ON SYMPTOM AMPLIFICATION Patient symptoms may be amplified by variables independent of injury or disease and some variables can be prevented and some aggravated by the treating physician.38,39 A patient’s emotional state determines how one perceives minor, day-to-day symptoms from life’s activities, including occupational sources. Patients have been shown, for example, to recall symptoms in a way that matches their current emotional state. If one asks someone who is currently distressed about headaches, the person will recall many more severe headaches episodes than when in a good mood. Studies show that the direction of the effect IS NOT that symptoms significantly affect one’s mood, but rather one’s mood affects symptoms and symptom recall.39,40 A patient will recall many symptoms during a period of emotional or psychological distress, and will underreport or have poor recall of symptoms in the more remote past when less distressed.40 In addition, anxiety and depression facilitate recall of unpleasant past events, negative experiences and, in particular, previous illnesses. For example, Croyle et al. induced positive or unpleasant mood among a group of subjects who were then asked to recall their prior symptoms in the last 30 days.41 Those who underwent an unpleasant mood induction recalled more symptoms than individuals who underwent a positive mood induction. Similarly, Cohen et al. showed that in otherwise healthy subjects who underwent exposure to a respiratory virus to induce illness, a higher psychological stress 597

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assessed before the viral challenge was associated with greater symptom scores in response to infection.42 Mood affects the perception of symptoms and the appraisal of one’s health.41 A negative mood makes illness-related memories more accessible and induces a poorer assessment of one’s overall state of health. It follows that a negative mood makes collisionrelated memories more accessible and leads a person to focus on symptoms that they are told are sequelae of the collision. Michelotti et al.43 further demonstrated that normal subjects, when in states of natural stress, have altered muscle function and tenderness about the jaw, a common problem in whiplash patients. Yet, these subjects suffered no injury and recovered as the psychological/emotional distress levels dropped. Similarly, Castro et al. were able to reproduce in a laboratory setting the acute whiplash syndrome in 20% of subjects who were falsely led to believe they had experienced a true motor vehicle collision.44 Despite the lack of any biomechanical forces to cause injury, the symptoms evoked were seemingly genuine in this setting, and their development was predicted by pre-experiment psychological measures of somatic focus and tendencies towards anxiety. Second, as Barsky reveals, what we believe to be the cause of our symptoms affects how severely we perceive those symptoms. Studies show that patients who believe they are injured will have an underestimation of symptoms in the period before the patients believe they were injured. Thus, it has been shown patients with whiplash underestimate their pre-injury history of neck symptoms.45 Finally, the close attention to symptoms will affect symptoms. Kasch et al.46 showed that patients with ankle sprains, when asked through questionnaires and repeated examinations to pay close attention to symptoms such as headache, neck pain, and back pain, will become just like whiplash patients in 3 months. They will report the same symptoms and even the same restricted range of neck motion even though ankle sprain patients did not begin with spinal pain and even though 100% of the ankle sprain pain resolved within 6 months. Could these subjects be amplifying life’s background noise of symptoms? The study reaffirms the prognosis for ankle sprain, but perhaps the reason ankle sprains are not a long-term socioeconomic patient disability is that even in United States most ankle sprains are supposed to cause acute pain but patients and physicians alike do not accept an ankle sprain as a cause or reason for chronic pain and disability. Worry and fear of long-term pain is aggravated by friends and physicians agonizing over the chronic nature of whiplash injury. Ankle

sprains, on the other hand, are considered a benign self-limiting process. Whatever the sources of WAD symptoms, the evidence suggests that patients symptoms will be aggravated in an environment that both promotes the seriousness of the symptoms and encourages the patient to focus on his or her symptoms.

THE EVIDENCE ON ACTIVE VERSUS PASSIVE COPING There is considerable chronic pain literature trying to explain why patients with similar pain levels can have such divergent outcomes, in which some recover from acute pain within days to weeks and others develop chronic pain and disability. Although high levels of initial pain in whiplash patients predict a poorer outcome, why do some but not all patients with high levels of initial pain develop chronic pain. Perhaps, rather than the initial level of pain, the ability of patients to cope with the pain is the most important predicting variable. Research by Carroll defines both active and passive coping (Table 54.4).47 Active coping refers to those coping strategies in which the patient takes responsibility for pain management and include attempts to control the pain or to function in spite of pain. Passive coping refers to strategies in which patients give the responsibility for pain management to an outside source or allow other areas of life to be adversely affected by pain. Passive coping is generally found to be associated with increased severity of depression, higher levels of activity limitation, and helplessness. Active coping has been found to be associated with less severe depression, increased activity level, and less functional impairment, but to be unrelated to pain severity. It is intuitively apparent that higher pain levels will stress any coping style, all the more so if the coping mechanisms are limited. Many patients use combinations of active and passive coping, but for any pain level, the higher the passive coping usage, the worse the outcome. Regardless of levels of active coping, Carroll et al.47 further showed that the development of disabling neck, low back pain, or both was strongly associated with the high use of passive coping strategies. Even if a person stays busy or active, and engages in physical exercise, the concomitant tendency to hold passive strategies, such as relying heavily on pain medications, frequently focusing on and discussing their pain with others, and canceling social activities, negates the beneficial effects of the active coping. Passive coping is hazardous to the outcome. Recent research with whiplash patients confirms the relevance of coping styles to recovery.48

Table 54.4: Markers of Active and Passive Coping Styles for Pain ACTIVE COPING Engaging in physical exercise or physical therapy Staying busy or active Clearing your mind of bothersome thoughts or worries Participating in leisure activities (such as hobbies, sewing, stamp collecting, etc.) Distracting your attention from the pain (recognizing you have pain, but putting your mind on something else) PASSIVE COPING Saying to yourself, ‘I wish my doctor would prescribe better pain medication for me’ Thinking, ‘This pain is wearing me down’ Talking to others about how much your pain hurts Restricting or canceling your social activities Thinking ‘I can’t do anything to lessen this pain’ Focusing on where the pain is and how much it hurts 598

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ADVICE FOR THE ACUTE WHIPLASH PATIENT Physicians should be truthful with their patients. Physicians can give advice based on their own convictions and their own clinical experience but they should also know and adhere to the evidence-based literature. The following is the algorithmic approach proposed by the authors, based on the literature and their own convictions. Based on the literature, the appropriate treatment for WAD 1 and 2 is shown in Figure 54.1. The following is a summary of the advice that may be given to patients with grade 1 or 2 WAD, based on the literature and on the authors’ personal convictions. 1. On the basis of your symptoms and the examination, you have grade 1 (or 2) whiplash. This means most likely that you have a sprain of muscles and ligaments and that you do not have a fracture, injury to nerves, or other serious damage that we can detect. The symptoms you are experiencing are normal and common for your type of injury. You need to know that the most people recover from this injury within 6 weeks, and you should have no long-term problems. You may hear, however, that a few people do go on to have chronic pain and trouble working or enjoying their usual lifestyle after the injury. It is important to know that there are things you may do that can reduce the chance of this happening, but there are other things you may do that will increase the chance of chronic pain happening. As long as you focus on what you can do to recover, you will do well.

Initial visit

Initial and next visits*

2. Maintain normal activities or modified activities as much as possible. It is usual for these activities to seem painful, but there is no evidence that normal activities will cause harm, but rather that they improve recovery. 3. Start with exercise and good posture maintenance early. Whiplash patients who exercise daily, despite the fact that these exercises may hurt initially, do better than those who rest and hope the pain will go away on its own. 4. Avoid using a collar. While this may offer temporary relief, we know that collar use prolongs recovery. 5. Avoid relying solely on non-exercise (passive) therapies. In general, whiplash patients who use passive therapies instead of exercise, or those who have the expectation that others will cure them, do not do well. Exercise, done daily and with dedication, offers a better chance of recovery. 6. Do not rely on medications to completely eliminate your pain. There is no evidence that medications speed recovery from whiplash injury, though if they assist in keeping you active and exercising, they may be helpful in the short term. Over-thecounter medications are known to be the safest and should be used first. Other pain killers and medications cause many side effects including sedation, dizziness, dry mouth, poor concentration, poor memory, ringing in the ears, visual disturbance, and headache. 7. Paying close attention to symptoms and worrying over symptoms will make your symptoms more severe.

Use history and physical examination to classify according to WAD grade.

Symptoms of Grade 1 with no signs

Symptoms and signs of Grade 2

Symptoms and signs of Grade 3

Reassure. Usual activities. Simple analgesics. No X-ray needed.

Confirm no fracture on X-ray. Reassure. Usual activities. Simple analgesics. Exercises.** Lumbar roll and posture advice.

Confirm no fracture on X-ray. Consider MRI or CT scan. Treat according to nature of neurological involvment. Consider specialist involvement.

X-ray evidence of fracture

Immediate specialist consultation.

3−6 weeks If unresolved, or little progress, reassess red flags and coping styles, medication adverse effects, anxiety, depression, causes for symptom amplification. Re-educate and consider specialist consultation to address barriers to recovery.

Ask questions: Is patient wearing a collar, relying heavily on analgesics, not doing exercises, not using lumbar roll, worried about something, depressed, keeping a pain diary, using passive therapies and expecting a “cure”, withdrawing from usual activities ...

* It may be necessary to repeat this advice, and use subsequent visits to identify red flags that become apparent over time. ** Exercises could be taught by the physician or part of a supervised program with an experienced exercise therapist.

Fig. 54.1 Management of whiplash-associated disorder. 599

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8. The more time you spend talking to others about how bad your pain is, the more you tend to focus on your pain than on your recovery, and the more severe your pain will become. 9. Do not assume that problems you notice months later are caused by the injury. You need to remember that aches and pains, headaches, and many other symptoms are common in life, especially if your life becomes stressed. Because you have been injured, it is natural that you will be paying closer attention to your body than you would have before, so it is natural you will notice life’s aches and pains more than you did before. The best distraction from your pain and this cycle of increased attention to symptoms is to continue your normal activities, do things you enjoy despite the hurt, and keep your stress levels down by keeping your usual schedule.

References 1. Spitzer WO, Skovron ML, Salmi LR, et al. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders. Spine 1995; 20(Suppl 8):1S–73S.

24. Ferrari R, Constantoyannis C, Papadakis N. Laypersons’ expectation of the sequelae of whiplash injury: a cross-cultural comparative study between Canada and Greece. Med Sci Mon 2003; 9:CR120–124. 25. Ferrari R, Lang C. A cross-cultural comparison between Canada and Germany of symptom expectation for whiplash injury. J Spinal Disord Tech 2005; 18:92–97. 26. Cassidy JD, Carroll L, Cote P, et al. Low back pain after traffic collisions: a population-based cohort study. Spine 2003; 28:1002–1009. 27. Cote P, Hogg-Johnson S, Cassidy JD, et al. The association between neck pain intensity, physical functioning, depressive symptomatology and time-to-claim-closure after whiplash. J Clin Epidemiol 2001; 54:275–286. 28. Cote P, Cassidy JD, Carroll L, et al. A systematic review of the prognosis of acute whiplash and a new conceptual framework to synthesize the literature. Spine 2001; 26:E445–E458. 29. Waddell G, Pilowsky I, Bond MR. Clinical assessment and interpretation of abnormal illness behaviour in low back pain. Pain 1989; 39:41–53.

2. Hartling L, Brison RJ, Ardern C, et al. Prognostic value of the Quebec Classification of Whiplash-Associated Disorders. Spine 2001; 26:36–41.

30. Sobel JB, Sollenberger P, Robinson R, et al. Cervical nonorganic signs: a new clinical tool to assess abnormal illness behavior in neck pain patients: a pilot study. Arch Phys Med Rehabil 2000; 81:170–175.

3. Versteegen GJ, van Es FD, Kingma J, et al. Applying the Quebec Task Force criteria as a frame of reference for studies of whiplash injuries. Injury 2001; 32:185–193.

31. Ferrari R. Comment on Polatin et al., Predictive value of Waddell signs [letter]. Spine 1999; 24:306.

4. Holm L, Cassidy JD, Sjogren Y, et al. Impairment and work disability due to whiplash injury following traffic collisions. Scand J Public Health 1999; 2:116–123.

32. Hoffman JR, Mower WR, Wolfson AB, et al. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma, for The National Emergency X-Radiography Utilization Study Group. N Engl J Med 2000; 343: 94–99.

5. Cassidy JD, Carroll L, Cote P, et al. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Eng J Med 2000; 342:1179–1186. 6. Brison RJ, Hartling L, Pickett W. A prospective study of acceleration–extension injuries following rear-end motor vehicle collisions. J Musculoskeletal Pain 2000; 8:97–113. 7. Suissa S, Harder S, Veilleux M. The relation between initial symptoms and signs and the prognosis of whiplash. Eur Spine J 2001; 10:44–49. 8. Hildingsson C, Toolanen G. Outcome after soft-tissue injury of the cervical spine. Acta Orthop Scand 1990; 61:357–359. 9. Gennis P, Miller L, Gallagher EJ, et al. The effect of soft cervical collars on persistent neck pain in patients with whiplash injury. Acad Emerg Med 1996; 3:568–573. 10. Gargan MF, Bannister GC. The rate of recovery following whiplash injury. Eur Spine J 1994; 3:162–164. 11. Mayou R, Bryant B. Outcome of ‘whiplash’ neck injury. Injury 1996; 27:617–623. 12. McKinney LA. Early mobilisation and outcome in acute sprains of the neck. Br Med J 1989; 299:1006–1008. 13. Borchgrevink GE, Kaasa A, McDonagh D, et al. Acute treatment of whiplash neck sprain injuries. A randomised trial of treatment during the first 14 days following car accident. Spine 1998; 23:25–31. 14. Schrader H, Obelieniene D, Bovim G, et al. Natural evolution of late whiplash syndrome outside the medicolegal context. Lancet 1996; 347:1207–1211. 15. Obelieniene D, Schrader H, Bovim G et al. Pain after whiplash – a prospective controlled inception cohort study. J Neurol Neurosurg Psychiatry 1999; 66:279–283. 16. Partheni M, Miliaris G, Constantayannis C, et al. Whiplash injury [letter]. J Rheumatol 1999; 26:1206–1207. 17. Partheni M, Constantoyannis C, Ferrari R, et al. A prospective cohort study of the outcome of acute whiplash injury in Greece. Clin Exp Rheumatol 2000; 18:67–70. 18. Bonk A, Ferrari R, Giebel GD, et al. A prospective randomized, controlled outcome study of two trials of therapy for whiplash injury. J Musculoskeletal Pain 2000; 8:123–132. 19. Keidel M, Baume B, Ludecke C, et al. Prospective analysis of acute sequelae following whiplash injury. World Congress on Whiplash-Associated Disorders; February 7–11, 1999; Vancouver, Canada. 20. Schnabel M, Ferrari R, Vassiliou T, et al. A randomized, controlled outcome study of active mobilization versus collar therapy for whiplash injury. Emerg Med J 2004; 21:306–310. 21. Dadoniene J, Uhlig T, Stropuviene S, et al. Disease activity and health status in rheumatoid arthritis: a case-control comparison between Norway and Lithuania. Ann Rheum Dis 2003; 62:231–235. 22. Zink A, Braun J, Listing J, et al. Disability and handicap in rheumatoid arthritis and ankylosing spondylitis – results from the German rheumatological database. German Collaborative Arthritis Centers. J Rheumatol 2000; 27:613–622.

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23. Ferrari R, Obelieniene D, Russell AS, et al. Laypersons’ expectation of the sequelae of whiplash injury. A cross-cultural comparative study between Canada and Lithuania. Med Sci Mon 2002; 11:728–734.

33. Stiell IG, Clement CM, McKnight RD, et al. The Canadian c-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med 2003; 349: 2510–2518. 34. Ferrari R. The whiplash encyclopedia. The facts and myths of whiplash. Gaithersburg, MD: Aspen Publishers; 1999:25–37. 35. Kjellman GV, Skargren EI, Öberg BE. A critical analysis of randomised clinical trials on neck pain and treatment efficacy. A review of the literature. Scand J Rehab Med 1999; 31:139–152. 36. Peeters GG, Verhagen AP, de Bie RA, et al. The efficacy of conservative treatment in patients with whiplash injury: a systematic review of clinical trials. Spine 2001; 26:E64–E73. 37. Pearson ND, Walmsley RP. Trial into the effects of repeated neck retractions in normal subjects. Spine 1995; 20:1245–1250. 38. Williams MM, Hawley JA, McKenzie RA, et al. A comparison of the effects of two sitting postures on back and referred pain. Spine 1991; 16:1185–1191. 39. Barksy AJ. Forgetting, fabricating, and telescoping. The instability of the medical history. Arch Intern Med 2002; 162:981–984. 40. Simon GE, Gureje O. Stability of somatization disorder and somatization symptoms among primary care patients. Arch Gen Psychiatry 1999; 56:90–95. 41. Croyle RT, Uretsky MB. Effects of mood on self-appraisal of health status. Health Psychol 1987; 6:239–253. 42. Cohen S, Doyle WJ, Skoner DP. Psychological stress, cytokine production, and severity of upper respiratory illness. Psychosom Med 1999; 61:175–180. 43. Michelotti A, Farella M, Tedesco A, et al. Changes in pressure–pain thresholds of the jaw muscles during a natural stressful condition in a group of symptom-free subjects. J Orofacial Pain 2000; 14:279–285. 44. Castro WH, Meyer SJ, Becke ME, et al. No stress – no whiplash? Prevalence of ‘whiplash’ symptoms following exposure to a placebo rear-end collision. Int J Legal Med 2001; 114:316–322. 45. Marshall PD, O’Connor M, Hodgkinson JP. The perceived relationship between neck symptoms and precedent injury. Injury 1995; 26:17–19. 46. Kasch H, Stengaard-Pedersen K, Arendt-Nielsen L, et al. Headache, neck pain, and neck mobility after acute whiplash injury: a prospective study. Spine 2001; 26:1246–1251. 47. Carroll L, Mercado AC, Cassidy JD, et al. A population-based study of factors associated with combinations of active and passive coping with neck and low back pain. J Rehabil Med 2002; 34:67–72. 48. Buitenhuis J, Spanjer J, Fidler V. Recovery from acute whiplash: the role of coping styles. Spine 2003; 28:896–901.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ ii: Whiplash

CHAPTER

Soft Tissue Injuries Following Whiplash

55

Paul H. Lento and William Sullivan

INTRODUCTION Cervical soft tissue injuries resulting from whiplash are often considered controversial. These injuries are presumed to be caused by an acceleration/deceleration injury that commonly occurs during many motor vehicle collisions.1 Although several structures may cause pain following a whiplash injury, patients with whiplash associated disorders (WAD) are often diagnosed as having an acute musculoligamentous injury referred to as a cervical sprain or strain.1–3 The tissues involved in this diagnosis are postulated to be the large, multisegmental muscles, the smaller one- or two-segment muscles, the fascia or connective tissue, and the spinal ligaments. Fortunately, the majority of these whiplash patients improve over time.4–6 However, a subset of patients with whiplash injuries continue to have pain complaints despite a lack of objective diagnostic evidence confirming the presence of an injury.7–9 Although pain generators such as the cervical disc and facet have been described elsewhere,10–14 and may contribute to referred or radicular pain and even cervicogenic headache, many of these patients with WAD have overlying muscular or soft tissue pain that may radiate into the shoulders and upper limb in a nonradicular pattern.8,15–17 Since soft tissue symptoms persist despite what would seem an adequate period of healing and, since abnormal pathology cannot be identified with advanced radiologic or electrophysiological testing, these patients may be diagnosed as malingerers or felt to be seeking financial compensation for their injuries. Yet, some studies have demonstrated that litigation may not be a clear risk factor for the continuance of symptoms.18,19 Therefore, patients are often diagnosed with myofascial pain, the etiology of which also continues to remain elusive and controversial.15,20 Recently, however, there have been theories that may better explain the persistence of these symptoms following whiplash injury. The purpose of this chapter is to describe the cervical soft tissue injuries incurred from an acute whiplash. In addition, mechanisms that produce these injuries will be discussed, including the evidence that proves the existence of soft tissue injury following whiplash. Finally, the possible theories that may explain the etiology of chronic persistent soft tissue cervical pain following whiplash will be presented.

ACUTE INJURY Overview Although there are accepted pain generators of the cervical spine, it is commonly observed following whiplash that the cervical musculoligamentous tissues may contribute to WAD of the cervical spine.1,2,7,8,21,22 The precise biomechanics of cervical whiplash have been discussed elsewhere and are more complex than a simple cantilever mechanism.23,24 However, the cervical acceleration and decel-

eration that occur during whiplash may help explain injury that is incurred by the supportive tissues. Although the full range of cervical motion is not exceeded during low–moderate cervical whiplash,25–27 it is implied that acceleration of the torso produces relatively forceful head extension. As this occurs, the anterior cervical muscles are lengthened when the acceleration force of the impact overpowers their tone.28 This eccentric force would theoretically create muscle fiber tearing and damage to surrounding vasculature, lymphatics, and even neural tissues.2,28 The brunt of the remaining force may then be taken up by passive structures such as the anterior longitudinal ligament (ALL).28 Following this acceleration phase, the head flexes as the torso decelerates. Flexion of the head may be potentiated by contraction of the neck flexors stimulated by the stretch reflex from the preceding acceleration phase.28 This combination may excessively load the posterior cervical structures. Studies in animal models29 have implicated that, during this deceleration phase, the upper cervical spine, serving as a pivot point, sustains the greatest injury as supportive structures serve to decelerate the head. By this mechanism the ligamentous structures such as the alar and transverse ligaments as well as the tectorial membrane, suboccipital, and upper cervical muscles may be traumatized.21,30–33 Other authors have reported that acceleration and deceleration force may also be associated with a significant amount of cervical axial loading and distraction.22,34 These forces may create irritation of more central nervous structures such as the spinal cord, brainstem, and nerve roots.35 This direct impact on neural structures, as well as the supportive musculoligamentous structures have been implicated in the development of acute pain and also the perpetuation of chronic pain following cervical whiplash, including the presence of adverse neural tension (Fig. 55.1) and central sensitization.35,36

MUSCULOLIGAMENTOUS INJURY Despite this theoretical overview, there is a relative paucity of strong in vivo evidence that supporting structures such as the cervical muscles and ligaments are damaged during whiplash injury. Although injury to these musculoligamentous structures is often implied when clinicians use the diagnosis of cervical strain or sprain following whiplash, most of the information regarding injury to these structures comes from animal research, cadaveric and radiologic studies, electromyographic data, and some reported clinical experiences.

Clinical experience Janes and Hooshmand2 in 1965 was one of the first to clinically report on the etiology of soft tissue pain following cervical flexion– extension injuries. They referred to these injuries as cervical sprains and inferred that in a rear-end collision, the patient is in a relaxed position, deprived of the protection usually achieved by contraction

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A

B

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Fig. 55.1 A physical examination maneuver to elicit adverse neural tension in the upper limb and cervical spine. The examiner depresses, abducts, and externally rotates the shoulder while extending and supinating the wrist. The elbow then can be extended slowly to see if any of the patient’s symptoms are recreated. If they are, the cervical spine can be laterally flexed side to side to lessen or worsen the symptoms.

of the cervical paraspinal musculature. In Janes’s experience, these ‘sprains’ were caused by injury to the cervical ligaments such as the interspinous ligaments, ligamentum nuchae, and ALL. They provided evidence for this statement by reporting on the surgical findings of 32 patients with cervical pain following cervical trauma. Twenty-three had experienced whiplash injuries. Upon surgical exploration, eight of these patients had definite rupture of the interspinous ligament at C6 or C7 with scar formation, while 13 had hypermobility of one or two spinous processes of the cervical vertebrae. Additionally, the ligamentum nuchae and interspinous ligaments had developed calcifications indicative of degenerative changes and scarring. Approximately 90% of patients in this case series had good to excellent outcomes with 1–7 year follow-up after posterior cervical fixation. Unfortunately, Janes and Hooshmand did not report on disc or zygapophyseal injuries in this case series but this report provided clear evidence that ligamentous damage may serve as a potential pain generator following a cervical whiplash. Hohl8,21 and later Hirsch et al.22 reported on clinical findings associated with soft tissue injury following whiplash based upon clinical observations. They concluded that acute cervical pain following whiplash was partly from soft tissue injury, namely musculoligamentous damage, but provided no new substantial clinical proof to support this theory. Like most, they postulated that rear-end collisions resulted in the most disability and that injury to the anterior or posterior musculature occurred during cervical acceleration and deceleration33,37 Front-end collisions, creating forward cervical flexion, it was felt, would result in injury mainly to the posterior musculature and ligaments.8,21,22 Interestingly, these authors were among the first to report that patients often had pain radiating into the upper limb that did not follow a radicular pattern and suggested that these unexplainable symptoms may be due to irritation of injured musculoligamentous structures. It is known that stimulation of these supportive structures with hypertonic saline produces somatic pain patterns.38–41 More recent clinical observations suggest that these nonradicular referral patterns may also be attributable to central neural irritation, as evidenced by adverse neural tension.36

Animal studies Despite these case series and clinical experiences, the majority of evidence suggesting damage to the musculoligamentous structures following cervical whiplash is found predominantly from animal studies. Macnab,19 utilizing a monkey model, simulated significant acceleration injuries to the cervical spine. His studies produced cervical muscular injuries that ranged from minor tears in the sternocleidomastoid to tears of the longus colli muscle and hem602

orrhage within the esophagus. In addition, damage to the longus colli resulted in associated retropharyngeal hemorrhage and damage to the cervical sympathetic nervous system. These findings may explain the clinical complaints of dysphagia, dizziness, and vertigo in patients following whiplash. These acceleration injuries also resulted in avulsion of the anterior longitudinal ligament and separation of the disc from the cervical vertebrae28 but these injuries never occurred without concomitant injury to the anterior cervical musculature. Although Macnab admitted that less severe injuries would not result in such significant soft tissue trauma, he was among the first to provide pathological evidence that the cervical muscle and ligaments could contribute to pain and cervical dysfunction following a whiplash injury. Wickstrom et al.,42 also utilizing a primate model, produced acceleration and deceleration injuries to the cervical spine. With this more accurate simulation of the whiplash injury, there was a high proportion of damage to the posterior ligamentous complex and cervical nerve roots. Inflammation and hemorrhage within the trapezius and splenius capitis muscles was detected in approximately 25% of the specimens. Additionally, Wickstrom et al.43 confirmed Macnab’s findings, demonstrating that the ALL may indeed be damaged during the acceleration phase of whiplash, separating from the anterior cervical disc and vertebral body. Understandably, these injuries were not identified by utilizing plain radiographs, suggesting that patients, even with significant soft tissue injury, will have negative radiographic examination. Unterharnscheidt29 was among the first to separate what damage would be created by the acceleration phase versus the deceleration phase of the whiplash. He remarked that the deceleration phase of whiplash produced hemorrhage and tearing to the origin of cervical musculature as well as damage to the posterior longitudinal ligament, tectorial membrane, transverse, and alar ligaments. Ironically, he failed to reveal any major alterations in the ligamentous structures during the acceleration phase but did confirm the presence of bleeding within the sternocleidomastoid. Liu et al.,44 as well as Bocci and Orso,30 have shown in experimental animal models that during the acceleration phase of whiplash, the cervical ALL, alar ligament, transverse ligament, and even PLL may be injured. This is noteworthy, as previous authors have implicated the role of deceleration as the cause of injury to these posterior structures.

Cadaveric studies Clinical evidence in humans confirming soft tissue injury after whiplash is relatively sparse and often relies on cadaveric or postmortem specimens to identify musculoligamentous injuries. However, it has

Section 3: Cervical Spine

been refuted that cadaveric specimens, although more anatomically accurate than an animal model, cannot adequately replicate normal living tissue since it lacks contractile muscle that may be protective during whiplash. Postmortem analysis has also been cited as not being representative of the typical whiplash mechanism since the majority of victims who die have sustained forces beyond what is considered typical for low to moderate velocity car collisions. Despite these arguments, Clemens and Burow45 subjected unembalmed cadavers to rear-end impacts with approximate average velocities of 19 km/h. Significant ligamentous injuries were observed with the majority of the injuries occurring about the C5–6 or C6–7 level. Injury to the ALL was found in 80%, while 10% of the cadavers had injury to the PLL, and 10% had injury to the ligamentum flavum. Dural attachments to these ligaments may generate tensile forces on nearby neural structures.46,47 These cadaveric studies lend credence to the belief that ligamentous injuries, in addition to muscular injury, are partly responsible for local and radicular pain following whiplash.46,47

Electromyographic evidence Although it was initially reported that the cervical muscles do not participate in protection during cervical whiplash,48 there has been subsequent electromyographic evidence to support the theory that the cervical musculature undergoes tremendous activation during a whiplash injury.49 This activation, particularly if occurring eccentrically, would potentially explain damage to supportive muscular structures. Additionally, it has been recognized that anticipatory contraction of supportive musculature prior to the collision may be protective since there is a reduction of head acceleration and angular displacement.50,51 Magnusson et al.52 were among the first to measure electromyographic activity from muscles during a simulated whiplash injury. Recordings from the SCM, trapezius, semispinalis capitis, splenius capitis, and levator scapulae revealed significant activity from all muscles. The first muscles to be activated were from the superficial muscles including the trapezius, levator scapulae, and SCM, while the deeper muscles, semispinalis capitis and splenius capitis, contracted later and for longer periods. The authors theorized that the larger superficial muscles with longer moment arms grossly stabilized the spine while the deeper muscles continued with sustained contractions to provide segmental control to the cervical spine during the acceleration and deceleration phases of whiplash. Kumar et al.49 confirmed these results, recording EMG activity from anterior and posterior musculature during rear-end impact of various velocities. Muscle responses were greater with higher levels of acceleration. The SCM generated up to 179% of its maximal voluntary contraction but awareness of impending impact significantly reduced the muscle response, whereas a lack of awareness had the opposite effect. This study confirmed that significant force is absorbed by the cervical supportive musculature and that knowledge of an impending collision may help reduce the injury to musculature incurred at the time of impact. Siegmund et al.,53 however, have stated that most laboratory EMG testing falsely represents what occurs during automobile collisions since participants in experiments are aware that at some point a collision will take place and may contract supportive musculature in anticipation. Therefore, to more accurately measure electromyographic data from muscles during whiplash, the following experiment was performed. Three subgroups of participants were subjected to a whiplash perturbation while having EMG activity recorded from their paraspinals and SCMs. The first group was completely aware that a collision was to occur, the second group knew that a collision was to occur but was unsure when, and the third group, as evidenced

by resting baseline electromyographic activity, was completely surprised when the collision took place. Siegmund et al. showed that the SCM and paraspinals in male subjects of the surprised group had a delay in onset of activation 7 ms and 5 ms, respectively, compared to the alerted participants. Cervical paraspinal amplitudes were also 260% higher in surprised male subjects and their flexion acceleration velocities were significantly greater. Although the purpose of this paper was to more accurately assess mechanics closer to a real-life situation, the kinematics and electromyographic data of these studies reveal the significant trauma that the cervical soft tissues may sustain during a whiplash injury.

Radiologic studies There have been few published articles demonstrating the importance of radiologic studies in understanding the mechanism and presence of cervical musculoligamentous lesions after a whiplash injury. Although there has been diagnostic ultrasound evidence of soft tissue injury following whiplash,54 Davis et al.55 reported on the soft tissue abnormalities utilizing MRI in nine whiplash patients. Three patients had injuries to the ligamentous structures, including two to the ALL and one to the interspinous ligament, a recognized pain generator. These injuries are compatible with the animal studies and cadaveric studies cited above. Utilizing CT scan imaging techniques, Dvorak and associates56 have indicated the importance of the alar ligaments in providing higher cervical level stability during whiplash. It was postulated that these ligaments may be irreversibly stretched or ruptured while the head is rotated and flexed during high-speed trauma, especially in a rear-end collision or unexpected impact. Although further studies are needed to confirm this potentially injurious mechanism, White and Panjabi34 have suggested that insufficient alar ligament support may lead to irritation of the spinal cord and brainstem elements, potentially contributing to pain and disability produced by soft tissue injuries. Many investigators are now realizing that this potential for central nervous system sensitization may, in addition to soft tissue injury, contribute to both acute and chronic pain following cervical acceleration, deceleration, axial compression, and distraction that occurs during whiplash injury (Table 55.1).34,36

Table 55.1: Summary of Soft Tissues Injured During the Phases of Whiplash Injury Based upon Animal, Cadaveric, Electromyographic, and Radiologic Studies Acceleration Phase

Deceleration Phase

Esophagus

Trapezius

Sternocleidomastoid

Splenius capitis

Longus colli

Semispinalis capitis

Anterior longitudinal ligament

Levator scapula

Alar ligament

Posterior longitudinal ligament

Transverse ligament

Alar ligament

Posterior longitudinal ligament

Transverse ligament

Cervical sympathetics

Tectorial membrane

Cervical nerve roots

Interspinous ligament Spinal cord/brainstem elements Cervical nerve roots

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CHRONIC PAIN FROM WAD WITH IMPLICATIONS FROM CENTRAL NEURAL MECHANISMS Although the majority of individuals improve over time, chronic pain following whiplash does indeed exist. Patients with chronic WAD, much like that occurring from acute whiplash, probably experience pain from many etiologies. The cervical disc, zygapophyseal joint, and soft tissue structures have all been implicated as potential pain generators and the complex interaction of these tissues may contribute to the perpetuation of chronic cases.11,12,57,58 However, many patients continue to experience persisting symptoms despite the absence of abnormalities on diagnostic tests, relief from therapeutic spine and soft tissue injections, and even cervical spine surgery. Many of these patients are labeled as myofascial pain patients, having a cadre of bizarre symptoms including sleep and psychological disturbances as well as nonradicular referred pain into the limbs and head.15 Although the exact etiology of chronic WAD remains elusive and a complete discussion of all the various causes is beyond the scope of this chapter, there are some recent theories to suggest that some patients may be experiencing a combination of cervical muscle and joint dysfunction as well as central neural hypersensitivity.15,36 Hopefully, an understanding of these potential pain mechanisms may help clinicians provide a more comprehensive treatment strategy for chronic WAD patients. Although persistent ligamentous damage may exist,2 some have found evidence of persistent dysfunction, reduced blood flow, and concomitant pain within the cervical musculature following whiplash injury. For example, Larsson et al.,59 using laser Doppler flowmetry, demonstrated that patients who had chronic neck pain following a car collision had impaired regulation of the microcirculation in painful trapezius muscles. During static contractions, the trapezius of these patients had a decreased microcirculatory flow compared to control subjects who actually demonstrated an increase in flow during activity. This relative reduction in flow may perpetuate muscular dysfunction secondary to the accumulation of metabolites, stimulation of afferents and associated gamma motor neurons, and reflex-mediated stiffness. However, Larsson et al. did not see an increase in neural excitability, but rather saw a reduction in EMG activity possibly related to pain inhibition or fatigue. Cervical muscular dysfunction has also been identified in patients with chronic WAD. In a study by Nederhand et al.,60 patients with chronic WAD type II were monitored with surface EMG during static postures, unilateral dynamic manual exercise, and upon relaxation after the exercises. Compared to control subjects, the whiplash patients had a decreased ability to relax the trapezius following activity. From this study, Nederhand at al. proposed that patients with WAD may acquire fear of movement and physical activity, which leads to guarding and a decrease ability to relax associated cervical musculature.61 Theoretically, this continued muscular contraction, reduction of blood flow, and perpetuation of muscle dysfunction, and fear-related avoidance lead to the vicious cycle of chronic pain following WAD. Therefore, an underlying disturbance in both the microcirculation with exercise and the inability for muscles to relax postexercise may contribute to the perpetuation of pain. Finally, there has been relative recent evidence to suggest the presence of abnormal central nervous system processing and central neural hypersensitivity following the whiplash injury.62,63 For example, Koelbaek et al.64 using pain pressure thresholds and VAS scores following infusion of saline both into painful and nonpainful tissues, reported that patients with chronic pain following whiplash had lower pressure pain thresholds and larger areas of pain with higher VAS scores compared to control subjects. These higher VAS scores and wider areas of pain following the saline infusion were present 604

Fig. 55.2 Causes of chronic soft tissue pain following whiplash include central nervous system hypersensitivity, muscle dysfunction, ligament damage, proprioception dysfunction, or more likely a complex interaction of these and other potential pain generators.

both in painful paracervical musculature as well as in nonpainful control muscles not involved in the whiplash such as the tibialis anterior. Similarly, Sterling et al.36 have found that these patients have heightened sensitivity to sensory stimuli such as heat and cold as well as increased mechanosensitivity of peripheral nerves to adverse neural tension, and deficits in proprioception of the head and cervical spine soon after injury. Difficulty with proprioception and hypersensitivity to sensory stimuli may help explain the perpetuation of symptoms not only from overlying muscle but deeper structures such as the cervical zygapophyseal joint and disc. Hypersensitivity of the nervous system and adverse neural tension, together with sclerotomal pain patterns referred from deeper structures, may also explain the myriad of nonradicular referral pain patterns seen in these perplexing patients.

SUMMARY In conclusion, cervical pain and upper limb symptoms following whiplash are usually due to cervical disc, zygapophyseal, and soft tissue injury. In the majority of cases, injury to soft tissue structures such as the supportive muscles and ligaments as evidenced by animal, cadaveric, and electromyographic studies occur due to the acceleration and deceleration. Fortunately, the majority of these injuries heal with time. Some patients, however, have continued symptoms and are often labeled as having myofascial pain. However, the clinician should also suspect persistent ligamentous injury, concomitant muscle and joint dysfunction, and possibly underlying central hypersensitivity as the cause of chronic WAD (Fig. 55.2).

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Cervical Spine ■ ii: Whiplash

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Epidemiology of Disc, Joint, and Root Pain in Whiplash

56

Yung Chen, Richard Derby and Byung-Jo Kim

INTRODUCTION Nearly 5% of the working population is significantly disabled by neck pain. It accounts for a significant proportion of occupational illness and disability and places a heavy load on insurance compensation systems. The etiology of neck pain is complex. The differential diagnosis of cervicalgia includes fracture, spondylosis, infection, tumor, congenital disorders, and inflammatory disorders such as rheumatoid arthritis. In the majority of the whiplash cases, pain is usually caused by mechanical disorders secondary to trauma. Neck pain resulting from a whiplash mechanism of injury is controversial and has attracted particular attention. A whiplash injury is typically defined as an injury to the cervical spine resulting from hyperextension and flexion of the head during a motor vehicle accident (Fig. 56.1). Sources of pain in whiplash patients are usually multifactorial. The primary affected anatomical structures of the cervical spine are perivertebral soft tissues, neuro-elements, intervertebral disc, and zygapophyseal joint (Fig. 56.2). Most whiplash-related neck pain is usually self-limiting, and can be adequately treated with conservative measures such as rest, nonsteroidal antiinflammatory agents, pain medications, muscle relaxants, and physical therapy. Patients failing to improve with this regimen may require further radiographic and interventional diagnostic work-ups. Although epidemiology in whiplash has been relatively well studied, few studies have adequately provided detailed analyses of the anatomical structures involved in chronic neck pain in whiplash patients. Increased knowledge about the size and extent of this problem is essential as it may facilitate predictions of the need for medical services.1 This chapter reviews the epidemiology of whiplash-induced neck pain and the studies addressing the anatomical structures involved.

EPIDEMIOLOGY OF WHIPLASH Motor vehicle accidents with a whiplash mechanism of injury are one of the most common causes of neck injuries, with an incidence of perhaps 1 million per year in the United States.2 The social and economic costs are tremendous. Twenty-five to 30 billion dollars are spent annually on treatment for neck discomfort without neurologic signs in whiplash patients in the United States alone.3 The costs of whiplash injury are expected to rise with increasing incidence. Whiplash injuries usually result in neck pain arising from injury to soft tissue, the disc, or zygapophyseal joint, and the etiology of this pain has been documented in animal and human studies. Headaches, reported in 82% of patients acutely, are usually of the muscle contraction type, and are often associated with greater occipital neuralgia related to C2 cervical nerve root injury, and less often to temporomandibular joint syndrome.4,5 Other frequent complaints include dizziness, paresthesia, postconcussion syndrome, and low back pain.6 Fifteen per-

cent of whiplash patients suffer severe pain for 1–3 years, and 26–44% of patients will develop long-term problems.7 Chronic whiplash has long been a source of controversy, in large part because most patients do not have a readily identifiable injury in either the acute or chronic stage. Chronic unremitting pain occurs in 5% of patients.8

Incidence and prevalence The incidence and severity of whiplash injury is increasing with the wider use of transport and the development of higher-velocity vehicles.9 Many epidemiologic studies have been reported from a number of countries utilizing automobile insurance company data. Considerable caution is necessary when comparing national statistics. Such statistics are dependent on complex social and legal variables, and cannot be used as an overall measure of incidence.10 The occurrence, severity, and duration of whiplash-related symptoms have been reported differently among different countries. Regional differences within the same country may also impact study results. Wide differences between countries in cultural attitude, insurance systems, or financial compensation may significantly impact statistical analyses. In an analysis of 300 cases showing lower whiplash incidence in Singapore relative to Australia,11 the author suggested that cultural differences in how whiplash was viewed in these two countries (e.g. as an illness, versus as an illness behavior) were a significant variable. A 1987 Quebec study showed increasing whiplash incidence.6 The overall incidence was 70 per 100 000 persons, but the rate in a Saskatchewan study was 700 per 100 000 persons. In this case, differences may be caused by regional variations in the insurance compensation system: a no-fault insurance system in Quebec versus a tort system in Saskatchewan. Legislation changes in Australia (the claimant now has to report the accident to the police and bear the first $317 of medical expense), afforded a substantial effect upon whiplash incidence. One year following the new law, whiplash reported incidences were 50–70% fewer than previous years, even though there presumably may have been more vehicles on the road. A recent study also supported the idea that financial compensation by insurance systems has a profound effect on the frequency and duration of whiplash claims, and that claimants recover faster if compensation for pain and suffering is not available. Cassidy et al.14 studied a population-based cohort of persons who filed insurance claims for traffic injuries in Saskatchewan, where the insurance system was changed from the tort compensation system to a no-fault system. After the introduction of no-fault, there was a 28% reduction in incidence, and the median time to the closure of claims was reduced by more than 200 days.

Prognosis Whiplash is associated with high costs and a prognosis that is variable and difficult to predict. A prospective study of 93 patients with 607

Part 3: Specific Disorders

Head rotates back

Head thrown forward

Seatback pushes torso forward

Fig. 56.1 (A) During a collision, the seat pushes the torso forward, resulting in hyperextension of the cervical spine, and (B) subsequent to the momentum of the restrained torso, the head is thrown forward resulting in hyperflexion of cervical spine. (Adapted, with permission, from an original image by Michael Melton, www.injuryresources.com)

Force from car seat B

A

cervical whiplash revealed that only 15% had persistent minor discomfort, but 43% of patients still had symptoms sufficiently severe to interfere with their ability to work 2 years after the injury.15 Many studies addressing prognostic factors have been published, but there have been various results. Hildingsson and Toolan15 found that acute symptoms, physical findings, forces and directions of impact, head rests, radiographs, and sex did not show prognostic

value. However, Evans2 suggested that some risk factors, including older age, interscapular or upper back pain, occipital headache, paresthesia at presentation, reduced range of cervical spine movement, objective neurologic deficits, preexisting degenerative osteoarthritic changes, and an upper-middle occupational category correlated with less favorable recovery. These data showed long-term disability in over 6% of patients, and patients with those risk factors did not

Areas of injury The rapid motion of the neck during a crash can result in a number of injuries – many of which are impossible to see on x-rays or MRI. Here are some of the injuries that have been shown after whiplash crashes 4

1. Rim lesions 2. Endplate avulsions 3. Tears of the anterior longitudinal ligament 4. Uncinate process

5

5. Articular subchondral fractures 6

6. Articular pillar

1 7. Articular process 2

8. Ligament tear

3 A

Facet joint

8 B

Intervertebral disc Neural element

Facet joint

7

Fig. 56.2 (A) Area of potential injury includes vertebral bodies, intervertebral disc, facet, and neuro-elements (Reproduced, with permission, from Lang J. Clinical Anatomy of the Spine 1993. Copyright Thieme Medical Publishers, New York). (B) The rapid motion of the neck during a crash can result in a number of injuries, many of which are impossible to see on X-rays or MRI. Here are some of the injuries that have been shown after whiplash crashes. 608

Section 3: Cervical Spine

return to work after 1 year. There was, however, only minimal association between poor prognosis and collision speed or severity and the extent of vehicle damage. In a recent study, risk factors for prolonged recovery time after whiplash injury were introduced.16 All vehicular-related injury reports and medical records of 4759 individuals, who sustained a whiplash injury in the province of Quebec, Canada, in 1987, were recruited, and the author followed these patients for up to 7 years. The author found that sociodemographic factors including older age, female sex, having dependants, and not being employed full-time each decreased the rate of recovery by 14–16%. Factors related to the crash conditions decreased the rate of recovery as follows: being in a truck or bus, 52%; being a passenger in the vehicle, 15%; colliding with a moving vehicle, 16%; and side or frontal collision, 15%. The median recovery time was 32 days, and 12% of subjects had still not recovered after 6 months. Signs and symptoms independently associated with slower recovery besides female gender and older age included neck pain on palpation, muscle pain, pain or numbness radiating from neck to arms, hands or shoulders, and headache. The presence of all these factors in females aged 60 predicted a median recovery time of 262 days, compared with 17 days for younger males aged without any of these factors. The author concluded that sociodemographic and crash-related factors, as well as several signs and symptoms, are predictive of a longer recovery period. An early intervention program was recommended to manage whiplash patients with these prognostic markers.

to evaluation. During separate evaluations, the joint was randomly blocked with either lidocaine or bupivacaine. Fifty-four percent of patients experienced neck pain relief, suggesting that cervical zygapophyseal joint pain was the most common source of chronic neck pain after whiplash. However, this study was limited, as the injection protocol may be compromised by placebo responses. A subsequent double blind, placebo-controlled study by the same group supported the importance of zygapophyseal joint pain.22 Two different local anesthetics and a placebo injection of normal saline were administered in random order in 68 consecutive patients referred for chronic neck pain. A positive diagnosis was made if the patient’s pain was completely and reliably relieved by each local anesthetic, but not by the placebo injection. This study showed that the cervical facet joints were the source of neck pain in 60% of the population with chronic pain after whiplash injury. The prevalence of C2–3 zygapophyseal joint pain was 50%, and the prevalence of lower cervical zygapophyseal joint pain was 49%. Although well-designed clinical studies have evaluated zygapophyseal joint as a possible source of chronic neck pain in whiplash patients, strong evidence correlating joint damage and neck pain in whiplash remain insufficient. To date, no controlled trials have examined whiplash patients closer to the time of injury, rather than years later. Further research studies are warranted to support the hypothesis of facet joints as pain generators for the chronic whiplash patients.

JOINT PAIN

During a whiplash injury, cervical nerve roots may be a secondary injury to disc protrusion or zygapophyseal joint trauma.24–26 The nerve roots are also susceptible to significant injury in the absence of more overt trauma to contiguous structures.25–27 During the extension phase of injury, the nerve root may become entrapped in a transiently narrowed neural foramen.25,26 Statistically significant reductions in the foramen diameter with increasing extension compared to the foraminal diameter at the neutral position have been observed.28 In addition, significant pressure increments have been related to head position. Farmer and Wisneski29 measured pressure in the neural foramina of C5, C6, and C7 nerve roots at various positions of the head and ipsilateral arm in eight fresh cadavers. Increasing neck extension led to significant pressure changes at each root tested, but the results with neck flexion were variable. The nerve initially compressed by neck extension may be subjected to a traction injury as the neck is thrown

The zygapophyseal joint has been considered as a possible source of whiplash patient pain (Fig. 56.3). Autopsy studies have shown structural spine damage, including joint injuries such as joint hemarthrosis, cartilage damage, and capsular ligament, in whiplash victims.17,18 Clinical studies have shown that cervical zygapophyseal joint pain is the most common etiology for chronic neck pain after whiplash, and the prevalence of specific cervical zygapophyseal joint involvement has also been reported. However, the studies have been limited, as this zygapophyseal joint-mediated pain was not diagnosed and confirmed using controlled diagnostic joint blocks.19–23 Barnsley et al.20 studied the prevalence of cervical zygapophyseal joint pain using double-blind, controlled, diagnostic blocks in 50 patients with a history of whiplash injury an average of 4 years prior

The cervical facet joints

ROOT PAIN

Normal gliding motion

Vertebral body

Facet joints

Intervertebral disc Front

Facet joints

Spinous process Front Fig. 56.3 The cervical facet joints. (Adapted, with permission, from an original image by Michael Melton, www.injuryresources.com) 609

Part 3: Specific Disorders

into a rebound flexion.25,26 This direct root trauma likely leads to intraneural vascular congestion and edema.25,26,30,31 Olmarker et al.30 studied edema formation in spinal nerve roots of the pig cauda equina following experimental compression at various rates, and found that edema formation was more pronounced after rapid onset of compression. They also found that intraneural edema may be more easily formed in nerve roots than peripheral nerves following compression injury.32 Few epidemiologic studies have evaluated root pain after whiplash. In 1953, Gay and Abbott25 reported that the most common complication after whiplash was cervical radiculopathy. In 50 patients who suffered from a whiplash injury to the neck for 4 years, 35 cases (70%) had intense pain in the posterior cervical region, with radiation of pain into the occipital region, shoulder girdle, or upper extremities. Pain was intermittent and often followed a pattern suggesting irritation of the fifth, sixth, or seventh cervical nerve root on one side. Eighteen cases (36%) had persistent cervical radiculopathic pain which was not improved by conservative treatment. Of these 18 cases, 13 had protruded intervertebral discs, and 5 had hypertrophic arthritis of the cervical spine confirmed by radiologic examination. All of these patients showed evidence of lower cervical root involvement. In a prospective outcome study, Jonsson et al.27 assessed the clinical and imaging findings of 50 patients (17 men, 33 women, mean age: 33 years) with whiplash-type neck distortions. Neck pain persisted in 24 patients (48%) and radiating pain developed within 6 weeks in 19 patients (38%). Eight patients with severe radiating pain and large disc protrusions on MRI had surgically confirmed fresh disc herniations. One recent study evaluated the outcome of therapeutic selective nerve root blocks for whiplash-induced cervical radicular pain. Of 21 patients with diagnosis confirmed by diagnostic selective nerve root injection, 12 patients (57%) demonstrated involvement of a single root, 8 patients (38%) of two roots, and 1 patient (5%) of three roots. The most commonly involved nerve root was C7 (40.6%) followed by C8 (25%), C6 (21.9%), C5 (9.4%), and T1 (3.1%). Of these patients, only 36.4% were working full time, and 81.8% were taking medication including opiates (22.7%) and prescription NSAIDs (31.8%). However, clinical efficacy of selective nerve root block for radicular pain after whiplash was not demonstrated.33

DISC PAIN Cervical discs have been suggested as one of the factors causing pain in both acute and late-phase whiplash. The most common site of disc injury is C5–6 in studies using radiographic evidence.27,34,35 This finding was supported by a recent kinematic analysis of cervical intervertebral discs during simulated whiplash.36 The authors suggested that whiplash trauma could potentially injure the cervical discs posteriorly via excessive 150° fiber strain and disc shear strain, or anteriorly via axial elongation. The 150° fiber and disc shear strains were the greatest at the posterior region of the C5–6 disc, consistent with previous reports that the vast majority of the disc injuries occurred at C5–6. Intervertebral disc damage has been consistently documented in pathologic and clinical investigations of whiplash injury patients. In an autopsy study, Taylor and Twomey18 showed clefts in the cartilage plates of the intervertebral discs in 15 of 16 spines from whiplash victims. Posterior disc herniation through a damaged anulus fibrosus was also found, suggesting that common disc injuries could cause the pain experienced by whiplash patients. Jonsson et al.27 demonstrated a high incidence of discoligamentous injuries in whiplash-type distortion through a 5-year follow-up outcome study. Fresh disc herniation was surgically confirmed in 20% of whiplash patients with persistent, severe radiating pain. In another long-term follow-up study, Watkinson et al.37 reviewed 10 years of whiplash patient follow-up data, and found that radiographically documented degenerative changes of the 610

cervical spine were present in 68% of patients, of whom 87% were symptomatic. The disc degeneration rate was higher in the whiplash patients when compared with age-matched controls. In a retrospective study, Hamer et al.38 provided evidence that whiplash patients are at an increased risk of premature disc degeneration. The incidence of previous whiplash injury in 215 unselected patients who underwent an anterior cervical discectomy and fusion was twice that of a control population of 800 general orthopedic outpatients. Another retrospective MRI study documented disc herniations causing cord impingement and occult anterior vertebral endplate fractures in whiplash patients.34 A clinical study demonstrated that 39% of whiplash patients without initial radiographic signs of disc degeneration developed degenerative changes within 5–10 years. Although this study was not an age-matched, controlled study, the results may support the hypothesis that whiplash trauma can accelerate disc degeneration.39 Although a few studies have reported pathologic MRI findings after whiplash injuries, there is only one published prospective study. Pettersson et al.35 performed clinical examination and MRI in 39 whiplash patients (20 women and 19 men, mean age: 32 years) at a mean of 11 days after trauma, and repeated the procedure at a 2-year follow-up visit. Thirty-three percent of whiplash patients (13 patients) showed herniated cervical discs with medullary impingement (15.4%) or dura impingement (17.9%) at the 2-year followup. Patients with medullary impingement had persistent or increased symptoms. The most common involved levels were C4–6, which corroborates previous studies.27,34,40 The authors suggested that MRI is a reliable study for deciding the treatment plan of patients with persistent arm pain, neurologic deficits, or clinical signs of nerve root compression. However, performing MRI in acute phase was not recommended due to the relatively high proportion of false-positive findings, although disc pathology was clearly one contributing factor to the development of chronic symptoms following whiplash injury.

SUMMARY A whiplash injury is typically defined as an injury to the cervical spine resulting from hyperextension and flexion of the head during a motor vehicle accident. Whiplash injury is one of the most common causes of neck injuries, with an incidence of perhaps one million per year in the United States. Five percent of whiplash patients have chronic, unremitting symptoms that may be attributed to unresolved injury, psychosocial factors, or the possibility of secondary gain. Although many studies have addressed this controversial subject, debate about the causes of chronic whiplash syndrome continues. In some patients, extensive studies in the absence of intense neck pain and prolonged aggressive therapy may promote the idea that something serious has occurred. To resolve the debate, more knowledge about the epidemiology of whiplash, including prevalence rates, real pathologic data, and prognostic markers are required. Studies of the individual anatomical structures which may be sources of chronic neck pain would help expand our knowledge of the pathophysiology of chronic whiplash syndrome, and permit the creation of practical clinical guidelines.

Acknowledgments We are grateful to Dr. Todd Billeci for editing the manuscript.

References 1. Guez M, Hildingsson C, Nilsson M, et al. The prevalence of neck pain: a populationbased study from northern Sweden. Acta Orthop Scand 2002; 73:455–459. 2. Evans RW. Some observations on whiplash injuries. Neurol Clin 1992; 10:975–997. 3. Kwan O, Fiel J. Critical appraisal of facet joint injections for chronic whiplash. Med Sci Monit 2002; 8:RA191–RA195.

Section 3: Cervical Spine 4. Keith WS. ‘Whiplash’-injury of the 2nd cervical ganglion and nerve. Can J Neurol Sci 1986; 13:133–137. 5. Packard RC. The relationship of neck injury and post-traumatic headache. Curr Pain Headache Rep 2002; 6:301–307. 6. Spitzer WO, Skovron ML, Salmi LR, et al. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining ‘whiplash’ and its management. Spine 1995; 20:1S–73S.

24. Borchgrevink GE, Smevik O, Nordby A, et al. MR imaging and radiography of patients with cervical hyperextension–flexion injuries after car accidents. Acta Radiol 1995; 36:425–428. 25. Gay JR, Abbott KH. Common whiplash injuries to the neck. JAMA 1953; 152:1698–1704. 26. Seletz E. Whiplash injuries: Neurophysiologic basis for pain and methods used for rehabilitation. JAMA 1958; 168:1750–1755.

7. Johnson G. Hyperextension soft tissue injuries of the cervical spine – a review. J Accid Emerg Med 1996; 13:3–8.

27. Jonsson H Jr, Cesarini K, Sahlstedt B, et al. Findings and outcome in whiplash-type neck distortions. Spine 1994; 19:2733–2743.

8. Macnab I. The ‘whiplash syndrome.’ Orthop Clin North Am 1971; 2:389–403.

28. Yoo JU, Zou D, Edwards WT, et al. Effect of cervical spine motion on the neuroforaminal dimensions of human cervical spine. Spine 1992; 17:1131–1136.

9. Schutt CH, Dohan FC. Neck injury to women in auto accidents. A metropolitan plague. JAMA 1968; 206:2689–2692. 10. Mayou R, Radanov BP. Whiplash neck injury. J Psychosom Res 1996; 40:461–474. 11. Balla JI. The late whiplash syndrome: a study of an illness in Australia and Singapore. Cult Med Psychiatry 1982; 6:191–210.

29. Farmer JC, Wisneski RJ. Cervical spine nerve root compression. An analysis of neuroforaminal pressures with varying head and arm positions. Spine 1994; 19: 1850–1855.

12. Awerbuch MS. Whiplash in Australia: illness or injury? Med J Aust 1992; 157: 193–196.

30. Olmarker K, Rydevik B, Holm S. Edema formation in spinal nerve roots induced by experimental, graded compression. An experimental study on the pig cauda equina with special reference to differences in effects between rapid and slow onset of compression. Spine 1989; 14:569–573.

13. McDermott FT. Reduction in cervical ‘whiplash’ after new motor vehicle accident legislation in Victoria. Med J Aust 1993; 158:720–721.

31. Rydevik B, Brown MD, Lundborg G. Pathoanatomy and pathophysiology of nerve root compression. Spine 1984; 9:7–15.

14. Cassidy JD, Carroll LJ, Cote P, et al. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 2000; 342:1179–1186.

32. Slipman CW, Lipetz JS, DePalma MJ, et al. Therapeutic selective nerve root block in the nonsurgical treatment of traumatically induced cervical spondylotic radicular pain. Am J Phys Med Rehabil 2004; 83:446–454.

15. Hildingsson C, Toolanen G. Outcome after soft-tissue injury of the cervical spine. A prospective study of 93 car-accident victims. Acta Orthop Scand 1990; 61: 357–359.

33. Slipman CW, Lipetz JS, Jackson HB, et al. Outcome of therapeutic selective nerve root blocks for whiplash-induced cervical radicular pain. Pain Physician 2001; 4:167–174.

16. Suissa S. Risk factors of poor prognosis after whiplash injury. Pain Res Manag 2003; 8:69–75.

34. Davis SJ, Teresi LM, Bradley WG Jr, et al. Cervical spine hyperextension injuries: MR findings. Radiology 1991; 180:245–251.

17. Jonsson H Jr, Bring G, Rauschning W, et al. Hidden cervical spine injuries in traffic accident victims with skull fractures. J Spinal Disord 1991; 4:251–263.

35. Pettersson K, Hildingsson C, Toolanen G, et al. Disc pathology after whiplash injury. A prospective magnetic resonance imaging and clinical investigation. Spine 1997; 22:283–287; discussion 288.

18. Taylor JR, Twomey LT. Acute injuries to cervical joints. An autopsy study of neck sprain. Spine 1993; 18:1115–1122. 19. Aprill C, Bogduk N. The prevalence of cervical zygapophyseal joint pain. A first approximation. Spine 1992; 17:744–747. 20. Barnsley L, Lord SM, Wallis BJ, et al. The prevalence of chronic cervical zygapophyseal joint pain after whiplash. Spine 1995; 20:20–25; discussion 26. 21. Bogduk N, Marsland A. The cervical zygapophyseal joints as a source of neck pain. Spine 1988; 13:610–617. 22. Lord SM, Barnsley L, Wallis BJ, et al. Chronic cervical zygapophyseal joint pain after whiplash. A placebo-controlled prevalence study. Spine 1996; 21:1737–1744; discussion 1744–1745.

36. Panjabi MM, Ito S, Pearson AM, et al. Injury mechanisms of the cervical intervertebral disc during simulated whiplash. Spine 2004; 29:1217–1225. 37. Watkinson A, Gargan MF, Bannister GC. Prognostic factors in soft tissue injuries of the cervical spine. Injury 1991; 22:307–309. 38. Hamer AJ, Gargan MF, Bannister GC, et al. Whiplash injury and surgically treated cervical disc disease. Injury 1993; 24:549–550. 39. Hohl M. Soft-tissue injuries of the neck in automobile accidents. Factors influencing prognosis. J Bone Joint Surg Am 1974; 56:1675–1682. 40. McKenzie JA, Williams JF. The dynamic behaviour of the head and cervical spine during ‘whiplash’. J Biomech 1971; 4:477–490.

23. Sapir DA, Gorup JM. Radiofrequency medial branch neurotomy in litigant and nonlitigant patients with cervical whiplash: a prospective study. Spine 2001; 26: E268–E273.

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PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ i: Cervical Radicular Pain

CHAPTER

Cervical Radicular Pain: An Algorithmic Methodology

57

Zacharia Isaac and Curtis W. Slipman

Employing an algorithmic methodology for the evaluation of cervical radicular pain has numerous clinical benefits. It simultaneously combines elegant simplicity with diagnostic meticulousness. It helps generate a comprehensive differential diagnosis in complex conditions and prioritizes these diagnoses. To use such an algorithm effectively, however, it is mandated that the clinician gain the necessary fund of knowledge behind the various branches in the decision tree so that each patient is treated individually to optimize functional outcome. The old adage that ‘a smart man knows the rules, but a wise man knows the exceptions’ holds true. The evaluation of cervical radicular pain employs an overall assessment of historical and examination features, electrodiagnostic testing, diagnostic imaging, and diagnostic anesthetization of a suspected pain generator. A basic tenet underpinning the use of the above tools is that an accurate diagnosis allows for specific treatment and therefore better outcomes. Cervical radiculopathy is defined as a dysfunction of a cervical spinal nerve root with resultant myotomal deficit or reflex change or an abnormal electromyographic study. In contrast, cervical radicular pain is pain that radiates in the distribution of a cervical dermatome or dynatome. By definition, there does not need to be focal myotomal deficit, reflex changes, or electromyographic evidence of radiculopathy. Hence, radicular pain can often exist without radiculopathy, and conversely, radiculopathy can be present at times without radicular pain. Involvement of the ventral spinal root results in myotomal deficit and electromyographic evidence of denervation. Involvement of the dorsal sensory nerve root fibers result in pain and does not result in a focal myotomal deficit and is not detectable on electromyography. There often is involvement of both, but the clinical presentation can be one where either motor or sensory symptoms predominate.

ANATOMY Anatomy of the cervical spine is covered in more detail in Chapter 46 by Russell Gilchrist. A brief discussion of the relevant cervical spine anatomy is discussed here to provide the reader with some background information. The cervical spine is the most mobile segment of the axial skeleton, and serves to support and move the head, and protects the neural elements within. There are seven cervical vertebrae which can be divided into upper (C1–2 or atlantoaxial joint) and lower segments (C3–C7). The C1 vertebrae (atlas) and the C2 (axis) are different in function than the lower segments. The atlas is a ring-like structure without a vertebral body. The lateral masses of C1 articulate with the occipital condyles above and the axis below. The axis has a vertebral body and an odontoid process which is the congenitally fused body of the atlas. The C1–2 joint allows for 58% of all cervical rotation, or 45° of rotation in either direction.1 The atlantooccipital articulation permits 10° of flexion and 25° of extension.2 The C2–3 segment represents a mechanically transitional area where flexion, extension, and lateral bending become increasingly permit-

ted, and is the most common zygapophyseal joint associated with whiplash-related cervicogenic headaches. The lower cervical vertebrae (C3–C7) articulate via the intervertebral discs anteriorly and the cervical zygapophyseal joints posteriorly. The zygapophyseal joint has a 45° orientation relative to the horizontal plane which allows for ipsilateral bending and rotation. Lateral bending occurs primarily at C3–4 and C4–5. The C3–C7 segments have articulations known as uncovertebral joints, or joints of Luschka, along the posterolateral border of the intervertebral disc, and are in the anteromedial portion of the intervertebral foramen. These articulations are not true synovial joints, but can hypertrophy with associated disc degeneration and result in a narrowing of the intervertebral foramen and potential neural compromise. Each spinal nerve arises from the spinal cord by two roots. The ventral root contains motor efferent fibers from alpha motor neurons in the ventral horn of the spinal cord. The dorsal root carries primary sensory afferent fibers from cells in the dorsal root ganglion. The dorsal and ventral spinal roots combine to form the spinal nerve. This spinal nerve then divides into two branches, a dorsal primary ramus and a ventral primary ramus. The dorsal ramus divides and supplies innervation to muscular, cutaneous, and articular branches for posterior neck structures and the ventral ramus supplies the prevertebral and paravertebral muscles and forms the brachial plexus which subsequently innervates the upper limb. Cervical facet syndrome can often mimic radicular pain and refer symptoms to the limb. The differentiation between facetogenic or radicular symptoms is facilitated by an awareness of two facts. Firstly, the axial neck symptoms are often more severe than extremity symptoms (Fig. 57.1).3–7 Secondly, the cervical facet joint does not refer symptoms distal to the elbow. Please see Figure 57.2, which illustrates pain referral patterns of the cervical zygapophyseal joints. The cervical zygapophyseal joints are innervated by medial branches of dorsal rami from C3–4 to C6–7 that run above and below a given level. The superficial medial branch of the C3 dorsal ramus, or the third occipital nerve, innervates the C2–3 joint.8 The ventral rami of C1 innervate the atlanto-occipital joint, and C2 rami innervate the atlantoaxial joint. The C1 nerve root contains motor fibers only and emerges from the spinal canal at the atlanto-occipital junction. The cervical intervertebral discs receive innervation in the outer third of the anulus. The anterior portion of the disc is innervated via the vertebral nerve (derived from the gray rami communicans of the sympathetic trunk at midcervical levels and the branches of the stellate ganglion at lower levels). The posterior and lateral portions of the disc receive innervation via the sinuvertebral nerve (recurrent nerve of Luschka, derived from a branch of the vertebral nerve and ventral ramus at each level). The sinuvertebral nerve innervates the disc and the disc above a given segment, the pedicle, posterior longitudinal ligament, posterior vertebral periosteum, epidural veins, and dorsal dura mater. The cervical spinal cord is approximately 10 mm 613

Part 3: Specific Disorders Neck pain> Arm pain

Constitutional symptoms? Yes

No

Evaluate with ESR, CBC, bone scan, MRI with gadolinium, age appropriate cancer screening, possible subspecialist referral

Trauma ?

No

Conservative care for 8 weeks Education Posture and activity modification NSAIDS Physical therapy Worksite ergonomic evaluation

Yes

Plain films, trauma series if acute flexion/extension views if no fracture and if symptoms are persistent then MRI C-spine

No fracture and no gross segmental instability

Fracture or gross instability

Conservative care for 8 weeks Education Posture and activity modification NSAIDS Physical therapy Worksite ergonomic evaluation

Cervical fusion

Failure to improve or frequent recurrence

MRI of the cervical spine

Medical etiology Institute appropriate diagnosis and treatment

Biomechanical disorder

Failure to improve or frequent recurrence

Fig. 57.1 Algorithm: extremity symptoms greater than axial symptoms.

Diagnostic Algorithm table

C2−3

C2−3 C2−3 C3−4

C4−5

C3−4

C3−4

C5−6

C5−6

C5−6 C6−7

Fig. 57.2 Facet joint pain referral patterns for cervical facet joints C2–3 through C6–7. 614

Section 3: Cervical Spine

in diameter, and the vertebral canal averages 17 mm in diameter. The cervical central canal is almost twice as wide laterally as it is in the anteroposterior direction and is widest at C3–5. In contrast, the thoracic spinal canal is more round and narrow. The radicular complex of ganglia, spinal nerve root, and surrounding sheath account for 20– 35% of the cross-sectional area of the foramen.9 The cervical foramen are widest at C2–3 and progressively decrease in size to the C6–7 level. This diminution in size, combined with the increased segmental motion in the lower cervical spine, likely affects the incidence of degenerative disc disease in the cervical spine and resultant cervical radiculopathy. Cervical radiculopathy secondary to spondylosis most commonly affects the seventh (60–70%), sixth (16–25%), eighth (4–10%), and fifth (2%) cervical spinal nerves.10–12 In younger patients, cervical radiculopathy is more commonly secondary to trauma or disc herniation whereas in older individuals it is often secondary to uncovertebral hypertrophy with resultant foramenal stenosis. Determining the symptomatic nerve root often begins with asking the patient to describe the areas of pain. Cervical dermatomal charts were first studied in the late nineteenth century by Sherrington;13,14 however, patients with radicular symptoms may have symptoms other than the dermatome implicated by imaging studies. A dynatome is a pattern of referred symptoms, and cervical dynatomes for cervical nerve roots C4 through C8 have been studied. Slipman et al.’s dynatomal mapping15 derived cervical spinal nerve root stimulation referral patterns by mechanically stimulating a given spinal nerve and asking patients to delineate areas of symptom referral (Fig. 57.3). It has been demonstrated that there is overlap between dermatomal and dynatomal maps; however, symptoms can be commonly referred outside of a given dermatome. This may be secondary to the high incidence of intrathecal anastomoses between cervical spinal nerve roots, as high as 61% between the dorsal nerve roots and 10% for the ventral roots.16 Please see Figure 57.4, which demonstrates different types of intrathecal anastomoses noted by Moriishi et al. This high incidence of anastomoses in the dorsal roots can result in atypical referral patterns. For example, the little finger is classically involved in patients with C8 radicular pain, however 30% of C6 nerve root stimulations can produce little finger symptoms. Also noted was that the index finger, classically involved in patients with C6 or C7 radicular pain, can be involved in 24% of C8 nerve root stimulations.15 Other possible factors that may confound the evaluation include somatic referral of axial pain which can often mimic radicular pain, conjoined nerve roots, multilevel neural compression, concomitant musculoskeletal diagnoses, concomitant peripheral entrapment syndromes, and psychological distress due to chronic pain.

PATHOPHYSIOLOGY OF RADICULAR PAIN The degenerative cascade that occurs with age likely begins with degeneration of the cervical intervertebral disc. Viscoelastic properties of the disc change trend toward desiccation as age-related alterations in the chemical composition of the nucleus pulposus and anulus fibrosus occur. The disc loses height and bulges posteriorly into the canal by a hoop tension effect. The loss of disc height anteriorly results in infolding of the ligamentum flavum and facet joint capsule posteriorly. This results in a decrease in both the size of the central canal and neural foramen. Osteophytes form around the disc margins, uncovertebral articulations, and the zygapophyseal joints. The uncovertebral articulations, which represent a degenerative cleft on the posterolateral and foramenal region of the vertebral body, hypertrophy, which results in foramenal narrowing. The resultant decrease in canal size can result in compromise of the spinal nerve roots or spinal cord. Mechanical compression of the nerve root may lead to motor weakness or sensory deficits. Radicular pain is generally thought to be secondary to an inflammatory response and subsequent involvement of the nerve

root. Increased permeability within intraneural blood vessels result in edema of the nerve root. The dorsal root ganglion has been implicated in the pathogenesis of radicular pain and radiculopathy. Chronic edema and fibrosis within the nerve root can increase the sensitivity of the nerve root to pain by lowering the excitation threshold.17 Much of the research investigating the biochemical pathophysiology of radiculopathy has been performed in the lumbar spine. The relative abundance of studies investigating lumbar radiculopathy reflects its higher clinical incidence compared to cervical radiculopathy. Given the relative paucity of studies examining the biochemical mediators involved in cervical radicular pain, one needs to make a leap of faith to conclude that parallels exist with the lumbar spine. While these parallels may exist for cervical radicular pain due to disc protrusions, it may not be the case in patients with cervical radiculopathy due to foramenal narrowing due to uncovertebral hypertrophy, or whiplash-induced posttraumatic radicular pain. A discussion of some of the salient research performed in the lumbar spine is included below. It may be reasonable to conclude that many of the same biochemical pathways are involved in some etiologies of cervical radicular pain. Biochemical mediators of pain released from the cell bodies of the sensory neurons located in the dorsal root ganglion lower the impulse propagation threshold and biochemical mediators released from the intervertebral disc activate the arachidonic acid cascade. There have been numerous studies demonstrating a biochemical inflammatory process mediating pain in radiculopathy. Saal et al. found elevated phospholipase A 2 in disc material obtained from patients treated surgically for radiculopathy.18 Phospholipase A2 is the rate limiting step in the arachidonic acid pathway, which subsequently generates prostaglandins and leukotrienes.19 Prostaglandin E2 has been shown to be elevated in disc material at the time of surgery, and it has been shown to play a role in sensitizing nociceptors to bradykinins.20 Additionally, phospholipase A 2 has been shown to be neurotoxic.21 In work by Takahashi and co-investigators, disc material obtained at surgery in humans was assayed and cultured. They studied disc protrusion, extrusion, and sequestration. They found that with disc protrusion there was an increased number of chondrocytes. In contrast, with extrusion and sequestration, there were an increased number of histiocytes, fibroblasts, and endothelial cells with relatively few chondrocytes.22 Cytokines are expressed by these cells and there is no apparent difference in the groups of cytokines produced when comparing disc protrusion, extrusion, or sequestration. Betamethasone added to the cell cultures of disc materials inhibited cytokine and prostaglandin E2 production. In a study by Doita et al., disc samples obtained from surgical patients with an extrusion or sequestration showed increased granulation tissue and increased monocytes expressing interleukin-1.23 Interleukin-1 is known to stimulate inflammatory mediators and proteolytic enzymes including plasminogen activator, collagenase, and stromelysis. Kang and investigators assayed and compared disc tissue from patients being operated on for scoliosis and a herniated disc. They observed elevated levels of matrix metalloproteinase, nitric oxide, prostaglandin E2, and interleukin-6 in the herniated disc group. Concentrations of interleukin-1, tumor necrosis factor and interleukin-1 receptor antagonist protein were not appreciably increased or different in either group.24 Matrix metalloproteinase-3, inhibitor of matrix metalloproteinase-1, calcitonin gene-related peptide, vasoactive intestinal peptide, and substance P have all been associated with disc degeneration.25–29 It has been postulated that these inflammatory mediators play a role in lumbar radicular pain. Immune responses to nucleus pulposus in the vascular space has been theorized to be a mechanism of chronic inflammation. Work by Gertzbein demonstrated significant elevation in the lymphocyte transformation test, a measure of the cellular immune response.30 IgM titers were also increased in 2 of 3 patients with discogenic back pain or sciatica.31 These changes in the biochemical milieu contribute to the inflammatory response and subsequent hypersensitivity of the nerve root to stimulation.32–36 615

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10 30 50 70 90

10 30 50 70 90

% 0 20 40 60 80 100

% 0 20 40 60 80 100

B

A

10 30 50 70 90

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C

% 0 20 40 60 80 100

D

Fig. 57.3 Dynatomal maps for cervical spinal nerve roots C4–7. Pain referral patterns for cervical spinal nerve roots undergoing provocative stimulation. (A) is spinal nerve root C4. (B) is spinal nerve root C5. (C) is spinal nerve root C6. (D) is spinal nerve root C7. 616

Section 3: Cervical Spine Type A

Type B

Type C

Type D

Dura mater

Posterior

Anterior Fig. 57.4 An illustration of several types of intrathecal anastomoses. The presence of intrathecal anastomoses may in part account for the variability of pain referral pattern in clinical settings.

Cervical radicular pain can occur in the absence of significant degenerative changes in patients with a history of trauma. Whiplash events can injure many structures in the spine including the muscles and ligaments, intervertebral disc, bony structures, zygapophyseal joints, and cervical spinal nerve roots. There is a paucity of literature focusing on nerve root injury secondary to a whiplash event. Keith in 1986 described an observational case series of 14 patients with persistent post-whiplash symptoms which included unilateral occipital and suboccipital pain, tenderness, and hypoesthesia. The author postulated a causative injury to the second cervical ganglion and nerve root.37 Örtengren et al. confirmed the presence of gangliar and radicular injury in whiplash in an experimental pig model. Using pigs in simulated flexion–extension whiplash events, Örtengren was able to show increased gangliar cytoplasmic uptake of Evans blue, a dye usually excluded from this intracellular region in healthy ganglion cells. Increased dye uptake was found most frequently in the C4–C7 spinal nerves, and was not found in a control group of pigs that underwent a sham whiplash simulation. The author postulated that transient elevations in intraforaminal pressure are the cause of the neural injury. These pressure increases are due to two factors: mechanical load on the foramen itself due to discordant supra- and subjacent vertebral motions, as well as spikes in intraforaminal venous pressure due to nearby alterations in pressure in the epidural venous plexa.38 Exact values for such pressures in humans have yet to be elucidated, if indeed this mechanism is the cause of spinal nerve injury in whiplash. Studies have described neuronal malfunction in response to axonal injury, leading some to consider distal axonal damage as a possible source of dorsal root ganglion injury in whiplash.39 The underlying cause of neural damage in whiplash remains unresolved. Symptomatology suggestive of radicular injury, including radiating pain, is reported widely in the literature. Objective dermatomal hypoesthesia has been a relatively rare finding, however.39,40 Cervical nerve root injury can occur in the absence of MRI correlate.41 In a study by Slipman et al., patients with clinical evidence of radicular pain, as demonstrated by a positive Spurling’s sign or a positive upper extremity root tension sign in combination with increased pain during extension or ipsilateral rotation, without any corroborative pathology with advanced cervical imaging, underwent diagnostic selective nerve root blocks to identify the pain generating spinal nerve. Subsequent therapeutic selective nerve root

blocks were given with only 14% of patients achieving a good or excellent outcome. A transient steroid effect was noted in 59% of patients. The authors concluded that selective nerve root blocks using glucocorticoid are not an effective treatment for whiplash-induced cervical radicular pain.42 The poor outcomes reported suggest an underlying etiology that does not include an inflammatory response, thereby illustrating that there is likely a multitude of mechanisms by which cervical radicular pain can develop and be perpetuated.

CLINICAL ASSESSMENT History Symptoms related to the cervical spine can be broadly categorized as predominantly axial pain, extremity pain, or myelopathy. Combinations of the above are often present, but making this initial categorization helps with generating a differential diagnosis and further instituting treatment. Patients with cervical radicular pain will often complain of symptoms in the upper limb which are worse than axial neck pain, and symptoms are typically exacerbated with sustained neck position, neck extension, neck rotation, and ipsilateral limb abduction with elbow extension. Symptoms are often alleviated by positional shifting, maintaining a neutral posture to the spine, avoidance of neck rotation, and overhead abduction with elbow flexion, also known as Bakody’s sign (Fig. 57.5). Conditions such as cervical discogenic pain/cervical internal disc disruption syndrome and cervical facet joint syndrome cause a predominance of axial neck pain but can refer symptoms to the limb without the compression or involvement of the cervical spinal nerve root. In contrast to cervical facet-mediated pain, the cervical disc can refer symptoms into the extremity that is distal to the elbow (Fig. 57.6).43 This mechanism is termed somatic referral, which was previously known as sclerotomal referral. This referred pain may be via central mechanisms. Patients with this syndrome will often describe axial pain to be greater than limb pain. In contrast, radicular pain will more commonly have limb pain greater than axial pain. Identifying whether the referred symptoms are secondary to radicular pain versus somatic referral can often be ascertained through clinical assessment. Cervical myelopathy can occur simultaneously with radiculopathy (myeloradiculopathy). The 617

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Fig. 57.5 Bakody’s overhead abduction sign. Patients with cervical radicular pain due to a herniated disc experience relief of discomfort in this position due to less tension on the cervical spinal nerve root.

identification of myelopathy is critical because a specific subset of patients will require surgery and their outcomes are improved when this decision is not delayed. Patients with myelopathy can present with different patterns in which upper motor neuron symptoms predominate secondary to injury to the spinal cord (Fig. 57.7): (1) transverse lesion syndrome, in which the corticospinal, spinothalamic, and posterior cord tracts were involved with almost equal severity and which is associated with the longest duration of symptoms, suggesting that this category may be an end stage of the disease; (2) anterior cord or motor system syndrome, in which corticospinal tracts and anterior horn cells are involved, resulting in motor weakness and spasticity with relative preservation of sensation – this is usually due to an anterior spinal artery infarction, which is a single artery located in the anterior median fissure and supplies the anterior two-thirds of the spinal cord; (3) central cord syndrome, in which motor and sensory deficits affected the upper extremities more severely than the lower extremities – this is usually seen in syringomyelia or hydromyelia, and trauma; (4) Brown-Séquard syndrome, which consists of ipsilateral motor deficits and ipsilateral loss of vibration and proprioception, with contralateral sensory deficits to pain and temperature – this is most commonly seen after trauma;. and (5) myeloradiculopathy or brachialgia and cord syndrome, which consists of radicular pain in the upper extremity along with motor and/or sensory long-tract signs.

An algorithmic approach Treatment of a patient’s pain complaints should employ a diagnosisspecific approach. Obtaining a specific diagnosis will ensure that the best treatment is instituted for a given complaint. Treatment of cervical radicular pain involves a spectrum of treatment options which include education for the patient, activity and postural and worksite modifications, therapeutic exercise, adjunctive modalities, cervical traction, pharmacologic measures, fluoroscopically guided injection procedures, and surgical decompression. Treatment should be individualized and goal oriented to ensure successful patient outcomes. Details of the different treatment options are discussed in more depth in Chapters 59–61. When historical and examination features are associated with corroborative imaging, the diagnosis is not a dilemma. However, in clinical

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situations where the affected nerve root is in question, such as when there is a lack of corroborative imaging abnormalities, or multiple compressive abnormalities are present and the examination is inconclusive, electrodiagnostic studies (EDX), including electromyography and nerve conduction studies, can help identify physiologic evidence of nerve injury. EDX can be helpful to identify the affected nerve root, or to discriminate other diagnoses that can mimic radicular pain, such as plexopathy or peripheral nerve entrapments. When electromyography is also inconclusive, functional testing can be employed to identify the pain generator. Diagnostic selective nerve root blocks can be helpful to identify radicular pain, and the specifically involved root. Employing a diagnostic algorithm to determine the affected root should emphasize minimizing the number of interventions so as to obtain a diagnosis with the fewest injections. In cases where a myotomal deficit is present or a depressed reflex is present, these are often the most useful clues to determine the affected spinal nerve root. Sensory disturbances are much less helpful because of the dual dermatomal innervation of a given skin segment, and the relatively common peripheral entrapments in the upper limb may further obscure the diagnosis. The pain referral pattern can be helpful and should be compared with known dermatomal and dynatomal maps. Sequential diagnostic selective nerve root blocks, described in more detail below, can be used to anesthetize the suspected injured nerve roots to determine which nerve root is a significant contributor to the patient’s pain. Patients with cervical spine complaints can be categorized into four groups that are determined by the presence or absence of spondylotic changes and whether or not there is a history of trauma. This schema creates the following four categories: (1) atraumatic spondylotic radicular pain, (2) traumatic spondylotic radicular pain, (3) traumatic nonspondylotic radicular pain, and (4) atraumatic nonspondylotic radicular pain. The diagnoses that cause radicular pain in each of these groups vary, and hence treatment is different.

Atraumatic spondylotic radicular pain Cervical degenerative disc disease is exceedingly common, and its incidence increases with aging. Over half of the middle-aged population has radiologic or pathologic evidence of cervical spondylosis.44,45 Only a minority of these individuals become clinically symptomatic and develop axial neck pain, cervical radicular pain, or cervical myelopathy. The etiology of axial neck pain is often secondary to either musculoskeletal sprain and strain, discogenic pain secondary to cervical internal disc disruption syndrome, or cervical facet syndrome. These disorders typically have a predominance of axial pain with relatively minor or no extremity symptoms. In contrast, patients with predominance of scapular and extremity symptoms more commonly have involvement of the cervical spinal nerve root or spinal cord itself. When determining the symptomatic spinal nerve root in patients with atraumatic cervical radicular pain, the clinician can often employ parsimony and thus one or two predominant pain generators can often be established. Many patients with atraumatic spondylotic cervical radicular pain present with typical historical and examination features, and corroborative imaging. For these patients, establishing a pain generator and an algorithm for treatment is more straightforward (Fig. 57.8). In the presence of severe weakness and/or progressive weakness, surgical decompression is considered the intervention of choice. Determining if the weakness is progressive requires skillful neurological testing, and a detailed understanding of the Medical Research Council 0 to 5 scale manual muscle testing technique. Additionally, the patient should be asked as to whether they are aware of progressive weakness and of any functional deficits relating to the affected limb. In the absence of progressive weakness, conservative options such as pharmacologic

Section 3: Cervical Spine C2–3 discogram pain referral map 10 30 50 70 90

% 0 20 40 60 80 100 N=9

C3–4 discogram pain referral map 10 30 50 70 90

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C4–5 discogram pain referral map 10 30 50 70 90

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Fig. 57.6 Cervical discogenic pain referral patterns based on provocative discography.

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% 0 20 40 60 80 100 N=27

C6–7 discogram pain referral map 10 30 50 70 90

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Fig. 57.6—Cont’d.

measures, physical therapy, and injections targeted toward the affected spinal nerve root can be used. If conservative measures fail to bring adequate pain relief and restoration of function, surgical options of percutaneous or open decompression may be considered.

Traumatic spondylotic cervical radicular pain In patients with traumatic cervical radicular pain, multiple spinal and extraspinal structures may be injured. Degenerative spondylotic changes that are present on imaging often predate the new injury and sometimes mislead the clinician as to the pain generator. In some cases, a new herniated disc may make obvious the pain generator, but this is the case in only a minority of patients. Spinal structures such as the muscles, tendons and ligaments of the spine, cervical zygapophyseal joints, spinal nerve roots, and the intervertebral disc itself can become injured and cause axial neck pain with or without an extremity component which may mimic radicular pain. Extraspinal structures such as the shoulder, elbow, and wrist can become concomitantly injured and mimic or be present along with radicular pain. 620

The diagnostic algorithm in this instance is more complicated and may require addressing multiple diagnoses (Fig. 57.9). This concept cannot be overemphasized. When making a medical diagnosis the law of parsimony is applied, but this rule could lead the spine clinician astray when evaluating a patient who sustained trauma. In determining the symptomatic spinal nerve root in patients with traumatic cervical radicular pain, attention to underlying degenerative narrowing may provide clues as to the spinal nerve roots that may be more readily injured. The patient’s pain referral pattern should be compared to known dermatomal and dynatomal maps, and examination should attempt to identify reflex changes and myotomal deficit to determine if the degenerative changes on imaging are of clinical relevance. In the absence of a correlation, electromyographic studies may be helpful to determine if radiculopathy is present. Unfortunately, in cases where reflexes and myotomal strength is normal, electromyographic studies are also often unrevealing. In these instances, fluoroscopically guided diagnostic selective nerve root anesthetization may be helpful in establishing a diagnosis of cervical radicular pain. Upon establishment of a diagnosis, therapeutic interventions such as pharmacologic

Section 3: Cervical Spine

Principal fiber tracts of spinal cord Fasciculus gracilis Fasciculus cuneatus

Septomarginal fasciculus (oval bundle) Interfascicular fasciculus (comma tract)

Dorsolateral tract (fasciculus) (of Lissauer)

Lateral corticospinal (pyramidal) tract (crossed)

Dorsal (posterior) spinocerebellar tract

Rubrospinal tract Lateral (medullary) reticulospinal tract

Lateral spinothalamic tract and spinoreticular tract Ventral (anterior) spinocerebellar tract

Ventral (anterior) or medullary (pontine) reticulospinal tract

Spinoolivary tract

Vestibulospinal tract

Spinotectal tract

Ventral (anterior) corticospinal tract (direct)

Ventral (anterior) spinothalamic tract

Tectospinal tract Medial longitudinal (sulcomarginal) fasciculi

Fasciculus proprius

Ascending pathways Descending pathways Fibers passing in both directions Areas affected

A

Principal fiber tracts of spinal cord Fasciculus gracilis Fasciculus cuneatus

Septomarginal fasciculus (oval bundle) Interfascicular fasciculus (comma tract)

Dorsolateral tract (fasciculus) (of Lissauer)

Lateral corticospinal (pyramidal) tract (crossed)

Dorsal (posterior) spinocerebellar tract

Rubrospinal tract Lateral (medullary) reticulospinal tract

Lateral spinothalamic tract and spinoreticular tract Ventral (anterior) spinocerebellar tract

Ventral (anterior) or medullary (pontine) reticulospinal tract

Spinoolivary tract

Vestibulospinal tract

Spinotectal tract

Ventral (anterior) corticospinal tract (direct)

Ventral (anterior) spinothalamic tract Fasciculus proprius

B

Tectospinal tract Medial longitudinal (sulcomarginal) fasciculi Ascending pathways Descending pathways Fibers passing in both directions Areas affected

Fig. 57.7 (A) Transverse cord syndrome: global involvement of the spinal cord with both motor and sensory affected. (B) Anterior cord syndrome: involvement of the anterior portion of the spinal cord resulting in predominantly motor weakness and spasticity due to involvement of the various corticospinal tracts, with relative preservation of sensory function since the fasciculus gracilis and cuneatus which carry proprioception, vibration, and discriminative touch are in the posterior portion of the spinal cord.

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Principal fiber tracts of spinal cord Fasciculus gracilis Fasciculus cuneatus

Septomarginal fasciculus (oval bundle) Interfascicular fasciculus (comma tract)

Dorsolateral tract (fasciculus) (of Lissauer)

Lateral corticospinal (pyramidal) tract (crossed)

Dorsal (posterior) spinocerebellar tract

Rubrospinal tract Lateral (medullary) reticulospinal tract

Lateral spinothalamic tract and spinoreticular tract Ventral (anterior) spinocerebellar tract

Ventral (anterior) or medullary (pontine) reticulospinal tract

Spinoolivary tract

Vestibulospinal tract

Spinotectal tract

Ventral (anterior) corticospinal tract (direct)

Ventral (anterior) spinothalamic tract

Tectospinal tract Medial longitudinal (sulcomarginal) fasciculi

Fasciculus proprius

Ascending pathways Descending pathways Fibers passing in both directions Areas affected

C

Principal fiber tracts of spinal cord Fasciculus gracilis Fasciculus cuneatus

Septomarginal fasciculus (oval bundle) Interfascicular fasciculus (comma tract)

Dorsolateral tract (fasciculus) (of Lissauer)

Lateral corticospinal (pyramidal) tract (crossed)

Dorsal (posterior) spinocerebellar tract

Rubrospinal tract Lateral (medullary) reticulospinal tract

Lateral spinothalamic tract and spinoreticular tract Ventral (anterior) spinocerebellar tract

Ventral (anterior) or medullary (pontine) reticulospinal tract

Spinoolivary tract

Vestibulospinal tract

Spinotectal tract

Ventral (anterior) corticospinal tract (direct)

Ventral (anterior) spinothalamic tract Fasciculus proprius

D

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Tectospinal tract Medial longitudinal (sulcomarginal) fasciculi Ascending pathways Descending pathways Fibers passing in both directions Areas affected

Fig. 57.7—Cont’d (C) Central cord syndrome: involvement of central portion of canal. Typically by syringomyelia or hydromyelia. Since it usually occurs in cervical spine, it causes weakness of the upper extremity with preservation of lower extremity function. (D) Brown-Sequard syndrome: a hemisection of the cord resulting in ipsilateral motor deficits, loss of vibration and position sense below the level of the lesion. Ipsilateral segmental anesthesia is also observed at the lesion level. Loss of pain and temperature is observed contralaterally below the level of the lesion.

Section 3: Cervical Spine Correlate MRI abnormalities with pain referral symptoms, reflex changes, strength and sensation. Obtain flexion/extension films to exclude segmental instability.

Etiology is confirmed on MRI imaging

No anatomic compression identified on MRI

Physical therapy Patient education Activity modifications NSAID/adjuvant analgesics Therapeutic selective nerve root block

measures, physical therapy, and therapeutic spinal injections can be implemented. If the affected nerve root has associated spondylotic changes that may be implicated as a compressive abnormality, surgical decompression can be considered in the event of failure of conservative care. However, in cases where post-traumatic radicular pain is present without evidence of an anatomic abnormality on MRI or CT-myelography, no specific surgical intervention is available.

Traumatic nonspondylotic cervical radicular pain Determining the pain generating structure in patients with suspected cervical radicular pain without significant cervical spondylotic changes can be diagnostic challenge. Injury to a variety of spinal and extraspinal structures may occur. In patients with a defined myotomal deficit or reflex change, diagnosing the affected nerve root can be straightforward, but often these examination features are not present. The differential diagnosis is similar to that of spondylotic cervical radicular pain. However, knowledge of pain referral maps for cervical discogenic pain, cervical facet syndrome, and cervical dermatomal and dynatomal maps for radicular pain are often the only clues to defining a diagnosis. MRI and EDX studies are usually negative (Table 57.1).

Atraumatic nonspondylotic radicular pain The differential for patients with atraumatic nonspondylotic cervical radicular pain is very broad and involves many categories of diagnoses, some involving the cervical nerve root and many that do not. Brachial plexopathy may occur, either secondary to malignancy (pancoast tumor, lung cancer), radiation, neurotoxic chemotherapeutic agents, viral syndromes (Parsonage-Turner), thoracic outlet syndrome (vascular or neurogenic), or vasculitis. Disorders of the peripheral nerve such as peripheral entrapment of the median, radial, or ulnar nerves, connective tissue disorders such as seen in polyarteritis nodosa which causes a vasculitis of the peripheral nerve, can cause extremity pain. Intrinsic shoulder problems such as impingement syndromes and

EMG/NCS identifies specific nerve root

Failure of conservative care or progressive weakness ?

Resolution of symptoms

If segmental instability present, consider surgical fusion.

EMG/NCS

E Fig. 57.7—Cont’d (E) Myeloradiculopathy: involvement of the spinal cord due to central canal stenosis resulting in any of the above syndromes but also involvement of the cervical spinal nerve root due to degenerative changes such as uncovertebral hypertrophy or disc herniation, thus resulting in mixed upper and lower motor neuron injury.

Multiple anatomic abnormalities on MRI identified

Physical therapy Patient education Activity modifications NSAID/adjuvant analgesics Therapeutic selective nerve root block

Decompressive surgery if compressive abnormality present and symptoms persist

EMG/NCS negative or inconclusive

Diagnostic selective nerve root blocks, see Algorithm based on pain referral pattern, Fig. 57.10

If diagnostic SNRB negative, then re-consider other etiologies

Fig. 57.8 Algorithm: cervical radicular pain.

rotator cuff tears, subdeltoid bursitis, SICK scapula syndrome, acromioclavicular joint osteoarthritis, and sternoclavicular joint arthritis can cause shoulder, upper arm, and trapezius symptoms. Central pain syndromes such as brain or spinal cord tumors, demyelinating diseases such as multiple sclerosis, cerebrovascular accidents involving the sensory cortex, or the thalamus (Dejerine-Roussy thalamic pain syndrome) can cause extremity pain, and careful examination can identify clues to centrally mediated pain. Complex regional pain syndromes type 1 and type 2 can cause extremity pain, with concomitant allodynia, color changes, edema, and atrophy. Pulmonary, gastrointestinal, and cardiac etiologies can refer symptoms to the shoulder, scapula, chest wall, and to the extremity.

Pain referral patterns Posterior neck and trapezius Patients with symptoms in the region of the posterior neck and trapezius can have a broad differential diagnosis. Axial neck complaints can be seen with spinal infection or malignancy. Trapezius symptoms can be referred from a host of visceral etiologies that may irritate the diaphragm, including hepatobiliary diseases, subphrenic abscess,

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Part 3: Specific Disorders Arm pain> Neck pain

Consider alternative diagnosis: Shoulder problem, elbow problem, tendinitis, plexitis, peripheral nerve entrapment

Normal MRI and EMG

Evaluate and treat

Dermatomal/dynatomal/somatic referral

MRI of the C-spine

Biomechanical disorder

Medical diagnosis: institute appropriate diagnosis and treatment

pancreatic pseudocyst, and pleural effusion. Trapezius symptoms can stem from referred pain from axial mechanical neck disorders such as cervical facet syndrome or internal disc disruption syndrome, referred pain from the shoulder, brachial plexitis/thoracic outlet syndrome, and cervical radicular pain. Cervical discogenic pain can refer symptoms to the trapezius from C3–4, C4–5, C5–6, C6–7 levels. The C2–3 and C7–T1 discs can refer symptoms to the neck. The C2–3 disc can often refer symptoms additionally to the occiput while the C7–T1 disc can refer symptoms to the interscapular region (Fig. 57.10). In evaluating patients with trapezius symptoms of possible cervical spinal nerve root origin, the trapezius can be divided into posterior and anterior regions. For patients with isolated trapezius symptoms the following frequencies can be helpful; however, in patients with a more distal referral pattern, the distal symptoms can often be more informative. Posterior trapezius symptoms are associated with the following spinal nerve roots: C4 (100%), C5 (92%), C7 (77%), C6 (74%), C8 (52%).15 Anterior trapezius symptoms are associated with the following spinal nerve roots: C6 (58%), C5 (50%), C4 (50%), C7 (37%).15

Deltoid Rapid progressive weakness

Surgical referral

Conservative care, see table and add cervical traction

Failure to improve or frequent recurrence

Algorithm, cervical radicular pain, Fig. 57.8 Fig. 57.9 Algorithm: patient with axial symptoms greater than extremity symptoms.

The differential diagnosis for deltoid pain again includes the brachial plexus, intrinsic shoulder pathology, and cervical radicular pain. Deltoid pain can be a diagnostic challenge because it is a very common area of referred pain with intrinsic shoulder pathology and nearly every spinal nerve refers pain to this region before radiating more distally into the limb. Etiologies of intrinsic shoulder pathology can be divided into intracapsular and extracapsular etiologies. Intracapsular etiologies include loose bodies, adhesive capsulitis, glenohumeral joint instability, shoulder dislocation/subluxation, and osteoarthritis of the glenohumeral joint. Extracapsular etiologies of shoulder pain include humeral fractures, subacromial bursitis, bicepital tendonitis, clavicular fractures, AC joint separation or osteoarthritis, impingement syndrome, heterotopic ossification, rotator cuff tendonopathy, scapular winging secondary to cranial nerve XI or long thoracic nerve palsy. The

Table 57.1: Probability Analysis by Predominant Pain Referral Pattern EVALUATION OF SCAPULAR PAIN Superior periscap C6 (51%), C7 (42%), C8 (38%), C5 (29%), C4 (25%) Inferior/middle scapular C8 (24/29%), C7 (17/17%), C6 (9/16%), C5 (7%/7%) EVALUATION OF NECK AND TRAPEZIUS Posterior trap C4 (100%), C5 (92%), C7 (77%), C6 (74%), C8 (52%) Anterior upper trap C6 (58%), C5 (50%), C4 (50%), C7 (37%) EVALUATION OF DELTOID PAIN Posterior deltoid C7 (79%), C5 (79%), C4 (75%), C6 (74%), C8 (71%) Anterior deltoid C6 (74%), C5 (57%), C7(48%), C8 (43%), C4 (25%)

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Section 3: Cervical Spine

Table 57.1:—Cont’d EVALUATION OF UPPER ARM PAIN Posterolateral C6 (79%), C7 (65%), C8 (62%), C 5(7%) anterolateral C6 (58%), C7 (42%), C5 (29%), C8 (14%) Anteromedial arm C8 (43%), C6 (30%), C5 7%) EVALUATION OF FOREARM PAIN Ventral radial forearm C6 (44%), C7 (23%), C5 (14%), C8 (10%) Dorsal radial forearm C6 (67%), C7 (58%), C8 (33%) Dorsal ulnar forearm C8 (67%), C7 (42%), C6 (23%) EVALUATION OF CHEST PAIN C7 (17%), C8 (14%), C6 (7%)

Imaging, examination and electromyography inconclusive Posterior neck and upper trapezius

Post upper trap

Ant upper trap

Dx SNRB C4 C5 C7 C6 C8

Dx SNRB C6 C5 C4 C7

Scapular pain

Superior periscap

Inferior/mid periscapular

Dx SNRB C6 C7 C8 C5 C4

Dx SNRB C8 C7 C6 C5

If compressive abnormality, correlate, then consider surgical decompression

Chest pain

Dx SNRB C7 C8 C6

If refractory symptoms

Deltoid

Upper arm

Forearm

Ant delt

Post delt

Post/lat upper arm

Ant/lat upper arm

Ant/med upper arm

Ventra radial forearm

Dorsal radial forearm

Dorsal ulnar forearm

Dx SNRB C6 C5 C7 C8 C4

Dx SNRB C7 C5 C4 C6 C8

Dx SNRB C6 C7 C5 C8

Dx SNRB C6 C7 C5 C8

Dx SNRB C8 C6 C5

Dx SNRB C6 C7 C5 C8

Dx SNRB C6 C7 C8

Dx SNRB C8 C7 C6

Therapeutic SNRB physical therapy NSAIDs/adjuvant analgesics

If refractory symptoms

If no compressive abnormality, then comprehensive pain modulation program

Fig. 57.10 Algorithm: pain referral pattern.

physical examination is important in defining the most likely etiology prior to proceeding with diagnostic testing. Shoulder impingement syndrome can be tested for using impingement tests such as Hawkin’s maneuver (Fig. 57.11) or with scaption (resisted shoulder abduction in the scapular plane with the elbow extended reproducing famil-

iar shoulder pain). Bicepital tendonitis can be identified by eliciting significant tenderness when palpating over the bicepital groove and Speed’s test (Fig. 57.12). Yergason’s test (resisted forearm supination with the elbow flexed at 90° producing anterior shoulder pain) can also be present in bicepital tendonitis (Fig. 57.13). O’Brien’s active 625

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626

Fig. 57.11 Hawkin’s sign. The examiner forward flexes the patient’s shoulder and internally rotates the shoulder. Reproduction of familiar shoulder symptoms is considered positive and suggestive of impingement of the rotator cuff.

Fig. 57.12 Speed’s test for bicepital tendonitis. The shoulder is forward flexed and the elbow is extended with the forearm supinated. The patient is asked to resist the examiners downward force. The reproduction of anterior shoulder pain is considered positive.

Fig. 57.13 Yerguson’s test for bicepital tendonitis. The biceps tendon is palpated to detect whether subluxation of the proximal bicepital tendon occurs when the patient flexes the elbow and externally rotates the shoulder against the examiner’s resistance. Familiar pain in the anterior shoulder is also produced when positive.

Fig. 57.14 O’ Brien’s test. The shoulder is forward flexed with the elbow extended and the forearm is pronated such that the thumb is pointed downward. The patient is asked to resist the examiner’s downward force. Reproduction of pain is considered positive and may be suggestive of a superior labral tear anterior and posterior (SLAP) lesion.

compression test can be helpful to identify a superior labral anterior and posterior (SLAP) tear (Fig. 57.14). Acromioclavicular joint osteoarthritis and sternoclavicular joint arthritis can be associated with tenderness to palpation of these structures. Adhesive capsulitis or frozen shoulder presents with a relatively abrupt onset and on examination the patient has pain at end range of glenohumeral. The decrease in range of motion is symmetric in all planes and involves the glenohumeral joint with sparing of scapulothoracic movement. The drop arm test can be seen in full-thickness rotator cuff tears of the supraspinatus, and the external lag sign suggests a posterior cuff tear. The empty can test elicits pain or weakness in patients with a rotator cuff tear in the affected shoulder. Nearly all cervical nerve roots can refer pain to the deltoid before radiating more distally into the extremity. The deltoid can be divided

into anterior and posterior regions to help with determining the likely involved nerve roots. In patients with isolated deltoid pain, the following frequencies may be helpful in generating a probability analysis. In patients with more distal symptoms, the distal symptoms may be more useful than the frequency of deltoid pain alone. The posterior deltoid is involved with the following frequency: C7 (79%), C5 (79%), C4 (75%), C6 (74%), C8 (71%).15 The anterior deltoid is involved with the following frequency: C6 (74%), C5 (57%), C7 (48%), C8 (43%), C4 (25%).15

Scapula Scapular pain is an extremely common presentation of various painful conditions. The broad differential includes visceral etiologies,

Section 3: Cervical Spine

brachial plexitis, scapulothoracic dyskinesia (SICK scapula syndrome), suprascapular neuropathy, referred pain from the shoulder, referred pain from the thoracic or cervical spine via somatic referral or radicular pain. Thoracic pain is more commonly midline or over the paraspinal muscles, rather than overlying the scapula itself. Thoracic radiculopathies secondary to spondylosis is rare in comparison to the lumbar and cervical spine. However, patients with diabetes mellitus, shingles, zoster-related herpetic neuralgia, or Lyme disease-related radiculopathy may be susceptible to a nonspondylotic thoracic radiculopathy and more commonly experience severe pain in a band-like distribution to the chest wall. Periscapular pain stemming from the cervical or thoracic regions can often be distinguished on examination since patients with thoracic radicular pain should not have symptom provocation with cervical spine range of motion, cervical Spurling’s test, or upper extremity root tension sign. Additionally, thoracic radiculopathies, with the exception of T1, should not be associated with any symptoms, reflex changes, or motor deficits referable to the upper limb. When evaluating patients with scapular complaints on the basis of cervical radicular pain, the scapula should be divided into three main areas: superior, middle, and inferior periscapular regions. The superior periscapular region is implicated by nerve root stimulation with the following frequency: C6 (51%), C7 (42%), C8 (38%), C5 (29%), C4 (25%).15 The inferior and middle scapular regions have the following frequencies respectively: C8 (24/29%), C7 (17/17%), C6 (9/16%), C5 (7%/7%).15 Scapular pain can also be referred on the basis of somatic referral rather than cervical discogenic pain or facet syndrome. The cervical intervertebral disc can somatically refer symptoms to the scapular. In order of decreasing frequency, the C6–7, C7–T1, C5–6, C4–5, and C3–4 discs can be involved. The C4–5 cervical facet joints can cause some symptom referral to the superomedial scapula, and the C5–6 and C6–7 facet joints can refer symptoms to the superior and middle scapula. The C6–7 facet joint can refer symptoms to the inferior scapula as well.

Upper arm Symptoms in the upper arm can be caused by intrinsic shoulder pathology, humeral bony involvement with fractures, infection, tumor, or neurologic involvement of the brachial plexus or thoracic outlet syndrome, referred visceral pain, and cervical radicular pain. It is not uncommon for a patient to have symptoms solely in the upper arm as a manifestation of cervical radicular pain. The upper arm should be divided into posterolateral, anterolateral, and anteromedial regions in order to generate a probability analysis. The posterolateral upper arm is affected with the following frequency: C6 (79%), C7 (65%), C8 (62%), C5 (7%).15 The anterolateral upper arm is affected with the following frequency: C6 (58%), C7 (42%), C5 (29%), C8 (14%).15 The anteromedial upper arm is affected with the following frequency: C8 (43%), C6 (30%), C5 (7%).15

Forearm and hand Forearm pain can be the result of musculoskeletal overuse-related tendinopathy, entrapment of a peripheral nerve, or cervical radicular pain. The two main tendinopathy syndromes include the misnomers, lateral and medial epicondylitis. Lateral epicondylitis is commonly referred to as ‘tennis elbow’ and more properly should be termed wrist extensor tendonosis. The extensor carpi radialis brevis (ECRB) tendon, rather than the lateral epicondyle, is the primary site of pathology on histological studies.46 Indeed, degenerative changes (consistent with angiofibroblastic hyperplasia) in the ECRB, extensor carpi radialis longus, and extensor digitorum communis, occur because of proximal wrist extensor overuse rather than

Fig. 57.15 Test for lateral epicondylitis. Patient extends the wrist and forefinger and middle finger against the examiner’s resistance. Reproduction of familiar pain in the dorsal forearm is considered positive for lateral epicondylitis.

inflammation. In chronic cases, inflammatory cells are rarely found, but microtears and scarring are observed. There is often tenderness to palpation in the region of the lateral epicondyle, and pain noted with resisted wrist extension with the elbow extended and with resisted long finger extension at the proximal interphalangeal joint (Fig. 57.15). Symptoms of proximal medial forearm and elbow pain, commonly referred to as ‘golfer’s elbow,’ have also been incorrectly termed medial epicondylitis Medial epicondylitis initially develops with a true tendonitis of the origin of the forearm flexor musculature and can be associated with pain and palpation tenderness over the medial epicondyle. Like lateral epicondylitis, in the chronic stages, the inflammatory component is significantly reduced, and the proximal wrist flexor tendons demonstrate degeneration and disorganized scarring. The common peripheral nerve entrapments that can cause forearm pain include median neuropathy, either proximal in the forearm (pronator teres syndrome or anterior interosseous syndrome) or distally (carpal tunnel syndrome). Carpal tunnel syndrome is by far the most common median nerve entrapment, and the most common upper extremity peripheral entrapment. Pain and paresthesias can be located in the palmar aspect of the hand involving the volar aspect of the thumb, index, long and radial half of the ring finger and can radiate proximally into the forearm, and rarely into the upper arm. Symptoms can be associated with a positive flick sign (flicking the wrist alleviates pain), and can be exacerbated with office work or wrist flexion, or nocturnal exacerbation. On examination, percussion at the carpal tunnel (Tinel’s) can elicit familiar hand symptoms or radiate symptoms proximally into the forearm or upper arm (vallieux phenomenon). When severe, thenar atrophy can be seen on examination. Ulnar neuropathy can occur at or near the elbow (arcade of Struther’s ligament, cubital tunnel, flexor carpii ulnaris aponeurosis, which is also known as the arcuate ligament) or the hook of the hamate in the wrist. Pain and paresthesias can occur in the ulnar aspect of the forearm and into the palmar and dorsal aspect of the small and half of the ring finger. Patients may complain of nocturnal pain. Symptoms can often be elicited by percussion over the course of the ulnar nerve at the cubital tunnel or over the hamate bone in the wrist. Atrophy can be seen in the adductor digiti minimi or first dorsal interossei. Symptoms can often be confused with a C8 radiculopathy. Radial neuropathy can occur proximally in the humerus and result in injury in the high axillary region (Saturday night palsy, honeymooner’s palsy, crutch palsy) or the spiral groove, or more distally 627

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in the forearm (supinator syndrome, Arcade of Frohse) and cause the posterior interossei syndrome. It is far less common than median or ulnar entrapments. Weakness of the finger extensors is seen in the posterior interosseous syndrome. The cervical nerve roots that cause pain commonly refer pain into three predominant patterns, the ventral radial forearm, the dorsal radial forearm, and the dorsal ulnar forearm. The ventral radial forearm is involved with the following frequency: C6 (44%), C7 (23%), C5 (14%), C8 (10%).15 The dorsal radial forearm is involved with the following frequency C6 (67%), C7 (58%), C8 (33%).15 The dorsal ulnar forearm is involved with the following frequency C8 (67%), C7 (42%), C6 (23%). The hand can also be involved in cervical radicular pain with the dorsal index finger being involved in C7 (52%), C6 (37%), and C8 (24%) of radiculopathies.15 Dorsal fifth digit symptoms were produced in C8 (48%), C7 (33%), and C6 (30%).15 Intrinsic hand pain can be seen in patient’s with Dequervain’s stenosing tenosynovitis. This condition will provoke symptoms along the radial aspect of the forearm and into the thumb and will have a positive Finkelstein’s test. Osteoarthritis of the carpal–metacarpal (CMC) joint can cause pain in the radial aspect of the wrist and hand and often has pain with range of motion or palpation of the CMC joint. These conditions can be distinguished from carpal tunnel syndrome or cervical radiculopathy based on examination features, electrodiagnostic testing, or diagnostic imaging.

Chest pain Numerous organ systems can cause chest pain or discomfort. Cardiac etiologies include coronary artery disease related ischemia/infarction, arrhythmia, or vasospasm related to Prinzmetal angina or drugs such as cocaine. Gastrointestinal etiologies include gastroesophageal reflux or peptic ulcer disease, which can be exacerbated in patients treated with nonsteroidal antiinflammatories and corticosteroids. Vascular etiologies such as dissecting thoracic aortic aneurysms can cause severe acute chest and back pain. Pulmonary etiologies including malignant and infectious etiologies can cause chest wall pain. Chest pain can be a manifestation of cervical or thoracic radicular pain. Thoracic radicular pain can often follow a band-like distribution from the back to the anterior chest wall. Spondylotic thoracic radicular pain is less common because of bony stability provided by the rib cage. Nonspondylotic thoracic radicular pain can occur in diabetic patients, and this can present as a polyradiculopathy. Shingles, or varicella-zoster can cause thoracic radicular pain and chest wall complaints but most commonly has an associated classical dermatomal distribution rash of grouped vesicles on an erythematous base. Chest pain is a less common feature of cervical radicular pain; however, cervical radicular pain may be considered in patients with symptoms inexplicable on the basis of a medical etiology. The cervical spinal nerve roots that can refer symptoms to the chest wall occur with the following frequency: C7 (17%), C8 (14%), C6 (7%).15

Fig. 57.16 Modified Spurling’s test. The neck is extended and the head is ipsilaterally rotated while the spine is axially loaded. Reproduction of symptoms beyond the shoulder is considered positive and indicative of cervical radicular pain due to a herniated disc or foramenal stenosis.

been performed comparing various examination findings to needle electromyography which can demonstrate physiological evidence of denervation and distinguish cervical radiculopathy from peripheral nerve entrapments. A study by Wainner et al.47 used electromyography as a gold standard for the diagnosis of cervical radiculopathy and studied examination features associated with cervical radiculopathy. The investigators found that examination maneuvers associated with acceptable diagnostic accuracy for cervical radiculopathy include the following with respective sensitivities/specificities: Elvey’s upper limb tension test A (0.97sn/0.22sp) (Fig. 57.18), cervical rotation to the involved side less than 60° (0.89sn/0.49sp), cervical flexion less than 55° (0.89sn/0.41sp), involved biceps muscle stretch reflex (0.24sn/0.95sp), neck distraction test reducing symptoms (0.44 sn/0.90sp), manual muscle testing involved biceps (0.24sn/0.94sp), Valsalva maneuver exacerbating pain

Physical examination Physical examination is an important tool in the diagnosis of cervical radicular pain and radiculopathy. Given the lack of a single test that is considered the gold standard for the diagnosis of cervical radiculopathy, establishing sensitivities and specificities for various maneuvers is difficult. Neurological examination involving manual muscle testing, muscle stretch reflexes, and sensory deficits are useful to determine the involved spinal nerve root or roots. Additionally, provocative tests such as Spurling’s maneuver, cervical range of motion, and upper limb dural tension tests can determine if pain can be elicited in a familiar distribution in the extremity using maneuvers that may irritate the spinal nerve root (Figs 57.16–57.18). Studies have 628

Fig. 57.17 Spurling’s test. The neck is ipsilaterally bent while the neck is forward flexed and a sustained axial load is provided. Reproduction of symptoms beyond the shoulder is considered positive and indicative of cervical radicular pain due to a herniated disc or foramenal stenosis.

Section 3: Cervical Spine

Fig. 57.18 Elvey’s upper limb root tension test. Abduction of the shoulder, extension of the elbow and contralateral rotation of the head reproduces extremity symptoms.

(0.22sn/0.94sp), Spurling’s test A exacerbating pain (0.50sn/0.86sp) (Fig. 57.17), shoulder abduction test alleviating pain (0.17sn/0.92sp), involved C5 dermatome sensation (0.29sn/0.86sp). The four following tests were analyzed as a test item cluster: Spurling’s test A, neck distraction, Elvey’s upper limb tension test A, involved cervical rotation less than 60°. The post-test probability for patients with two, three, or four tests positive was 21%, 65%, and 90%, respectively. Tong et al.48 assessed the utility of the cervical Spurling’s test. Spurling’s test was scored positive if it reproduced symptoms distal to the shoulder. Electrodiagnostic examination was used as a reference. The sensitivity of the Spurling’s maneuver was 30% and its specificity was 93%. The results of the Spurling’s test was positive in 16% of patients with a normal electrodiagnostic study, 3.4% of patients with nerve disorders other than radiculopathy found on electromyelogram (EMG), 37.5% of patients with possible radiculopathy on EMG, and 40% of patients with certain electrodiagnostic evidence of radiculopathy. Manual muscle testing, side-to-side comparison of muscle stretch reflexes, and sensory testing can be helpful in identifying the affected nerve root. The least reliable of these is sensory deficit as there is significant dermatomal overlap in a given region of skin. Sensory disturbances can follow a classic dermatomal distribution, or a dynatomal distribution, discussed in more detail elsewhere in this chapter. Detailed knowledge of the spinal nerve root and peripheral nerve innervating a given muscle tested is required to determine the structure. Although much myotomal overlap exists with upper extremity tested muscles, the authors find the following muscles useful to test either with manual muscle testing or with needle electromyography. The most specific muscle group is in italics. ●

●

●

C4 radiculopathy: weakness of levator scapular and trapezius. Clinically, patients may have weakness of shoulder elevation (Fig. 57.19). There is no reliable reflex test. C5 radiculopathy: rhomboid, deltoid, bicep, and infraspinatus weakness. This clinically may be associated with shoulder abduction and external rotation weakness (Figs 57.20–57.22). The biceps reflex may be diminished. C6 radiculopathy: can easily be confused for C5 or C7 radiculopathy. Weakness can overlap with the C5 or C7 muscles. Muscles

Fig. 57.19 Manual muscle testing technique for trapezius C4 myotome. The patient elevates the shoulder against the examiner’s downwardapplied resistance. Commonly, the patient will simultaneously shrug both shoulders, but only one is demonstrated here to illustrate the motion.

●

●

affected include: infraspinatus, biceps, brachioradialis, pronator teres and tricep (Figs 57.23–57.25). The bicep or brachioradialis reflex may be diminished. C7 radiculopathy: this is the most common electrophysiologically identified radiculopathy and can result in weakness of the triceps, pronator teres, flexor carpi radialis (Fig. 57.26) There may be a diminished triceps reflex. C8 radiculopathy: weakness can be present in the opponens pollicis, flexor digitorum profundus, flexor pollicis longus, and hand intrinsic muscles (Fig. 57.27). Clinically, patients present with symptoms similar to an ulnar neuropathy and can have weakness of finger abductors and grip strength as well as a median motor neuropathy. No reliable reflex test is available.

Fig. 57.20 Manual muscle testing for deltoid. Axillary nerve, C5 myotome. The patient is asked to abduct the shoulder against the examiner’s resistance.

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Fig. 57.21 Manual muscle testing for biceps brachii. Musculocutaneous nerve, C5 and C6 myotome. The patient is asked to flex the elbow against the examiner’s resistance while the forearm is supinated.

Fig. 57.22 Manual muscle testing for infraspinatus. Suprascapular nerve, C5 and C6 myotome. The patient is asked to externally rotate the humerus against the examiner’s resistance. The examiner must be careful that the patient does not substitute deltoid muscle groups and abduct the shoulder.

Diagnostic imaging In the acute trauma setting, especially when an injury to the head or neck has occurred, plain radiographs of the cervical spine are performed because of their rapid availability, relative low cost, and sufficient sensitivity for fractures. The trauma series includes anteroposterior, right and left oblique, odontoid view, and cross-table lateral view. All five views in combination have a 92% sensitivity for fracture. However, sensitivity can be significantly decreased with films of poor technique. In patients with a history of remote trauma, spondylolisthesis, or surgery, flexion and extension films can be used to diagnose gross instability. Sagittal plane translation of a vertebral body on flexion–extension films represents segmental instability. Greater 630

Fig. 57.23 Manual muscle testing for brachioradialis, radial nerve, C6 and C7 myotome. The patient is asked to flex the elbow with the radial portion of the forearm pointed upward.

Fig. 57.24 Manual muscle testing for pronator teres. Median nerve, C6 and C7 myotome. The patient has the elbow at approximately 90°, and is asked to pronate the forearm against the examiner’s resistance.

than 3 mm of translation between flexion and extension or angulation of more than 11° at a single spinal segment may necessitate spinal fusion. In patients with acute or chronic neck pain with no history of trauma, plain films add little to the diagnostic work-up. The cervical MRI is often the study of choice in patients with radicular and axial neck pain. Indications for obtaining an MRI include when symptoms are associated with constitutional symptoms of fevers, nocturnal exacerbation of pain, percussion tenderness, or weight loss. In patients who have not improved with conservative care or have symptoms that are severe, disabling, or associated with progressive weakness, further interventions are necessary and thus imaging is required. This latter clinical situation is where spine specialists are often consulted to help further with management, and MRI

Section 3: Cervical Spine

Fig. 57.25 Manual muscle testing for triceps. Radial nerve C6, C7, and C8. The patient is asked to extend the elbow against the examiner’s resistance. The examiner must be careful not to be fooled by substitution by pectoralis and anterior deltoid muscle groups. The position displayed above helps to isolate the triceps.

Fig. 57.26 Manual muscle testing for flexor carpi radialis. Median nerve, C7 and C6 myotome. The patient is asked to flex the wrist against the examiner’s resistance.

offers the best noninvasive imaging. It can diagnose degenerative disc disease, central or foramenal stenosis secondary to osseous structures versus herniated nucleus pulposus, spondylolisthesis, malignancy, or infection. The addition of gadolinium contrast is useful in the diagnosis of postsurgical epidural fibrosis, infection, or tumor.49–52 Given the high sensitivity of MRI for a wide range of pathology, it has become the study of choice. However, anatomic abnormalities such as disc protrusion or extrusion are present in up to 30% of asymptomatic individuals.53,54 These anatomic abnormalities may lack clinical, but not radiologic, specificity for pain complaints. Implicit in that observation is that astute clinical correlation with the history, examination, neurophysiologic, and functional tests is necessary to establish a precise diagnosis and ultimately offer specific treatment.

Fig. 57.27 Manual muscle testing for opponens pollicis. Recurrent branch of median nerve, C8 myotome. The patient is asked to oppose the thumb, bring the thumb toward the little finger against the examiner’s resistance.

Bone scintigraphy studies using radiolabeled isotopes allow assessment of the physiologic processes within the skeletal system as a whole. The isotope is incorporated by osteoblasts into the hydroxyapatite crystals in bone. Areas of high metabolic turnover show increased uptake. This can be effective in screening for infection or malignancy. While useful as a screening tool, its limited specificity may often require additional imaging for definitive diagnosis. Focal uptake within the zygapophyseal joints may be associated with the cervical facet syndrome. Positive bone single photon emission computed tomography (SPECT) scans demonstrating uptake in the zygapophyseal joints can be associated with a good short-term benefit with intra-articular steroid injections when compared to bone SPECT scan-negative patients.55 CT-myelography can be a complementary tool in the evaluation of cervical radicular pain. However, disadvantages of the study include that it is invasive and can be associated with postdural puncturerelated headaches. MRI and CT-myelographic evaluation of cervical spinal stenosis by using current qualitative methods results in significant variation in image interpretation.56 Shafaie et al. compared the diagnostic ability of MRI and CT-myelogram for degenerative cervical disorders such as radiculopathy and stenosis. They found varying results, with CT generally grading abnormalities more severe than that appreciated with MRI. For most parameters of interpretation, the degree of concordance between CT-myelography and MRI is only moderately good, with discrepancies noted especially in the differentiation of disc and bony pathology.57 These methods should be viewed as complementary studies. CT-myelograms may be more sensitive compared with standard noncontrast MRI in the identification of nerve root avulsion.58 The overlapping coronal–oblique slice MRI procedure may provide comparable sensitivity with CT-myelogram for the identification of nerve root avulsion.59

Electromyography and nerve conduction studies Needle electromyography and nerve conduction studies (EMG/ NCS) can be useful adjunctive diagnostic tools in the evaluation of cervical radiculopathy. Needle electromyography is the single most useful electrophysiologic test for the identification of cervical radic631

Part 3: Specific Disorders

ulopathy. The needle electromyography portion of the EDX study involves the percutaneous insertion of a needle into muscles in the upper limb and cervical paraspinal muscles. Muscle with an axonal injury to its innervating nerve root or peripheral nerve will demonstrate membrane instability, manifested as fibrillation potentials, and positive sharp waves. Needle electrode examination can detect as little as a 4% loss of motor axons.60 When injury has been present for a more sustained time, the process of reinervation will manifest itself as polyphasic motor unit potentials. The electromyographer, through a detailed understanding of anatomy, can determine whether the constellation of injured muscles represent the distribution of a cervical spinal nerve root, peripheral nerve injury, or plexus lesion. The nerve conduction portion of the examination involves the administration of an electrical impulse along the course of a motor, sensory, or mixed peripheral nerve and measuring the velocity, amplitude, and duration of the transmitted impulse. This can identify peripheral entrapments, plexopathy, peripheral neuropathy, or demyelinating disease. The needle portion of the EMG/NCS is the most useful test to identify cervical radiculopathy but will only identify radiculopathy and its associated radicular pain when motor axonal injury is present. Cervical radicular pain can exist in the absence of axonal injury. Irritation of the dorsal root ganglion and the dorsal sensory afferent fibers can result in pain without motor injury. Another issue is that the sensitivity of the needle EMG increases with the number of muscles sampled. Dillingham et al. demonstrated that sampling six upper limb muscles along with the paraspinal muscles was sufficient to identify a cervical radiculopathy by EMG.61 Sampling more than that had marginal increases in sensitivity, and sampling less than that had a decrease in sensitivity. An in-depth discussion of this concept is provided by Dillingham in Chapter 8. In patients with prior laminectomy, sampling cervical paraspinal muscles can often demonstrate abnormalities due to local incisional denervation. In these patients, eight extremity muscles are necessary to achieve optimal identification. Another limitation is that myotomal overlap between nerve roots can often make determination of the affected nerve root difficult, and although physiologic evidence of radiculopathy can be demonstrated, the specific nerve root which should be injected or decompressed surgically may not be clear.62,63

Functional testing Ambiguity in diagnosis may exist because of discordant findings on history, examination, imaging, and electrodiagnostic testing. Functional studies performed by a trained spine specialist can play a key role in the diagnosis and management of patients with chronic and recurrent neck and radicular pain. Implementing an efficient algorithm will ultimately provide a specific diagnosis and thus allow for treatment directed to this diagnosis, and not simply modulate pain complaints. Focused treatment obviates the performance of unnecessary procedures and necessarily institutes the treatment required to obtain a successful result. Based on the composite of history, examination, neurophysiologic, and imaging studies, a statistical likelihood of the etiology of the patient’s pain can be formulated for the individual patient. In a stepwise and methodical fashion, the likely structures are anesthetized under fluoroscopic guidance to ascertain whether symptom relief is obtained. Each patient completes a visual analog scale (VAS) pre- and postprocedure. The VAS consists of a horizontal bar measuring 100 mm which is marked by the patient to grade the severity of pain. Toward the 100 mm mark represents more severe pain. If the VAS reduction is greater than 80% after a diagnostic block, the block is considered positive and the anesthetized structure is considered to be the etiologic structure. Subsequently, therapeutic injections are offered as treatment. If the diagnostic block 632

does not provide 80% relief, then the next most likely structure is investigated. Diagnostic selective nerve root blocks (SNRBs) have been studied in the lumbar spine and have demonstrated a high sensitivity and specificity for identifying the pain-generating spinal nerve. This has been demonstrated in studies correlating positive blocks with identification of an anatomic abnormality at the time of surgery. The sensitivity of diagnostic lumbar SNRB ranges 87–100% and the specificity ranges 94–100%.64–68 At least three studies have been done looking at cervical diagnostic selective nerve root blocks which supported their specificity.69–71 Using methodical technique, it is likely that these techniques can also be useful in the cervical spine for the evaluation of cervical radicular pain. It has been demonstrated that higher volumes of injectate will diminish the specificity of the diagnostic selective nerve root block.72 If a patient has possible facet-mediated pain, diagnostic facet joint injections or medial branch blocks can be used to determine the pain generator. However, such injections, in contrast to SNRB, reportedly have a false-positive diagnostic block rate of approximately 27%.73 This false-positive rate may be attributable to a placebo effect or inadvertent anesthetization of nearby structures or from extra-articular extravasation of anesthetic injectate. The placebo effect can be minimized by using a patient-blinded, placebo-controlled, doubleblock injection the facet joint or its medial branches or time-dependent anesthetic blockade to the medial branches. Informed consent and an explanation of the rationale for this meticulous approach is necessary so that patients do not feel they have been misled.

CONCLUSION An algorithmic methodology adds efficiency and efficacy for the evaluation and treatment of complex painful spine disorders. Treatment of a patient’s pain complaints should employ a diagnosis-specific approach. Obtaining a specific diagnosis helps ensure that the best treatment for a given complaint is instituted. Cervical spine complaints should be categorized into axial, radicular, and myelopathic features. Identification of myelopathic features should lead the clinician to consider surgical options early to ensure optimal neurologic and functional outcome. In the absence of myelopathy, most spine disorders can be managed conservatively. Determining the paingenerating cervical spinal nerve root in patients with radicular pain affects treatment with interventional procedures, physical therapeutic exercises, and surgical options. Treatment of cervical radicular pain involves a spectrum of treatment options which include education for the patient, activity and postural and worksite modifications, therapeutic exercise, adjunctive modalities, cervical traction, pharmacologic measures, fluoroscopically guided injection procedures, and surgical decompression. Treatment should be individualized and goal oriented to ensure successful patient outcomes.

References 1. White AA, Punjabi MM. Clinical biomechanics of the spine. 2nd ed. Philadelphia: Lippincott; 1990. 2. Jofe M, White A, Punjabi M. Clinically relevant kinematics of the cervical spine. In: Sherk H, Dunn E, Eismont F, eds. The cervical spine. 2nd edn. Philadelphia: JB Lippincott; 1989:57–69. 3. Bogduk N, Marsland A. The cervical zygapophyseal joints as a source of neck pain. Spine 1988; 13:610–617. 4. Aprill C, Bogduk N. The prevalence of cervical zygapophyseal join pain – A first approximation. Spine 1992; 17:744–747. 5. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns I: A study in normal volunteers. Spine 1990; 15:453–457. 6. Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal joint pain patterns II: A clinical evaluation. Spine 1990; 6:458–461.

Section 3: Cervical Spine 7. Slipman CW, Isaac Z, Thomas J, et al. Cervical zygapophyseal joint syndrome and referral to the head and face: preliminary data from 100 patients. Proceedings of the Cervical Spine Research Society 2002 Annual Meeting, December 2002; 68. 8. Bogduk N, Marsland A. On the concept of third occipital headache. J Neurol Neurosurg Psychiatry 1986; 49:775–780.

36. Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990; 15:674–678. 37. Keith WS. ‘Whiplash’ – Injury of the 2nd cervical ganglion and nerve. Can J Neurol Sci 1986; 13:133–137.

9. Hadley LA. Anatomicroradiographic studies of the spine: changes responsible for certain painful back conditions. New York J Med 1939; 39:969–974.

38. Örtengren T, Hansson HA, Lovsund P, et al. Membrane leakage in spinal ganglion nerve cells induced by experimental whiplash extension motion: A study of pigs. J Neurotrauma 1996; 13:171–180.

10. Marinacci AA. A correlation between operative findings in cervical herniated disc with electromyograms and opaque myelograms. Electromyography 1966; 6:5–20.

39. Waxman SG, Rizzo MA. The whiplash (hyperextension–flexion) syndrome: A disorder of dorsal root ganglion neurons? J Neurotrauma 1996; 13:735–739.

11. Yoss RE, Corbin KE, MacCarthy CS, et al. Significance of signs and symptoms in localization of involved roots in cervical disc protrusion. Neurology 1957; 7: 673–683.

40. Jonsson H Jr, Cesarini K, Sahlstedt B, et al. Findings and outcome in whiplash-type neck distortions. Spine 1994; 19:2733–2743.

12. Levin KH, Maggiano HG, Wilbourn AJ. Cervical radiculopathies: comparison of surgical and EMG localization of single root lesions. Neurology 1996; 46:1022–1025.

41. Slipman CW, Lipetz JS, Jackson HB, et al. Outcomes of therapeutic selective nerve root blocks for whiplash induced cervical radicular pain. Pain Phys 2001; 4(1): 1–7.

13. Sherrington CS. Experiments in examination of the peripheral distribution of the fibers of the posterior roots of dome spinal nerves. Part I. Phil Trans Roy Soc London 1893; Ser. B. 184:641–763.

42. Slipman CW, Lipetz JS, DePalma MJ, et al. Therapeutic selective nerve root block in the nonsurgical treatment of traumatically induced cervical spondylotic radicular pain. Am J Phys Med Rehabil. 2004; 83(6):446–454.

14. Sherrington CS. Experiments in examination of the peripheral distribution of the fibres of the posterior roots of some spinal nerves. Part II. Phil Trans Soc London 1898; Ser. B. 190:45–187.

43. Slipman CW, Furman M, Plastaras C, et al. Provocative cervical discography symptom mapping. Pending publication in The Spine Journal 2005.

15. Slipman CW, Plastaras CT, Palmitier RA, et al. Symptom provocation of fluoroscopically guided cervical nerve root stimulation. Are dynatomal maps identical to dermatomal maps? Spine 1998; 23(20):2235–2242.

44. Hughes JT, Brownell B. Necropsy observations on the spinal cord in cervical spondylosis. Riv Patol Nerv Ment 1965; 86:196–204. 45. Paltis C, Jones AM, Spillane JD. Cervical spondylosis: Incidence and implications. Brain 1954; 77:274–289.

16. Moriishi J, Otani K, Tanaka K, et al. The intersegmental anastomoses between spinal nerve roots. Anatom Rec 1989; 224:110–116.

46. Regan W, Wold LE, Coonrad R, et al. Microscopic histopathology of chronic refractory lateral epicondylitis. Am J Sports Med 1992; 20(6):746–749.

17. Bogduk N, Windsor M, Inglis A. The innervation of the cervical intervertebral discs. Spine 1988; 13:2–8.

47. Wainner RS, Fritz JM, Irrgang JJ, et al. Reliability and diagnostic accuracy of the clinical examination and patient self-report measures for cervical radiculopathy. Spine 2003; 28(1):52–62.

18. Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990; 15:674–678. 19. Franson RC, Saal JS, Saal JA. Human disc phospholipase A2 is inflammatory. Spine 1992; 17:S129–132. 20. Wilburger RE, Wittenberg RH. Prostaglandin release from lumbar disc and facet joint tissue. Spine 1994; 19:2068–2070. 21. Ozaktay AC, Cavanaugh JM, Blagoev DC, et al. Phospholipase A2 induced electrophysiologic and histologic changes in rabbit dorsal lumbar spine tissues. Spine 1995; 20:2659–2668.

48. HC Tong, Haig A, Yamakawa K. The Spurling test and cervical radiculopathy. Spine 2002; 27(2):156–159. 49. Bundschuh CV, Modic MT, Ross JS, et al. Epidural fibrosis and recurrent disk herniation in the lumbar spine: MR imaging assessment. Am J Roentgenol 1988; 150:923–932. 50. Frocrain L, Duvauferrier R, Husson JL, et al. Recurrent postoperative sciatica: evaluation with MR imaging and enhanced CT. Radiology 1989; 170:531–533.

22. Takahashi H, Suguro T, Okazima Y, et al. Inflammatory cytokines in the herniated disc of the lumbar spine. Spine 1996; 21:218–224.

51. Ross JS, Masaryk TJ, Schrader M, et al. MR imaging of the postoperative lumbar spine: assessment with gadopentetate dimeglumine. Am J Roentgenol 1990; 155:867–872.

23. Doita M, Kanatanni T, Harada T, et al. Immunohistologic study of the ruptured intervertebral disc of the lumbar spine. Spine 1996; 21:235–241.

52. Colletti PM, Dang HT, Deseran MW, et al. Spinal MR imaging in suspected metastases: correlation with skeletal scintigraphy. Magn Reson Imaging 1991; 9:349–355.

24. Kang JD, Gergescu HI, McIntyre-Larkin L, et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 1996; 21:271–277.

53. Boden SD, McCowin PR, Davis DO, et al. Abnormal magnetic-resonance scans of the cervical spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg [Am] 1990; 72:1178–1184.

25. Kanemoto M, Hukuda S, Komiya Y, et al. Immunohistochemical study of metalloproteinase-3 and tissue inhibitor of metalloproteinase-1 in human intervertebral discs. Spine 1996; 21:1–8.

54. Teresi LM, Lufkin RB, Reicher MA, et al. Asymptomatic degenerative disk disease and spondylosis of the cervical spine: MR imaging. Radiology 1987; 164:83–88.

26. Ashton IK, Roberts S, Jaffray DC, et al. Neuropeptides in the human intervertebral disc. J Orthop Res 1994; 12:186–192. 27. Konniten YT, Gronblad M, Antti-Poika I, et al. Neuroimmunohistochemical analysis of periodical nociceptive neural elements. Spine 1990; 15:383–386. 28. Cornefjord M, Olmarker K, Farley DB, et al. Neuropeptide changes in compressed spinal nerve roots. Spine 1995; 20:670–673. 29. Weinstein J, Claverie W, Gibson S. The pain of discography. Spine 1988; 13: 1344–1348. 30. Gertzbein SD. Degenerative disk disease of the lumbar spine. Clin Orthop Rel Res 1977; 129:68–71. 31. Marshall LL, Trethewie ER, Curtain CC. Chemical radiculitis. Clin Orthop Rel Res 1977; 129:61–67.

55. Dolan AL, Ryan PJ, Arden NK. The value of SPECT scans in identifying back pain likely to benefit from facet joint injection. Br J Rheumatol 1996; 35(12): 1269–1273. 56. Stafira JS, Sonnad JR, Yuh WT, et al. Qualitative assessment of cervical spinal stenosis: observer variability on CT and MR images. Am J Neuroradiol 2003; 24(4): 766–769. 57. Shafaie FF, Wippold FJ 2nd, Gado M, et al. Comparison of computed tomography myelography and magnetic resonance imaging in the evaluation of cervical spondylotic myelopathy and radiculopathy. Spine 1999; 24(17):1781–1785. 58. Morenski JD, Avellino AM, Elliott JP, et al. Bilateral multiple cervical root avulsions without skeletal or ligamentous damage resulting from blast injury: case report. Neurosurgery 2002; 50(6):1368–1370

32. Chabot MC, Montgomery DM. The pathophysiology of axial and radicular neck pain. Semin Spine Surg 1995; 7:2–8.

59. Doi K, Otsuka K, Okamoto Y, et al. Cervical nerve root avulsion in brachial plexus injuries: magnetic resonance imaging classification and comparison with myelography and computerized tomography myelography. J Neurosurg Spine 2002; 96(3):277–284.

33. Ashton IK, Roberts S, Jaffray DC, et al. Neuropeptides in the human intervertebral disc. J Orthop Res 1994; 12:186–192.

60. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley & Belfus; 1995: 523–584.

34. Imai S, Konttinen Y, Tokunaga Y, et al. An ultrastructural study of calcitonin gene related peptide immunoreactive nerve fibers innervating the rat posterior longitudinal ligament: a morphologic basis for their possible efferent actions. Spine 1997; 22:1941–1947.

61. Dillingham TR, Lauder TD, Andary M, et al. Identification of cervical radiculopathies: optimizing the electromyographic screen. Am J Phys Med Rehabil 2001; 80:84–91.

35. Cornefjord M, Olmarker K, Farley DB, et al. Neuropeptide changes in compressed spinal nerve roots. Spine 1995; 20:670–673.

62. Levin KH. Cervical radiculopathies: comparison of surgical and EMG localization of single root lesions. Neurology 1996; 46:1022–1025.

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Part 3: Specific Disorders 63. Brendler S. The human cervical myotomes: functional anatomy studied at operation. J Neurosurg 196;. 28(2):105–111. 64. Schutz H, Loughweed WM, Wortzman G, et al. Intervertebral nerve root in the investigation of chronic lumbar disc disease. Can J Surg 1973; 16:217–221. 65. Krempen JF, Smith BS. Nerve root injection: a method for evaluating the etiology of sciatica, JBJS 1974; 56A:1435–1444. 66. Dooley JF, McBroom RJ, Taguchi T, et al. Nerve root infiltration in the diagnosis of radicular pain. Spine 1988; 13(1):79–83. 67. Van Akkerveeken PF. The diagnostic value of nerve root sheath infiltration. Acta Orthop Scan 1993; (Suppl 251):61–63. 68. Stanley D, McLaren MI, Euinton HA, et al. A prospective study of nerve root infiltration in the diagnosis of sciatica: a comparison with radiculography, computed tomography, and operative findings. Spine 1990; 15(6):540–543.

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69. Anderberg L, Annertz M, Brandt L, et al. Selective diagnostic cervical nerve root block – correlation with clinical symptoms and MRI-pathology. Acta Neurochir (Wien) 2004; 146(6):559–565; discussion 565. Epub 2004 Apr 26. 70. Strobel K, Pfirrmann CW, Schmid M, et al. Cervical nerve root blocks: indications and role of MR imaging. Radiology 2004; 233(1):87–92. 71. Macadaeg K, Sasso R, Nordmann D. Selective nerve root injections can accurately predict level of nerve impairment and outcome for surgical decompression: a retrospective analysis. Pain Med 2001; 2(3):245–246. 72. North RB, Kidd DH, Zahurak M, et al. Specificity of diagnostic nerve blocks: A prospective, randomized study of sciatica due to lumbosacral spine disease. Pain 1996; 65:77–95. 73. Barnsley L, Lord SM, Wallis BJ, et al. False positive rates of cervical zygapophyseal joint blocks. Clin J Pain 1993; 9124–9130

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ i: Cervical Radicular Pain

CHAPTER

Rehabilitation Methods in Cervical Radicular Pain

58

David A. Lenrow and Jeffrey Ostrowski

Treatment of cervical radiculopathy spans the spectrum from medication and activity modulation through surgical decompression. Treatment recommendations are based on the specific patient’s history and physical findings. The wide variation in the approach to similar patterns of patient symptoms, history, and findings is indicative of the lack of clear evidence-based practice algorithms. The armamentarium of treatments available includes medications, activity modification, rest, physical therapy, bracing, complementary medicine techniques, spinal injections and percutaneous procedures and surgery.1–8 Nonsurgical treatment has been shown to be effective and safe for cervical radiculopathy, with outcomes similar to those for surgical intervention.1,2,5,7 The decision of which treatment to recommend and its timing is primarily based on the physician’s experience and training, with little conclusive empirical evidence in most cases. Approaching treatment based on history and exam and response to treatment with reevaluation and modification of the treatment plan as indicated is a sensible approach.

EVALUATION History and physical examination should focus on musculoskeletal and neurologic evaluation and, as always, should be expanded depending on the patient’s history and exam. The prior treatment and responses should be noted. Depending on the duration and extent of symptoms, neurologic deficits and presence or absence of provocative maneuvers, an initial treatment plan will be formulated. Patients may already have had diagnostic studies and others will need imaging, electrodiagnostic studies, or other tests performed. If there is a clear diagnosis of radiculopathy with concordant history, exam, and diagnostic studies, treatment is instituted.

MEDICATIONS There are many classes of medications available to treat cervical radicular pain.2,6 For pain and presumed inflammation nonsteroidal antiinflammatory drugs (NSAIDs) are often used as the first line of medication therapy. Traditional NSAIDs are generally recommended unless there is a contraindication such as a history of ulcer disease or upper GI bleed. The controversy surrounding the use of COX-2 selective antiinflammatory agents continues to evolve. At issue are cardiovascular adverse events, which led to the voluntary withdrawal of Vioxx by Merck on September 30, 2004. The recent FDA hearings (February 2005) seem to suggest that these drugs should be restricted to use in patients who are in the category of those patients at elevated risk for GI adverse events with low CV risk factors. At the time of the final edit of this chapter the formal outcome of the hearings and the recommendations/package insert changes were not known. Narcotic medications are the mainstay of treatment for pain unresponsive to NSAIDs. The American Pain Society recommends

opioids for acute pain when non-opioids fail.9 For episodic pain or short-term usage, short-acting narcotics are effective. Patients with constant moderate to severe pain are better treated with long-acting narcotic medications (sustained release) for a stable level of pain control. They avoid the peaks and troughs often associated with short-acting prn medications. Adjuvant medications are often useful for pain management to help decrease narcotic usage and, in certain cases, control pain without narcotics. Tricyclic antidepressants (TCAs) are the most studied medicine for neuropathic pain. They are utilized in lower doses than would be given for depression.10 Selective serotonin reuptake inhibitor (SSRI) antidepressants may be beneficial for pain management in some patients. One of the benefits of TCAs is their sedating effect on most patients. Patients often have difficulty sleeping so if the TCA is taken at night it serves a dual purpose. Gabapentin has been helpful in treating neuropathic pain as have other anticonvulsants.11 Steroids orally and via spinal injections are another medication option. Oral steroids may be beneficial when NSAIDs fail2,6 but treat a focal problem with a systemic treatment. Muscle relaxers, major tranquilizers, and hypnotics may also be tried for pain relief. There are also other pain medications which are often helpful such as tramadol, a non-scheduled pain medication which acts at the opioid receptors.

DIAGNOSTIC STUDIES A patient with radicular pain that brings them to the doctor, for the most part, requires diagnostic work-up to identify the cause of the radiculopathy. In general, X-rays with dynamic views and MRI imaging are helpful to evaluate for instability and to identify any neural impingement. If MRI is not an option, CAT scan may be helpful to elucidate the anatomy and cause of the radiculopathy. If there is a question of a systemic process, bone scan and lab studies are indicated. In patients without a clear localization of radiculopathy to a specific root level, or if there is a question of plexopathy, peripheral entrapment or polyneuropathy, EMG and NCS are often helpful.12

BRACING For comfort, a soft cervical collar may be worn, particularly when traveling. The negative effect is that it may lead to further deconditioning of the neck muscles. A soft collar may also help with sleep. For sleep, keeping the neck in a neutral position with pillows or a cervical pillow is beneficial. Rigid collars have also been used to treat cervical radiculopathy.2,4,5,13 There are no controlled studies showing a beneficial effect compared to no treatment but use of a collar has been part of a conservative treatment program that was effective. In one study, cervical collars were shown to have the same outcome at 16 months as surgery or physical therapy.5 635

Part 3: Specific Disorders

PHYSICAL THERAPY Introduction Because the superiority of any one rehabilitation method for cervical radiculopathy has not been firmly established, many physical therapists use a combination of conservative interventions. Some of the methods and techniques are evidence-based, while others are anecdotal or traditional. These interventions may include repeated movement exercise, manual techniques, modalities, traction, neural mobilization, dynamic stabilization exercise, postural training, patient education and ergonomics. Although research is inconclusive, there have been a number of studies published advocating the effectiveness and success of conservative rehabilitation treatment.1–3,14,15 The success of any rehabilitation treatment plan begins with the evaluation. An effective evaluation utilizes signs and symptoms, which the clinician identifies during the history and physical examination to govern clinical decision-making.16,17 Treatment decisions are made based upon a patient’s symptom response to movement and the mechanical stresses that reproduce these symptoms.16,17 This type of interactive evaluation enables the clinician to develop a treatment algorithm. The algorithm presented in this chapter can be used to direct treatment, categorize patients into different treatment paradigms, and determine the most appropriate intervention to create an objectively based treatment program.

Patient evaluation The evaluation should consist of an accurate patient history, a physical exam, an assessment, and an appropriate treatment selection. Physician referrals should include the medical diagnosis and appropriate precautions. The physical exam should include posture analysis, range of motion measurements, neurological examination, and repeated movement testing. Posture analysis is typically performed by observing the patient in various positions. Neutral spine posture can be defined as ‘a vertical line passing through the lobe of the ear, the seventh cervical vertebra, the acromion process, the greater trochanter, just anterior to the midline of the knee, and slightly anterior to the lateral malleolus.’18 Postural abnormalities may be the result of habitual adoption of poor posture or the result of an acquired deformity. The common habitual postural abnormality that the clinician should be aware of is termed the forward head position. In this position, kyphosis or flexion of the lower cervical and upper thoracic spine causes a compensatory extension or excessive lordosis in the upper cervical spine to achieve a level head position.19 Over time, excessive upper cervical lordosis may be a source of headaches, and excessive lower cervical kyphosis may lead to cervical radicular pain.19–21 There are two acquired cervical postural deformities associated with cervical radiculopathy: kyphosis and torticollis.16,22,23 In both cervical kyphosis and acute cervical torticollis, patients become locked in a protective position and are unable to move out of this acquired deformity. The physical examination continues with a range of motion assessment, which is divided into physiologic and accessory motion. The physiologic motion, or the normal gross movements of the cervical spine, includes retraction and protrusion, sagittal plane extension and flexion, transverse plane rotation and coronal plane lateral flexion (side-bending) (Table 58.1). Accessory motion is the gliding of one cervical segment on another. Assessment of accessory motion is segment specific and assists the clinician in determining the possible level of the pathology. Neurologic and specialized cervical spine testing is essential when evaluating and treating patients with cervical radiculopathy. The neurologic exam should consist of myotome, dermatome, neural tension signs, and muscle stretch reflex testing. Patients experiencing 636

Table 58.1: Chart of normal cervical spine motion Movement

Range of normal motion

Upper cervical flexion and extension

1–15°

Cervical flexion

80–90°

Cervical extension

70°

Cervical rotation

70–90°

Cervical lateral flexion

20–45°

radicular symptoms must have their myotomes and reflexes tested at each visit to monitor any changes. Special testing for the cervical spine includes Spurling’s, vertebral artery insufficiency and instability testing. Repeated movement testing evaluates patient responses to precisely controlled, repetitive spinal motion. Repeated movements causing pain to retreat to a more central location are favorable toward treatment outcomes, and those causing pain to travel more peripherally are undesirable.16,24–28 Centralization is the process by which pain, originating from the spine, retreats to a more central location and remains as a result of performing certain repeated movements, or adopting certain positions.16 Centralization of referred pain can be utilized as a diagnostic tool, as well as a means of identifying patients who will respond to conservative rehabilitation.24–27 Repeated movement testing begins with establishing pre-testing, to determine baseline symptoms. The patient is instructed to perform one repetition of the designated motion. The physical therapist then assesses symptom response to that motion. If baseline symptoms are no worse as a result, the patient is to perform that motion repeatedly. Typically, 10–15 repetitions are performed and symptoms are reassessed. If there is no effect on the baseline symptoms, additional sets of 10–15 repetitions are performed with assessment after every set. Usually, three sets, in one direction, are enough to stress the lesion and gain a symptom response. If the radicular symptoms begin to improve and centralize, the appropriate movement has been identified, and movement in that direction should be continued until symptoms resolve. If the radicular symptoms begin to peripheralize and become worse, that movement and associated posture are discontinued, and other movements are evaluated. If after three sets there has been no effect in the baseline symptoms, the clinician must ensure the motion has been adequately performed. To accomplish this task, movements must reach end range. The clinician may need to manually apply overpressure or examine sustained positions to fully stress tissues with a particular movement. If baseline symptoms still remain unaffected, movement in the opposite direction of the test movement should be examined. If a limitation of motion has been produced, as a direct result of repeatedly performing the test movement, that test movement is considered unfavorable and should be abandoned. If there was no effect with the test movement and no loss of motion in the opposite direction, that movement is cleared and other movements need to be examined. Sagittal plane movements are exhausted prior to examining coronal and transverse plane movements. Once the repeated movement test is complete, the clinician assesses the patient’s response and can utilize the algorithm to direct treatment. This pattern of assessment as part of a thorough evaluation process will allow the clinician to properly classify the patient into certain treatment patterns and therefore determine the most effective treatment interventions. These treatment interventions will be explained in more detail in the remaining portion of this chapter. Table 58.2 and Figure 58.1

Section 3: Cervical Spine

Table 58.2: Suggested treatment choices based on evaluation classification Treatment program one

Treatment program two

Treatment program three

Acute

Subacute

Chronic

Acute

Subacute

Chronic

Acute

Subacute

Chronic

X

X

X

X

X

X

X

X

X

Cold

X

X

X

X

X

X

X

Heat

X

X

X

X

X

X

X

Ultrasound

X

X

X

X

X

X

Electric Stimulation

X

X

X

X

X

X

X

X

X

X

X

X

X

X

X

X

Posture Correction Modalities

Traction

X

Repeated Movements

X

X

X

Manual Therapy

X

X

X

X

X

X

X

X

Patient Education

X

X

X

X

X

X

X

X

X

Ergonomics

X

X

X

X

X

X

X

X

X

X

X

X

X

X

X

X

X

X

Neural Mobilization

X

Exercise Stabilization Cardiovascular

X

X

X

X

X

X

Flexibility

X

X

X

X

X

X

Strength

X

X

X

X

X

X

present the fundamental clinical reasoning of the experienced clinician. The algorithm provides a structured method of assessing patient symptoms and selecting an appropriate treatment pattern (Fig. 58.1). Epidemiological evidence and time frame of injury have been used to generalize acute, subacute, or chronic injury and, to some extent, treatment. However, physical therapy treatment should be based on clinical presentation and response to repeated movement testing. Three treatment patterns have been established based upon patient response to repeated movement testing (Table 58.2). Each treatment pattern contains a variety of

techniques used to treat cervical radiculopathy. Treatment patterns one and two are designed for patients who respond positively to repeated movements and/or sustained positions and postures. Patients in this category typically have a better prognosis.24,25,27,29 Treatment pattern three is designed for severely irritable tissues. Patients in this category are unable to tolerate repeated movements or sustained positions and postures. All movements and postures tend to worsen symptoms or have no effect. Patients may require further medical treatment prior to initiating a rehabilitation program or even fail conservative treatment measures.26

Repeated movement testing

Symptoms improve

Yes Treatment pattern number 1 for acute, subacute and chronic patients

Symptoms worsen or no effect

Symptoms worsen

Symptoms improve with sustained positions/postures Yes

No Treatment pattern number 3 for acute, subacute and chronic patients. *Possibility that conservative care will fail. The patient may need to be referred back to the physician.

Treatment pattern number 2 for acute, subacute and chronic patients Fig. 58.1 Treatment algorithm.

637

Part 3: Specific Disorders

REHABILITATION METHODS FOR CERVICAL RADICULOPATHY The individualized treatment of cervical radiculopathy relies heavily upon clinical reasoning. There are no set techniques or predetermined protocols. If a patient’s condition is too acute or irritable to tolerate movement testing, symptom management takes precedence. The intent is to decrease the symptoms enough to allow the patient to tolerate the evaluation and treatment process. Symptoms may need to be managed passively through postural correction, modalities, and gentle manual techniques before initiating repeated movements.

Posture Correction of abnormal posture is used as a treatment tool to reduce abnormal and unnecessary strain, to aid in the resolution of nerve root irritation and to prevent recurrence. Patients with an acute condition will use positioning and posture to alleviate pain. The goal is to minimize pain and create an optimal healing environment for the damaged tissues. Once the condition is no longer acute and the patient is able to tolerate movements, attempts of attaining and maintaining a neutral cervical spine posture may begin. It has been reported that through the performance of an exercise program one can change one’s resting spinal posture.30,31 It has been recommended that through performing repeated cervical retraction exercises, pulling the head and neck posteriorly into a position in which the head is aligned more directly over the thorax, one can decrease the forward head posture, achieve a more neutral resting cervical spine position, increase the diameter of the neural foramen, and reduce nerve root irritation.16,18,30,32,33 This kinesthetic awareness, of achieving and maintaining a neutral cervical spine posture, is critical in the maintenance and possibly in the prevention of recurrent cervical radiculopathy.

Modalities Modalities refer to physical agents and electrotherapy methods. Physical agents are tissue cooling and heating techniques, including ultrasound. Additionally, there is a multitude of electrotherapy techniques available to the clinician. Modalities produce physiologic effects, such as promoting increased tissue extensibility, increased blood flow, spasm reduction, and pain relief that may be useful in the treatment of cervical radiculopathy. It is incumbent upon the clinician to understand the physiologic effects of the available modalities and apply them appropriately, relative to the patient’s condition. The use of heat and ice is often indicated in the early stages of treatment. The goal of their application is twofold: break the pain–muscle spasm cycle, and promote early use of movement-oriented treatment techniques. As such, their application and efficacy, while continually debated, is justified. The choice of heat or ice is empirical and largely depends on patient comfort. Cooling and heating effects of superficially applied modalities change tissue temperatures at minimal depths, and likely do not effect change at the depth of the nerve root. The depth of penetration of superficial heat has been reported to be 1–2 cm at best and insufficient to reach deep soft tissue structures.34 Application of therapeutic heat produces an increased tissue extensibility with resultant decreased stiffness, pain relief, reduction of muscle spasm, reduction of inflammation, and enhanced blood flow.35 Deep heating, through the use of ultrasound has been purported to be beneficial in increasing tissue extensibility through its thermal effects. Therefore, it may play a role in improving range of motion in the restricted cervical spine. Cryotherapy, or the application of therapeutic cold, is used when cooling effects on tissue are desired. Typically, cold is applied in early stages of injury. Analgesia may occur when tissue temperatures are decreased. Motor 638

nerve conduction velocity and muscle spindle firing has been shown to decrease when tissue temperatures drop to 10–15°C.36 This may produce desired relaxation of muscle spasm. Vasoconstriction occurs with the application of cold. That is the rationale for using cold for the reduction of inflammation and edema. Certain heating modalities may not be warranted for patients with an acute cervical radiculopathy. The stage of the patient’s condition and the results of the evaluation must be taken into account for proper selection and application of modalities. Various forms of electrical therapy have been used to modulate pain. The electrical current can be effective in disrupting the pain and spasm cycle by stimulating the afferent neural pathways, thereby inhibiting protective muscle guarding. Early reduction of pain from electrotherapy, albeit temporary, is a starting point toward a more active rehabilitation process. While the use of modalities specifically for the treatment of cervical radiculopathy has not been extensively studied, they offer the clinician commonly used and viable adjuncts to active treatment techniques. Therapeutic modalities as described here may be used as an adjunct to active intervention, but for the most part their efficacy has not been subjected to intensive clinical trials.37 Nonetheless, sufficient empirical and anecdotal evidence exists, which suggests that these agents do play a role as part of a clinic-based rehabilitation program. In the chronic patient, passive modalities have not been determined to be an effective treatment.16,38,39 Therefore, it is imperative that an active treatment program be initiated as soon as tolerated while the use of modalities is de-emphasized.

Cervical traction Cervical traction is often used in the treatment of radiculopathy.2,8,40–43 The rationale for traction is based on elongation of the spine, resultant increase in intervertebral space, relaxation of spinal muscles, opening of the neural foramen, and relief of nerve root compression.44–46 With cervical traction, the reduction of compressive forces theoretically serves to create space for the inflamed or compressed nerve root, thereby diminishing structural impingement and improving fluid dynamics. The efficacy of traction has not been conclusively proven in a randomized, controlled trial, but it is commonly used and thought to be beneficial in the treatment of cervical radiculopathy.47,48 Many clinicians advocate manual traction as a means of assessing the patient’s response to the technique prior to employing mechanical devices and as a treatment technique itself. Figure 58.2 represents application of manual traction. The variables of duration, direction of force, and position can be rapidly assessed and easily changed dependent on the pain response. The clinician will be looking for pain to move from a distal to a proximal location and decrease in intensity as a favorable response. Once it has been determined that the response is favorable, mechanical treatment devices can be employed. Should cervical traction produce a desirable effect, home traction units are available. Concerning duration of traction forces, Colachis and Strohm showed that nearly all vertebral separation occurs during the first seven seconds of force application, but that up to 20–25 minutes is necessary to produce muscle relaxation.40–42 Intermittent traction produces twice the amount of separation as sustained traction and as a result it is currently the mode of choice.49 If improvement is realized, parameters of time and traction force can be increased on a slow gradient until maximum benefit as measured by symptom relief is achieved. With regard to positioning, traction is typically performed with the patient sitting or supine. The supine position has been shown to provide greater separation of intervertebral spaces from C4 to C7 than sitting, when the angle of pull and force were controlled.50

Section 3: Cervical Spine

Table 58.3: Repeated movements and manual techniques Procedures

Plane of Movement

Retraction (with/without Patient-generated, sagittal plane, overpressure, sitting or standing) weight-bearing movement

Fig. 58.2 Manual traction.

This suggests that the supine position is superior for the desired separation effect. The angle of pull must be correct to get the desired therapeutic effect. Flexion of 20–30° is advocated to obtain the greatest benefit of posterior muscular elongation and enlargement of the intervertebral foramina.51 There is no firm consensus on the amount of traction force needed to produce a desired clinical result. It appears that at least 25–30 pounds of force are required to produce measurable separation of the cervical vertebrae.41,42,52 The traction force must be at least the weight of the head to produce any significant decompression. Traction is contraindicated in the presence of any disease resulting in structural compromise or instability.53 Examples include tumor, infection, and rheumatoid arthritis. Further, any condition for which movement is contraindicated also is a contraindication for traction.54 Relative contraindications include acute strains and sprains that would be aggravated by traction.19 Traction applied to patients with joint instability may cause further strain and should be carefully monitored if applied at all. Other relative contraindications may include pregnancy, osteoporosis, hiatal hernia, and claustrophobia. A careful patient history should be taken before employing cervical traction to rule out absolute and relative contraindications. It is strongly advised to consult dynamic X-rays first to clear the patient of instabilities that could be aggravated by traction. Unstable spondylolisthesis or atlanto-axial instability is a contraindication for traction. When applying cervical traction, one must be aware of additional risk factors including increased blood pressure, respiratory compromise and temporomandibular joint compression due to the required harness for certain mechanical devices.

Repeated movements and associated manual techniques As soon as the patient is able to tolerate motion, movements that centralize the radicular symptoms are employed. Refer to Table 58.3, repeated treatment movements and the associated manual techniques. When utilizing repeated movements and associated manual techniques, there is a progression of force that should be followed. Patient generated forces in mid range and then end range are performed first. If the centralization process plateaus, more force is required to fully resolve the patient’s symptoms. Patient generated overpressure can be applied at the end range of motion. If symptoms continue to centralize but plateau once again, additional force, beyond the patient’s capabilities, may be required. At this point, therapist generated forces are necessary to fully resolve symptoms. Therapist

Retraction and extension (with/without overpressure, sitting or standing)

Patient-generated, sagittal plane, weight-bearing movement

Retraction and extension (with overpressure, lying supine or prone)

Patient-generated, sagittal plane, nonweight-bearing movement

Retraction and extension with traction and rotation (lying supine)

Therapist-generated, sagittal plane, nonweight-bearing mobilization

Extension mobilization (lying prone)

Therapist-generated, sagittal plane, nonweight-bearing mobilization

Retraction and lateral flexion (with/without overpressure, sitting, standing or supine)

Patient-generated, coronal plane, weight-bearing or nonweightbearing movement

Lateral flexion mobilization and manipulation (sitting or lying supine)

Therapist-generated, coronal plane, weight-bearing or nonweight-bearing mobilization and manipulation

Retraction and rotation (with/without overpressure, sitting or standing)

Patient-generated, transverse plane, weight-bearing movement

Rotation mobilization and manipulation (sitting or lying supine)

Therapist-generated, transverse plane, weight-bearing or nonweight-bearing mobilization and manipulation

Flexion (with/without Patient-generated, sagittal plane, overpressure, sitting or standing) weight-bearing movement Flexion mobilization (lying supine)

Therapist-generated, sagittal plane, nonweight-bearing mobilization

applied overpressure is performed first. If little to no improvement has been made, more reductive force is indicated. Mobilization and if necessary manipulation may be added to the regimen. After each therapist applied technique, symptoms are reassessed and the patient is instructed to repeat the movements unaided. Sagittal plane movement and techniques, in weight bearing, are exhausted before performing movements in the coronal plane, transverse plane, and non-weight bearing positions. One exception is a patient who presents with postural torticollis. In most cases, postural torticollis will require lateral flexion and rotational techniques.16 Patients with an acute injury and/or postural torticollis or kyphosis may not be able to tolerate movements in weight bearing. In these cases, patients are treated in a lying position. Lying unloads the motion segment and places it in slight traction, producing less pain with movement. Evidence suggests that symptom reduction is more stable when treated in a weight bearing position.23 Therefore, movements are to be performed in weight bearing whenever possible. Once a directional preference is found, movements in that direction are to be performed for 10 repetitions every 2 hours. The reduction of symptoms is maintained through repetition and posture correction. The correct posture is determined by the directional preference of the treatment. Any adverse strain has the ability to revert compression back upon 639

Part 3: Specific Disorders

the cervical nerve root. As symptoms become intermittent and more stable, the repetitions can be reduced by half. When the patient is pain free for 3–4 days the exercises only need to be performed a few times a day and as needed. At this time, the patient may begin restoration of function. The patient is instructed to move in those directions that were once avoided. This is done to restore full range of motion and soft tissue flexibility. Cervical stabilization exercises may safely begin. Finally, the patient is educated in prevention techniques, warning signs of symptom return, and self-treatment techniques. Treatment plans based on patient response to repeated movements have been found to yield better results in symptom reduction, symptom elimination, and restoration of function when compared to other conservative interventions.28 In addition, when centralization is observed, a favorable treatment result is expected.25,27,29 Centralization is often seen when the injury is acute (less than 8 weeks), symptoms are intermittent, and the patient demonstrates no significant neurological deficits.16,29 Donelson et al. investigated the usefulness of the centralization phenomenon in evaluating and treating referred pain. It was determined that 87% of patients, in whom symptoms centralized, had excellent outcomes with relief of pain and functional recovery.25 If a directional preference is not found and symptoms do not centralize within 2–3 weeks, minimal improvements are expected and the risk of developing chronic disability is greater.24,26,29 It has been recommended that non-centralizers receive additional medical treatment for either physical or non-physical factors that could delay symptom resolution.26 Patients should also be instructed in performing an active exercise program emphasizing return to function and avoiding activities that increase or produce radicular pain.26

Fig. 58.3 End-range traction, retraction extension mobilization.

niques are designed to stretch and glide the nerve root. This can be accomplished by performing upper limb neural tension tests. Neural mobilization techniques are applied either actively or passively. Because these techniques are designed to mobilize restricted neural elements, a temporary peripheralization of symptoms will occur.

Manual therapy techniques There are a variety of manual techniques utilized to treat cervical radiculopathy.16,22,23,55,56 Manual therapy may be used in an acute or stable condition. In the acute stage, gentle manual techniques are used to reduce pain and enable patients to begin movement on their own. In the latter stages of treatment, it is used to achieve and maintain full range of motion and function. Mobilization techniques are applied either actively or passively. Active mobilization includes proprioceptive neuromuscular facilitation and muscle energy techniques. Passive mobilization is a repetitive, passive movement of varying amplitude and low acceleration applied at different points in the range of motion.57 Manual techniques should begin with the spine positioned in a relatively pain free posture. A mobilizing force is locally applied to the designated vertebral segment. The direction of the mobilizing force is governed by patient response. In the presence of a radiculopathy, the exacerbation of distal symptoms should be avoided.58 The direction of application, the rate, the rhythm and the force used to produce motion and symptom changes must be meticulously monitored. Techniques can be individualized to appropriately treat the patient’s condition. The force of the mobilization will vary from very gentle and barely perceptible, in painful situations, to maximal force at end range of motion as symptoms become less irritable. As radicular symptoms decrease, treatment may be progressed to increase motion and resolve remaining axial pain. Figure 58.3 presents an end-range mobilization utilized to restore extension range of motion.

A

Neural mobilization techniques Neural mobilization techniques are a combination of upper limb and cervical spine movements used to free nerve root restrictions and restore normal mobility to the nervous system.55 Refer to Figure 58.4 for an example of an upper limb nerve glide and stretch. These tech640

B Fig. 58.4 (A) Starting position of a median nerve bias dural glide. (B) Midposition of nerve glide.

Section 3: Cervical Spine

Exercise

C Fig. 58.4 (C) End-range position of nerve glide.

The production of peripheral symptoms should cease shortly after the treatment technique has been performed. Symptoms must not remain worse as a result of treatment. If the radicular symptoms remain exacerbated, the mobilization was applied too strenuously. In a patient in whom the radicular symptoms remain worse and cervical spine motion becomes limited in the opposite direction to the neural mobilization, the cervical spine movement, associated with the neural mobilization, could be aggravating the condition. The patient may have a directional preference and an underlying condition that will improve with repeated movements in that direction. Such a patient should be treated with repeated gentle movements until the symptoms are stable, and resume the neural mobilization techniques if a restriction still exists.16 When treating acute symptoms, the neural techniques should be performed passively, in a relaxed, pain relieving posture, far removed from the symptom area.55 The techniques are to be performed through as much of the range of motion as possible as long as symptoms are not reproduced. Butler and Jones recommend a sequence of gentle oscillations for approximately 20–30 seconds.55 After each sequence, symptoms must be monitored and reassessed. As the patient improves, pain free range of motion will improve. As this occurs, the treatments need to become more aggressive to have a therapeutic effect. Progression of the applied neural mobilization techniques may include: performing the technique actively, moving closer to or at the lesion site, placing tension on the neural system as the glides are being performed, increasing the grade of the mobilization and performing the oscillations at end range. Unlike treatment of the irritable condition, some degree of pain and symptom reproduction is expected and necessary to fully restore the neural movement. Symptoms must be constantly monitored to ensure that they are improving. The techniques are continued until full range of motion and function has been achieved. The mechanism by which neural mobilization effectuates symptom resolution is unknown. The leading hypothesis is that ‘mobilization of the nervous system has a mechanical effect on the vascular dynamics, axonal transport systems and mechanical features of the nerve fibers and connective tissues.’55 Studies have been published that support this theory and the use of neural mobilization techniques for treating radicular pain.59–63 Although we are believers in this conceptual model and apply the techniques, there is no peer-reviewed literature that substantiates either the mechanism of action or that the treatment is effective.

Once the patient’s symptoms have centralized, or if centralization has not occurred in approximately 2–3 weeks, restoration of function through an exercise program may begin.24,26,29 Care is taken to avoid production or exacerbation of radicular symptoms.26 Cervical spine stabilization techniques have been theorized to allow the patient to gain neuromuscular control over movements and eliminate mechanical sources of pain.6 The approach begins with identifying the neutral position of the spine. This neutral position is defined as the pain free position in which the patient can perform necessary functional activities. Starting in the neutral position, the patient is guided through a gradient of simple isometric exercises. Addition of upper limb and body movements can be incorporated to challenge the patient to maintain neutral cervical spine posture during simulated functional activities.64 Refer to Figure 58.5 for examples of cervical stability exercises. Patients are only progressed to more advanced positions when the basic exercises are pain free. Slow progression that is advanced as tolerated and focuses more on functional activities has been shown to yield better results.17 Others believe that the exercise should not be overly aggressive and efforts should focus toward progressively reducing the patient’s pain and advancing function.2 As the patient improves, strengthening may progress to isotonic or isokinetic techniques.

A

B Fig. 58.5 (A) Intermediate cervical stabilization exercise. (B) Advanced cervical stabilization exercise. 641

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Ergonomics and patient education Ergonomics is an essential adjunctive component of treatment. Many activities, both in the workplace and at home, require sustained positions that may compromise recovery and cause relapse.16,20,32 Activities requiring sustained positions tend to promote detrimental postures and increase radicular symptoms.16,32,55 Preventing sustained working postures is an integral aspect of the rehabilitation program.65 Appropriate work area design and body mechanics training should be performed to offer the patient the best possible chance of a maintaining recovery and function. Patient education is one of the most important tools used to treat cervical radiculopathy. Patients instructed in the clinical reasoning process and given the proper education can competently begin self-treatment and help prevent future injuries.6,16 This training encourages the patient to become an active participant in the rehabilitation process. As a result, patients are able to evaluate their symptom response during activities and situations, utilize self-treatment techniques, and prevent recurrence.6,16,66 An appropriate quote by Mckenzie states, ‘If there is the slightest chance that patients can be educated in a method of treatment that enables them to reduce their own pain and disability using their own understanding and resources, they should receive that education.’16 In conclusion, the success of any physical therapy rehabilitative treatment plan begins with the evaluation. An effective evaluation utilizes signs and symptoms, identified during the history and physical examination, to govern clinical decision-making.16,17 The individualized treatment of cervical radiculopathy relies heavily upon clinical reasoning. There are no set techniques or predetermined protocols. Once the evaluation is complete, the clinician assesses the patient’s response and utilizes the algorithm to direct treatment. The algorithm provides a structured method of assessing patient symptoms and selecting an appropriate treatment pattern. Because the efficacy of any one treatment philosophy has not been firmly established, a variety of techniques, based on the patient’s response to movement testing, should be used to deliver the most comprehensive and effective treatment. The clinical approach also may vary depending on the acuity of the radicular pain and the etiology. Comorbidities and age are also taken into account when formulating a treatment plan including medication management and rehabilitation techniques. Communication with the patient and treating physician are integral parts of providing safe and effective treatment for patients with cervical radicular pain. Effective medication management including pain relief and reduction of inflammation are part of an effective rehabilitation program. They allow the physical therapist to progress treatment and contribute to the resolution of symptoms. Randomized, controlled trials evaluating rehabilitation techniques for the treatment of cervical radicular pain are necessary to better identify the techniques that are the most effective.

Example 1 A patient has cervical radicular pain that is mild to moderate and has been decreasing over the past several weeks with mild myotomal and dermatomal deficits in a pattern consistent with the MRI findings. The initial approach to treatment would be NSAIDs if not contraindicated, activity modification, physical therapy, and ergonomic education. If the patient’s sleep was disturbed secondary to pain a short-acting narcotic medication would be prescribed for use prior to sleep. Sleeping position modifications would be recommended. If neuropathic pain was a prominent complaint a TCA or neurontin would be considered. 642

If the patient’s symptoms did not improve over the next 3–4 weeks, or if the symptoms escalated, the next step would be selective nerve root blocks.

Example 2 A patient presents with severe radicular pain, inability to function at work, and mild neurologic deficits in a pattern consistent with their imaging studies. This patient would benefit from treatment with NSAIDs, narcotic analgesia on a prn basis, and early intervention with spinal injections, specifically selective nerve root blocks. If the symptoms do not improve or if the weakness progresses surgical evaluation is indicated.

Example 3 Patients with progressive neurologic deficits, marked weakness, and those with evidence of myelopathy or cord contusion require prompt surgical evaluation. The degree of urgency will depend on the duration of symptoms, history of trauma, and clinical findings.

CONCLUSION As in nearly all medical conditions, treatment depends on history, exam, and response to treatment offered. There are no proven algorithms to approach treatment of cervical radiculopathy, as better studies have yet to be performed. The algorithms offered are based on the author’s experience and the limited evidence available – one of the many examples of the art of medicine waiting for the science to lead to evidence-based algorithms. Treatment of an individual patient remains a moving target with further interventions dependent on the progression or resolution of symptoms and signs, along with diagnostic data and forthcoming evidence-based medicine. The astute clinician bases practice on a combination of experience and evidence-based medicine to help guide recommendations to patients. The more informed we make our patients, the better position they are in to make treatment decisions and understand their options. Barring progression of neurologic deficits or development of myelopathy, a trial of rehabilitative techniques to treat cervical radiculopathy is an accepted, and now recommended, course of treatment. A detailed neurologic exam, activity modification, and antiinflammatory medications are the initial approach. Bracing, physical therapy, traction, and other modalities are often useful with oral steroids and selective nerve root blocks used for patients who do not improve after 4 weeks of treatment or those who cannot tolerate physical therapy. When to image a particular patient varies by clinician. Prior to sending patients for physical therapy or performing traction, the minimum diagnostic study would be a set of X-rays with dynamic views. If there are motor deficits, reflex changes, symptoms that last more than 2–3 weeks without improvement, or if the patient is being sent for spinal injections, MRI imaging is indicated. Patients with progressive weakness or persistent symptoms in spite of an appropriate conservative program should be referred for a surgical evaluation as should patients with myelopathy. Patients with painless weakness present another category of patients for whom early surgical decompression is often recommended. Theoretically, these patients have nerve root compression without significant inflammation and no sensory nerve root irritation. A literature search did not produce any evidence supporting early decompression in these patients. Regularly scheduled follow-up appointments and clear instructions to patients to be aware of changes in strength, bowel and bladder function, sensation, and gait are critical to monitor a patient’s response to treatment. Rehabilitation methods are an effective treatment for cervical radiculopathy. The timing of specific interventions and the efficacy of specific methods require further investigation.

Section 3: Cervical Spine

References 1. Heckmann JC, Lang CJ, Zobelein I, et al. Herniated cervical intervertebral discs with radiculopathy: an outcome study of conservatively or surgically treated patients. J Spinal Disord 1999; 12:396–401. 2. Saal JS, Saal JA, Yurth EF. Nonoperative management of herniated cervical intervertebral disc with radiculopathy. Spine 1996; 21:1877–1883. 3. Sampath P, Bendebba M, Davis JD, et al. Outcome in patients with cervical radiculopathy: prospective, multicenter study with independent clinical review. Spine 1999; 21:591–597. 4. Persson LC, Moritz U, Brandt L. Cervical radiculopathy: pain, muscle weakness and sensory loss in patients with cervical radiculopathy treated with surgery, physiotherapy or cervical collar. A prospective, controlled study, Eur Spine J 1997; 6:256–266. 5. Persson LC, Carlsson CA, Carlsson JY. Long-lasting cervical radicular pain managed with surgery, physiotherapy, or a cervical collar: A prospective, randomized study. Spine 1997; 22:751–758. 6. Wolff MW, Levine LA. Cervical radiculopathies: conservative approaches to management. Phys Med Rehab Clin N Am 2002; 13:589–608. 7. Fouyas IP, Statham PF, Sandercock PA. Cochrane review on the role of surgery in cervical spondylitic radiculomyelopathy. Spine 2002; 27:736–747. 8. Ellenberg MR, Honet JC, Treanor WJ. Cervical radiculopathy. Arch Phys Med Rehabil 1994; 75:342–352. 9. American Pain Society. Principles of analgesic use in the treatment of acute pain and cancer pain, 5th edn. Glenview, IL: APS; 2003. 10. Simdrup SH, Jensen TS. Efficacy of pharmacological treatment of neuropathic pain: an update and effect related to mechanism of drug action. Pain 1999; 83:389–400. 11. Backonja M, Glanzman RL. Gabapentin dosing for neuropathic pain: evidence from randomized placebo-controlled clinical trials. Clin Ther 2003; 25:81–104. 12. Dillingham TR. Electrodiagnostic approach to patients with suspected radiculopathy. Phys Med Rehabil Clin N Am 2002; 13:567–588. 13. Redford JB, Patel A. Orthotic devices in the management of spinal disorders. Spine: State of the Art Reviews 1995; 9:673–688. 14. Radhakrishnan K , Litchy WJ, O’Gallon WN, et al. Epidemiology of cervical radiculopathy: a population-based study from Rochester, Minnesota, 1976 through 1990. Brain 1994; 117(Part 2):325–335. 15. Mochida K, Hiromichi K, Atsushi O, et al. Regression of cervical disc herniation observed on magnetic resonance images. Spine 1998; 23:990–995. 16. Mckenzie RA. The cervical and thoracic spine,1st edn.Waikanae, New Zealand: Spinal Publications (NZ) Limited; 1990. 17. Piva SR, Erhard RE, Al-Hugail M. Cervical radiculopathy: a case problem using a decision-making algorithm. JOBST 2000; 30(120):745–-754. 18. Goebel A, Fater D, Kernozek T. The effects of cervical retraction exercise on forward head posture and cervical range of motion in an asymptomatic population. The Mckenzie Journal; 10:24–29. 19. Saunders DH, Saunders R. Evaluation, treatment and prevention of musculoskeletal disorders. Spine 1993; 3:1. 20. Braun BL. Postural differences between asymptomatic men and women and craniofacial patients. Arch Phys Med Rehabil 1991; 72:653–656. 21. Griegel-Morris P, Larson K, Mueller-Klaus K, et al. Incidence of common postural abnormalities in the cervical, shoulder and thoracic regions and their association with pain in two age groups of healthy subjects. Phys Ther 1992; 72:425–431. 22. Cyriax JH, Cyriax PJ. Cyriax’s illustrated manual of orthopaedic medicine, 2nd edn. OM Publications; London: Butterworth Heinemann 1993. 23. Mulligan BR. Manual therapy ‘NAGS’, ‘SNAGS’, ‘MWMS’ etc, 4th edn. Wellington, New Zealand: Plane View Services; 1999. 24. Werneke M, Hart DL. Discriminant validity and relative precision for classifying pain patients with nonspecific neck and back pain by anatomic pain patterns. Spine 2003; 28(2):161–166. 25. Donelson R, Silva G, Murphy K. Centralization phenomenon: its usefulness in evaluating and treating referred pain. Spine 1990; 15:211–213. 26. Werneke MW, Hart DL, Cook D. A descriptive study of the centralization phenomenon: a prospective analysis. Spine 1999; 24:676–683. 27. Long AL. The centralization phenomenon: its usefulness as a predictor of outcomes in conservative treatment of chronic low back pain (a pilot study). Spine 1995; 20:2513–2521.

30. Pearson ND, Walmsley RP. Trial into the effects of repeated neck retractions in normal subjects. Spine 1995; 20(11):1245–1251. 31. Scannell JP, McGill SM. Lumbar posture – should it, and can it be modified? A study of passive tissue stiffness and lumbar position during activities of daily living. Phys Ther 2003; 83(10):907–917. 32. Abdulwahab SS, Sabbahi M. Neck retractions, cervical root decompression, and radicular pain. J Ortop Sports Phys Ther 2000; 30:4–12. 33. Lentell G, Kruse M, et al. Dimensions of the cervical neural foramina in resting and retracted positions using magnetic resonance imaging. J Ortop Sports Phys Ther 2002; 32(8):380–390. 34. Michlovitz S. Thermal agents in rehabilitation. Philadelphia: FA Davis; 1996. 35. Hunter J, Mackin E, Callahan A (eds). Rehabilitation of the hand: surgery and therapy. St. Louis, MO: Mosby; 1995. 36. Fisher E, Solomon S. Physiological responses to heat and cold. In: Licht S, ed. Therapeutic heat and cold. Baltimore: Waverly Press; 1965. 37. Quebec Task Force on Spinal Disorders. Scientific approach to the assessment and management of activity-related spinal disorders: A monograph for clinicians. Report of the Quebec Task Force on Spinal Disorders. Spine 1976; 1:127–134. 38. Rosonoff H, et al. Chronic cervical pain: radiculopathy or brachialgia. Spine 1992; 17(suppl): S362. 39. Tan J, Nordin M. Role of physical therapy in the treatment of cervical disc disease. Orthop Clin North Am 1992; 23:435. 40. Harris PR. Review of literature and treatment guidelines. Phys Ther 1977; 57: 910–915. 41. Colachis SC, Strohm BR. A study of tractive forces and angle of pull on vertebral interspaces in the cervical spine. Arch Phys Med Rehabil 1965; 46: 820–829. 42. Colachis SC, Strohm BR. Relationship of traction time to varied tractive forces with constant angle of pull. Arch Phys Med Rehabil 1965; 46:815–819. 43. Stratton SA, Bryan JM. Dysfunction, evaluation and treatment of the cervical spine and thoracic inlet. In: Bonatell, B, Wooden M, eds. Orthopaedic physical therapy, 2nd edn. New York: Churchill Livingstone; 1993:77–122. 44. Hood J, Hart DL, Smith HG, et al. Comparison of electromyographic activity in normal lumbar sacrospinous musculature during continuous and intermittent pelvic traction. J Orthop Sports Phys Ther 1981; 2:137–141. 45. Murphy MJ. Effects of cervical traction on muscle activity. J Orthop Sports Phys Ther 1991; 13:220–225. 46. Colachis SC, Strohm BR. Effect of duration of intermittent cervical traction on vertebral seperation. Arch Phys Med Rehabil 1986; 47:353–359. 47. Dreyer SJ, Boden SD. Nonoperative treatment of neck and arm pain. Spine 1998; 23:2746–2854. 48. Van der Heijden GJ, Beurskens AJ, Koes BW, et al. The efficiency of traction for neck and back pain, a systematic blinded review of randomized clinical trial methods. Phys Ther 1995; 75:93–104. 49. Zybergold RS, Piper MC. Cervical spine disorders: a comparison of three types of traction. Spine 1985; 10:857–871. 50. Deets D, Hands KL, Mupp SS. Cervical traction: a comparison of sitting and supine positions. Phys Ther 1977; 57:255–261. 51. Crue BL, Todd EM. The importance of flexion in cervical halter traction. Bull Los Angel Neuro Soc 1965; 30:95–98. 52. Judovich BD. Herniated cervical disc: a new form of traction therapy. Am J Surg 1952; 84:446–456. 53. Yates D. Indications and contraindications for spinal traction. Physiotherapy 1972; 58:55. 54. Esses SI. Textbook of spinal disorders. Philadelphia: JB Lippincott Company; 1995. 55. Butler DS, Jones MA. Mobilization of the nervous system. London: Longman Group UK Limited; 1991. 56. Maitland GD. Vertebral manipulation, 5th edn. London: Butterworth; 1986. 57. Gross AR, Kay TM, Dennedy C, et al. Clinical practice guidelines on the use of manipulation or mobilization in the treatment of adults with mechanical neck disorders. Man Ther 2002; 7(4):193–205. 58. Conley MS, Meyer RA, Bloomber JJ, et al. Noninvasive analysis of human neck muscle function. Spine 1995; 20(13):2505–2512.

28. DiMaggio A, Mooney V. Conservative care for low back pain: What works? J Musculoskeletal Med 1987; 4:9.

59. Kornberg C, Lew P. The effect of stretching neural structures on grade I hamstring injuries. JOBST 1989; June:481–487.

29. Werneke MW, Hart DL. Centralization phenomenon as a prognostic factor for chronic low back pain. Spine 1999; 24:758–765.

60. Bora FW, Richardson S, Black J. The biomechanical responses to tension in a peripheral nerve. J Hand Surg 1980; 5:21–25.

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62. Lundborg G. Nerve injury and repair. Edinburgh: Churchill Livingstone.

65. Jacobs K, Bettencourt CM. Ergonomics for therapists. London: ButterworthHeinemann; 1995:140–141.

63. Totten PA, Hunter JM. Therapeutic techniques to enhance nerve gliding in thoracic outlet syndrome and carpal tunnel syndrome. Hand Clin 1991; 7(3):505–520.

66. Slipman CW, Isaac Z, Patel R, et al. Chronic neck pain: the specific syndromes. J Musculo Med 2003; 24–33.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ i: Cervical Radicular Pain

CHAPTER

Cervical Radicular Pain: Injection Procedures

59

Jason S. Lipetz

INTRODUCTION This chapter will review the literature pertaining to the use of epidural space steroid injection (ESI) in the treatment of cervical radicular pain. Epidural injections are utilized to introduce corticosteroid and anesthetic to the epidural compartment and the suspected site of neural injury. There is a plethora of literature describing ESI in the treatment of lumbar radicular and axial pain, and this topic will be comprehensively addressed in a dedicated chapter of this text. Injection therapy has found a particular role in the treatment of lumbar radiculopathy, as a growing body of literature has supported a biochemical and inflammatory injury component in the case of lumbar radicular disorders.1–5 Recent prospective uncontrolled6–9 and controlled lumbar studies10–12 have suggested a significant beneficial response when transforaminal epidural steroid injections (TFESI) are utilized in the treatment of radiculopathy. While the role of inflammation in the injury process of cervical radiculopathy has largely been extrapolated from this lumbar literature base, several studies have similarly highlighted the biochemical processes likely at play in cervical radicular disorders. In a study of cervical disc specimens removed during discectomy for radiculopathy,13 when compared to control disc samples, significant increases in matrix metalloproteinase, nitric oxide, prostaglandin E2, and interleukin-6 were observed. A later study by this same author14 revealed herniated cervical disc specimens to be biologically responsive with resultant increased levels of nitric oxide, interleukin-6, and prostaglandin E2 when exposed to interleukin-1β. A more recent immunohistochemical investigation of herniated cervical intervertebral discs15 has revealed the presence of inflammatory processes and neovascularization, increased levels of matrix metalloproteinase, and a marked increase in nitric oxide production when compared to control samples. Similar to the lumbar literature, which has revealed abnormal radiographs and compressive lesions in asymptomatic individuals,16–18 studies of the cervical spine also reveal abnormal radiographic findings in patients without cervical pain or symptoms of radiculopathy.17,19,20 In a cervical MRI study of asymptomatic patients,19 20% of subjects over 40 years of age were observed to have foraminal stenosis, and 10% of cases under 40 years of age revealed a herniated disc. In an earlier study of asymptomatic subjects employing cervical myelography,17 21% of cases were observed to have nerve root filling defects. These significant radiographic and potentially compressive findings in asymptomatic individuals suggest that a purely mechanical injury construct is too simplistic. Also, parallel to the lumbar radiographic literature,21–24 which has revealed regression of symptomatic disc lesions with a tendency for symptoms to improve prior to radiographic regression, cervical studies have demonstrated a regression of symptomatic cervical disc pathology.25–27 Both CT26 and MRI25,27 studies have revealed the

largest disc herniations to reduce most in size. In greater than 75% of cases a 35–100% size reduction in disc lesions has been observed, and a greater likelihood of resolution is realized in cases of disc extrusion. In combination, these cervical-specific biochemical and radiographic studies set the stage for a mechanochemical injury construct in cases of cervical radiculopathy. It is the biochemical or inflammatory component of neural injury that is the intended target of ESI therapy. The remainder of this chapter will review the available literature addressing this treatment approach in cervical radicular disorders.

BACKGROUND LITERATURE Similar to lumbar ESI, injections to the cervical spine can be performed through either an interlaminar or transforaminal approach. During the performance of interlaminar injections, medication is most reliably placed in the epidural space with the use of fluoroscopic guidance. This fact has been established in the lumbar spine injection literature. White28 revealed a 25% miss rate when interlaminar injections were performed by an experienced anesthesiologist without the use of fluoroscopy. The inaccuracy of cervical interlaminar injections performed without guidance has more recently been reported.29 In this multicenter retrospective analysis, a first-attempt miss rate of 53% was observed when the typical loss of resistance technique was utilized. When medication was successfully introduced to the epidural space, ventral spread of medication was observed in only 28%. While interlaminar ESI can be performed with technical success, particularly with the use of fluoroscopic guidance, there are anatomic advantages to performing ESI through a transforaminal approach.30 With interlaminar injections, medication is typically deposited dorsally, posterior to the thecal sac. The spinal pathology that serves as the intended target of ESI is typically located in the ventral spinal canal. TFESI provides the interventionist an opportunity to better control the flow of injectant and target the specific level of segmental pathology. In addition, and of particular importance in the cervical spine, the transforaminal injection approach allows for foraminal and extraforaminal spread of medication. The complexity of the cervical anatomy requires fluoroscopic guidance if TFESI is to be performed. In addition, and similar to ESI in the lumbar spine, the use of fluoroscopic guidance and contrast enhancement allows the interventionist to avoid vascular uptake, which would prevent the successful placement of medication at the injury site. Indeed, this is a significant issue for two reasons. The general notion is that a local instillation of glucocorticoid provides greater benefit than using an oral or parenteral route. If the medication is infused intravascularly, this proposed benefit will be obviated. A second and potentially more important reason to avoid intravascular uptake is the possibility of inadvertent arterial injection with resultant neural injury. Such complications 645

Part 3: Specific Disorders

will be further reviewed in the concluding section of this chapter. Several studies underscore the importance of using fluoroscopy during spinal injection procedures. An 11.2% incidence of venous uptake has been observed by fluoroscopy during lumbar TFESI, necessitating needle repositioning to achieve a satisfactory epidurogram.31 An earlier study of fluoroscopically guided lumbar injections32 revealed a 10.9% and 10.8% incidence of vascular uptake during transforaminal and caudal injections, respectively, compared with a 1.9% incidence when utilizing an interlaminar approach. In a prospective study of 337 cervical TFESI,33 the overall rate of fluoroscopically visualized venous uptake was 19.4%. Observation of blood in the hub of the injection needle was determined to be unreliable in the detection of vascular uptake, with a 97% specificity but only a 45.9% sensitivity observed. These studies highlight the role of fluoroscopic visualization as the only reliable means of observing venous uptake, as the sensitivity of blood observed in the spinal injection needle or tubing is unacceptably poor. While the majority of background literature addressing cervical ESI describes an interlaminar injection approach, performed with and without fluoroscopic guidance, more recent clinical studies employ fluoroscopically guided TFESI. While there is an apparent trend for more recent cervical literature to describe a transforaminal (TF) approach, there remains a wide discrepancy in cervical injection techniques employed by the interventional spine community. A recent national survey of anesthesia practices found that fluoroscopic guidance is employed during cervical ESI in 73% of private practices but in only 39% of academic institutions.34 Similarly, TFESI was more likely to be employed by 61% of private practices but only 15% of academic centers.

INTERLAMINAR INJECTION LITERATURE Cervical ESI clinical outcome studies have been published, but the body of literature is not as vast as that addressing lumbar ESI. To date, the overwhelming majority of these studies are uncontrolled and retrospective. The introduction of cervical epidural injections initially arose as a result of the described successes in treating lumbar axial and radicular pain with epidural injections of corticosteroid. The earliest reference to cervical epidural injection therapy was in a 1972 study describing the role of intra- and extradural corticosteroids.35 In the 1980s, several studies reported clinical outcomes following cervical epidural injection therapy.36–40 These studies included patients with a variety of clinical presentations including radiculopathy, cervical pain, reflex sympathetic dystrophy, postherpetic neuralgia, and viral brachial plexitis. Three uncontrolled studies published in 1986 which included a total of 180 patients describe a combined result of greater than 90% pain relief in 20–24% of patients and little to no response in 12–24% of cases.37–40 In these studies, an interlaminar injection approach was performed without fluoroscopic guidance. In one of these studies38 that retrospectively analyzed 25 patients receiving an average of 1.5 injections, patients with superior outcomes were more likely to present with radicular pain and sensorimotor deficits on examination. In a 1988 study41 of 16 patients presenting with suspected cervical radicular symptoms without a radiographic correlate, up to three blind interlaminar ESI were performed. After 1 year and questionnaire follow-up, 12 patients described their pain as improved and 50% of those patients with initial neurological deficits reported improvement in these symptoms. Additional outcome studies published in the 1990s36,40,42 describe approximately 40% of 100 combined patients realizing relief of 70% or greater. In one of these studies,36 which included 58 patients followed for 6 months, 41.4% demonstrated an excellent response, defined as greater than 90% pain relief. An excellent outcome was described to be more likely in 646

those patients with radiographic evidence of spondylosis or subacute cervical strains. A 1993 retrospective analysis of 100 patients43 receiving cervical interlaminar ESI attempted to identify patient characteristics that would serve as reliable predictors of clinical outcome. In each case, a mean of 2.35 injections were performed in a nonfluoroscopically guided (blind) fashion at the level of suspected segmental pathology. Forty-one percent of the total patient population described greater than 50% pain relief and at least a partial return to normal activities at a mean of 14.7 months follow-up. Symptom duration prior to injection and a history of trauma did not prove reliable in predicting clinical outcomes. Older patients and those with radicular pain were observed to realize more lasting pain relief. In this study, patients with a herniated disc or a motor deficit were observed to do worse. Patients with cervical spondylosis or stenosis demonstrated a superior outcome. The authors concluded that patients with clinical radiculopathy or radicular pain were more likely than patients with axial pain alone to realize relief from cervical ESI. Complications in this study included a 2% incidence of dural puncture and 4% incidence of vasovagal events. In a 1996 study of 26 patients44 treated nonsurgically for cervical radiculopathy associated with a herniated disc, 20 patients demonstrated a good or excellent outcome. Each of these patients was fully satisfied with the outcome and reported little to no residual pain or activity limitation. Nineteen of these 20 successes initially presented with cervical disc extrusion. The outcomes following injection therapy in this study cannot be presented with any certainty, as only nine of these patients received a single fluoroscopically guided cervical ESI performed in either an interlaminar or transforaminal fashion. Other nonsurgical treatment approaches employed in this study included relative rest, icing, the use of a cervical collar, nonsteroidal anti-inflammatory agents, and in most cases, an oral corticosteroid taper. Similarly, in a frequently referenced 1999 study45 which prospectively studied 246 patients nonrandomly assigned to either conservative or surgical treatment for cervical radiculopathy, cervical injection therapy was employed in the conservative care group. Spinal injections employed were described as nerve blocks, ESI, or facet blocks. The body of the paper suggests that injections were utilized in 13% of patients, and therefore outcomes following injection therapy in this paper are unclear. In this paper, both groups of patients realized significant improvements in pain and functional status.

DIAGNOSTIC SELECTIVE NERVE ROOT INJECTION While there are many references alluding to the utility of lumbar diagnostic selective nerve root block (SNRB), performed through a fluoroscopically guided transforaminal approach, the role of diagnostic cervical injections remains poorly defined. The specificity and sensitivity of lumbar diagnostic nerve root injections has been estimated at 87–100%46,47 and 99–100%,48,49 respectively, with corroborative surgical lesions observed. In a study of patients treated with anterior cervical decompression and fusion,50 75 patients demonstrated a positive response to a preoperative diagnostic cervical SNRB. Diagnostic injections were performed with fluoroscopic guidance, contrast enhancement, and 1 cc of 1% lidocaine. The study describes 65 of 75 patients realizing immediate postoperative relief during a recovery room assessment. In a more recent report,51 the preoperative diagnostic utility of lumbar and cervical selective nerve root injections has similarly been assessed. In this study, 101 patients were included, but only 18 were cervical patients. Nerve root localization was confirmed with both contrast enhancement and symptom provocation utilizing a nerve root stimulator. Anesthetization was performed utilizing

Section 3: Cervical Spine

0.5–0.75 cc of 2% lidocaine. A 90% reduction in symptoms during the postinjection assessment was considered a positive response. Of those patients who underwent surgery with a positive preoperative diagnostic injection, 91% reported a successful surgical outcome. Of the 10 patients who demonstrated a negative response to preoperative injection, 60% reported a successful surgical outcome. This difference in outcomes was statistically significant (p=0.05). In a novel study,52 the symptoms resulting from cervical nerve root provocation during diagnostic SNRB were recorded and dynatomal maps described. In this study, 87 patients underwent 134 cervical nerve root stimulations. The C4 through C8 nerve roots were studied and symptom distributions recorded utilizing more than 1000 bits of data compiled upon a 793-body-sector bit map containing 43 clinically relevant body regions. The resultant dynatomal maps differed considerably from the classic cervical dermatomes described by Foerster53 and Keegan and Garrett.54 Highlights from the dynatomal maps include C5 root stimulation resulting in symptoms radiating as distal as the forearm in only 14%, C6 symptoms incorporating the ulnar hand and fifth digit in 37% and 30%, respectively, C7 symptoms uniquely referred to the anterior head and to the chest as frequently (17%) as to the middle finger, and C8 symptoms extending to the thumb as often as digit five (Fig. 59.1). As the authors explain, these differences between the dynatomal maps and more classically described dermatomal distributions likely arise in part from limitations in the more classic studies’ methodology, the more frequent existence of cervical intrathecal anastomoses,55,56 and varying nerve root contributions to the brachial plexus.

A

In the author’s practice, diagnostic cervical SNRB are employed when diagnostic uncertainty remains. As described later in this chapter, the level of segmental pathology is often clarified through a review of radiographs and a detailed physical examination. In those cases in which diagnostic uncertainty remains, electrodiagnostic studies can be utilized. When electrodiagnostic studies fail to confirm a level of segmental pathology, SNRB can be utilized in an effort to more definitively identify the pain generator. In the cervical spine in particular, where dynatomal overlap is more frequently observed, the clinician needs to be cautious in assigning a level of radicular involvement when the physical examination and radiographs are not clearly corroborative. In other cases, radicular pain may be clinically suspect, but a radiographic correlate is not appreciated, i.e. following whiplash or in the setting of a chemical radiculitis. In such instances, diagnostic SNRB are employed. It is the author’s goal during diagnostic injections to achieve a contrast pattern which reveals the exiting nerve root and dorsal root ganglion without epidural spread to adjacent levels. This can often best be achieved by positioning the spinal needle adjacent the posteriorly situated superior articular process but with a more inferior and lateral position in the foramen (Fig. 59.2). Anesthetization is performed with 0.8–1.0cc of 2% lidocaine. The patient’s response to diagnostic injection is considered positive if an 80% symptomatic reduction is realized during the postinjection assessment performed approximately 20 minutes after injection. Pain ratings and diagrams are completed before and after injection, and typically provocative maneuvers are performed during the assessment phase.

B

Fig. 59.1 (A) C6 dynatomal map. Symptom distribution along the anterior and posterior torso and upper limb depicted. Darker shading indicates more frequent occurrence of symptoms. (B) C7 dynatomal map. 647

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A

B

TRANSFORAMINAL INJECTION LITERATURE AND DIAGNOSTIC SUBSETS A 1996 prospective uncontrolled study of 68 consecutive cervical radiculopathy patients reported outcomes following injection therapy.57 Each patient described radicular pain that radiated at least as distally as the forearm. All patients except for one presented with an associated neurologic deficit in the form of either reduced strength, sensation, or a diminished reflex. The average duration of symptoms was approximately 2 months. All but one patient demonstrated a radiographic finding which was believed to correlate with symptoms. In 70% of cases a corroborative intervertebral disc protrusion or herniation was described, and in 30% spondylotic foraminal encroachment was observed. The patients in this study were treated with three possible injection techniques. Initially, a cervical or brachial plexus block was performed using anatomic landmarks without image guidance. If this injection technique proved helpful, it was repeated. Otherwise, a fluoroscopically guided contrast enhanced TFESI was performed. Once again, if this approach proved helpful it was repeated. If this failed to offer relief, a fluoroscopically guided interlaminar ESI was performed. Each patient received an average of 2.5 injections, and in 62% of cases a TFESI was employed. Twenty-nine percent improved with the plexus block approach and 16% received interlaminar injections. No complications were reported in this study. The average time to clinical discharge in this study was 7 months. At that time an average VAS of 0.6 was recorded, all patients had returned to work, and partial or full neurologic recovery was described in 47% and 46%, respectively. An additional phone interview was conducted with 93% of patients at an average of 39 months following treatment. By this survey, 76% of patients were pain free and the other 24% reported an average pain score of 2/10. Eighty-six percent reported an absence of parasthesias, and 73% reported no residual weakness. No patient required surgical intervention. In addition to these described clinical outcomes, the authors share an interesting observation in the discussion section of their paper. This same group of investigators performed a study with similar methodology and interventions in the treatment of patients with lumbar radiculopathy.58 In that study, 14% of patients ultimately required surgical intervention, leading the authors to speculate that the prognosis for recovery following injection therapy might be more favorable for the cervical radiculopathy population. In a 2001 prospective study of 32 patients with cervical radiculopathy,59 fluoroscopically guided TFESI were similarly employed. Inclusion criteria included a persistence of symptoms for at least 2 months, high radicular pain scores on a 10 point scale, and a radio648

Fig. 59.2 (A) Oblique view demonstrating needle position for diagnostic right C7 SNRB. (B) Posteroanterior view demonstrating epidurogram during diagnostic right C7 SNRB.

graphic correlate such as a focal disc lesion or degenerative foraminal stenosis. In 26 of 32 cases, spondylosis was described rather than a disc herniation. Injections were performed in the seated position and with fluoroscopic guidance but without contrast enhancement. Patients were clinically followed for 6 months. In 27 of the 34 levels treated only one injection was performed, and in the remaining seven, a second injection was administered. At 6-month follow-up, a good or excellent result, defined as at least 50% pain relief and requiring little to no medical treatment, was observed in 56% of patients. No long-term complications were reported. These outcomes are inferior to those described by the previous 68 patient study in which no patients described ongoing debilitating pain. There are several differences between these studies in methodology and patient populations. First, the majority of the patients in this study presented with radiculopathy suspected as arising from corroborative degenerative foraminal stenosis as opposed to a herniated disc. Additionally, contrast enhancement was not utilized during injections, and repeat injections were not employed in the majority of cases. Transforaminal injections performed with CT guidance have been utilized in a retrospective study of 30 patients presenting with cervical radiculopathy.60 In this study, 16 patients presented with suspected corroborative degenerative foraminal stenosis and 14 with a focal disc protrusion. Patients were excluded if a strength deficit was evident. The average symptom duration prior to injection therapy was 2.7 months. Patients were evaluated at 2 weeks and 6 months after injection therapy and the pain response was assessed. Injection procedures were performed with CT guidance and contrast enhancement. The mean visual analog score prior to injection therapy was 6.5, and this was significantly reduced (p<0.001) to 3.3 at 2 weeks after the injection procedure. An outcome of excellent was assigned to those with greater than 75% pain relief and good for those with at least a 50% pain reduction. Eighteen patients realized a good or excellent outcome 2 weeks after the first injection and this was sustained at 6 months without further injection therapy. Only 3 of 12 patients who realized an initial fair or poor outcome received a second injection. Two of these patients realized excellent outcomes that were sustained at the 6-month follow-up. Initial pain intensity, symptom duration, and radiographic correlates were not found to reliably predict clinical outcomes. No procedural complications were reported. In an additional study of CT-guided transforaminal injection therapy for radicular pain,61 outcomes of 160 patients were retrospectively analyzed. In 18 of these cases, patients presented with cervical radicular pain. The remainder of the patients were treated for symptoms of thoracic or lumbar origin. Patients presented with variable radiographic correlates in this study, including degenerative foraminal

Section 3: Cervical Spine

stenosis, disc herniation, postoperative fibrosus, or no visible radiographic abnormalities. The majority of patients, approximately 80%, received only a single injection. Eleven of these 18 patients (61%) realized symptomatic improvement, and it is extrapolated from the data that in 80% of these cases a greater than 50% reduction in radicular pain was realized. It would also appear after a review of this report that approximately 66% of those cases with improvement demonstrated sustained relief by phone interview at a mean of 110 days following treatment. For the study group as a whole, there was no apparent correlation between radiographic findings at the symptomatic level and outcomes. There was a suggestion of greater efficacy of injections for cervical patients, in which 57.9% of injections were categorized as effective, when compared to thoracic and lumbar patients, in which a 50% and 48% efficacy were assigned, respectively. In an effort to assess outcomes following cervical TFESI in a more diagnosis-specific fashion, the author’s research group retrospectively analyzed the data in three separate studies.62–64 The first of these three studies62 included 20 subjects with cervical radicular pain arising from atraumatic spondylotic foraminal stenosis. Each patient presented with radiographic evidence of foraminal stenosis at the symptomatic level. A diagnosis of level-specific radiculopathy was confirmed either by a corroborative myotomal strength deficit or reflex abnormality, electrodiagnostic evidence of myotomal denervation, or a positive response to a confirmatory diagnostic SNRB. Patients’ average symptom duration prior to treatment was 5.8 months. At initial presentation, the average VAS was 6.9. Follow-up data collection was performed by an independent reviewer by phone interview at an average of 21.2 months. An average of 2.2 injections was performed in each case. At the time of follow-up, six patients (30%) had proceeded with surgical decompression. An overall good or excellent result was described by 12 patients (60%). To be categorized as a good or excellent outcome, patients needed to demonstrate a pain score of four or less on a ten point scale, be working full time, utilizing no more than prescription NSAIDs to control pain, and demonstrate high patient satisfaction scores. The average recorded verbal pain score at the time of follow-up was 2.0. A significant improvement ( p=0.001) in the average pain score was observed. A significant reduction ( p=0.0005) in medication usage was also observed at the time of follow-up. At follow-up, only one patient was requiring opioid analgesics and nearly 86% were utilizing no medications or over-the-counter agents. An analysis of patient characteristics at initial presentation, including associated weakness and distal extent of radicular pain, did not predict clinical outcomes with statistical significance. A significant relationship was noted between patient age and satisfaction with treatment, with younger patients providing the highest patient satisfaction scores ( p=0.0047). In the second and third published studies, patients with a traumatic symptomatic onset were described. In the second paper,63 the efficacy of cervical TFESI was retrospectively analyzed in 22 patients who presented with radicular pain following a whiplash event and whose imaging did not reveal a radiographic correlate at the symptomatic level. In this study, patients were excluded if their examination revealed a strength or reflex abnormality or if electrodiagnostic studies revealed denervation. Each patient demonstrated an initial positive response to a diagnostic SNRB to confirm the symptomatic level. Patients’ average symptom duration prior to diagnostic injection was 6 months. Follow-up data were collected by phone interview at an average of 33 weeks after the final therapeutic injection. Outcome categorization was based upon a consideration of work status, medication use, and Oswestry scores. An overall 14% good or excellent outcome was observed. To be labeled good or excellent, the patient was required to be working at least full time with modifica-

tions, utilizing no more than prescription NSAIDs for pain control, and demonstrate an Oswestry score of 21–40, suggestive of more ‘moderate’ disability. When considering patient stratification before and following treatment, a significant change was not observed. In patients with initial higher levels of function, a more pronounced pain reduction was reported at the time of follow-up. The third64 of these three studies similarly investigated patients with a traumatic symptomatic onset but with radiographs revealing degenerative foraminal stenosis at the symptomatic level. This study included 15 patients presenting with a median symptom duration of 13 months. The symptomatic level was determined by the presence of a corroborative strength deficit or reflex abnormality, electrodiagnostic evidence of myotomal denervation, or a positive response to a diagnostic SNRB. An average of 3.7 injections was performed at each symptomatic level, and follow-up data were collected by phone interview at an average of 20.7 months following treatment. Similar to the first of these three studies, outcomes were determined through a consideration of work status, pain scores, medication use, and patient satisfaction. While a significant reduction ( p=0.0313) in pain scores was observed, an overall good or excellent outcome was observed in only 20%. Six patients underwent surgery, and only one of these realized a good or excellent postoperative outcome. The outcomes from these three studies as well as the previous cervical TFESI studies described in this chapter are summarized in Table 59.1. In this author’s practice, transforaminal injections are employed for patients with cervical radicular pain and radiculopathy. Often, prior to injection therapy, patients have failed trials of nonsteroidal anti-inflammatory agents and analgesics, physical therapy, oral corticosteroids, and interlaminar epidural injections performed with or without fluoroscopic guidance. In other cases in which the patient presents with a more painful or pronounced radiculopathy, transforaminal injections are introduced earlier in the treatment algorithm. The algorithmic approach to the patient with cervical radicular pain is comprehensively addressed in Chapter 57 by Dr. Zacharia Isaac and Curtis Slipman and will only be touched upon here. An important guiding principle is that prior to performing a therapeutic transforaminal injection, the level of segmental pathology is confirmed. Intuitively, this is an appealing notion as the purpose of the injection is to deliver the therapeutic substance as close to the site of pathology as possible. Devoting the time required and employing the appropriate diagnostic modalities to the identification of the proper target is a necessary component of providing the best possible treatment. The level of nerve root involvement is typically confirmed in one of three ways. The patient can present with radiographs revealing of a focal compressive lesion, i.e. disc protrusion or degenerative foraminal stenosis (Fig. 59.3), and a corroborative myotomal strength deficit or reflex abnormality. In cases in which radicular pain is suspect, but the exam remains intact and imaging less conclusive, i.e. multilevel foraminal compromise, electrodiagnostic studies can be employed to confirm the level of pathology. If such testing also does not prove to be diagnostic, diagnostic SNRB offers a third means of confirming the level of involvement. In those cases in which the patient presents with a history and examination consistent with cervical radicular pain, a normal neurologic exam, and a highly corroborative radiograph, i.e. single-level disc extrusion with pronounced foraminal compromise and nerve root compression, the level of pathology is also appropriately assigned. Therapeutic injections are typically performed 2 weeks apart with a reevaluation scheduled 2 weeks after the second injection. In those cases in which patients present with more debilitating pain, the first two injections can be performed at 1-week intervals. If progress is realized after the initial two injections, a third is scheduled. If pain relief is complete after one or two injections, no further injections are performed. A fourth and final injection is reserved for 649

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Table 59.1: Cervical TFESI Outcome Studies in Chronological Order Lead Author

Year

Methodology

Population

Clinical Outcomes

Bush

1996

Prospective uncontrolled

68 patients 30% with TFESI performed 62% foraminal stenosis 70% with disc protrusion 76% pain free 24% minimal pain

None proceeded to surgery

Berger

1999

Retrospective uncontrolled

18 patients with radicular pain CT guided injections performed

Significant response in 57.9%

Slipman

2000

Retrospective uncontrolled

20 patients with spondylotic foraminal stenosis, atraumatic

Good or excellent outcome in 60%

Vallee

2001

Prospective uncontrolled

26 of 32 patients with spondylotic foraminal stenosis

Good or excellent result in 56%

Slipman

2001

Retrospective uncontrolled

22 patients, whiplash induced radicular pain, no radiographic correlate

Good or excellent outcome in 14%

Slipman

2004

Retrospective uncontrolled

15 patients with whiplash induced radicular pain and foraminal stenosis

Good or excellent outcome in 20%

Cyteval

2004

Retrospective uncontrolled

16 with spondylotic foraminal stenosis, 14 with focal disc protrusion CT guided injections performed

Good or excellent outcome in 60%

those patients with sustained and incremental, but incomplete, relief after the initial three. Patients with successful therapeutic outcomes typically receive between two and three injections. This is in agreement with the lumbar6,10 and cervical57,62 injection literature describing superior clinical outcomes. While observed clinically, it is atypical for the cervical radiculopathy patient to realize complete lasting relief after the first injection. The author questions whether recently published cervical59,60 and lumbar65 TFESI studies describing inferior outcomes have done so, in part, as a result of terminating treatment after a single injection rather than offering a series of injections in accordance with the patient’s clinical response. Injections are typically performed in conjunction with a diagnosis-specific physical therapy regimen coordinated by an experienced mechanical therapist. During therapy, an emphasis is placed upon symptom centralization and strengthening of the myotomal strength deficit.

A

The author’s experience is in agreement with the cervical injection literature in that patients with radicular pain arising from degenerative foraminal stenosis are often successfully treated with injection therapy, but are more likely to have persistent or recurrent symptoms than the patient with an acute discogenic radiculopathy. This contradicts findings of interlaminar ESI papers36,43 that suggest superior outcomes in the setting of degenerative spondylosis. The 60% success rate described for patients with spondylotic radicular pain is essentially in agreement with the author’s clinical experience. In those patients with persistent spondylotic radicular pain, it would appear that the stenosis serves as an ongoing mechanical stressor less likely to be ameliorated through chemical therapies. Those patients with radicular pain following trauma, i.e. whiplash, without a radiographic correlate may present with the worst prognosis due to an intrinsic and less reversible neural injury following a transient but

B

Fig. 59.3 (A) Focal protrusion/herniation of nucleus pulposus to the left at C6–7 with associated compromise of the entrance zone of the neural foramen, compression of the exiting C7 nerve root axilla, and deformation of the anterolateral spinal cord. (B) Degenerative spondylotic and advanced stenosis of the right C5–6 neural foramen. Arrowheads indicate the minimal residual T2 signal observed within the foramen. 650

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potentially profound compressive or traction type insult.66 Outcomes in the author’s practice for this challenging population have been poor and have mirrored the data from the author’s whiplash studies.63,64 While one report41 has described more positive outcomes following ESI for patients with cervical radicular pain without a radiographic correlate, these ‘radiculitis’ patients were not described as post-traumatic. The author would also agree with the observations of other authors suggesting that outcomes following TFESI for patients with acute discogenic cervical radiculopathy are superior to those observed for patients with lumbar radiculopathy.57,61 Controlled studies of lumbar transforaminal injection therapy for mixed patient populations with stenotic and discogenic radiculopathy suggests a 71–84% success rate.10,12 The author’s experience with patients presenting with discogenic cervical radiculopathy is consistent with a long-term success rate at the higher end of this range. This also holds true for patients presenting with more severe radicular pain, even when a more pronounced myotomal strength deficit is initially evident. In contrast to43 and in agreement with38 previous interlaminar ESI studies, the author has not found a sensorimotor deficit at initial presentation to portend a worse nonsurgical outcome. In those cases where the extent of weakness presents a greater clinical concern, patients are concurrently evaluated by a surgical associate and their progress more closely followed. This apparent greater resilience of the cervical nerve roots and increased likelihood of successful outcomes following medical rehabilitation and interventional spine treatment in patients with cervical discogenic radiculopathy, if true, has led the author to consider possible explanations for this discrepancy. Firstly, cervical discogenic radiculopathy might be more likely to resolve than a similar lumbar syndrome secondary to the relatively lower mechanical loads to which the cervical intervertebral discs are routinely subject. Mechanical disc loading should be less relevant in cases of extrusion or sequestration when compared to contained protrusions, and further analysis of outcomes in these particular cases might offer additional clarification. A second factor which might theoretically contribute to cervical nerve root recovery is the proximity of the neural injury site to both the motor and sensory cell bodies. The cervical nerve roots are most typically affected in the neural foramen and in the more immediate proximity of the dorsal root ganglion and anterior horn cell. It is questionable if this proximity to both the motor and sensory bodies might render the cervical nerve root more resilient due to a greater and more immediate availability of protective and regenerative factors. Finally, it will be interesting to see if newer injectable medications are introduced over the coming years. While the current cocktail of corticosteroid and local anesthetic would appear to be effective in treating patients with radicular pain syndromes, basic scientific research has uncovered other potential targets in both the inflammatory cascade67 and the pain generating cycle.68 It will require welldesigned and controlled clinical trials to determine if in fact newer agents can offer a more potent and cost-effective means of treating the biochemical injury component of cervical and lumbosacral radiculopathies.

COMPLICATIONS More minor complications following interlaminar cervical ESI including nausea, vomiting, dizziness, facial flushing, hypotension, and increased cervical pain have been reported.69–71 Complications arising from fluoroscopically guided interlaminar ESI have been described in a retrospective study of 345 injections in 157 consecutive patients.72 Injections were performed at the C6–7 or C7–T1 level utilizing 2 cc of 1% lidocaine and 80 mg of triamcinolone acetonide. Patients were surveyed by telephone 24 hours after

injection procedures and asked to complete a standardized questionnaire. Clinical chart notes were also reviewed for the 3-week period following injections. A transient increase in neck pain was described in 6.7%, nonpositional headaches which resolved in 24 hours in 4.6%, insomnia the night of the injection in 1.7%, vasovagal reactions in 1.7%, facial flushing in 1.5%, fever the night of the procedure in 0.3%, and dural puncture in 0.3%. The authors concluded that interlaminar ESI appear to be a safe treatment approach for patients with cervical radiculopathy. Before proceeding with a discussion focusing on more injection site-specific complications arising from ESI, it should be highlighted that many of the more minor ‘complications’ described actually represent symptoms arising from a transient systemic corticosteroid effect. Insomnia, facial flushing, and nausea69–72 are fairly commonly described in the author’s practice and more notably when less particulate corticosteroid compounds, i.e. betamethasone as opposed to methylprednisolone, are administered. Resultant elevations in blood glucose levels remain a particular concern in diabetics receiving injection therapy. Similarly, and as reported in the literature, persistent hiccups73 and dysphonia74 have been observed on more limited occasion following epidural injection of corticosteroid. The systemic corticosteroid effect which frequently arises after epidural injection by any route raises the possibility that a component of the therapeutic effect realized might similarly arise from a more systemic as opposed to a local process. While this is an issue for further study and consideration, in the author’s experience many patients realize relief through ESI after failing one or two oral corticosteroid tapers. While limited in methodology, a small placebo-controlled study75 comparing oral dexamethasone to placebo in the treatment of lumbosacral radicular pain did not demonstrate a significant therapeutic effect. In this author’s opinion, while the possibility remains that a systemic corticosteroid effect contributes in small part to the therapeutic response following ESI, it can be stated with much greater certainty that these systemic effects contribute to the profile of minor ‘complications’ often observed. Additional and more serious complications following interlaminar ESI have also been reported. Cases of severe pain suggestive of neural injury following an interlaminar ESI have been described.76,77 In three of these cases, a blind C6–7 approach was complicated by a complex regional pain syndrome (CRPS) affecting the upper extremity contralateral to the symptomatic side in two cases. In these cases, symptoms resolved over a 3-week to 3-month period and were presumed to arise from either spinal cord or nerve root trauma. A 1998 paper69 reports two cases of intrinsic spinal cord damage following interlaminar injection. In each of these cases, intravenous sedation was utilized and the injection was performed with fluoroscopic guidance. In each case the initial injection attempt resulted in suspected subarachnoid placement without a response from the sedated patient. Postprocedural imaging did reveal an abnormal signal within the spinal cord in both cases. In the first case, the patient was left with symptoms consistent with an iatrogenic right C7 radiculopathy and paresthesias affecting the bilateral lower extremities. In the second case, the patient suffered from a severe left upper extremity CRPS and paresthesias affecting the right thigh. Epidural abscess,78 epidural hematoma,30,79–81 and subdural hematoma82 have similarly been described as complications arising from interlaminar cervical ESI. In several of these cases, the patients required emergent cervical laminectomy and decompression for progressive neurologic deterioration. In two of these cases, a postoperative return to neurologic baseline is reported,78,79 and in another82 the patient succumbed to cardiac arrest following an acute meningitis. Complications following cervical TFESI have been highlighted in the more recent literature. Complications associated with both 651

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cervical and lumbar TFESI have been reported in a prospective, nonrandomized, controlled study.83 In this paper, 151 patients received 306 transforaminal injections. Concurrently, 60 patients who were evaluated, but who did not receive injection therapy served as the control group. Side effects and complications were recorded by an independent reviewer through patient questionnaires completed immediately following, at 1 week, and 3 months following each injection. The control group also completed the same questionnaire on one occasion. In this study, 37 patients received 89 cervical TFESI. Ninety-one percent of the study group as a whole described no complications or side effects during the injection procedure. Light headedness was reported by 2.2% of patients, nausea by 1.1%, and dural puncture was also suspected in 1.1%. Immediately following cervical injection procedures, 22.7% reported increased pain at the injection site, 18.2% described increased radicular pain, 13.6% light headedness, 9.1% increased axial pain, 4.5 % non-specific headache, and 3.4% nausea. At the 1-week interview there was no difference in reporting between the cervical injection patients and the control group except for increased pain at the injection site which was reported in 30.3% of injection patients. At 3 months, two patients reported increased neck pain and one reported heartburn and fluid retention. Of the two patients with increased neck pain, one stated that he or she would not repeat the injection when considering the outcome. No patients in the study group reported more serious complications. Complications associated with fluoroscopically guided cervical TFESI have also been reported in a retrospective fashion.84 In this study, a total of 357 injections were performed. Fluoroscopically guided contrast-enhanced injections were performed utilizing 1–2 cc of 1% lidocaine and 6–12 mg of betamethasone. Charts were reviewed from the time of injection for as long as 3 years following treatment to identify complications. Two complications were reported. In one case, a patient lost consciousness for 2 minutes, followed by 2 hours of nausea and vomiting which then resolved. In the second case, the patient reported a headache and cervical stiffness that persisted for 3 months following the injection with a subsequent complete resolution. These authors concluded that cervical TFESI are a relatively safe treatment option. As this study was retrospective in nature, the possibility remains that additional complications, and in particular those of a short-term nature, were experienced but not recorded through a more comprehensive and ongoing process of patient inquiry. A more recent retrospective review85 describes the complications associated with 1036 cervical TFESI performed over a 4year period. In this report, no catastrophic neurologic events are described. Seventeen minor complications (1.64%) including dizziness, numbness, pain, transient weakness, and one case of transient global amnesia were described. Of particular interest in this study is the authors’ efforts to correlate complications with needle tip placement as observed in the frontal and lateral fluoroscopy images. Their data suggest that deeper needle placement, i.e. more medial in the frontal plane, did not correlate with the incidence of minor complications. A significant relationship ( p=0.04) is described between minor complications observed and improper needle positioning in the lateral plane. More anterior or ventral placement of the needle tip within the neural foramen appeared to correlate with the incidence of transient complications. Severe neurological complications following cervical TFESI have also been reported and the pathophysiology behind these events has been the focus of recent discussion and debate.86–91 The complex vasculature of the cervical spine is illustrated in Figure 59.4. Three cases of fatalities arising from either spinal cord or brain injury following TFESI have been reported in the literature.88,91,92 In the first of these cases,91 an anterior spinal artery syndrome following a C6 injection is 652

described. In this case, a 22-gauge spinal needle was reportedly successfully passed into the right C5–6 foramen. A satisfactory contrast pattern is described, and the injection was performed utilizing 0.5 cc of 0.5% bupivacaine and 0.5 cc of triamcinolone. Within 2 minutes the patient developed a flaccid four-extremity paralysis and respiratory compromise. An MRI of the cervical spine revealed increased signal within the spinal cord from C2 to T1. The patient ultimately recovered sensation without improvement in his motor exam, and within 1 month the patient expired from medical complications. In the second reported case,88 a 48-year-old female was treated with a C6 transforaminal injection utilizing contrast enhancement and a satisfactory epidurogram is similarly described. A 25-gauge, 2” spinal needle was utilized to inject 2 mL of 0.25% bupivacaine and 80 mg of triamcinolone. Upon transfer from the procedure table, the patient became unresponsive. Within 1 hour she regained consciousness but remained with pronounced bilateral lower and right upper extremity weakness. The patient underwent surgical brainstem decompression in the setting of an apparent massive cerebellar infarct. She expired the following day. Intraoperative findings were significant for an anomalous tortuous vertebral artery. Pathology revealed bilateral cerebellar and left occipital cortex infarction with thromboembolism within a leptomeningeal artery adjacent to the left occipital cortex, consistent with an injury to the vertebral artery or an associated branch. In a third fatality case,92 a left C7 TFESI was performed utilizing a 25-gauge, 312-" spinal needle. Following needle placement in the foramen, initial aspiration was ‘heme positive’ and the needle was therefore repositioned. A satisfactory epidurogram of the C7 nerve root was then appreciated after the injection of contrast, and a 3 cc solution of 80 mg methylprednisolone and 0.75% bupivacaine was injected. The patient immediately became unresponsive. CT imaging revealed a large brainstem hemorrhage, obstructive hydrocephalus, and extensive bleeding throughout the pons and midbrain. The patient expired the following day. Postmortem examination revealed dissection and thrombosis of the left vertebral artery suspected to have resulted from vertebral artery puncture during the injection procedure. In addition to these three reported fatalities, it has been reported that 15 other cases of death or severe neurologic sequelae have followed cervical TFESI.86,87 The details of cases have yet to be presented or published as they remain sub judice. In one reported case of a marked adverse neurologic complication, a patient suffered from cortical blindness, a partial right homonymous hemianopsia, following TFESI at the C5–6 level.93 In this case, vertebral artery puncture was also suspected, based upon an initial aspirate, and 1 cc of air was intentionally introduced by the authors in an effort to confirm needle placement within the epidural space. Contrast agent was then injected and an unsatisfactory epidurogram was observed. Within seconds, the patient developed nystagmus and, within 45 minutes, total bilateral blindness which ultimately improved. An initial MRI of the brain revealed widespread occipital lobe enhancement, and follow-up imaging on day 4 revealed edema within the left occipital cortex. The authors of this case speculate that complications arose from either direct vertebral artery injury, radiocontrast agent toxicity following intra-arterial injection, or air embolization.82,94 Inadvertent injection of a crystalloid corticosteroid solution into a radicular artery has been theorized as a likely mechanism of injury in those cases where an acute vascular insult to the spinal cord is suspected.86,87,89,90 In these cases it is speculated that a larger-caliber radicular or segmental medullary artery which more critically reinforces the anterior spinal artery becomes compromised during the TFESI. These more critical radicular arteries are located within the neural foramen and can arise variably at the C3 to C8 levels.95,96 Potential mechanisms of radicular artery insult include direct intra-

Section 3: Cervical Spine Arterial distribution: schema Right posterior spinal artery

Sulcal (central) branches to right side of spinal cord

Peripheral branches from pial plexus

Posterior radicular artery

Sulcal (central) branches to left side of spinal cord

Anterior segmental medullary artery

Left posterior spinal artery Zone supplied by penetrating branches from pial plexus

Pial artery plexus Anterior and posterior radicular arteries

Zone supplied by central branches Zone supplied by both central branches and branches from pial plexus

Anterior spinal artery

Posterior radicular artery A

Plial arterial plexus

Anterior segmental medullary artery

Posterior cerebral artery Superior cerebellar artery Basilar artery Anterior inferior cerebellar artery Posterior inferior cerebellar artery Anterior spinal artery Vertebral artery Anterior segmental medullary artery Cervical vertebrae Ascending cervical artery Deep cervical artery Subclavian artery B

arterial injection, transient vasospasm, arterial compression from a foraminal fluid bolus, or iatrogenic dissection.86–89,91 Contrast flow patterns consistent with inadvertent arterial penetration have been published in which the radicular artery either terminates in multiple spinal cord branches or joins with the anterior spinal artery.86,87 In these cases where such contrast flow was observed, the procedure was terminated secondary to vascular penetration concerns.86,87 In another case, while such arterial flow was not visualized after the injection of contrast, radicular artery injection was suspected, based upon the patient’s response to an initial injection of anesthetic.89 In this case, a satisfactory epidurogram was depicted with the needle placed within the right C6–7 foramen. Injection of 0.8 cc of 2% lidocaine was then performed with a suspected resultant venous flow pattern contralaterally as the ipsilateral periradicular dye was blushed. Over the subsequent 3 minutes, the patient lost motor control of all four extremities as well as sharp sensation, while fine touch sensation and proprioception were preserved. All symptoms, consistent with

Fig. 59.4 (A) Arterial supply of the ventral cervical spine. Note the radicular and segmental medullary arteries. (B) Arteries of the cervical spine and brainstem, ventral view.

those arising from an anterior spinal artery syndrome, resolved without sequelae within 20 minutes. The transient nature of these pronounced deficits was likely related to the half-life of the anesthetic agent. Corticosteroid was not subsequently injected. Concurrent injection of corticosteroid in this case may have resulted in a less reversible injury. The authors in the second fatality case above88 further investigated the potential relationship between corticosteroid particle size and neurologic injury resulting from intra-arterial injection. The authors theorized that injection of the corticosteroid preparation might have contributed to arterial thrombus formation and vascular occlusion. Five commonly utilized corticosteroid preparations were subjected to microscopic study. Following manual agitation, the particles in dexa- and betamethasone tended to be lucent and rod-like, whereas those in the triamcinolone and methylprednisolone samples were amorphous and opaque. Additionally, over time, the particles in the samples of methylprednisolone and triamcinolone tended to form 653

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A

B

large aggregates in excess of 100 micrometers. The authors speculate that such aggregate formation might be a factor contributing to occlusion of the microvasculature. Direct intraneural spread of injectate along the spinal nerve to the spinal cord has also been suggested as a potential mechanism of spinal cord injury during injection.87,97 Fortunately, after hundreds of cervical TFESI performed in the author’s practice, there have been no significant complications. Candidates for cervical TFESI are carefully selected. Cervical TFESI are utilized predominantly for patients with true radicular pain. Unlike lumbar TFESI, which are often utilized for patients with axial pain, cervical TFESI are less frequently employed for patients without a radicular component. Patients are fully conscious during injections and are repeatedly questioned regarding symptoms during the procedure. Injection needles utilized can range from 22-gauge to 25-gauge, and all agents are injected through microbore tubing to eliminate needle movement during syringe changes. To assure proper and posterior foraminal entry, the desired oblique view is sequentially created from the lateral plane. Once achieved, magnification and columnation are utilized (Fig. 59.5). A dedicated chapter of this text will more completely address cervical TFESI technique. Contrast injection is observed in real time to confirm satisfactory flow and to rule out vascular uptake. Prior to the introduction of corticosteroid and following observation of a satisfactory dye flow pattern, a test dose of local anesthetic, approximately 1 cc of 1% lidocaine, is injected. The patient is then briefly monitored and questioned for any adverse response including an exacerbation of pain complaints in the affected limb, headache, lightheadedness, or other sensorimotor symptoms affecting the upper or lower extremities. While there has been a national shortage of betamethasone suspensions, this agent has been available in limited quantities in the author’s practice and, when available, remains the corticosteroid of choice for cervical injections. The corticosteroid and anesthetic solution is manually agitated prior to injection. By administering all medications through tubing, a lower-pressure injection is performed, likely minimizing transient increases in foraminal pressures and maximizing patient comfort during injection. The use of tubing throughout the injection procedure obviates the need for syringe changes at the interface with the spinal needle and minimizes the likelihood of needle position change during the procedure. The recent apparent increase in reports describing complications associated with cervical TFESI is likely multifactorial in origin. In part, this increase might parallel an overall increase in the numbers of TFESI performed as this technique is embraced by greater numbers in the interventional spine community. Any interventionist performing cervical TFESI should either first complete dedicated fellowship training or reach a level of greater lumbar procedural 654

Fig. 59.5 (A) Oblique view demonstrating needle position for therapeutic right C7 transforaminal injection. (B) Posterioanterior view demonstrating epidurogram during therapeutic right C7 transforaminal injection. From Slipman CW, et al.52 with permission of Lippincott, Williams & Wilkins.

experience prior to including this injection approach in the treatment armamentarium. With further standardization of injection technique and training for cervical TFESI, complication rates might be further reduced. The complications reported to date have in large part been vascular in nature. The available case reports reveal devastating incidents resulting from either direct trauma to or injection of the vertebral artery. Other cases are highly suggestive of disruption of a critical penetrating radicular artery, through direct intra-arterial injection, needle trauma, or vasospasm following injection. In the setting of the betamethasone shortage, the possibility remains that the use of corticosteroid solutions containing larger and aggregate-forming particles has contributed to vascular occlusion in some cases. It should be noted that betamethasone has similarly been implicated in a case of suspected vascular insult resulting in a lower thoracic spinal cord injury and paraplegia following a midlumbar TFESI.98 The details of other adverse event cases remain unavailable, but the possibility also exists that some neurologic complications have resulted from more grossly misplaced needles or ill-advised procedural technique. To date, the available literature pertaining to cervical TFESI is predominantly uncontrolled and retrospective in design. These studies suggest a favorable outcome in 60–76% of patients with nontraumatic cervical radiculopathy. Prospective, controlled studies are needed to more conclusively demonstrate the efficacy of this interventional approach. In the author’s practice, cervical TFESI remains an integral component in the cervical radiculopathy therapeutic algorithm. Cervical TFESI is often effective in patients who have previously failed trials of nonsurgical therapies including targeted rehabilitation, oral corticosteroids, and interlaminar injections. The success rate is particularly high in patients with radiculopathy arising from acute disc protrusion with or without an associated strength deficit. Interventionists must remain aware of, and patients informed of, the serious complications, albeit rare, which are possible with cervical transforaminal injections. The intricate vascular and neuroanatomy of the cervical spine demands consistent and meticulous procedural technique if complication rates are to be minimized.

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81. Catchlove RFH, Braha R. Clinical reports: the use of cervical blocks in the management of chronic head and neck pain. Can Anaesth Soc J 1984; 31:188–191. 82. Reitman CA, Watters W. Subdural hematoma after cervical epidural steroid injection. Spine 2002; 27:E174–E176. 83. Huston CW, Slipman CW, Garvan CW. Complications and side effects of cervical and lumbosacral selective nerve root injections. Arch Phys Med Rehab 2005; 86:277–283. 84. Brady RD. Complications of transforaminal cervical epidural steroid injections. Proceedings of the North American Spine Society. 14th Annual Meeting. 1999; 142–143. 85. Ma D, Gilula L, Riew D. Complication of fluoroscopically guided extraforaminal cervical nerve blocks – an analysis of 1036 injections. Spine J 2004; 4:5S–21S. 86. Baker R, Drefuss P, Mercer S, et al. Cervical transforaminal injection of corticosteroids into a radicular artery: a possible mechanism for spinal cord injury. Pain 2003; 103:211–215. 87. Rathmell JP, Aprill C, Bogduk N. Cervical transforaminal injection of steroids. Anesthesiology 2004; 100:1595–1600. 88. Tiso RL, Cutler T, Catania JA, et al. Adverse central nervous system sequelae after selective transforaminal block: the role of corticosteroids. Spine J 2004; 4: 468–474. 89. Karasek M, Bogduk N. Temporary neurologic deficit after cervical transforaminal injection of local anesthetic. Pain Med 2004; 5:202–205. 90. Kloth DS. Risk of cervical transforaminal epidural injections by anterior approach. Pain Phys 2003; 6:392–393. 91. Brouwers PJAM, Kottink EJBL, Simon MAM, et al. A cervical anterior spinal artery syndrome after diagnostic blockade of the right C6-nerve root. Pain 2001; 91: 397–399. 92. Rozin L, Roman R, Koehler SA, et al. Death during transforaminal epidural steroid nerve root block (C7) due to perforation of the left vertebral artery. Am J Foren Med Path 2003; 24:351–355. 93. McMillan MR, Crumpton CR. Cortical blindness and neurologic injury complicating cervical transforaminal injection for cervical radiculopathy. Anesthesiology 2003; 99:509–511.

73. Slipman CW, Shin CH, Patel RK. Persistent hiccup associated with thoracic epidural injection. Am J Phys Med Rehab 2001; 80:618–621.

94. De Cordoba JL, Bernal J. Cervical transforaminal blocks should not be attempted by anyone without extensive documented experience in fluoroscopically guided injections. Anesthesiology 2004; 100:1323–1324.

74. Slipman CW, Chow DW, Lenrow DA. Dysphonia associated with epidural steroid injection: a case report. Am J Phys Med Rehab 2002; 83:1309–1310.

95. Chakravorty BG. Arterial supply of the cervical spinal cord (with special reference to the radicular arteries). Anat Rec 1971; 170:311–330.

75. Haimovic IC, Beresford HR. Dexamethasone is not superior to placebo for treating lumbosacral radicular pain. Neurology 1986; 36:1593–1594.

96. Turnbull IM, Brieg A, Hassler O. Blood supply of the cervical spinal cord in man. A microangiographic study. J Neurosurg 1966; 21:951–965.

76. Field J, Rathmell JP, Stephenson JH, et al. Neuropathic pain following cervical epidural injection. Anesthesiology 2000; 93:885–888.

97. Selander D, Sjostrand. Longitudinal spread of intraneurally injected local anesthetics. Acta Anaesth Scand 1978; 22:622–634.

77. Siegfried RN. Development of complex regional pain syndrome after cervical epidural steroid injection. Anesthesiology 1997; 86:1394–1396.

98. Houten JK, Errico TJ. Paraplegia after lumbosacral nerve root block: a report of three cases. Spine J 2002; 2:70–75.

78. Huang RC, Shapiro GS, Lim M, et al. Cervical epidural abscess after cervical epidural steroid injection. Spine 2004; 29:E7–E9. 79. Stoll A, Sanchez M. Epidural hematoma after epidural block: implications for its use in pain management. Surg Neurol 2002; 57:235–240.

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80. Tuel SM, Meythaler JM, Cross LL. Cushing’s syndrome from epidural methylprednisolone. Pain 1990; 40:81–84.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ i: Cervical Radicular Pain

CHAPTER

Surgery for Cervical Radicular Pain

60

Frederick A. Simeone

INTRODUCTION Historical notes The first recognized case of cervical radiculitis caused by herniation of the nucleus pulposus was operated on by Professor Angelo Chiasserini, one of the founders of Italian neurosurgery, in January 1937. Previously, cases of cervical ‘chondromas’ had been described but the specific pathophysiology of discogenic cervical radiculitis was not recognized.1 Cervical disc disease was initially treated by posterior foraminotomy or discectomy, similar to that which had already been performed in the lumbar region. The advent of the Smith−Robinson technique, later popularized with methodology by Cloward, led to a dramatic shift of the direction of treatment for cervical radiculopathy from posterior to anterior. Indeed, Angevine et al. reported that the United States national rates for cervical discectomy with and without anterior fusion had changed dramatically during the 1990s with a marked increase in the inclusion of a fusion procedure.2 There was a significant geographic distribution in the rate of fusion for cervical disc disease, with the South having the highest fusion rate. Although the rate of surgery for cervical disc disease did not increase significantly during the 1990s, the rates of fusion procedures did rise significantly.

Indications The reasons for surgery for cervical radicular pain are: 1. The development of neurological deficit, in the distribution of a specific cervical nerve root. 2. Unremitting radicular pain, which has not responded to nonoperative measures. The nonoperative measures which usually precede surgery for cervical radiculopathy are described elsewhere in these pages, and will not be discussed at this point. The indications for treatment of cervical radiculopathy for weakness vary somewhat with the nerve root involved. Generally speaking, a surgeon is more aggressive with C5 radiculopathy, during which paralysis of the deltoid muscle could evolve and which ultimately is disabling. Similarly, surgery for a C8 radiculopathy is generally not delayed because intrinsic hand muscle weakness can essentially disable fine movement hand functions. However, C6 and C7 motor deficits are less disabling. Furthermore, surgery for cervical radiculopathy depends on the acuity of the onset and the severity. Neurological deficit of a mild to moderate degree, which has evolved over several days or weeks, can be treated nonoperatively, at least in its initial phases. Acute cervical radiculopathy with profound weakness is generally considered an

urgent surgical matter, and nonoperative measures are likely to be ineffective. With acute and profound weakness, there is only a small window of time during which decompression can be effective before permanent neural damage evolves. In view of the relative safety of these operative procedures with modern techniques, permanent loss of cervical nerve root motor function, particularly C5 and C8, should not be risked by attempts to relieve the syndrome with nonoperative measures. Generally speaking, nonoperative measures are more effective for pain relief than for relief of neurological deficit. Although spontaneous improvement in pain may occur, patients could be left with permanent neurological deficit if treatment is inordinately delayed.

Contraindications There are definite and, in the author’s opinion, controversial contraindications to surgery. The definite contraindications, of course, are patient’s ill health which will not tolerate an operative procedure. Another contraindication for surgery for improvement of strength would evolve if the patient had profound weakness for a long interval of time, with atrophy, as a result of which permanent nerve damage is suspected. Obviously, cervical nerve root decompression would not be effective in patients with permanent injury. The patients may request that something be done to help them regain their strength, but after a long duration of profound weakness in any cervical nerve root, the surgeon should either refuse the operation or at least indicate to the patient that recovery is unlikely, depending on his assessment of each individual case. The relative contraindications, as discussed below, are, in the author’s opinion, important but somewhat controversial.

Workmen’s compensation There are now ample data which indicate that patients who believe that their radiculopathy is the result of a work-related accident, for which they believe they should be compensated, do significantly worse than patients who are not compensated for their cervical radiculopathy. The reasons for this are complex and sometimes difficult to understand. In many instances there may be a conscious effort on the part of a patient to prolong the symptoms while getting reimbursement without working. In other instances, however, it seems that the mere involvement in the compensation system is sufficient to cause a patient to believe that he or she has been ‘injured’ and should be paid while recovering from these injuries. Assessment of such patients is complex. Many do not appear to be pure malingerers. Others indicate that they are an intensely interested in returning to work yet all treatment modalities, including surgery, fail. Still others will apparently recover from their cervical radicular surgery, which 657

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apparently proceeded with good results, yet still be unable to return to work although they can function in almost any other environment. The conscientious surgeon, who analyzes the outcome of the surgery, must consider a patient who continues to complain of pain and cannot work as a surgical failure. Too often, a surgeon will assume that his obligation has been completed when he performs an effective surgery with good clinical and radiographic indications. In patients not encumbered with psychosocial factors, one can generally expect good results in 95% of cases. If surgery is performed, however, and the patient cannot return to work, and is still receiving compensation payments, the surgeon must wonder whether he or she has really performed any useful service, particularly if relief of pain and return to normal activity are the personal outcome requirements. There is overwhelming evidence that patients covered by workmen’s compensation claims did generally poorer than individuals who believe that their cervical radiculopathy is the result of a natural process. The references for this are extensive, and many of them will include patients with lumbar radiculopathy whose response, when under workmen’s compensation, is similarly affected negatively.

Litigation The patients involved in active litigation, similarly, do poorly if they believe that their cervical radiculopathy is the result of an injury caused by another responsible party. The exact explanations for this are difficult to ascertain definitively. What comes to mind, initially, is that there is a form of malingering which is designed to enhance an economic reward. In many cases this may be true. However, in other cases it is apparent that the individual is somehow involved in the ‘system’ and that there are conflicting forces which are both rewarding and penalizing for prompt relief of symptoms following surgery. Furthermore, in some patients there appears to be a genuine feeling of being injured, perhaps permanently, by the negligence of another party or organization. Proof of this is the fact that, quite counterintuitively, the poor results with surgery may persist even after the case is settled. In fact, patients involved in litigation, which is settled still do worse than average in terms of relief of cervical radiculopathy following surgery. There is a remarkable cultural difference in patients’ response to surgery for pain. In countries where litigation, compensation, and other ‘reimbursement’ for their injury are not part of the culture, improvement with surgery is more likely regardless of the patient’s concept of the initiating cause. The process of litigation will often send the patient to physicians who work for the plaintiff ’s attorney or even for the defense. The attitudes of these physicians alter the patients’ response to surgery, although one would like to assume that the system is entirely impartial. There is no doubt, that at least in the US, this is an adversarial system in which the plaintiff and the plaintiff ’s expert must produce evidence of disability while the defense claims the opposite. The patient becomes mired in this process, sometimes being sent for physical therapy, multiple consultations, and frequently a variety of drug therapies. This takes us to our next subject.

Addiction Patients who are chronically addicted to narcotic drugs may not be able to relinquish their pain despite the fact that the cause of the pain has been relieved. Narcotics are excellent drugs for the treatment of acute pain or for the management of pain in patients who have terminal disease, where increasing doses of narcotics do not necessarily impact negatively on the quality of life. However, chronic narcotics users soon become embroiled in the pain/habituation cycle and, after a certain amount of narcotics, over a certain period of time, the 658

patient will soon develop two problems. He will have not only the cervical radiculopathy, but also drug addiction. Drug addiction is not cured by a surgical procedure. In situations where the patient can be managed nonoperatively, i.e. if pain is without advanced neurological deficit, it is wise to undergo a detoxification process first. The patient should be weaned from the drug, sometimes with professional help, and the narcotics can be supplanted by non-narcotic agents. Naturally, the patient will complain that these drugs are not as effective as the narcotics, and his argument may be definitive and persistent. Nevertheless, the patient is to understand that if he or she wants to have relief of the cervical radiculopathy he or she must undergo surgery while free from narcotics. It is less reasonable to anticipate detoxification in immediate postoperative period because evaluation of the success of the operation becomes extremely difficult. Patients addicted to narcotics, even after a successful nerve root decompression, will still be addicted to narcotics. The only way they can get these drugs is to develop pain of some sort, usually the same pain for which they were operated on, but, remarkably, also for another perhaps unrelated discomfort, which requires narcotics for relief. In those instances where a patient is addicted to narcotics but requires urgent surgery, say for rapid development of neurological deficit, the surgery can be followed by a narcotic withdrawal regimen. The end-point in this operation, however, is the relief of the weakness, which can be measured objectively. Relief of pain, however, is difficult to determine simply because of the addiction. In the author’s experience, the best results for treatment of genuine compressive cervical radiculopathy happen when the patient is free from addicting doses of narcotics prior to operation.

Depression Patients with longstanding depression may not be able to relinquish their cervical radiculopathy symptoms following surgery. Acute depression, depression associated with the cervical radiculopathy and its limitations, or depression related to some recent emotional experience is not the kind of depression discussed here. Rather, we often find that patients who have been depressed for several months and more, despite the etiology, will do better when they have been on sufficient doses of antidepressant medicine for a significant period of time prior to undergoing surgery. If the depression can be lifted medically prior to operation, the overall results will be improved. Depressed patients continue to complain regardless of the effectiveness of the operation of decompression of the cervical nerve root. It is important that the chronic depression be treated medically or through psychotherapy prior to considering surgery for cervical root pain.

TECHNIQUE Posterior cervical nerve root decompression In the author’s opinion, this highly effective operation is dramatically underused in the United States for reasons which remain mysterious. The posterior operation provides nerve root decompression, long-term relief of radicular symptoms, without the necessity to fuse the cervical spine. The complication rate is substantially less than anterior discectomy. The procedure, however, cannot be used for midline cervical disc herniations where a spinal cord compression is the principal pathology (Figs 60.1–60.8). The patient is placed on the operating table in a kneeling position so that the cervical spine is above the right atrium. This requires tilting the table in a reversed Trendelenburg fashion to an appropriate distance, and that the patient be adequately fixated to avoid sliding during this table positioning.

Section 3: Cervical Spine

Fig. 60.1 Posterior cervical foraminotomy. Axial view of cervical spine showing disc herniation. The shaded area shows the extent of the foraminotomy and medical facetectomy.

Fig. 60.3 Posterior cervical foraminotomy. The extent of the ‘keyhole’ prior to foraminotomy.

Fig. 60.2 Posterior cervical foraminotomy. The patient is placed in the prone position with the cervical region elevated above the level of the right atrium to reduce venous pressure. Head fixation is by Mayfield tongs.

For a single-level nerve root decompression, an incision of approximately 2.5 cm is made over the affected spinous processes. The level is confirmed radiographically, intraoperatively. The cervical muscles on one side are dissected free from the lamina and held in place with the retractor. Under microscopic control, the inferior margin of the lamina of the superior vertebra and the superior margin of the lamina of the inferior vertebra are removed with drills or rongeurs so that the top of a ‘keyhole’ is visualized. The bottom of the keyhole, of course, is the bony structures over the affected nerve root. Under microsurgical control, the dorsal portion of the intervertebral foramen through which the affected nerve root passes is drilled down to a thin eggshell which is then removed with a small curette. Alternatively, a small Kerrison rongeur can be used to complete the foraminotomy without compressing the underlying nerve root. At the end of this procedure, one should easily be able to pass an instrument through the foramen and determine that there is no pressure on the nerve

Fig. 60.4 Posterior cervical foraminotomy. Right-angle rongeur beginning the ‘keyhole’ opening.

root. This dissection can be carried out pedicle-to-pedicle and generally involves only the medial half of the facet joint. As such, instability has not been demonstrated when the procedure is performed unilaterally. In young patients with an acute history, and in preoperative studies, where one suspects a free disc fragment, it is possible to 659

Part 3: Specific Disorders

Fig. 60.5 Posterior cervical foraminotomy. A probe is inserted into the foramen to determine its degree of stenosis.

Fig. 60.7 Posterior cervical foraminotomy. Overlying the nerve root are veins which can be cauterized in order to visualize the dura.

Fig. 60.8 Posterior cervical foraminotomy. Under microscopic guidance, the nerve root is gently retracted to expose the posterior surface of the bulging or extruded disc, which is then removed with fine instruments such as a Rosen knife or microsurgical Penfield elevator. Fig. 60.6 Posterior cervical foraminotomy. When the foramen is tight, the overlying bone is drilled first until it is thin and then chipped away with a right-angle curette. The right-angle rongeur should not be forced through the foramen in order to decompress the root.

remove the extruded disc material to obtain even more immediate relief. Generally, it is necessary to coagulate the overlying venous cuff in order to expose the disc herniation. When the herniation is incised there can be a spontaneous extrusion of the disc material, and in the author’s experience, this generally portends an excellent result with immediate relief of arm pain. When the pathology is ‘hard,’ that is secondary to an osteophyte, a wide decompression as described above is sufficient to relieve the patient’s symptoms permanently. It is not necessary to attempt to flatten, remove, or otherwise manipulate the anterior osteophytes since the pathology is apparently a ‘sandwich’ 660

effect and removing one portion of the sandwich on either side adequately releases the pressure of the foraminal contents. As discussed elsewhere in this book, this procedure can be performed using even more minimally invasive techniques. Narrow retractors which access the foramen by splitting the paraspinous muscles through an even smaller incision (1.5 cm) have facilitated a less painful recovery. There are several advantages to this approach over the anterior operation specifically for cervical radiculopathy. First of all, several roots can be examined, and it is frequent that multiple roots are involved, without fusing multiple spine segments and thereby applying undue stress on the remaining non-fused motion segments. Secondly, the mechanics of the spine are not altered by surgical immobilization. Furthermore, the risk to the esophagus, larynx, and adjacent structures is eliminated because the approach will only involve the paracervical musculature before the level of the pathology is reached.

Section 3: Cervical Spine

Anterior cervical disc excision and fusion The anterior operation is apparently the most widely used for cervical radiculopathy, although the previously mentioned operation is safer, simpler, and produces fewer long-term effects than the anterior discectomy about to be described (Figs 60.9–60.14). In the anterior

Fig. 60.11 Anterior cervical discectomy and fusion. Caspar screws have been inserted into the vertebrae above and below the planned discectomy. The disc has been removed and the anterior surface of the adjacent vertebra are burred in order to gain better access to the deeper portion of the operative field.

Fig. 60.9 Anterior cervical discectomy and fusion. The paracervical structures had been retracted medially and laterally to expose the entire anterior surface of the cervical vertebra.

Fig. 60.10 Anterior cervical discectomy and fusion. With self-retaining retractors in the place, the longus colli muscles are separated from the anterior surface of the cervical spine.

operation, the neck is prepared and the cervical spine is exposed through a transverse incision in a neck crease. The carotid sheath, sternocleidomastoid muscle, esophagus, and trachea are identified and held aside with retractors. Then the radiographic marker is inserted in the appropriate interspace and the level is identified. Under microsurgical control, a complete discectomy is done at that level with care taken to make sure that the disc material is removed from the foramen. After as complete a discectomy as possible has been performed, a bone graft or cage is inserted into the interspace. The bone graft can be from the patient’s iliac crest or can come from a prepared cadaver bone, usually fibula. Anterior fixation ‘cages’ are frequently used in the cervical spine and come in different forms and material composition. There are apparently no definitive data as to which of these techniques is better at producing a long-term radiographic fusion for single-level disease, nor is there any evidence that one technique is better than the other in terms of cervical radicular pain relief but, here again, we now are discussing the fusion more than the nerve root decompression. For radicular pain relief, it is important to achieve adequate nerve root decompression either directly or indirectly via restoration of the disc and foraminal height with the interbody device. After the patient’s own bone (autograft), cadaver bone (allograft), or mechanical cage is inserted, an anterior plate may be screwed into the vertebra above and below the fusion for added stability. Some patients do not require the use of a postoperative collar when an anterior fusion is supported by an anterior plating device. Recently, there has been a trend to avoid autograft because of pain at the donor site, but still some surgeons prefer autograft over allograft or mechanical devices. This is a matter of choice and analysis of one’s own outcomes. Because of this controversy over technique, the following summarizes the author’s views on which operation is preferred for each of the following cervical disc disease syndromes. 1. Posterior foraminotomy and/or discectomy: A. Monoradicular arm pain. 661

Part 3: Specific Disorders

Fig. 60.12 Anterior cervical discectomy and fusion. After the Caspar screws have been separated under some tension the intervertebral disc space is enlarged by curettes or a drilling burr.

B. Multiradicular arm pain. C. Radicular neurological deficit. 2. Anterior cervical discectomy and fusion: A. Disc herniation with cord compression as well as radicular compression. B. When cervical radiculopathy is associated with demonstrable cervical spine instability or localized kyphosis. C. When nerve root decompression is required on both sides at the same level. Complications of each technique are worthy of note. 3. Posterior cervical foraminotomy: A. Infection. B. Nerve root injury. C. Complications related to patient position. D. Cerebrospinal fluid leak. 4. Anterior discectomy and fusion: A. Laryngeal nerve injury. B. Esophageal injury. C. Spinal cord injury at the time of discectomy or graft insertion. D. Nerve root injury and spinal fluid leak. E. Infection. F. Failure of fusion. G. Complications from graft insertion, plating, etc. H. Cerebrospinal fluid leak. 662

Fig. 60.13 Anterior cervical discectomy and fusion. An intervertebral spacer of appropriate size is inserted into the interspace while the Caspar retractor is opening the interspace. Force should not be applied in order to seat the spacer. An anterior plate is then affixed to the adjacent vertebral bodies.

As one can see, the complications from the anterior surgery are more significant than those from a posterior surgery. The most frequent complication of the anterior operation, however, is long term. It has been clearly demonstrated that patients who undergo a fusion of one or more cervical motion segments, will, in time, develop accelerated degenerative disc disease at the adjacent levels which may require a second surgery at the adjacent level because of unrelenting symptoms. With posterior surgery, it is not necessary to fuse the spine in order to relieve compression on an individual nerve root. Spine surgeons should familiarize themselves with the technique of cervical foraminotomy and learn its benefits, as described in several large series, which show excellent results without long-term complications. Regardless of the chosen approach, patients generally experience relief of cervical radicular pain in about 95% of cases, although the results can be less if affected by compensation, litigation, addiction, or depression (Table 60.1). Generally speaking, the pain pattern follows the sensory deficit so that, for instance, a C5 nerve root compression syndrome will produce pain radiating across the shoulder and partially down the arm. Reflex abnormalities relate to those muscle groups of which reflexes can be detected. These are principally C6 (loss of biceps reflex) and C7 (loss of triceps reflex). The order of progression of clinical findings due to nerve compression is: 1. Pain. 2. Numbness.

Section 3: Cervical Spine

be carried out until it is obvious that they are not working or until the deficit becomes a problem for the patient. For pain with acute profound neurological deficit, surgery is generally performed urgently. This is particularly true if the C5 (deltoid muscles) or C8 (intrinsic hand muscles) are involved. These are the most disabling nerve roots when dysfunctional, and prompt surgery is indicated with profound or acute weakness. If there is acute but not profound deficit, the patient should be followed very carefully as the threshold for surgery on these roots is low. For neurological deficit without pain, a neurological evaluation for alternative causes other than cervical radiculopathy is indicated. If compressive cervical radiculopathy is demonstrated, the degree, severity, and duration of the weakness have to be considered. At this point, it becomes the patient’s decision as to what kind of ‘chance’ he wants to take while undergoing nonoperative therapy, recognizing that neurological deficit of long duration, or acute profound neurological deficit, may not be relieved by surgical decompression. Radiographic abnormalities can either be an acute soft disc herniation or some form of foraminal stenosis, either secondary to bony foraminal hypertrophy or an osteophytic spur. Prior to reviewing the radiographs, the surgeon should determine what nerve root is involved and should only consider surgery if that nerve root is clearly affected. The role of surgery in patients who have multiple radiographic abnormalities is controversial. Sometimes, the clinical pattern will indicate overlapping roots, in which case two levels should be explored. This is particularly true with the combination of C5–6 with C6–7 root involvement. It is common to explore both of these roots in patients who have arm pain radiating towards the thumb, index, and middle finger with associated numbness. Again, the superiority of the posterior approach allows multiple roots to be explored without inducing multiple fusions. Fig. 60.14 The anterior operation is apparently the most widely used for cervical radiculopathy, although the previous mentioned operation is safer, simpler, and produces fewer long-term effects than the anterior discectomy about to be described.

3. Reflex change. 4. Weakness. An algorithm for the surgical indications in cervical radiculopathy is as follows: For patients with pain alone, nonoperative measures should be extended for a reasonable period of time or until the patient cannot tolerate the pain any longer. Long-term use of narcotics should be avoided. Nonoperative measures are discussed elsewhere. For pain with neurological deficit, if the neurological deficit is mild and chronic, nonoperative methods, as discussed elsewhere, should

OUTCOMES Outcomes for posterior cervical foraminotomy and discectomy One of the largest original series of this operation, including 736 consecutively operated cases, was reported in 1983.3 In this series, there was a 96% incidence of significant relief of arm pain and paresthesias, and a 90% incidence of resolution of preoperatively present motor deficit. Most of these operations were preceded by Pantopaque myelography, the study of choice for cervical disc disease at that time. Fifteen percent of the cases involved two or more levels. There was no significant difference regarding the results or recurrences among patients with so-called hard disc protrusion, soft disc protrusion, or spondylotic radiculopathy. The median time to return to normal activities was 9.4 weeks with an average follow-up time of 2.8 years.

Table 60.1: Clinical syndromes of cervical radiculopathy Root

Motor

Sensory

C3

No detectable motor deficit

Numbness around mastoid, ear lobe, and anterior neck

C4

No detectable motor deficit

Numbness across the shoulder top but not extending over arm

C5

Deltoid and partial biceps

Numbness over the shoulder top extending partially down lateral aspect of the arm

C6

Biceps (partial deltoid)

Numbness of thumb and index finger, dorsum of hand

C7

Weakness of the triceps muscle

Numbness involving middle finger, but may also involve thumb and index finger whereas C6 does not involve the middle finger

C8

Weakness of intrinsic hand muscles

Numbness of ring and small finger 663

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A prior study, which included 383 cases of ‘lateral disc’ was reported in 1976 by Scoville et al.4 The results were good to excellent in 95% of these patients. There were no recurrences or serious complications, and the study specifically focused on posterolateral soft disc ‘sequestration.’ Aldrich studied 53 patients. In 36 of these, the disc was sequestered (nonconfined), and was posterolateral to the disc space as seen on imaging studies.5 Most of these patients had distinct motor weakness. They were treated by posterior partial facetectomy and removal of the disc fragments under direct microscopic vision. Pain relief was immediate and sensory deficit and residual motor loss improved within 6 months. There were no complications. Hospital stay averaged 2 days and follow-up period averaged 26 months. Rodrigues et al. reported 81 patients who underwent posterior treatment for soft disc herniation between 1990 and 1999.6 Total relief of pain was obtained in 49 of these 51 patients (96%). Motor improvement resulted in 35 of the 46 patients (76%) who had motor deficits, and sensory improvement was seen in 22 of the 35 patients (62.8%) who presented with sensory findings. Perhaps the longest follow-up study, consisting of 170 patients operated on between 1959 and 1991 with a 96% follow-up, was reported by Davis in 1996.7 He used the Prolo outcome rating scale to determine the results. Eighty-six percent of patients had good relief as defined as a Prolo score of 8 or better. Of the 10 patients with Prolo scores under 5, seven did strenuous work and had compensation claims. The remainder had legal claims or were at psychological risk for surgery. This author favored the Prolo Outcome Scale as a standard. The Witzmann et al. study of 67 surgically treated patients for cervical radiculopathy from the posterior approach reported complete disappearance of symptoms in 93% of the cases followed up to 3 months after surgery.8 Only 10% of these patients retired prematurely. He also favored the Prolo functional economic outcome rating scale, and 60% of the patients showed excellent economic outcomes. As one might expect, variations in surgical technique of the posterior foraminotomy have evolved. One technique favored a large bony decompression as suggested by Jodicke et al.9 They reported that all 39 patients improved. There were two early relapses and residual pain was observed in three patients within 30 days postoperatively, necessitating surgical revision. They believed that the failure was associated with residual mediolateral disc protrusion in one case and generalized spondylosis in the other. These results are significantly less favorable than those reported in large series. More favorable results were reported by Fessler and Khoo.10 They recommend a ‘microendoscopic foraminotomy’ approach which they used from March 1998 to 2001 in 25 patients with cervical root compression from either foraminal stenosis or disc herniation. Symptomatic relief was seen in 92% of the patients. By the end of the minimum of 1-year follow-up, 92% had experienced resolution or improvement of the symptoms, whereas 8% were unchanged. These results were slightly better than the patients on whom the standard approach was used, of which 88% either resolved or improved. There was no significant difference in the outcome of the procedures, but they do report two durotomies among 25 patients who were treated with microendoscopic foraminotomy, and contradistinction to the negligible report of this complication among other posterior foraminotomy approaches.

Outcomes of anterior approach cervical disc surgery The controversies generated by the anterior operation are significantly more complex than those involving the posterior approach. The controversies include: 664

1. To fuse or not fuse? 2. Does the fusion, if it is used, endanger the adjacent discs for premature degeneration, both symptomatic and unsymptomatic? 3. Could a cervical disc prosthesis be inserted safely, and would it prevent adjacent disc degeneration? In addition to the controversy, the list of complications is significantly greater with anterior cervical surgery, and include difficulty with swallowing, hoarseness, and a variety of other worries not seen in the posterior surgery. However, as mentioned previously, anterior cervical surgery for a midline cervical disc herniation is the procedure of choice, particularly when there is cord compression, and there is little controversy in this situation. Numerous studies have discussed the outcomes in anterior surgery for degenerative disc disease. The results have been similar to those of posterior surgery since the original description of the procedure by Smith and Robinson.11 More recent studies, such as those of Zoega et al., used a variety of questionnaires up to 2 years postoperatively, including the modified Million Index, the Oswestry Index, and the visual analogue scale.12 The results were analyzed by an unbiased observer using Odom’s criteria. The study is reported because of the variety of testing methods used to determine the outcome of surgery. In this series, 81% of patients were satisfied with the outcome of surgery. Most significantly, they reported a good correlation among the different methods of analysis listed above. Anterior discectomy without cervical fusion was a significant consideration in the many series. In retrospective analysis, of the 42 patients who underwent anterior cervical discectomy without fusion between 1988 and 1994, good results were achieved in 93% of patients with soft disc and 59% of patients with hard disc disease. In postoperative films, gaps of the disc space were seen in 43% of these patients and 28% seemed to have radiographic fusion. Despite this, Lieu and Howng indicated that anterior discectomy without fusion is a treatment of choice for soft disc disease.13 Jacobs et al., utilized an extensive search strategy to review papers dated between 1996 and 2004 involving various methods of anterior cervical disc surgery. Ultimately, they reported 14 studies involving 939 patients and evaluated three comparisons of different fusion techniques. Anterior discectomy alone had a shorter operation time, shorter hospital stay, and a shorter postoperative absence from work than discectomy with fusion. There was no significant difference in pain relief or rate of fusion. The authors concluded that fusion techniques that use allograft gave better fusion results than those using interbody devices such as cages, but the utility of cervical fusion was questioned in comparison with simple anterior cervical discectomy.14 Donaldson and Nelson reported in 2002 on 64 consecutive patients who underwent anterior cervical discectomy without interbody fusion. The results were comparable, 91% with good to excellent outcomes, to other studies, and they concluded that interbody fusion is not necessary in the surgical management of cervical disc disease.15 To demonstrate the divergence of opinion on this matter, it is now common, if not routine, throughout the United States to perform anterior discectomy with some type of fusion material and anterior plating. Wang et al. showed increased fusion rates with cervical plating for two-level cervical discectomy and fusion among the 60 patients who were treated with and without fusion. Remarkably, 25 of the patients who were not plated had pseudoarthrosis, whereas none of the patients who were plated had a pseudoarthrosis. It is not clear from this paper whether the clinical results were different between the two groups.16 Wirth et al. concluded in 2000, in his comparison of treatment of cervical radiculopathy with posterior cervical foraminotomy, anterior discectomy without fusion, and anterior discectomy with fusion,

Section 3: Cervical Spine

that all procedures gave relief of symptoms and signs postoperatively during the follow-up period. The number of patients in the study, however, was small and the conclusions rather general.17 Any discussion of outcomes must consider the very real and worrisome history of adjacent disc degeneration once one or more cervical vertebrae are fused. Studies are many indicating adjacent disc degeneration, often symptomatic, in a period of years after anterior cervical fusion. This, in the author’s opinion, is a major detraction from the anterior procedure for radiculopathy. Although the immediate results for cervical radiculopathy are good, one must consider the late complications. For instance, Matsunaga et al. noticed that shear strain on adjacent segments increased 20% on the average 1 year after fusion.18 Wu et al., in a pre- and postoperative fast spin echo magnetic resonance imaging (MRI) study, determined that among 68 patients during the average time of 37 months, there was a significant incidence of disc herniations and osteophyte formation in the levels immediately above and below the fused group.19 Kulkarni et al. determined, on a postoperative MRI study with a mean duration of 7.5 months, in 44 patients, that the levels adjacent to the fused segment exhibited more pronounced degenerative changes in 75% of the patients who had undergone a two-level anterior corpectomy.20 In one of the largest studies, Goffin et al. examined 180 patients who were treated with anterior cervical interbody fusion with the follow-up of approximately 6 months.21 The patients were examined clinically and radiographically by independent investigators. A radiologic ‘degeneration score’ was compared initially and at the time of long-term follow-up. At the late follow-up interval, anterior cervical interbody fusion showed additional radiologic degeneration at the adjacent disc levels in 92% of the patients and varying degrees of clinical deterioration. The longer the time interval since surgery, the greater the radiological degeneration. Katsuura et al. found that degenerative changes were present on radiological examination adjacent to the fused segment in 50% of their patients, eight of whom also demonstrated neurological deterioration. They believed that the tendency for adjacent disc degeneration was aggravated by preoperative conditions, such as kyphosis or sigmoid curvature.22 In order to address the very real issue of adjacent disc degeneration, there has been recent interest in the development of an artificial cervical disc which would move somewhat normally and theoretically prevent adjacent disc degeneration which is felt to be the result of the additional load when fusion interferes with normal motion. The results of the studies with use of artificial cervical disc will not be discussed here because long-term follow-up is not available and much controversy exists among spine surgeons as to the utility of this technique. One cannot help comment, however, that the entire issue of cervical disc replacement because of the deleterious effects of anterior fusion on adjacent cervical spine in patients with cervical radiculopathy could be avoided simply by performing posterior cervical foraminotomy. It would appear that the artificial disc, in cases of unilateral radiculopathy, evolved from the unnecessary requirement of the fusion to simply relieve pressure on the cervical nerve root.

syndrome and correlative radiographs in properly selected patients. In these patients, both the anterior and posterior approaches are associated with high patient satisfaction. The posterior approach is associated with less risk of iatrogenic complications and is preferred in patients with no axial neck pain and a paracentral herniated discs. The anterior approach is preferred for midline disc herniation or in patients with spondylotic compression and axial neck pain. The anterior approach may or may not be accompanied by fusion.

References 1. Brunori A, Decaro GMF, Giuffre R, et al. Successful cervical disc surgery by Professor Angelo Chiasserini Sr of Rome 1937. J Hist Neurosci 1998; 7(3):219–224. 2. Angevine PD, Arons RR, McCormick PC. National and regional rates and variation of cervical discectomy with and without anterior fusion, 1990–1999. Spine 2003; 28(9):931–939. 3. Henderson CM, Hennessy RG, Shuey HM Jr, et al. Posterior-lateral foraminotomy as an exclusive operative technique for cervical radiculopathy: a review of 846 consecutively operated cases. Neurosurgery 1983; 13(5):504–512. 4. Scoville WB, Dohrmann GJ, Corkill G. Late results of cervical disc surgery. J Neurosurg 1976; 45(2):203–210. 5. Aldrich F. Posterolateral microdisectomy for cervical monoradiculopathy caused by posterolateral soft cervical disc sequestration. J Neurosurg 1990; 72(3):370–377. 6. Rodrigues MA, Hanel RA, Prevedello DM, et al. Posterior approach for soft cervical disc herniation: a neglected technique. Surg Neurol 2001; 55(1):17–22. 7. Davis RA. A long-term outcome study of 170 surgically treated patients with compressive cervical radiculopathy. Surg Neurol 1996; 46(6):523–530. 8. Witzmann A, Hejazi N, Krasznai L. Posterior cervical foraminotomy. A follow-up study of 67 surgically treated patients with compressive radiculopathy. Neurosurg Rev 2000; 23(4):213–217. 9. Jodicke A, Daentzer D, Kastner S, et al. Risk factors for outcome and complications of dorsal foraminotomy in cervical herniation. Surg Neurol 2003; 60(2):124–129. 10. Fessler RG, Khoo LT. Minimally invasive cervical microendoscopic foraminotomy: an initial clinical experience. Neurosurgery 2002; 51(5 Suppl):S37–S45. 11. Robinson RA, Smith GW. Anterolateral cervical disc removal and interbody fusions for cervical disc syndrome. Bull Johns Hopkins Hosp 1955; 96:223–224. 12. Zoega B, Karrholm J, Lind B. Outcome scores in degenerative cervical disc surgery. Eur Spine J 2000; 9(2):137–143. 13. Lieu AS, Howng SL. Clinical results of anterior cervical discectomy without interbody fusion. J Med Sci 1998; 14(4):212–216. 14. Jacobs W, Anderson P, Limbeek J, et al. Single or double-level anterior interbody fusion techniques for cervical degenerative disc disease. Cochrane Database Syst Rev 2004; 18(4):CD004958. 15. Donaldson JW, Nelson PB. Anterior cervical discectomy without interbody fusion. Surg Neurol 2002; 57(4):219–224. 16. Wang JC, McDonough PW, Endow KK, et al. Increased fusion rates with cervical plating for two-level anterior cervical discectomy and fusion. Spine 2000; 25(1):41–45. 17. Wirth FP, Dowd GC, Sanders HF, et al. Cervical discectomy. A prospective analysis of three operative techniques. Surg Neurol 2000; 53(4):340–346. 18. Matsunaga S, Kabayama S, Yamamoto T, et al. Strain on intervertebral discs after anterior cervical decompression and fusion. Spine 1999; 24(7):670–675. 19. Wu W, Thuomas KA, Hedlund R, et al. Degenerative changes following anterior cervical discectomy and fusion evaluated by fast spin echo MR imaging. Acta Radiol 1996; 37(5):614–17. 20. Kulkarni V, Rajshekhar V, Raghuram L. Accelerated spondylotic changes adjacent to the fused segment following cervical corpectomy: magnetic resonance imaging study evidence. J Neurosurg Spine 2004; 100(1):2–6.

SUMMARY

21. Goffin J, Geusens E, Vantomme N, et al. Long-term follow-up after interbody fusion of cervical spine. J Spinal Disord Tech 2004; 17(2):79–85.

Surgery to decompress cervical nerve roots is a highly successful procedure when performed on patients with a clear-cut clinical

22. Katsuura A, Hukuda S, Saruhashi Y, et al. Kyphotic malalignment after anterior cervical fusion is one of the factors promoting the degenerative process in adjacent intervertebral levels. Eur Spine J 2001; 10(4):320–324.

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SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ i: Cervical Radicular Pain

CHAPTER

Surgical Decompression for Foraminal Stenosis

61

Mark A. Knaub, Douglas S. Won and Harry N. Herkowitz

INTRODUCTION Cervical spondylosis is a common, occasionally disabling condition that occurs as a consequence of the natural aging process that affects a large portion of the adult population. Symptomatic cervical spondylosis can be arbitrarily divided by the findings at initial presentation. These symptomatic patients present with axial neck pain, radiculopathy, myelopathy, or most commonly a combination of these symptom complexes. This chapter will focus on the surgical treatment of cervical radiculopathy, specifically decompression of foraminal stenosis related to spondylotic changes. An initial review of the normal anatomy and pathologic changes responsible for the development of foraminal stenosis will be followed by a discussion on the clinical presentation and evaluation of these patients. The rationale, specific surgical techniques, potential complications, and clinical results of both anterior and posterior surgical approaches will be described in detail.

Intervertebral foramen

Joint of luschka Uncinate process

Fig. 61.1 The bony anatomy of the neural foramen on an oblique Inferior articular view of a cervical process functional spinal unit. The neural foramen is bordered superiorly and inferiorly by the adjacent pedicles. Anteriorly, the foramen Superior articular is bordered by the uncovertebral joint, the process intervertebral disc, and a portion of the vertebral body. The posterior Transverse process margin of the neural foramen is composed of the facet joint and adjacent lateral mass.

ETIOLOGY OF FORAMINAL STENOSIS The cervical functional spinal unit consists of two vertebral bodies joined by an intervertebral disc anteriorly and two synovial facet joints posteriorly. The cranial surface of the vertebral body is typically concave from side-to-side and convex in the anteroposterior direction. The inferior surface is convex from side-to-side and concave in the anteroposterior direction. A projection on the lateral aspect of the superior surface of the inferior vertebral body is called the uncus. The uncus is intimately related to the convex lateral inferior surface of the cephalad vertebrae. This projection off the cephalad vertebral body is referred to as the enchanure or anvil. The ‘articulation’ between these two structures is referred to as the ‘uncovertebral joint’ or ‘joint of Luschka.’ Cervical nerve roots exit the spinal canal through the neural foramen in an anterolateral and inferior direction. The boundaries of the neural foramen are formed superiorly and inferiorly by the adjacent pedicles. The medial aspect of the facet joint and an adjacent portion of the articular column form the posterolateral border of the neural foramen. The anterolateral border is formed by the posterolateral portion of the uncus, the intervertebral disc, and the inferior portion of the superior adjacent vertebrae. Figure 61.1 shows a cervical spine model, viewed in an oblique projection, which illustrates the bony confines of the neural foramen. Neurologic symptoms that arise from cervical spondylosis are the result of a cascade of degenerative events that likely begins in the intervertebral disc. Age-related changes within the disc lead to an alteration in the chemical composition of the nucleus pulposus. A decrease in the proteoglycan and water content in the nucleus alters the biomechanical properties of the disc itself, as well as those of the functional spinal unit. As a result, the disc loses height and bulges posteriorly

into the spinal canal. The vertebral bodies physically move closer to one another as a result of the loss of disc height. This alteration in the normal anatomic relationships of the vertebral bodies, in combination with the altered biomechanical properties of the intervertebral disc, results in altered loading of the facet and uncovertebral joints. This increase in load through the facet and uncovertebral joints leads to the formation of osteophytes around these articulations and at the margins of the disc space. Neural foraminal narrowing can occur as a result of both static and dynamic processes. Abnormal biomechanics that result from biochemical changes in the intervertebral disc may lead to microinstability that contributes to dynamic neural foraminal narrowing. Changes in the bony architecture of the borders of the foramen lead to static narrowing of the neural foramen. Posteriorly protruding disc material, uncovertebral osteophytes, or thickened soft tissues within the foramen may result in extrinsic compression of the nerve root. An oblique radiograph of the cervical spine illustrates the anatomic borders of the foramen and how uncovertebral joint osteophytes can result in narrowing of the foramen. Both Figure 61.1 and Figure 61.2 demonstrate how osteophyte formation from the facet joint could result in narrowing in the anterior–posterior dimension. The height of the foramen may also be compromised as the intervertebral disc loses its biomechanical integrity and loses height. As mentioned earlier, the vertebral bodies move closer together, causing the adjacent pedicles to move closer, thereby narrowing the cephalad–caudad dimension of the neural foramen. Surgical treatment of neural foraminal stenosis must address the anatomic structures that are responsible for narrowing of the foramen and may include an arthrodesis to eliminate any dynamic foraminal narrowing. 667

Part 3: Specific Disorders Intervertebral foramen

Joint of Luschka

Inferior articular process

Uncinate process

Superior articular process

Fig. 61.2 An oblique radiograph of the cervical spine showing the anatomic borders of the foramen. This radiograph demonstrates how posterior uncinate process osteophytes can narrow the anterior– posterior dimensions of the foramen. Osteophyte formation of the facet joint can also affect the size of the neural foramen.

CLINICAL PRESENTATION AND PATIENT EVALUATION Foraminal stenosis typically results in cervical radiculopathy which refers to symptoms that occur in a specific dermatomal pattern in the upper extremity. Patients typically describe sharp pain and tingling or burning sensations in the involved area. Diminished sensation and motor loss corresponding to the involved nerve root may be present, as may diminished deep tendon reflexes. Patients typically have neck and arm pain that prevents them from finding a comfortable position. They may find comfort by placing their forearm on top of their head, the so-called ‘shoulder abduction sign.’1 Extension or lateral rotation of the head to the side of the pain (Spurling’s maneuver) may aggravate the symptoms. This finding may assist in the differentiation of radicular pain from other sources of shoulder pain and muscular neck pain. It is also paramount to remember that multiple sources of neck and upper extremity pain are extremely common and that neural compression may very well be occurring at two distinct locations.2,3 Adaptations to the initial radiculopathy symptoms may result in secondary pathologic changes in the shoulder, carpal tunnel, and ulnar nerve that may cloud the clinical picture and persist long after the cervical radiculopathy has resolved. In a series of 736 patients with cervical radiculopathy treated operatively, Henderson et al. reported the clinical signs and symptoms at presentation. They found that 99.4% had arm pain, 85.2% had sensory deficits, 79.7% had neck pain, 71.2% had diminished deep tendon reflexes, 68% had motor weakness, 52.5% had periscapular pain, 17.8% had anterior chest pain, and 9.7% had headaches. The neurologic deficits at presentation correlated with the offending disc level in approximately 80% of the patients.4 As always, patient evaluation begins with a complete history and detailed physical examination. A complete neurologic exam of all four extremities should included motor and sensory examinations, as well as an assessment of deep tendon reflexes. Special attention should be given to the presence of pathologic reflexes in the lower extremities to rule out the possibility of coexistent myelopathy. Provocative tests such as Spurling’s maneuver should be performed. The presence of 668

Lhermitte’s sign should be sought. Relief of radicular complaints with neck flexion and rotation away from the painful upper extremity may occur, as this motion opens the neural foramen. Similarly, direct axial cervical traction may lessen the radicular symptoms. In addition, it is necessary to assess for other etiologies of shoulder and/or arm pain such as peripheral nerve entrapment syndromes, intrinsic shoulder pathology, and vascular insufficiency. Radiographic evaluation begins with plain cervical spine films in the anteroposterior and lateral projections. Oblique radiographs are at times helpful in assessing for foraminal narrowing from uncovertebral osteophytes, but are not routinely obtained. Dynamic (flexion– extension) lateral radiographs should be considered but are not necessary in every patient. Based on the patient’s presenting symptoms and history, the physical examination, and initial radiographs, the spine surgeon should have a good idea of what will be found on additional imaging studies or at the time of surgery. The decision to proceed with further imaging or diagnostic testing should be made by the surgeon based on the suspected diagnosis, the duration and severity of the symptoms, and other individual patient factors. Additional studies that should be considered include bone scan, myelography combined with computed tomography (CT), electrodiagnostic testing, and magnetic resonance imaging (MRI). Consideration for bone scans should be given in patients with suspected malignancy, infection, or occult trauma realizing that bone scan may be normal in the setting of multiple myeloma. Myelography combined with computed tomography was the study of choice for the evaluation of suspected cervical stenosis until the widespread availability of MRI. Myelo/CT studies are still useful in those patients with contraindications to MRI and in potential revision situations. MRI has become the gold standard imaging modality for evaluation of patients with cervical radiculopathy and myelopathy. The advantages of MRI are that it provides complete visualization of the vertebrae, intervertebral discs, nerve roots, subarachnoid space, and spinal cord, including any intraspinal cord pathology. Multiplanar images are also routinely generated by this noninvasive, readily available imaging modality. It provides exquisite sensitivity in detecting subtle anatomic abnormalities. Axial images at the level of the neural foramen provide excellent contrast between the cerebrospinal fluid (CSF)-filled nerve root sleeve and the surrounding bony and soft tissue structures. Foraminal narrowing from disc herniation, uncovertebral osteophyte, facet hypertrophy, and in-folded ligamentum flavum can be visualized on these axial T2 images. An example of foraminal stenosis caused by uncovertebral osteophytes can be seen in Figure 61.3.

SURGICAL DECOMPRESSION OF FORAMINAL STENOSIS Patients presenting with symptoms of cervical radiculopathy and imaging studies that coincide with the physical exam findings should be considered for active treatment. Medical rehabilitation and interventional spine treatment modalities including nonsteroidal antiinflammatories, mild narcotic analgesic medications, physical therapy, cervical epidural steroid injections, and selective nerve root blocks should be utilized initially for most patients. Absolute indications for surgical decompression of isolated foraminal stenosis are lacking although patients presenting radicular symptoms in combination with progressive myelopathy should be treated surgically. Strong indications for surgical intervention include profound muscle weakness and atrophy. Surgical decompression should also be considered if a patient has undergone a prolonged period of conservative management without resolution of their symptoms. A trial of 6–12 weeks of nonoperative modalities is considered adequate by most surgeons. The severity of the patient’s pain and the degree of muscle

Section 3: Cervical Spine

Fig. 61.3 T2-weighted axial MRIs demonstrating normal-appearing intervertebral foramen (A) and bilateral neural foraminal narrowing from uncovertebral joint osteophytes (B).

weakness play a role in the decision to abort conservative treatment and proceed with surgical intervention. Once the decision has been made to treat a patient surgically, the surgeon is faced with the decision as to which approach is most suitable given the patient’s symptoms and the exact etiology of the foraminal narrowing. Anterior and posterior surgical approaches for foraminal stenosis have been described and excellent results have been reported with both. In general, patients with axial neck pain should be treated with anterior discectomy and fusion. Motion-sparing procedures such as posterior foraminotomy may not address alternative axial pain generators, such as the intervertebral disc and facets. Patients with isolated radicular symptoms may be treated with any of the abovementioned procedures. Reports of excellent results with all procedures can be found in the literature. The theoretical advantages of each of the approaches will be discussed in the following sections of the chapter.

ANTERIOR CERVICAL DISCECTOMY AND FUSION The anterior approach to the cervical spine allows for direct access to the compressive pathology responsible for foraminal stenosis. Bulging or herniated disc material and uncovertebral osteophytes lie anterior to the spinal cord and the nerve roots and can therefore be directly removed from an anterior approach. Figure 61.4 shows how these offending anterior structures are directly accessible for removal via

A

B

Fig. 61.4 Axial T2 MRI images demonstrating the location of the offending structure, in this case a disc herniation, anterior to the spinal cord. Direct removal of this pathology can be accomplished, safely, via an anterior approach. Manipulation of the spinal cord would be necessary to directly remove this pathology from a posterior approach.

an anterior approach. Robinson and Smith initially described anterior cervical discectomy and fusion in 1955.5 The anterior approach avoids direct manipulation of the neural elements. This original procedure relied on indirect decompression of the spinal cord and neural foramen by distraction of the disc space. Progression of spondylotic spur formation was prevented by stabilization of the segment and the authors believed that regression of these osteophytes occurred as a result of the arthrodesis. In 1958, Cloward published an alternative technique for anterior cervical discectomy and fusion in which direct decompression of the neural elements was performed.6 There are no comparative studies in the literature to support the clinical superiority of direct or indirect decompression of the neural elements in spondylotic radiculopathy. Individual surgeons must make a decision as to which philosophy they subscribe. The surgeon’s training as well as personal experience likely influence this decision. Numerous modifications of the original Smith–Robinson and Cloward bone grafting techniques have been described. The Smith– Robinson technique involves an autogenous tricortical corticocancellous horseshoe graft placed into the evacuated disc space. The cortical component of the graft provides structural support that maintains the disc-space height while the cancellous portion facilitates graft incorporation. The original technique involved simply removing the cartilaginous endplate and incomplete decortication. More aggressive decortication, beyond simple cartilaginous endplate removal, has been demonstrated to improve fusion rates.7,8 Cloward’s autogenous graft was harvested from the iliac crest with an oversized hole saw. The oversized dowel graft was then impacted into an undersized hole at the level to be fused. The unicortical surface of this dowel graft was placed anteriorly, resting just posterior to the anterior surface of the vertebral bodies. Bailey and Badgley described a technique in which a ‘keystone- shaped’ corticocancellous graft was utilized.9 This trapezoidal-shaped graft is mortised into the prepared disc space. Excellent results with this technique were reported by Simmons in 1969.10 Contemporary choices for graft material include autograft, allograft, and synthetic cage devices. Good results have been reported with all of these graft choices when utilized for one-level discectomy and fusion without instrumentation, although the current literature does not support the superiority of any one single graft material or device.7,11–15 Higher rates of radiographic arthrodesis have been reported with the use of autogenous iliac crest grafts, especially with multiple-level discectomies.12,16 Higher radiographic fusion rates with autogenous grafts do not occur without consequences. Complications related to graft harvest include hematoma formation, infection, injury to the lateral femoral cutaneous nerve, iliac wing fractures, and, most importantly, persistent iliac crest pain have been reported.17,18 Silber et al. reported iliac crest graft site harvest complications in a series of patients undergoing one-level anterior cervical discectomy and fusion (ACDF). Twenty-six 669

Part 3: Specific Disorders

percent of patients reported chronic pain at the donor site and nearly half of these chronically used pain medications. They also report functional impairment in 13% of the patients studied.17 Allografts have been used in anterior cervical spine surgery since the 1950s. Cloward reported a 94% fusion rate in 44 patients who underwent ACDF with a dowel-shaped, frozen allogeneic iliac crest graft.6 Schneider utilized freeze-dried allogeneic iliac crest bone for ACDF with the Cloward technique. He reported an arthrodesis rate of 93% with one-level procedures and an 85% fusion rate for multiple-level discectomy and fusion.19 The use of allograft iliac crest grafts with the Smith–Robinson has also been reported in the literature. Rish reported a fusion rate of 80% in single-level and 69% in multiple-level patients undergoing a Smith–Robinson-type ACDF with freeze-dried allogeneic iliac crest.20 A 94% fusion rate was reported by Brown et al. in patients undergoing the same procedure with allogeneic, frozen iliac crest grafts.21 They also reported a high rate of graft collapse when allogeneic iliac crests are used. As a result of concerns over the compressive strength of allograft iliac crest grafts, some authors began utilizing fibular allograft for anterior cervical discectomy and fusion. Martin et al. reported on 289 patients who underwent ACDF with freeze-dried fibular allograft without instrumentation.11 Radiographic fusion was obtained in 90% of those undergoing one-level fusions. After two-level procedures, only 72% showed radiographic fusion at all levels. Although there was a trend towards higher rates of nonunion in those patients who were smokers, the difference was not statistically significant. The authors concluded that freeze-dried allogeneic fibula is an effective substrate for obtaining fusion following anterior cervical discectomy without instrumentation. In an attempt to increase the likelihood of solid arthrodesis, many authors have advocated the addition of an anterior cervical plate, especially for multiple-level procedures. Radiographs of a two-level anterior discectomy and fusion with an anterior cervical plate are shown in Figure 61.5. Instrumentation increases the stability across the operative segment and decreases the motion between the graft and vertebral endplate, thereby increasing the chance of solid arthrodesis. The addition of anterior cervical instrumentation has been shown to decrease the rate of pseudoarthrosis in both single and multiplelevel ACDFs. Nonunion rates ranging 11–63% have been reported depending on the number of levels at attempted fusion, the type of graft material used, and whether or not anterior instrumentation was utilized.12,22–25 Wang and colleagues reviewed the clinical and radiographic results of 80 patients treated with single-level ACDF.26 Pseudoarthrosis rates of 4.5% and 8.3% were reported for instrumented and noninstrumented, respectively. Patients stabilized with an anterior plate had significantly less graft collapse and kyphosis than those without a plate. The clinical outcomes based on Odom’s criteria were not significantly different between the two groups. In two separate reports, the same senior authors have also reported retrospectively on the use of anterior cervical plates in two- and three-level ACDFs.27,28 Autogenous tricortical iliac crest grafts were used in all patients in each study. In the review of two-level procedures, a statistically significant difference in pseudoarthrosis rate was found in the instrumented group (0%) compared to the noninstrumented group (7%).27 The use of a cervical plate did not alter clinical outcomes but those patients who developed a pseudoarthrosis had poorer clinical results. In the third report by this group, the results of three-level ACDF were reviewed.28 Forty of the fifty-nine patients were stabilized with an anterior cervical plate. Pseudoarthrosis developed in 18% (7/40) of the plated patients and 37% (7/19) of those treated without a plate. This difference was not statistically significant, perhaps because of the small number of patients, but the authors point out that the rate of nonunion in the noninstrumented group is nearly twice that of 670

A

B

Fig. 61.5 Lateral and anteroposterior radiographs of a patient who underwent a two-level anterior cervical discectomy and fusion with autogenous iliac crest bone graft. An anterior cervical plate was utilized to increase the immediate stability of the construct and to increase the likelihood of solid arthrodesis.

the instrumented group. Once again, the development of a pseudoarthrosis resulted in poorer clinical outcomes. Other groups have analyzed the results of both one- and two-level ACDFs treated with and without plates.29,30 Caspar et al. retrospectively reviewed the charts of 356 patients who underwent one- and two-level ACDF with and without anterior instrumentation for degenerative disorders.30 Six percent of those undergoing noninstrumented fusions required reoperation for pseudoarthrosis compared to 0.7% in whom an anterior cervical plate was used. Two (out of 146) patients in whom a plate was used required a revision procedure secondary to hardware failure prior to fusion. The authors concluded that the use of anterior instrumentation for one- and two-level ACDFs results in a significant reduction in reoperation rates. In a retrospective manner, Kaiser et al. compared the radiographic results of a group of patients stabilized with anterior cervical plates following one- and two-level ACDF with a historical cohort of patients that were treated without plates.29 Cortical ring allograft struts were utilized in each of the groups. The fusion rates for one- and two-level ACDF with anterior instrumentation were 96% and 91%, respectively. Significantly

Section 3: Cervical Spine

lower fusion rates were found in those one- and two-level procedures (90% and 72%, respectively) that were not stabilized by an anterior plate.11 No infectious, neurologic, or graft-related complications were reported in the instrumented group. Statistical analysis revealed a higher graft complication rate in the noninstrumented group from the historical cohort. The authors conclude that the improved fusion rates and negligible complication rates justify the routine use of anterior cervical plating in the treatment of cervical spondylosis.

Surgical technique The patient is positioned in the supine position on a regular operating room table. General anesthesia is utilized for all patients. An orogastric tube or esophageal probe is placed into the esophagus to help identify the esophagus if needed during the dissection. A towel roll is placed longitudinally between the patient’s scapulae to help extend the cervical spine. The shoulders are taped in a depressed position after the arms have been well padded and tucked by the patient’s side. This allows for better visualization of the lower cervical spine on the localizing lateral radiograph. The head is then rotated to the right side to allow easier access to the left side of the neck for the surgical approach. The authors prefer the left-sided approach because of the more consistent course of the recurrent laryngeal nerve, in the tracheoesophageal grove, on this side. Headlights and loupe magnification are utilized in all cases. Transverse skin incisions are utilized for all one- and two-level procedures. The location of this incision is chosen by identification of palpable landmarks on the anterior neck. Exposure for three or more level procedures is easier through an oblique incision that is placed at the medial border of the sternocleidomastoid muscle belly. After incising the skin and subcutaneous tissues the platysma muscle fibers are split transversely. The superficial layers of the deep cervical fascia are entered just medial to the medial border of the sternocleidomastoid muscle. Utilizing the plane lateral to the trachea and esophagus and medial to the carotid sheath the anterior portion of the spine is exposed. The longus coli muscles are identified under the prevertebral fascia, which is then split in the midline and pushed away with blunt dissection. Palpation of the carotid tubercle on the anterior portion of the C6 transverse process allows for preliminary identification of the level for the planned surgery. A marker or spinal needle is placed into the disc space at the presumed level for radiographic confirmation. Once the appropriate level has been identified, the longus coli muscles are elevated and retracted laterally. A self-retaining cervical retractor is placed with its teeth under the longus coli muscle bellies. Retraction superficial to the longus coli muscles, which can result in damage to the sympathetic chain with resultant Horner’s syndrome, should be avoided. The sympathetic chain is at highest risk of injury at C6. Anterior osteophytes from the adjacent vertebral bodies are removed with a Leksell rongeur. This will assist with access to the disc space in patients with significant spondylosis and disc space collapse and also allows the anterior cervical plate to sit flat across the disc space. A scalpel is used to incise any portion of the anterior anulus remaining. Disc material is removed with a straight pituitary rongeur. Pins for a cervical distractor are screwed into the center of the adjacent vertebral bodies, taking care to avoid penetration of the adjacent endplate. Alternatively, a small cervical lamina spreader may be utilized to provide distraction across the disc space. The remaining disc material is removed with a pituitary rongeur. The up-sloping uncinate processes must be exposed bilaterally. This may be accomplished by removing disc material with a Kerrison rongeur or a cervical curette. Removing the cartilaginous endplates with cervical curettes begins preparation of the endplates. The longitudinal fibers of the posterior

longitudinal ligament are identified at the dorsal aspect of the disc space. Spondylotic bars and uncovertebral joint osteophytes can be visualized and removed with Kerrison rongeurs, cervical curettes, or a high-speed burr. The foramen can be located and explored with a nerve hook. Removal of uncovertebral osteophytes in the foramen is accomplished with a Kerrison or a curved cervical curette. In cases where foraminal stenosis is caused by disc space collapse and uncovertebral osteophytes, the PLL is left intact and the interspace is now ready to accept the graft. If a soft disc herniation is suspected from preoperative imaging, a rent in the PLL is sought. If one is found, it can be explored with a small nerve hook. Free fragments of disc are removed with a pituitary rongeur. The PLL is then removed from of the adjacent vertebral bodies with a Kerrison rongeur. A nerve hook is then passed under the adjacent vertebral bodies and out into the foramen to assure that all free fragments of disc have been removed. Endplate preparation began with removal of the cartilaginous portion of the endplate with curettes prior to the actual decompression. A large Kerrison rongeur is now utilized to remove any anterior overhang from of the inferior surface of the superior vertebral body. Alternatively, a high-speed burr may be used to remove this bone. Removal of this bone creates a flat host bone surface on the inferior aspect of the superior vertebral body to accept the graft. The highspeed burr is also used to remove some of the hard, subchondral bone of the endplate in an attempt to stimulate fusion. Care must be exercised with this step to avoid removing too much subchondral bone and exposing the cancellous bone of the vertebral body. This may predispose the construct to excessive settling of the graft into the adjacent vertebral bodies. The authors’ choice of graft material is patellar allograft. The articular cartilage of the patella is removed prior to preservation leaving a tricortical graft with thick, strong cortices for biomechanical strength and osteoconductive cancellous bone to facilitate osseous integration of the graft. The graft is cut with an oscillating saw to a thickness of about 8–9 mm depending on the size of the disc space after distraction and the discectomy. The graft is tapered slightly from front to back in an attempt to facilitate maintenance of the normal cervical lordosis. The depth of the graft is determined by measuring the depth of the vertebral body after the decompression has been completed. As with an iliac crest graft, the three cortical surfaces are placed anteriorly and laterally leaving the cancellous surface posteriorly. The shaped patellar allograft is tamped into place while distraction is continued through the pin distractor. The anterior portion of the graft is recessed 2–3 mm posterior to the anterior cortex of the vertebral bodies. To confirm the depth of the graft, a nerve hook is passed beside the graft and the free space between the PLL and the posterior aspect of the vertebral body is palpated. Any remaining anterior osteophytes are removed with a rongeur or high-speed burr. This will allow the cervical plate to lie flat against the anterior aspect of the spine, thereby avoiding any possible issues with dysphagia from the instrumentation. Failure to completely remove this abnormal bone also results in the plate resting on the osteophytes with the screws obtaining some of their purchase in this soft bone. The distraction across the disc space is released and the distraction pins are removed. To provide additional compression of the graft, the neck is brought out of extension by placing a towel behind the occiput. The authors’ choice of plating systems is a slotted, dynamic plate that allows for both dynamic compression of the graft as the screws are tightened, and linear settling of the graft as the cranial screws slide through the slots in the plate. During the insertion of the plate care must be taken to assure that the cranial screws are entering the vertebral body at the graft–host bone junction. Failing to do so may result in damage to the superior adjacent segment as the operative level settles and the cranial edge of the plate approaches 671

Part 3: Specific Disorders

the disc space proximal to the fusion. This is more of a concern with multiple-level discectomies but should not be neglected with onelevel fusions. An appropriate length of plate is placed flat against the anterior aspect of the spine. The drill holes are drilled for the inferior screws first with a drill bit with a stop at the appropriate length. The length of these screws is determined by the overall size of the patient and by preoperative radiographs. Alternatively, the depth of the vertebral body may be determined intraoperatively after the discectomy and decompression have been completed. Unicortical screws typically range 12–16 mm in length. The drill guide for the inferior screws is a ‘static’ guide, which places the screw in the center of the hole in the plate. The two caudal screws are placed but not tightened securely to the plate, thereby avoiding tipping the superior end of the plate anteriorly. The guide for the cranial screws is a ‘dynamic’ drill guide, which preferentially drills the guide hole eccentrically in the slot of the plate. The superior screws are placed but are also not secured tightly to the plate. Once all four screws have been placed, the inferior, or ‘static,’ screws are fully tightened. As the ‘dynamic’ screws at the top of the slots at the cranial end of the plate are tightened, a compressive force is place across the graft. Lastly, the screw-locking mechanism is engaged to prevent back-out of the screws. A lateral radiograph is obtained to confirm the position of the plate, the maintenance or recreation of the cervical lordosis, and the position of the screws. The self-retaining retractor is removed and sidewalls of the wound are inspected for any bleeding. The wound is irrigated with antibiotic saline and a small Jackson-Pratt drain placed directly over the plate and passed out the superior or lateral aspect of the wound. The platysma is closed with absorbable sutures followed by a running subcuticular closure of the skin. Because of the used of routine anterior cervical plating, all single-level discectomies are placed into a soft cervical collar that is worn for comfort only. Multilevel discectomies and corpectomies are placed into a semirigid cervical orthosis.

Posterior cervical foraminotomy Approaching cervical foraminal stenosis from a posterior approach allows for decompression of the neural elements without fusion of the involved motion segments. Motion preservation theoretically avoids the potential long-term complication of adjacent segment degeneration and disease. Proponents of laminoforaminotomy also stress that the posterior approach does not put vital structures such as the trachea, esophagus, and carotid sheath at risk during the surgical exposure. Since a fusion is not performed there is no risk of pseudoarthrosis or graft extrusion. Also, no risk of bone graft donor site morbidity or disease transmission from an allograft exists when a posterior foraminotomy is performed for foraminal stenosis. Concern exists over the large amount of muscle stripping and damage that must be done to perform a standard, open laminoforaminotomy. Higher rates of infection and postoperative neck pain have been reported in patients undergoing posterior procedures compared to anterior procedures.31 As a result of the concern over the large amount of muscle dissection, some have advocated a minimally invasive approach to posterior laminoforaminotomy. Fears of wrong-level surgery, creation of iatrogenic instability by excessive resection of the facet joint, and inadequate decompression also sway the surgeon away from performing laminoforaminotomies. Direct manipulation of the neural elements is also required to remove the offending pathologic structures that arise anterior to the nerve root. Theoretically, higher rates of neurologic complications should exist, although this has not been widely reported in the literature. While conventional wisdom suggests that motion preservation is a clear benefit of laminoforaminotomy, preservation of motion in patients with a combination of radiculopathy and neck pain will likely not alleviate and may even exacerbate preexisting neck pain. Anterior 672

discectomy and fusion operations, which remove the proposed ‘pain generator’ (thought by many to be the disc itself) and do not allow for motion of potentially diseased facet joints, are more suited for patients with coexistent neck pain. Clinical indications for posterior foraminotomy are similar to those outlined in the earlier portion of this chapter. Isolated radiculopathy in patients with imaging-confirmed neural compression that has failed to respond to conservative treatment modalities should be considered for operative treatment. Patients with any neck pain should be offered anterior decompression and fusion. Pathoanatomic indications for posterior cervical foraminotomy include posterolateral soft disc herniations, cervical lateral recess or foraminal stenosis from spondylosis, facet arthropathy with foraminal compression, continued radiculopathy following ACDF, and cervical disease in patients whom anterior approaches are contraindicated. As mentioned earlier, posterior cervical foraminotomy should also be considered when the cervical disease is located at the anatomic extremes, such as cervicothoracic junction or in the proximal cervical segments. Contraindications to foraminotomy include patients with vertebral body spondylotic bars, large central disc herniations, myelopathy, preexisting instability, and ossification of the posterior longitudinal ligament. Patients with significant kyphotic deformities should also not undergo posterior foraminotomies because of the nature of their neurologic compression. Posterior decompression in this setting, without correction of the deformity, may result in continued neurologic symptoms as the neural elements remained draped over the anterior compressive pathology. The indications and contraindications to posterior foraminotomy are summarized in Table 61.1. The effectiveness of the posterior cervical foraminotomy has been well documented in the literature over the past four decades.4,32–39 Scoville and associates reported 95% good or excellent results in patients who had lateral disc herniations.32 Rothman and Simeone reported 98% success rate in a group of patients that were followed for up to 8 years.33 Between 1963 and 1980, Henderson and Hennessy performed 846 posterior foraminotomy for cervical radiculopathy. They reported a 96% incidence of relief of significant arm pain and/or paresthesia and a 98% incidence of resolution of preoperative motor deficit.4 They also stated that there was no significant difference postoperatively regarding results or recurrence between the patients with suspected soft or hard disc protrusions and those with strictly spondylotic radiculopathy. Simeone and Dillin subsequently reported 96% good or excellent outcomes in their series of patients.34

Table 61.1: Indications and contraindications to posterior laminoforaminotomy Indications

Contraindications

Posterolateral soft disc herniations

Neck pain

Foraminal stenosis from uncovertebral joint osteophytes

Large central disc herniations

Facet arthropathy with foraminal compression

Myelopathy

Continued radiculopathy following ACDF

Preexisting instability

Disease at anatomic extremes (C2–3 or C7–T1)

Ossification of the PLL

Anterior approach contraindicated

Kyphotic sagittal alignment

Section 3: Cervical Spine

Herkowitz, et al. prospectively compared anterior and posterior approaches for the treatment of cervical radiculopathy caused by soft disc herniations.35 Seventeen patients were randomized to undergo anterior fusion while sixteen patients had a posterior foraminotomy. Good to excellent results occurred in 85% of those undergoing an anterior discectomy and fusion and in 75% of patients treated with posterior foraminotomy. This difference was not statistically significant. Wirth et al. randomized 72 patients with acute radiculopathy from a unilateral cervical disc herniation to undergo posterior cervical foraminotomy, ACDF, or anterior cervical discectomy without fusion (ACD).40 All three procedures yielded excellent relief of symptoms in nearly all of the patients. Complications, operative time, length of hospital stay, and the use of analgesics in the immediate postoperative period were similar in all three groups. At 2-month follow-up, nearly all of the patients reported excellent pain relief and approximately 90% were back to work. Telephone interviews more than 2 years after the procedure showed a decrease in the percentage of patients in each group with complete pain relief although 79–92% were able to work. Return trips to the operating room for a disc operation at the same level were more common in the foraminotomy group while a higher incidence of adjacent segment disc problems requiring an operation occurred in the ACDF group. Proponents of motion-sparing procedures may argue that this is due to stress transfer to the adjacent segments when a fusion is performed. In 1993, Zeidman and Ducker presented the results of posterior cervical foraminotomies performed in 172 patients with cervical radiculopathy.39 Some patients had multilevel disease and had multilevel foraminotomies; thus, a total of 243 foraminotomies were performed during 7-year period. Relief of radicular pain was obtained in 167 patients (97%). Recovery of motor deficit to baseline function was achieved in 36 of the 39 (93%) patients with preoperative motor weakness. Although the majority of patients who underwent singlelevel foraminotomy had improvement of their preoperative sensory abnormalities, the patients who had multilevel foraminotomies had minimal recovery of their sensory deficit. Also, no patient with depressed reflex had a recovery of this reflex after the operation. More recently, Harrop et al. reported on the effectiveness of treating cervical radiculopathy via posterior approach.41 They found reduction of radicular pain from a mean score of 7.45 of 10 preoperatively to 0.2 postoperatively. Although preoperative neck pain was not as severe as the radicular pain, there was a reduction of preoperative neck pain from mean score of 2.55 of 10 to 0.5 postoperatively. Both of these differences were statistically significant. Because of the concerns over the amount of muscle stripping needed to perform an open posterior foraminotomy, some have advocated the use of less invasive surgical techniques. The feasibility of a minimally invasive endoscopic approach (MED) to a posterior cervical laminoforaminotomy was evaluated in a cadaveric study.31 The authors compared the decompression provided by a minimally invasive approach with that of a standard open technique. The procedure time tended to be longer in the MED group and the laminotomy defect created with this minimally invasive technique larger. The average amount of the facet joint removed in the MED procedure was 37.5±12% versus 32.8±6.0% in the open group. This difference was statistically significant. Based on the biomechanical studies by Raynor and Zdeblick, this amount of facet removal does not lead to iatrogenic instability.42,43 Postprocedure CT myelography documented adequate neural decompression of the nerve roots at each level in both the open and MED groups. One dural laceration occurred during minimally invasive procedure but the authors felt that this was a ‘learning curve phenomenon.’ The authors concluded that the MED system provided adequate exposure and allowed for decompression equal to that of an open approach.

The clinical results of minimally invasive posterior foraminal decompression have been reported as well. Adamson reported results of 100 consecutive cases of posterior microendoscopic laminoforaminotomy used for the treatment of unilateral cervical radiculopathy secondary to disc herniation and/or spondylotic foraminal stenosis.44 Excellent or good results were obtained in 97 patients, with all returning to their preoperative occupation or level of functioning between 1 day and 4 weeks postoperatively. All patients were discharged from the hospital no later than postoperative day 1 with 90 of the patients being discharged the day of the procedure. Pain relief was excellent in a vast majority of patients, with 84 patients requiring no additional prescription medication after the first week. Fessler et al. reported their initial clinical experience with minimally invasive cervical microendoscopic foraminotomy (MEF) using the MED system.45 The MEF technique was performed on 25 patients with cervical radiculopathy from spondylotic foraminal stenosis or soft disc herniation. A group of 26 patients who underwent open cervical laminoforaminotomy for similar indications served as a comparison group. They reported that MEF group had lower overall operative times (115 versus 171 minutes), less blood loss (138 versus 246 mL per level), shorter postoperative hospital stay (20 versus 68 hours), and lower postoperative narcotic medication requirements (11 versus 40 equivalents) when compared to the patients who underwent open laminoforaminotomy. The first 12 patients in the MEF group were positioned in the prone position while the remaining 13 were placed in the seated position. Utilizing the seated position resulted in significantly shorter OR time, reduced blood loss, and shorter hospital stays. Outcomes were not significantly different between the two groups, with each achieving greater than 90% symptomatic improvement after the procedure.

Surgical techniques Anatomic considerations Posterior compression of the nerve root within the vertebral foramen can occur from the superior articular process, the ligamentum flavum, and the periradicular fibrous tissues.46 These compressive structures are easily removed via a posterior approach. In fact, one-quarter to one-half of the facet joint must be removed to ‘unroof ’ the neural foramen during a posterior foraminotomy (Fig. 61.6). Anterior compressive structures such as uncovertebral osteophytes (unless very large) may be difficult to visualize and remove via the posterior approach. Nerve root decompression in this setting is provided by simply ‘unroofing’ the foramen. Soft disc herniations within the foramen may be visualized by gently retracting the nerve root cephalad to reveal the disc fragment. Compression of the neural structures medial to the foramen can simply not be addressed from the posterior approach, as this would require direct manipulation of the spinal cord itself. The foraminal decompression afforded by an anterior approach is often overestimated secondary to difficulty in lateral visualization. Pathology that exists far lateral within the foramen (for example, a soft disc herniation that has migrated laterally out of the interspace) can be easily overlooked unless careful scrutiny of the root anatomy is performed. This requires exposure of the vertebral artery and puts this structure at significant risk of injury. A thorough discussion of the advantages and limitations of both the anterior and posterior approaches was written by Raynor in 1983.47 Concerns over the stability of the cervical functional spinal unit after foraminotomy prompted biomechanical evaluation of the effects of resection of progressively larger portions of the cervical facets on the acute stability of the cervical spine. Progressive facet joint resection resulted in segmental hypermobility when 50% of both facet joints was removed. The authors of both studies recommended limiting resection of the facet joints to less than 50% to avoid iatrogenic instability after 673

Part 3: Specific Disorders

A

B

C

Fig. 61.6 Axial CT scan image (A) through the cervical spine in an asymptomatic young patient without degenerative changes. Simulated bone removal provided by a posterior laminoforaminotomy (B). Postoperative CT myelogram (C) of a patient treated with an open laminoforaminotomy for unilateral radiculopathy from spondylotic changes.

laminoforaminotomy.42,43 If more than 50% of the facet joint must be excised to perform an adequate decompression, serious consideration must be given to adding an arthrodesis to the procedure.

Open posterior cervical foraminotomy Patients undergoing posterior foraminotomy can be positioned in either the prone or seated position. This choice is largely dependent on surgeon’s familiarity with the positioning and his or her training and personal preference. The advantages of the seated position are: gravity-assisted drainage of the operative field, minimal venous bleeding, and a comfortable operating position for the surgeon. A potential disadvantage is the risk of venous air embolism. The prone position may result in engorgement of the epidural veins which may in turn lead to excessive bleeding which may hinder operative visualization of the offending pathology. Many surgeons, however, are more familiar and comfortable with prone position because of its widespread use in the lumbar spine. To a great extent, venous engorgement can be countered by raising the head of the table so that the cervical spine is roughly parallel to the floor. The head is stabilized with either Gardner-Wells tongs and traction or a Mayfield pin head holder. The neck is placed in slight flexion to effectively ‘un-shingle’ the posterior elements of the spine and ease access to the foramen. Precordial Doppler ultrasonography and end-tidal CO2 monitoring are used by some surgeons to detect air emboli within the atrium. Intraoperative somatosensory evokedpotential monitoring of the operated dermatome as well as of distal distributions to examine spinal cord integrity and electromyographic recordings can also be used to assess motor integrity of the involved root as well. A spinal needle is inserted percutaneously and a lateral radiograph is taken to assess the position of the needle and guide the ultimate placement of the midline incision. A standard midline incision is made down to the level of the fascia. The relatively avascular midline raphe is identified and deep dissection carried out in this plane to the tips of the spinous processes. The paraspinal muscles are gently stripped unilaterally, taking care to expose out to the lateral edge of the lateral mass. Care should be taken to avoid complete destruction of the facet joint capsules during the exposure. Once the appropriate level has been identified, bone removal is initiated in the interlaminar window near the junction of the lamina and the lateral mass. A high-speed burr is used to remove the medial portion of the inferior articular facet at the junction of the lamina and the lateral aspect of the lamina itself. A curette or nerve hook can be placed underneath the superior articular facet to act as 674

a depth guide while burring. The superior articular facet is thinned until the anterior cortex is translucent. The remainder of this cortical bone can be removed with a small Kerrison rongeur with the foot of the Kerrison rongeur placed into the foramen. Undercutting the facet with small angled curettes can further decompress the roof of the foramen. Removal of the ‘roof ’ of the foramen will allow for visualization of the leash of epidural veins that lie around the nerve root. Bipolar electrocautery may be utilized to control epidural bleeding. With the exposure of the root, it is followed into the foramen, and the root is decompressed posteriorly, superiorly, and inferiorly so that it is no longer being compressed. If the foraminal stenosis is being caused by uncovertebral osteophytes, the foraminal decompression has been completed by ‘unroofing’ the foramen. If the neural compromise is caused by a soft disc herniation, the nerve root is gently retracted cephalad, and a nerve hook is used to sweep ventral to the root to identify and remove displaced disc fragments. More commonly, herniated disc fragment is trapped underneath the PLL. To remove the disc fragment, the posterolateral aspect of the PLL can be incised. Then, the disc fragment can be removed with toothed forceps. Hemostatis is obtained with bipolar electrocautery and thrombin soaked Gelfoam. Finally, a layered closure should be performed with careful closure of the fascia and underlying muscles to prevent separation of the muscle layers, which may result in significant indentation at the operative site. Sterile dressings are applied and the patient may be placed into a soft cervical collar. The soft collar is utilized for a short period of time (3–5 days) to allow for soft tissue healing. Since this is a motion-sparing procedure, prolonged immobilization should be avoided.

Microendoscopic foraminotomy The patient positioning and set-up for this minimally invasive approach is the same as that used for the open technique. Monitoring for venous air embolism and for neurologic injury may also be performed as in the open procedure. Once the patient is positioned, a fluoroscope is brought into the operative field to localize the operative level with a spinal needle prior to a skin incision. A skin incision is made approximately 1 cm off midline at the level of the pathology. Under fluoroscopic guidance, a K-wire is inserted to the facet or lateral mass of the level of the pathology. It is imperative to dock the guide wire directly on the bone to avoid inadvertent dural penetration. A small incision is placed around the wire to allow the passage of a series of dilators through the soft tissues. These dilators must be docked directly onto the facet complex to minimize interference of visualization from the

Section 3: Cervical Spine

adjacent muscle tissue. Lateral fluoroscopic images should be obtained frequently to insure a proper working trajectory throughout this process. Finally, the tubular retractor is anchored to the operating room bed via a specific retractor arm. The working end of the retractor must be positioned at the junction of the lamina and lateral mass. Magnified visualization can be provided with an endoscope, an operative microscope, or with loupes. If loupe magnification is utilized, a retractor system with a built-in light source makes visualization much easier. Once the tubular retractor is set in the desired position, any remaining soft tissue overlying the working area is removed with electocautery and pituitary rongeurs. The exact position of the retractor is adjusted, if necessary, to allow for visualization of the medial facet and lateral laminofacet junction. Once the bony landmarks are clearly identified, a high-speed burr is used to perform the facetectomy as described above in open laminoforaminotomy. The anterior cortex of the superior facet is burred until it appears translucent. Then, an endoscopic curette and small Kerrison rongeur is used to remove remaining thinned cortex. Bleeding from epidural veins in the foramen is controlled with a long endoscopic bipolar electrocautery forceps. The adjacent pedicles are palpated with a small nerve hook. Foraminotomy is completed with a small angled endoscopic Kerrison rongeur and microcurettes. The adequacy of the decompression should be confirmed by palpating the root along its course with a small nerve hook. If a soft disc herniation is present, a small nerve hook is used to sweep ventral to the root to allow for removal of the fragment with a small pituitary rongeur. After confirming the nerve root is adequately decompressed, the tubular retractor is removed and the wound is closed in two layers. A soft cervical collar may be used for a short period of time for patient comfort but is not necessary, given the minimally invasive nature of the procedure. Most patients may be discharged from the hospital on the same day.

A

CASE STUDIES Example 1 A 52-year-old man presented with a 2-month history of right arm pain and neck pain. He had been treated initially by his primary care physician with ibuprofen and physical therapy. Plain radiographs and an MRI were obtained; images of interest are presented in Figure 61.7. The axial MRI image shows right, unilateral foraminal stenosis from uncovertebral osteophytes. Mild deformation of the spinal cord is also present on the right as a result of a spondylotic bar from the inferior portion of the C6 vertebral body. The patient was sent for a series of cervical epidural steroid injections which gave him partial, temporary relief of his symptoms. After 5 months of symptoms, the patient wished to discuss surgical treatment. Because of his neck pain and the mild amount of spinal cord deformation, he was offered an ACDF with instrumentation as described in detail above. The procedure was performed without incident. In the recovery room, the patient reported that his arm pain was 90% improved compared to pre-op and that his neck pain was completely absent. He was immobilized in a soft cervical collar until his 2-week postoperative visit. At this visit, his arm pain had completely resolved. He had radiographic evidence of a solid arthrodesis at his 6-month postoperative visit. He is now 15 months out from surgery and has had no recurrence of arm pain or neck pain.

B

Example 2 A 38-year-old female was seen in the emergency room complaining of severe, burning pain on the radial side of her right forearm and hand. She had no complaints of neck pain. Plain radiographs showed mild disc space narrowing at C5–6 and C6–7. An MRI (Fig. 61.8) showed a lateral soft disc herniation at C5–6 with no central spinal canal

C

Fig. 61.7 Plain lateral radiograph (A), sagittal T2 MRI (B), and axial T2 MRI through the C7 foramen (C) of a 52-year-old man who presented with right C7 radiculopathy and axial neck pain. Anterior cervical discectomy and fusion with instrumentation was performed in this patient with resolution of both his arm pain and neck pain. 675

Part 3: Specific Disorders

A

Fig. 61.8 Sagittal (A) and axial (B) T2 MRI images of a 38-year-old female who presented with severe right-sided C6 radiculopathy but no neck pain. The images show a lateral soft disc herniation at the C5–6 level. She was treated with an open, posterior laminoforaminotomy with excellent relief of her preoperative symptoms.

B

stenosis. She was initially treated with NSAIDs and physical therapy without any resolution of her symptoms. Selective nerve root blocks failed to lessen her C6 radiculopathy. Surgical intervention was discussed because of ongoing symptoms that interfered with her ability to work. Her lack of neck pain and the presence of a lateral soft disc herniation made her a perfect candidate for an open posterior laminoforaminotomy. The procedure was performed with the patient in the prone position. After ‘unroofing’ the foramen as described above, a large free fragment of disc was identified in the axilla of the C6 nerve

root. A small, blunt nerve hook was passed under the C6 root and the fragment was removed with a small pituitary rongeur. The patient’s arm pain and paresthesias were completely absent when the patient was seen in the recovery room. She was discharged the following morning in a soft cervical collar. She returned to the office 2 weeks after surgery without her collar and with complaints of mild neck pain. Her neck pain resolved completely by her 6-week postoperative visit. She is now 9 months out from surgery and has no arm or neck pain.

Symptomatic cervical radiculopathy

History, physical examination, and plain radiographs No neurologic deficit

Conservative treatment (PT/NSAIDs)

Neurologic deficit No improvement

Additional imaging (MRI/CT myelo) Improved

HNP/foraminal stenosis Improvement

ESI/SNRI No improvement

Observation Surgical treatment

Axial neck pain and radiculopathy

ACDF

676

Radiculopathy alone

Posterior foraminotomy

Fig. 61.9 An algorithm for the treatment of symptomatic, cervical foraminal stenosis.

Section 3: Cervical Spine

CONCLUSIONS

14. van Limbeek J, et al. A systematic literature review to identify the best method for a single level anterior cervical interbody fusion. Eur Spine J 2000; 9(2):129–136.

Successful surgical treatment of refractory radiculopathy from isolated cervical foraminal stenosis can be accomplished from both anterior and posterior surgical approaches. A simple algorithm is presented in Figure 61.9. After an appropriate trial of nonoperative management, usually lasting at least 6 weeks, patients will be considered for operative intervention. Any patient with neck pain is offered an anterior cervical discectomy and fusion with instrumentation. Patients with central spinal canal stenosis from either a soft disc herniation or spondylosis are not candidates for a posterior decompression and are also offered an anterior procedure. The available literature does not support the superiority of one graft type or plate. The authors use tricortical, patellar allograft to avoid the morbidity of harvesting iliac crest autograft and because of the theoretical advantages mentioned above. The authors’ choice of anterior cervical plate is a slotted, dynamic plate that allows limited, linear settling of the graft. Patients with only radicular complaints and isolated foraminal stenosis from either a lateral, soft disc herniation or spondylosis may be offered a posterior laminoforaminotomy. The authors have no experience with the microendoscopic technique described above. The authors perform the open procedure with the patient in the prone position with the head stabilized in Mayfield tongs. In the authors’ practices, the great majority of patients are treated with anterior cervical discectomy and fusion. There are two major reasons for this. Most patients do not meet the strict criteria for posterior laminoforaminotomy, in that many patients present with some neck pain or osteophytes that lie medial to the area that can be safely decompressed from a posterior approach. More importantly, anterior cervical discectomy and fusion with instrumentation is a procedure with reliable and reproducible clinical results.

15. Floyd T, Ohnmeiss D. A meta-analysis of autograft versus allograft in anterior cervical fusion. Eur Spine J 2000; 9(5):398–403.

References 1. Davidson RI, Dunn EJ, Metzmaker JN. The shoulder abduction test in the diagnosis of radicular pain in cervical extradural compressive monoradiculopathies. Spine 1981; 6(5):441–446. 2. Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet 1973; 2(7825):359–362. 3. Massey EW, Riley TL, Pleet AB. Coexistent carpal tunnel syndrome and cervical radiculopathy (double crush syndrome). South Med J 1981; 74: 957–959. 4. Henderson CM, et al. Posterior-lateral foraminotomy as an exclusive operative technique for cervical radiculopathy: a review of 846 consecutively operated cases. Neurosurgery 1983; 13(5):504–512. 5. Robinson R, Smith G. Anterolateral cervical disc removal and interbody fusion for cervical disc syndrome. Bull Johns Hopkins Hosp 1955; 96:223–224.

16. Bishop RC, Moore KA, Hadley MN. Anterior cervical interbody fusion using autogeneic and allogeneic bone graft substrate: a prospective comparative analysis. J Neurosurg 1996; 85(2):206–210. 17. Silber JS, et al. Donor site morbidity after anterior iliac crest bone harvest for singlelevel anterior cervical discectomy and fusion. Spine 2003; 28(2):134–139. 18. Kurz LT, Garfin SR, Booth Jr RE. Harvesting autogenous iliac bone grafts. A review of complications and techniques. Spine 1989; 14(12):1324–1331. 19. Schneider JR, Bright RW. Anterior cervical fusion using preserved bone allografts. Transplant Proc 1976; 8(2 Suppl 1):73–76. 20. Rish BL, McFadden JT, Penix JO. Anterior cervical fusion using homologous bone grafts: a comparative study. Surg Neurol 1976; 5(2):119–121. 21. Brown MD, Malinin TI, Davis PB. A roentgenographic evaluation of frozen allografts versus autografts in anterior cervical spine fusions. Clin Orthop 1976; 119:231–236. 22. Boker DK, et al. Anterior cervical discectomy and vertebral interbody fusion with hydroxy-apatite ceramic. Preliminary results. Acta Neurochir (Wien) 1993; 121(3–4): 191–195. 23. Brown CW, Orme TJ, Richardson HD. The rate of pseudarthrosis (surgical nonunion) in patients who are smokers and patients who are nonsmokers: a comparison study. Spine 1986; 11(9):942–943. 24. Emery SE, Fisher JR, Bohlman HH. Three-level anterior cervical discectomy and fusion: radiographic and clinical results. Spine 1997; 22(22):2622–2624; discussion 2625. 25. Mutoh N, et al. Pseudarthrosis and delayed union after anterior cervical fusion. Int Orthop 1993; 17(5):286–289. 26. Wang JC, et al. The effect of cervical plating on single-level anterior cervical discectomy and fusion. J Spinal Disord 1999; 12(6):467–471. 27. Wang JC, et al. Increased fusion rates with cervical plating for two-level anterior cervical discectomy and fusion. Spine 2000; 25(1):41–45. 28. Wang JC, et al. Increased fusion rates with cervical plating for three-level anterior cervical discectomy and fusion. Spine 2001; 26(6):643–646; discussion 646–647. 29. Kaiser MG, et al. Anterior cervical plating enhances arthrodesis after discectomy and fusion with cortical allograft. Neurosurgery 2002; 50(2):229–236; discussion 236–238. 30. Caspar W, et al. Anterior cervical plate stabilization in one- and two-level degenerative disease: overtreatment or benefit? J Spinal Disord 1998; 11(1):1–11. 31. Roh S., et al. Endoscopic foraminotomy using MED system in cadaveric specimens. Spine 2000; 25(2):260–264. 32. Scoville WB, Whitcomb BB. Lateral rupture of cervical intervertebral disks. Postgrad Med 1966; 39(2):174–180. 33. Rothman R, Simeone FA, eds. The spine, 2nd edn. Philadelphia: WB Saunders; 1982. 34. Dillin W, et al. Cervical radiculopathy. A review. Spine 1986; 11(10):988–991.

6. Cloward R. The anterior approach for removal of ruptured cervical disks. J Neurosurg 1958; 15:602–617.

35. Herkowitz HN, Kurz LT, Overholt DP. Surgical management of cervical soft disc herniation. A comparison between the anterior and posterior approach. Spine 1990; 15(10):1026–1030.

7. Bohlman HH, et al. Robinson anterior cervical discectomy and arthrodesis for cervical radiculopathy. Long-term follow-up of one hundred and twenty-two patients. J Bone Joint Surg [Am] 1993; 75(9):1298–1307.

36. Epstein JA, et al. Cervical spondylotic radiculopathy. The syndrome of foraminal constriction treated by foramenotomy and the removal of osteophytes. Clin Orthop 1965; 40:113–122.

8. Emery SE, et al. Robinson anterior cervical fusion comparison of the standard and modified techniques. Spine 1994; 19(6):660–663.

37. Fager CA. Posterolateral approach to ruptured median and paramedian cervical disk. Surg Neurol 1983; 20(6):443–452.

9. Bailey RW, Badgley CE. Stabilization of the cervical spine by anterior fusion. J Bone Joint Surg [Am] 1960; 42:565–594.

38. Aldrich F. Posterolateral microdisectomy for cervical monoradiculopathy caused by posterolateral soft cervical disc sequestration. J Neurosurg 1990; 72(3):370–377.

10. Simmons EH, Bhalla SK. Anterior cervical discectomy and fusion: a clinical and biomechanical study with eight-year follow-up. J Bone Joint Surg [Br] 1969; 51:225–237.

39. Zeidman SM, Ducker TB. Posterior cervical laminoforaminotomy for radiculopathy: review of 172 cases. Neurosurgery 1993; 33(3):356–362.

11. Martin GJ Jr, et al. Anterior cervical discectomy with freeze-dried fibula allograft. Overview of 317 cases and literature review. Spine 1999; 24(9):852–858; discussion 858–859.

40. Wirth FP, et al. Cervical discectomy. A prospective analysis of three operative techniques. Surg Neurol 2000; 53(4):340–346; discussion 346–348. 41. Harrop JS, et al. Cervicothoracic radiculopathy treated using posterior cervical foraminotomy/discectomy. J Neurosurg 2003; 98(2 Suppl):131–136.

12. Zdeblick TA, Ducker TB. The use of freeze-dried allograft bone for anterior cervical fusions. Spine 1991; 16(7):726–729.

42. Zdeblick TA, et al. Cervical stability after foraminotomy. A biomechanical in vitro analysis. J Bone Joint Surg [Am] 1992; 74(1):22–27.

13. Cauthen JC, Theis RP, Allen AT. Anterior cervical fusion: a comparison of cage, dowel and dowel-plate constructs. Spine J 2003; 3(2):106–117; discussion 117.

43. Raynor RB, Pugh J, Shapiro I. Cervical facetectomy and its effect on spine strength. J Neurosurg 1985; 63(2):278–282.

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Part 3: Specific Disorders 44. Adamson TE. Microendoscopic posterior cervical laminoforaminotomy for unilateral radiculopathy: results of a new technique in 100 cases. J Neurosurg 2001; 95(1 Suppl):51–57. 45. Fessler RG, Khoo LT. Minimally invasive cervical microendoscopic foraminotomy: an initial clinical experience. Neurosurgery 2002; 51(5 Suppl):37–45.

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46. Tanaka N, et al. The anatomic relation among the nerve roots, intervertebral foramina, and intervertebral discs of the cervical spine. Spine 2000; 25(3):286–291. 47. Raynor RB. Anterior or posterior approach to the cervical spine: an anatomical and radiographic evaluation and comparison. Neurosurgery 1983; 12(1):7–13.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ ii: Cervical Axial Pain

CHAPTER

An Algorithmic Methodology for Cervical Axial Neck Pain

62

David W. Chow and Curtis W. Slipman

INTRODUCTION Fluoroscopically guided cervical injection procedures are commonly used for the nonsurgical management of cervical axial neck pain that has been nonresponsive to a reasonable trial of physical therapy, nonsteroidal antiinflammatory drugs (NSAIDs), activity modification, time, and relative rest. Although recent studies investigating the utility of diagnostic and therapeutic cervical injections have provided useful information in the management of cervical axial neck pain, clinical pathways incorporating this information have not developed in such a manner that provides an accurate diagnosis allowing for specific treatment and minimizing unnecessary procedures. This chapter will provide an algorithmic paradigm for the clinician to systematically formulate a differential diagnosis and treatment plan. These diagnostic and therapeutic pathways have incorporated recent peer-reviewed literature investigating the utility of cervical injection procedures in the management of cervical spinal disorders such as cervical facet joint syndrome (CFJS) and cervical internal disc disruption syndrome (CIDD).

HISTORICAL ASPECTS Fluoroscopically guided cervical injections have been utilized in the clinical management of cervical axial neck pain for several decades. It is only over the past decade and a half that these techniques have been systematically employed for diagnostic and therapeutic purposes. Smith and Nichols1 first described cervical discography in 1957 as a diagnostic tool for the evaluation of cervical intervertebral disc degeneration. A year later, Cloward2 reported the indications for diagnostic cervical discography. In 1964, Holt3 suggested that discography did not have diagnostic value. In contrast, Simmons and Segil4 reported that cervical discography was a reliable diagnostic tool in the determination of a symptomatic cervical disc level in the setting of degenerative disc disease of the cervical spine. Bogduk and Marsland,5 in 1986, identified the value of local anesthetic blockade of the medial branch nerves to the cervical facet joints, implicating CFJS as a cause of cervicogenic headaches. In 1987, Whitecloud and Seago6 demonstrated the validity of cervical discography as a diagnostic tool. A year later, Bogduk and Marsland7 determined that cervical facet joints could cause neck and/or head pain. This study generated pain referral patterns that were constructed from cervical regions from which patients obtained symptom relief after local anesthetic blockade of the cervical facet joints. In 1990, Dwyer et al.8 described pain referral maps of the cervical facet joints in normal volunteers by distending the joint capsule with contrast injected under fluoroscopy. April et al.9 then assessed the accuracy of the pain referral maps. The location of symptomatic cervical facet joints in patients with cervicogenic neck pain were predicted from the pain referral maps and then assessed with confirmatory local anesthetic blockade of the cervical facet joint. In 1993, Barnsley et al. investigated the diagnostic value of comparative local anesthetic blockade of the cervical facet joints.10

They reported that false positives were present with single diagnostic cervical facet joint injections.11 Barnsley et al., in 1994, reported that intra-articular facet joint steroid injections were efficacious in less than 50% of patients for whiplash-induced cervical facet joint pain syndrome leading to chronic neck pain.12 Also in 1994, Dreyfuss et al.13 determined that the atlanto-occipital and atlantoaxial joints may be nociceptive structures. Subsequently, pain referral maps of the atlanto-occipital and atlantoaxial joints were constructed from this study of asymptomatic volunteers.14 In 1995, Lord et al.15 investigated the value of comparative local anesthetic cervical facet joint blocks in the diagnosis of cervical facet joint pain in relation to placebo-controlled cervical facet joint injections. Fluoroscopically guided placebo-controlled local anesthetic injections were utilized by Barnsley et al.16 and Lord et al.17 to investigate the prevalence of whiplash-induced chronic cervicogenic neck pain and headaches. Slipman et al. reported on the outcomes of intra-articular cervical facet joint steroid injections for traumatically induced C2–3 headache.18 In 1995, Saal19 showed favorable outcomes for nonoperative treatment including the use of cervical epidural space steroid injections for painful cervical disc herniations and radiculopathy. Schellhas et al.20 reported that magnetic resonance imaging (MRI) cannot reliably identify the source(s) of cervical discogenic pain and that significant cervical disc annular tears demonstrated by discography often escape MRI detection. Within that study, they also reported upon the distribution of pain referral patterns for the C3–4 to C6–7 disc levels. That same year, Lord et al.17 demonstrated the efficacy of percutaneous radiofrequency neurotomy for patients with neck pain due to CFJS in a double-blinded, placebo-controlled trial. In 1999, McDonald et al.21 described the long-term effectiveness of cervical radiofrequency neurotomy for chronic neck pain and demonstrated that repeat radiofrequency ablation will reinstate the same degree of pain relief if the pain returned after a successful initial procedure. In 2000, Grubb and Kelly22 reported that cervical discograms frequently identified abnormal concordantly painful fissured discs at multiple disc levels in more than 50% of the 173 patients examined, suggesting that treatment decisions based on fewer discs injected during discography should be reconsidered until more disc levels have been assessed. In 2003, Slipman et al.23 reported upon the various cervical discogenic pain referral maps provoked during cervical discography in the first large multicenter prospective study investigating discogenic pain referral patterns and laterality of pain referral.

ALGORITHMIC METHODOLOGY A working knowledge of the anatomic interrelationships in the cervical spine is important in understanding the pathomechanism of cervical spinal disorders that cause cervical axial neck pain. Similarly, understanding the epidemiology, etiology, and pathophysiology of these disorders is helpful in organizing a differential diagnosis, initiating a logical systematic treatment plan, and ultimately formulating diagnostic and 679

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Table 62.1: Historical categorization Axial pain

Limb pain

Cervical sprain / strain

Musculoskeletal

Disc herniation

Radiculopathy

Fibromyalgia

– Disc herniation

Myofascial pain syndrome

– Stenosis

Whiplash syndrome

therapeutic treatment algorithms. This chapter will focus on cervical axial neck pain that has been nonresponsive to a reasonable trial of physical therapy, NSAIDs, acute pain medications, activity modifications, time, and relative rest. Musculoskeletal entities such as muscular strains will not be discussed since these entities typically resolve within 2 months of appropriate nonoperative treatments (Table 62.1).24–26

Clinical assessment Traumatic versus atraumatic In formulating an accurate differential diagnosis, obtaining a comprehensive history is the initial step. A detailed history is critical because it will provide the clinical basis of any diagnostic and treatment paradigm and as well as offer prognostic implications. For instance, a history of trauma provides the possibility that more than one structure sustained a traumatic injury. It has been well documented that whiplash injuries can injure a cervical facet joint, intervertebral disc, cervical nerve root, or a combination of these structures.16,27–34 A common cervical intervertebral disc injury that occurs as a result of whiplash is a transverse tear near the anterior vertebral rim.29,30 This ‘rim lesion’ is caused by distraction and shearing at the annular–endplate interface by sudden cervical extension.35–37 Rim lesions have been shown to predispose the disc to premature degeneration.30,31,38–40 Other injuries that can occur may include disc contusion or herniation, facet hemarthroses, cervical nerve root shearing, or fractures of the articular processes.16,27–33,36,41–47 Organizing the history as traumatic versus atraumatic is useful when attempting to formulate a differential diagnosis. It is reasonable to assume that traumatically induced cervical axial neck pain may arise from more than one structure. For nontraumatic cases, the law of parsimony is applied and it is assumed that there is only one structure responsible for the painful symptoms.

Segmentation of pain The next step in formulating a differential diagnosis within the framework of a diagnostic algorithm is segmenting the distribution of pain into quadrants: head, neck, upper back or periscapular, upper arm, and forearm. The relative distribution of pain in these regions assists in determining whether the pain is axial or radicular. Cervical axial pain includes the neck, head, and/or interscapular regions. Radicular pain refers to upper limb symptoms that are greater or more pronounced than axial complaints. Understanding the various pain referral patterns or dynatomes of the cervical nerve roots will assist in properly interpreting the segmented distribution of painful symptoms. For instance, upper back or periscapular pain that is more intense than neck pain in the patient without arm symptoms can be of radicular etiology despite its relative axial location. A more detailed discussion regarding the historical and examination features of cervical radicular pain and how to differentiate that from cervical axial pain is contained in Chapter 57. It is also generally considered that cervical axial neck pain that is greater in intensity than extremity pain is typically caused 680

by cervical facet joint syndrome or cervical internal disc disruption. However, ipsilateral lower cervical neck pain may be caused by injury to the fourth or fifth cervical nerve root.48 In these more challenging clinical scenarios, physical examination findings can provide additional information to further rank order the differential diagnosis. For example, physical examination findings of increased focal suboccipital pain during 45 degrees of cervical flexion and sequential rotation would suggest pain emanating from the C1–2 joint.13,14

Upper versus lower cervical axial neck pain Formulating a probability analysis within each grouping, axial or radicular, is the next critical step in successfully implementing treatment algorithms to arrive at an accurate diagnosis. For instance, a history of unilateral occipital headaches more intense than neck pain following a traumatic injury is more suggestive of upper cervical facet joint syndrome than cervical internal disc disruption.16,33 Upper cervical neck pain may be due to cervical internal disc disruption or from an upper cervical facet joint (C2–3, C3–4, C1–2).33 In this scenario, a history of trauma, unilateral symptoms, or the presence of occipital headaches tends to favor the presence of cervical facet joint syndrome involving an upper cervical facet joint. Similarly, an atraumatic history, bilateral symptoms, or the absence of occipital headaches, would more likely suggest cervical internal disc disruption syndrome as the cause of upper cervical axial neck pain. Lower cervical neck pain may be caused by a lower cervical facet joint, intervertebral disc, or an injury to the fourth or fifth cervical nerve root.16,27–33 One may suspect cervical facet joint syndrome more than internal disc disruption if there is focal tenderness following palpation of an isolated cervical facet joint or if the patient is able to point to the painful area corresponding to the distribution of pain reported for a particular facet joint.49 However, one cannot make the diagnosis of CFJS just on the presence of focal tenderness of the cervical paraspinal muscles in the region of a cervical facet joint. In traumatic injuries such as whiplash, cervical facet joint syndrome maybe more common than an injury to an upper cervical nerve root;33,50 however, this may be a consequence of the paucity of epidemiologic data for whiplash-induced cervical radicular pain.

Periscapular and interscapular pain If symptoms are primarily in the upper back, interscapular, or periscapular region then the differential diagnosis may include CFJS, CIDD, cervical radicular pain and, less likely, thoracic internal disc disruption. If the interscapular or periscapular pain is reproduced by a provocative maneuver such as the Spurling’s test, then nerve root involvement rather than facet joint syndrome or internal disc disruption syndrome is of higher probability. CFJS rarely refers pain below the elbow;8,9 therefore, forearm or hand symptoms would suggest nerve root or disc injury. The differentiating facts would include the relative degree of neck pain versus arm pain and whether ipsilateral neural foramenal closure maneuvers trigger upper extremity complaints. For patients with upper limb greater than cervical axial neck pain, positive provocative maneuvers for radicular pain, such as the Spurling’s test, are suggestive of cervical nerve root involvement.51,52 Information from a positive provocative maneuver is particularly helpful in the absence of a detectable myotomal deficit or reflex change in a patient with an uncharacteristic dermatomal distribution of upper limb pain. In a patient that has a positive nerve root tension maneuver in the setting of a negative Spurling’s maneuver, brachial plexus involvement should be considered. A nerve root tension maneuver is positive when upper limb pain is provoked with contralateral cervical rotation, and/or lateral bending, or forward flexion.53 Provocative

Section 3: Cervical Spine

maneuvers are an important part of the physical examination armamentarium and can provide useful information to help formulate an accurate differential diagnosis.

Laterality of symptoms The differential diagnosis is further organized depending upon whether the symptoms are unilateral or bilateral. Unilateral symptoms of occipital headaches, or neck, or upper back pain are more suggestive of cervical facet joint syndrome than internal disc disruption provided there is an exquisitely tender foci overlying a facet joint. In the absence of that complaint and finding on examination, then either the facet joint or the disc could be the culprit. Unilateral cervical axial neck pain (without periscapular symptoms) more intense than headaches could emanate from a cervical facet joint or an intervertebral disc. In our experience, bilateral cervical axial upper neck pain without headaches can be caused by CIDD rather than CFJS. Grubb and Kelly’s study22 supports our clinical observations as they reported bilateral cervical axial neck pain in 34–50% of cervical discs injected at each disc level with provocative diagnostic cervical discography. Additionally, data from a similar, but more detailed study by Slipman23 revealed that 30–62% of discs produced bilateral cervical axial neck pain during cervical discography. In contrast, the study by Dwyer et al.8 investigating the pain referral patterns of cervical facet joints in normal volunteers did not demonstrate any bilateral pain from unilateral facet joint distention. The follow-up study by Aprill et al.9 reported resolution of painful bilateral symptoms in three out of ten patients at C3–4, C6– 7, and C7–T1. Slipman and Chow’s study of cervical pain mapping also reported resolution of bilateral symptoms with local anesthetic blockade of the cervical facet joints.55 In general, bilateral symptoms of neck or upper back pain, headaches, or symmetric upper arm pain are no more suggestive of cervical internal disc disruption than unilateral symptoms of cervical facet syndrome (Table 62.2). Although the facet joint can trigger bilateral pain it is rarely considered equally intense on both sides. In contrast, cervical disc pain can elicit pain intensity that is perceived to be equal on each side. If there are complaints that are distributed sometimes on the right and at other instances on the left and the remaining episodes symmetric, this is likely discogenic unless there is a traumatic history. If trauma to the cervical spine led to the aforementioned symptoms then one would have to postulate that at least two structures were injured if the symptoms were not discogenic in origin. For that reason, our algorithm begins with addressing the disc unless, of course, there was a definitive description of focal facet pain corroborated during the examination. One potential morsel of historical data that could be helpful is getting a sense that the symptoms are located in the perfect midline. If the patient can reliably articulate

that such occurs, then the probability analyses should weigh heavily toward disc-generated pain. As previously alluded to, a similar description of pain over a facet joint with provoked pain to manual palpation would lend credence to the joint as the painful site. It is unusual for physical therapy to induce increased axial pain; however, this is a common complaint with facet joint-mediated pain. This seems to be particularly relevant when there are associated headaches. Almost invariably, intractable facet joint-mediated neck pain and headaches is dramatically intensified with cervical traction. When this occurrence is described, the authors invariable consider the facet joint as probable locus of pain.

Diagnostic testing Once a differential diagnosis has been formulated, treatment may then be instituted. The treatment plan will initially consist of general measures and in some circumstances specific interventions. However, when a patient fails a reasonable course of nonoperative treatment with medications and physical therapy, diagnostic testing is frequently needed prior to initiating additional treatment. Typically, the initial diagnostic tool is an imaging study. In patients with a history of a traumatic event such as a whiplash injury, cervical flexion and extension radiographs should be obtained. In nontraumatic cases, cervical spine radiographs are rarely required due to its minimal diagnostic yield. Accordingly, MRI is the initial imaging study of choice because of its high sensitivity to detect soft tissue pathology such as a focal disc protrusion or bony pathology such as neuroforaminal stenosis.56–60 While MRI has demonstrated high sensitivity, there are concerns about its clinical specificity. Several studies have reported that a significant percentage of individuals with focal disc protrusions or foraminal stenosis are asymptomatic.61–64 This issue of clinical specificity reinforces the importance of correlating each patient’s history and examination findings with the imaging study to formulate an accurate differential diagnosis and ultimately the correct clinical diagnosis. In patients with a traumatic history, MRI findings of degenerative disease of the CFJS and CIDD is common. Nontraumatic CFJS patients will typically also have MRI results that are not localizing. Patients with traumatic or nontraumatic CIDD may have MRI findings of a focal disc protrusion, annular disc tear, or a broad-based degenerative concentric annular disc bulge with loss of disc height and disc desiccation. These discogenic MRI findings may or may not be clinically symptomatic in patients whom the clinical suspicion of CIDD is high. Nevertheless, these MRI findings should not be ignored as they may be clinically symptomatic in a patient with CIDD and can offer an initial starting point in determining which disc level to treat if the patient is a candidate for a fluoroscopically guided cervical epidural steroid injection.

Cervical facet joint syndrome

Table 62.2: Current categorization Axial pain

Limb pain

Cervical sprain / strain

Musculoskeletal

Annular disc tear

Radiculopathy

CIDD

– Disc protrusion

CFJS

– Spondylosis

Deconditioning / overuse

Radiculitis

Traumatic v. atraumatic

Neurogenic Somatic referral Traumatic v. atraumatic

Patients with cervical axial neck pain and a high clinical suspicion of CFJS, who have failed a reasonable trial of conservative treatment, are candidates for a fluoroscopically guided diagnostic facet joint injection. When upper cervical facet joint syndrome from trauma or whiplash is suspected, diagnostic facet joint blocks are performed sequentially at C2–3, C3–4, and C1–2, until the offending site is identified. This sequence is based from clinical experience and epidemiologic studies.16,33 In particular, Lord demonstrated that 50% of all patients with chronic whiplash-induced cervicogenic headaches experience symptoms of cervical facet joint arthralgia/synovitis emanating from the C2-3 joint. Whiplashinduced lower neck pain emanating from a facet joint was most common at C5–6.16,33 681

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Diagnostic and therapeutic injections

Radiofrequency ablation

Fluoroscopically guided diagnostic facet joint blocks are performed in sequential fashion once the diagnostic algorithm has been constructed. If a diagnostic facet joint block is positive, then a fluoroscopically guided therapeutic intra-articular steroid facet joint block is offered. Barnsley et al.12 reported on the ineffectiveness of intraarticular facet joint steroid injections for the treatment of chronic cervical facet joint pain in patients who were involved in a motor vehicle accident. However, this study used a singular outcome measure and only evaluated the efficacy of one intra-articular steroid injection per joint without restricting provocative physical activities or physical therapy. Despite the flaws in the Barnsley et al. study,12 the use of intra-articular facet joint steroid blocks have been discouraged for the treatment of chronic pain due to CFJS. Unfortunately, this is in part due to the paucity of well-designed studies investigating the efficacy of intra-articular steroid injections for chronic pain due to CFJS. In our experience, fluoroscopically guided therapeutic intra-articular steroid injections have been effective in the treatment of CFJS. Slipman et al.18 demonstrated good to excellent results in 61% of patients treated with intra-articular facet joint steroid injections who experienced daily, unremitting headaches emanating from the C2–3 facet joint following a whiplash injury. This study used multiple outcome measures including work status, change in VAS, and reduction in analgesic usage with an average follow-up period of 19 months.

If the patient failed to improve with therapeutic intra-articular steroid facet joint blocks because of a true nonresponse, then radiofrequency ablation or dorsal rhizotomy is considered. Lord et al.17 reported on the efficacy of radiofrequency rhizotomy in patients diagnosed with CFJS confirmed with double-blind, placebo-controlled local anesthetic blockade. McDonald et al.21 then demonstrated that radiofrequency rhizotomy provided statistically and clinically significant long-term pain abatement, and that repeat ablation can reinstate the same degree of pain reduction if the symptoms returned after a successful initial procedure.

Placebo-controlled blocks If a patient experiences greater than 90% relief of symptoms after a therapeutic intra-articular facet injection that lasts until the date of a planned second, third, or even fourth subsequent injection, then the intervention is cancelled. Such relief typically heralds the onset of continued symptom relief provided the patient adheres to specific activity prohibitions and patiently returns to a normal activity level. As previously alluded to, this is conducted under direct physician supervision and must be individualized. Overall, it can take 6–12 months after the final injection before pre-morbid activities and habits can be resumed. If a patient fails to obtain satisfactory relief from a therapeutic intra-articular facet joint block following an initial positive diagnostic facet joint or medial branch block, the major question that must be addressed is whether the patient failed because of an incorrect diagnosis or if he/she is a true nonresponder. The former issue is raised because single diagnostic facet joint blocks have a 27% falsepositive rate.11 Consequently, it is possible that the initial diagnostic block was a false-positive response. In these instances, single-blind, placebo-controlled diagnostic facet joint blocks are recommended. These are performed with 2.0% lidocaine intra-articularly and with saline extra-articularly, though others advocate a different paradigm. Some interventional spine physicians prefer to conduct medial branch blocks. This can be performed as a placebo-controlled trial or using a comparative control paradigm. In the latter instance, two different local anesthetics of varying durations are used. Single-blind, placebocontrolled diagnostic facet joint blocks are considered positive if the lidocaine injection relieved the pain and the saline injection did not. If the single-blind, placebo-controlled diagnostic injections are negative, then the next suspected structure in the diagnostic algorithm should be addressed. If the single-blind, placebo-controlled diagnostic blocks are positive, then the patient is a true nonresponder and is a candidate for radiofrequency ablation of the medial branches of the dorsal rami supplying the involved facet joint.

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Cervical internal disc disruption syndrome For those patients suspected of experiencing symptoms of cervical internal disc disruption syndrome, a fluoroscopically guided transforaminal steroid injection at the suspected symptomatic disc level is recommended. If the MRI reveals multilevel disc disease or does not demonstrate an obvious symptomatic disc level, a fluoroscopically guided C7 transforaminal steroid injection on the symptomatic ipsilateral side for patients with lower neck pain is suggested in order to bathe the posterior surface of the lower intervertebral discs, posterior longitudinal ligament, and other nearby innervated structures. This procedure is performed at C4 or C5 for patients with upper neck pain with or without headaches. If a steroid effect is not realized after two injections, then the patient should undergo cervical discogram to determine if there is internal disc disruption. If the discogram reveals one or two successive disc levels with posterior annular fissures and concordant pain responses, then the patient may be a candidate for surgical fusion. If the discs do not demonstrate a posterior annular tear with a concordant pain response, then the discogram is negative and internal disc disruption is unlikely. In this scenario, the next suspected structure in the diagnostic algorithm should be tested. If the discogram reveals three or more positive disc levels, two positive disc levels with an intervening normal disc, or if any concordantly painful discs are lobular, then a chronic pain modulation program is suggested. If a diagnosis has not been established at the end of the diagnostic algorithm, then the patient will need to be re-evaluated to determine if the correct diagnostic algorithm was utilized or if a diagnosis was missed.

SUMMARY In the past decade and a half, there have been numerous research studies investigating the utility of cervical injection procedures in the treatment of cervical spinal disorders. The majority of these studies have investigated disorders involving one of three primary cervical structures; zygapophyseal joint, intervertebral disc, and nerve root. An algorithmic paradigm is offered that incorporates the use of fluoroscopically guided cervical spinal injections in the treatment of painful cervical spinal disorders that will refine the selection of injection procedures performed. This algorithmic methodology achieves that end by providing the clinician with a mechanism to systematically formulate a differential diagnosis and treatment plan, and minimizing unnecessary interventional procedures. This process necessitates continuous revision as new information is published, thereby implying plasticity to these algorithms.65 Nevertheless, they have been employed successfully at several institutions and clinical practices.

Section 3: Cervical Spine

References 1. Smith GW, Nichols P. The technique of cervical discography. Radiology 1957; 68:718–720. 2. Cloward RB. Cervical discography: technique, indications and use in diagnosis of ruptured cervical disc. Am J Roentgenol 1958; 79:563–574. 3. Holt EP. Fallacy of cervical discography. JAMA 1964; 188:799–801. 4. Simmons EH, Segil CM. An evaluation of discography and the localization of symptomatic levels in discogenic disease of the spine. Clin Orthop 1975; 108:57–68. 5. Bogduk N, Marsland A. On the concept of third occipital headache. J Neurol Neurosurg Psychiatry 1986; 49:775–780. 6. Whitecloud TS, Seago RA. Cervical discogenic syndrome: results of operative intervention in patients with positive discography. Spine 1987; 12:313–316. 7. Bogduk N, Marsland A. The cervical zygapophysial joints as a source of neck pain. Spine 1988; 13:610–617.

30. Taylor JR, Twomey LT. Acute injuries to cervical joints. An autopsy study of neck sprain. Spine 1993; 1115–1122. 31. Algers G, Pettersson K, Hildingsson C, et al. Surgery for chronic symptoms after whiplash injury. Follow-up of 20 cases. Acta Orthop Scand 1993; 64(6):654–656. 32. Davis SJ, Teresi LM, Bradley WG Jr, et al. Cervical spine hyperextension injuries: MR findings. Radiology 1991; 180(1):245–251. 33. Lord SM, Barnsley L, Wallis BJ, et al. Chronic cervical zygapophysial joint pain after whiplash: a placebo-controlled prevalence study. Spine 1996; 21(15):1737–1745. 34. Spitzer WO, Skovronmm ML, Salmim LR, et al. Scientific monograph of the Quebec Taskforce on Whiplash Associated Disorders: redefining ‘whiplash’ and its management. Spine 1995; 20,10S–68S. 35. Macnab I. Acceleration extension injuries of the cervical spine. In: Rothman R, ed. The spine, 2nd edn. Philadelphia: WB Saunders; 1982:647–660. 36. Macnab I. Acceleration injuries of the cervical spine. J Bone Joint Surg [Am] 1964; 46:1797–1799.

8. Dwyer A, Aprill C, Bogduk N. Cervical zygapophysial joint pain patterns I: a study in normal volunteers. Spine 1990; 15:453–457.

37. Crowell RR, et al. Mechanisms of injury in the cervical spine: experimental evidence and biochemical modeling. In: The cervical spine, the Cervical Spine Research Society, 2nd edn. Philadelphia: JB Lippincott; 1989:70–90.

9. Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal joint pain patterns II: a clinical evaluation. Spine 1990; 15:458–461.

38. Vernon-Roberts B, Pirie CJ. Degenerative changes in the intervertebral discs of the lumbar spine and their sequelae. Rheumatol Rehab 1977; 16:13–21.

10. Barnsley L, Lord SM, Bogduk N. Comparative local anesthetic blocks in the diagnosis of cervical zygapophysial joint pain. Pain 1993; 55:99–106.

39. Davis SJ, Teresi LM, et al. Cervical spine hyperextension injuries: MR findings. Radiology 1991; 180:245–251.

11. Barnsley L, Lord SM, Wallis BJ, et al. False positive rates of cervical zygapophysial joint blocks. Clin J Pain 1993: 9124–9130.

40. Osti OL, Vernon-Roberts B, Fraser RD. Annulus tears and intervertebral disc degeneration: an experimental study using an animal model. Spine 1990; 15:762–767.

12. Barnsley L, Lord SM, Wallis BJ, et al. Lack of effect of intra-articular corticosteroids for chronic cervical zygapophysial joint pain. N Engl J Med 1994; 330:1047–1050.

41. Gay JR, Abbott KH. Common whiplash injuries to the neck. JAMA 1953; 152: 1698–1704.

13. Dreyfuss P, Michaelsen M, Fletcher D. Atlanto-occipital and lateral atlanto-axial joint pain patterns. Spine 1994; 19(10):1125–1131.

42. Seletz E. Whiplash injuries. Neurophysiological basis for pain and methods used for rehabilitation. JAMA 1958; 168:1750–1755.

14. Dreyfuss P, Rogers J, Dreyer S, et al. Atlanto-occipital joint pain. A report of three cases and description of an intra-articular joint block technique. Reg Anesth 1994; 19(5):344–351.

43. Jonsson H, Cesarini K, et al. Findings and outcome in whiplash-type neck distortions. Spine 1994; 19:2733–2743.

15. Lord SM, Barnsley L, Bogduk N. The utility of comparative local anesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophysial joint pain. Clin J Pain 1995; 11:208–213. 16. Barnsley L, Lord SM, Wallis BJ, et al. Chronic cervical zygapophysial joint pain after whiplash: a prospective prevalence study. Spine 1995; 20:20–26. 17. Lord SM, Barnsley L, Wallis B, et al. Percutaneous radiofrequency neurotomy for chronic cervical zygapophyseal joint pain. N Engl J Med 1996; 335:1721–1726. 18. Slipman CW, Lipetz JS, Plastaras CT, et al. Outcomes of therapeutic zygapophyseal joint injections for headaches emanating from the C2–C3 joint. Arch Phys Med Rehabil 2001; 81(8):1119–1122. 19. Saal JS. The role of inflammation in lumbar pain. Spine 1995; 20(16):1821– 1827. 20. Schellas KP, Smith MD, Cooper RG, et al. Cervical discogenic pain: prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers. Spine 1996; 21(3):300–312. 21. McDonald GJ, Lord SM, Bogduk N. Long-term follow-up of patients treated with cervical radiofrequency neurotomy for chronic neck pain. Neurosurgery 1999; 45(1):61–67. 22. Grubb SA, Kelly CK. Cervical discography: clinical implications from 12 years of experience. Spine 2000; 25(11):1382–1389. 23. Slipman CW, Patel RJ, Chow DW, et al. Cervical disc pain: provocative pain maps, (Manuscript submitted). 24. Maimaris C, Barnes MR, Allen MJ. Whiplash injuries of the neck: a retrospective study. Injury 1988; 19:393–396. 25. McDowell GS. Acute cervical sprain. In: Snider, RK, ed. Essentials of musculoskeletal care. Rosemont: American Academy of Orthopaedic Surgeons; 1997:509–511. 26. Cole AJ, et al. Functional rehabilitation of cervical spine athletic injuries. In: Kibler WB, Herring, SA, Press, JM, eds. Functional rehabilitation of sports and musculoskeletal injuries. Chicago: Aspen; 1998:127–148. 27. Alker GJ Jr, Young SO, Leslie EV, et al. Postmortem radiology of head and neck injuries in fatal traffic accidents. Radiology 1975; 114:611–617. 28. Rasuschning W, McAfee PC, et al. Pathoanatomical and surgical findings in cervical spinal injuries. J Spinal Disord 1989; 2(4):213–222. 29. Taylor JR, Finch P. Acute injury of the neck: anatomical and pathological basis of pain. Ann. Acad Med Singapore 1993; 22(20):187–192.

44. Cain CM, et al. Cervical spine injuries in road traffic crashes in south Australia. Aust NZ J Surg 1989; 59:15–19. 45. Yoo JU, et al. Effects of cervical spine motion on neuroforaminal dimension of the human cervical spine. Spine 1992; 17:1131–1136. 46. Lu J, et al. Cervical intervertebral disc space narrowing and size of intervertebral foramina. Clin Orthop Relat Res 2000; 370:259–264. 47. Farmer JC, Wisneski RJ. Cervical spine nerve root compression. Spine 1994; 19: 1850–1855. 48. Slipman CW, Plastaras CT, Palmitier RS, et al. Symptom provocation of fluoroscopically guided cervical nerve root stimulation: Are dynatomal maps identical to dermatomal maps? Spine 1998; 23(20):2235–2242. 49. Jull G, Bogduk NK, Marsland A. The accuracy of manual diagnosis for cervical zyagpophysial joint pain syndromes. Med J Aust 1988; 148:233–236. 50. Slipman CW, Plastaras CT, Huston CW, et al. Outcomes of nerve root blocks for whiplash induced cervical radiculitis. Presented at North American Spine Society, 11th Annual Meeting, 1996. 51. Ellenberg MR, Honet JC, Treanor WJ. Cervical radiculopathy. Arch Phys Med Rehab 1994; 75(3):342–352. 52. Levitz CL, Reilly PJ, Torg JS. The pathomechanics of chronic, recurrent cervical nerve root neurapraxia: the chronic burner syndrome. Am J Sports Med 1997; 25(1):73–76. 53. Uchihara T, Furukawa T, Tsukagoshi H. Compression of brachial plexus as a diagnostic test of cervical cord lesion. Spine 1994; 19(19):2170–2173. 54. Elvey RL. Brachial plexus tension tests and the pathoanatomical origin of arm pain. In: Idczak RM, ed. Biomechanical aspects of manipulative therapy. Carlton, Australia: Lincoln Institute of Health Sciences; 1981. 55. Slipman CW, Chow DW, et al. Lower cervical zygapophyseal joint pain maps. (Manuscript in preparation) 56. Modic M, Masaryk TJ, Mulopulos G, et al. Cervical radiculopathy: prospective evaluation with surface coil MR imaging, CT with metrizamide, and metrizamide myelography. Radiology 1986; 161:753–759. 57. Hedberg MC, Drayer BP, Flom RA, et al. Gradient echo (GRASS) MR imaging in cervical radiculopathy. Am J Roentgenol 1988; 150:683–689. 58. Tertti M, Paajanen H, Laato M, et al. Disc degeneration in magnetic resonance imaging: a comparative biochemical, histologic, and radiologic study in cadaver spines. Spine 1991; 16:629–634.

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Part 3: Specific Disorders 59. Brown BM, Schwartz RH, Frank E, et al. Preoperative evaluation of cervical radiculopathy and myelopathy by surface-coil MR imaging. Am J Roentgenol 1988; 151:1205–1212. 60. Larsson EM, Holtas S, Cronqvist S, et al. Comparison of myelography, CT myelography and magnetic resonance imaging in cervical spondylosis and disc herniation: pre- and postoperative findings. Acta Radiol 1989; 30:233–239. 61. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic resonance scans of the cervical spine in asymptomatic subjects: a prospective investigation. J Bone Joint Surg [Am] 1990; 72:1178–1184.

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62. McRae DL. Asymptomatic intervertebral disc protrusions. Acta Radiol 1956; 46:9–27. 63. Teresi LM, Lufkin RB, Reicher MA, et al. Asymptomatic degenerative disk disease and spondylosis of the cervical spine: MR imaging. Radiology 1987; 164:83–88. 64. Matsumoto M, Fujimura Y, Suzuki N, et al. MRI of cervical intervertebral discs in asymptomatic subjects. J Bone Joint Surg [Br] 1988; 80(1):19–24. 65. Slipman CW, Chow DW, et al. An evidenced-based algorithmic approach to cervical spinal disorders. Crit Rev Phys Rehab Med 2001; 13(4):283–299.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ ii: Cervical Axial Pain

CHAPTER

Rehabilitation Methods

63

Anthony R. Cucuzzella and Julie Marley

INTRODUCTION About two-thirds of all people will experience neck pain at some point in their lives.1 Diverse rehabilitation methods and techniques are employed by various healthcare clinicians to treat individuals experiencing neck pain. Most of the treatments applied lack substantial scientific support for their application, with very limited information available from randomized, controlled trials into the effectiveness of individual treatment modalities. As substantial healthcare resources are utilized for this condition, more high-quality studies are needed to determine which of these interventions are effective and provide long-term pain reduction and improvement in function. Rehabilitation for neck pain primarily encompasses exercise, manual therapy, educational strategies, and physical modalities. The purpose of this chapter is to review these treatments, purported methods of action, and review evidence for and against their use. Acute nontraumatic, acute traumatic, and chronic neck pain will be discussed separately, as inherent differences in each of these subcategories may necessitate variations in management strategy. Neck pain may resolve within days or weeks but often recurs and can become chronic.1 The true natural history, or the frequency and timing of its recovery without treatment, is unknown. In one study, 90% of patients with mild neck pain reported improvement within 30 days, while 76% of those with moderate pain reported improvement at 90 days, independent of treatment.2 Although acute episodes often improve, spinal pain is frequently recurrent, with 43% in one survey reporting 11 or more episodes over a year.3 The frequency with which neck pain becomes chronic and unrelenting is thought to be about 10% and causes severe disability in 5%.1 There is very limited evidence regarding prognostic factors.4 Whiplash injuries are more likely to cause continuing symptoms, with up to 40% reporting continued symptoms 15 years after the injury.1 Primary aims of rehabilitation of acute neck pain include assisting in recovery from the episode without creating dependency, maintaining activities of daily living, reducing absenteeism from work, and preventing development of long-term symptoms. Due to the recurrent nature of neck pain, prevention of future episodes should also be a main goal of intervention. Once symptoms become chronic, treatment may still focus initially on pain reduction, but will quickly move to recovery of strength and function as symptoms allow. As there is little scientific evidence supporting the use of any of the current physical modalities and ample evidence that the application of movement provides the best stimulus for repair, this chapter focuses on delineating exercise and manual therapy approaches for the interventional spine physician. Exercise and maintenance of normal activity have support in systematic reviews,1,5–8 while most conclude that rest and passive therapy can have a negative effect. There are numerous concepts of utilizing exercise and manual therapy with some overlap in reasoning and techniques of application. The authors

will highlight features of commonly used approaches that have some support for their efficacy. Additionally, the authors present algorithms for clinical decisionmaking in rehabilitation of acute nontraumatic, acute traumatic, and chronic neck. Although no specific approach has been proven to be most effective, these algorithms are in line with current evidencebased guidelines. The authors emphasize active over passive intervention whenever possible, decision-making based on an understanding of chemical and mechanical pain, and specific exercise based on a thorough evaluation of a patient’s mechanical presentation.

SOURCES OF NECK PAIN In the clinical practice of treating acute neck pain, it is difficult to base treatment on a pathoanatomic model. The source of pain could be discogenic, zygapophyseal, ligamentous, myofascial, or a combination. Radiologic imaging cannot conclusively determine the pain generator. Neck pain correlates poorly with spondylosis as it is equally present in those with and without neck pain. Furthermore, many patients with neck pain show no signs of spondylosis.9,10 Magnetic resonance imaging cannot reliably identify discogenic pain. Schellhas found normal-appearing discs on magnetic resonance imaging (MRI) proved to have painful annular tears with discography.11 Additionally, injuries to the zygapophyseal joints frequently are undetectable with X-ray or MRI.9 Many diagnoses later confirmed with diagnostic injections exhibit similar initial symptomatology, with overlap between zygapophseal, discogenic, and myofascial pain patterns.12,13 Just as radiology does not always conclusively provide a diagnosis, neither does a clinical examination.12 Often, a structural source is suspected based on particular pain behaviors and clinical presentation, but no clinical tests have conclusively been shown to prove the structural source of the pain. Tender points or trigger points are neither reliable nor a valid sign of the cause of neck pain.12 Clinicians often speculate that patients who present with a large obstruction to movement in one direction that lessens with repetition of that movement, as well as centralization of pain with repeated movements, have pain of discogenic origin. Likewise, studies have shown that abnormal quality of movement, abnormal end feel, and pain reproduction upon examining the passive accessory movements of the joint are predictive of zygapophyseal joint pain.14 Speculation and hypotheses about pain sources should not be interpreted as dogmatic certainties. In the case of chronic symptoms, further diagnostic information may be available from diagnostic injections or cervical discography. Despite the potential for these procedures to assist in diagnosis, it should be kept in mind that both a symptomatic disc and a symptomatic zygapophyseal joint have been identified in a high percentage (41%) of chronic neck pain patients.9 Furthermore, Bogduk et al. also reports a potentially high false-positive rate with provocation discography.12 685

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Another complicating factor in diagnosing an anatomical pain generator is that due to alterations that occur in the central nervous system with chronic pain, there may be less of a direct relationship between the pathology and the resultant symptoms. If pain persists beyond the normal healing time, persistent nociceptive input from the peripheral nervous system may cause changes in the central nervous system, ultimately reducing thresholds for pain and causing increased responses to afferent input. Generalized muscle hyperalgesia has been shown to occur in chronic whiplash syndrome, confirming this central hyperexcitability.15,16 As a result of the altered nervous system, nociceptive signals can be initiated, producing a ‘phantom’ pain in an area that previously had tissue damage.9 Changes in the muscular control system have been shown to occur, which may be a contributing factor in chronic neck pain. Irrespective of the initial tissue injury, increased muscle fatigability, altered muscle activation patterns, and decreased neuromuscular efficiency have all been shown to occur.15 Rehabilitation may need to address these multiple physiologic changes. Some, although certainly not all, patients with chronic pain become distressed, inactive, and deconditioned. Their condition may cause them to suffer economic and social deprivations. In patients with persistent symptoms, it is important to recognize the possibility that these psychosocial factors may complicate the rehabilitation process. Despite these numerous difficulties in diagnosing the anatomic ‘pain generator,’ clinicians often can still provide effective treatments based on a thorough evaluation of the patient’s presentation. This necessitates a clear understanding of the process of inflammation and subsequent repair, as well as an ability to differentiate mechanical and chemical activation of nociceptors. This allows the application of treatment in a structured fashion directed at the type of pain, rather than just providing symptomatic treatment in an ad hoc fashion. Regarding diagnosis, physicians and researchers continue to make progress with the availability of more-sophisticated imaging techniques. Studies are accumulating that compare clinical evaluation methods to diagnostic injections and discography, which add valuable evidence helpful in improving one’s ability to determine the pain generator.

The McKenzie method of mechanical diagnosis and therapy One commonly applied method of determining what type of exercise to provide is called Mechanical Diagnosis and Therapy, developed by Robin McKenzie. McKenzie developed an assessment tool that utilizes repetitive motion in cervical flexion, extension, sidebending, and rotation.21 The symptomatic and mechanical response to these motions gives the clinician a framework to determine how to most effectively apply movement or exercise. Many times, a movement is found during assessment that causes the pain to reduce in intensity, or other times to ‘centralize’ and then subsequently to resolve. Centralization, first observed by McKenzie, describes a ‘situation in which pain arising from the spine and felt laterally from the midline or distally is reduced and transferred to a more central or near midline position when certain movements are performed.’22 This process occurs in those with arm pain as well as in those with axial pain only (Fig. 63.1). Pain that is referred into the scapular and upper trapezius region may localize to the midline of the cervical spine. Ultimately, the midline pain is also eliminated with continued performance of the centralizing movement. In a sample of 86 neck pain patients, Donelson et al.23 found centralization occurred in 45.3% of patients. Sixty-seven percent centralized with extension tests while 33% centralized with flexion.

REHABILITATION INTERVENTIONS Exercise for acute nontraumatic neck pain Exercise interventions are deemed essential for the effective management of patients with neck pain and are commonly used by clinicians in the treatment of acute nontraumatic neck pain. Regardless of the involved musculoskeletal tissue, the beneficial effects of early motion are well supported in the literature. Early motion results in strengthening tendons and ligaments, restoring full range of motion, preventing adhesion formation, improving collagen alignment, and preserving articular cartilage.17,18 The optimal function of musculoskeletal structures is restored and maintained by activity. Exercise involves active participation of the patient and has been shown to be superior to passive treatments.1 Active participation gives the patient a sense of control over his or her symptoms and helps lessen the fear of movement. Those who fear movement and re-injury often avoid activity, thus creating disability and depression.19 According to Vlaeyen,20 those who confront their pain and follow a progressive return to normal activity are more likely to make a full recovery. Active range of motion, stretching of scapulothoracic and cervical spine musculature, strengthening, motor control, proprioceptive exercises, and overall aerobic conditioning are all used currently to treat cervical pain. Due to the paucity of well-conducted studies, there has been a lack of consensus on whether specific exercises are needed, or whether general advice to ‘stay active’ is just as effective. Some exercise approaches have mounting support for their efficacy and will be outlined below. 686

Fig. 63.1 Drawing of centralization.

Section 3: Cervical Spine

The examiners in this trial only assessed flexion and extension. As centralization also may occur with lateral movements, including these in the assessment may have increased the centralization rate. Centralization most commonly occurs in patients with a significant obstruction to one movement. As the pain centralizes, the obstruction to movement in that direction progressively becomes less, creating a symptom and mechanical response that occur together. McKenzie theorizes that mechanical displacement or internal derangement is lessening as centralization is occurring.21 Centralization may occur immediately during the first assessment or may occur more gradually over a few days of repetitive motion applied in one direction. This rapid change in the patient’s condition is inconsistent with the slower recovery more often observed with natural history. Werneke24 assessed 289 acute cervical and lumbar patients for the occurrence of centralization. Thirty percent centralized in one session, while another 46% were classified into a ‘partial reduction’ group. This group had a slower movement of their pain toward the midline, occurring in anywhere from 2 to 7 sessions. When a direction of movement is found that causes the pain to centralize or to be abolished, the patient is taught to perform frequent exercises in the direction that created the improvement. Many patients can centralize their pain with sitting extension, while other patients need unloaded supine extension. Those with unilateral or asymmetrical pain may require lateral excercises initially and progress to extension once the pain is central. A smaller number rapidly improve with flexion. Whatever direction of movement creates rapid improvement or centralizes the pain is commonly termed the mechanically determined directional preference. The exercise is performed until the pain remains abolished and it becomes apparent that the condition is stable enough to be moved in other directions. When one direction of movement causes centralization to occur, the opposite direction of movement often causes a worsening of the pain; hence, patients are taught to avoid these movements until the process of reduction is complete. If centralization and abolition of the pain occurs rapidly, it makes the use of any other type of treatment for the pain unnecessary, as the patient has learned to eliminate the symptoms independently. Such favorable findings should clearly guide the patient’s treatment by instructing the patient to continue to utilize the exercise that centralized or eliminated the symptoms. For instance, if a patient can eliminate the symptoms with lower cervical extension (Fig. 63.2) (i.e. retraction followed by extension), the patient is instructed to perform this exercise hourly and maintain very erect posture in between the performance of the exercise. An erect posture is very important, as a slouched sitting position will allow the lower cervical spine to fall into flexion, thus creating a return of symptoms. If at any point the pain begins to return, the patient independently performs the exercise that returns the pain to the midline and then abolishes it. Centralization has been associated with greater improvements in pain severity, improved functional disability scores, and better return to work rates.25,26 In Werneke’s study, the centralizers had fewer visits than noncentralizers (3.9±4 versus 8±0.4). Patients categorized into centralization or partial reduction had greater improvements in pain intensity and perceived function than noncentralizers. Conversely, failure of centralization has been associated with poor outcomes and is highly predictive that the patient will not make improvements with this type of exercise approach.25 Werneke found if centralization did not occur by the seventh visit, no improvement in pain intensity or perceived function occurred. The performance of repeated movements also helps distinguish chemical from mechanical pain. One movement in each direction often does not provide enough information to distinguish between mechanical and chemical pain. Chemicals (histamine, bradykinin, serotonin, etc.)

are released by cells in damaged tissue and cause pain production when their concentration is sufficient to irritate free nerve endings. Mechanical pain occurs when normal tissue is held for prolonged periods at end range (as in the case of poor posture), when displacement occurs within the motion segment causing increased tension on certain structures, or when stress is placed on tissue that has healed in a shortened position.22 If pain is primarily chemical in nature, the pain will be constant and repeated movements in all directions will aggravate the pain.27 In these cases, mechanical therapy will be unsuccessful until the chemical component is addressed. Mechanical pain, on the other hand, may be constant or intermittent and the repetitive movement assessment will reveal what increases and decreases mechanical deformation. The information gained about the behavior of the lesion allows the clinician to specifically tailor the treatment to addressing the chemical component or correcting the faulty mechanics.

Segmental stabilization exercises Another emerging method of applying exercise is based on the work of an Australian group of researchers, including Sterling, Falla, and Jull.27–29 They have published a series of research papers investigating motor activity in patients with neck pain. Prior to their work, a reduction in strength of the cervical flexors and extensors had been shown in those with neck pain.30–32 Vernon33 also found a progressive anteriorto-posterior muscle imbalance, with the cervical flexors becoming

A

B Fig. 63.2 Cervical retraction followed by extension. (Adapted from Figure 16.1 in McKenzie, 1990)21.

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relatively weaker as compared to the extensors. The Australian group’s contribution is their series of studies showing that both those with insidious-onset neck pain and those with whiplash-associated disorder develop deficits in motor activity and control. This manifests itself as altered patterns of cervical muscle recruitment and deficits in particular groups of muscles.29 Maintenance of the stability of the cervical lordosis requires action of the superficial larger muscles that cross more than one joint, such as the sternocleidomastoid and the scalenes, as well as action of the segmental vertebral muscles, the longus colli, and the longus capitus muscles. Winters and Peles34 showed, using a computer model, if only the superficial muscles were used to produce movement of the neck, regions of local segmental instability were produced. Muscle activity of the deep segmental muscles was required to stiffen or stabilize the segments, especially in functional midranges. Jull et al.35 and Falla et al.36 have found dysfunction in the neck flexor muscles in both traumatic and insidious-onset neck pain. They developed the craniocervical flexion test (CCF), or nodding of the head (Fig. 63.3), which is a task that in normals utilizes the deep cervical flexors (longus colli, longus capitus, rectus capitis anterior, and rectus capitis lateralis) and the superficial neck flexors (scalenes and sternocleidomastoid).37 During performance of the CCF test, a pressure unit was inserted behind the neck to monitor the flattening of the cervical lordosis that accompanies this motion. Subjects were asked to progressively increase the pressure in the unit by performing five repetitions of CCF, increasing the pressure by 2 mmHg with each repetition. The control group was able to do this quite accurately, while patients with neck pain demonstrated large pressure shortfalls. With electromyogram (EMG) recordings, they demonstrated that the diminished ability to perform this task accurately resulted from reduced activity in the deep cervical flexors. EMG recordings also found increased activation of the superficial neck flexors. This deficit in the deep neck flexors has been shown to occur within 1 month following whiplash injury, but the timing of its onset has yet to be determined in those with a spontaneous onset of neck pain. In the lumbar spine, Hides et al.38 found deficits in the deep segmental stabilizers (transverse abdominus and multifidus) occurred early within an episode of acute back pain. The Australian researchers advocate having patients perform exercises in an attempt to restore the action of the deep cervical flexors and minimize the action of the superficial flexors.28 Patients perform

craniocervical flexion exercises through their full range of motion in an attempt to retrain the segmental cervical muscles. They are given feedback to minimize the contraction of the superficial flexors. The theory is that performance of these exercises will minimize recurrent episodes of neck pain. This is based on research in the lumbar spine which demonstrated that deficits of the segmental stabilizers (the transverse abdominus and the multifidus) remained following an acute low back pain episode despite resolution of pain.39 In a follow-up study, patients were given a specific exercise program to train the deep stabilizers of the lumbar spine. Recurrence rates over the next year were 30% for those who performed the specific exercises, compared to 80% for those who did not. Future studies in the cervical spine will need to address if deep stabilizer deficits spontaneously resolve with pain, if specific exercises are needed, and if these exercises have an effect on recurrence rates. In addition to training the deep cervical flexors, these authors advocate exercises to train the tonic postural function of the scapular muscles.40 The forward head position, so commonly adopted by those with neck pain, involves increased thoracic kyphosis and abduction of the scapula. The scapular stabilizers, in particular the lower trapezius and serratus anterior, play a postural supporting role when sitting in an erect position, holding the scapula in a relatively adducted and depressed position. It is proposed by some authors41 that those who chronically sit with forward head and thoracic kyphosis lose the postural function in the scapular muscles, although there is no research evidence to support this finding. Exercises for these scapular muscles are similar to training of the deep cervical flexors; training initially involves holding a low-level static contraction to improve tonic postural control. Patients are taught to retract and depress their scapula in a prone position and then attempt to carry it over to a sitting position.

Evidence for exercise for acute nontraumatic neck pain Most randomized, controlled trials (RCTs) of exercise for acute neck pain have studied patients with whiplash. However, there is some evidence that specific exercises may help certain patients recover faster from acute neck pain episodes. The work of Donelson et al.23 and Werneke et al.24 showed a frequent occurrence of directional preference. In acute spinal pain, many studies24–26 have indicated that patients with a directional preference recover more swiftly and predictably using exercises, posture, and activity modifications determined by their directional preference. In one RCT that included patients with acute and chronic neck pain, Kjellman et al.42 compared three groups. Group one received exercise prescribed utilizing the McKenzie method, group two received general exercise, and group three received ultrasound. The McKenzie group had a more rapid improvement in pain intensity during the first 3 weeks and lower pain scores at 6 months. At 12-month follow-up, all three groups showed significant improvement with no significant difference among the groups. This study adds more evidence that directional preference exercise may help patients recover faster, but also shows the tendency for most acute neck pain to get better with time, irrespective of treatment.

Exercise for acute traumatic neck pain

Fig. 63.3 Craniocervical flexion exercise with feedback from a pressure biofeedback unit. 688

Traumatic neck pain most commonly involves whiplash, or a sudden acceleration–deceleration injury secondary to an automobile accident. Traumatic injuries also occur as a result of sporting injuries or falls, albeit with different forces on the neck than with an automobile accident. As whiplash is the most common traumatic incident, and all available studies focus on the sequelae to it, this section will focus on rehabilitation of whiplash-associated disorders (WAD), although the concepts could be applied to any traumatic neck injury.

Section 3: Cervical Spine

Most systematic reviews of treatment for whiplash injury conclude that an active approach is superior to passive treatment.43,44 The optimal management of whiplash-associated disorders is unknown, but some concepts for improving outcomes are emerging. Musculoskeletal dysfunctions observed following whiplash are a decreased ability to move the cervical spine, altered patterns of muscle recruitment, and deficits in kinesthetic awareness, balance and eye movement control.15 Rehabilitation of these deficits will be addressed in this chapter in those with neck pain, decreased range of movement, and/or point tenderness with no neurological signs (Quebec Task Force grade II).45 The authors present evidence in support of an early active approach to management. Lesions may occur in virtually any cervical structure including the ligaments, muscles, discs, zygapophyseal joints, and the bony elements. Experimental studies have shown that with rear-end collisions the torso motion causes the vertebrae to extend from the lowest vertebra to the upper vertebrae, causing the inferior articular facet to collide with the superior facet of the lower vertebrae.46 Kaneoka et al. hypothesized that this collision impinges on and inflames the synovial fold in the zygapophyseal joint. In fact, painful facet joints have been found in 54% of those with chronic pain associated with whiplash.46 Other common injuries are reported to be posterior disc herniations and anterior annular rim lesions.47 Just as with nontraumatic neck pain, radiologic imaging does not provide a conclusive diagnosis. Yoganandan et al.48 simulated a whiplash injury in four cadavers. The purpose was to determine type of injuries sustained with whiplash and whether these injuries could be viewed with conventional imaging. Impact speed was comparable to 75–90% of those who suffer a whiplash injury. There results suggest that multiple injuries occur that cannot be visualized with X-ray or CT scan. These included capsular tears of the zygapophyseal joints, tears of the ligamentum flavum, and disc anulus ruptures. Regardless of which tissue is injured, a uniform sequence of events shaping repair is set in motion. When developing a rehabilitation program for optimizing repair and preventing chronicity, determining the stage of healing and understanding the primary events occurring will improve outcomes. The primary means of tissue repair is by formation of granulation scar tissue.49 The formation of scar tissue is a three-phase cycle and is a normal reparative process following an injury. A review of this highly organized process and the role of graded movement in assisting optimal healing make it apparent why active rehabilitation of whiplash injuries appears to be superior to passive rehabilitation. Tissue healing following injury starts immediately with the inflammatory phase and generally lasts 1–5 days.49 Vasodilation and a release of prostaglandins and histamines in the area of damage results in increased blood flow. Peripheral neutrophils and monocytes migrate into the injured area to destroy bacteria and maintain a clean environment.49 These tissues create an inflammatory edema that seals the area to allow healing to occur. Neovascularization brings increased oxygen to the damaged area. Optimal management includes rest of the structures involved for this very short period of time. Excessive inflammatory edema causes larger quantities of scar tissue.19 Ice during this phase will help minimize edema. Ensuring a good sitting, standing, and sleeping posture (as opposed to the commonly adopted forward head position with increased thoracic and cervical kyphosis) decreases the stress placed on the tissues and subsequently decreases pain. The fibroblastic phase begins in the middle of the first week following injury.50 This is when the necessary components for repair are accumulated and the architectural make-up of the tissue is being formed.49 Scar tissue is created and strength is imparted to the tissue, depending on the forces placed on it. Fibroblasts synthesize collagen, which is the substance of scar tissue, and glycosaminoglycans, which fill in the space in and around collagen fibers. The glycosaminoglycan ground substance

provides lubrication and acts as a spacer between moving collagen fibers. Immobilization during this phase causes a loss of ground substance, which creates cross-links between the collagen fibrils, rendering them immobile.51 Additionally, fibrofatty tissue proliferates within the joint and forms adhesions as it matures into scar tissue. Articular cartilage joins with this tissue and degrades.52 Ligaments have been shown to loose their orientation, and their insertions into bone are weakened. Mobilization during this phase is essential. The joints and cartilage are stretched and lubricated by synovial fluid and their metabolic activities are enhanced.52 Cartilage repair in injured joints that were subsequently treated with CPM showed marked improvement in the rate and end point of the healing process.51 DePalma et al.53 noted that early motion and weight bearing had a beneficial effect on the repair of full-thickness cartilage defects. Salter54 and Houlbrooke et al.55 have also reported on the beneficial effects of early passive motion on joints and articular cartilage. Regular passive motion in progressively increasing ranges kept the needed space between collagen fibers and allowed better alignment of collagen and cros- links. Early mobilization has also been shown to improve outcomes in tendon repair.51 To gain the beneficial effects of movement during this phase, movements should be started once the initial inflammatory stage is nearing completion and the fibroblastic phase is underway. Several authors21,56 have outlined programs to determine how much movement to apply during healing. To allow the patient to gain confidence and to prevent a return to the inflammatory phase, movement should start in midrange with low repetitions, with a progression to end range movement as the patient tolerates it. If movement is too painful in a loaded position, the patient may need to lie down. If a movement hurts as it is occurring, but the pain ceases when the movement is complete, an acceptable amount of movement has occurred. If pain continues for more than a few minutes after the movement is complete or the pain becomes constant in nature, the movement was likely too far and the repetitions or the vigor with which they are being applied should be decreased. The remodeling phase begins at about 21 days following injury and provides the final form to the scar. All of the collagen mass is assembled, but the tensile strength is only 15% of normal.49 This process of scar remodeling continues for up to 12 months as collagen turnover rearranges the scar tissue, depending on the stresses placed on it. Many authors have demonstrated that the absence of controlled stress results in a weak, fibrous scar.54,57 Other researchers have shown that the application of stress during healing can lengthen a scar and positively influence the characteristics of the collagen repair. In response to internal and external influences, scar differentiates to become quasi-specific. One of the goals of motion during this phase is to enhance the potential of the scar to resemble its original tissue. During this phase of healing it is important to progress movement further into the range to restore full mobility. Once mobility has been achieved, stresses should be increased to attempt to increase the strength of the scar tissue. This may include cervical and scapulothoracic strengthening as well as encouraging the patient to return to all previous functional activities, as tolerated. Additionally, a mechanical assessment using repeated movements may be a helpful adjunct at this phase of treatment, as just with insidious onset neck pain, some patients exhibit a directional preference for one movement.

Motor control exercises The Whiplash and Cervical Spine Research Unit at the University of Queensland, Australia, has provided a significant amount of new information about physical and psychological changes with acute whiplash injuries. They followed 76 whiplash patients from a few 689

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weeks until 6 months postinjury and found changes in motor control, kinesthetic awareness, and certain psychological factors which might help predict chronicity. Changes in motor function develop early after a whiplash injury and may need to be addressed in a rehabilitation program.58 Changes in motor activity and control observed are the same as for insidious-onset neck pain: increased EMG activity of the superficial neck flexors, and decreased activity of the deep segmental neck stabilizers. Altered patterns of muscle recruitment were apparent in all whiplash patients within a month of injury and persisted to 6 months even in those patients who reported full recovery of pain. Altered patterns of muscle activation have also been shown in the shoulder girdle with chronic WAD.59–61 The Whiplash and Cervical Spine Research group propose having patients perform craniocervical flexion exercises for WAD just as described for insidious-onset neck pain prior to a general strengthening program. The efficacy of such an exercise program has yet to be investigated in whiplash patients. Sterling et al.58 have shown that kinesthetic disturbances occurred soon after injury. Joint position error (JPE) was measured by blindfolding subjects and then asking them to perform a series of movements and then return to their original head position. JPE was compared between the whiplash group and the controls. In those with moderate to severe symptoms, there was a statistically significant higher JPE, present within a month of injury and persisting at 6 months of injury. Whether specific exercises addressing these deficits improves outcomes in acute whiplash patients is still to be addressed. Sterling15 have also found some sensory and psychological changes which they believe may help predict chronicity of WAD. Local cervical mechanical hyperalgesia (decreased pressure pain thresholds using pressure algometry) occurred in the acute stage of whiplash injury, but resolved by 2–3 months in those who recovered and those with persisting mild symptoms. In contrast, those with persisting moderate to severe symptoms not only had local hyperalgesia, but widespread mechanical and thermal hypersensitivity soon after injury. According to Sterling et al., optimal initial management of this subgroup would include pharmaceutical management, and a slower approach to restoring movement with minimal pain provocation. Additionally, the early presence of moderate levels of acute posttraumatic stress was a distinguishing factor of those who became chronic in their group of patients. The whiplash research group gave all participants a battery of questionnaires measuring psychological distress. The group that had persistent moderate or severe symptoms could be distinguished from the others even a few weeks after injury. All whiplash patients displayed initial psychological distress, but the group with significant persistent symptoms had one distinguishing factor. They had moderate levels of acute post-traumatic stress as measured on the Impact of Events Scale.62 Sterling et al. proposes that utilization of psychological testing scales would help institute early psychological referral for this subgroup who might benefit from a multiprofessional approach to their management. Traditionally, this type of treatment has not been instituted until it becomes clear that symptoms are not resolving.

direction of movement might be more beneficial than others. There was also a third group that performed the active intervention but waited until 2 weeks postinjury to begin the exercises. At 6 months postinjury, the groups that moved frequently, instead of gradually after a period of rest, had significantly greater pain reduction. The group that did the best was the one that started movement the earliest. Most importantly, only 10% of the actively treated patients had symptoms at 6 months, compared to 50% of the patients who were given standard of care. The active group only required an average of 4 visits, and no passive modalities were used with any of these patients. More information can be gained when comparing this study to the RCT of Sodelund et al.63 Two groups of acute whiplash patients performed range of motion exercises three times daily. One group also received kinesthetic exercises. At 6-months follow-up, the average patient in both groups remained in pain and disabled. Comparing the study of Sodelund et al. to that of Rosenfeld et al. may provide information on dosage. Only 10% of subjects in the Rosenfeld et al. study who exercised their necks hourly remained in pain at 6 months, whereas most subjects in the Sodelund et al. study who exercised their necks three times a day remained in pain at 6 months. Additionally, exercises in the Rosenfeld et al. study were not standardized to all patients, but tailored, based on each patient’s specific response. Most studies looking at the efficacy of soft collars do not support their use.64,65 Immobilization not only has physiologic ramifications, but enhances fear of movement and disability. When immobilization in a soft collar combined with time off of work was compared to a group who were told to act as usual during the first 14 days following injury, there was a significantly better outcome for the act-as-usual group in terms of pain, memory, and concentration.66 Two other studies have been published comparing early movement to use of a collar. Pennie and Agambar67 found no difference at 2year follow-up between a group given a collar with instructions for subsequent self-mobilization to a group that received traction and physical therapy. Crawford et al.68 placed one group in a collar for a few days and another group in a collar for 3 weeks and then had them both perform self-mobilization exercises. The group in the collar for the shorter time returned to work much earlier (17 versus 34 days) although there was no difference in pain and range of motion at 1-year follow-up. These studies highlight that wearing a collar certainly adds no benefit, and in 4 out of 5 studies it caused a worse outcome on most measures. In the studies where the collar groups did as well as the other groups in terms of pain and function, both groups received mobilization exercises, which may have negated the initial immobilization effects of the collar.

Summary of exercise for acute neck pain ●

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Evidence for exercise interventions in acute traumatic neck pain 56

In a randomized, controlled trial, Rosenfeld et al. compared an early active movement program to instruction to rest for 2 weeks with optional use of a collar, followed by movement of the head 2–3 times a day. The active group performed cervical rotation every hour starting 2–3 days after injury. If symptoms were still present at 20 days, the evaluation was supplemented by a mechanical evaluation using repeated movements, as described by McKenzie, to determine if any 690

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A substantial portion of patients with acute neck pain can centralize and abolish their pain rapidly with performance of repeated motion in one direction. At least three studies24,41,56 have shown that prescribing exercise based on centralization of pain provides quicker relief of pain and improves outcomes. With traumatic neck pain, early, frequent movement has been shown to provide superior outcomes. There may be a role for providing segmental stabilization exercises for patients with acute neck pain.

Exercise for chronic or recurrent neck pain Exercise for chronic neck pain has more support in the literature than for other interventions, although what type of exercise, and the optimal amount and frequency, have yet to be determined. In reality, the type of exercise prescribed for chronic neck pain varies widely.

Section 3: Cervical Spine

McKenzie method for chronic neck pain patients Just as with acute neck pain, assessment of repetitive movements helps the clinician understand the ‘lesion behavior’ and thus develop a rehabilitation strategy. Although occurring less frequently in chronic neck pain, there may be one direction of movement that, when performed repeatedly, causes centralization to occur. Initiating the exercise program with this direction may help minimize the pain and make it easier to address any other musculoskeletal deficits. In other patients with chronic neck pain, avoidance of particular movements secondary to pain or poor posture can create shortened or dysfunctional tissue.21 In this case, repetitive motions reveal a particular pattern of symptom production: movement into the shortened end range produces pain which ceases once the movement is complete. In these cases, the patient is taught to exercise into the direction or directions that are limited, producing the pain with each repetition as long as the pain stops when the exercise is ceased. This is an effective way to remodel tissue without creating microtrauma. It is not unlike a patient restoring elbow flexion and extension after a fracture once the cast has been removed. To gain motion, patients must perform the movements frequently.

General strengthening programs Numerous studies have shown reduced strength and endurance in the cervical flexor and extensor muscles in patients with neck pain.28 There are many methods available to perform strengthening. Strengthening programs currently used run the gamut from extremely low-tech to extremely high-tech. Most exercise programs focus on the cervical muscles as well as the scapular stabilizers. A typical low-tech strengthening program either involves isometrics or utilizing a head lift in supine and prone positions to strengthen the flexors and the extensors, respectively. Resistance can be increased with a free weight or by elastic bands. Scapulothoracic exercises may involve free weights or closed-chain exercises, such as push ups. The difficulty of closed-chain exercises can be increased infinitely by decreasing the stability of the surface (exercise balls) or performing them unilaterally, tasks for the very highly fit. Two companies, MedX and DBC International, have developed equipment that is used to test isometric strength and strengthen the cervical musculature through a full range of motion. MedX equipment was developed in the United States, while DBC equipment was developed in Finland. Both systems have machines that provide resistance through the range of cervical extension and cervical rotation. Patients use the machines 2 times a week for 8–12 weeks. Clinical trials conducted by DBC and MedX have shown that biweekly sessions maximize tissue adaptation while minimizing risk of overstimulation and increased pain. Utilizing the machines three times per week in the lumbar spine increased risk threefold and increased cost by 50% without additional benefit. The machines provide controlled, periodic, and specific overload to isolated musculature. Resistance is progressively increased. In addition to cervical muscular strengthening, both systems have patients use scapulothoracic machines to strengthen these muscles, and the MedX corporation advocates having patients become involved in a cardiovascular conditioning program as well.

Motor control exercise program As stated earlier in the chapter, deficits in motor control occur early with insidious and traumatic-onset neck pain, and have been shown to continue with chronic neck pain. In addition to a disturbance of the neck flexor synergy, those with chronic neck pain have shown an increased fatigability of the superficial cervical flexor muscles. Research has demonstrated that those with chronic neck pain have

increased EMG activity of the scalenes, the sternocleidomastoid, and the upper trapezius during the performance of a repetitive upper extremity task.69–71 Additionally, after the task was completed, patients with neck pain were unable to relax the sternocleidomastoid, the anterior scalene, and upper trapezius muscles. Research in healthy subjects has shown that during rapid arm movements the cervical muscles are coactivated within 50 ms of the onset of deltoid activity. Falla et al. have shown that in chronic patients with neck pain, there is a delayed onset of the deep and superficial cervical flexor muscles.69 The deep cervical flexors demonstrated the longest delay of onset. Based on these series of research studies, the Australian group advocates an alternative approach to the general strengthening model. Prior to starting high-load strengthening, they specifically address the coordination between the layers of the neck flexor muscles exercises.69 Patients perform the craniocervical flexion exercises and scapular depression/retraction exercises as described previously. General strengthening is not recommended in the early stages as it thought that this will only facilitate continuation of substitution by superficial muscles. General strengthening is addressed after patients have reeducated the deep and postural muscles, as evidenced by their ability to perform the CCF exercises properly. A recent RCT using this exercise approach for treatment of chronic headache and neck pain found a statistically significant reduction in pain at 12-month follow-up compared to a control group.40

Proprioceptive exercises Revel et al.72 demonstrated that cervicocephalic kinesthesia, or the ability to relocate the head accurately on the trunk after movement, was significantly reduced in patients with chronic neck pain. Thus, they designed an exercise program involving eye–neck coordination and head repositioning activities. They performed an RCT comparing a group who utilized these exercises to a control group for patients with chronic (>3 months) neck pain. At 10-week follow-up, there was a statistically significant decrease in neck pain, improvement in head repositioning ability, and functional improvement in the intervention group.

Evidence for exercise for chronic neck pain One RCT by Taimela et al.73 compared three groups: 12 weeks of participation in the DBC cervicothoracic exercise program (combined with proprioceptive exercises); extensive instructions in home exercise; and advice to exercise with no specific instruction. The home exercises were listed as stretching and strengthening, but it was not clear what was strengthened or how. The results showed that the average selfexperience total benefit was highest in the DBC group at 3 months and at 12 months, next in the home exercise group, and lowest in the no specific instruction group. At 3 months post-treatment, the active and home exercise group had significantly lower pain scores than the control group, but by 12 months there was no statistical difference among the three groups (all continued to have lower scores than initially). Bronfort et al.74 compared three groups: spinal manipulation combined with low-tech stretching and strengthening, manipulation combined with MedX, and manipulation alone. Both groups with exercise had greater subjective improvements and objective improvements, although there was no difference in the high-tech and low-tech exercises. While both of these studies lend support to the use of exercise for chronic neck pain, they do not determine that the high-tech expensive equipment provides better outcomes. Current costs for 8–12 weeks of utilization of the extension and rotation MedX machines are substantial, necessitating further research to validate if use of this type of equipment improves outcomes over lower-tech strengthening equipment. 691

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In another recent RCT,75 180 women with chronic non-specific neck pain were randomized to either neck strength training, endurance training, or a control group. The strength training group used an elastic rubber band in sitting to resist 15 repetitions of neck flexion, rotation, and extension. The aim was to maintain the level of resistance at 80% of their maximum isometric strength, which was recorded at the start of the program and at follow-up visits. They also performed upper extremity exercises with a dumbbell for one set of 15 repetitions with the highest load possible. The endurance group exercised the neck flexors and extensors by actively lifting their head up from the supine and prone position for three sets of 20 repetitions. They performed upper extremity exercises with a 2 kg dumbbell for three sets of 20 exercises. The control group was advised to perform cardiovascular exercise three times a week for a half hour as well as stretching three times a week for 20 minutes. All three groups could perform their exercise programs at home and were asked to continue the exercises for 1 year. At the 12-month follow-up, all groups had a decrease in neck pain and disability, but there was a statistically significant greater improvement in both the strength and endurance training group over the control. The strength training group did the best with greatest decreases in their pain and disability scores, with concomitant maximum improvement in strength and range of motion. Wailing et al.76 also compared strength and endurance training to a control group. Both exercise groups performed scapulothoracic strengthening and did not utilize specific cervical strengthening. The Wailing et al. strength training group used a lower intensity of weight training than the strength training group in Ylinen et al.’s previously mentioned study, and found that both strength and endurance groups improved relative to the control, with no significant difference between groups. Randlov et al.77 also found equal improvements with intensive and light neck and shoulder exercises. Systematic reviews conclude that exercise is the only intervention that has evidence to support its use for treatment of chronic neck pain. Sarig-Bahat78 concludes in his review article of exercise for mechanical neck disorders, ‘findings revealed significant evidence to support the effectiveness of exercise in two main fields of mechanical neck disorders, whiplash-associated disorders and chronic neck pain.’ The Philadelphia Panel for Evidence-Based Clinical Practice Guidelines concluded that there is good evidence to include supervised exercise programs in rehabilitation of chronic neck pain.7 The British Medical Journal’s Guidelines also concludes ‘active physiotherapy reduces pain compared with passive treatments, and exercise reduces pain compared with stress management.’1 From the studies reviewed, it appears that supervision (even of a home exercise program) is important to maintain compliance. Although Ylinen et al.’s patients performed a home exercise program, they had significant training at the beginning, with a 12-day institutional program to start. Patients also kept exercise diaries that were reviewed at 2 and 6 months into the program. Other studies that did not show benefit with exercise therapy only briefly taught patients home exercise programs with no substantial follow-up.79 It has been well established that results achieved by strength training disappear if training is performed only for a short term.

Summary of exercise for patients with chronic neck pain ●

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A mechanical assessment using repetitive motions is still an excellent first starting point for patients with chronic neck pain as a substantial number can still centralize their pain. Strengthening cervical and scapulothoracic musculature has support in the literature for patients with chronic neck pain.

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Some studies suggest there may be some role for segmental stabilization prior to strengthening of global muscles (muscles that cross more than one joint). There is some evidence that higher-intensity strengthening versus endurance training is more effective for treatment of chronic neck pain. Guidance with an exercise program with follow-up to ensure compliance, correct technique, and adjust dosage appears to provide better outcomes.

EDUCATION STRATEGIES Static work positions and repetitive occupational tasks have been found to be risk factors for insidious-onset neck pain. A forward head posture has consistently been linked with cervical pain.21,31,41 A forward head position leads to sustained end range stretch of collagenous structures which, when occurring frequently enough, can produce pain even without damage to the tissue. 21 Prolonged sustained positions may eventually cause tissue damage resulting in a more significant episode of neck pain that doesn’t necessarily resolve solely with correction of the offending posture. With acute and sometimes chronic neck pain, correction of posture often eliminates or lessens pain. When this is the case, correction of the provocative postures appears to be an essential component of rehabilitation to hasten recovery and prevent recurrence, regardless of the pain generator. An assessment of varying spinal and head positions often reveals a position where a patient can minimize, centralize, or abolish the pain. Use of the slouch/overcorrect procedure (Fig. 63.4) as well as exploring varying positions of cervical retraction can help identify this posture. If a reductive position is found, showing patients cause and effect by having them alternately assume the provoking posture and the reductive posture helps them learn the control they have over the amount and location of their symptoms. Patients have substantial incentive to maintain this position once they realize their own ability to control their symptoms. As many people adopt positions in daily life at a computer that involves lower cervical flexion and upper cervical extension (protrusion), often supporting the lumbar lordosis, decreasing the thoracic and subsequent cervical kyphosis, and retracting the upper cervical spine results in reduction of symptoms. Use of supportive rolls can help maintain a correct position during long periods sitting at a computer. Taping (Fig. 63.5) can also be particularly helpful for providing reinforcement for those who require more feedback for maintenance of an erect position. Ergonomics, body mechanics, and other postural factors, such as sleeping position may need to be addressed as well. Nighttime aggravation of the pain may occur secondary to mechanical or chemical factors. If there appears to be a mechanical component to nighttime pain (i.e. the patient can relieve the pain by a change of position or by providing additional support) use of a supportive neck roll or a change to a different pillow may have a beneficial effect on symptoms. The information and advice that healthcare professionals give to patients are potent elements of the intervention. Educational experts advise a coordinated approach, in which physicians and therapists all give the same information.80 Conflicting information has been found to contribute to fear avoidance beliefs and pessimism about future recovery. Current guidelines suggest advice to continue ordinary activities as much as possible. For acute pain, there is also evidence that patients may benefit from general diagnos-

Section 3: Cervical Spine

A

B

C

Fig. 63.4 The slouch/overcorrect exercise. (A) The patient assumes the extreme of flexion. (B) The patient assumes the extreme of extension. (C) The patient releases by about 15% for correct sitting posture.

tic information stating that there is ‘no sign of serious disease’ and less specific diagnostic information.80 Patients with back pain who were given a specific diagnosis for a work-related injury were more likely to progress to chronicity.81

MANUAL THERAPY Historically, manual therapy has been a frequently used modality for treatment for neck pain. Manual therapy covers a whole host of treatment techniques applied by medical practitioners, chiropractors, and many factions within physical therapy. There are currently over 90 different named systems of manual procedures.82 Purported methods of action of techniques differ depending on the philosophy

Fig. 63.5 Taping of the thoracic region for posture correction. If the patient slouches, the tape gives immediate feedback to return to an erect position.

of the group applying the treatment. Manual therapy theories state that mobilization or manipulation may cause neuromodulation of nociceptive activity, stretch or release adhesions, increase motion of the joint, or decrease displacement within the joint.83 In systematic reviews attempting to determine its efficacy, manual therapy is frequently lumped together as one type of treatment. In reality, contrasts in philosophies may render the resultant treatment menu quite different. Variations in clinical reasoning result in diverse examination methods, patient and technique selection, and dosage differences. Some concepts advocate manual therapy for a select number of patients who are not progressing independently, while other concepts utilize manual technique on most if not all patients. What is provided in addition to the manual therapy (i.e. exercise or modalities) will differ depending on approach. Thus, for research purposes, it is difficult to view all of manual therapy as one entity. Manual therapy approaches are ever evolving, with overlap from one concept of treatment to another, rendering them not completely separate entities. For a comprehensive review of manual therapy available for neck pain, it is important to provide a brief account of some current philosophies. Manual therapy encompasses manipulation and mobilization of the spinal joints. The speed of the technique differentiates manipulation from mobilization.84 Manipulation is a high-velocity thrust that can be exerted through a short or long lever arm. According to one definition, short lever-arm techniques are low-amplitude thrusts that aim to affect a specific level of the vertebral column, while longlever techniques move many vertebral articulations simultaneously.84 Mobilization involves low-velocity passive motion to vertebral segments. Theoretically, manipulation and mobilization differ in effect as the rate of vertebral joint displacement in manipulation does not allow the patient to prevent joint movement, while the slower rate of movement in mobilization allows the patient to stop the movement.84 In the late nineteenth century, organized orthodox medicine did not recognize any value in manipulation, so two competitive systems utilizing manipulation developed, namely osteopathy and chiropracty. In the practice of osteopathy, joints are mobilized for increasing motion and the techniques are very specific. Osteopaths palpate the spinal joints seeking limited spinal movement and muscle spasm and direct their manual treatment to the segment that they believe to be fixed in 693

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a faulty position.85 In 1895, Daniel David Palmer founded chiropracty based on the view that vertebrae may become subluxed and manipulation may restore correct alignment and function. Chiropractors palpate for vertebral displacement.85 James Mennell introduced manipulation to physical therapists in 1916 at St. Thomas’s Hospital in the United Kingdom. Subsequently, Dr. James Cyriax, who followed Dr. Mennell at St. Thomas’s, trained most of today’s present-day leaders in manual therapy. Osteopath Dr. Allan Stoddard also had a significant influence. In 1961, Freddy Kaltenborn of Norway was the first physical therapist to develop and publish concepts and techniques of joint manipulation. Subsequent physical therapists continued to develop the arts of mobilization and manipulation and developed their own ‘concepts of treatment.’ Some approaches are based on a biomechanical analysis of articular dysfunction, while others rely more on analysis of pain response to movement. Instruction in manual therapy varies by country and school. For example, entry level physical therapy programs in Australia teach the Maitland Concept, while Norwegian therapists learn Kaltenborn’s approach. In the United States the majority of programs give an introduction to many philosophies. Numerous postgraduate continuing education courses are available, with some being eclectic and others focusing on one particular approach. Orthopedic manual therapy is considered a specialized area of physical therapy, requiring completion of postgraduate education. Many named systems of manual therapy have their own fellowship program, such as The Maitland Concept, The McKenzie Institute, and the University of St. Augustine (Stanley Paris’s program), to name but a few. The International Federation of Orthopedic Manipulative Therapists represents groups of manual therapists around the world and has set educational standards for postgraduate programs. For an understanding of the most common manual therapy approaches being practiced, a brief review of concepts of treatment is provided. A recent survey asked physical therapists in the United States which individuals have had the most influence in orthopedic physical therapy.86 The rankings of manual clinicians in descending order were Robin McKenzie, James Cyriax, MD, Geoffrey Maitland, Stanley Paris, Brian Mulligan, and Freddy Kaltenborn. It should be noted that although the techniques and philosophies of manual treatment are discussed in this section, the vast majority of manual therapists provide exercise in addition to the manual therapy.

Robin McKenzie Robin McKenzie’s approach was partially discussed in the exercise section of this chapter, but also has a manual therapy component. The McKenzie approach is actually a marriage between exercise and manual therapy, with a goal of making patients independent of clinicians.87 McKenzie was trained by the experts of the time (including Cyriax, Stoddard, Maitland, Kaltenborn, and Mennell) as a manipulative therapist and at one time considered himself to be an ardent manipulator. His approach was altered with his observation that patient-generated forces could bring about a change in the condition often more rapidly than clinician-generated forces. He determined that the majority of patients could get better with self-treatment and only a minority needed mobilization or manipulation. According to his philosophy, performing exercise in a rhythmic fashion, repeatedly to end range in the direction of preference, is actually a mobilization, only performed by the patient and not the clinician. The method of determining what exercise to prescribe has been described early in this chapter. When symptoms do not fully abolish, or the movement is not fully gained, McKenzie advocates performing mobilization, and manipulation only in a select few who require more force. Manual techniques are performed based on symptomatic and mechanical response, and observation for the occurrence of centralization. Manual techniques are performed only a minimal number of times, until the patient can get the desired benefit with his own self-generated force (Figs 63.6, 63.7). McKenzie believes teaching patients to treat themselves whenever possible is superior to providing manipulative therapy to all patients as risks of aggravating the condition are lowered, and self-management encourages independence and may reduce full-blown recurrences.

Geoffrey Maitland Maitland’s concept of manual therapy is one of the standard approaches to spinal techniques. Maitland studied worldwide with osteopaths,

James Cyriax, MD Dr. James Cyriax is generally considered to be the father of orthopedic medicine. His impact on the field of manual therapy has been profound. He has had the most influence on all other manual therapists discussed here and has taught his methods to thousands worldwide. Dr. Cyriax was a British orthopedist who started teaching physical therapists manual techniques in 1938. Cyriax’s work is based on the principles that all pain arises from a lesion, and that all treatment must reach and exert a beneficial effect on the lesion.85 Cyriax believed that there was no place for diffuse massage, superficial or deep heat, or general exercise for non-specific spinal disorders. He stressed that to understand the lesion and treat it appropriately, each patient must be studied individually with re-evaluation at each session to assess any alteration in the physical signs. Cyriax originated the concept of referred pain and was among the first to recognize the intervertebral disc as a source of pain. His treatment techniques consisted of manipulation, friction massage, traction, and injection. Cyriax taught manipulative techniques, often performed with manual traction, with the intent of restoration of pain-free movement. In his methods, the normal joints are moved until the resistance of the blocked joint is felt, with a final thrust of tiny amplitude applied at this point.85 694

Fig. 63.6 Lateral flexion mobilization. (Adapted from Figure 12:7 in McKenzie, 1990.)

Section 3: Cervical Spine

Fig. 63.7 Retraction and extension with traction and rotation. (Adapted from Figure 12:4a in McKenzie, 1990.)

Fig. 63.9 Atlantoaxial rotation mobilization. (Adapted from Figure 10.83 in Maitland, 1995.).

chiropractors, medical doctors, and physical therapists. The Maitland Concept of Manipulative Physiotherapy emphasizes continuous evaluation and assessment. In clinical decision-making, Maitland emphasizes giving the greatest weight to the unique individual combination of the abnormal signs and symptoms rather than the diagnosis.88 Additionally, Maitland presented and emphasized a clear differentiation between manipulation and mobilization and has been a strong advocate of the use of gentle passive mobilizations prior to the more traditional forceful techniques of manipulation. In Maitland’s system, active, passive, and passive accessory movements are assessed to find the most painful sign or segmental stiffness. When an active or passive movement is identified that hurts, the joint is mobilized (Figs 63.8, 63.9). Reassessment is performed to see if the movement hurts less. If there is no positive change in the physical sign, the technique is modified until the desired intention is achieved. Maitland emphasizes grading the degree of applied movement according to the presenting signs and symptoms. Gentle initial techniques are emphasized with a gradual progression to stronger techniques only if necessary.88 Maitland’s techniques are specific, attempting

to mobilize one joint at a time. Mobilizations are performed while the joint surfaces are distracted, compressed, or in neutral.

Stanley Paris Paris, originally from New Zealand, trained with Cyriax, Stoddard, and Kaltenborn. He was instrumental in founding The International Federation of Orthopedic Manipulative Therapy and teaches manual therapy in the program he founded in the United States. He has been responsible for physical therapists in the United States becoming skilled in manual therapy. Paris teaches a version of manual therapy with specific techniques that emphasize restoration of normal mechanics and de-emphasizes pain. Paris breaks active movements into their component motions and assesses joint play for the purpose of evaluation and treatment.

Brian Mulligan Brain Mulligan was one of the founders of the New Zealand Manipulative Therapists’ Association and developed some commonly used mobilization techniques, some of which are called ‘mobilization with movement.’89 All of Mulligan’s mobilizations are done with the patient bearing weight. He believes this to be very important as often improvements gained from manual therapy are lost when the patient returns to a weight-bearing posture. If successful, his techniques bring about an immediate improvement in the condition. If there is no immediate improvement, he discards the technique for that patient. ‘NAGS’ is an acronym for ‘natural apophyseal glides’ and are facet mobilizations. Mulligan describes these techniques as extremely useful for those with a gross loss of movement and the elderly (Fig. 63.10). ‘SNAGs,’ or ‘sustained natural apophyseal glides,’ are sustained mobilizations performed in the plane of the facet while the patient is moving. For example, if a patient has a painful loss of left rotation, the mobilization is performed above the suspected site of the lesion while the patient turns her head to the left (Fig. 63.11). If the ‘SNAG’ is successful, the patient will gain full left rotation without pain. If this is effective, the patient is taught to perform a ‘self-SNAG’ at home (Fig. 63.12). ‘SNAGs’ can also be performed to gain cervical side flexion, extension, and flexion.

Freddy Kaltenborn Fig. 63.8 Posterior–anterior lower cervical mobilization. (Adapted from Figure 10.61 in Maitland, 1995.)

Kaltenborn went from Norway in 1952 to study with Cyriax. Subsequently, he taught thousands of physicians and physical thera695

Part 3: Specific Disorders

Fig. 63.10 ‘NAGS’ to the upper cervical spine. (Adapted from Figure 1a in Mulligan, 1995.)

Fig. 63.12 Self-‘SNAG’ for restricted rotation. (Adapted from Figure 15b in Mulligan, 1995.)

pists manual therapy, and was instrumental in getting manipulation included in Norway’s physical therapist’s charter in 1957. Together with another physical therapist, Olaf Evjenth, Kaltenborn developed the Kaltenborn–Evjenth Concept, which is now taught in many countries. Kaltenborn’s approach to manual therapy is based on biomechanical principles of movement. Kaltenborn’s assessment includes active and passive movement testing as well as segmental mobility testing by palpation in an attempt to identify directions of joint restrictions. Palpation is also utilized to assess soft tissue. Kaltenborn’s manual techniques utilize biomechanical principles of movement.

ies had a mixture of patients with acute and chronic neck pain, and will be reviewed in the section on chronic neck pain. Nordemar et al.90 compared three groups being treated for acute neck pain. One group received muscle energy technique mobilizations, one group received transcutaneous electrical nerve stimulation (TENS), and one group wore a collar. At 10 weeks post-treatment, there was no significant difference between groups. This one study does not support the use of this type of mobilization (muscle energy techniques), but does not provide any evidence about other differing concepts in which mobilization is applied. In addition, the mobilization group wore a collar, which may have counteracted any beneficial effects of the mobilization. Howe et al.91 compared 1–3 manipulations to a no-treatment control and found greater pain relief in the manipulation group at 1 week, and no difference at 3 weeks. At least five systematic reviews have assessed the efficacy of manipulation and mobilization in neck pain.5–8,92 For acute neck pain, they all conclude that there are few studies and the evidence is currently inconclusive.

Evidence for manual therapy for acute nontraumatic neck pain Many systematic reviews of manual therapy literature have been published which have reviewed the literature comprehensively. These reviews, as well as a search of MEDLINE and CINAHL subsequent to their publication, only revealed two small randomized, controlled trials of manual therapy for acute neck pain. Some of the other stud-

Evidence for manual therapy for acute traumatic neck pain

Fig. 63.11 ‘SNAG’ with left rotation. (Adapted from Figure 3 in Mulligan, 1995.) 696

Evidence is lacking on the effects of manual therapy on acute traumatic neck pain. Only two studies have looked at the use of manual therapy for acute traumatic neck pain.64,65 Both had the patient perform exercise, so it is impossible to determine if noted benefits of movement in both studies were supplemented by the specific mobilization techniques performed. Manual therapy may be helpful in acute pain from whiplash when the patient has too much pain to begin to restore movement on his or her own or has a fear of movement. Sometimes a movement that is very painful can become substantially less painful when some form of manual technique is applied during the movement or prior to application of the movement. Manual treatment may just involve assisting the patient in performing the movement independently and can be applied to the upper and lower cervical spine The authors’ opinion is that not every patient needs manual therapy following whiplash, with this type of treatment being reserved for those patients who are having difficulty restoring movement independently. Manual therapy should be used judiciously with an aim of restoring the patient to self-treatment. A systematic review of manual therapy and

Section 3: Cervical Spine

subsequent clinical practice guidelines93 concludes that manual therapy should be used in conjunction with exercise rather than in isolation.

Evidence for manual therapy for chronic neck pain The body of literature for manual therapy for chronic neck pain is much more substantive than for acute neck pain, although many of the studies are not considered to be of high quality. The Cochrane Collaborative Reviews,6 which have received the highest quality rating of methodological rigor, selected 33 randomized or quasi-randomized, controlled trails that investigated the use of manipulation or mobilization as a treatment for mechanical neck disorders. This review included manual therapy provided by any type of practitioner. Of these 33 selected trials, 42% were considered high-quality trials when the Jadad scale was used, and 24% were considered high-quality when the van Tulder scale was used. Common methodological weaknesses were a failure to describe appropriate concealment of treatment and lack of effective blinding procedures. Three randomized, controlled trials assessed the effect of one session of manipulation,94–96 all determining that single sessions of manipulation do not result in significant pain relief for acute, subacute, or chronic mechanical neck disorders. Five trials were found that compared the effects of anywhere from 6 to 20 sessions of manipulation over a 3–11 week period74,97–100 to a variety of interventions including soft-tissue treatments, high-technology exercise, low-technology exercise, medication, low-voltage electrical acupuncture, and standard physical therapy. In every case, the manipulation group showed no statistically significant benefit over the control, and in one case the group that received manipulation alone fared worse to other treatment groups.74 In this study, manipulation alone (manipulation as described by Frymoyer) was compared to manipulation combined with lowtechnology exercise. The group that also had exercise showed a clinically worthwhile cumulative advantage over manipulation alone. Four trials have compared mobilization and manipulation techniques.101–104 Overall, no difference in pain relief and functional improvement at short-term follow-up was found when comparing a very limited number of manual therapy techniques. Hurwitz et al. compared manipulation to mobilization and found no difference between groups.105 When mobilization and manipulation were compared to placebo, there was no evidence of difference in pain and function between the two groups.106 Mobilization was compared to use of a cold pack107 with no difference between groups at short-term follow-up. Mobilization was also compared to acupuncture. David et al.108 in a high-quality RCT, with long-term follow-up, compared one group receiving Maitland mobilizations performed once a week for 6 weeks to another group receiving acupuncture. Both groups had a decrease in pain scores that were not statistically significant from one another. Ernst published a systematic review of chiropractic spinal manipulation.109 Four studies met his inclusion criteria. Two of these trials were of a single treatment session and two were studies of multiple sessions of high-velocity thrusts of the upper cervical spine. None of the four trials demonstrated the superiority of chiropractic manipulation over the control interventions. The Cochrane Review reports that there is strong evidence for maintained long-term benefit from mobilization or manipulation in combination with exercise. This is based on the findings of six RCTs.40,74,110–113 Patients were more satisfied with manual therapy plus exercise than either alone. Interestingly, although satisfaction was greater with multimodal treatment, outcomes for pain relief and improvement in function were not different in those who received exercise alone compared with those who received exercise and manual therapy.

In summary, the evidence does not support the use of mobilization or manipulation alone or with any type of modalities other than exercise. Manual therapy has been shown to be most effective when used in combination with exercise.114 Long-term treatment with spinal manipulative therapy in isolation has been shown to be no more effective than placebo in the treatment of mechanical neck pain. Manual therapy should be used prudently so patients do not become dependent on this care, with the emphasis on the exercises that the patient can perform independently.

Risks associated with cervical spine manipulation Cervical spine manipulation occasionally is associated with vascular and neurological complications. The exact risk is unknown, but in 1997 Di Fabio84 reported on 177 cases found throughout the literature, Ernst115 reported 31 cases just between 1995 and 2001, and Haldeman116 reported 117 cases related to manipulation in the English language literature. Additionally, underreporting is likely to significantly distort the evidence.115 Ernst cites a recent unpublished survey of neurologists that found 35 cases of neurological complications occurring within 24 hours of cervical spine manipulation. Additionally, an audience poll was taken at a meeting of the Stroke Council of the American Heart Association, where 360 unreported cases of stroke after spinal manipulation were reported.84 All estimates of incidence of serious complications for manipulation are based on weak evidence and range anywhere from 1 in 20 000 to 5 in 10 000 000.92 Smith and Johnston studied all patients under age 60 with cervical arterial dissection at two stroke centers between 1995 and 2000 and compared them to controls to determine whether spinal manipulative therapy (SMT) is an independent risk factor for cervical artery dissection. In both univariate and multivariate analysis, patients with dissection were more likely to have had SMT within 30 days prior to their CVA.117 Thus, it was considered an independent risk factor for vertebral artery dissection. Although the most frequently reported complication is vertebral artery dissection causing stroke, other complications have been reported, such as internal carotid artery dissection, phrenic nerve injury, subdural hematoma, prolapse of disc, and retinal artery embolism. Di Fabio reports that 18% of the cases he reviewed resulted in death. The specific type of manipulation was not described in 46% of cases, but when it was described it often involved a rotational thrust technique in the upper cervical spine. It is thought that a stroke could result from manipulation by mechanical compression or excessive stretching causing tearing of the arterial wall. The artery is thought to be most vulnerable where it takes its circuitous course at the atlantoaxial articulation when stretched in end range rotation. Screening for signs of vertebral artery compromise is taught to all practitioners of manipulation to attempt to reduce the frequency of complications. Screening involves sustained positioning of the upper cervical spine in end range rotation and extension, watching for any signs of brainstem ischemia or blood flow impedance. Recent studies have shown that these tests may not actually significantly reduce vertebral artery flow as previously postulated, and this testing is unlikely to distinguish who may have a complication with SMT.118 Some injuries are thought to occur as a result of tearing, which would not be predicted by this type of screening. Other authors have suggested that cervical manipulation may have been administered to patients who already had spontaneous dissection in progress.116 No factors included in the patient history, including arteriosclerosis, have been shown to be risk factors.116 697

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Complications currently appear to be unpredictable. Even with high estimates, the risk of an adverse event is extremely small. Yet complications do occur, cannot be predicted, and often are quite serious, leaving permanent neurologic injury. This has led Di Fabio as well as experts from the RAND group to recommend mobilization over manipulation, as there is no compelling evidence that manipulation achieves better clinical outcomes than mobilization. If manipulation is used, practitioners have a legal and ethical obligation to provide information and gain consent, with current guidelines reflecting these recommendations.118

Soft tissue manual therapies Another arm of manual therapy includes those philosophies and techniques that focus on treatment of soft tissue. Massage attempts to decrease pain by focusing on painful sites in soft tissue. Massage encompasses a variety of techniques ranging from superficial to deep. Many patients report temporary lessening of pain following massage. In a recent survey in the United States of those with back and neck pain,119 65% of those who received massage reported it to be very helpful. According to many recent systematic reviews, massage has not been shown to influence outcome in terms of either pain or disability.1,7,8,120,121 Most studies have not studied massage exclusively, but as part of a multimodal treatment regimen. It appears that in some patients massage provides a temporary symptomatic benefit, but it is unclear if it affects the clinical course of the episode of pain in any way. Myofascial therapy is a philosophy of care utilized by a wide variety of practitioners. Myofascial release’s roots lie in the concepts of Andrew Taylor Still, the founder of osteopathic medicine, and were subsequently developed further by the work of other osteopaths. Myofascial models began to gain more attention with the work of Janet Travell, MD, who discussed the presence of myofascial pain syndromes and trigger points. Myofascial release is a stretching technique that attempts to detect subtle restrictions within individual myofascial units. The goal is to facilitate maximum relaxation of tight or restricted tissues. According to the Myofascial Release Manual (C.J. Manheim, The Myofascial Release Manual 3rd edn, unpublished work), ‘the hands of the therapist continually search for areas of restricted tissue that impede efficient motion through feedback from the kinesthetic link with the patient.’ It also defines active myofascial trigger points as ‘specialized soft tissue restrictions that prevent smooth muscle contraction throughout the length of the muscle.’ One of the goals of myofascial release is to minimize or eliminate these restrictions. Few research articles about myofascial release have appeared in peer-reviewed journals. There continues to be debate between two philosophies: (1) that the muscles and trigger points themselves constitute a cause for chronic pain, and (2) that the pain located in the muscle region is referred pain from an underlying pathology of the disc or the zygapophyseal joint. If there is some underlying pathology, treatment of the soft tissue may temporarily relieve symptoms but would not create any lasting change in the condition. Bogduk states, ‘The questions that remain for practitioners in this field is when a patient is said to have a cervical trigger point, how valid is the diagnosis and how reliably has it been made?’12

Summary of manual therapy for neck pain ●

● ●

698

There are numerous methods of manual therapy available, and the most commonly used methods by physical therapists have been reviewed here. Manual therapy used in isolation does not have support in the literature. There is some support for manual therapy in combination with exercise.

●

Cervical manipulation carries some risks which has caused a few authors to advocate mobilization over manipulation.

PHYSICAL MODALITIES Clinical rationales for the use of physical modalities primarily encompass two areas. One theory is that the modality has some effect on the inflammatory and subsequent repair process. The other theory is that the modality provides a temporary modulation of pain by affecting central mechanisms of pain production. Modalities have most frequently been used in combination with or as a preparation for other treatments. Therapeutic modalities are not considered cures but as adjuncts to a comprehensive rehabilitation program. Many of the claimed effects of modalities are empirical, as none of the modalities has been shown to provide any long-term effects on pain or to accelerate or improve the healing process following injury. The Cochrane Back Group’s review of physical modalities concludes ‘all therapeutic modalities have not been studied in enough detail to adequately assess efficacy or effectiveness.’121 A key question remains with the application of any treatment modality. Is the modality solely palliative in nature or is it actually affecting the clinical course of the disorder? The goal of this chapter is to review the most commonly used modalities and their purported effects. As high-quality studies of modalities are few, their use for acute and chronic pain are considered together.

Thermal modalities Superficial heat has frequently been applied to musculoskeletal conditions using hot packs and wraps. Superficial heat can heat tissue to a depth of 2–3 cm.122 The physiologic effects of heat are a temporary increase in collagen extensibility, decreased joint stiffness, pain and muscle spasm relief, and increased blood flow. Some patients report temporary pain modulation with heat. Postulated mechanisms of relief are vasodilation with decreased ischemia-induced pain or flushing of pain mediators; endorphin-mediated response; or an alteration in cell membrane permeability.122 Heat is contraindicated with acute inflammation because of increased bleeding and edema formation. No study has shown that heat prior to the application of manual treatment or exercise improves outcomes. Ultrasound has been used for its thermal and nonthermal effects. Ultrasound is available in most physical therapy departments and one survey reports that most use it on a daily basis.123 Despite this, ultrasound remain unproven in management of neck pain or any other musculoskeletal disorder. For acute injuries, low-intensity pulsed ultrasound has been advocated for relief of inflammation, swelling reduction, acceleration of tissue repair, increased circulation, and scar modification.124 Evidence is lacking on whether any of these events actually occur. In an animal experiment, ultrasound was shown to have no antiinflammatory effect. Ultrasound is also used at higher intensities for thermal effects for tissues deeper than 2 cm. No studies were found that utilized ultrasound for acute neck pain, but studies utilizing ultrasound for acute musculoskeletal problems in the extremities do not support its use.123 Certain studies conclude that ultrasound may actually be harmful at high intensities within what has been considered the therapeutic range, causing vasoconstriction and increased histamine response and consequently producing more inflammatory exudates.124 As for chronic neck pain, one RCT comparing ultrasound to placebo for chronic myofascial trigger point neck pain found no difference in pain between the groups.125 Based on this study, the Philadelphia Panel7 reported that there was good scientific evidence that showed no benefit of therapeutic ultrasound as an intervention for chronic neck pain. They concluded that

Section 3: Cervical Spine

there is not enough evidence to include or exclude ultrasound as an intervention for chronic neck pain. Cold application via ice packs, ice massage, cold water immersion, and other various methods is another common adjunct to treatment. Cutaneous vasoconstriction follows icing and is indicated for acute musculoskeletal trauma. It has been shown to depress acute inflammation, which is beneficial, as too much inflammatory exudates promote large quantities of scar tissue. Cooling may also have a temporary pain-relieving effect by cutaneous counter-irritation, diminished nerve conduction, or reflex muscle relaxation.122 Other than for acute inflammation, ice has not been shown to have any long-term effect on treatment outcomes for acute or chronic neck pain.

Cervical traction Cervical traction may be administered by a variety of means. These include manual traction, mechanical motorized traction, or a variety of home cervical traction units used with an over-the-door pulley system or supine with weights or inflatable pumps that distract the joint surfaces. Traction is used intermittently and in a sustained fashion. The rationale for traction is that spinal elongation will increase the intervertebral space and relax spinal muscles. The proposed mechanisms of action have not been supported by research. The Philadelphia Panel for Evidenced-Based Guidelines for treatment of neck pain found four RCTs but excluded them all as methodological quality was poor. There has been one systematic review specifically of traction that concluded that the available studies of traction do not allow clear conclusions due to design flaws. The reviewers state that available evidence does not show the efficacy of traction but also does not show that traction is an ineffective therapy for neck pain.126 Anecdotally, it does appear in some specific cases of acute neck pain that manual traction helps facilitate movement in a patient who otherwise is having much difficulty regaining motion. The authors’ opinion is that traction applied in combination with manual technique may help facilitate restoration of movement in patients who have too much pain to gain motion independently. Traction followed by mechanically reductive forces appears to be the most beneficial. Some patients with acute neck pain present stuck in a forward head position and are in substantial pain and unable to move in any direction. Without the use of manual traction, it is usually virtually impossible to begin to regain motion. Manual traction alone or, if possible, followed by supine retraction and extension often can quickly help the patient restore a normal head position. If movement is unable to be attained, sustained traction in flexion may be helpful.

Electrotherapy Electrotherapy encompasses a variety of currents used for therapeutic purposes. Direct current is commonly used with topical antiinflammatory drugs to promote their resorption (iontophoresis). Alternating current or TENS is used for pain relief, utilizing the ‘gate control’ theory of inhibiting pain-related potentials at the spinal and supraspinal level. Alternating current is also used for muscle contraction and strengthening. Finally, pulsed electromagnetic fields (PEMF) is another form of electrotherapy used for pain control. One randomized, controlled trial comparing TENS to use of a collar and analgesics for acute neck pain found no significant difference in pain reduction between the two groups at 1 and 3 months.90 Overall, three systematic reviews all conclude that electrical stimulation modalities have little evidence of effectiveness and no evidence for more than a transient benefit.7,8,120 Electric stimulation for chronic pain could not be assessed due to a lack of controlled studies.

Pulsed electromagnetic therapy One study evaluated the effects of pulsed electromagnetic therapy (PEMT) on whiplash patients. The professed effects include vasodilation, increased oxygen partial pressure of tissue, increased rate of blood flow in capillaries, and increased polarization of cell membranes.121 Foley-Nolan et al.127 compared 6 weeks of wearing a soft collar with a PEMT unit to wearing a collar with a placebo unit. A significant shortterm reduction of pain was found in the PEMT group, but it disappeared by 12 weeks. The results are similar for chronic neck pain. Two high-quality studies128,129 compare PEMT to placebo for chronic neck pain, and both report better short-term pain relief with PEMT. There is no available information on long-term pain relief.

Percutaneous neuromodulation therapy Percutaneous neuromodulation therapy (PNT) combines TENS and electroacupuncture by using acupuncture-like needles positioned 2–4 cm into soft tissue. Patients then receive electrical stimulation that provides the maximum tolerable ‘tapping’ without producing muscle contractions130 to stimulate peripheral sensory nerves at the dermatomal levels corresponding to the local pathology. The exact mechanism of action remains unknown, but the proposed effects are that this type of stimulation may effect the neuronal feedback systems involved in the regulation and maintenance of pain. Proponents of this type of therapy hypothesize that it may be effective in treating pain resulting from central sensitization by activating large-diameter deep somatic afferents.131,132 Current ongoing, as yet unpublished, studies are focusing on whether those who are believed to have a diagnosis consistent with a centrally mediated pain source (myofascial pain or fibromyalgia) versus a diagnosis associated with a recurrent structural source (disc protrusion) have different outcomes with PNT. The difficulty with this theory is the controversy over whether myofascial pain is due to central mediation causing continuing pain or due to some underlying structural source that cannot be determined by conventional radiography causing referred pain. No published studies were found that measured the efficacy of this type of therapy for acute or chronic neck pain.

Acupuncture Acupuncture is a widespread complementary treatment for neck pain. Results from studies are contradictory and have not provided evidence for the efficacy of acupuncture in the treatment of acute or chronic neck pain. A systematic review performed in 1998, which did not separate acute and chronic neck pain, established that the outcomes of 14 randomized, controlled trials were equally balanced between positive and negative.133 Only eight were considered high quality and five of these were negative. These authors concluded that the evidence does not support the hypothesis that acupuncture is efficacious in the treatment of neck pain, but that further studies are justified. Another review of the literature134 concluded that there is strong evidence that acupuncture is not effective for treating chronic neck pain. Subsequent to both of these systematic reviews, a controlled trial on acupuncture for chronic neck pain was published.135 It compared nine sessions of acupuncture to nine sessions of sham acupuncture. Both the real and sham treatments significantly reduced pain at 16-weeks follow-up, without significant differences between the two.

Other physical modalities Both low-power laser and infrared light have been used with less frequency in treatment of acute neck pain, all without evidence of their benefit. Low-power laser has been advocated for pain control and soft tissue healing, but is not currently used in most rehabilitation 699

Part 3: Specific Disorders

Indeed, corticosteroid facet joint injections, corticosteroid transforaminal and intralaminar epidural injections, and facet ablation procedures may be considered as a type of therapeutic modality. A spine physical therapist, faced with a patient with limited range of motion and not responding to exercise or manual techniques, may suggest therapeutic injection treatment for this patient. Following the cervical injection procedures, the patient may be referred back to the therapist. The injections may have improved the chemical component to the pain, but many patients may continue to have pain of a mechanical nature. Approximately 2 weeks after an injection, a mechanical evaluation utilizing repeated movements may help determine if the patient is amenable to mechanical treatment. If a movement is found that lessens the pain, a patient may be taught to perform this movement as part of a home exercise program. Finite periods of manual therapy may be helpful to facilitate performance of the home exercise program. Furthermore, after a helpful injection,

clinics. The physiologic effects attributed, but not scientifically proven, to low-power laser include an acceleration of collagen synthesis, an increase in vascularization of healing tissue, and a decrease in microorganisms.136 No RCTs were found that address the use of lasers for patients with acute neck pain. Two RCTs exist that compare lasers to placebo for chronic neck pain.137,138 In the high-quality study the placebo group did better than laser. In the low-quality study the laser group did better than placebo. One small RCT compared infrared light with placebo with subacute neck pain and found no significant treatment effect.139

Therapeutic injections as a modality Although many clinicians use fluoroscopic facet joint injections and selective nerve root blocks as diagnostic procedures, most patients are interested in the therapeutic benefits of these procedures.

Acute/subacute neck pain

Mechanical assessment using repeated movements

Centralization or reduction of symptoms with repeated movements?

Yes

Treat with exercise in direction of movement that helped symptoms and posture correction

No Does there appear to be a significant chemical component?

Yes

No

Are symptoms fully abolished? Are manual techniques helpful?

MDP Yes

Recover function

No

Yes Range of motion

Strength

Yes

Yes

Improvement?

Is posture adequately maintained?

No Recovery of function

No

Are manual techniques helpful?

Return to mechanical assessment

Education/ taping

Consider flouroscopically guided corticosteroid injection

Fitness No

Yes Education for prevention of occurrence

Recover function

Helpful?

Is an antiinflammatory helpful?

Yes

Recover function Yes

No

No

Recovery of function within limits of symptoms

If symptoms continue past natural history, consider flouroscopically guided corticosteroid injection

Further intervention with spine physician

MDP

Recover function Yes

Recover function

700

No

No

Consider flouroscopically guided corticosteroid injection

Fig. 63.13 Algorithm for treatment of acute nontraumatic neck pain.

Section 3: Cervical Spine

specific exercises to address motor control deficits and improve the segmental stability of the spine may also decrease the chances of pain recurring once the patient returns to regular functional activities. Utilizing therapy in this fashion after an injection may also help the patient understand that injections in isolation are not the only intended treatment. Indeed, the injection is a tool to improve range of motion to allow the patient to participate more successfully in therapeutic exercise that may provide sustained relief.

●

● ●

●

SUMMARY This chapter has outlined the most commonly used treatment modalities for rehabilitation of neck pain. The authors have presented the available evidence and the conclusions from many systematic reviews relating to each method, and several summary algorithms pain (Figs 63.13–63.15). None of the available treatments for acute or chronic neck pain has been studied in enough detail to scientifically prove its benefit. Many treatments continue to be used despite evidence that they are not likely to be effective. Some overall conclusions emerge based on the evidence: ● All treatment methods need to be studied with more high-quality, trials.

●

● ● ●

There may be subgroups of patients who can be identified that respond best to different treatment approaches. Exercise has more support for its use than any other treatment modality. Exercise methods need to be studied in greater detail to determine what type and dosage is most effective. Evidence is emerging that exercises tailored to each individual patient, based on a sound evaluation of the patient’s condition, provide superior results to general exercise. Patients need guidance. Advice to stay active, in isolation from a complete management strategy, has been shown not to have much impact on pain and disability. Patients report more satisfaction with a multimodal treatment program including manual therapy and exercise, but manual therapy in isolation has not been shown to provide long-term benefits. Manual therapy includes many concepts of treatment. It would be beneficial to compare treatment approaches. Manual therapy should be applied within a larger treatment context of exercise and patient education. If modalities are used, it should be short term to enhance functional rehabilitation efforts and facilitate the patient’s response to active treatment.

Acute/traumatic neck pain

Rest/ice 24–48 hours

Start range of motion exercises within patient tolerance. Approximately 5 repetitions hourly

At 21 days, is the patient largely symptom free and fully recovered function ? Yes

Presenting with measurable acute posttraumatic stress

Perform mechanical asssessment using repetitive motions

Does patient need segmental stabilization exercises ?

Continue exercises as home exercise program

No

No

Yes

No

symptoms centralize ?

Yes

See tree 1 acute algorithm

No

Consider multiprofessional approach to management

Continue progressive mobility program

Progress to recovery of function as per acute/subacute algorithm

Return to mechanical assessment

And manual therapy if helpful

If symptoms continue consider flouroscopically guided corticosteroid injection or further treatment with spine physician

Fig. 63.14 Algorithm for treatment of acute traumatic neck pain. 701

Part 3: Specific Disorders Chronic neck pain

Mechanical assessment using repeated movements

Centralization or reduction of symptoms Yes

No

See acute/subacute algorithm − tree 1

Give patient option

1

Address potential central sensitization

Acupuncture

Pharmacology

2

3

Trial with manual techniques plus

Percutaneous neuro-modulation therapy

Segmental stabilization followed by general strengthening

Address chemical component

MDP

Or

Followed by 2 +/–1

Strengthening of central and scapulothoracic musculature

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Fig. 63.15 Algorithm for treatment of chronic neck pain.

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20. Vlaeyen WS. Behavioral analysis, fear of movement (re)injury and behavioral rehabilitation in chronic low back pain. In: Vleeming A, Mooney V, Tilsher H, et al., eds. 3rd Interdisciplinary World Congress on Low Back and Pelvic Pain. Vienna; 1998:57–68.

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113. Hoving JL, et al. Manual therapy, physical therapy, or continued care by a general practitioner for patients with neck pain. Ann Internal Med 2002; 136(10): 713–722. 114. Bronfort G, Haas M, Evans RL, et al. Efficacy of spinal manipulation and mobilization for low back pain and neck pain: a systematic review and best evidence synthesis. Spine J 2004; 4(3):335–356. 115. Ernst E. Manipulation of the cervical spine: a systematic review of case reports of serious adverse events, 1995–2001. MJA 2002; 176:376–380. 116. Haldeman S, Kohlbeck FJ, McGregor M. Unpredictability of cerebrovascular ischemia associated with cervical spine manipulation therapy. Spine 2002; 27: 49–55.

92. Hurwitz EL, Aker PD, Adams AH, et al. Manipulation and mobilization of the cervical spine: a systematic review of the literature. Spine 1996; 21:1746–1760.

117. Smith WS, Johnston SC, Skalabrin EJ, et al. Spinal manipulative therapy is an independent risk factor for vertebral artery dissection. Neurology 2003; 60(9): 1424–1428.

93. Gross AR, Kay TM, Kennedy C, et al. Clinical practice guideline on the use of manipulation or mobilization in the treatment of adults with mechanical neck disorders. Man Ther 2002; 7(4):193–205.

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SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ ii: Cervical Axial Pain

CHAPTER

Therapeutic Injections for the Treatment of Axial Neck Pain and Cervicogenic Headaches

64

Steven P. Cohen and Milan P. Stojanovic

INTRODUCTION The treatment of chronic neck pain remains one of the most challenging problems pain management specialists are confronted with. Defined as continuous pain persisting for more than 6 months, an estimated 16–22% of adults suffer from chronic neck pain, with the condition having a higher prevalence in women than men.1,2 Among patients with chronic neck pain, approximately 30% report a history of neck injury, which is most commonly the result of a motor vehicle accident.1 Although neck pain is by definition perceived in the region of the body bounded laterally by the lateral margins of the neck, superiorly by the superior nuchal line and inferiorly by a line transecting the T1 spinous process,3 this does not presuppose it is caused by pathology in this area. Pain in the neck may be referred from visceral and somatic structures in the thorax, or even extremities (Table 64.1). Similarly, pathology in the neck may lead to symptoms elsewhere in the body, such as a herniated cervical disc causing pain in an arm, or upper cervical spine disease causing pain in the occiput. The latter scenario is particularly relevant, as cervicogenic headaches affect 0.4–2.5% of the general population, and 15–20% of chronic headache sufferers.4 The first attempt at setting guidelines for the diagnosis of cervicogenic headache was made in 1990 by Sjaastad et al.5 Since then, the diagnostic criteria have been updated, with the major change being that an analgesic response to anesthetic blocks in the neck is now obligatory.6 Thus, this chapter focuses on the use of interventional blocks in the cervical spine to treat axial neck pain and cervicogenic headaches.

AO joint is flexion and extension in a sagittal plane (i.e. nodding of the head). While flexion at the AO joint is usually limited to around 10°, the degree of extension is considerably greater, approaching 25°.7 The range of motion in the anteroposterior plane is generally restricted to less than 20° rotation. The innervation of the AO joint is from the ventral ramus of C1, with the second dorsal cervical nerve supplying the AO synovial space.8,9

Mechanisms of injury Perhaps owing to the relative weight of the cranial contents and the stress induced by frequent movements of the head, atlanto-occipital mediated joint pain has been described in a variety of different inflammatory diseases including rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis.10,11 Trauma is another common cause of AO joint pain, with hyperextension of the skull, with or without damage to the tectorial membrane, being the proposed mechanism of action. Interestingly, restriction of normal articular motion is also hypothesized to result in pain emanating from the AO joint.12 Proposed etiologies of this type of injury include intra-articular adhesions, capsular scarring, and localized muscle hypertonicity.11

Clinical presentation The presentation of patients with AO joint pain is protean, with no known pathognomonic features.13 The International Headache Society’s (IHS) diagnostic criteria for cervicogenic headache include:6 ● ●

ATLANTO-OCCIPITAL JOINT BLOCKS Anatomy and function The first cervical vertebra, atlas, is unique in the sense that it possesses neither a body nor spinous process. It consists of an anterior and posterior arch extending between two lateral masses, forming a closed triangular ‘ring’ that accommodates the brainstem. Each lateral mass contains superior and inferior facets. Since no discs separate the atlas from adjacent bony structures, these facets function to connect C1 to the occiput above, and the axis below. The cranial articular surfaces are large and concave, articulating with the condyles of the occipital bone to form the two atlanto-occipital (AO) joints. The transverse processes of C1 are long, protruding structures containing triangular foramina, through which the vertebral arteries pass on their way to the brain. The posterior arch, devoid of a spinous process, lies deep beneath the skin, making manual palpation difficult. The articulations of the occipital-atlanto-axial complex are among the most complex in the human body. The primary function of the

● ● ●

Head and neck pain, with or without radiation into an extremity; Pain precipitated by neck movement, awkward head positioning, or external pressure over the upper cervical or occipital region; Unilaterality of pain; Pain described as moderate to severe, nonthrobbing, and nonlancinating; and Relief of pain by diagnostic anesthetic blocks.

According to the IHS, cervicogenic headaches tend to occur more frequently in females, are often accompanied by a history of trauma, and show a poor response to nonsteroidal antiinflammatory drugs and medications used to treat migraines, such as ‘triptans’ and ergotamine. Of import, the IHS criteria do not distinguish between the various pain generators involved in cervicogenic headaches. In a study assessing the response to lateral AO joint injections in five asymptomatic volunteers, Dreyfuss et al. found considerable variability in the provoked pain patterns, with the most inferior area of pain approximating the C5 vertebral level, and the most superior area extending almost to the vertex of the skull.8 In one patient, only temporal pain was produced. Most subjects tended to have pain limited to the upper neck and suboccipital regions. The induced pain was typically characterized as being ‘dull,’ ‘aching,’ or ‘pressure-like,’ and 707

Part 3: Specific Disorders

Table 64.1: Common and uncommon causes of neck pain Soft tissue injuries

INFECTIOUS Osteomyelitis

Cervical strain

Epidural abscess

Anterior scalene syndrome

Septic arthritis

Pectoralis minor syndrome

Discitis

Torticollis

Meningitis

Viral myalgia

Pharyngitis

Soft tissue calcium deposits and the 1st or 2nd cervical vertebrae

Tonsillitis Mumps, parotiditis

BONY PATHOLOGY Hyoid bone syndrome

Tuberculous spondylitis

Cervical rib

Lymphadenitis

Paget’s disease

VASCULAR

Ossification of the posterior longitudinal ligament or longus collis

Vertebral artery aneurysm Carotid body tumor

Diffuse idiopathic skeletal hyperostosis (DISH)

Inflamed thyroglossal duct Subclavian artery aneurysm

Fractures

REFERRED PAIN FROM THE THORAX

Spondylosis Esophageal pathology (esophagitis, inflamed diverticulum, etc.)

NEUROLOGIC Thoracic outlet syndrome

Thyroid pathology (thyroiditis, thyroid cystadenoma, etc.)

Nerve injuries

Mediastinal pain (pneumomediastinum, mediastinitis, etc.)

Myelopathy

Greater occipital neuralgia Radiculopathy

Angina

Syringomyelia

MALIGNANT

Arnold–Chiari malformation

Primary or metastatic tumors of the cervical spine Spinal cord tumors

Cervical acute herpes zoster or postherpetic neuralgia TRAUMATIC

Pancoast’s tumor

Epidural hematoma

Bronchial tumors

Dislocations

RHEUMATOLOGIC

Subluxation

Rheumatoid arthritis

Acute herniated disc

Osteoarthritis

Ligamentous injury

Ankylosing spondylitis Polymyalgia rheumatica

Cervical strain MISCELLANEOUS

Crystal arthropathies including gout

Branchial cleft remnant

Fibromyalgia

Psychogenic pain

MUSCLE AND OTHER SOFT TISSUE DISORDERS

Postural disorders Synovial cyst

Tendonitis

Temporomandibular disorder

Myofascial pain syndrome

unilateral in distribution. In a study by Fukui et al., whose aim was to determine the pain referral patterns for all levels of cervical zygapophyseal joint injections, in the 10 patients with neck and occipital pain who underwent lateral AO joint blocks, pain was referred into the ipsilateral upper posterolateral cervical region in all cases, and into the occipital area in 30% of patients.14 708

Outcome studies While it is widely acknowledged that the AO joint can be a source of head and/or axial neck pain, there is scant evidence to support the therapeutic use of intra-articular joint blocks. In a paper by Dreyfuss et al., they reported three patients with upper neck pain

Section 3: Cervical Spine

and/or occipital headaches who obtained complete relief after local anesthetic and steroid injections of the AO joints.15 In one patient, two injections were needed. However, in two of the patients, atlantoaxial (AA) and C2–3 injections were performed in addition to the AO injections. In the third patient, an AA joint injection was concurrently done. In an abstract by Busch and Wilson, the authors presented two patients who obtained significant pain relief following combined repeat AO and AA joint injections.16 The first patient was a 41-year-old male who presented with right occiput, neck, and jaw pain stemming from a waterskiing accident. This patient underwent three successive right-sided AO and AA joint injections with local anesthetic and steroid, each of which provided several weeks of dramatic pain relief and increased range of motion in his neck. He eventually underwent an occiput to C2 fusion, which resulted in 100% pain relief. The second patient was a 70-year-old woman with a long history of pain in the left side of the neck, head, and eye. Over the course of 2 years, she received multiple, bilateral AO and AA joint blocks with local anesthetic and steroid, each of which resulted in excellent pain relief. The patient refused surgical stabilization, preferring to continue treatment with repeat injections. Potential complications of AO blocks include epidural and intrathecal injection, intravascular injection into the adjacent venous plexus, vertebral artery or carotid artery, and brief periods of ataxia.

ATLANTOAXIAL JOINT BLOCKS Anatomy and function The most distinctive feature of the second cervical vertebra, axis, is the dens or odontoid process. It is a vertical conical structure containing two articular facets, one oriented anteriorly to link up with the anterior arch of the atlas (i.e. the median atlantoaxial joint), the other situated posteriorly, corresponding to the transverse atlantal ligament extending between the two lateral masses of C1. The median AA joint functions as a pivot: the atlas pivots around the dens, carrying the head with it. On the lateral sides of the dens are two transverse processes, with laterally inclined upper articular surfaces that connect to the lateral masses of the atlas (i.e. the lateral atlantoaxial joints). Together, these structures form the three AA joints, one of the most intricate articulation complexes in the human body. The AA complex provides the widest range of motion among all joints in the cervical spine. In the sagittal plane, the dens allows for 5–10° of flexion and 10° of extension. In the horizontal plane, the AA joint permits 60–90° rotation.17,18 Hence, pain arising from the AA joints is often exacerbated by turning of the head. The innervation of the AA joint is from the ventral ramus of C2.

Presentation Pain caused by AA arthropathy, like that for AO-mediated pain, is variable and inconsistent. Frequently, the AA joints are implicated in occipital pain radiating in the distribution of the greater occipital nerve (GON) because of the close proximity of the posterior branches of the C2 and C3 nerve roots, which join together to form the GON.19,20 Other articles have described AA joint pain as referred pain involving the medial branches of the C1–3 dorsal rami (the greater occipital and third occipital nerves for C2 and C3, respectively), and their convergence with trigeminal afferents in the trigeminocervical nucleus.18 This latter theory would explain studies implicating the AA joint in pain extending to the face.16 Consistent with the IHS criteria for cervicogenic headaches,6 in most studies on AA joint headache patients the pain tends to be unilateral.21 In the study by Dreyfuss et al. in which five asymptomatic volunteers were subjected to provocative injections of their AO and AA

joints, evoked pain patterns for AA injections were much more uniform than for C0–1 blocks.8 The pain area in these five subjects was located primarily lateral and slightly posterior to C1–2. In the cervical Z-joint pain referral study by Fukui et al., the pain was referred to the occipital region in 3 of the 10 patients with chronic neck and occipital pain who underwent provocative lateral AA joint injections, and to the upper posterolateral cervical region in 100% of these subjects.14 These findings are consistent with those of the Dreyfuss study in asymptomatic individuals.8

Outcome studies Even though there are many reports in the literature regarding the therapeutic benefit of AA joint blocks with steroid and local anesthetic for chronic neck and occipital pain, the conclusions that can be drawn regarding this procedure are limited by the absence of any randomized clinical trials. In a retrospective study by Glemarec et al., the authors injected a lateral AA joint in 32 patients with chronic neck pain, with or without radiation in the GON distribution.21 Twenty-six patients, receiving 36 joint injections, were available for follow-up. Eighteen of these patients reported relief following the injection, with the mean pain score improvement being 52.3% (range 0% to 100%). The average duration of pain relief was 13.1 months (range 3 days to 48 months). In this study, the authors found that both the degree and duration of pain relief were greater in patients with inflammatory disorders than in those with mechanical causes of cervicalgia. In a case series by McCormick, the author treated two patients with rheumatoid arthritis and four with osteoarthrosis with C1–2 injections using lidocaine and steroid.22 Five of the six patients obtained immediate pain relief, attributable to the local anesthetic. In three patients, pain relief lasted 3–7 months. In one patient, excellent pain relief was obtained for 2 weeks, after which the patient underwent a posterior fusion. In the patient who did not obtain pain relief, subsequent injection of the C2–3 facet joint resulted in excellent analgesia. The results of studies assessing AO and AA joint blocks as a treatment for neck pain are summarized in Table 64.2.

CERVICAL ZYGAPOPHYSEAL JOINT INJECTIONS Anatomy and function The cervical zygapophyseal joints (Z-joints) are true diarthrodial synovial joints, replete with a joint space, hyaline cartilage surfaces, a synovial membrane and fibrous capsule, that serve to connect adjacent vertebral bodies. The joints are inclined at roughly 45° from the horizontal plane and angled 85° from the sagittal plane. This alignment functions to prevent excessive anterior translation and assist the discs in weight-bearing. The C3–4 through C7–T1 facet joints each receive dual innervation from the medial branches of cervical posterior rami, one at the level of the joint itself and the other from the segmental level above. These nerves arise from the dorsal rami in the cervical intertransverse spaces, then wrap around the waists of their respective articular pillars where they can easily be anesthetized. The C2–3 facet joint differs somewhat in that its nerve supply derives from the C2 dorsal ramus and the third occipital nerve (TON), which is one of two medial branches from the C3 dorsal ramus. The TON is the larger and more superficial of the C3 medial branches. The medial branches of the cervical posterior rami differ from those in the lumbar spine in that their main function is to supply the cervical Z-joints, with only small, discrete branches innervating the posterior neck muscles. It therefore seems logical that using cervical medial branch blocks (MBB) as a diagnostic tool for cervical facet arthropathy would carry a lower false-positive rate than lumbar MBB, although this has not been studied. The density of mechanoreceptors 709

Part 3: Specific Disorders

Table 64. 2: Clinical evaluations of atlanto-occipital and atlantoaxial joint blocks First Author, Year

Type of Study

Number of Patients (pts)

Blocks Performed

Outcomes

Comments

McCormick 198722)

Case series

3 pts with RA and 3 with osteoarthrosis

Unilteral AA blocks with steroid & LA

Good to excellent pain relief ranging from 3–7 months.

1 pt who did not obtain good relief subsequently responded to C2–3 injection.

Chevrot 19959

Prospective observational study

100 pts with neck and/or occipital pain

AA blocks with steroid

Not designed to measure outcomes. In the pilot study involving 30 pts, 18 obtained clinical improvement lasting weeks to months.

Arthrographic abnormalities were seen in most pts with radiographic abnormalities.

Dreyfuss 199415

Case series

3 pts with upper neck pain and occipital H/A

AO, AA & in 2 pts, C2–3 blocks with steroid & LA

Complete pain relief lasting between 6 mon and 1 yr.

1 pt required 2 sets of injections, with the 2nd set of injections including periarticular infiltration.

Aprill 200223

Not mentioned

34 pts with neck pain and (sub) occipital H/A

Lateral AA blocks with steroid and LA

21 pts obtained complete temporary pain relief. Duration of relief not given.

Pts whose pain was exclusively cervical were less likely to respond to the injections than those whose symptoms extended into the occiput.

Lamer 199124

Case studies

2 pts with ear pain and C-spine DJD

Unilateral AA blocks with steroid and LA

In 1 pt, complete and sustained relief of pain and numbness. In the 2nd pt, significant pain relief obtained.

Periauricular numbness persisted in the 2nd pt.

Glemarec 200021

Retrospective study

26 pts with neck Lateral AA injection pain with or with steroid without radiation into occiput. 16 had a mechanical disorder and 10 an inflammatory disorder

18 pts obtained pain relief (mean 52%, range 0–100%). Mean duration of pain relief 13.1 mon (range 3 d to 48 mon).

Degree (79% vs 36%) and duration (17 mon vs 2.2 mon) of pain relief greater in inflammatory than mechanical group.

Busch 198916

Case studies

2 pts with neck and head pain

Unilateral (n=1) and B/L (n=1) AO and AA blocks with steroid and LA

Both pts obtained significant pain relief and improved range of motion.

1 pt underwent repeat injections every 2–4 mon when her pain returned, the other was pain-free after a C0–2 fusion.

Ehni 198425

Letter to the Editor

7 pts with unilateral suboccipital pain

Unilateral injection of LA and steroid

Relief lasting up to 1 month.

Injection technique or outcomes not discussed. One pt obtained relief from a C2 rhizotomy, another from fusion, and two from a combination of the two.

RA, rheumatoid arthritis; DJD, degenerative joint disease; H/A, headache; LA, local anesthetic.

in cervical facet joints is higher than that in the lumbar region.26 In one study, the most common levels for symptomatic cervical facet joints were C2–3 and C5–6.27

Mechanism of injury The most common cause of neck pain is whiplash injury. One of the earliest studies on this phenomenon was conducted by Severy et al., who subjected human volunteers to two rear-impact collisions at 13 kph and 15 kph, respectively.28 This seminal experiment demonstrated the importance of phasing differences between the vehicle and various body parts of the passenger during acceleration and deceleration as a source of injury. The peak acceleration of the vehicle preceded that of the torso, which in turn preceded that of the neck and head. This established that a critical element of whiplash 710

involved inertial loading of the neck, as the torso abruptly moved forward under an initially stationary head. In the early 1970s, Clemens and Burow performed a cadaveric study whereby 21 human corpses underwent 25 kph rear-end motor vehicle collisions with and without head rests.29 After the collisions, anatomical dissection was used to determine the site and extent of injuries. In the cadavers that underwent rear-end impacts without head rests, injuries to the cervical intervertebral discs were noted in 90% of cases, tears of the anterior longitudinal ligament in 80%, tears of the cervical Z-joint capsules were found in 40% of cadavers, and fractures of the vertebral bodies in 30%. In the cadavers protected by head rests, no injuries were found. Modern studies on the biomechanics of whiplash injury have focused on high-speed photography and cineradiography. In an eloquent review by Bogduk and Yoganandan, the authors conclude that

Section 3: Cervical Spine

instead of the articular processes of the cervical Z-joints gliding across one another, the inferior articular processes of the moving vertebrae chisel into the superior articular processes of their supporting vertebrae during whiplash-type injuries.30 The posterior compression within the facet joints occurs about 100 msec after impact. Although this hypothesis is supported by volunteer and cadaver studies, several questions remain unanswered. The main question remains: why some whiplash victims suffer no pain or pain that quickly disappears, whereas others proceed down the path of years and years of suffering. Other causes of cervical facet pain include sports injuries, work-related accidents, and wearing head gear.

Presentation and prevalence The main challenge in treating patients with cervical facet arthropathy in general, and whiplash in particular, is that no correlation has ever been established between symptoms and radiologic imaging. Consequently, the clinician must rely on other means to obtain a diagnosis. For lumbar facet arthropathy, recent studies have shown that there are no historical or physical examination findings that allow one to definitively identify the Z-joints as pain generators.31,32 This issue has not been adequately investigated in cervical pain, but at least one study has shown that a thorough physical examination can accurately diagnose the presence or absence of cervical Z-joint pain, and the level of involvement, as determined by diagnostic blocks.33 Signs of possible facet-mediated pain include limited range of motion, tenderness to palpation, and pain during intervertebral movement. Clinical studies have been conducted in both normal volunteers and patients with suspected cervical facet pain to determine pain referral pattern from the joints.14,34,35 The results of these experiments are strikingly consistent. From C2–3, the pain pattern generally extends rostrally to the upper cervical region and suboccipital area. Infrequently, symptoms will extend towards the ear or further up the scalp. From C3–4, pain is referred to the upper and middle posterior neck, with occasional radiation into the lower occiput. From C4–5, the most common referral pattern is into the lower posterior cervical region, although in a significant percentage of people it extends into the middle posterior neck and suprascapular region. Pain from C5–6 is typically distributed to either the suprascapular region or lower neck, but can sometimes extend to the shoulder joint or midposterior neck. From C6–7, pain is usually referred into the upper scapula or lower neck. Pain from the C7–T1 Z-joint most frequently extends further down into the midscapula area. There have been several studies done to determine the prevalence of cervical facet joint pain. In a retrospective study involving 318 patients with intractable neck pain who underwent cervical Z-joint blocks, provocative discography, or both, Aprill and Bogduk made a definite diagnosis of cervical facet pain in 25% of patients, while noting that another 38% of patients may have suffered from cervical Z-joint pain but were not appropriately investigated.36 Overall, 64% of the 128 patients who underwent single, intra-articular facet injections obtained significant pain relief. Bogduk’s group from Newcastle, Australia, conducted two double-blind, controlled trials in the mid-1990s assessing the prevalence of cervical Z-joint pain in whiplash patients.27,37 In the first study, painful facet joints as determined by definite or complete pain relief using confirmatory MBB with lidocaine and bupivacaine were found in 54% of the 50 study subjects.27 In a later study, Lord et al. used three blocks to make a diagnosis of cervical Z-joint pain in the 68 study patients – confirmatory double blocks with lidocaine and bupivacaine, coupled with a negative response to placebo injections.37 In this paper, the overall prevalence of cervical facet pain was found to be 60%.

Outcomes for intra-articular injections As is the case for lumbar Z-joint blocks, the International Spinal Injection Society (ISIS) advocates controlled diagnostic blocks as the only definitive means of diagnosing cervical facet joint pain.38 For diagnostic purposes, medial branch blocks have been shown to be as accurate as intra-articular injections provided contrast is used to prevent venous uptake. Due to the high incidence of false-positive blocks,39,40 ISIS recommends using either confirmatory blocks or placebo-controlled injections in order to increase the specificity.38 Although previous uncontrolled studies have reported prolonged pain relief from cervical facet blocks using steroid and local anesthetic,41,42 a double-blind, placebo-controlled study by Barnsley et al. failed to demonstrate a beneficial effect for intra-articular corticosteroids.43 In patients who respond to diagnostic intra-articular or medial branch blocks, radiofrequency denervation of these nerves has been shown in several uncontrolled44–48 and one placebo-controlled study49 to provide effective long-term pain relief. Radiofrequency procedures are discussed in detail in elsewhere within this book.

THIRD OCCIPITAL NERVE BLOCKS One of the putative causes of headache and upper neck pain is osteoarthritis of or injury to the C2–3 zygapophyseal joint. Because pain from this facet joint is largely mediated through the third occipital nerve (TON), these headaches are often referred to as third occipital nerve headaches.50 In a prevalence study involving chronic neck pain in 100 patients following whiplash injury, Lord et al. found approximately 27% suffered from TON headache.51 The criteria for the diagnosis of TON headache in this study was complete eradication of head pain with two consecutive TON blocks done with lidocaine and bupivacaine, with the bupivacaine blocks providing longer pain relief than the lidocaine blocks. Of the 27 subjects diagnosed with TON headache, headache was the predominant complaint in 21 patients, and neck pain was the main complaint in 6. The C2–3 facet joint is innervated by the third occipital nerve, the larger and more superficial of the two medial braches of the C3 dorsal ramus, and the C2 dorsal ramus. The C2–3 Z-joint may be particularly prone to injury in that it represents a transition zone between the atlantoaxial joint which accommodates rotation of the head, and the lower cervical spine which promotes flexion and extension of the neck. The history and physical examination are relatively non-specific in the diagnosis of third occipital neuralgia. Patients typically present with occipital headaches and neck pain, often after whiplash injury. Tenderness overlying the C2–3 facet joint may be the only sign suggesting this disorder.51 Third occipital nerve blocks have been advocated as the most reliable screening tool for headaches mediated by the TON.50,51 Nerve blocks performed with local anesthetics and steroids may provide prolonged pain relief in some patients, though this is unreliable. Radiofrequency denervation of the third occipital nerve is the best treatment option for patients who experience short-term pain relief with diagnostic injections. However, the one study that specifically addressed TON radiofrequency neurotomy in C2–3 Z-joint pain found a high failure rate.48 Ataxia is the main side effect of this procedure.

CONCLUSIONS Despite its prevalence and the high toll it exacts on society, neck pain remains poorly understood, inadequately diagnosed, and extremely difficult to treat. In an attempt to alleviate the suffering of patients with neck pain, many clinicians turn to nerve blocks. Ideally, these blocks should be performed in the context of a multidisciplinary 711

Part 3: Specific Disorders

approach to therapy, which includes functional restoration, pharmacological treatment and, when indicated, alternative approaches to pain management. What is most surprising is how little research has been completed to understand the mechanisms underlying disorders causing neck pain. It is also striking that there is little evidence to support the use of many nerve blocks that are routinely done to treat neck pain. Presently, the primary use of nerve blocks in axial neck pain is for diagnostic purposes. Except for one placebo-controlled trial published in 1996 showing efficacy for radiofrequency denervation in the treatment of cervical zygapophyseal joint pain, the evidence supporting the other treatments outlined in this chapter is anecdotal. It is imperative that further research be done, both preclinically to help elucidate the mechanisms behind the various causes of neck pain, and clinically to justify specific treatments.

23. Aprill C, Axinn MJ, Bogduk N. Occipital headaches stemming from the lateral atlanto-axial (C1–2) joint. Cephalagia 2002; 22:15–22.

References

30. Bogduk N, Yoganandan Y. Biomechanics of the cervical spine Part 3: minor injuries. Clin Biomech 2001; 16: 267–275.

1. Guez M, Hildingsson C, Stegmayr B, et al. Chronic neck pain of traumatic and nontraumatic origin: a population-based study. Acta Orthop Scand 2003; 74 576–579. 2. Guez M, Hildingsson C, Nilsson M, et al. The prevalence of neck pain: a populationbased study from northern Sweden. Acta Orthop Scand 2002; 73:455–459. 3. Merksey H, Bogduk N. Classification of chronic pain. Descriptions of chronic pain syndromes and definition of pain terms. 2nd edn. Seattle: IASP Press; 1994:103–111. 4. Haldeman S, Dagenais S. Cervicogenic headaches: a critical review. Spine J 2001; 1:31–46. 5. Sjaastad O, Fredriksen TA, Pfaffenrath V. Cervicogenic headache: diagnostic criteria. Headache 1990; 30:725–726. 6. Sjaastad O, Fredriksen TA, Pfaffenrath V. Cervicogenic headache: diagnostic criteria. Headache 1998; 38:442–445. 7. Racz GB, Sanel H, Diede JH. Atlanto-occipital and atlantoaxial injections in the treatment of headache and neck pain. In: Waldman SD, Winnie AP, eds. Interventional pain management. Philadelphia: WB Saunders; 1996:219–222. 8. Dreyfuss P, Michaelsen M, Fletcher D. Atlanto-occipital and lateral atlanto-axial joint pain patterns. Spine 1994; 19:1125–1131. 9. Chevrot A, Cermakova E, Vallee C, et al. C1–2 arthrography. Skeletal Radiol 1995; 24:425–429. 10. Santavirta S, Konttinen YT, Lindqvist C, et al. Occipital headache in rheumatoid cervical facet joint arthritis. Lancet 1986; 20:695. 11. Bogduk N, Corrigan B, Kelly P, et al. Cervical headache. Aust Med J 1985; 143: 202–207. 12. Vernon H. Spinal manipulation and headaches of cervical origin. J Manual Med 1991; 6:73–79. 13. Bogduk N. The anatomy and pathophysiology of neck pain. Phys Med Rehabil Clin N Am 2003; 14:455–472.

25. Ehni G, Benner B. Occipital neuralgia and C1–2 arthrosis. N Engl J Med 1984; 310:127. 26. Bogduk N, Twomey L. Clinical anatomy of the lumbar spine. 2nd edn. New York: Churchill Livingstone; 1991. 27. Barnsley L, Lord SM, Wallis BJ, et al. The prevalence of chronic cervical zygapophyseal joint pain after whiplash. Spine 1995; 20 20–26. 28. Severy DM, Mathewson JH, Bechtol CO. Controlled automobile rear-end collisions, an investigation of related engineering and medical phenomena. Can Serv Med J 1955; 11:727–759. 29. Clemens JH, Burrow K. Experimental investigation on injury mechanisms of cervical spine at frontal and rear-frontal vehicle impacts. In: Proceedings of the 16th Stapp Car Crash Conference, Detroit, MI, 1972: 76–104.

31. Jackson RP, Jacobs RR, Montesano PX. Facet joint injections in low back pain: a prospective statistical study. Spine 1988; 13:966–971. 32. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–1137. 33. Jull G, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygapophyseal joint pain syndromes. Med J Aust 1988; 148:233–236. 34. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns I: a study in normal volunteers. Spine 1990; 15:453–457. 35. Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal joint pain patterns II: a clinical evaluation. Spine 1990; 15:458–461. 36. Aprill C, Bogduk N. The prevalence of cervical zygapophyseal joint pain. A first approximation. Spine 1992; 17:744–747. 37. Lord SM, Barnsley L, Wallis BJ, et al. Chronic zygapophyseal joint pain after whiplash: a placebo-controlled prevalence study. Spine 1996; 21:1737–1744. 38. Bogduk N. International Spinal Injection Society guidelines for the performance of spinal injection procedures. Part I: zygapophyseal joint blocks. Clin J Pain 1997; 13:285–302. 39. Barnsley L, Lord SM, Wallis BJ, et al. False-positive rates of cervical zygapophyseal joint blocks. Clin J Pain 1993; 9:124–130. 40. Barnsley L, Lord S, Bogduk N. Comparative local anesthetic blocks in the diagnosis of cervical zygapophyseal joint pain. Pain 1993; 55:99–106. 41. Roy DF, Fleury J, Fontaine SB, et al. Clinical evaluation of cervical facet joint infiltration. J Can Assoc Radiol 1988; 39:118–120. 42. Slipman CW, Lipetz JS, Plastaras CT, et al. Therapeutic zygapophyseal joint injections for headaches emanating from the C2–3 joint. Am J Phys Med Rehabil 2001; 80:182–188.

14. Fukui S, Ohseto K, Shiotani M, et al. Referred pain distribution of the cervical zygapophyseal joints and cervical dorsal rami. Pain 1996; 68:79–83.

43. Barnsley L, Lord SM, Wallis BJ, et al. Lack of effect of intraarticular corticosteroids for chronic pain in the cervical zygapophyseal joints. N Engl J Med 1994; 330:1047– 1050.

15. Dreyfuss P, Rogers J, Dreyer S, et al. Atlanto-occipital joint pain: a report of three cases and description of an intraarticular joint block technique. Reg Anesth 1994; 19:344–351.

44. Schaerer JP. Radiofrequency facet denervation in the treatment of persistent headache associated with chronic neck pain. J Neurol Orthop Surg 1980; 1:127–130.

16. Busch E, Wilson PR. Atlanto-occipital and atlanto-axial injections in the treatment of headache and neck pain. Reg Anesth 1989; 14 (Suppl 2):45. 17. Jofe M, White A, Panjabi M. Clinically relevant kinematics of the cervical spine. In: Sherk H, Dunn E, Eismont F, et al, eds. The cervical spine. 2nd edn. Philadelphia: JB Lippincott; 1989:57–69. 18. Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine 1982; 7: 319–330. 19. Bogduk N. The anatomy of occipital neuralgia. Clin Exp Neurol 1981; 170: 167–184. 20. Lazorthes G. Les branches posterieures des nerfs rachidiens et le plan articulaire vertebral posterieur. Ann Med Phys 1972; 25:193–202 (in French). 21. Glemarec J, Guillot P, Laborie Y, et al. Intraarticular glucocorticoid injection in the lateral atlantoaxial joint under fluoroscopic control. Joint Bone Spine 2000; 67: 54–61. 22. Mccormick CC. Arthrography of the atlanto-axial (C1–C2 joints): techniques and results. J Intervent Radiol 1987; 2:9–13.

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24. Lamer TJ. Ear pain due to cervical spine arthritis: treatment with cervical facet injection. Headache 1991; 31:682–683.

45. Sluijter ME, Koetsveld-Baart CC. Interruption of pain pathways in the treatment of the cervical syndrome. Anaesthesia 1980; 35:302–307. 46. van Suijekom HA, van Kleef M, Barendse GAet al. Radiofrequency cervical zygapophyseal joint neurotomy for cervicogenic headache: a prospective study of 15 patients. Funct Neurol 1998; 13:297–303. 47. Sapir DA, Gorup JM. Radiofrequency medial branch neurotomy in litigant and nonlitigant patients with cervical whiplash. A prospective study. Spine 2001; 26: E268–E273. 48. Lord SM, Barnsley L, Bogduk N. Percutaneous radiofrequency neurotomy in the treatment of cervical zygapophyseal joint pain: a caution. Neurosurgery 1995; 36:732–9. 49. Lord SM, Barnsley L, Wallis BJ, et al. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med 1996; 335:1721–1726. 50. Bogduk N. Marsland A. On the concept of third occipital headache. J Neurol Neurosurg Psychiatry 1986; 49:775–780. 51. Lord SM. Barnsley L. Wallis BJ, et al. Third occipital nerve headache: a prevalence study. J Neurol Neurosurg Psychiatry 1994; 57:1187–1190

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ ii: Cervical Axial Pain

CHAPTER

Sympathetic System

65

Sara Haspeslagh and Maarten Van Kleef

STELLATE GANGLION BLOCK Clinical syndrome ‘Sympathetically maintained pain’ is defined as ‘pain that is maintained by sympathetic efferent innervation or by circulating catecholamines (especially norepinephrine).’1 This presents an assumed pain mechanism, not a clinical syndrome, and therefore it can be present in different pain syndromes. The most common places where it occurs are the extremities and the face. Disturbances in the mechanism of the sympathetic system of the face and the upper extremity can give the following symptoms: swelling, hyperhidrosis, disturbances in the temperature regulation of the skin, and changes in skin coloring. There are several diseases and syndromes that can show disturbances in the sympathetic innervation. One example is the complex regional pain syndrome type 1 (CRPS-1) that is characterized by continuing pain after an initiating noxious event or after an immobilization, allodynia, or hyperalgesia with which the pain is disproportionate to any inciting event.2 There is a growing controversy on the value of sympathetic blocks in CRPS-1 and 2. A recent review raises questions on the efficacy of local anesthetic sympathetic blockade as a treatment of CRPS. In this review it was concluded that less than one-third of patients involved in trials obtained full pain relief.3 Further studies are needed to clarify this indication. Furthermore, there is typically evidence of edema, alteration in skin blood flow or abnormal pseudomotor activity in the part of the body the pain is experienced. In all instances, other potential diagnoses that can mimic the symptoms of CRPS must be excluded.

Indications and contraindications Indications for the performance of a stellate ganglion block with local anesthetic are similar to those for recommending radiofrequency (RF) lesioning. These include: 1. Chronic pain syndromes in the facial and/or cervicobrachial region in which the sympathetic system is hypothesized to be involved (as denoted by symptoms of swelling, cyanosis, changed warmth/cold sensations and/or hyperhidrosis);4,5 2. Vascular diseases, e.g. Raynaud’s disease, arterial embolism in the area of the arm, preoperatively before vascular surgery in the upper extremity; 3. Acute herpes zoster of the face and/or the lower cervical and upper thoracic dermatomes; 4. CRPS type 1 and causalgia (CRPS type 2) of the upper extremity; 5. Failed neck surgery syndrome with a CRPS-like condition; and 6. Some atypical facial pain states and post-traumatic headaches.6 Contraindications to perform a stellate ganglion blockade include: anticoagulant therapy or coagulation disorders (since the needle is

inserted near important vascular structures such as the carotid artery, and an inadvertent vascular puncture is possible); local infection in the overlying soft tissue or systemic infection; recent cardiac infarction; marked impairment of the cardiac stimulus conduction, since a stellate ganglion block blocks the cardiac acceleration nerves (the sympathetic fibers of T1 to T4) creating a risk of intractable bradycardia; and contralateral pneumothorax or pneumonectomy, since a known complication of the stellate ganglion block is pneumothorax. A relative contraindication is glaucoma since repeated stellate ganglion blocks can provoke glaucoma.

Side effects and complications Side effects of a stellate ganglion block are temporary ipsilateral Horner’s syndrome (miosis, ptosis, and enophtalmia), conjunctival injection, nasal congestion, and facial anhidrosis. Furthermore, temperature differences between the blocked arm and the contralateral arm (raised skin temperature in the ipsilateral arm) and visible engorgement of the veins on the ipsilateral hand and forearm can occur. Each of these alterations provides proof that the sympathetic system is blocked. In this fashion, an accurate assessment about the response to a diagnostic block can be made. One of the most serious complications can occur if there is an unintentional injection involving the vertebral and/or the carotid artery,7 as seizures that are difficult to treat will result. Accidental injection intrathecally will lead to respiratory failure and the requirement of mechanical ventilation.8–11 In anticipation of these potential complications, it is advised that an intravenous line be in place prior to the blockade. A less serious but quite disconcerting side effect results from inadvertent diffusion of local anesthetics into nearby nerve structures. In particular, blockade of the recurrent laryngeal nerve typically results in hoarseness, the sensation of a mass in the throat, and sometimes a subjective shortness of breath. Of course, this complication can be dangerous when the blockade has been performed bilaterally in patients with preprocedural respiratory impairment.12 In other instances, a partial blockade of the brachial plexus with temporary paralysis of arm musculature can result.13 If the phrenic nerve is blocked, a temporary unilateral paralysis of the diaphragm transpires with resultant respiratory impairment.14 Another complication that can lead to respiratory impairment occurs when the apex of the lung is pierced and a pneumothorax ensues. This is more likely to occur if an anterior technique at the C7 level is used as compared to other approaches.

Outcomes There are only a handful of published studies regarding the efficacy of a stellate ganglion block. In 1983, Bonelli et al. performed a randomized, controlled trial in patients with reflex sympathetic 713

Part 3: Specific Disorders

dystrophy (RSD) of the upper extremity in which they compared the efficacy of stellate ganglion block using 15 ml bupivacaine 0.5%, up to a total of eight blocks, with treatment by a regional intravenous sympathetic block using 20 mg guanethidine every 4 days up to a total of four blocks.15 They concluded that there was a significant improvement in the visual analogue scale (VAS), skin temperature, and skin plethysmography as compared to baseline. There were no significant baseline differences between the two groups. Malmqvist et al. published a randomized controlled trial in 1992 which assessed the efficacy of stellate ganglion blocks using different concentrations and volumes of local anesthetic and different sites of injection.16 They called the sympathetic block ‘complete’ if the following five criteria were met: the presence of a change in skin temperature, skin blood flow, resistance response and skin resistance level, and the symptoms of Horner’s syndrome. They concluded that it is difficult to perform a block that meets all the five criteria since only six of the 54 blocks met all five criteria. They claimed that injection toward C7 (instead of injection toward C6) and a high concentration were more likely to achieve a successful block. The volume seemed of less importance. There has been only one study performed addressing RF lesioning of the stellate ganglion for the treatment of pain in the upper extremity caused by RSD.17 It was a poorly designed retrospective study. In 1998, Price et al. published a study with a small number of participants in which they compared the efficacy of a sympathetic ganglion block using 1% lidocaine/bupivacaine and a block with normal saline in patients with CRPS-1 using a double-blinded, cross-over paradigm.18 Four of the seven patients received a stellate ganglion block, and three received a lumbar sympathetic block. In both the local anesthetic group and the saline group there was a large reduction in pain relief accompanied by the reversal of mechanical allodynia 30 minutes after the block in six in of the seven patients. There was no significant difference in the initial peak reduction between the groups. The mean duration of pain relief was significantly longer in the local anesthetic group. The authors concluded that both magnitude and duration of pain relief should be closely monitored to provide optimal efficacy in procedures that use local anesthetics to treat CRPS. Forouzanfar et al. published a retrospective study in 2000 in which they reviewed 86 stellate ganglion RF ablation procedures used in different chronic pain syndromes.19 They concluded that this technique is most likely to benefit patients suffering from CRPS-2, ischemic pain, cervicobrachialgia, or post-thoracotomy pain. They emphasized that the clinical efficacy of this technique still remains to be proven in a randomized, controlled trial.

THORACIC SYMPATHETIC BLOCK Clinical syndrome Sympathetic fibers provide innervation to the vasculature, sweat glands, and pilomotor muscles of the skin. This is why disturbances in the coloring and temperature regulation of the skin as well as in the sweating of the skin can be observed in syndromes with a dysregulation of the sympathetic system. The cardiac plexus receives sympathetic innervation via the T1–4 nerves (acceleration nerves) and blocking of these nerves causes bradycardia. The abdominal viscera get their sympathetic innervation via the splanchnic sympathetic nerves (T5–12), from the celiac ganglion. Pain emanating from the upper abdomen can be sympathetically mediated via the celiac plexus. The aortic plexus consists of the aorticorenal ganglion and the superior and the inferior mesenteric ganglia (coming from fibers from T12–L2) and provides sympathetic fibers to different lower abdominal viscera. 714

Indications and contraindications Indications to perform a thoracic sympathetic block are: 1. Sympathetically mediated pain of the upper thorax, chest wall and the thoracic, and upper abdominal viscera; 2. Hyperhidrosis, especially palmar hyperhidrosis; 3. Intractable cardiac arrhythmia,20,21 cardiac angina (Prinzmetal’s vasospastic angina pectoris),22–24 and abdominal angina; 4. Acute (e.g. acute vascular occlusions) or chronic vascular diseases (e.g. Raynaud’s disease);25,26 5. CRPS type 1 and causalgia (CRPS type 2) of the upper extremity; 6. Post-thoracotomy pain; 7. Acute herpes zoster; 8. Postherpetic neuralgia; and 9. Phantom breast pain after mastectomy. Contraindications to performing a percutaneous thoracic sympathectomy are similar to those for a cervical sympathectomy with the addition of extensive hyperhidrosis as a relative contraindication. In this instance, it has been shown to carry a greater risk of severe compensatory hyperhidrosis.27

Side effects and complications Side effects include excessive hand dryness and/or excessive facial drying after a T2 and T3 lesion. Another side effect of these high thoracic lesions can be a (lasting), partial Horner’s syndrome. The most common complication of this technique is causing a pneumothorax. Therefore, a postoperative chest radiograph is recommended. Furthermore, there is the possibility of a self-limited intercostal neuritis. In a study performed by Wilkinson, this seemed to occur when a new technique that was developed in 1988 was employed. With this technique, three RF lesions were made rostrocaudally at each ganglion site under neuroleptanalgesia with superficial local anesthesia.27

Outcomes In 1996, Wilkinson published a study in which he performed 148 percutaneous radiofrequency sympathectomies in 110 patients.27 The patient population treated was diagnosed with a variety of syndromes including hyperhidrosis, vascular occlusion, Raynaud’s disease or other chronic vasculopathies, painful causalgia or reflex dystrophy or Prinzmetal’s angina. In 27 of the 110 patients a failure and major recurrence of sympathetic activity occurred over the 15 years of follow-up. He ‘improved’ his technique twice during the 15 years and noticed that the four severe recurrences of the sympathetic activity occurred by using the first two techniques. Most of the patients with recurrence requested a subsequent RF procedure and cited the simplicity and the limited discomfort of this procedure. The incidence of a pneumothorax was 24% (6 out of 247 procedures). Raj et al. reviewed retrospective data on 110 T2 and T3 sympathectomies performed in 27 patients with different syndromes including CRPS-1 of the upper extremity, brachial plexus injury, postmedication neuritis of the brachial plexus, phantom limb pain, deafferentation pain after dorsal root entry zone lesioning, and chest wall pain.28 They reported an incidence of pneumothorax of 1.82% (2 out of 110 procedures). They did not report the efficacy of the procedure.

LUMBAR SYMPATHETIC BLOCK Clinical syndrome Pain in the lower abdominal region, pelvic region, or the lower extremities can be mediated by sympathetic hyperactivity. The clinical symptoms of disturbances in the sympathetic system as described in the cervical subsection pertain here.

Section 3: Cervical Spine

Indications and contraindications Indications include: 1. Ischemic pain and circulatory insufficiency of the lower extremity, e.g. Raynaud’s disease, arteriosclerosis of the vessels of the leg, and Buerger’s disease; 2. CRPS-I or -2 of the leg, phantom pain, and postamputation residual limb pain; 3. Hyperhidrosis; and 4. Pain syndromes of the viscera of the lower abdomen or of the pelvis (e.g. urogenital pain). Contraindications to performing the lumbar sympathetic block are coagulation disorders or intake of anticoagulants, local infection, or systemic infection.

Side effects and complications Side effects after the lumbar sympathetic blocks with local anesthetics are: vasodilatation (engorgement of the veins), increased temperature, and reduction of edema. These are all signs of a good block. An annoying side effect for the patient is the possibility of postoperative paravertebral muscle spasms and backache. An important complication is neuralgia of the genitofemoral nerve, especially following chemical sympathicolysis.29,30 This complication is less common when performing an RF lesioning technique. This diminished probability is due to the technique used. The position of the needle is checked with contrast dye (no spread of dye should be observed lateral of the contours of the vertebra) and an electrical stimulation test is performed before definitive lesioning. When the needle is placed too laterally or posteriorly, a block of the genitofemoral nerve or the lumbar plexus within the psoas muscle may occur. The possibility of intravascular or subarachnoid injection is low when the correct technique is followed. The use of contrast and real-time imaging is recommended to avoid this complication.

Outcomes Several retrospective studies have been performed to determine the efficacy of RF denervation of the lumbar sympathetic chain in peripheral vascular disease and ischemic pain. In 1991, Dominkus et al. published a study of 30 patients with inoperable diabetic angiopathies treated with percutaneous RF thermolesion of the lumbar sympathetic chain (PRFS).31 They reported good results when compared to surgical sympathectomy. The relevant outcome measure was that the percentage of patients requiring amputation by 2 years. They conclude that the PRFS is a good alternative to surgical sympathectomy, as there is no need for general anesthesia. We should point out that the convalescence is dramatically easier with RF lesioning as compared to an open surgical sympathectomy. That same year, Haynsworth and Noe compared chemical lysis of the lumbar sympathetic chain with phenol to RF denervation.32 They found that 89% of patients in the phenol group showed signs of sympathetic blockade at 8 weeks, while this was observed in only 12% of the RF group. They conclude that although the incidence of postsympathetic neuralgia seemed to be less with RF denervation, further refinement of needle placement to ensure complete lesioning of the sympathetic chain will be required before the technique can offer an advantage over the phenol technique. A few years later, Noe and Haynsworth presented a modified technique of lumbar RF sympatholysis and compared it with the results of chemical sympatholysis.33 In 1995, Rocco reported a clinical trial in which patients with sympathetically mediated pain who previously responded to sympathectomy or sympathetic blocks were treated with lumbar RF sympatholysis.34 He concluded that long-lasting pain relief was difficult to obtain after a single treatment

with RF sympatholysis in patients with sympathetically maintained pain. In 2002, Cepeda et al. published a meta-analysis in which they evaluated the efficacy of lumbar sympathetic blocks with local anesthetics in the treatment of complex regional pain syndromes.3 They concluded that approximately 30% of patients obtained full pain relief. But they correctly stated that this efficacy is mainly based on case series without a control group. Thus, there is an overestimation of the treatment response. To date, no studies concerning the use of RF denervation of the lumbar sympathetic chain for patients with a proven diagnosis CRPS have been published.

References 1. Stanton-Hicks M, Janig W, Hassenbusch S. Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain 1995; 63:127–133. 2. Merksey H, Bogduk N. Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms. 2nd edn. 1994, Seattle. 3. Cepeda M, Lau J, Carr D. Defining the therapeutic role of local anesthetic sympathetic blockade in complex regional pain syndrome: a narrative and systematic review. Clin J Pain 2002;18(4):216–233. 4. Rauchfuss V, Bohland W, Sauer D. Stellate block in diseases in the area of the upper limb. Zbl Chir 1971; 54(5):567–570. 5. Carron H, Litwiller R. Stellate ganglion block. Anesth Analg 1975; 54(5):567–570. 6. Sluijter M. Chapter 7: Sympathetic blocks in the cervical region. Meggen (LU), Switzerland: Flivopress SA; 2003. 7. Ellis J, Ramamurthy S. Seizure following stellate ganglion block after negative aspiration and test dose. Anesthesiology 1986; 64:533–534. 8. Bruyns T, Devulder J, Vermeulen H, et al. Possible inadvertent subdural block following attempted stellate ganglion blockade. 1991; 46:747–749. 9. Stannard C, Glynn C, Smith S. Dural puncture during attempted stellate ganglion block. Anaesthesia 1990; 54:952–954. 10. Ono H, Mochizuki K, Matsumoto T. A rare complication of stellate ganglion block – high spinal anesthesia caused by an inadvertent subarachnoid injection. Masui 1975; 24(4):386–390. 11. Maritano M, Marchisio O, Zaccagna C, et al. High subarachnoid (C5–C6) anesthetic block as a complication of stellate ganglion infiltration. Description of a case. Minerva Anesthesiol 1968; 34(5):594–598. 12. Scott D, Ghia J, Teeple E. Aphasia and hemiparesis following stellate ganglion block. Anesth Analg 1993; 62:1038–1040. 13. Stohr M, Mayer K, Petruch F. Armplexusparese nach stellatum blockade und plexusanasthesie. Dtsh med Wschr 1978; 103:68–70. 14. Sawyer R, Turnbull D, Richemond M, et al. Assessment of diaphragm function after stellate ganglion block using magnetic stimulation. Anaesthesia 2002; 57(1):70–76. 15. Bonelli S, Conoscente F, Movilia P, et al. Regional intravenous guanethidine vs. stellate ganglion block in reflex sympathetic dystrophies: a randomized trial. Pain 1983; 16(3):297–307. 16. Malmqvist E, Bengtsson M, Sorensen J. Efficacy of stellate ganglion block: a clinical study with bupivacaine. Reg Anesth 1992; 17(6):340–347. 17. Geurts J, Stolker R. Percutaneous radiofrequency lesion of the stellate ganglion in the treatment of pain in the upper extremity reflex sympathetic dystrophy. Pain Clin 1993; 6:17–25. 18. Price D, Long S, Wilsey B, et al. Analysis of peak magnitude and duration of analgesia produced by local anesthetics injected into sympathetic ganglia of complex regional pain syndrome patients. Clin J Pain 1998; 14:216–226. 19. Forounzafar T, van Kleef M, Weber WEJ. Radiofrequency lesions of the stellate ganglion in chronic pain syndromes. Retrospective analysis of clinical efficacy in 86 patients. Clin J Pain 2000; 16(2):164–168. 20. Pitkin G. Cervical and thoracic nerves. Philadelphia: JB Lippincott;1946. 21. Wilkinson H, Bryant G The supraventricular tachycardias: management by interruption of cardiac sympathectomies. JAMA 1961; 175:672–676. 22. Dos S. Cardiac sympathectomy for angina pectoris. Ann Thorac Surg 1978; 25: 178–179. 23. Baille Y, Siwalt M, Waillant A, et al. Resultats a distance de la chirurgic de l’angor de Prinzmetal. Ann Chir 1982; 36:613–614. 24. Henrard L, Pierard L, Limet R. Traitment par sympathectomie thoracique de l’angor de Prinzmetal a coronaries saines. Arch Mal Chur 1982; 75:1317–1319.

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Part 3: Specific Disorders 25. Montorsi W, Ghringhelli C, Amoni F. Indications and results of surgical treatments of Raynaud’s phenomenon. J Cardiovasc Surg 1980; 21:203–210. 26. Adson A, Brown G. The treatment of Raynaud’s disease by resection of the upper thoracic and lumbar sympathetic ganglia and trunks. Surg Gynecol Obstet 1929; 48:557–603. 27. Wilkinson HA. Percutaneous radiofrequency upper thoracic sympathectomy. Neurosurgery 1996; 38(4):715–725. 28. Raj P, Lou L, Erdine S, et al. T2 and T3 sympathetic nerve block and neurolysis. Philadelphia: Churchill Livingstone; 2004. 29. Cousins M, Reeve T, Glynn C. Neurolytic lumbar sympathetic blockade: duration of denervation and relief of rest pain. Anaesth Intensive Care 1979; 7:121–135. 30. Boas R. Sympathetic blocks in clinical practice. Anesthesiol Clin 1978; 16:149–182.

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31. Dominkus M, Kepplinger B, Bauer W, et al. Percutaneous radiofrequency thermolesion of the sympathetic chain in the treatment of peripheral vascular disease. Acta Medica Austriaca 1991; 18(Suppl)1:69–70. 32. Haynsworth RF Jr, Noe CE. Percutaneous lumbar sympathectomy: a comparison of radiofrequency denervation versus phenol neurolysis. Anesthesiology 1991; 74(3):459–63. 33. Noe CE, Haynsworth RF Jr. Lumbar radiofrequency sympatholysis. Journal of Vascular Surgery official publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter 1993; 17(4):801–806. 34. Rocco AG. Radiofrequency lumbar sympatholysis. The evolution of a technique for managing sympathetically maintained pain. Reg Anesth 1995; 20(1):3–12.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ ii: Cervial Axial Pain

CHAPTER

Cervical Spine

66

Sara Haspeslagh, Jan Van Zundert and Maarten Van Kleef

CERVICAL ZYGOAPOPHYSEAL PAIN Clinical syndrome Patients with cervical zygapophyseal (facet) joint pain present commonly with a dull and aching bilateral neck pain. Pain emanating from the cervical facet joints can refer into the occiput, interscapular, or shoulder girdle regions dependent on the cervical facet joint involved in the patient’s pain syndrome.1–4 Pain from the higher cervical facet joints may end up causing cervicogenic headache.5 On physical examination one may find a reduced range of motion of the cervical spine if the higher facet joints are involved. Marked paravertebral tenderness to palpation suggests regional soft tissue changes in response to the underlying injured facet joint, but these findings are not pathognomonic. X-rays, computed tomography (CT), and magnetic resonance imaging (MRI) scans may reveal morphological abnormalities; however, there is no direct relationship between anatomical findings and pain.6–8

Indications and contraindications The indications to perform a radiofrequency (RF) denervation of the medial branches that innervate the cervical facet joints are identical for nontraumatic and post-traumatic neck pain. In whiplash-associated cervical pain the periosteal tearing of the facet joints due to muscle ligamentous sprain is thought to be the most common cause of neck pain.9–11 Atraumatic cervical pain can be due to progressive degenerative facet disease (for example, joint arthritis) or postural changes. Cervicogenic headache (CH) is another possible indication of performing an RF denervation of the medial branches of the cervical facet joints. It is typically described as a unilateral headache localized in the neck or occipital region and sometimes projecting to the forehead. The referred pain originates from the cervical structures, which in some instances is singularly from the facet joints. This distinct headache syndrome was described as early as 1926. Sjaastad et al. were the first to name it CH and to propose diagnostic criteria.5,12 RF denervation of the cervical medial branches tend to reduce nociceptive output from structures such as spinal facet joints and spinal nerve roots, so this intervention has been proposed to be an effective treatment of CH.13 The contraindications of facet joint denervation are systemic infection, local infection in the overlying soft tissue, and coagulation disorders. Other contraindications include are an allergy to the injected medication and refusal of the patient to undergo the procedure.

Side effects and complications A common side effect (in 13% of the patients) of the RF denervation of cervical facet joints is a transient increase in pain in the neck

that resolves in 2–6 weeks.14 Vervest and Stolker also reported 4% of patients with occipital hypesthesia, which resolves in 3 months. They suggest this side effect is caused by a lesion of the third occipital nerve. Another side effect that is described after RF denervation of the third occipital nerve is a transient ataxia and unsteadiness, probably secondary to a partial blockade of the upper cervical proprioceptive afferents.3 Since the vertebral artery and the cervical segmental nerves lie just anteriorly to the cervical facet joints, there is the possibility of making contact with them if the needle is entered too anteriorly. Since the epidural space lies immediately medially to the facet joint, a deviation of the needle toward the midline should be avoided because of the risk of penetration into the epidural space or subarachnoid space.

Outcomes In 1980, Sluijter and Koetsveld-Baart15 concluded that RF lesioning of the cervical facet joints and/or dorsal root ganglion can be of considerable help in a selected group of patients. This judgment was based on observing 61% of patients obtaining in excess of 40% symptom relief following RF, while obtaining no benefit from prior treatments. In an open prospective study in 1995, Lord et al. evaluated the pain relief in the upper and lower cervical region using RF lesions of the medial branch of the posterior primary ramus (RF-PFD) in 19 patients using a posterior approach.16 Patient selection was based on comparative local anesthetic blocks. The procedure was effective in the lower region in 7 of 10 (70%) patients but only in 4 of 9 (44%) patients in the higher region, i.e. the C2–3 facet joint. That study concluded that the encouraging results of RF lesions at the medial branch of the dorsal ramus at the lower cervical levels justified a randomized, double-blind, controlled trial. One year later, Lord et al. performed a randomized, double-blind, controlled trial in patients with chronic pain of the lower cervical facet joints after whiplash injury.11 This study revealed that, in patients with chronic facet joint pain, confirmed with double-blind, placebo-controlled local anesthetic blocks, percutaneous RF neurotomy with multiple lesions of target nerves could provide lasting pain relief and was not a placebo effect. In 1999, McDonald et al.17 published a double-blinded, controlled study to determine the long-term efficacy of percutaneous radiofrequency medial branch neurotomy in the treatment of chronic neck pain. They only performed the neurotomy (using the posterior parasagittal approach) in patients with a positive response to either comparative or placebo-controlled blocks. Their conclusion was that the relief of neck pain obtained by percutaneous radiofrequency neurotomy can be clinically satisfying, but of limited duration. They also stated that the effects of these procedure could be reinstated if pain recurs. 717

Part 3: Specific Disorders

The prospective study of Sapir and Gorup, published in 2001,18 compared the efficacy of radiofrequency medial branch neurotomy to treat cervical zygapophyseal joint pain in patients with whiplash who were either litigants or nonlitigants. They found no difference in outcomes following radiofrequency treatment in patients with the potential of secondary gain. They also concluded that radiofrequency neurotomy is efficacious for the treatment of traumatic cervical facet arthropathy. Geurts et al. concluded that there is limited evidence for RF facet denervation in the treatment of chronic cervical pain following a whiplash event.19 Radiofrequency lesioning of the cervical facet joints in the treatment for neck pain and headache was performed in several studies.20,21 These studies suggest that RF can offer a tangible benefit, but that the results are modest and not compelling. In a recent open prospective study, Van Suijlekom et al. evaluated the effect of headache relief in patients with cervicogenic headache after RF-PDF at the levels C3–6.13 In that study the lateral approach was used. They demonstrated that RF cervical facet denervation leads to a significant reduction in headache severity, number of days with headache, and analgesic intake in patients with cervicogenic headache diagnosed according to the criteria of Sjaastad et al.5 In 2004 Stovner et al. published a randomized, double-blind, sham-controlled study to determine whether RF denervation of facet joints C2–3 could be a good treatment of cervicogenic headache.22 They could include only 12 patients in total and did a follow-up of 24 months. They found some improvement in the neurotomy group at 3 months, but later on there were no marked differences between the RF group and the sham group. Their conclusion was that the procedure is probably not beneficial in cervicogenic headache. At this juncture, in the authors’ view, a definite conclusion about the clinical efficacy of the procedure can only be made following a randomized, controlled trial including a large number of patients.

CERVICAL RADICULAR PAIN Clinical syndrome Cervicobrachialgia is a widespread pain syndrome. Bland estimates that 9% of all men and 12% of all women experience this pain at some times in their lives.23 In 1994, Radhakrishnan et al. published a population-based survey.24 In this epidemiological survey an annual incidence of cervical radiculopathy of 83.2 per 100 000 in a population between 13 and 91 years was found. The pain in cervicobrachialgia is described as a continuous, dull aching pain in the neck (most commonly localized in the mid- and lower cervical area) traveling beyond the gleno-humeral joint into the arm with referral to a particular spinal segment. Segmental pain in the upper extremity can be related to discogenic pathology such as a cervical disc protrusion or irritation of the spinal nerve. Spinal nerve irritation can be caused by narrowing of the intervertebral foramen by spondylosis. The most common nerve levels involved, are C6 and C7 and less C5. The levels C4 and C8 are uncommon. The involved spinal level can be estimated by the dermatome in which the pain is radiating and can be determined by prognostic nerve blocks.25–27 In the International Association for the Study of Pain (IASP) classification of chronic pain, Merskey and Bogduk considered radicular pain and radiculopathy as two distinct entities.28 Cervical radicular pain is defined as pain perceived as arising in the upper limb caused by ectopic activation of nociceptive afferent fibers in a spinal nerve or its roots or other neuropathic mechanisms. Cervical radiculopathy is defined as the objective loss of sensory and/or motor function 718

as a result of conduction block in axons of a spinal nerve or its roots. The two conditions may nonetheless coexist and may be caused by the same lesion, or radiculopathy may follow radicular pain in the course of the disease. Ectopic activation may occur as a result of mechanical deformation of a dorsal root ganglion (DRG), mechanical stimulation of previously damaged nerve roots, inflammation of a DRG, and possibly by ischemic damage of DRG.28–31 Any lesion that causes conduction block in axons of a spinal nerve or its roots, either directly by mechanical compression of the axons or indirectly by compromising their blood supply and nutrition, may be the cause of radiculopathy. Clinical entities that may cause cervical radicular pain or radiculopathy include: foraminal stenosis, prolapsed intervertebral disc and radiculitis due to arteritis, infection or inflammatory exudate. The diagnosis of cervical radicular pain and/or radiculopathy requires a thorough history taking; clinical diagnosis using standardized test methods of physical examination, medical imaging, electrophysiologic investigation, and determination of the causative level by means of selective nerve root blocks. Many authors state that cervical radicular pain is a common clinical diagnosis.32–35 As with other types of spinal pain, if the pain does not spontaneously resolve within 3 months, medical diagnoses such as vertebral column infection and cancer should be considered before further symptomatic treatment is offered. Furthermore, abnormalities that may benefit from percutaneous disc decompression or an open surgical procedure, such as cervical disc prolapse or other serious pathological abnormalities should be excluded before radiofrequency DRG is performed. In medical history, the location and pattern of pain, altered sensation or paresthesias, and motor deficits were thought to be definitive for cervical radicular pain.36–38 As described elsewhere in this book, there are numerous instances in which the painful symptoms are located in region that is not classically associated with a particular nerve. Neurological examination includes testing of strength, muscle stretch reflexes, and sensation.39 The cervical range of motion is frequently assessed when examining patients with complaints of neck pain and these measurements may be used as an indicator of treatment effectiveness.40,41 Provocative tests for patients with cervical radicular pain and radiculopathy may induce or alleviate mechanical deformation by the following mechanisms: enlargement or narrowing of the neural foramen,42,43 peripheral neural elements placed on slack or stretch,44–46 and an increase in intrathecal pressure.47 Five different provocative tests have been reported as useful for the diagnosis of cervical radicular pain: (1) Spurling’s test,42 (2) shoulder abduction test,44 (3) Valsava’s maneuver,47 (4) neck distraction,48 and (5) Elvey’s upper limb tension test.46 The Spurling test is one of the few clinical tests that has been validated in a controlled trial using electromyography (EMG) as confirmation. This test had a sensitivity of 30% but a specificity of 93%, illustrating its value in confirming cervical radicular pain and radiculopathy.49 The most commonly used complementary diagnostic tools to establish the etiology of cervical radicular pain and radiculopathy are imaging and electrophysiological studies. Imaging studies provide information relative to anatomic abnormalities, while electrophysiological studies allow detection of dysfunction. The primary role of plain radiography is to rule out other insidious disease processes and the delineation of osteophytes when used in conjunction with MRI.50,51 Myelography is used to assess the effect of a space-occupying lesion on the dural sac, the nerve roots, and the spinal cord.52 A CT scan is particularly useful for enhancement of bony margins. It is more sensitive than MRI to bony changes but has

Section 3: Cervical Spine

limited ability to detect soft tissue lesions.50,53,54 MRI is noninvasive and more sensitive to changes of the disc, spinal cord, nerve root, and surrounding soft tissue structures.53 Some authors state that MRI is the imaging method of choice, which appears to be consistent with current practice patterns.55 Because imaging procedures may show a number of dramatic abnormalities that produce no signs or symptoms, interpretation of any imaging finding must be done in the context of the patient’s clinical presentation.56 Although often collectively referred to as electromyography (EMG), in practice the electrophysiological examination consists of needle electromyography and a variety of evoked potential procedures. Needle electromyography is used to sample motor unit behavior in selected limb muscles as well as the cervical paravertebral muscles in order to detect neural pathophysiology and localize it to a cervical nerve root or roots.57 Nerve conduction studies are also performed in conjunction with EMG in order to rule out other causes of symptoms such as a diffuse peripheral neuropathy or more distal mononeuropathy.57 All diagnostic modalities provide excellent information of the morphological pathology and its relation to the neuraxis but do not reveal its clinical significance. Therefore, selective diagnostic nerve root blocks are recommended before deciding which level should be treated. The technique, injecting a local anesthetic adjacent to the DRG, controlled by means of contrast injection, has been described by van Kleef et al.25

Indications and contraindications The indications to perform a radiofrequency (RF) lesioning of a cervical DRG differ from level to level. 58 It must be emphasized that a diagnostic segmental cervical nerve block always has to be performed prior to an RF procedure to predict the effect of blocking a certain segmental nerve and to identify the involved level(s). The C2 and C3 levels are performed for cervicogenicand neck-related headache, for post-traumatic headache, and in cases where there is persisting pain in the suboccipital region or the upper neck region after a noneffective medial branch procedure. The C2 level is also performed in true occipital neuralgia with sensory loss in the C2 dermatome. An indication for the level C4 is really exceptional. The C5, C6, C7, and C8 levels can be performed in cases of acute herniation at the involved level with clinically significant radicular pain. This may occur when radiculopathy results from narrowing of the foramen, although uncommon at the C8–T1 level, or when there is a clearly defined radicular pain without any anatomical findings. Lastly, a C5 dorsal root ganglion RF treatment can be performed, as described by Sluijter, when there is shoulder pain caused by pathology in or around the joint. The contraindications are the same as described above in the part ‘Cervical zygapophyseal pain.’

Side effects and complications A side effect that is often seen (40–60%) is a mild burning sensation (some deep neck soreness) in the treated dermatome that subsides spontaneously within 1–3 weeks.25 Some sensory changes, such as a slight hypesthesia may occur, but invariably disappears within 3–4 months.59,60 Known complications of a blockade of a cervical segmental nerve are injections of local anesthetics epidural, intrathecal and intravascular. It can be injected in the adjacent venous plexus, in the vertebral artery or even in the carotid artery. Since the proximity to the brain in the higher cervical levels, there is the risk of local anesthetic

central nervous system toxicity although only a low volume of local anesthetic is used.

Outcomes In 1991, Vervest and Stolker published a retrospective study in 53 patients with prolonged cervical pain eventually radiating to the occipital region, head, shoulder, or arm not responding to conservative treatment.14 If there was local tenderness at the facet joints, a percutaneous cervical facet joint denervation was performed. If this was not successful and there was cervical pain with referral to the occipital region or arm, indicating segmental irritation, diagnostic segmental nerve blocks were performed. A positive diagnostic block was followed by an RF-DRG. The results were good to excellent in 80.5% of treatments. After a follow-up of 1.5 years 44 patients (84.5%) still had satisfactory pain relief. Van Kleef et al. investigated the outcomes following the performance of this procedure in the cervical region. In an open prospective study of 20 consecutive patients with chronic intractable pain in the cervical region with referral to the head, shoulder, and/or arm, RF-DRG provided pain relief in 75% of patients at 3 months and in 50% of patients at 6 months.61 The results revealed that initial pain relief was acceptable, but there was a tendency for pain to recur at 3–9 months. In 1996, Van Kleef et al. showed that RF lesions adjacent to the DRG for cervicobrachial pain could result in a significant alleviation of pain in chronic cervicobrachial pain.25 In this prospective, double-blind, randomized study, the outcomes revealed a positive benefit during the first 8 weeks after the procedure. Slappendel et al. suggested, in a recent double-blind, randomized study with follow-up of 3 months, that treatment with 40°C RF application to the DRG is equally effective as treatment at 67°.59 In a recent systematic review Geurts et al. concluded that there is limited evidence that RF-DRG is more effective than placebo in chronic cervicobrachialgia.19 Niemisto et al. performed a systematic review and arrived at the same conclusion.62 In 2003, Van Zundert et al. published a clinical audit of 18 patients with cervicogenic headache or cervicobrachialgia who failed conservative treatment. This cohort underwent PRF, the least destructive RF modification adjacent to the involved cervical DRG.60 In 72% of the patients there was a minimum reduction of pain at least 50% at 8 weeks. At 1 year 33% of the patients continued to report the treatment outcome as good or very good. There were no neurological side effects or complications observed.

References 1. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns. I: A study in normal volunteers. Spine 1990; 15(6):453–457. 2. Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal joint pain patterns. II: A clinical evaluation. Spine 1990; 15(6):458–461. 3. Bogduk N, Marsland A. The cervical zygapophyseal joints as a source of neck pain. Spine 1988;1 3(6):610–617. 4. Fukui S, Ohseto K, Shiotani M, et al. Referred pain distribution of the cervical zygapophyseal joints and cervical dorsal rami. Pain 1996; 68:79–83. 5. Sjaastad O, Fredriksen TA, Pfaffenrath V. Cervicogenic headache: diagnostic criteria. Headache 1990; 30(11):725–726. 6. Gore D, Sepsic S, Gardness G. Roentgenographic findings of the cervical spine in asymptomatic people. Spine 1986; 11(6):521–524. 7. Schellhas KP, Smith MD, Gundry CR, et al. Cervical discogenic pain. Prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers. Spine 1996; 21(3):300–11. 8. Mayer E, Hermann G, Pfaffenrath V. Functional radiographics of the craniocervical region and the cervical spine. A new computer-aided technique. Cephalalgia 1985; 5(4):237–243. 9. Barnsley L, Lord S, Wallis B, et al. The prevalence of chronic cervical zygapophyseal joint pain after whiplash. Spine 1995; 20(1):20–26.

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Part 3: Specific Disorders 10. Lord S, Barnsley L, Wallis B, et al. Chronic cervical zygapophyseal joint pain after whiplash. A placebo-controlled prevalence study. Spine 1996; 21(15):1737–1745. 11. Lord SM, Barnsley L, Wallis BJ, et al. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med 1996; 335(23): 1721–12726.

38. Warfield C, Biber M, Crews D, et al. Epidural steroid injection as a treatment for cervical radiculitis. Clin J Pain 1988; 4:201–204.

12. Barre M. Sur un syndrome sympathique cervical posterieur et sa cause frequente: l’arthritide cervicale. Rev. Neurol. 1926; 33:1246–1248.

39. Fager C. Identification and management of radiculopathy. Neurosurg Clin N Am 1993; 4:1–12.

13. van Suijlekom HA, van Kleef M, Barendse GA, et al. Radiofrequency cervical zygapophyseal joint neurotomy for cervicogenic headache: a prospective study of 15 patients. Funct Neurol 1998; 13(4):297–303.

40. Youdas J, Carey J, Garrett T. Reliability of measurements of cervical spine range of motion – comparison of three methods. Phys Ther 1991; 71:98–104; discussion 105–106.

14. Vervest A, Stolker R. The treatment of cervical pain syndromes with radiofrequency procedures. Pain Clin 1991; 4:103–112.

41. Lowery W Jr, Horn T, Boden S, et al. Impairment evaluation based on spinal range of motion in normal subjects. J Spinal Disord 1992; 5:398–402.

15. Sluijter ME, Koetsveld Baart CC. Interruption of pain pathways in the treatment of the cervical syndrome. Anaesthesia 1980; 35(3):302–307.

42. Muhle C, Bischoff L, Weinert D, et al. Exacerbated pain in cervical radiculopathy at axial rotation, flexion, extension, and coupled motions of the cervical spine: evaluation by kinematic magnetic resonance imaging. Invest Radiol 1998; 33:279–288.

16. Lord SM, Barnsley L, Bogduk N. Percutaneous radiofrequency neurotomy in the treatment of cervical zygapophyseal joint pain: a caution. Neurosurgery 1995; 36(4):732–739.

43. Spurling R, Scoville W. Lateral rupture of the cervical intervertebral discs: a common cause of shoulder and arm pain. Surg Gynecol Obstet 1944; 78:350–358.

17. McDonald G, Lord S, Bogduk N. Long-term follow-up of patients treated with cervical radiofrequency neurotomy for chronic neck pain. Neurosurgery 1999; 45(1):61–68.

44. Davidson R, Dunn E, Metzmaker J. The shoulder abduction test in the diagnosis of radicular pain in cervical extradural compressive monoradiculopathies. Spine 1981; 6:441–446.

18. Sapir A, Gorup J. Radiofrequency medial branch neurotomy in litigant and nonlitigant patients with cervical whiplash. Spine 2001; 26(12):E268–E273.

45. Elbey R. The investigation of arm pain: signs and adverse responses to the physical examination of the brachial plexus and related tissues. New York: Churchill Livingstone; 1994.

19. Geurts JW, van Wijk RM, Stolker RJ, et al. Efficacy of radiofrequency procedures for the treatment of spinal pain: a systematic review of randomized clinical trials. Regl Anesthes Pain Med 2001; 26(5):394–400. 20. Hildebrandt J. Percutaneous nerve block of the cervical facets – a relatively new method in the treatment of chronic headache and neck pain. Man Med 1986; 2: 48–52. 21. Schaerer JP. Radiofrequency facet rhizotomy in the treatment of chronic neck and low back pain. Internat Surg 1978; 63(6):53–59. 22. Stovner L, Kolstad F, Helde G. Radiofrequency denervation of facet joints C2–C6 in cervicogenic headache: A randomized, double-blind, sham-controlled study. Cephalagia 2004; 24:821–830. 23. Bland J. Cervical spine syndromes. J Muskuloskel Med 1986; 3:23–41. 24. Radhakrishnan K, Litchy W, O’Fallon W, et al. Epidemiology of cervical radiculopathy. A population-based study from Rochester, Minnesota, 1976 through 1990. Brain 1994; 117(Pt 2):325–335. 25. van Kleef M, Liem L, Lousberg R, et al. Radiofrequency lesion adjacent to the dorsal root ganglion for cervicobrachial pain: a prospective double blind randomized study. Neurosurgery 1996; 38(6):1127–1131.

46. Saal J, Saal J, Yurth E. Nonoperative management of herniated cervical intervertebral disc with radiculopathy. Spine 1996; 21:1877–1883. 47. Rothstein J, Roy S, Wolf S. The Rehabilitation Specialist’s Handbook. Philadelphia: FA Davis; 1991. 48. Viikari-Juntura E, Porras M, Laasonen E. Validity of clinical tests in the diagnosis of root compression in cervical disc disease. Spine 1989; 14:253–257. 49. Tong H, Haig A, Yamakawa K. The Spurling test and cervical radiculopathy. Spine 2002; 27:156–159. 50. Brown B, Schwartz R, Frank E, et al. Preoperative evaluation of cervical radiculopathy and myelopathy by surface-coil MR imaging. Am J Roentgenol 1988; 151:1205– 1212. 51. Nakstad P, Hald J, Bakke S, et al. MRI in cervical disk herniation. Neuroradiology 1989; 31:382–385. 52. Wilmink J. Clinical relevance of cervical disk herniation diagnosed on the basis of MR imaging. Am J Neuroradiol 1989; 10:1278–1279. 53. Jahnke R, Hart B. Cervical stenosis, spondylosis, and herniated disc disease. Radiol Clin North Am 1991; 29:777–791.

26. Van Kleef M, Sluijter M. Radiofrequency lesions in the treatment of pain of spinal origin. In: Gildenberg P, Tasker R, eds. Textbook of stereotactic and functional neurosurgery. New York: McGraw-Hill; 1998:1585–1599.

54. Modic M, Masaryk T, Mulopulos G, et al. Cervical radiculopathy: prospective evaluation with surface coil MR imaging, CT with metrizamide, and metrizamide myelography. Radiology 1986; 161:753–759.

27. Stolker R, Groen G. Clinical review: The management of chronic spinal pain by blockades: a review. Pain 1994; 58:1–20.

55. Wainner R, Gill H. Diagnosis and nonoperative management of cervical radiculopathy. J Orthop Sports Phys Ther 2000; 30:728–744.

28. Merksey H, Bogduk N, (eds). Classification of chronic pain: Descriptions of chronic pain syndromes and definitions of pain terms. Monograph for the Sub-Committe on Taxonomy, International Association for the Study of Pain. 2nd edn. Seattle, International Association for the Study of Pain.

56. Healy J, Healy B, Wong W, et al. Cervical and lumbar MRI in asymptomatic older male lifelong athletes: frequency of degenerative findings. J Comput Assist Tomogr 1996; 20:107–112.

29. Howe J, Loeser J, Calvin W. Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pain of nerve root compression. Pain 1977; 3:25–41. 30. Howe J. A neurophysiological basis for the radicular pain of nerve root compression. New York: Raven Press; 1979. 31. Murphy R. Nerve roots and spinal nerves in degenerative disk disease. Clin Orthop 1977: 12(129):46–60. 32. Ahlgren B, Garfin S. Cervical radiculopathy. Orthop Clin North Am 1996; 27: 253–263. 33. An H. Cervical root entrapment. Hand Clin 1996; 12:719–730. 34. Ellenberg M, Honet J, Treanor W. Cervical radiculopathy. Arch Phys Med Rehabil 1994; 75:342–352. 35. Caplan L. Management of cervical radiculopathy. Eur Neurol 1995; 35:309–320. 36. Cloward R. Cervical diskography. A contribution to the etiology and mechanism of neck, shoulder and arm pain. Ann Surg 1959; 150:1052–1064.

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37. Michelsen J, Mixter W. Pain and disability of shoulder and arm due to herniation of the nucleus pulposus of cervical intervertebral disks. N Engl J Med 1944; 231: 279–287.

57. Dimitru D. Electrodiagnostic medicine. Philadelphia: Hanley & Belfus; 1995. 58. Sluijter M. The medial branch procedure. In: Sluijter M (ed.) Radiofrequency Part 2: Thoracic and cervical region, headache and facial pain. Meggen. Flivo Press SA. 2003; pp. 99–110. 59. Slappendel R, Crul BJ, Braak GJ, et al. The efficacy of radiofrequency lesioning of the cervical spinal dorsal root ganglion in a double blinded randomized study: no difference between 40 degrees C and 67 degrees C treatments. Pain 1997; 73(2):159–163. 60. van Zundert J, Lamé I, de Louw A, et al. Percutaneous pulsed radiofrequency treatment of the cervical dorsal root. ganglion in the treatment of chronic cervical pain syndromes: a clinical audit. Neuromodulation 2003; 6(1):6–14. 61. van Kleef M, Spaans F, Dingemans W, et al. Effects and side effects of a percutaneous thermal lesion of the dorsal root ganglion in patients with cervical pain syndrome. Pain 1993; 52(1):49–53. 62. Niemisto L, Kalso E, Malmivaara A, et al. Radiofrequency denervation for neck and back pain: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2003; 28(16):1877–1888.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ ii: Cervical Axial Pain

CHAPTER

Cervical Discography: Diagnostic Value and Complications

67

Richard Derby, Renée Melfi, Gul Talu and Charles Aprill

INTRODUCTION

Sensitivity and specificity

Diagnostic procedures can confirm specific diagnoses. Establishing a correct diagnosis should allow prediction of outcome following appropriate treatment. To evaluate the diagnostic value of a procedure one must determine how well the test can discriminate between the diseased and nondiseased state. A diagnostic test is accepted or rejected after evaluating evidence, based on an accepted methodology. One must ask, is there historical need for the test, are there studies that validate acceptable specificity and sensitivity, are there other comparable, less invasive procedures, is the test clinically useful, is the incidence of significant morbidity low, and finally are serious complications preventable?1 In the case of cervical discography, the diseased state is the presence of a symptomatic disc. Ideally, discography would always be positive at a symptomatic disc and always be negative in an asymptomatic disc. A perfect procedure would be inexpensive, relatively painless, and free of serious complications. Cervical discography is not perfect. If sensitivity and specificity are acceptable and the results of this test can predict outcome of treatment, then in the absence of another less invasive test that will provide comparable information, one can justify the cost and risk of this less than perfect diagnostic procedure.

Since neck pain from a painful disc is not life-threatening and cervical spine fusion is not a benign treatment, the ideal diagnostic test should have high specificity (i.e. a low false-positive rate). To establish the specificity and sensitivity of provocative discography requires a randomized, blinded trial in a group of patients with chronic axial neck pain. The predictive variable would be the result of discography as defined by strict criteria. The outcome variable would be the presence or absence of a painful disc as determined by a gold standard. Unfortunately, no gold standard exists. Therefore, one cannot directly determine either the specificity or sensitivity of cervical discography. We can indirectly evaluate the specificity of cervical discography. Specificity is the measure of how well cervical discography can rule out a disc as a pain generator when the pain is caused by some other structure. Specificity equals true negative divided by (false positive + true negative). Ideally, one would perform discography on patients with chronic axial neck pain and patients with neck pain referred from other body regions. A less robust design would be to perform discograms on asymptomatic volunteers. This design, however, might give a higher false-positive rate because concordance of pain cannot be evaluated in asymptomatic volunteers. As with lumbar discography,17–19 a significant proportion of asymptomatic individuals with degenerated discs will have low-level pain during disc injection. A positive response should include a limiting verbal pain score (e.g. > 6–7/10 pain). Provoked pain below that level does not constitute a positive response. Alternatively, one could identify patients with painful Z-joints as the source of neck symptoms and perform discography on them. Patients with a positive discogram response who also had complete relief of their pain following placebo-controlled analgesic medial branch blocks are discogram false-positive responders. Soon after the separate introduction of cervical discography by Smith and Cloward in the late 1950s, Holt reported on the ‘fallacy of cervical discography.’ He performed discography on 50 ‘normal’ subjects who were inmates at the Missouri State Penitentiary.12 A total of 148 discs in 50 subjects were studied using 22-gauge needles placed in the neck blindly, using X-rays to document needle placement in the discs. Each ‘extremely co-operative’ inmate was given either Demerol or Nembutal 20 minutes before the procedure. Each disc was injected with 50% sodium diatrizoate (Hypaque sodium) and ‘… even in 0.2 cc amounts, great pain was produced in every subject at every space.’ Holt reported that every disc hurt when injected (i.e. the specificity was 0%). He observed that the pain lasted 5 minutes then subsided. Pain was variously described as ‘being hit in the back of the neck with a maul,’ ‘like sticking a knife into the base of my neck,’ or ‘a hot poker between the shoulder blades.’ He described almost 100% incidence of contrast extravasation despite a volumes of only 0.2–0.3 mL. According to Holt, only one inmate reported to sick call and all others resumed normal activity the next day without

Historical need Ralph Cloward acknowledged that George Smith performed the first cervical discography in1952, but both independently described the technique and use of cervical discography in the late 1950s.2–4 These surgeons were performing anterior cervical fusions for chronic axial pain and were searching for a procedure to identify the painful cervical discs. Both were frustrated by the insensitivity of available diagnostic tests. Plain film could diagnose disc degeneration but there was poor correlation with pain. Myelography with Pantopaque could identify central and paracentral disc herniation but the false-positive incidence was high, and myelograms were insensitive to lateral lesions. Both surgeons felt that reproduction of a patient’s usual pain during disc injection was evidence that the disc was symptomatic. Cervical fusions were performed based on this information. They recognized that most discs were anatomically disrupted,3,5 but not all were painful. Controversy arose because many surgeons felt that cervical spine surgery should not be performed for neck pain without radiculopathy. Cervical discography was berated because of the high prevalence of structurally abnormal cervical discs and because injection into most cervical discs provoked pain.2–16 None of the early reports mentioned the imprecise methods used to perform and evaluate discography. Many surgeons perceived cervical discography as a useless procedure.9,12,16 On the other hand, there were others who believed in discogenic pain, used discography to identify painful discs, and fused cervical segments found to be positive.3,5,7,13

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apparent problems. He did conclude that cervical discography might be made relevant by a radical change in contrast media and ‘techniques of performance.’ He politely conceded that further studies should be done to establish objective findings, including control patterns in normal individuals. A decade later in 1975, Holt reflected on the value of cervical discography by rehashing his previous observations and commenting on Struck’s study of 1200 patients undergoing cervical discography followed by about 800 surgical fusions.20 Holt comments, ‘Colorado has had statehood slightly less than 100 years. It is hard to conceive of so many ruptured cervical discs in all its history.’ He called for a ‘hard and fast moratorium on cervical discography.’21 Other early observational studies also noted a high incidence of painful disc injections. Meyer discounted the use of cervical discography because almost all the radiographic patterns were abnormal and he felt ‘there was no good correlation of pain radiation with the patient’s clinical symptoms or the roentogenographic findings.’10 Klafta and Collis discounted the 89% of positive pain provocation in patients because injection of contrast into cervical discs shown to have disc herniation on myelography did not usually reproduce the patient’s radicular pain.16 Despite negative bias, suboptimal imaging, and the use of irritating contrast, cervical discography was criticized but not challenged with new data for many years. In 1993, Shinomiya et al. in Japan partially reconfirmed Holt’s findings.22 These authors performed discography on 128 patients with spondylotic mylelopathy and radiculopathy. In the 72 patients with neck pain, 65% had reproduction of their usual pain. However, in the control group who had only neurologic symptoms, 50% reported pain provocation during injection. In the same year, Aprill and Bogduk found a potential source of the high false-positive rate of cervical discography while studying the prevalence of Z-joint and discogenic pain in patients with chronic axial neck pain.23 The authors performed both diagnostic medial branch blocks using a double-block protocol and cervical discography on a series of patients. Forty-one percent of patients had a positive discogram, but also had full relief of their axial neck pain for the duration of the local anesthetic following medial branch block with 0.5 mL of bupivacaine. These were false-positive discograms. In 1996, Kurt Schellhas, an experienced interventional radiologist, reported a 0% false-positive rate by using more precise methods and strict criteria for defining a positive response.24 He published a prospective observational study in which discography was performed on 40 discs in 10 asymptomatic volunteers and compared the results to 10 symptomatic patients. He used modern discography technique including 25-gauge needles, fluoroscopic guidance, and nonirritating contrast material. He also precisely graded pain intensity on a 10-point verbal pain scale, recorded the exact pain referral pattern, disc morphology, and pain concordance in patients. A minimum of four levels were studied in each patient. The mean age of the volunteers was 30 years. The disc morphology was abnormal in 35 of the 45 discs studied. While most abnormal discs did produce pain, the average pain was 2.42/10 (SD = 1.5). The most frequent response (14 discs) was 2–2.5/10 intensity. Pain intensity was 0–3/10 in 27 discs and 3–6/10 in 9 others. An intensity of 6/10 pain was reported in only one disc. By comparison, there were only two morphologically normal discs in the symptomatic group, but the average pain intensity and standard deviation was not calculated. The patient raw data show that there were 12 discs with minimal (0–3/10) pain responses, 11 with moderate (4–6/10) pain, and 17 discs with severe pain (7–10/10). In those moderately painful discs which might be most likely to be false-positive responses less than 50% (5/11) had concordant pain. The results are a ‘best case’ scenario. The stimulus intensity is manual and operator dependent. One would expect that the author 722

very carefully injected the asymptomatic volunteers. In addition, the volunteers were not chronic pain patients and were probably not blinded to the purposes of the study. If one accepts that a 7/10 intensity of pain provocation is required for a positive response, there was a 0% false-positive rate. If on the other hand, one logically infers that a 4–6/10 intensity of pain could easily be reported as 7/10 or greater intensity by a chronic pain patient, nine of the discs might have been reported positive, resulting in a false-positive rate of about 20–25%. But since 50% of these discs had nonconcordant pain, the actual false-positive rate is likely to be less than 20%. Lastly, in 2000, Ohnmeiss and Guyer indirectly commented on the specificity of cervical discography by comparing the post-discogram computed tomography (CT) image and the pain response in 269 discs in 161 patients. They found a significant relationship between radiographic degree of disc disruption and the occurrence of clinical pain provocation. In only 14.3% of the normal discs was concordant pain provoked during injection. On the other hand, 77.8% of the disrupted discs were clinically painful. Although some of the degenerated and leaking discs in the older patients were not symptomatic, injection into most disrupted discs provoked concordant pain. Unfortunately, only pain concordance and disc disruption was evaluated. No data were on the intensity of pain provocation.

Competing diagnostic tests If there is a less invasive, safer diagnostic test that will determine whether the disc is a source of pain, discography is not needed. Magnetic resonance imaging (MRI) scans are used to evaluate the structural morphology of cervical discs and have mostly replaced myelography and CT scans for imaging of the cervical spine. MRI can identify disc protrusions and degrees of disc degeneration. MRI scans are routinely used for surgical planning; not all patients are studied with discography.

MRI Structural correlation Patients with predominately axial neck pain, who have failed conservative care, and have unacceptable persistent symptoms may be surgical candidates. A surgeon must determine which level or levels are causing the pain prior to any operation. Because of the high sensitivity of MRI, some authors suggest that MRI can replace discography.25,26 MRI does demonstrate disc morphology, disc degeneration, and the contour of the outer anulus. But the clinical significance of these abnormalities in the absence of neural compression and radiculopathy is unclear. Are MRI findings of disc degeneration or minor protrusion of clinical importance?27,28 The presence of annular tears and loss of hydration are non-specific findings and many asymptomatic individuals have significant degenerative MRI structural abnormalities.29 Normal discs are uncommon after the mid-twenties and the development of posterior lateral fissures through the uncinate region are present in the majority of mature cervical discs.30 Since the early use of cervical discography, authors have reported the high incidence of annular tears in most cervical discs,2–12,31 but the sensitivity of an MRI scan compared to discography for detecting degeneration and annular tears in cervical discs is still debated. Gibson et al. examined 22 patients with both MRI and discography and on the basis of gross degeneration reached the conclusion that MRI scan was better for detecting gross degeneration.25 On the other hand, Schellhas et al. prospectively correlated MRI imaging and discography in 10 asymptomatic subjects and 10 patients

Section 3: Cervical Spine

with chronic axial pain.24 The authors found that various degrees of annular disruption were common in both symptomatic and asymptomatic subjects. The ruptures were usually posterolateral and fullthickness tears and leaks into the epidural space occurred in about 50% of the discs. Annular tears were identified during discography in 23 of 24 discs judged normal on MRI scans.

Pain provocation correlation If one could predict pain provocation during discography based on the degree of signal changes, annular tears, or minor posterior annular contour abnormalities, discography is not necessary. Although prior studies correlating MRI findings with pain provocation during lumbar discography suggest that dark discs are often associated with positive pain provocation,32,33 this relationship in the cervical spine is less clear. Parfenchuk and Janssen correlated the relationship between the MRI and CT scan obtained after cervical discography.34 They found no correlation between the MRI scan and the post-discogram CT scan to the pain response during discography. Although there was a significant correlation between the patterns seen on the MRI scan and discography, MRI had a high false-positive and false-negative rate compared to discography. They found that unlike lumbar discs, 63% of the ‘white’ cervical discs (normal) studied by discography had a positive pain response. The authors concluded that dark discs need not be studied by discography, but their study included few dark discs. Their findings were not supported by Zheng et al., who found only 63% of the dark discs were symptomatic.35 Furthermore, Schellhas et al. found that in their symptomatic patient group, 16 discs that were clearly abnormal on MR were negative to discographic testing, and 8 of 10 discs with normal MRI scans were shown to have fissures and provoke concordant pain during discography. In the asymptomatic group, 21 of 40 discs had abnormal morphology and none was symptomatic during discography.24

Surgical predictive value based on MRI compared to discography If one is to use MRI to identify a painful disc, all must agree on what MRI criteria will be used to select a symptomatic disc. The levels in question are those with lesser degrees of structural abnormalities, and not those with significant structural abnormalities that will be included in proposed fusion regardless of the discogram findings. Furthermore, we assume that other pain generators such as the Z-joints have been ruled out using appropriate analgesic testing. To compare outcome of surgery based on MRI scan alone or MRI plus discography, one would ideally randomize patients with similar clinical axial pain symptoms and similar structural pathology to undergo planned surgery based on either selection method and compare outcomes at various time intervals after surgery. There are no prospective randomized studies, but Zheng et al. indirectly arrived at the possible false-negative and false-positive rate for surgery based on MRI scans.35 This study retrospectively reviewed surgical outcome of 55 patients, between 1990 and 1995, who had clinically diagnosed cervical discogenic pain for at least 6 months and underwent an anterior cervical discectomy and fusion using a Simmons keystone technique and were available for follow-up at a minimum of 2 years. All had a preoperative MRI scan, discography, and a post-discogram CT scan. MRI disc morphology was classified as white, speckled, or dark and the integrity of the posterior anulus described as flat, bulging, torn, or small herniation. Discs that were thought to be symptomatic included dark herniated, dark torn, dark bulging, speckled herniated, speckled torn, and white herniated discs. Discography was performed by expert interventionists at an average of 2.9 levels using standard modern techniques. Discography was positive if injection of contrast

provoked moderate or severe familiar pain. The MRI findings in 13 of 55 (24%) patients and 103 of 161 (64%) injected discs correlated completely with the results of discography. In the 79 discs with a normal MRI scan 58 (73%) had painful (positive) disc injections. Discography spared 21 asymptomatic discs from being fused and identified 21 discs that were deemed symptomatic but had a normal MRI scan. Since 58 of 79 levels with positive discography were abnormal on MRI, the MRI scan sensitivity was 73.4% (or a false-negative rate of 26.6%). There were 82 levels with negative discography and 40 of these levels had normal MRI scans resulting in an MRI specificity of only 49% when compared to positive discogram responses. Fifty-five patients had a total of 79 levels fused with overall clinical results of excellent in 49%, good in 27%, fair in 18%, and poor in 6%. The results showed that positive discography occurred in 59% of small herniated and torn discs, 35% of bulging discs, and 29% of flat discs. Dark discs with small herniations were the most commonly fused levels and 67% of these discs had a positive discogram. Because discography was used as the criterion standard, levels with positive discograms and ‘negative’ MRI scans were fused and therefore there is no way of telling whether the results would have been the same, better, or worse if the segment was not fused.

Nerve root block Kikuchi et al. combined cervical discography with diagnostic transforaminal nerve root sleeve injections to help localize symptomatic levels when the available imaging including routine radiography, flexion–extension films, myelography, phlebography, or epidurography was inadequate36 These authors felt provocation of pain at discography alone was inadequate because of the frequent occurrence of disrupted discs, the sensitivity of the anterior and posterior longitudinal ligaments, and the irritation caused by contrast material. They also warned about false-positive responses caused by placing the needle close to the endplate. They did, however, feel that reliable information could be obtained by using a nonirritating injectate such as normal saline or local anesthetic and by infiltrating the anterior longitudinal ligament with contrast prior to injection. Relieving the patient’s pain by local anesthetic infiltration of the nerve root sleeve confirmed the diagnosis, ‘even if there was no clinical evidence of impaired conduction in the roots.’

Analgesic discography Analgesic discography is relief of pain rather than provocation and was first described by Roth in 1976.37 Between 1968 and 1974 he preformed cervical analgesic discography in 71 consecutive patients having the ‘clinical diagnosis of medically intractable cervical-discogenic syndromes.’ All patients underwent plain roentgenograms, myelograms, provocative discograms, and analgesic discograms. Analgesic discograms were performed only when the patient was symptomatic (actively painful), without sedation, and at one level at a time. One mL of a 2% ‘analgesic solution’ was injected into the disc through a 22-gauge needle. After each injected level the patient was passively and actively tested, and painless manipulation was considered a positive response. All 71 patients had a least one positive level. In comparison, Roth states that only 21 patients, or 30% of the same group, experienced characteristic pain patterns during provocative discography. He reported that following fusion 93% of the patients had minimal or no symptoms and returned to work. In 1987, Osler reported an 81% excellent or good result after cervical fusion based on the results of analgesic cervical discography.38 No other studies have been published validating these two studies. This technique is used in unclear cases by some interventionists, including the two senior authors (R.D. and C.A.). 723

Part 3: Specific Disorders

CLINICAL UTILITY Cervical fusions are most commonly performed in patients with chronic unresolved axial neck pain and referred upper extremity pain. Many of these patients are in the worker’s compensation and legal system and surgical results may be less than optimal because of the significant influence of psychosocial factors on outcome.39 An average of 66–75% success rate may be the best one can achieve by fusing the affected segments but outcome will obviously depend on the criteria used to define success. Although advanced imaging studies provide improved threedimensional anatomic definition, low specificity has precluded the use of imaging studies alone for selecting surgical levels when chronic axial, mechanical neck pain is a dominant complaint. Consequently, there is a need for provocative and analgesic diagnostic cervical injections (i.e. discography and cervical zygapophyseal joint block) on which to base selection of the level to be fused when history and examination suggest a patient to be an operative candidate.

Selecting fusion levels Garvey et al. retrospectively compared patient-perceived outcome following cervical fusion for predominately mechanical cervical axial pain.40 Of 87 patients meeting the inclusion criteria and available for follow-up, 66 had undergone cervical discography. A ‘clean pattern’ was defined as significant, concordant reproduction of pain at the affected levels with little or no pain at the adjacent levels studied. If these criteria were not meet, the discogram was classified as ‘nonclassic.’ Of the 66 patients, 35 (53%) had a clean pattern and 31 (46%) a nonclassic pattern. Good to excellent outcomes were reported in 91% of the clean group compared to 68% of the nonclassic pattern (p= 0.016). Twenty-one (24%) of the 87 patients did not undergo discography. They generally showed obvious grossly abnormal discs with normal discs above and below; 18 (86%) had good to excellent outcomes. Earlier less rigorous retrospective surgical outcome studies also reported good outcomes following cervical fusions based on discography. In 1975, Simmons and Segil determined the levels to fuse based on the results of provocative discography performed by experienced radiologists.41 Discography was deemed positive if concordant pain was provoked using a standard anterolateral technique. Emphasis was given to repeat testing and making sure the patient was blinded to the level injected. Other than discography, at that time, only clinical impressions and myelography were available to determine the symptomatic levels. There was significant disagreement between the levels selected on the basis of clinical impression and myelography versus discography. Good surgical results were obtained in 30 of the 31 patients operated at levels determined by discography, ‘all having immediate lessening of symptoms and complete relief of symptoms by 1 week.’ Whitecloud and Seago retrospectively evaluated their results of cervical fusions in 40 patients with chronic mechanical neck pain of 27 months duration on average.42 Surgery was based on the results of cervical discography performed by the surgeon first author. A positive result was determined when the patient reported intense concordant pain provocation with injection of no more than 0.5 mL of contrast medium, followed by ‘prompt relief of the patient’s symptoms’ after injection of 0.2 cc Xylocaine. Usually, three levels were studied in a random, patient-blinded fashion. No details were provided regarding the intensity of pain required to be classified as positive. Structural abnormalities were for the most part ignored, but care was exercised in not allowing a leak through the outer anulus which the author thought would result in a false-positive response. At a minimum of 12 months, 34 of the 40 patients were available for follow-up. Using 724

Odom’s criteria, ten patients (32%) had excellent results, 13 (38%) good, 4 patients (12%) fair, and 6 (18%) had poor results. Finally, the frequent occurrence of multiple concordant painful levels may in fact be one of the most important uses of cervical discography because it often persuades the patient and surgeon not to pursue a surgical solution. Grubb and Kelly found that in patients with positive discography, 75% had two positive levels and 54% had three or more positive levels.31 Similarly, Parfenchuk and Janssen34 found a 57% positive rate at multiple levels. Connor and Darden43 found an 84% positive rate at multiple levels in 33 patients. Since many surgeons will not operate for discogenic pain when three or more levels are involved, these patients may be spared a potential failed surgery. In fact, of 173 patients studied by Grubb and Kelly, only 37 (20%) were felt to be surgical candidates. This high rate of multilevel positive responses supports a protocol of performing discograms on a minimum of four levels or on all accessible levels.31

Complications All invasive tests have inherent risks. Placing a needle into a cervical disc has the potential to cause serious complications including infection, spinal cord injury, and bleeding. Because the disc is an avascular structure with poor defenses, infection should be and is the most common serious complication. Disc infections can spread to the adjacent epidural space and cause epidural abscess and cord compression. Cord injury can occur if the discographer passes a needle through the disc and into the spinal cord. Pressurizing a disc with contrast material or saline could potentially cause a disc herniation which could compromise the cord at a stenotic segment. Passing a needle through the carotid artery could potentially cause a plaque to be dislodged or significant bleeding that would cause airway compromise. The actual reported incidence of these potential serious complications is low.

Infection In 1987, Fraser et al. inoculated sheep lumbar discs with contrast alone (control discs) and with contrast mixed with various concentrations of Staphylococcus epidermidis.44 None of the control discs developed discitis. All of the discs inoculated with an estimated seven or more bacteria developed a bacterial discitis after 2 weeks. This report also included a review of human disc infection after discography using two different techniques. Discitis occurred in 2.7% of cases when discography was performed with a single large unstyletted needle. The discitis rate was only 0.7% when a double needle technique with styletted needles was employed. The authors concluded that ‘all cases of discitis after lumbar discography were initiated by infection, introduced by the needle tip.’ In a follow-up study, Osti et al. found no cases of disc space infection in 46 sheep discs inoculated with bacteria when either prophylactic antibiotics were given i.v. or mixed with the injected contrast.45 In addition, the authors prospectively followed 127 consecutive patients undergoing lumbar discography using the styletted two-needle technique and with the addition of cephazolin at 1 mg per mL to the contrast material. None of the 127 patients developed any clinical or radiographic signs of discitis. Contamination of a needle tip could occur from a cough or sneeze by the patient, operator, or support personnel, or contamination could occur by passage of the needle through a contaminated structure such as the esophagus, trachea, or hypopharynx. However, the most common reported causative organism in disc space infection is S. epidermidis and therefore the skin is probably the most common source of needle contamination.46,47 Mixed oropharyngeal flora have been isolated and there are case reports of subdural abscess48 and retropharyngeal abscess.49

Section 3: Cervical Spine

Of the 1986 patients reported in case series,43,46,47,49,50,51 14 were found to have discitis, for an incidence of 0.7% per patient with a range of 0% to 3.2%. Zeidman et al.47 reported the incidence of discitis in their study plus five other studies to be between 0.5% and 2%. Recently, Guyer et al.49 reported two cases of discitis in 269 disc injections for an incidence of 0.74% per disc and 1.24% per patient. Prophylactic antibiotics were not routinely used. Both infected patients had a past medical history of diabetes mellitus. One case was found incidentally on a presurgical lateral X-ray film. In the other case, increased neck pain and arm pain were reported 3 days after cervical discography. Both patients had good clinical outcome with spontaneous fusion at the affected level. Zeidman et al. have reported the largest series: 4400 disc injections in 1357 patients.47 There were eight complications (seven cases of discitis and one retropharyngeal abscess) for an incidence of 0.18% infections per disc injection and 0.59% per patient. Prophylactic antibiotics were used in four out of the eight patients. They identified male gender, presence of a beard, and a short, thick neck as risk factors. All eight patients had good outcomes. One case of discitis in 456 disc injections in 114 patients (0.22% per disc and 0.88% per patient) was reported by Simmons et al.41 Whitecloud and Seago identified one case of discitis out of 34 patients for an incidence of 0.296% per patient.42 In 1988, Guyer et al. reported two cases of cervical disc infection in 362 disc injections, for an incidence of 0.55% per disc.46,49 In 1993, Shinomiya and Segil documented no complications in 401 disc injections in 144 patients.22 A report by Connor and Darden noted four complications in 31 patients for an incidence of 12.9%.43 ‘Discitis’ reportedly occurred in one patient. Increased neck pain several days post-procedure preceded acute onset of tetraplegia 5 days after cervical discography. MRI indicated an anterior epidural mass from C3 to C7. Epidural abscess was suspected, but at surgery the mass was found to be firm, fibrous tissue. There was no purulent material; Gram stain revealed no bacteria and cultures were negative (personal chart review by C.A.). The patient was hypertensive, diabetic, and suffered with severe uncontrolled gout. The etiology of the fibrous anterior epidural mass is not clear. Other complications included a patient with a severe vasovagal episode and one patient who had exacerbation of symptoms and was operated on several days after discography. It should be noted that it is normal to have residual discomfort for as long as 1 week following discography. Connors reported a complication rate 78% higher than the next highest series reporting complications. This difference could be the result of either marginal technique or incredibly bad luck.

Epidural abscess and miscellaneous rare complications Smith and Kim reported an increase in the size of a disc herniation after cervical discography.50 The patient had a past medical history of a moderate-sized central/left lateral herniated disc at C6–7. On injection of C6–7, the patient reported immediate severe concordant neck and arm pain. The following day, the patient had a temperature of 99.4°F orally, WBC of 12 700, ESR 55 mL per hour. Repeat ESR was 70 mL per hour. MRI obtained 18 hours after discography revealed fluid within the substance of an enlarged C6–7 disc herniation. Anterior corpectomy at C6 indicated thickened and a swollen posterior longitudinal ligament. Review of clinical history and MRI images is more suggestive of infection than an increased herniation size. The patient’s long-term outcome was good. There are reports of paralysis/paresis after cervical discography. Lownie and Ferguson reported a case in which there was presentation of neck pain with bilateral radicular pain, low-grade temperature

and progressive tetraparesis within 1 week of cervical discography.48 The patient was found to have a subdural empyema from C5 to T12 and continued to have spastic paresis at 1-year follow-up. Eismont et al.52 reported a patient who had increased neck pain, weakness in all four extremities, and urinary incontinence 4 weeks after cervical discography. The patient had discitis with purulent encephalomeningitis, with continued tetraparesis at 5-year follow-up. Laun et al. reported on two patients with paralysis related to discography; one with postinjection discitis and the other who developed tetraplegia within seconds of disc injection.51 Discography was contraindicated in both patients. The patient with discitis was found to have granulocytopenia and an intragluteal abscess premorbidly. The patient who suffered the immediate tetraplegia had a past medical history of myelopathy manifest by increased tone in all four extremities, weakness, and paresthesias. Premorbid myelogram showed arrest of contrast medium at the C4 disc space, confirming severe central stenosis. On injection, the patient reported excruciating pain. Within seconds, numbness and tetraparesis ensued. At surgery, one large and many small sequestered disc fragments were removed from the epidural space. In the discussion, one learns that the contrast was ‘injected very easily without exerting any pressure and was evenly distributed in the spinal canal.’ This statement raises the question of injection into the spinal cord. Regardless, cervical discography is contraindicated in a patient with cervical stenosis and myelopathy. Minor complications were also reported by Guyer in 1997,49 including headache and anterior cervical hematoma. Cervical hematomas causing airway obstruction have not been reported. Other theoretical but undocumented risks include pneumothorax when performing discography at C7–T1 or direct injection into the spinal cord.

Prevention, diagnosis, and treatment Infection Meticulous sterility is the first step. One should consider a full surgical prep and drape combined with surgical attire, including cap, mask, and double gloves. Although some have advocated a two-needle technique,49 most discographers use a single-needle technique with a styletted 23- or 25-gauge needle.53 Today, most discographers routinely use prophylactic antibiotics. The first senior author (R.D.) has noted only one case of cervical discitis since he began using intravenous antibiotics in 1990. That case was incidentally found on presurgical lateral X-rays. The second senior author (C.A.) personally reports no cases of cervical discitis since he began using intradiscal antibiotics in 1993. The published literature on cervical disc space infections following cervical discography reports the use of antibiotics in only the review by Zeidman et al.47 Prophylactic antibiotics were given only to patients deemed to be at high risk. Included were patients with beards, diabetes, and mitral valve prolapse. It is interesting to note that three cases of discitis were in male patients with beards who were given prophylactic antibiotics. The route of antibiotic administration was not mentioned in the study. Since antibiotics were administered only for cases thought to be at risk, one might speculate that only intravenous antibiotics were administered. The dose and timing of administration are critical. To be effective the antibiotic must be delivered in high dose with medication started well before the disc injection and continuing through the injection procedure.45 Failure to maintain high blood level may result in insufficient intradiscal concentration of antibiotic. Although most interventionists performing cervical discography use prophylactic antibiotics, there is no consensus on the route of administration, dose, or specific antibiotic. Both the North American Spine Society54 and the International Spine Intervention Society53 725

Part 3: Specific Disorders

recommend the routine use of antibiotics given either i.v., combined with the injected contrast, or both.

Intravenous administration A single dose of perioperative antibiotics reduces the incidence of postoperative disc space infection. Since the disc is an avascular structure, penetration into the disc is dependent on diffusion. The penetration and distribution of antibiotics into the avascular intervertebral disc is significantly influenced by the charge of the antibiotic. Positively charged antibiotics such as gentamicin, vancomycin, and clindamycin are able to penetrate into the negatively charged nucleus pulposus, while negatively charged antibiotics such as penicillin and cephalosporins can penetrate into the neutrally charged anulus fibrosus, but not the nucleus.52–54 Fraser et al. showed penetration of cefazolin at 1% of the blood levels in 4 or 5 sheep disc anuli but only 1 of 5 nuclei. Despite the poor penetration, no discitis resulted in the inoculated sheep discs.44 In human discs, Boscaidin et al. found that there was penetration of cefazolin into 40 lumbar discs and found that 25 of the 37 discs exposed 15–220 minutes post infusion had detectable levels.57 Rhoten et al. found that the most reliable penetration of cefazolin into cervical discs was achieved by administering 2 g of cefazolin approximately 60 minutes prior to disc space manipulation with the highest levels achieved at 45–57 minutes. Cefazolin has a half-life of 20–60 minutes, with maximum serum levels occurring 5–15 minutes after intravenous infusion.

Intradiscal administration Combining antibiotics with the injected contrast is appealing because significantly higher doses can be achieved without the inconsistencies of intravenous administration. Because disc space infections are most commonly caused by S. epidermidis, cefazolin is probably the most commonly used prophylactic antibiotic. Clindamycin, however, is often used when patients are allergic to cephalosporins. When these antibiotics are combined with contrast there in no decrement in their mean inhibitory concentration (MIC) and in fact iohexol used at 300 mgI/mL will achieve at least a level of two times the MIC.58 Doses of 1 mg/mL for gentamicin and cefazolin will exceed the MICs determined against Escherichia coli B, S. aureus, and S. epidermidis by more than 10-fold.58 Because clindamycin is bacteriostatic rather than bacteriacidal, a dosage of at least 7.5 mg /mL is required to achieve 10 times the MIC. The primary concern regarding the intradiscal use is the potential for toxicity. In cultured human disc cells from surgically removed disc anulus, cefazolin, gentamicin, cefamandole, and vancomycin all caused decrements in cell viability and proliferation when used in concentrations above 1 mg/mL. Whether higher doses are toxic when injected into a disc nucleus or whether the effect is only transitory is unknown.

Diagnosis and treatment Signs and symptoms of disc space infection are often subtle. Most patients have increased pain for several days to several weeks following cervical discography; however, the most common and reliable hallmark of discitis is an increase in axial pain. The onset of significantly increased pain is usually delayed by several days. Any patient who has a sudden increase in pain 2–3 days up to several weeks after cervical discography should be seen and evaluated. In fact, any patient who calls in with complaints of significantly increased pain should be evaluated. Although fever is a usual hallmark of infection, in disc space infections fever is not common. There may be a vague complaint of night sweats or chills. Early in the course, physical examination will reveal limited spontaneous movement of the head 726

and neck, decreased range of motion due to severe pain, and pain with firm local palpation over the spinous process or with vertical neck compression. Mandatory lab work includes a complete blood count, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). CPR is the most sensitive test and is elevated early. ESR is usually elevated later in the course of the infection. In some cases only the ESR will be elevated. Any patient with either test elevated and with increased pain should have an MRI scan. Within 3–7 days of the onset of discitis, subchondral marrow space edema becomes apparent. Endplate erosion is conclusive but occurs later. Enhanced signal within the epidural space indicates epidural involvement or abscess. If the MRI scan is negative, continue to follow the patient, and if symptoms do not improve over several weeks, or if they become worse, repeat the CRP, ESR, and if either is elevated, repeat the MRI scan. If discitis is diagnosed, in most cases the patient should be admitted to hospital and consultation with an infectious disease specialist should be considered. If there is epidural involvement, surgical consultation must also be considered. Most infections can be treated successfully with intravenous antibiotics in hospital for several days and continued for 5–6 weeks of self-administered home i.v. treatment. Infectious disease consultants usually want a direct tissue culture. Obtaining disc material by repeat needle aspiration or biopsy in the cervical disc is, however, usually unreliable and most often result in a negative culture. Once the endplates are penetrated and the disc is vascularized, the more benign infections such as S. epidermidis are sterilized.45 There are some who feel that most cases of cervical discitis are self-limited and spontaneously resolve. ‘Patients can be treated with antibiotics and bed rest and/or neck bracing with radiological evidence of spontaneous fusion developing over several weeks.’47

Cord injury Check the lateral fluoroscopic image prior to injection. Injecting contrast and especially contrast containing cephalosporin into the spinal cord is not a good thing. It is not difficult to pass a needle through the disc and into the cord and it is imperative to recognize this technical error. Usually, the patient will respond violently as they experience a sharp radiating pain into the upper and lower extremities. If this occurs, immediately withdraw the needle 1 cm and check the lateral fluoroscopic view. Depending on the patient’s build, checking the lateral view at the lower cervical levels may be difficult. In these cases, one should have considered touching the vertebral body above or below the disc to be sure of the depth before passing the needle into the disc. If the shoulders cannot be retracted enough to visualize the disc space and identify a needle the procedure should be aborted at that level. Using a short needle (e.g. 2–2.5 inch) will help one recognize when the needle has been advanced too far, and the short length will hopefully not reach the cord. Injection of cephalosporin-containing contrast material into the CSF might cause seizures. Cephalosporins are highly irritating to the cord. But, since one should only inject 0.1–0.2 mL at a time, and if one recognizes that the disappearing contrast is either in a vein or large fluid-containing space, 0.1 mL will probably not be a problem. However, failure to recognize injection into the CSF and injecting more solution is a problem. Cord injury due to injected contrast causing cord compression by enlarging or further herniating disc material into the central canal is rare. Interestingly, in patients suspected to have spinal cord compression, Ralph Cloward stated that ‘the pain experienced by disc injection also included a shock-like sensation “like electricity” which spread down the middle of the spine as far as the coccyx in one patient, and all the way to the toes in another.’4 This is the L’Hermitte’s phenomenon.

Section 3: Cervical Spine

Although Cloward may be excused for this questionable practice, one should be very careful about injecting a disc at a severely stenotic level or at a level with a large disc protrusion.

Bleeding Although the carotid artery is displaced during needle insertion, one can expect that in a patient with a large, short neck, a needle may on occasion pass through the artery and may result in several days of pain and swelling in the patient’s anterolateral neck (‘throat’) and discomfort when swallowing. A hematoma is often seen on a postdiscogram CT scan. Ice packs and reassurance are all that is necessary. Bleeding causing airway obstruction has not to our knowledge been reported, but the first senior author (R.D.) was told of one anecdotal account of a post-discogram obstruction occurring several hours after the discogram and requiring emergency intubation. Even though most hematomas will not cause airway compromise, one should consider stopping all medication and supplements that interfere with clotting an appropriate time before the procedure.

SUMMARY Cervical discography is far from an ideal test and, because of a possible significant false-positive rate and the potential morbidity, the test is controversial. There are, however, no other diagnostic tests that will confirm that a particular disc is a source of pain, and as such cervical discography remains the standard test. The sensitivity of the test is unknown, but the specificity is probably between 60% and 80%. Almost all mature cervical discs have fissures extending through the uncinate region at the posterolateral disc margin. When opened by injected contrast material, these will cause pain in symptomatic and asymptomatic subjects. One should therefore discount any pain provoked during the initial opening of the fissure and only secondary pressurizations causing concordant pain at 7/10 intensity or more should be called a positive response. Specificity will obviously vary with the pain tolerance and ability of a patient to discriminate pain concordance. A control-level disc that provokes pain less than 4/10 or clearly discordant pain will lower the chance of a false-positive response. Because multiple positive responses are common, cervical discography may be the best tool to rule out a surgical solution. Z-joint pain should be ruled out by an analgesic block protocol before performing cervical discography. During pressurization of the cervical discs, movement of the segment is often observed. Since Z-joint pain is common in the cervical spine,23 one could argue that the Z-joints should be blocked immediately before discography to make sure disc pain and not Z-joint is reproduced during pressurization causing segmental movement. The test should be used only when the information is needed and other tests are inconclusive. Discography is usually not needed when surgery is being performed for radicular pain unless the source of radicular pain is unclear or the patient also has significant axial pain and the surgeon needs to know the status of the discs adjacent to a proposed fusion. When the patient’s report of pain is felt to be unreliable, relief of pain following analgesic discography might provide evidence that the disc is a source of pain. Finally, the procedure should ideally only be performed by interventionists that perform the procedure on a regular basis. Meticulous asepsis and prophylactic intradiscal antibiotics should reduce the incidence of discitis to less than 0.2%, and other serious complications should be rare and mostly preventable. While there are no data to prove or disprove long-term negative consequences from puncturing the anulus of a cervical disc or injecting contrast-containing antibiotics,

using smaller-gauge needles and limiting the concentration of antibiotic injected is prudent.

References 1. Warren S, Browner TBN, Steven R, et al. Designing a New study: diagnostic tests. In: Stephen Hulley SC, ed. Designing clinical research. Baltimore, MD: Williams & Wilkins; 1988:87–97. 2. Smith GW, Nichols P Jr. The technique of cervical discography. Radiology 1957; 68(5):718–20. 3. Cloward RB. Cervical diskography. A contribution to the etiology and mechanism of neck, shoulder and arm pain. Ann Surg 1959; 150:1052–1064. 4. Cloward RB. Cervical discography. Acta Radiol Diagn (Stockh) 1963; 11:675–688. 5. Smith GW. The normal cervical diskogram; with clinical observations. Am J Roentgenol Radium Ther Nucl Med 1959; 81(6):1006–1010. 6. Cloward RB. The clinical significance of the sinu-vertebral nerve of the cervical spine in relation to the cervical disk syndrome. J Neurol Neurosurg Psychiatry 1960; 23:321–326. 7. Stuck RM. Cervical discography. Am J Roentgenol Radium Ther Nucl Med 1961; 86:975–982. 8. Cloward RB. New method of diagnosis and treatment of cervical disc disease. Clin Neurosurg 1962; 8:93–132. 9. Sneider SE, Winslow OP Jr, Pryor TH. Cervical diskography: is it relevant? JAMA 1963; 185:163–165. 10. Meyer RR. Cervical diskography. A help or hindrance in evaluating neck, shoulder, arm pain? Am J Roentgenol Radium Ther Nucl Med 1963; 90:1208–1215. 11. Schaerer JP. Cervical discography. J Int Coll Surg 1964; 42:287–296. 12. Holt EP Jr. Fallacy of cervical discography. Report of 50 cases in normal subjects. JAMA 1964; 188:799–801. 13. Herbert JJ. [Diagnosis of cervical disk hernias by discography and their surgical treatment]. Rev Chir Orthop Reparatrice Appar Mot 1965; 51:619–630. 14. Schaerer JP. Cervical discography and whiplash injury. Med Trial Tech Q 1965; 11:53–68. 15. DePalma AF, Subin DK. Study of the cervical syndrome. Clin Orthop Relat Res 1965; 38:135–142. 16. Klafta LA Jr, Collis JS Jr. An analysis of cervical discography with surgical verification. J Neurosurg 1969; 30:38–41. 17. Carragee EJ, et al. The rates of false-positive lumbar discography in select patients without low back symptoms. Spine 2000; 25 (11): 1373–1380; discussion 1381. 18. Derby R, et al. Comparison of discographic findings in asymptomatic subject discs and the negative discs of chronic LBP patients: Can discography distinguish asymptomatic discs among morphologically abnormal discs? Spine J 2005; 5(4):389–394. 19. Derby R, et al. Pressure-controlled lumbar discography in volunteers without low back symptoms. Pain Med 2005; 6(3):213–221. 20. Stuck RM. Neurological diagnosis of ruptured cervical discs. Proc Aust Assoc Neurol 1968; 5(3):455–457. 21. Holt EP Jr. Further reflections on cervical discography. JAMA 1975; 231(6): 613–614. 22. Shinomiya K, et al. Evaluation of cervical diskography in pain origin and provocation. J Spinal Disord 1993; 6(5):422–426. 23. Bogduk N, Aprill C. On the nature of neck pain, discography and cervical zygapophysial joint blocks. Pain 1993; 54(2):213–217. 24. Schellhas KP, et al. Cervical discogenic pain. Prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers. Spine 1996; 21(3):300–311; discussion 311–3112. 25. Gibson MJ, et al. Magnetic resonance imaging and discography in the diagnosis of disc degeneration. A comparative study of 50 discs. J Bone Joint Surg [Br] 1986; 68(3):369–373. 26. Nachemson A. Lumbar discography – where are we today? Spine 1989; 14(6): 555–557. 27. Modic MT, et al. Magnetic resonance imaging of the cervical spine: technical and clinical observations. Am J Roentgenol 1983; 141(6):1129–1136. 28. Modic MT, Masaryk TJ, Weinstein MA. Magnetic resonance imaging of the spine. Magn Reson Annu 1986; 37–54. 29. Boden SD, et al. Abnormal magnetic-resonance scans of the cervical spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg [Am] 1990; 72(8):1178–1184.

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Part 3: Specific Disorders 30. Hirsch C, Schajowicz R, Galante J. Structural changes in the cervical spine. A study on autopsy specimens in different age groups. Acta Orthop Scand 1967; Suppl 109:7–77. 31. Grubb SA, Kelly CK. Cervical discography: clinical implications from 12 years of experience. Spine 2000; 25(11):1382–1389. 32. Horton WC, Daftari TK. Which disc as visualized by magnetic resonance imaging is actually a source of pain? A correlation between magnetic resonance imaging and discography. Spine 1992; 17(6 Suppl):S164–S171. 33. Bernard TN Jr. Lumbar discography followed by computed tomography. Refining the diagnosis of low-back pain. Spine 1990; 15(7):690–707. 34. Parfenchuk TA, Janssen ME. A correlation of cervical magnetic resonance imaging and discography/computed tomographic discograms. Spine 1994; 19(24): 2819–2825. 35. Zheng Y, Liew SM, Simmons ED. Value of magnetic resonance imaging and discography in determining the level of cervical discectomy and fusion. Spine 2004; 29(19):2140–2145; discussion 2146.

44. Fraser RD, Osti OL, Vernon-Roberts B. Discitis after discography. J Bone Joint Surg [Br] 1987; 69(1):26–35. 45. Osti OL, Fraser RD, Vernon-Roberts B. Discitis after discography. The role of prophylactic antibiotics. J Bone Joint Surg [Br] 1990; 72(2):271–274. 46. Guyer RD, et al. Discitis after discography. Spine 1988; 13(12):1352–1354. 47. Zeidman SM, Thompson K, Ducker TB. Complications of cervical discography: analysis of 4400 diagnostic disc injections. Neurosurgery 1995; 37(3):414–417. 48. Lownie SP, Ferguson GG. Spinal subdural empyema complicating cervical discography. Spine 1989; 14(12):1415–1417. 49. Guyer RD, et al. Complications of cervical discography: findings in a large series. J Spinal Disord 1997 10(2):95–101. 50. Smith MD, Kim SS. A herniated cervical disc resulting from discography: an unusual complication. J Spinal Disord 1990; 3(4):392–394; discussion 395.

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52. Eismont FJ, et al. Antibiotic penetration into rabbit nucleus pulposus. Spine 1987; 12(3):254–256.

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55. Riley LH 3rd, et al. Tissue distribution of antibiotics in the intervertebral disc. Spine 1994; 19(23):2619–2625. 56. Currier BL, Banovac K, Eismont FJ. Gentamicin penetration into normal rabbit nucleus pulposus. Spine 1994; 19(23):2614–2618. 57. Boscardin JB, et al. Human intradiscal levels with cefazolin. Spine 1992; 17 (6 Suppl):S145–S148. 58. Klessig HT, Showsh SA, Sekorski A. The use of intradiscal antibiotics for discography: an in vitro study of gentamicin, cefazolin, and clindamycin. Spine 2003; 28(15):1735–1738.

PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ ii: Cervical Axial Pain

CHAPTER

Fusion Surgery for Axial Neck Pain

68

Timothy A. Garvey

INTRODUCTION For those suffering from cervical radiculopathy or myelopathy, there is little debate that an anterior cervical discectomy and fusion (ACDF) is a viable treatment option.1–20 However, patients who present with their chief complaint being ‘neck pain,’ with or without referred or radicular symptoms, often are told that there is nothing that can be done surgically. This is wrong! The purpose of this chapter is to enhance the reader’s understanding of the surgical peer-reviewed literature, which leads to a rational decision-making process (Fig. 68.1). For many patients, that decision will be that surgical intervention is a reasonable option with a predictable statistical chance of success. The time-honored adage ‘that it is the decision, not the incision, which is most important,’ cannot be overemphasized.

DOMINANT NECK PAIN

Surgical consult

Active rehab

If present

Not done

INDICATIONS – PATIENT SELECTION While covered in previous chapters, a brief review of the epidemiology and natural history of neck pain is in order. Prevalence studies have noted 35% of the general Norwegian population to have neck pain complaints within the preceding year, with 14% of respondents reporting those symptoms to have lasted longer than 6 months.21 In the Saskatchewan Health and Back Pain Survey, reported in 2000, it was documented that 54% of respondents had experienced neck pain in the preceding 6 months, with almost 5% perceiving themselves to be ‘highly disabled’ by their pain.22 When one looks at the literature of whiplash-associated disorders, it is apparent that while the majority of injured individuals do have spontaneous resolution of their symptoms, a small percentage, yet a significant number of human beings, do develop chronic neck pain.23,34 As with all medical ailments, it is important to appreciate the natural history of a condition. One approaches the patient with a ‘common cold’ with a vastly different sense of urgency than in comparison to an individual with suspected acute meningitis. We must then realize that in studies of natural history many with neck pain never seek out evaluation. Therefore, there is an inherent selection bias to more self-perceived impairment in those who seek out medical care. In an average 15.5-year follow-up study, Gore et al. reported on those presenting with neck pain.35 Seventy-nine percent of patients noted improvement with nonoperative care, with 43% reporting pain-free status and 32% continuing to report modest to severe pain. The severity of initial presenting symptoms, and the report of a significant injury, were more indicative of those with long-term complaints. In a series of patients with neck-only, or neck and arm pain, DePalma et al. noted 45% of those treated nonoperatively to have satisfactory long-term outcome.36,37 In a surgical series report, DePalma et al. reported that at 3-month follow-up those presenting with dominant neck pain had 21% complete relief and 22% no relief

Psych consult

Stay non-op

Thorough evaluation, exclude tumor, infection, significant decreased neurologic function, i.e. myelopathy

Failure at 12 months; non-operative strategies which have specifically included active rehabilitation

Psych issue

No psychosocial contraindications

No

Patient perceives severity to point of requesting surgical option

Objectification

RATIONAL SURGICAL DECISION MAKING

History and physical exam

Selective nerve root block, discography, facet blocks

Radiographs – AP, lateral, flexion-extension, MRI, CT, myelography

Specific anatomic diagnosis

Discogenic pain

– Facet arthrosis – Degenerative listhesis – Instability

Stenosis posterior rami distribution

ACDF at affected levels

Fusion affected level, posterior vs. anterior

Decompression

Fig. 68.1 Algorithmic approach.

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Part 3: Specific Disorders

with nonoperative care.36 At a 5-year follow-up time, Rothman noted 23% of patients continued to be partially or totally disabled due to significant cervical symptoms stemming from disc degeneration.36,38 In a review of those presenting with cervical radiculopathy, it was noted that while patients do not typically progress to myelopathy with nonoperative care, they often (two-thirds of the group) will have persistent symptomatology of some degree.39,40 The whiplash literature reveals a common pattern of a small group reporting persistent intrusive symptoms.23,34 In a textbook chapter, McNab and McCulloch summarized ‘about those who had suffered a whiplash injury, approximately 10–20% are left with discomfort of sufficient severity to interfere with their ability to do work and to enjoy themselves in leisure hours.’41 Thus, it must be acknowledged that while many who seek out medical care for neck pain will improve with nonoperative management, a finite low percentage of patients will still have symptoms of sufficient magnitude to cause them to seek out a surgical solution. It is for this group of patients that we need to have a rational surgical decision-making process.

OFFICE EVALUATION History When a patient presents for initial evaluation, we ask for their chief complaint, as this will focus our line of questioning and examination. In this chapter, we are concerned with those who complain of ‘axial neck pain.’ However, the typical patient does not say, ‘I have dominant axial pain;’ they state rather that they have neck pain, with or without arm pain. Patients who yield an ultimate diagnosis of myelopathy or radiculopathy will often present with a complaint of neck pain.8,40,42,43 It is up to the medical evaluation to elicit the historical features that will lead to a specific diagnosis. Several critical decisions must be made at the initial evaluation. Is this mechanical or non-mechanical pain? Mechanical pain is typically worse with certain activities, i.e. flexion usually increases discogenic pain, while extension increases the pain from facet arthrosis, and the patient can usually find a position of comfort. Non-mechanical pain suggests tumor, infection, or other etiologies which require a different investigation. This often is the patient with rest pain, night pain, no position of comfort, and they may present with constitutional symptoms of weight loss, fever, chills, malaise, etc. One needs to answer, is this pain local, referred, or radicular? Local pain is just that, focal, localized neck pain. Referred pain, that is pain felt away from the tissue of site of origin, is often inter- or periscapular, upper trapezial, or basioccipital. Radicular pain is the classic radiating pain along the course of the nerve root. This typically is into the brachium with radiation distally such as to the dorsal radial forearm, thumb, and index finger to suggest a C6-type distribution. It is often forgotten, however, that while this classic distribution is along the course of the ventral rami, there also does exist the dorsal rami along which path patients can also perceive pain. This ‘dorsal radicular’ pain can/does often get lumped together with axial symptomatology. One needs to assess whether the patient is intact neurologically or has deficits. From the historical perspective, we ask about paresthesias, numbness, weakness, ataxia, and bowel and bladder dysfunction. For those with significant myelopathy or progressive loss of neurologic function, an urgent surgical consultation is recommended. We finally need to answer whether there are significant psychosocial contraindications to elective surgical treatment for pain management. This is based on depression, frank psychosis, secondary gain issues, or unrealistic expectation, all of which need to be considered. Thus, this chapter is focusing on the individual who has dominant axial mechanical neck pain that is primarily local or referred, who is intact neurologically, and who has no obvious psychosocial contra730

indication to proceed with a surgical work-up. We must realize that patients present with signs and symptoms on a continuum. Some will have 100% arm pain in a C6 distribution while others will present with 100% neck pain with no periscapular or arm pain. Most, however, will have some combination of both. I believe it is vital to have the patient decide if the neck pain is greater than, the same as, or less than the arm pain. I query specifically about a percentage, i.e. 70% neck pain and 30% arm pain. While this is not exact, it does help us understand what the patient wants addressed. Simplistically, we think the more arm pain there is, the more nerve root decompression is required; the greater the neck pain, the more the patient has a joint problem which can be addressed with a fusion of the affected joint (in the near future, potential arthroplasty). I typically ask about fevers, chills, night pain, etc. If tumor or infection is suspected, the patient needs an urgent laboratory evaluation and a magnetic resonance imaging (MRI) diagnostic work-up. Questions about the timing of onset, that being acute and/or traumatic, i.e. whiplash, versus gradual or progressive onset help in the differential diagnosis. Provocative or ameliorative motions can suggest a source, i.e. worsening pain with flexion activities with progressive pain throughout the day that is relieved with rest, tends to suggest a discogenic etiology. Patients who cannot turn to one side and describe unilateral pain when looking over their shoulder (i.e. Spurling’s maneuver) suggest a foraminal radicular etiology. I question about neurologic function. For myelopathy, I ask about generalized weakness, decreased fine motor dexterity, stumbling or ataxia, sphincter dysfunction such as urinary urgency, and paresthesias which may be nondermatomal. For radiculopathy, often a specific root pattern of numbness, pain, or specific weakness can be elicited. If these symptoms are present, they can help focus the differential to a specific cervical diagnosis. For psychosocial issues, we review the patient intake forms for depression, look for expectations of treatment, and solicit information about worker’s compensation status and litigation as these all may have a bearing on the patient-perceived pain. Specific psychologic treatment may be recommended. It is of interest that our last cervical fusion study did not correlate the presence of worker’s compensation or litigation with poor outcome.9

Physical examination The physical examination should be straightforward. Range of motion is documented. If flexion hurts more than extension, think discogenic; if extension hurts more than flexion, think facet arthrosis or stenosis. If rotation or lateral flexion is preferentially limited to one side, it suggests a unilaterality of pathology. Spurling’s maneuver, i.e. lateral flexion, extension, and rotation which causes provocation of symptoms, suggests foraminal nerve root compression. If this reproduces the patient’s ‘neck pain,’ particularly into the upper trapezial or periscapular region, think nerve root pain. Assess the reflexes: hyperactive suggests upper motor neuron pathology, hypoactive suggests lower motor neuron pathology; and compare right side versus left side. Check for strength and sensation. If the examination documents pathology to suggest myelopathy or dense radiculopathy, the evaluation focuses on the neurologic deficit. An MRI or myelogram computed tomography (CT) scan should then be sought out. Often, those with dominant neck pain will have some component of arm symptomatology, just as those with ‘radiculopathy’ often have substantial complaints of neck pain.2,7,8,19,44,45

IMAGING After a history is obtained and a physical examination is performed, one should start with basic radiographs. I prefer anteroposterior (AP), lateral, and flexion extension cervical spine radiographs. I do

Section 3: Cervical Spine

not routinely obtain an open mouth view or oblique views. One looks to exclude the obvious destruction of tumor and/or infection. We check for dynamic instability by the measurement of listhesis and angular deformity.43,46 We note obvious spondylosis by assessing disc space height, sclerosis, and osteophyte formation.47–49 While it is recognized that with increasing age there is an increasing presence of radiographic spondylosis, the films are helpful. If a young patient has multilevel spondylosis, we think less of a surgical approach; if a single level is involved, we think more of a surgical solution. If gross instability is seen, the patient needs to be counseled about the risks of nontreatment. The MRI is now my next recommendation. Exquisite detail about tumors, infection, neurologic compression, and disc morphology is obtained. However, for this group of patients with axial neck pain, the history and physical examination did not suggest tumor or infection. The disc spaces are assessed for morphology, annular tears, and frank herniations. If the patient has a contraindication to MRI, i.e. pacemaker, metal in the eye, etc., a myelogram CT scan would be recommended and should yield similar diagnostic value.

ADVANCED INVASIVE DIAGNOSTICS Based upon the evaluation, when one has a patient with chief complaint of neck pain, who is grossly normal neurologically, who has failed a prolonged course of nonoperative management, who has no psychosocial contraindication, and who believes the symptoms are severe enough to contemplate surgical intervention, advanced invasive diagnostic testing can be critical in objectifying the pathologic source of the patient’s symptoms. Surgeons cannot ‘cut out pain.’ They can decompress nerves or spinal cords, stabilize unstable joints, and fuse (replace) bad joints. It is the objectification process which allows us to educate a patient about the statistical chance of success for a given procedure. In some patients, the history, physical examination, radiographs, and MRI will suffice. For example, a patient may present with a chief complaint of neck pain, which came on acutely, with initially severe arm pain, that now has settled into chronic axial neck pain, 80%, with 20% arm pain into the thumb and index finger. Flexion activities typically increase the pain, and the patient can find positions of comfort at rest. The patient has mild weakness of wrist extension with mild decrease of the brachioradialis reflex. The MRI shows mild to moderate degeneration of C5–C6 with a central to right-sided herniated nucleus pulposus, and all other segments are pristine appearing. In this case, if nonoperative treatment has failed (which may have included a C6 selective nerve root block), I would not typically do more testing. A single-level ACDF may be recommended. However, this clean a scenario is uncommon. Most often, the patient with axial pain will have several levels of degenerative change on an MRI study or noted on the X-rays. In those whose history and examination suggest a discogenic source, a discogram can be a very valuable tool. While the selection of this ‘older technology’ of discography still emotes controversy in some, I find it to be particularly useful in the surgical evaluation of those with axial pain. Data from our center has shown a statistical association with patient-perceived outcome.9 Numerous other authors have cited the utility of discography in patient selection.9,17,20,45,50–60 Most often, the MRI alone will not suffice. There are a substantial number of asymptomatic individuals who have MRI-documented pathology, which increases with age.60–63 In a prospective correlation of MRI and discography, in asymptomatic subjects and pain sufferers, Schellhas et al. concluded that MRI often misses annular tears and cannot reliably identify the source of discogenic pain.62 While many asymptomatic individuals had

degenerative changes, only 3/40 discs studied in this group elicited a pain response, suggesting a high specificity and positive predictive value.62 Pragmatically speaking, the issue is, does the discogram yield information that reliably predicts outcome, and do published reports document this? The answer is yes, Table 68.1 documents such. What is hard to report upon is when the discogram keeps the patient out of surgery. For example, when every level hurts and there is no control, surgical intervention will not typically yield good results. The clean discographic surgical patient will have significant (greater than 6/10) concordant reproduction of pain at the affected level/levels, with little or no pain and normal appearance at the control level.9 A selective nerve block can be useful in determining a surgical level. Such a patient may have neck, upper trapezial, and periscapular pain that increases with Spurling’s maneuver, has foraminal stenosis on MRI, and appears to have symptoms that are more often unilateral. In this patient, I often proceed to a selective nerve block. The selective nerve root block can be both diagnostic and potentially therapeutic. If in the first 30–60 minutes, during the lidocaine anesthetic phase, the patient reports significant diminution, i.e. 70–100% relief of typical pain, that specific nerve root is indicated as a primary pain generator. If steroids give long-term relief, all will be happy.64 If the patient has great relief with the selective nerve root block, unilateral pain, foraminal stenosis, and no instability, then a posterior laminoforaminotomy may be a favored option. If there is bilateral pain, and an additional ‘discogenic component,’ then one may proceed with an ACDF at the affected level. True facet blocks or medial rami branch blocks are not uncommon in the work-up of patients with neck pain, particularly post-traumatic pain.24,65–68 To date, I know of no study to base fusion surgery on this diagnostic tool. Conceptually, one would think, if the patient had excellent temporary relief of the pain with this injection at a specific joint, that fusion of that joint may relieve the pain. If one were to use this intuitive reasoning to base the surgical decision, I would recommend that it be done in a study fashion with attendant IRB approval.

SURGICAL TREATMENT FOR SPECIFIC ANATOMIC DIAGNOSES When the ultimate clinical diagnosis for a patient with chronic axial mechanical pain is that of discogenic pain, an anterior cervical discectomy and fusion is a very reasonable treatment option (Fig. 68.1). The patient will have symptoms of dominant neck pain with or without referred symptoms to the basioccipital region, upper trapezial region, or interscapular region. The patient may also have a component of arm pain with mild neurologic signs of dysfunction. The X-rays will often show spondylosis with no gross instability. The MRI and discography will pinpoint specific joints as the ‘painful levels.’ The more clean the diagnosis, i.e. one or two levels of concordant reproduction of pain, which matches the MRI appearance of degeneration, with a normal nonpainful adjacent segment, the higher is the likelihood that the patient will favorably respond to an anterior cervical decompression and fusion. Having more levels involved does not preclude the surgical option, but it does raise the risk of the patient reporting nonsuccessful outcome and pseudoarthrosis. Therefore, the patient needs to clearly understand this preoperatively. On the other hand, in an older population with advanced degeneration, these joints have less motion, and my experience has been favorable.9 The physiologically younger patient with expectation of high physical demand will be less satisfied with attempts at multilevel treatment. To answer a patient’s question about what they may expect from surgical management, the reader needs to assess their level of satisfaction with the current surgical literature support for that treatment. 731

Part 3: Specific Disorders

A

C

B

EF

D

F

G

Fig. 68.2 This case represents a common presenting scenario. The patient is a 39-year-old female first seen in November 2000 with a 9-month history of 90% neck pain and headaches and 10% arm pain. She was seen again in early 2003 with continued symptoms which are progressively worse. (A, B) These show flexion extension radiographs which reveal moderate cervical spondylosis at C5–C6 with no obvious instability. (C) This shows a sagittal MRI with small posterior protrusion at C5–C6 with disc desiccation. There appears to be small annular thickening posteriorly at C3–C4. There is no gross cord compression. (D) Transverse image at the same level shows no gross cord compression. (E) The patient underwent discography with 10/10 concordant reproduction of pain at C5–C6, with small pressure sensations at other levels. (F, G) These show flexion extension radiographs 1 year postoperatively with solid arthrodesis at C5–C6 and no obvious degenerative change or stability at the adjacent segments. Her pain was substantially improved. She was working full-time and taking no pain medication.

732

Section 3: Cervical Spine

A clever paper by Smith and Pell, titled ‘Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials,’ points out that advocates of evidence-based medicine ought not to neglect the information we obtain from observational studies.69 When we see similar reports of good to excellent outcomes spanning six decades, from various centers, utilizing similar diagnostic evaluations and surgical interventions, we can place greater confidence in the predictability of those data (Table 68.1).9,17,20,45,50–58,60 The pioneers of ACDF surgery, Robinson and Smith, reported on 56 patients in their 1962 paper.16,17 Fortyfive of 56 had neck pain, 38 of 56 had traumatic etiology, 25 of 56 had occipital pain, 26 of 58 had interscapular pain, and discography was done in 47 of 56 patients. They reported 73% good to excellent results, 22% fair, and 5.5% poor outcome, with 9 of 56 patients having pseudoarthrosis. Highlighting the data from a recent series from our center can give an appreciation of what to expect from this type of surgical approach.9 Out of a prospective series of 112 patients with axial mechanical neck pain, 87 were available at average 4.4-year follow-up which included an extensive self-reported outcome data questionnaire. This series documented that 82% (71/87) self-rated their outcome to be good, very good, or excellent. Pain improvement was evidenced by an average diminution of the VAS from 8.4 preoperative to 3.8 at followup, and was seen in 93% of individuals. The average 3.8 follow-up score includes those with recurrent pain, new injury, and who did not respond, thus reflecting a higher average VAS. Self-rated function improved 50% as documented on both a cervical-modified Oswestry and Roland and Morris disability index. We specifically looked at our use of discography in the selection process (Table 68.2). If a clean anatomic pattern was present, that is greater than or equal to 6/10 concordant reproduction of pain, with little or no pain at an anatomi-

Table 68.1: Outcomes of surgical treatment Author

Number of patients

Reported outcome

Zheng

60

55

76% good or excellent, 18% fair, 6% poor

Garvey9

87

82% good or excellent, 16% fair, 2% poor

20

85% satisfaction

Ratliff54 Motimaya

14

78.6% satisfaction

Palit53

38

79% satisfactory, 21% not satisfactory

Whitecloud19

34

70% good or excellent, 12% fair, 18% poor

Roth56

71

93% good or excellent, 1% fair, 6% poor

White46

28

62% good or excellent, 23% fair, 23% poor

Riley45

93

72% good or excellent, 18% fair, 10% poor

Simmons57

30 neck pain 51 neck and arm

78% good or excellent, 15% fair, 7% poor

William20

15

7% excellent, 20% good, 33% fair, 40% poor

Dohn50

34

62% good or excellent, 24% fair, 15% poor

Robinson17

56

73% good or excellent, 22% fair, 5% poor

52

Table 68.2: Surgical outcome – discography Discographic pattern

Excellent/good

Fair/poor

No follow-up

Clean

32

3

8

Not clean

21

10

7

No discography

18

3

10

Clean is ≥6 of 10 concordant pain with validating level.

cally near-normal control level, and all of the affected levels were treated, 91% (32/35) reported good to excellent outcome. In those with ‘nonclean anatomic pattern,’ i.e. most commonly greater than or equal to 6/10 nonconcordant pain at what will become a proposed adjacent segment with mild to moderate morphologic abnormality, only 68% (21/31), reported good to excellent outcome. In the group where we did not utilize discography, i.e. those with single- or twolevel pathology on MRI with a lesser component of clinically correlating radicular pain, 86% (18/21) self-reported good to excellent outcome. The take-home message is that the better one can objectify the pathology, the more likely is it that surgery can remedy the patient’s symptomatic complaints. The reader can review similar reports of surgical outcomes that span six decades from multiple centers (Table 68.1).9,17,20,45,50–58,60 These authors report remarkably similar outcomes and what appears to be a similar diagnostic grouping. This gives greater confidence that these studies do cumulatively support this type of surgical approach for discogenic neck pain. Although the majority of my surgical practice for those with axial neck pain complaints is secondary to a discogenic etiology, a distinct group presents with complaints of neck pain, secondary to spondylosis, with facet arthrosis, facet ganglion cysts, rheumatoid arthritis, and/or instability as evidenced by degenerative listhesis. The caveat in this group is that a high percentage of radiographic spondylosis is seen in the asymptomatic population.47,69–71 In this group, one would potentially be a candidate either for an anterior decompression and fusion and/or a posterior cervical approach to specific joint pathology. This algorithmic breakout of ‘posterior-based’ pain would include those with rheumatoid arthritis who are more prone to subaxial instability. As noted earlier, if obvious arthrosis is seen at these joints, temporary relief is obtained with anesthetic blocks, treatment at these levels appears rational, but peer-reviewed validation is lacking. Finally, a third group is seen in those with chief complaint of neck pain. These are the individuals with a radicular etiology, in whom a decompressive procedure would be indicated. Often, they will be more unilateral in their complaints. Upon more focused historical review, their pain will typically have more upper trapezial and periscapular radiation, on exam the symptoms will be typically made worse with Spurling’s maneuver, and the pain most often will be temporarily significantly reduced with a selective nerve root block. In this group, a posterior laminoforaminotomy with nerve root decompression is a rational surgical choice. They can also be managed with an anterior cervical decompression and fusion, but the fusion in this group may not be required. This posterior rami-based group also involves the upper cervical roots (C2, C3, and C4) which often have been neglected.42,72,73

SUMMARY Patients who present with a chief complaint of chronic axial neck pain do have a surgical option available to them when nonoperative treatment, specifically including an active rehabilitative approach, has not yielded successful adequate resolution of the symptoms, and the patient feels that these symptoms are so severe that they would 733

Part 3: Specific Disorders

wish to entertain a surgical option with a typical 70–80% chance of good to excellent outcome. In this case, surgical diagnostic work-up should ensue. This includes the history and physical examination, radiographs, MRI or CT, and very often advanced diagnostic injections leading to objectification. In these patients, the rational surgical decision-making process will most often yield gratifying patientperceived outcomes.

26. Gargan M, Bannister G. Long-term prognosis of soft-tissue injuries of the neck. J Bone Joint Surg [Br] 1990; 72(5):901–903.

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24. Barnsley L, Lord S, Wallis B, et al. The prevalence of chronic cervical zygapopyhsial joint pain after whiplash. Spine 1995; 20(1):20–26.

55. Riley L. Various pain syndromes which may result from osteoarthritis of the cervical spine. Maryland State Med J 1969; 18:103–105.

25. Carroll C, McAfee P, Riley L. Objective findings for diagnosis of ‘whiplash.’ J Musculoskeletal Med 1986; 57:76.

56. Roth D. A new test for the definitive diagnosis of the painful-disk syndrome. JAMA 1976; 235(16):1713–1714.

Section 3: Cervical Spine 57. Simmons E, Bhalla S, Butt W. Anterior cervical discectomy and fusion. A clinical and biomechanical study with eight-year follow-up. With a note on discography: technique and interpretation of results. J Bone Joint Surg [Br] 1969; 51:225–237.

65. Bogduk N, April C. On the nature of neck pain, discography and cervical zygapophysial joint blocks. Pain 1993; 54:213–217.

58. Whitecloud T, Seago R. Cervical discogenic syndrome. Results of operative intervention in patients with positive discography. Spine 1987; 12(4):313–316.

66. Lord S, Barnsley L, Wallis B, et al. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med 1996; 335(23): 1721–1726.

59. Zeidman S, Thompson K. Cervical discography. In: The Cervical Spine Research Society. The Cervical Spine. 3rd edn. Philadelphia: Lippincott-Raven; 1998: 205–216.

67. Manchikanti L, Boswell M, Singh V, et al. Prevalence of facet joint pain in chronic spinal pain of cervical, thoracic, and lumbar regions. BMC Musculoskeletal Disord 2004; 5(1):15.

60. Zheng Y, Liew S, Simmons E. Value of magnetic resonance imaging and discography in determining the level of cervical discectomy and fusion. Spine 2004; 29: 2140–2145.

68. McDonald G, Lord S, Bogduk N. Long-term follow-up of patients treated with cervical radiofrequency neurotomy for chronic neck pain. Neurosurgery 1999; 45(6):1499–1500.

61. Boden S, McCowin P, Davis D, et al. Abnormal magnetic resonance scans of the cervical spine in asymptomatic subjects. J Bone Joint Surg [Am] 1990; 72: 1178–1184.

69. Smith G, Pell J. Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials. Br Med J 2003; 327:1459–1461.

62. Schellhas K, Smith M, Gundry C, et al. Cervical discogenic pain: prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers. Spine 1996; 21(3):300–311.

70. Friedenberg Z, Miller W. Degenerative disc disease of the cervical spine. J Bone Joint Surg [Am] 1963; 45:1171–1178.

63. Teresi L, Lufkin R, Reicher M, et al. Asymptomatic degenerative disk disease and spondylosis of the cervical spine: MR imaging. Radiology 1987; 164:83–88. 64. Ferrante M, Wilson S, Iacobo C, et al. Clinical classification as a predictor of therapeutic outcome after cervical epidural steroid injection. Spine 1993; 18(6): 730–736.

71. Hitselberger W, Witten R. Abnormal myelograms in asymptomatic patients. J Neurosurg 1968; 28:204–206. 72. Poletti C. The neglected roots: C4, C3, C2. In: Cervical Spine Research Society. Atlanta, GA; 1998. 73. Toshimasa T. Cranial symptoms after cervical injury: aetiology and treatment of the Barre-Lieou syndrome. J Bone Joint Surg [Br] 1989; 71:283–287.

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PART 3

SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ iii: Other Disorders of the Cervical Spine

CHAPTER

Cervicogenic Headache

69

Sarjoo M. Bhagia, Curtis W. Slipman and Craig D. Brigham

INTRODUCTION It is a common experience in clinical practice to encounter syndromes that are diagnosed and treated using a variety of methods despite limited research and/or a lack of evidence-based medical consensus. Cervicogenic headache (CH) is one of these entities. Although there is long-standing notion that headaches can originate from structures in the neck and can be treated by interventions directed at the cervical spine, it is only during the past two decades that the topic has gained attention in mainstream medical literature. CH is a syndrome and not a distinct disease process. Its symptoms constitute a ‘final common pathway’ for pain emanating from a variety of cervical biomechanical and/or inflammatory disorders. It is a diagnosis of exclusion and more serious pathology should be ruled out. Specific spinal structures such as nerves, nerve root ganglia, uncovertebral joints, intervertebral discs, facet joints, ligaments, and even muscle may give rise to similar symptoms ultimately diagnosed as CH.1,2 The absence of pathognomonic symptoms, physical findings, or imaging studies makes the diagnosis and treatment of CH challenging to the clinician. This chapter will review the history, epidemiology, pathophysiological basis, diagnostic criteria, and treatment of CH.

HISTORICAL PERSPECTIVE One of the earliest references describing a relationship between headache and the cervical spine was a series of lectures by Hilton occurring between 1860 and 1862, which were reported by Pearce.3 Almost 90 years later, a case series published by Hunter and Mayfield4 in 1949 formed the intellectual rationale for interventional techniques to treat cervicogenic headaches. Hunter and Mayfield reported that occipital neuralgia could be an important cause of headaches, with pain radiating from the occiput to the periorbital and jaw areas. Their theory was used to justify the injection of analgesics around the occipital nerves in an attempt to relieve these headaches. That same year, Bartschi-Rochaix5 coined the term ‘cervical migraine’ to label headaches presumed to derive from the neck. In 1955, Kovacs6 postulated that motion restriction of the cervical spine could lead to muscle spasm, thereby compromising the vertebral artery and nerves, and manifesting as a headache. This premise helped popularize osteopathic, chiropractic, and manual treatment of the cervical spine to relieve CH. Bogduk and Marsland7 in 1986 put forth their theory of ‘third occipital headache’ and advocated surgical intervention to treat it. This paper provided the first compelling scientific evidence that headaches could indeed develop as a consequence of a cervical spine biomechanical disorder. The term ‘cervicogenic headache’ was initially introduced into the medical lexicon in 1983 by Sjaastad et al.,8 to describe patients with a headache associated with disorders of the neck. In 1988, the International Headache Society (IHS)9 amended its diagnostic classi-

fication system to include a category for CH. In 1990, Sjaastad et al.1 published specific diagnostic criteria for CH. Less stringent diagnostic criteria for CH was subsequently published by the International Association for the Study of Pain (IASP) in 1994,10 and by the Quebec Headache Study Group in 1995.11 In 1998, Sjaastad et al.12 revised their diagnostic criteria for CH based on more extensive clinical research.

EPIDEMIOLOGY Few epidemiologic studies exist and these have only been done in the last decade.13–20 These studies support that CH is common. However, there is a great deal of variation in the perceived prevalence of CH. In the general population, for example, prevalence rates ranged from 0.4% to 2.5%,13,14 whereas studies looking at all patients with a complaint of headache reported estimates of 15–20%.9,14–16 The highest variation was among headache center patients, with prevalence estimates of 0.4–80%.17,18 The wide variation in reported prevalence can be attributed to the different diagnostic criteria used to define CH. The population pool each of the publications drew from was not comparable. Another factor influencing prevalence rates in headache centers is the overlap between the diagnosis of CH, tensiontype headache (TTH), and common migraine headache (MH). Bono et al.19 report that 75% of patients fulfilling IHS criteria for MH also met most of the criteria for CH. One study of headache center patients reported that whereas only 16.1% were diagnosed with CH, an additional 20.1% were diagnosed with both MH and CH, for a total prevalence of 36.2%.16 Another study reported that 56.4% of CH diagnoses occur in combination with other headaches, including MH, TTH, and drug-induced headache.20 Analysis of patient descriptive data from studies where such information was given reveals that there is a preponderance of female patients with CH,21–23 with an average gender distribution of 79.1% female and 20.9% male. The mean age was noted to be 42.9 years, and the mean duration of symptoms was 6.8 years.24

NEUROANATOMIC BASIS AND PATHOPHYSIOLOGIC MECHANISMS Convergence theory There is compelling circumstantial evidence that substantiates the theory of convergence to explain how cervical spine pathology can manifest as CH. The basic premise of convergence is that when primary afferents from two separate regions in the body converge on the same second-order neurons in the spinal cord, nociceptive activity along one of the afferent nerves can be perceived as pain in the other afferent nerve.25 Anatomically, both cervical and cranial afferent nerves innervate the head and face. The greater occipital, lesser 737

Part 3: Specific Disorders

occipital, and greater auricular nerves may innervate as far as the coronal sutures. Pain perceived in the forehead could be due to convergence between the trigeminal and upper cervical afferents. The cervicotrigeminal interneuron relay conveys nociceptive information to the upper cervical cord neurons. The trigeminal nucleus begins in the pyramidal decussations and descends as far caudad as C4 as the nucleus caudalis. The trigeminal nucleus is morphologically and functionally associated with the upper cervical cord and the cells form a column which is continuous with the posterior horn of the cervical cord. These anatomical relationships clearly demonstrate convergence between the trigeminal and cervical cord (Fig. 69.1). This convergence may also help to explain the systemic and sympathetic nervous system features accompanying CH. Kerr26 discussed the relationship of the descending tract of the trigeminal nerve to the upper cervical roots following his dissection and analyses of adult cats. He observed that trigeminal afferents formed a bundle (trigeminosolitary bundle) with the solitary nucleus leading him to conclude that the trigeminal nerve provides a visceral component to the head and neck. The descending afferent trigeminal tract was identified as far caudal as the third cervical root. Trigeminal fibers were found at the low medullary, first, and third cervical cord levels. The second cervical root of the trigeminal fibers descends to the upper half of the cervical segment, but rapidly disappeared.26 Sectioned dorsal rhizotomy specimens demonstrated that the first cervical root traversed the trigeminal tract. There was no evidence of afferent fibers descending to the fourth through sixth cervical roots.26 The spinal tract of the trigeminal nerve entered the cervical cord in Lissauer’s tract as far down as the uppermost area of the

Gasserian ganglion

V1

Lesser occipital nerve (C2 and C3 ventral ramus)

V2

V3

Third occipital nerve

Fig. 69.1 The cervicotrigeminal interneuronal relay. A potential overlap of central neuronal connections occurs between the spinal nucleus of the trigeminal nerve and the upper cervical cord neurons. The trigeminal nucleus develops from the pyramidal decussations and descends to the level of C2, and perhaps as caudad as C4, as the nucleus caudalis, which primarily subserves pain and temperature function to the head and neck. This trigeminal nucleus is morphologically and functionally associated with the upper cervical segments, and its cells form a column continuous with the column of cells that form the posterior horn in the cervical cord. 738

Cervical facet joint The zygapophyseal joints are implicated as a major source for cervicogenic headaches. The medial branch of the dorsal ramus above and below its location innervates the facet joints, except C2–3. The C2–3 is innervated by the superficial medial branch of the C3 dorsal ramus, also known as the third occipital nerve (TON).25,30 Pain patterns from stimulation of the cervical zygapophyseal joints have been studied in normal volunteers31 and from clinical evaluation.32,33 These studies suggest that the cervical zygapophyseal joints produce characteristic pain patterns according to the segmental distribution.31,32 The prevalence of zygapophyseal joint pain after whiplash has been reported as high as 50% in the C2–3 joint and 49% in the lower cervical joints.34,35

Cervical discs

Greater occipital nerve (C2 distal ramus)

Spinal nucleus and tract of CNV

third cervical cord. These cadaveric findings provide the anatomic basis for convergence theory (Kerr principle) and may explain why cervicogenic pain can occur ipsilaterally or bilaterally. Almost every structure in the cervical spine has been implicated as a cause of headaches. Similarly, the mechanism of action may be due to degenerative changes, a direct result of trauma or without any underlying biomechanical basis. Current theories of anatomic causes of CH are based on retrospective observation, of either a reproducible finding on clinical examination, a response to stimulation of the structure, or relief of symptoms after treatment directed at the structure. Examples include the response of patients to surgery for disc disease,27 injections of posterior facets with local anesthetics,28 and injections of cervical muscles with botulinum toxin.29

Cervical discs have been implicated as a possible source of cervicogenic headache.25,36 Provocative discography is required to diagnose a painful cervical disc. In provocative discography, approximately 1 cc of radiopaque contrast is injected into the nucleus pulposus and the patient’s pain response is documented.37 Grubb and Kelly38 reported the prevalence of cervical pathology and referral patterns over a 12year period. There were characteristic pain patterns depending on the level of the intervertebral disc. The C2–3 disc level referred pain into the upper cervical area, often extending into the occipital region and head, possibly accompanied by headaches in the occiput or frontal region. The pain pattern at the C3–4 level was similar to the C2–3 pain, but extended less into the occiput; and fewer patients experienced headache. More than 50% of the patients had three levels that had concordant responses, which may change clinical decisions to operate. Schellhas et al.,39 while correlating MRI findings with discography results, found a significant number of annular tears on discography that magnetic resonance imaging (MRI) was unable to detect. They concluded that magnetic resonance imaging is not reliable to delineate annular tears and should be used only as screening tool. Slipman et al.40 performed symptom mapping on 41 patients who underwent provocative discography at 101 levels to outline the pain referral patterns. The pain pattern on provocation of the C2–3, C3–4, C4–5, and C5–6 disc levels involved the occipital and/or facial areas, implicating the cervical discs as a possible source of CH.

Cervical segmental nerves Diagnostic blocks of segmental nerves C2 and C3 have been routinely performed to confirm the diagnosis of cervicogenic headache.41 Bovin et al.28 performed an anesthetic blockade of the C2–5 spinal nerves to determine their involvement in the pathogenesis of cervicogenic headache. They reported that the most convincing relief occurred with a blockade of the C2 nerve. No patients responded completely

Section 3: Cervical Spine

to isolated blockades of nerves C3, C4, or C5. The C2 and C3 pain dermatomes were well described by Poletti in 1991.42

Occipital nerves Another commonly implicated structure is the occipital nerve. The greater occipital nerve originates from the dorsal ramus of the C2 spinal nerve, the lesser occipital nerve from the ventral ramus of C2 and C3 spinal nerves via the cervical plexus, and the third (least) occipital nerve is the superficial medial branch of the C3 dorsal ramus (Fig. 69.2).43 Attributing occipital pain to irritation of the greater and lesser occipital nerve was common in the past. There is no compelling evidence that occipital pain is the result of irritation of the greater or lesser occipital nerve. Lancinating occipital neuralgia is recorded as a feature of temporal arteritis,44 in which case inflammation of the occipital artery could affect the companion nerve. In the majority of cases of so-called ‘occipital neuralgia,’ however, no such

Hypoglossal nerve (XII) in hypoglossal canal

pathology is evident. The commonly held but inaccurate view is that occipital neuralgia is caused by entrapment of the greater occipital nerve where it pierces the trapezius. Surgical studies do not provide any evidence of this.45–47 The medial branch of C2 dorsal ramus, known conventionally as the greater occipital nerve, at first runs transversely across obliquus inferior. Near the origin of the obliquus inferior, the greater occipital nerve turns upwards across the dorsal surface of rectus capitis posterior major (see Fig. 69.2). Here it receives a communicating branch from the third occipital nerve. It emerges onto the scalp, not by piercing the trapezius, but by passing above an aponeurotic sling. This sling blends medially and laterally, with the aponeurotic insertions of trapezius and sternocleidomastoid, respectively, and thereby attaches to the superior nuchal line. Along its middle portion, the sling lies suspended from the superior nuchal line, leaving an aperture between it and the bone, through which the greater occipital nerve and the occipital artery emerge, leaving the plane deep to trapezius and sternocleidomastoid to enter

Hypoglossal nucleus

Great occipital nerve

Greater occipital nerve Lesser occipital nerve Inferior ganglion of vagus nerve Ventral rami of C1,2,3 form ansa cervicalis of cervical plexus Least (3rd) occipital nerve Superior cervical sympathetic ganglion Superior root of ansa cervicalis

Internal carotid artery

Fig. 69.2 A sketch of a posterolateral view of the left third occipital nerve (TON) seen crossing the lateral aspect and then the dorsal aspect of the lower half of the C2–3 zygapophyseal joint. Articular branches to the joint arise from the deep aspect of the third occipital nerve or from the communicating loop to the C2 dorsal ramus. 739

Part 3: Specific Disorders

the scalp.47 When the trapezius and sternocleidomastoid muscles contract, there is a ‘sling effect’ that actually relieves pressure on the greater occipital nerve. The cardinal diagnostic criterion for greater occipital neuralgia seems to be response to blocks of the greater occipital nerve; but these blocks are not target specific when they involve volumes such as 5 mL45 or 10 mL.48,49 In such volumes, they do not selectively implicate the greater occipital nerve. Bogduk and Marsland first explained the concept of the third occipital nerve (TON) headache.7 They provided a detailed description of the anatomy of the C3 dorsal ramus. The superficial medial branch of the C3 ramus (also known as the third occipital nerve) crosses the lateral and dorsal aspects of the lower half of the C2–3 zygapophyseal joint (see Fig. 69.2). It then passes across the lamina of C3 before turning backwards and upwards to pierce semispinalis capitis and splenius capitis to become cutaneous over the suboccipital area.7 In a later study, 100 consecutive patients with neck pain for more than 3 months were examined to determine the prevalence of TON headache.50 Seventy-one patients complained of headache associated with neck pain; in 40 of these patients, headache was the dominant complaint. In 31 patients, headache was the ‘secondary’ complaint. The prevalence of TON headache was 27%. Of those patients with headache as the dominant complaint, the prevalence was 53%.50

Dural attachments Another theory of CH etiology comes from anatomical studies showing an attachment of the suboccipital tissues to the dura mater at the cervical–cranial junction, and the observation that mechanical traction on these tissues can cause movement of the dura.51–53 The rectus capitus posterior minor muscle53 and ligamentum nuchae52 have been shown to have direct connections to the suboccipital dura on very delicate dissection in a small number of cadavers. This suggests the possibility of the dura as a nociceptive structure in CH.

Inflammation Recent studies have implicated inflammation as the cause of various spine-related conditions, including CH. When intervertebral discs are injured they have been found to release inflammatory mediators.54–56 Interleukin (IL)-1β and TNF-α increase the molecular events of inflammation.57 As well, a marked increase in the nitric oxide (NO) pathway has been demonstrated in patients with migraines or cluster headaches.58 Martelletti et al. observed increased levels of IL-1β and TNF-α in patients experiencing cervicogenic headaches during periods of spontaneous fluctuating basal pain and during mechanically induced attacks. There were statistically significant differences in cytokine levels as compared to controls.59,60 An increase in NO formation in the presence of reactive oxygen species may interact with IL-1β and TNF-α. This signals a cascade of proinflammatory/ pain mediators such as prostaglandin and bradykinin, which play a role in neuronal sensitization. These interactions and responses implicate CH as an inflammatory consequence of cervical trauma. More importantly, they suggest that a myriad of pathological processes in different structures can manifest with similar or identical symptomatology (CH). The inability to find a singular involved anatomic structure or pathology as the cause of CH has led some to believe that CH does not represent a single pathological entity, but rather a pain syndrome resulting from the nociceptive stimulation of almost any structure in the cervical spine.61

740

Differential diagnosis Other headaches, such as cluster headache, migraine (MH), chronic paroxysmal hemicrania (CPH), hemicrania continua (HC), and tension-type headache (TTH) must be included in the differential diagnosis (Table 69.1). Intracranial pathology, infection, neoplasm must be ruled out prior to assigning the patient the diagnosis of CH. Headaches associated with sinusitis, temporomandibular joint syndrome, and visual or auditory disturbances are rarely confused with CH because each possesses unique distinguishing characteristics.

CLINICAL PRESENTATION AND DIAGNOSTIC CRITERIA The term CH, although adopted by a number of organizations, is not universally accepted. Given this lack of consensus it is not surprising that a variety of labels are used to discuss headaches associated with disorders of the cervical spine. Perusal of literature published prior to 1983 emphasizes this point. Before that date, a number of terms such as vertebragenous headache,62 vertebrogenic headache,63 spondylotic headache,64 cervical spine syndrome,65 cervical migraine,66 cervical headache,67 cervicogenic syndrome,68 greater occipital neuralgia,69 and third occipital headache8 appear to have referred to the same clinical entity. Providing a consistent label for CH is not the only aspect of this entity that has been afflicted by a lack of unanimity. A similar problem arises when one considers the diagnostic criteria for CH. The most widely used diagnostic criteria are those proposed by Sjaastad in 1990, which were subsequently updated in 1998.12 These criteria have been adapted by the Cervicogenic Headache International Study Group (Table 69.2). Three other expert groups, the International Headache Society (Table 69.3),9 the Quebec Headache Group,11 and the International Association for the Study of Pain10 have published their own criteria. Table 69.4 summarizes the prominent features of the diagnostic criteria published by various expert groups. Obtaining an accurate history is the initial step in formulating a differential diagnosis. A history of neck/head trauma should be considered to be of importance, especially if there is a possible whiplash mechanism.2,12 It has been reported that whiplash injuries usually affect the cervical facet joint, intervertebral disc, cervical nerve root, or a combination of these structures.34,70–72 Prior to the modification of the diagnostic criteria by Sjaastad et al. in 1998,12 CH had been defined as a unilateral headache spreading to the neck and the ipsilateral shoulder/arm, triggered by head/neck movements and posture. A strict unilaterality requirement has been softened in the updated CH diagnostic criteria.12 Since CH is a syndrome, the pathologic process can involve the contralateral side, potentially presenting as a bilateral headache. Even in the typical unilateral case, pain may eventually spread to the opposite side particular when the headache becomes severe. Nevertheless, the symptom intensity will remain greater on the original side.12 Other diagnostic features of CH include signs and symptoms of neck involvement. Such signs are biomechanical precipitation of attacks, whether iatrogenically and subjectively induced, reduced active range of motion (ROM) in the neck in one or more directions, diffuse ipsilateral neck/shoulder/arm pain of nonradicular nature, and occasionally, seemingly radicular arm pain (see Table 69.2). Pain may be reproduced iatrogenically by external pressure (1) over the tendinous insertions in the occipital area, (2) along the course of the major occipital nerve, (3) over the groove immediately behind the mastoid process, (4) over the upper part of the sternocleidomastoid muscle on the symptomatic side, and (5) over the lateral aspect of a cervical zygapophyseal joint. Pain may be precipitated intrinsically by

Section 3: Cervical Spine

Table 69.1: Differences and Similarities Between the Different Types of Headaches Symptoms and Signs

CPH

HC

CH

M

TTH

Unilaterality + of pain without sideshift

+

+

+

Unilaterality usually with sideshift

–

Male + preponderance

+

+

–

+

–

Pain topography

Stemming from the neck, spreading to the oculofrontotemporal area

Oculotemporal area and forehead

Oculofrontotemporal area

Oculofrontotemporal area

Oculotemporal area and forehead

Bandlike

Temporal pattern

Episodes of varying duration, or fluctuating continuous pain

Multiple and relatively short-lasting attacks

Long-lasting attacks toward chronicity (fluctuating continuous pain)

Clustering

Attacks of varying duration, usually 4 to 72 h

Long-lasting attacks toward chronicity

Pain characteristics

Moderate–severe, nonexcruciating

Lancinating, excruciating

Moderate–severe, nonexcruciating

Throbbing, excruciating

Pulsating

Dull–pressing

Reduction of the range of motion in the neck

+

–

–

–

–

–

Mechanical precipitation of attacks

+

+/–

–

–

–

–

(Long-lasting provocation; the onset of attacks takes 1 hour or more)

(Short-lasting provocation with the onset of CPH attacks within a few minutes)

Shoulder and arm pain

+

–/+

–

–

–

–

Neck trauma

+/–

–

–

–

–

–

Effect of anesthetic blockades

+

–

–

–

–

–

Response to indometacin and/or sumatriptan/ ergotamine

–

(A partial response could be present, with a rather clear response only in sporadic cases)

Absolute response to indometacin

Absolute response to indometacin

Response to sumatriptan/ ergotamine

Close to absolute response to sumatriptan/ ergotamine

–

Few and only moderately expressed

+ (also ‘local’)

Few and only moderately expressed

+ (also ‘local’)

+

Few and only moderately expressed

Autonomic symptoms and signs

CEH

CEH, cervicogenic headache; CH, cluster headache; CPH, chronic paroxysmal hemicrania; HC, hemicrania continua; M, migraine without aura; TTH, tension-type headache. Plus sign (+) indicates present. Minus sign (–) indicates absent. From Sjaastad et al.

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Part 3: Specific Disorders

Table 69.2: The Cervicogenic Headache International Study Group I. MAJOR CRITERIA OF CERVICOGENIC HEADACHE A. Symptoms and signs of neck involvement 1. Precipitation of head pain, similar to the usually occurring one a. By neck movement and/or sustained awkward head positioning, and/or b. By external pressure over the upper cervical or occipital region on the symptomatic side 2. Restriction of the range of motion in the neck 3. Ipsilateral neck, shoulder, or arm pain of a rather vague non radicular nature or, occasionally, arm pain of a radicular nature It is obligatory that one or more phenomena in point (A) are present. Point (1) suffices as the sole criterion positivity within group (A); points (2) or (3) do not (Table 2). B. Confirmatory evidence by diagnostic anesthetic blockades Obligatory point in scientific works. C. Unilaterality of the head pain, without side shift For scientific work this point should be preferably adhered to. II. HEAD PAIN CHARACTERISTICS A. Moderate–severe, nonthrobbing, and nonlancinating pain, usually starting in the neck B. Episodes of varying duration, or C. Fluctuating, continuous pain III. OTHER IMPORTANT CHARACTERISTICS A. B. C. D.

Only marginal effect or lack of effect of indomethacin Only marginal effect or lack of effect of ergotamine and sumatriptan Female sex Not infrequent occurrence of head or indirect neck trauma by history, usually of more than only medium severity None of the single points under (II) and (III) are obligatory.

IV. OTHER FEATURES OF LESSER IMPORTANCE A. Various attack-related phenomena, only occasionally present, and/or moderately expressed when present 1. Nausea 2. Phonophobia and photophobia 3. Dizziness 4. Ipsilateral ‘blurred vision’ 5. Difficulties in swallowing 6. Ipsilateral edema, mostly in the periocular area From Sjaastad et al.13

Table 69.3: International Headache Society Criteria for Headache Associated with Disorder of the Neck I. Pain localized to the neck and occipital region. May project to forehead, orbital region, temples, vertex, or ears II. Pain is precipitated or aggravated by special neck movements or sustained neck posture III. At least one of the following: Resistance to or limitation of passive neck movements Changes in neck muscle contour, texture, tone, or response to active and passive stretching and contraction Abnormal tenderness of neck muscles IV. Radiologic examination reveals at least one of the following: Movement abnormalities in flexion/extension Abnormal posture Fractures, congenital abnormalities, bone tumors, rheumatoid arthritis, or other distinct pathology (not spondylosis or osteochondrosis) Comment: Cervical headaches are associated with movement abnormalities in cervical intervertebral segments. The disorder may be located in the joints or ligaments. The abnormal movement may occur in any component of intervertebral movement, and is manifest during either active or passive examination of the movement. Adapted from IHS, Headache Classification Committee of the International Headache Society. Cephalalgia 1988.9

742

Section 3: Cervical Spine

Table 69.4: The Characteristics and Definitions of Cervicogenic Headache Criteria/Group

Cervicogenic Headache International Study Group13

International Headache Society9

Quebec Headache Study Group11

International Association for the Study of Pain10

Location of pain (region)

Starts in neck Ipsilateral vague, nonradicular neck, shoulder, arm pain or radiculopathy

Neck, occipital

Occipital

Starts in the neck/occiput Forehead Temporal Whole hemicranium

Pain characteristics

Unilateral without sideshift Moderate–severe Nonthrobbing Nonlancinating

Unilateral or bilateral

Unilateral without sideshift Becomes more continuous Moderately severe Varying duration

Pain increased with

Neck movemenet Awkward head positioning Pressure over ipsilateral cervical/occipital area

Subjective

Neck movement Posture

Neck movement

Objective Cervical spine range of motion

Decreased passive range of motion

Palpation findings

Tender neck muscles Changes in neck muscle properties

Response to blockade

Pain on C2–3 facet palpation C2–3 dermatome cellulalgia

Occipital nerve facets, or nerve roots abolish pain

Radiologic findings

Occipital nerves or nerve roots relieve pain Flexion/extension abnormalities Fracture Congenital anomaly Tumor/rheumatoid arthritis, not spondylosis

Neck trauma

Yes

Other

Nausea/vomiting Edema/ flushing Dizziness Phono/photophobia Blurred vision Dysphagia No effect with indomethacin, ergotamine, or sumatriptan

neck movements and/or sustained, awkward head positioning, especially during sleep. The duration of pain attacks, a few hours to a few weeks, and pain intensity, vary widely in CH with a strong tendency toward chronicity. CH can present as episodic in the initial phase becoming chronic in later stages. The pain usually starts in the neck, eventually spreading to the oculofrontotemporal area. Symptoms may actually be more intense in this latter location than in the occipital or cervical region.1,12 The duration of pain episodes for CH is frequently longer than in common migraine; the pain intensity is moderate and nonexcruciating, unlike cluster headache, and it is usually of a nonthrobbing nature. Autonomic symptoms and signs, such as photophobia, phonophobia, nausea, vomiting, and ipsilateral periocular

Normal or arthrosis

edema, are generally less frequent and less marked than in common migraine, but they can occur.1,2,12,21,22,73 Swallowing difficulty is reported, albeit rarely occurring associated phenomenon.74 There have also been cases with features consistent with a CH picture, but with additional dizziness/vertigo and vertebral drop-attacks.8,73 In the revised criteria, among the ‘Other Important Characteristics’ (see Table 69.2), the lack of complete response to indomethacin, sumatriptan, and ergotamine has also been introduced.

Authors’ recommendation Formulating a probability analysis of the structures involved is the most important step in the diagnostic and therapeutic algorithm 743

Part 3: Specific Disorders

facilitate closure or narrowing of the neuroforamina, are positive, then nerve root involvement rather than facet joint syndrome or internal disc disruption syndrome is of higher probability. In whiplash injuries, CFJS may be more common than upper cervical nerve root injury;34,76 however, this may be a consequence of the paucity of epidemiological data for whiplash-induced cervical nerve root injury.

(Fig. 69.3). Unilateral symptoms of occipital headaches greater than neck pain following a traumatic event is more suggestive of cervical facet joint syndrome (CFJS) than internal disc disruption.34,70 Similarly, one may suspect CFJS more than internal disc disruption if there is focal tenderness following palpation of an isolated cervical joint or if the patient is able to point to the painful area corresponding to the distribution of pain reported for a particular facet joint.75 Examination finding of increased focal suboccipital pain with terminal cervical flexion and sequential lateral rotation suggests pain emanating from a C1–2 joint. Bilateral symptoms of neck pain with headaches would be more suggestive of cervical internal disc disruption (CIDD) syndrome. Reproduction of symptoms by provocative maneuvers, which

Diagnostic testing Cervical spine radiographs are not a sensitive method for diagnosing CH, because no specific radiologic abnormalities are usually found.77,78 In patients with a history of whiplash injury or traumatic

Cervicogenic headache

Symptoms bilateral, symmetric

Symptoms primarily unilateral

Clinical exam and imaging consistent with cervical nerve root affection

C5TF

Discography (+)

Fusion

Palpable facet or symptom location correlating with CFJS pain map

(–)

**

Diagnostic SNRB Yes

No

Chronic pain modulation program

(+) Therapeutic SNRB

Diagnostic C2–3 FJB (–)

Diagnostic FJB correlating

(–) (+)

(–)

Surgery

Diagnostic C3–4 FJB (–) Diagnostic C1–2 FJB

Target other two facet joints

Therapeutic FJB (–)

(–)

(–) (–)

Diagnostic single blind double FJB

C5TF

(+)

(–) Radiofrequency ablation

Discography

(+)

Fusion

(–)

Re-evaluate

**

Chronic pain modulation program

** - positive discogram with > 2 concordant disc levels or with 2 concordant non contiguous disc levels or any lobular disc with a concordant pain response

744

Fig. 69.3 Therapeutic algorithm for cervicogenic headache.

Section 3: Cervical Spine

insult, cervical flexion and extension radiographs should be obtained. CH is a diagnosis of exclusion, and more serious pathologies must be ruled out. Magnetic resonance imaging is indicated to search for causes of pain that may require surgery or other more aggressive forms of treatment (i.e. Arnold–Chiari malformation, herniated intervertebral disc, spinal or neural foraminal stenosis, vertebral or facet fracture, and intramedullary or extramedullary spinal tumors).79,80 Although MRI has a high sensitivity to detect focal disc protrusions, foraminal stenosis, facet joint arthropathy or other pathology, there are concerns about its clinical specificity. Several studies have demonstrated that a significant percentage of individuals with focal protrusions or foraminal stenosis are asymptomatic.39 This issue of clinical specificity underscores the importance of correlating each patient’s symptoms and examination findings with the imaging study to obtain an accurate clinical diagnosis. If the patient is claustrophobic, then a high-quality open MRI is obtained. If this is unavailable, then a multi-planar computerized tomography (CT) scan is requested. Diagnostic anesthetic blockade is required to confidently render a diagnosis of cervicogenic headache. Diagnostic blockade can be directed to several anatomic structures such as the greater occipital nerve (dorsal ramus C2), lesser occipital nerve, atlanto-occipital joint, atlantoaxial joint, cervical segmental nerve roots, third occipital nerve (dorsal ramus C3), zygapophyseal joint(s), or intervertebral discs based on the clinical characteristics of the pain and the physical examination.41 Fluoroscopic guidance with and without contrast is necessary to assure accurate and specific localization of the pain source.28,81,82 Diagnostic blocks use small amounts of local anesthetic that are infused into or around the suspected nerve or structure with the goal of temporarily interrupting head pain. Because diffusion of the anesthetic to adjacent structures would muddle the results, it is essential to use the least amount of local anesthetic feasible to limit the anesthetic affect to the target site. The most recent diagnostic criteria for cervicogenic headache require the use of confirmatory nerve blocks.12 Although this approach is quite appealing it does not offer 100% accuracy.41,83 False-negative and false-positive responses to diagnostic blocks do occur and can result due to technical failure, placebo response (see Ch. 19), administration of sedative agents before or during the diagnostic block, concurrent pharmacologic treatment, and secondary psychosocial factors.

TREATMENT The successful treatment of cervicogenic headache requires a multifaceted approach using pharmacologic, nonpharmacologic, manipulative, anesthetic, and occasionally surgical interventions (Table 69.5). Some have suggested that the multidisciplinary treatment team consist of a primary treating physician, interventional spine physician, a physical therapist or physician appropriately trained to provide manipulative treatments, and a psychologist.63,84–87 Medications alone are often ineffective or provide only modest benefit. Positive diagnostic blocks, as outlined in diagnostic testing, may direct treatment toward more invasive interventional or neuroablative therapy. The diagnostic and treatment algorithm as recommended by the authors is outlined in Figure 69.3.

Interventional, anesthetic, and ablative treatment Cervical zygapophyseal joints Of the potential sources of CH, the zygapophyseal joints have been considered a common source of referral to the head and face. Prior studies have noted significant variations in the referral patterns of

the zygapophyseal joints. Dwyer et al. distended the C2–3 to C6–7 zygapophyseal joints in asymptomatic patients to report that only the C2–3 zygapophyseal joint referred symptoms to the head.31 Aprill et al. investigated the C2–3 to C7–T1 zygapophyseal joints and reported that the C2–3, C3–4, and C4–5 zygapophyseal joints could refer to the head.32 Dreyfuss et al. stimulated the atlanto-occipital and atlantoaxial joints by injection of radiopaque contrast with subsequent distention of the joint capsule. Both joints tended to refer pain into the ipsilateral occipital or suboccipital area, with possible referral into the face.88 Bogduk et al. performed medial branch and zygapophyseal joints blocks in 24 symptomatic patients from C1–2 to C5–6 levels and reported that the C2–3 zygapophyseal joints refers to the head and face while the C3–4 zygapophyseal joints only refers to the head.89 Slipman et al., reviewing data from 100 patients demonstrated that C4–5 and C5–6 zygapophyseal joints can refer pain to the head and the C1–2, C2–3, and C3–4 zygapophyseal joints can also refer pain to the face.33 The cervical facet joints, except for the C2–3 level, are innervated by the medial branch of the dorsal ramus above and below its location. At the C2–3 level, two medial branches innervate the joint: the C3 medial branch (deep) and the C3 medial branch (superficial), also known as the TON.25,61,90 Confirmation of joint involvement in CH is through unequivocal relief of head pain after the local anesthetic block of the joint. When upper CFJS is suspected, diagnostic blocks are performed sequentially at C2–3, C3–4, and C1–2 levels, until the offending site is identified. This sequence is based on clinical experience and is supported by epidemiological studies.70 If a diagnostic facet joint block is positive, fluoroscopically guided therapeutic intra-articular steroid injections are offered. Barnsley et al. investigated the effectiveness of intra-articular corticosteroid injections for chronic pain in the cervical zygapophyseal joints.91 Less than half the patients reported relief of more than 1 week and less than one in five patients reported relief for more than a month. They concluded that intra-articular injections with betamethasone was an ineffective treatment for pain in the cervical zygapophyseal joints. However, this study used one outcome measure, i.e. verbal pain score, and only evaluated the efficacy of one intra-articular steroid injection per joint without restricting physical activities or physical therapy. In our experience, fluoroscopically guided therapeutic intra-articular steroid injections have been efficacious in the treatment of CFJS. Slipman et al.92 demonstrated good to excellent results in 61% of patients treated with intra-articular steroids who experienced daily unremitting headaches emanating from the C2–3 facet joint subsequent to a whiplash injury. In that study, the average duration of symptoms was 3 years and no patient obtained relief with any analgesics prior to the injections. Most patients received 1–3 injections per joint. Although the change in average pain score (5.5 at follow-up compared with 8.2 at the time of initial presentation) does not seem to be a significant clinical difference, the frequency of patient’s headaches and their responsiveness to analgesic use were clearly improved. Patients with previous employment restrictions were observed to return to full-time work status. During treatment, patients in this study92 were advised to avoid forceful, rapid, or sustained cervical extension or rotation whenever possible. The basis for such a strict protocol is the observation that CFJS, especially when associated with whiplash injury, may be associated with subchondral fractures,93,94 joint capsule ruptures,95,96 and intraarticular hemorrhages.71,95 These structural insults may be responsible in triggering zygapophyseal joint headaches when stressed by overactivity or exercise. When the symptoms are reduced, the patient gradually returned to engaging in normal physical tasks rather than letting the patient participate in unregulated physical activities. 745

Part 3: Specific Disorders

Table 69.5: Potential Treatment Interventions for Cervicogenic Headache PHARMACOLOGIC Tricyclic antidepressants: amitriptyline, nortriptyline, doxepin, and others Antiepileptic drugs: gabapentin, topiramate, carbamazepine, divalproex sodium Muscle relaxants: tizanidine, baclofen, cyclobenzaprine, metaxalone, and others Nonsteroidal anti-inflammatory drugs Nonselective: ibuprofen, naproxen, indometacin, and others COX-2 selective: valdecoxib, celecoxib NONPHARMACOLOGIC Manipulative therapies Physical therapy Transcutaneous electrical nerve stimulation Biofeedback/relaxation therapies Individual psychotherapy INTERVENTIONAL Anesthetic blockades Spinal roots, nerves, rami, or branches Zygapophyseal joints Trigger points Neurolytic procedures Radiofrequency thermal neurolysis Cryoneurolysis Botulinum toxin injections SURGICAL Neurectomy Dorsal rhizotomy Microvascular decompression Nerve exploration and ‘release’ Zygapophyseal joint fusion

If a patient experiences greater than 90% relief of symptoms after a therapeutic intra-articular facet injection that lasts until the date of a planned second, third, or even fourth subsequent injection, then the intervention is cancelled. Such relief typically heralds the onset of continued symptom relief provided the patient adheres to specific activity prohibitions and patiently returns to a normal activity level. As previously alluded, this regimen is conducted under direct physician supervision and must be individualized. Overall, it can take 6–12 months after the final injection before premorbid activities and habits can be resumed. Patients who have responded to diagnostic/therapeutic blocks of the zygapophyseal joints with unequivocal but unsustained relief of head and neck pain may be good candidates for radiofrequency (RF) neurotomy. Because the authors perform intra-articular injections following a single positive diagnostic injection, the major question that must be addressed when a patient fails to improve following therapeutic injections is whether the patient failed because of an incorrect diagnosis or if he or she is a true nonresponder with a false-positive placebo response. The former issue is raised because there is a false-positive rate of 27% with single diagnostic facet joint blocks.97 Therefore, it is conceivable the initial diagnostic block 746

was a false-positive response. Accordingly, the authors advocate a double-blind, double-block diagnostic injection utilizing 2% lidocaine intra-articularly and normal saline extra-articularly for definitive confirmation of the diagnosis, before undertaking ablative procedure. This double block is considered positive if the lidocaine injection relieves the pain and the saline injection does not. In summary, all the patients progressing to double block have had a positive single block, have been treated with intra-articular steroids and failed to progress, and then participate in this double block procedure. So the authors are essentially doing a triple-block paradigm. If the double block is positive, the patient is a candidate for RF ablation of the medial branches of the dorsal rami supplying the involved facet joint. If the double block is negative, the next suspected structure in the diagnostic algorithm should be assessed. The use of RF techniques in treating cervicogenic headache resulting from cervical zygapophyseal joint is described by Hapeslagh and van Kleef in Chapter 65. An RF cannula is inserted to the target nerve under fluoroscopic guidance. An RF generator then heats the surrounding tissue under controlled conditions that allows the formation of a discrete lesion to interrupt all sensory pathways to the joint. Two to three lesions at 75–80°C for 60–90 seconds are

Section 3: Cervical Spine

typically made because the exact location of the nerve may vary.98 In a randomized, double-blind trial, Lord et al.99 demonstrated that the pain relief realized following percutaneous RF neurotomy in patients with chronic cervical zygapophyseal joint pain confirmed with double-blind, placebo-controlled local anesthesia, is real and not a placebo effect. The median time that elapsed before the pain returned to at least 50% of the preneurotomy level in the activetreatment group was 9 months as compared to 1 week in the shamcontrol group. Using a prospective cohort methodology McDonald et al.100 subsequently reported complete relief of pain in 71% of properly selected patients. The median duration of relief after a first procedure was 219 days when failures were included, but 422 days when successful cases were considered. Repeat procedures were effective in each instance. They concluded that RF neurotomy provides a clinically significant period of freedom from pain, and its effects can be reinstated if pain recurs. Patients whose pain was not relieved by the first procedure did not respond well to a second procedure. It is interesting to note that the outcome was not affected by litigation, status, or type of diagnostic block used. The contention that the potential for secondary gain does not influence response to treatment was further demonstrated by Sapir and Gorup101 in their prospective study of 46 patients with cervical zygapophyseal joint pain from whiplash treated with RF medial branch neurotomy. Radiofrequency cervical medial branch neurotomy markedly reduced the pain from whiplash in the study patients (both litigation and nonlitigation group) with an overall reduction of VAS 5.7±1.8. At 1 year the combined reduction from baseline in VAS score of 4.6±1.8 was still significant. When evaluating the reduction in pain from baseline at 1 year there was a statistical difference between groups, with the litigant group having a tendency for greater return of pain. This difference, however, is only a change in a VAS score of 1.4 between groups, which would be clinically difficult to differentiate. The overall change at 1 year from the pre-RF (baseline) score was still greater than 4 VAS points for the litigation group compared with 5.5 VAS points for the nonlitigation group. Clinically both represent significant reductions in pain. In a retrospective study evaluating the effectiveness of percutaneous radiofrequency neurotomy in the treatment of cervical zygapophyseal joint pain, Lord et al.98 noted a high failure rate of third occipital neurotomy for the treatment of C2–3 zygapophyseal joint pain. Of the 10 patients who underwent third occipital neurotomy, only four obtained relief lasting for more than 6 months. Ataxia was a regular side effect of third occipital neurotomy. It is unclear from the study whether ataxia was associated with long-lasting pain relief or occurred even in absence of sustained pain relief. All patients with ataxia were able to accommodate it by relying on visual cues, some within a few hours but others after 2–3 days. One patient continued to experience disorientation whenever challenged by visually complex situations, such as walking down stairs or turning quickly. The cause of ataxia is unclear. The rate of technical failure was considerably higher for third occipital neurotomies than for lower cervical medial branch neurotomies in the study by Lord et al.98 In this regard, Lord et al.98 recommend that third occipital neurotomy be abandoned until the technical problems can be overcome. Possible reasons for this high rate of failures include the relatively larger diameter of the nerve (1.5–2.0 mm) and its variable course. In contrast to the lower cervical medial branches that course around the concave waists of the cervical articular pillars, the TON curves around the convex capsule of the C2–3 joint. Thus, its course may vary, running higher or lower than the equator of the joint. In addition, because the TON lies superficial to the joint capsule, an electrode placed immediately adjacent to the bony margin of the joint may fail to incorporate the nerve by passing deep to the cap-

sule, thereby displacing the nerve from the electrode. The authors routinely perform radiofrequency ablation of the TON for C2–3 joint pain, following positive diagnostic blocks and failure of steroid response as outlined above. In the authors’ experience, the results of third occipital neurotomies are comparable to lower cervical medial branch neurotomies and ataxia is not a major reported side effect. There is sufficient merit in the third occipital neurotomy procedure to justify a randomized, double-blind, controlled trial.

Atlanto-occipital and atlantoaxial joints The atlanto-occipital and atlantoaxial joints are involved, respectively, in the flexion–extension and horizontal rotation of the head. These two joints are innervated by the C1, C2, and C3 spinal nerve roots and can be a source of CH.25,32,88 Racz et al.102 reported that the atlanto-occipital and atlantoaxial joint headaches are rarely seen and frequently misdiagnosed. Aprill et al.103 tested the hypothesis that C1–2 headaches are a rare entity. Thirty-four patients with suspected C1–2 pain underwent diagnostic blocks of the joint with a local anesthetic and steroid. Twenty-one patients obtained complete relief of headache. Pain relief lasted for the duration of the injected local anesthetic. The overall incidence of carefully selected patients who had pain in the occipital or suboccipital region resulting from atlantoaxial joint pain was reported as 16%. The technique for injecting these joints has been described by Racz et al.102 and Dreyfuss et al.104 Potential complications include: (1) injury to the brain stem, vertebral artery, or spinal cord; (2) intravascular injection of anesthetic or steroids that results in central nervous system toxicity or stroke; and (3) inadvertent epidural and intrathecal injections. Because of the close proximity of these joints to major neural and vascular structures, these procedures should only be performed by physicians who have great experience in the use of fluoroscopic-guided injection techniques. Apart from corticosteroid injections, there do not seem to be any other reliable therapeutic options. A specific RF procedure or other neuroablative techniques for the atlantoaxial and atlanto-occipital joints have not been developed.105

Cervical discs Cervical discs have been implicated as a possible source of cervicogenic headache,25,36 and cervical epidural steroid injections (CESIs) are preferred treatment of discogenic pain by many clinicians. CESIs have been used with success rates ranging from 40% to 75% for treatment of axial and radicular neck symptoms.106,107 However, the use of CESIs in the diagnosis and treatment of CH remains controversial. Cronen and Waldman reported the efficacy of CESIs in the treatment of pain secondary to tension-type headaches108 and as a diagnostic tool in the evaluation of head, neck, and face pain.109 Martelleti et al., who advocated the theory of the role of inflammation in CH, presented a small series on CESI and reported some relief.110 Reale et al.111 further suggested that epidural steroids are an effective treatment for CH because of their antiinflammatory effects combined with their direct effect on C fibers to block their nociceptive transmission. They report short-term (2 months) pain relief with few risks or side effects. However, van Suijlekom41 pointed out that a cervical epidural nerve block is not selective, can result in life-threatening situations, and should not be used in the standard diagnostic workup for cervicogenic headache. The authors concur with that view for two reasons. First, an epidural injection anesthetizes in a widespread and indiscriminate fashion, precluding any determination as to which anatomic structure is the offending site. Second, a large deposition of glucocorticoid will affect these numerous structures and may even 747

Part 3: Specific Disorders

748

have a systemic effect. Any alleviation of symptoms could very well be a consequence of this systemic response. Despite the absence of controlled, prospective, double-blind studies to assess the therapeutic benefit of CESIs in the treatment of head and neck pain, they are the preferred treatment of many clinicians. As elucidated in the chapter by Kenneth Botwin, extreme caution needs to be used when planning to do a cervical epidural injection. All CESIs should be performed under real-time fluoroscopic guidance using contrast to avoid intravascular injection which can result in potentially devastating neurological consequences. Potential complications of CESIs include: (1) inadvertent dural puncture with postdural puncture headache or intrathecal injection of local anesthetic and steroids; (2) intravascular injection, epidural hematoma, or abscess resulting in spinal cord compression; and (3) direct trauma to the spinal cord or nerve root. Similar to other nerve blocks in the cervical region, routine sedation should be avoided or kept to a minimum. The authors prefer using the transforaminal approach to the epidural space. For those patients suspected of experiencing CH symptoms secondary to discogenic etiology, a fluoroscopically guided transforaminal steroid injection at the C5 level on the symptomatic ipsilateral side is recommended to bathe the posterior surface of the upper intervertebral discs, posterior longitudinal ligament, and other nearby innervated structures. The insertion point for this injection is predicated upon the locations of symptoms and the likely disc levels that are involved.112 The C5 level is chosen when the headaches extended beyond the posterior occiput. When the headache symptoms involve the prefrontal/supraorbital distribution or the face, a C6 approach is use. In the former circumstance the therapeutic agents need to cover from C5 and cephalad. In the latter circumstance, the spread should be viewed cephalad and at least one level caudal such that it reaches the C7 vertebral body. Another critical aspect is insuring that flow is ventral and not dorsal to the spinal cord. When the aforementioned steps have been undertaken and a steroid effect is not realized after two injections, the patient will require provocative cervical discography to determine if there is internal disc disruption, answering the questions of whether the diagnosis was accurate, which levels are involved and whether surgery is a viable alternative. If the discogram reveals one or two successive disc levels with concordant pain responses, the patient may be a candidate for surgical fusion. If the discogram demonstrates discs without concordant pain responses, the next suspected structure in the diagnostic algorithm should be tested. When a discogram reveals three or more concordant disc levels, two disc levels with an intervening normal disc, or if any concordantly painful discs are lobular, the patient is not considered as a surgical candidate. Blume113 has reported the use of multiple RF lesions to the cervical disc at the C2–3 and C3–4 level. Six to eight lesions at 80°C for 3 minutes were performed. He described complete to partial relief of CH for 2–6 months. Side effects of cervical disc RF lesions include disc infection, nerve root injury, and temporary postoperative neuritis. Potential side effects and complications associated with this procedure, when weighed against the outcome, justify the lack of popularity of RF lesions of upper cervical discs for CH.

Management of the greater and lesser occipital nerves has varied greatly. Diverse treatments have included infiltration of the affected nerves with local anesthetic and steroids,16,46,114 occipital neurectomy,115 occipital neurolysis,45,116 RF denaturation of the greater, lesser, and least occipital nerves,113 microsurgical C2 ganglionectomy,117 partial posterior rhizotomy of C1–3 nerve,118 and peripheral nerve stimulation (PNS).119,120 Many patients with occipital neuralgia will respond to infiltration of local anesthetic and steroids in the distribution of the GON and LON. A number of small case series have reported on the injection of the occipital nerves where short-term improvement was noted in 50–90% of patients.16,28 A more permanent neuroablative technique can be considered for intractable occipital neuralgia that consistently responds to diagnostic nerve block. Performing neurolytic blocks using alcohol, or phenol, and surgical occipital neurectomy have lost favor because of recurrence, deafferentation syndrome, and neuroma formation. Liberation of the greater occipital nerve initially relieves headache in approximately 80% of cases, but the relief has a median duration of only 3–6 months.45 Excision of the greater occipital nerve provides relief in approximately 70% of patients, but this has a median duration of only 244 days.46 Reports of the treatment of intractable, idiopathic occipital neuralgia are mixed. Dorsal rhizotomy at C1–3 or C1–4 has provided some patients with complete relief for 1–4 years; nevertheless some patients suffer recurrences.121 Partial posterior rhizotomy at C1–3 seems to achieve good relief while preserving touch sensation, but not all patients respond adequately.118 Unfortunately, these procedures are so radical that they provide little insight into the mechanisms of occipital neuralgia, except to warn that even complete deafferentation of the affected region does not guarantee relief of pain. Hence, the authors do not routinely include diagnostic work-up or treatment of the greater and lesser occipital nerves in the authors’ algorithm.

Cervical segmental nerve

CONCLUSIONS

For a patient suspected of CH emanating from a cervical nerve root who has MRI or CT scan evidence of a disc protrusion or stenosis at the nerve root level, a fluoroscopically guided diagnostic selective nerve root block (SNRB) is required for corroborative evidence. If the diagnostic injection is negative, then the next suspected structure in the diagnostic algorithm should be tested. If the diagnostic SNRB is positive, then fluoroscopically guided therapeutic SNRB can

Despite a growing body of literature on CH and an increasing acceptance that headaches can originate from the cervical spine, there remains considerable controversy and confusion concerning most aspects of this topic. Anesthetic blockade plays an essential role in the diagnosis and treatment of cervicogenic headache. A positive or negative response to a diagnostic block must be considered in conjunction with the complexity of the patient with chronic headache,

be performed. In this instance, a therapeutic intervention is centered on the root and DRG. In comparison, when a transforaminal epidural is performed the focus of treatment primarily entails the dorsal aspect of the disc and posterior longitudinal ligament. Given these differences it is not surprising that the proper placement for the therapeutic agent differs. It is ventral to the cord for disc-generated pain (transforaminal epidural) and along the root and DRG for nerve root symptoms (SNRB). Surgical referral for discectomy or decompression and foraminotomy is recommended when there is lack of steroid effect and intractable pain when a corroborative structural lesion is present. Klein105 reported, in a nonpeer-reviewed publication, that percutaneous radiofrequency lesions of the cervical dorsal root ganglion at the C2 and C3 levels may be helpful in the treatment of C2- and C3-pattern headache. The goal of RF of the dorsal root ganglion is to interrupt the pain pathways carried by small fiber systems while maintaining sensory and motor function. He reported no significant side effects. However, this technique has not gained in popularity. The authors suspect this is because there is not a single peer-reviewed publication remotely substantiating this procedure.

Greater occipital nerve and lesser occipital nerve

Section 3: Cervical Spine

the placebo effect, and concurrent medical therapy before proceeding with more invasive interventional or neuroablative treatment. It is essential to have a profound knowledge of the anatomy of the cervical spine, an understanding of the pathophysiologic mechanisms of cervicogenic headache and a high degree of technical skill before performing these procedures. Serious life-threatening and neurologic injuries have been reported and this must be weighed against the benefits of treatment. Conservative therapeutic options should be attempted first. Acknowledging that conducting randomized, double-blind, controlled surgical trials are difficult, it is important that further studies are done if interventional techniques are to become standard and accepted therapies for cervicogenic headache. As the literature on this topic grows in volume and quality, the debate will intensify and, hopefully, will result in the clarification of the cause, diagnosis, and treatment of CH.

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22. Pfaffenrath V. Cervicogenic headache – the clinical picture, radiological findings and hypotheses on its pathophysiology. Headache 1987; 27:495–499. 23. Vincent M. Cervicogenic headache: a comparison with migraine and tension-type headache. Cephalgia 1999; 19(Suppl 25):11–16. 24. Haldeman S, Dagenais D. Cervicogenic headaches: a critical review. Spine J 2001; 1:31–46. 25. Bogduk N. Cervicogenic headache: anatomic basis and pathophysiologic mechanisms. Curr Pain Headache Rep 2001; 5:382–386. 26. Kerr FWL. Relation of the trigeminal spinal tract to upper cervical roots and the solitary nucleus in the cat. Exp Neurol 1961; 4:134–148. 27. Fredriksen T, Salvesen R, Stolt-Nielsen A, et al. Cervicogenic headache: long-term postoperative follow-up. Cephalgia 1999; 19(10):897–900. 28. Bovim G, Berg R, Dale L. Cervicogenic headache: anesthetic blockades of cervical nerves (C2–C5) and facet joint (C2/C3). Pain 1992; 49(3):315–320. 29. Freund B, Schwartz M. Treatment of chronic cervical-associated headache with botulinum toxin A: a pilot study. Headache 2000; 40(3):231–236. 30. Silverman S. Cervicogenic headache: Interventional, anesthetic, and ablative treatment. Curr Pain Headache Rep 2002; 6:308–314. 31. Dwyer S, April C, Bogduk N. Cervical zygapophyseal joints pain patterns I: A study in normal volunteers. Spine 1990; 15:453–457. 32. April C, Dweyer A, Bogduk N. Cervical zygapophyseal joint pain patterns II: A clinical evaluation. Spine 1990; 15:458–461. 33. Slipman C, Isaac Z, Thomas J, et al. Abstract: Cervical zygapophyseal joint syndrome and referral to the head and face. Preliminary data from 100 patients. Arch Phys Med Rehabil 2002; 83:1665. 34. Lord S, Barnsely L, Wallis B, et al. Chronic cervical zygapophyseal joint pain after whiplash. A placebo-controlled prevalence study. Spine 1996; 21(15): 1737–1745. 35. Lord S, Barnsely L, Wallis B, et al. The prevalence of chronic cervical zygapophyseal joint pain after whiplash. Spine 1995; 20(1):20–23. 36. Biondi D. Cervicogenic headache: diagnostic evaluation and treatment strategies. Curr Pain Headache Rep 2001; 5:361–362. 37. April C. Diagnostic disk injection. In: Frye A, Moyer J, eds. The adult spine: principles and practice. New York: Raven Press; 1991:403–440. 38. Grubb S, Kelly C. Cervical discography: Clinical implications from 12 years of experience. Spine 2000; 25:1382–1389. 39. Schellhas K, Smith S, Gundry C, et al. Cervical discogenic pain. Prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers. Spine 1996; 21:300–312. 40. Slipman C, Bhagia S, Plastaras C. Provocative cervical discographic symptom mapping. Chicago: Presented at the Annual meeting of the Am Acad Phys Med Rehab; October 2003. 41. van Suijlekom J. Cervicogenic headache: techniques of diagnostic nerve blocks. Clin Expl Rheumatol 2000; 18(Suppl 19):S39–S44. 42. Poletti C. C2 and C3 pain dermatomes in man. Cephalgia 1991; 11:155–159. 43. Netter F. Suboccipital triangle. In: Netter F, ed. Atlas of human anatomy. 2nd edn. 2000: Plate 164. 44. Jundt J, Mock D. Temporal arteritis with normal erythrocyte sediment rates presenting as occipital neuralgia. Arthritis Rheum 1991; 34:217–219. 45. Bovim G. Neurolysis of the greater occipital nerve in cervicogenic headache: a follow-up study. Headache 1992; 32:175–179. 46. Anthony M. Headache and the greater occipital nerve. Clinical Neurol Neurosurg 1992; 94:297–301. 47. Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine 1982; 7(4): 319–330. 48. Saadah H, Taylor F. Sustained headache syndrome associated with tender occipital nerve zones. Headache 1987; 27:201–205. 49. Gawel M, Rothbart P. Occipital nerve block in the management of headache and cervical pain. Cephalgia 1992; 12:9–13.

19. Bono G, Antonaci F, Ghirmai S, et al. The clinical profile of cervicogenic headache as it emerges from a study based on the early diagnostic criteria (Sjaastad et al. 1990). Funct Neurology 1998; 13(1):75–77.

50. Lord S, Barsley L, Wallis B, et al. Third occipital nerve headache: a prevalence study. J Neurol Neurosurg Psychiatr 1994; 57:1187–1190.

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85. Nilsson N. A randomized controlled trial of the effect of spinal manipulation in the treatment of cervicogenic headache. J Manipul Physiol Ther 1995; 18(7): 435–440.

55. Franson R, Saal J, Saal J. Human disc phospholipase A2 is an inflammatory. Spine 1992; 17(Suppl):129–132.

86. Nilsson N. The effect of spinal manipulation in the treatment of cervicogenic headache. J Manipul Physiol Ther 1997; 20:326–330.

56. Kang J, et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 1996; 21:271–275.

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57. Martelletti P, La Tour D, Giacovazzo M. Spectrum of pathophysiological disease in cervicogenic headache and its therapeutic indications. Neuromusculoskeletal Symp 1995; 3:182–187.

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58. Martelletti P, Stirparo G, Favilla M. Expression of NOS-2, COX-2, and Th1/Th2 cytokines in migraine. J Headache Pain 2001; 2:S51–S56.

90. Barnsley L. Comparative local anesthetic blocks in the diagnosis of cervical zygapophyseal joint pain. Pain 1993; 55:99–106.

59. Martelletti P. Proinflammatory pathways in cervicogenic headache. Clin Exp Rheumatol 2000; 18(2):S33–S38.

91. Barnsley L, Lord S, Wallis B, et al. Lack of effect of intraarticular corticosteroids for chronic pain in the cervical zygapophyseal joints. N Engl J Med 1994; 330:1047–1050.

60. Martelletti P, Stirparo G, Giacovazzo M, et al. Proinflammatory cytokines in cervicogenic headache. Funct Neurol 1999; 14(3):159–162. 61. Bogduk N. The anatomical basis for cervicogenic headache. J Manipul Physiol Ther 1992; 15(1):67–70.

92. Slipman C, Lipetz J, Plastaras C, et al. Therapeutic zygapophyseal joint injection for headaches emanating from the C2–3 joint. Am J Phys Med Rehabil 2001; 80(3):182–188.

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94. Woodring JH. Fractures of articular processes of the cervical spine. Am J Roentgenol 1982; 139:341–344.

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95. Jonsson H Jr, Rauschning W, et al. Hidden cervical spine injuries in traffic accident victims with skull fractures. J Spinal Disord 1991; 4:251–263.

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96. Buonocore E, Nelson CL. Cineradiograms of cervical spine in diagnosis of soft tissue injuries. JAMA 1966; 198:143–147. 97. Barnsley L, Lord SM, Wallis BJ, et al. False positive rates of cervical zygapophyseal joint blocks. Clin J Pain 1993: 9:124–130. 98. Lord S. Percutaneous radiofrequency neurotomy in the treatment of cervical zygapophyseal joint pain: a caution. Neurosurgery 1995; 36:732–739. 99. Lord S, Barnsley L, Wallis B, et al. Percutaneous radiofrequency neurotomy for chronic cervical zygapophyseal joint pain. N Engl J Med. 1996; 335:1721–1726.

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100. McDonald G. Long-term follow-up of patients treated with cervical radiofrequency neurotomy for chronic neck pain. Neurosurgery 1999; 45:61–67.

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101. Sapir A, Gorup J. Radiofrequency medial branch neurotomy in litigant and nonlitigant patients with cervical whiplash. Spine 2001; 26(12):E268–E273.

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72. Spitzer WO, Salmi LR, Cassidy JD, et al. Scientific monograph of the Quebec Taskforce on Whiplash associated discorders: Redifining whiplash and its management. Spine 1995; 20:10S–68S. 73. Fredriksen T. Cervicogenic headache (CEH): notes on some burning issues. Funct Neurol 2000; 15:199–203. 74. Michler R. Disorder in the lower cervical spine. A cause of unilateral headache? Headache 1991; 31:550–551. 75. Jull GB. The accuracy of manual diagnosis for cervical zygapophyseal joint pain syndromes. Med J Aust 1988; 148:233–236. 76. Slipman C, Plastaras CT, Huston CW, et al. Outcomes of nerve root blocks for whiplash induced cervical radiculitis. Presented at the 11th annual meeting of the North American Spine Society. 1996.

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77. Pfaffenrath V, et al. Cervicogenic headache: results of a computer-based measurements of cervical spine mobility in 15 patients. Cephalgia 1988; 8:45–48.

108. Cronen M. Cervical steroid epidural nerve blocks in the palliation of pain secondary to tension-type headaches. J Pain Symptom Manage 1990; 5:379–381.

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Section 3: Cervical Spine 115. Murphy J. Occipital neurectomy in the treatment of headache results in 30 cases. Maryland State Med J 1969; 8(6):62–66.

119. Weiner R. Peripheral neurostimulation for control of intractable occipital neuralgia. Neuromodulation 1999; 2:217–221.

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120. Stojanovic M. Stimulation methods for neuropathic pain control. Curr Pain Headache Rep 2001; 5(2):130–137.

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118. Dubuisson D. Treatment of occipital neuralgia by partial posterior rhizotomy at C1–C3. J Neurosurg 1995; 82:581–586.

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SPECIFIC DISORDERS

Section 3

Cervical Spine ■ iii: Treatment ■ iii: Other Disorders of the Cervical Spine

CHAPTER

Surgical Treatment of Cervical Myelopathy

70

David H. Kim and Alexander R. Vaccaro

INTRODUCTION This chapter will review current concepts regarding surgical planning, technique, and perioperative management for patients with cervical myelopathy. The pathophysiology, evaluation, and nonoperative management of this condition have been discussed in previous chapters.

INDICATIONS Surgical treatment is indicated for patients with moderate to severe myelopathic signs and symptoms such as functional weakness, loss of dexterity, or gait abnormality and who are otherwise sufficiently healthy to withstand the physiological stress of anesthesia and surgery. There is no consensus regarding the optimal treatment of mild forms of myelopathy such as patients with mild sensory alteration and hyperreflexia. Early surgical intervention can be considered a reasonable option for patients with radiographic evidence of static cord compression and clinical signs and symptoms of early myelopathy, with the goal of preserving neurological function and limiting the risk of future spinal cord injury. A period of nonoperative observation is an option for patients with clinical signs of early myelopathy but no significant functional compromise. In the absence of overt clinical signs or symptoms or myelopathy, surgical treatment of radiographic findings such as mild cord compression on magnetic resonance imaging (MRI) should be entered into with caution, given evidence that such findings may be present in as many as 16% of asymptomatic subjects under 64 years of age and in 26% aged 65 years and older.1 Mild, moderate, or severe forms of myelopathy remain clinical impressions without clearly defined criteria. Clinical studies have employed various scales including the Nurick grading system and the Japanese Orthopaedic Association system. Benzel’s modification of the JOA scale (mJOA) is more applicable to Western populations. (These classifications systems are outlined in previous chapters.) Using this system, an mJOA score <12 can be considered moderate myelopathy, while severe myelopathy is reflected by a score <7 (maximum score=18).2

PREOPERATIVE PREPARATION Patient evaluation includes obtaining a thorough history and examination as well as reviewing updated plain radiographs and advanced imaging studies of the cervical spine. Selection of an anterior or posterior surgical approach as well as the specific surgical technique depends in part on the location of predominant compressive lesions and the patient’s sagittal spinal alignment. The patient’s maximum active flexion and extension arc may suggest whether standard intubation methods will be safe or whether fiberoptic awake intubation should be utilized. Patients with myelopathy frequently have significant medical comorbidities, and a preoperative evaluation by appropriate medical specialists may

be necessary. Given the increased risk of catastrophic spinal cord injury, we often provide a hard collar to patients with moderate to severe cervical myelopathy and suggest that they wear it when riding in motor vehicles or are in situations in which they may experience acceleration– deceleration forces to their head and neck.

ANTERIOR SURGERY An anterior surgical approach is an option when spinal cord compression results from anterior pathology such as herniated disc material, endplate or uncinate process osteophytes, or ossification of the posterior longitudinal ligament (OPLL). The anterior approach is ideal for compression limited in extent to one or two spinal levels, and may provide superior results over posterior approaches by allowing direct excision of the offending pathology (Fig. 70.1). Although a posterior approach can achieve indirect decompression of the spinal cord in many patients, the surgery often must be extended over a greater number of levels. In patients with significant cervical kyphosis and anterior cord compression, a posterior-only approach will not achieve sufficient decompression, and in most cases anterior surgery is required. For the majority of anterior surgical procedures, we favor use of a standard operating table. Patients with severe myelopathy or canal stenosis should undergo anesthetic induction on the operating table to minimize manipulation while the patient is unconscious. Fiberoptic intubation is preferred to limit extension of the neck. Neurophysiologic spinal cord monitoring employing both sensory and motor evoked potentials is a potentially useful adjunct. A baseline measurement should be obtained prior to anesthetic induction and patient positioning. The patient is placed supine in 15–30° reverse Trendelenburg to reduce intraoperative bleeding. For one- to two-level discectomy or a one-level corpectomy, a 4 cm transverse skin incision is used from the midline to the medial border of the sternocleidomastoid muscle. For surgery involving three or more levels a transverse incision can be used but for difficult exposure, partial or complete transaction of the omohyoid muscle will improve exposure. A longer oblique incision is an alternative used along the medial border of the sternocleidomastoid muscle but it is less cosmetic. To reduce risk of injury to the recurrent laryngeal nerve, some surgeons prefer a left-sided incision and approach due to the more consistent anatomic location of the nerve on the left side within the tracheoesophageal groove. Superficial dissection consists of incision through skin, subcutaneous tissue, and platysma. Deep dissection then proceeds through a natural anatomic plane between the trachea and esophagus medially and the sternocleidomastoid muscle and the carotid sheath neurovascular bundle containing the internal jugular vein, vagus nerve, and carotid artery laterally. Gentle retraction of the trachea and esophagus medially and blunt dissection through the intervening middle layers of the deep cervical fascia reveals the longus colli muscles and prevertebral fascia overlying the anterior cervical spine. Subperiosteal elevation of this 753

B

A

D

C

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Fig. 70.1 Fourty-five-year-old male with cervical myelopathy and single-level anterior spinal cord compression resulting from herniated intervertebral disc tissue. (A) Sagittal MRI image demonstrates localized anterior cord compression. (B) Axial image through level of compression. (C) Postoperative lateral radiograph following anterior surgical discectomy and instrumented fusion. (D) Postoperative anteroposterior radiograph.

Section 3: Cervical Spine

muscle and fascia layer allows placement of self-retaining retractors and sufficient visualization to proceed with decompression. A simple intraoperative maneuver once the retractors are in place and opened is to deflate and then reinflate the endotracheal cuff to more evenly distribute pressures within the endolarynx and possibly minimize excessive pressure on branches of the recurrent laryngeal nerve, especially for a right-sided approach. Dysphagia and hoarseness are the most frequent immediate postoperative complaints following the anterior approach but typically resolve over the course of several days, although dysphagia may last several weeks to months. Persistent hoarseness or voice change lasting longer than several weeks is less common and can reflect injury to the recurrent or superior laryngeal nerve. Patients who undergoing a second anterior surgery through a contralateral approach should undergo preoperative laryngoscopic evaluation to confirm that vocal cord function is normal and to avoid the risk of bilateral vocal cord paralysis and the requirement of postoperative tracheostomy. Postoperative wound infections are rare following anterior cervical spine surgery. Significant injury to major vascular structures is also rare, but spinal decompression can lead to persistent bleeding from epidural vessels or decorticated bone surfaces resulting in postoperative hematoma formation. Given the limited space available in the cervical soft tissue, a moderate-sized hematoma can cause lifethreatening airway compression, and for this reason, if postoperative bleeding is considered a possibility, patients should be admitted for overnight observation. Esophageal injury is another major concern, and unrecognized intraoperative perforation can lead to delayed lifethreatening appearance of mediastinitis.

Anterior decompression In general, anterior decompression can be performed through the disc space, i.e. discectomy, or the vertebral body and adjacent disc spaces, i.e. corpectomy, or a combination of the two. Selection of the ideal technique for anterior decompression is based largely on the anatomic location of compressive pathology and planned reconstruction strategy.

Discectomy For stenosis and cord compression mostly limited to the disc space, i.e. disc bulges, disc herniations, and endplate osteophytic ridges, discectomy should provide adequate access for removal of compressive pathology while allowing preservation of the vertebral endplates to allow for stable reconstruction. Following surgical exposure of the anterior cervical spine, an anterior annulotomy is performed with a scalpel, and disc tissue is removed using a combination of curettes and Kerrison rongeurs. The vertebral arteries are located immediately lateral to the uncinate processes, and are vulnerable to injury if the decompression is extended too laterally. The discectomy is continued until the posterior longitudinal ligament (PLL) is visualized. A Kerrison rongeur can then be used to remove osteophytes from the posterior aspect of the adjacent endplates and uncinate processes as required. If imaging studies suggest the presence of extruded disc material behind the PLL, or if there is ossification causing compression, this ligament is resected, otherwise it is often retained to preserve additional stability. A micronerve hook is then used to confirm adequate decompression of the canal and adjoining neuroforamen.

Corpectomy When compressive pathology is located posterior to the vertebral bodies, discectomy alone may not provide adequate relief, and corpectomy is indicated. Corpectomy allows excision of all sources of anterior compression including vertebral osteophytes, disc material, and OPLL. The surgical approach is identical to that for discectomy.

For single-level corpectomy we favor a transverse incision, while multilevel corpectomies are more easily performed through an oblique incision medial to the sternocleidomastoid muscle. Following surgical exposure of the involved vertebral bodies, subtotal discectomies are performed of the disc spaces above and below the planned corpectomy as well as any intervening disc spaces if a multilevel corpectomy is planned. It is vital that the anatomic midline is identified and carefully maintained during subsequent bone removal to avoid straying too far lateral and causing injury to a vertebral artery. A minimum 165 mm corpectomy channel provides adequate decompression of the cervical spinal canal. A Leksell rongeur is used to resect vertebral body bone which can then be morselized and utilized as autologous bone graft during reconstruction. Once the posterior aspect of the vertebral body is approached, a high-speed burr is used to continue through the remaining cancellous bone. Upon reaching posterior cortical bone, a less aggressive diamond-tipped burr may be used to remove remaining bone and reduce the risk of a dural tear. Others find the use of a high-speed cutting burr safe and effective, especially with an intact posterior longitudinal ligament. To complete the decompression, the posterior longitudinal ligament may be removed, if necessary, with use of a micronerve hook, 1-0 and 2-0 Kerrison rongeurs, and a 3-0 cervical curette. In cases of OPLL, an attempt should be made to remove any ossified tissue contributing to compression of the spinal cord or nerve roots. In cases of severe compression, localized areas of dural erosion may be present when overlying tissue is removed. Even with an apparently intact subarachnoid membrane, postoperative cerebrospinal fluid (CSF) leakage and delayed formation of durocutaneous fistulas may occur, and consideration should be given to patching such defects with muscle or fascia and placing a lumbar subarachnoid shunt.3 Radiographic signs of dural penetration by the ossified posterior ligament have been suggested, including the ‘C’ sign and single-layer sign on plain radiographs or the double-layer sign on computed tomography.4 When these signs are present, an option is to avoid complete removal of overlying ossified tissue and leave free-floating patches attached to small areas of suspected dural penetration. This is accomplished by releasing the posterior longitudinal ligament laterally and allowing the thinned-out remaining ossified ligament to float forward, decompressing indirectly the spinal canal. An oblique corpectomy is an alternative technique that can be performed to achieve anterior decompression without the need for concomitant fusion. Proponents of this procedure suggest ideal candidates for this procedure as having asymmetric cord compression from spondylotic bars that are predominantly unilateral in location.5 The intervening disc space must be dehydrated and collapsed to limit the risk of postoperative instability. Bilateral foraminal stenosis is a contraindication. The skin incision and initial soft tissue dissection for oblique corpectomy are the same as for standard corpectomy. Retraction of midline structures, including the trachea and esophagus, is less forceful due to a more lateral surgical approach and may reduce postoperative dysphagia and hoarseness. The sympathetic chain and vertebral artery must be identified and protected. A burr is then used to remove, in an oblique fashion, a wedge-shaped posterior portion of the vertebral body. The central canal and ipsilateral neuroforamen can be decompressed through this approach, but the contralateral neuroforamen cannot be safely accessed. Due to preservation of the anterior half of the vertebral body, no fusion is required. With this technique, the rate of significant complications approaches 30% and therefore limits its potential application. Horner’s syndrome occurs transiently in up to 57% of patients but can be permanent in up to 9%.6 A prospective study of 26 patients treated by this technique resulted in 76.9% good to excellent results with 84.6% improvement in any preoperative radicular symptoms.5 755

Part 3: Specific Disorders

Discectomy–corpectomy A combination of discectomy and corpectomy can be utilized for anterior decompression when compressive pathology extends over three motion segments but is localized primarily to the disc spaces and one vertebral body. Preservation of one intervening vertebral body allows application of a plate using segmental screw fixation and significantly enhanced postoperative stability compared with multilevel corpectomy and long anterior plate stabilization without the need for supplemental posterior fixation.

Anterior reconstruction Following anterior discectomy or corpectomy, restoration of anterior column height allows preservation of sagittal alignment and avoidance of postoperative kyphosis. Reconstruction can be accomplished utilizing autologous structural bone graft, allograft bone, or titanium cage implants filled with autologous bone graft. Structural tricortical iliac crest autograft is well suited for anterior reconstruction following single-level or multilevel discectomy or single-level corpectomy. Following two-level corpectomy or more extensive decompression procedures, structural fibular allograft can be used with good results. The potential for significant bone graft harvest site morbidity, including chronic pain, numbness, infection, and hematoma, has led to the increased use of allograft bone in place of autologous iliac crest bone graft. Both cortical bone and dense cancellous bone products have been used with success. Titanium cages have the advantage of material strength, but significant mismatch in material properties between titanium and bone may increase the risk of endplate fracture and subsidence, particularly in osteoporotic bone. A problem with both autologous and allograft bone reconstruction is the need to place these relatively straight grafts in an inherently less stable anterior position to avoid spinal cord impingement. Precontoured titanium mesh cages are available for longer reconstructions that allow more central positioning on endplates while preserving a degree of lordosis.7 The concept of motion-sparing technology as an alternative to spinal fusion is appealing in theory, and numerous artificial disc replacement devices are currently available, mostly for use in the lumbar spine. At this time, spinal disc arthroplasty for the cervical spine is being performed in the United States in the setting of clinical trials only. Preliminary short-term results for some devices have reportedly been positive in the setting of myelopathy, but long-term outcome data are unavailable. A concern is that the theory of allowing continued motion in the setting of a decompressed dysfunctional myelopathic cord may not prevent continued shear injury and therefore continued apoptotic cell death in this setting.

Anterior plating Supplemental cervical plate and screw fixation is routinely recommended following multilevel anterior discectomies and corpectomy procedures. Plate fixation for single-level discectomy and fusion obviates the use of postoperative cervical brace but there is no clear evidence that it is superior to in situ fusion. If patient bone quality allows adequate fixation strength, instrumentation provides immediate stability, reducing early postoperative pain and in many cases obviating the need for weeks of postoperative hard collar or halo vest immobilization. Long-term outcome studies have demonstrated significantly improved fusion rates and decreased rates of graft-related complications associated with use of anterior plates.8,9 In the absence of instrumentation, 50% of patients undergoing single- or two-level corpectomy experience localized kyphosis of 10° or more as a result of graft subsidence.10 Preservation of cortical endplates can minimize 756

such subsidence but requires the use of anterior plates to prevent graft extrusion and may increase the risk of pseudoarthrosis.

POSTERIOR SURGERY The two principal surgical options for posterior decompression surgery are laminectomy and laminoplasty. Both techniques require preoperative cervical spinal alignment that is neutral or lordotic because both accomplish indirect decompression of the spinal cord by allowing the cord to migrate posteriorly in an expanded canal. Laminectomy involves removal of posterior laminar bone en bloc while laminoplasty involves elevating the laminar bone on an attached hinge. For posterior surgical approaches, Mayfield-type cranial tongs are used to immobilize the cervical spine. This allows stabilization of the head and neck in the so-called ‘military position’ with the head slightly forward flexed and in neutral alignment. The arms are typically tucked at the side with protective padding around the elbows to avoid direct compression of the ulnar nerves. As with anterior surgery, a 15–30° reverse Trendelenburg position is utilized to reduce blood loss. Although not yet accepted as the standard of care, intraoperative spinal cord monitoring through both motor and sensory tract evoked potentials is recommended. A baseline reading should be obtained prior to patient positioning and rechecked immediately after the patient has been positioned on the operating table. Potentials should then be monitored regularly throughout the procedure. The use of intraoperative steroids is not routinely recommended, given the lack of clinical evidence that they provide a positive risk–benefit effect in the absence of a discrete spinal cord injury event. The posterior surgical approach to the cervical spine is standard for both laminectomy and laminoplasty. Following a midline longitudinal skin incision, dissection proceeds in the midline through the subcutaneous tissue and ligamentum nuchae. Subperiosteal exposure of the posterior cervical spine is then performed using a combination of cervical Cobb elevators and electrocautery. Care is taken to avoid injury to any facet joint capsule that will not be fused. Stabilizing muscular attachments to the spinous process of C2 are typically preserved unless the C2 level is to be fused to limit postoperative kyphosis. Alternatively, the muscular attachments to C2 can be removed en bloc with a piece of spinous process and suture repaired at the conclusion of the procedure through a hole in the spinous process base.

Laminectomy Cervical laminectomy has been associated with a 20% incidence of late postoperative kyphotic deformity in the adult patient.11 Preoperative kyphosis is therefore a contraindication for laminectomy unless concomitant anterior reconstruction can restore at least neutral sagittal alignment. In patients with preoperative neutral or lordotic sagittal alignment, laminectomy is technically straightforward and yields typically good results in conjunction with a posterior fusion procedure (Fig. 70.2). Ideal candidates have multilevel stenosis that would be difficult to reconstruct following anterior decompression. Patients with extensive OPLL are also candidates to avoid the risk of dural tears with anterior decompression. The operation is also well suited for elderly and debilitated patients who may not tolerate a longer anterior procedure with potential for greater blood loss. Patients with significant calcification of the ligamentum flavum causing posterior cord compression are also good candidates.

Technique The posterior cervical spine is exposed to include all involved levels. Care is taken to avoid injury to the facet capsules of any levels that are not to be surgically fused. If an instrumented fusion is planned, then we recommend preparing screw holes for all implants prior to

Section 3: Cervical Spine

A

B

performing the actual laminectomy in order to minimize the risk of iatrogenic cord injury during instrumentation. The interspinous ligaments are resected proximal and distal to the levels to be decompressed. The laminectomy margins are defined anatomically by the longitudinal border between the lateral masses and the laminar bone. A high-speed burr is used to sequentially divide the laminar bone along this border on one side. Although this step is not typically associated with significant blood loss, an extensive epidural plexus of veins is concentrated near the junction of the lamina and lateral mass, and excessively lateral burring of the troughs can lead to substantial hemorrhage. We recommend placement of the troughs 2 mm medial to the junction of the lamina and lateral mass to minimize this risk. A Kerrison rongeur can be used to complete resection of the inner cortical bone. The contralateral laminar bone is then divided in similar fashion. With division of the ligamentum flavum, the resected laminar bone can be elevated sequentially and removed en masse, completing the laminectomy. Because of the increased incidence of postoperative C5 and C6 root palsy, a concomitant C5 and C6 foraminotomy is routinely prophylactically performed.

Laminoplasty Development of cervical laminoplasty was pioneered by Japanese surgeons for treatment of OPLL and first reported in the English

C

Fig. 70.2 Sixty-year-old male with multilevel cervical spondylotic myelopathy and preserved cervical lordosis. (A) Preoperative MRI. (B,C) Postoperative anteroposterior and lateral radiographs following posterior cervical laminectomy and instrumented fusion.

language by Hirabayashi et al. in 1983.12 Extensive anterior decompression and reconstruction procedures were associated with high failure rates and motivated development of a posterior approach that was less destabilizing and did not require complex reconstruction techniques. The surgical indications were subsequently expanded successfully to include patients with more generic spondylotic myelopathy as well. Laminoplasty results in lower rates of postoperative kyphosis compared to laminectomy without fusion. Elevating the laminar bone on a hinge expands the sagittal diameter of the spinal canal, allowing the spinal cord to migrate posteriorly, accomplishing an indirect decompression (Fig. 70.3). In patients with OPLL, postoperative imaging demonstrates posterior cord translation of up to 6 mm accompanied by increased transverse cord area, both of which correlate with improvements in myelopathy.13 Following the original description of the procedure by Hirabayashi et al., now referred to as ‘open-door’ laminoplasty, several modifications including ‘French-door’ and ‘skip’ laminoplasty have been reported and are currently being practiced.14–16 In general, the reduced operative time and blood loss associated with laminoplasty compared with both anterior decompression and fusion or laminectomy and fusion make it an appealing option for high-risk surgical patients. Theoretically, retention of the dorsal laminar bone may also limit formation of postoperative epidural fibrosis and tethering of the dura to paraspinal muscles. 757

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A

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C

D

Fig. 70.3 (A,B) Preoperative sagittal and axial MRI images and (C,D) postoperative MRI images following C3–7 laminoplasty for cervical spondylotic myelopathy.

Prior to surgery, careful assessment of a lateral radiograph in the neutral position must be made. Kyphotic sagittal alignment is considered by many to be a contraindication for laminoplasty. Either neutral or lordotic alignment is acceptable, although in patients with excessive lordosis there may be a risk of overexpansion of the canal diameter. Due to potentially increased risk of C5 palsy in patients with severe lordosis and excessive posterior cord migration, limiting the amount of laminar elevation to approximately 12 mm may minimize the degree of neural stretch. Preoperative spondylolisthesis is not considered a contraindication for laminoplasty, as 85% of spon758

dylolisthesis cases have been observed to resolve or improve within 1 year following surgery.17 In terms of prognosis, however, posterior spondylolisthesis may be associated with lower rates of postoperative neurological recovery. Patients with significant axial neck pain complaints may not be ideal candidates for laminoplasty, given relatively high rates of persistent neck pain following this procedure. In such patients, an anterior decompression and fusion for one- to two-level disease or a posterior laminectomy and fusion for three-level or greater disease may be better tolerated.

Section 3: Cervical Spine

Following completion of the C3–7 laminoplasty, if compression persists proximally at C2 or distally at T1, a laminectomy can be performed at the affected level(s) without significantly compromising spinal stability. In order to retain stabilizing muscular attachments to the C2 spinous process, a dome-shaped laminectomy of C2 can be performed utilizing a burr and Kerrison rongeur. Spontaneous closure of the hinged laminae can occur in the postoperative period and may compromise surgical results. Several techniques for maintaining laminar elevation have been developed. Small titanium plates and screws can be placed at each level or alternating levels to maintain the laminae in an open position. In patients with normal lordotic alignment, nonabsorbable sutures may be used to secure the opened laminae to the adjacent facet. Titanium plates and screws may be used in patients with neutral sagittal alignment when a more rigid block to hinge closure is desired. Another application is for patients with significant lordosis where more controlled expansion of the canal may be advantageous to avoid C5 root palsy.

Minimally invasive surgery

E Fig. 70.3 Cont’d (E) Axial CT image demonstrating hinged segment with bone graft strut.

Technique During posterior surgical exposure, violation of the intervertebral facet capsules is avoided, as spontaneous fusion may result and preservation of joint motion is a surgical goal. At the beginning of the procedure the tips of the spinous processes may be removed to prevent impingement of these structures during neck extension. A high-speed burr is utilized to create bilateral longitudinal troughs at the junction between the laminae and the lateral masses from C3 through C7. On the side to be opened, the trough is completely extended through both cortices of bone, and the ligamentum flavum is divided with a Kerrison rongeur to open the spinal canal. On the hinge side of the laminae, the trough is extended to but not through the anterior cortex of the laminae. Elevation of the laminae creates a controlled ‘greenstick’ fracture on the hinge side and expands the posterior dimension of the canal, allowing indirect decompression of the cord. Sutures can be used to maintain the hinged laminae in the open position, or spacers made of various materials, including spinous process bone, allograft bone, or hydroxyapatite, or miniature titanium plates can be utilized to block open the laminae. When fashioning allograft spacers to support the opened posterior arch, an ideal height of 10–15 mm allows adequate cord decompression while at the same time limiting the extent of posterior migration and possibly reducing the risk of C5 root palsy.18 In the setting of coexisting myeloradicular deficits or symptoms, careful assessment of the cervical neuroforamen should be performed on the preoperative MRI or computed tomography (CT)-myelogram images. The presence of significant foraminal stenosis that correlates with anatomic distribution of radiculopathy indicates the need for concomitant foraminotomies. Technical aspects of performing cervical foraminotomies are covered in a separate chapter. Individual nerve roots can be decompressed before or after creating the longitudinal bone troughs for laminoplasty, but should be performed prior to elevation of the lamina. If the number of foraminotomies is limited, performing them prior to creating the longitudinal troughs may be safer and allow greater preservation of stability.

Minimally invasive surgical techniques are being developed for treatment of cervical myelopathy but are as yet not widely practiced. Yabuki and Kikuchi have described their experience with endoscopic partial laminectomy in a series of 10 patients.19 Their strategy is based on Japanese reports that segmental laminotomy or fenestration performed in open fashion can yield outcomes similar to those following laminoplasty but with even less disruption of laminar integrity.20 Segmental laminotomy is not a procedure that has been generally accepted in the United States for treatment of cervical spondylotic myelopathy, so assessment of the endoscopic version of the technique is difficult. In the method described, a posterior approach is utilized with the patient in the prone position. Lateral fluoroscopy is utilized to guide placement of a 20 mm incision 20 mm off midline. After placement of a guidewire through the posterior fascia and musculature to the lamina proximal to the level of pathology, a series of dilators is used to place an 18 mm tubular retractor. Endoscopic partial laminectomy is then performed with a high-speed burr and a 1 or 2 mm Kerrison rongeur. The study group consisted of 8 patients with spondylotic myelopathy and 2 with myelopathy due to calcium pyrophosphate deposition in the ligamentum flavum. Surgery consisted of a two-level decompression in six cases and a one-level decompression in four cases. All patients reported subjective improvement, and the group experienced mean improvement in JOA score from 11.6 to 14.1 at mean follow-up of 14.9 months. The investigators concluded that operative time was increased (mean 164 minutes) but that blood loss was reduced (mean 46 mL) and there were no observed complications or cases of neurological worsening. Although the feasibility of safe endoscopic surgery was demonstrated, the limited anatomic decompression achieved by this technique would appear to make it inappropriate for most cases of myelopathy involving significant canal stenosis.

Instrumented fusion Following extensive anterior surgery, the role of posterior fusion is to provide additional stability and reduce the risk of implant failure and nonunion. In patients with neutral or minimally lordotic alignment, posterior implants can prevent development of postoperative kyphotic deformity. Specific patient populations with athetoid movement disorders, rheumatoid arthritis, and destructive spondyloarthropathy may benefit from the added stability of posteriorly positioned implants. Mild to moderate segmental instability that is 759

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not traumatic in origin does not necessarily require supplemental posterior fusion. It is often recommended to perform a posterior instrumented fusion following three-level or greater anterior decompression, particularly when segmental anterior instrumentation is not performed (Fig. 70.4). It is also recommended to perform an instrumented fusion when a multilevel laminectomy is performed to reduce the risk of postoperative instability or kyphosis.

Lateral mass screws For segmental posterior fixation in the subaxial cervical spine, C3– 6 lateral mass screw fixation, and C7 and T1 pedicle screws, and C2 isthmus or pedicle screw are the favored forms of internal fixation. Several techniques for lateral mass screw placement have been described. The technique described by An is frequently used, which provides excellent fixation strength while minimizing risk of injury to the vertebral artery and exiting nerve root (Fig. 70.5). The screw entry point is 1 mm medial to the midpoint of the lateral mass, and the screw trajectory is directed 15° rostral and 30° lateral. Typical screw lengths are 14–16 mm.

Fig. 70.5 Computed tomography axial image showing position of leftsided cervical lateral mass screw at C6.

Pedicle screws At the C2 and C7 levels, pedicle screw fixation is frequently used (Fig. 70.6). Variable coursing of the vertebral artery through the C2 vertebra makes lateral mass screw placement risky at C2, and the smaller size of the C7 lateral mass reduces fixation strength of lateral mass screws at this level. Pedicle screws are angled medially through the vertebral pedicle towards the vertebral body. Longer screw

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B Fig. 70.4 Anterior and posterior instrumented fusion including C3 through C7 vertebral levels following three-level anterior C4 through C6 corpectomies for cervical myelopathy. 760

Fig. 70.6 Computed tomography axial image showing position of leftsided cervical pedicle screw at C7.

Section 3: Cervical Spine

lengths can typically be utilized and achieve substantially greater fixation strength. Laminoforaminotomies can be created at the C6–7 level to allow direct palpation of the pedicles from within the canal prior to drilling of the screw holes. The isthmus of C2 may be easily palpated by dissecting along the superior border of the C2 lamina laterally to the junction of the C2 isthmus. Although the use of pedicle screw fixation in intervening vertebrae from C3 through C6 has been reported, the relatively small size of these pedicles and proximity of the vertebral artery significantly increases the risk of pedicle screw placement at these levels.

POSTOPERATIVE CARE Following lengthy anterior procedures, particularly those involving multiple levels, consideration should be given to continuing airway intubation overnight. Anterior soft tissue swelling and endolaryngeal edema may lead to airway compromise in the immediate postoperative period and patient ventilation should be carefully monitored. Risk factors for postoperative airway complications include age >65 years, morbid obesity, severe neurological deficit, asthma, proximal surgery extending to the C2 level, significant CSF leak, operative time >10 hours, and blood transfusion >4 units.21 Anteroposterior surgery may be another risk factor.22 The ‘leak test’ described by Emery et al. is useful for determining whether patients can safely be extubated following extensive cervical spine procedures.23 Patients with a dural defect or CSF leak identified at the time of surgery should be maintained at strict bed rest with the head of bed no lower than 45° for 1–5 days, depending on the extent of the defect. A persistent CSF leak is suggested by the presence of severe headache, neck swelling, dysphagia, stridor, or overt durocutaneous fistula formation.3 These patients may require dural repair with or without placement of a lumbar subarachnoid drain. Six to 12 weeks of postoperative hard collar immobilization may provide supplemental stability following vulnerable reconstructions such as might occur in osteoporotic bone. In general, for instrumented single- or two-level fusions or stable anteroposterior fusions, hard collar immobilization is optional. There is limited evidence that minimizing the period of postoperative collar immobilization may reduce the incidence of neck and shoulder pain following laminoplasty.

COMPLICATIONS Neurological New postoperative neurological deficits occur 7–8% of the time following surgery for cervical myelopathy.24–26 Clinical deterioration of myelopathy can occur but is relatively uncommon. Most often, new neurological deficits are isolated C5 or C6 distribution nerve root palsies that may appear at any time up to a month following surgery and typically take the form of isolated deltoid or regional upper extremity weakness. In most cases, these deficits resolve spontaneously without the need for specific intervention. Time to recovery may be 1 week to over 1 year. With respect to cervical laminectomy and laminoplasty, it has been suggested that posterior migration of the decompressed cord leads to extradural tethering of the C5 and C6 nerve roots. However, preoperative sagittal alignment does not appear significantly different among those developing postoperative palsy.27 Another theory is that excessively narrow laminectomy margins or a relatively medial laminoplasty hinge creates an edge effect as the cord migrates posteriorly and roots impinge on the bone margins. In support of this theory, anatomic studies have demonstrated that posterior translation of the cord by onethird its diameter results in direct contact of the C5 root with the laminectomy margin.28

There are no reliable tests for predicting patients at risk for developing postoperative root palsies. Abnormal preoperative deltoid muscle electromyogram (EMG) studies do not predict the occurrence of postoperative C5 palsy.27 On the other hand, the C5 and C6 motor segments originate within the cord at the C3–4 and C4–5 spinal levels, and the presence of MRI signal abnormalities within the cord at these levels may be a risk factor.29 It may be possible to reduce the risk of postoperative root palsy by performing bilateral 7–8 mm partial foraminotomies at the C5 and C6 root levels. In one retrospective study of 305 laminoplasty cases, performance of such foraminotomies reduced the incidence of postoperative C5 palsy from 4.0% to 0.6%.27 Although widely considered a specific complication of posterior cervical decompression, C5 nerve root palsy is also associated with extensive anterior decompression procedures, particularly when performed for myelopathy secondary to degenerative conditions. In general, rates appear comparable with those reported for posterior decompression with multiple series reporting rates of postoperative root palsy from 2.8% to 17%, with an average incidence of approximately 8%.7,30–35 Muscle weakness or paralysis of the deltoid is the dominant deficit, although both C5 and C6 root deficits with biceps and wrist extensor weakness often coexist. As with posterior surgery, symptoms typically improve spontaneously over the course of 3 months. The risk of C5 palsy can be reduced by limiting the corpectomy width to 15 mm, suggesting that anterior cord migration and nerve root traction may be to blame.33 Advanced patient age also appears to be a risk factor and may be related to increased perineural fibrosis tethering the nerve roots.36

Implant failure A technical concern with anterior strut graft and cage reconstruction is postoperative settling. This problem can be identified on plain radiographs by the appearance of 2 mm or more of vertical penetration into the adjacent vertebral body.37 Settling decreases construct stability, leads to progressive kyphotic deformity, and increases the risk of nonunion and eventual implant failure. Osteoporosis significantly increases the risk of graft or cage settling, and therefore we consider osteoporosis to be a relative contraindication for anterior cage reconstruction without supplemental posterior stabilization. Without instrumentation, single- or two-level corpectomy has been associated with localized kyphotic change of greater than 10° in 50% of patients.38 Progression of kyphosis is uncommon after 1 year. Early plate migration may be the result of graft or cage subsidence. On the other hand, delayed screw loosening and plate migration may indicate the presence of postoperative pseudoarthrosis. Significant screw back-out can lead to esophageal injury and consideration should be given to revision or removal of the instrumentation. Minimal screw back-out that does not progress following successful fusion is typically asymptomatic and can be observed. Plate migration that results in significant impingement of adjacent unfused vertebrae may be associated with development of delayed postoperative neck pain and ossification and may be an indication for plate removal. The risk of implant failure following two-level corpectomy is 9%.39 Anterior fusion following three-level or greater corpectomy without supplemental posterior stabilization has been associated with failure rates of up to 45%.40–42 It is therefore recommended in this situation to consider supplemental posterior instrumented fusion in all patients undergoing corpectomies of three or more levels.

Three-level or greater anterior decompression Assertions that laminoplasty is associated with lower risks of surgeryspecific complications should be viewed with caution. These claims are largely based on early reports that compare laminoplasty with 761

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older and outdated techniques of anterior reconstruction, i.e. corpectomy and noninstrumented fusion.43,44 The risk of graft migration, extrusion, and nonunion associated with multilevel anterior reconstruction can be significantly reduced by appropriate utilization of modern implant technology, including anterior plating and supplemental posterior instrumentation.

Kyphosis The risk of postlaminectomy kyphosis is increased in children and in patients with preoperative kyphotic alignment. Even in patients with nearly normal preoperative lordosis, progressive kyphotic deformity may occur with recurrent myelopathy, neck pain, and difficulty maintaining horizontal gaze (Fig. 70.7). Salvage surgery in this situation is risky and technically challenging, and for this reason it is typically recommended to include an associated instrumented fusion in this setting. Postoperative kyphosis may also develop following laminoplasty and has a negative impact on clinical outcomes in patients with spondylotic myelopathy. In patients with OPLL, kyphotic alignment appears to develop in up to 12.5% of patients 5 years following laminoplasty, but is not associated with the same adverse effect, possibly due to more restricted cervical motion.45

Neck pain The association between laminoplasty and postoperative neck pain remains controversial, with studies reporting increased rates as well as no significant difference in rates comparing laminoplasty to laminectomy and fusion or anterior decompression and fusion.34,46,47 High rates of chronic postoperative neck pain have been reported following laminoplasty regardless of surgical technique. Five-year rates of persistent neck and shoulder pain have been reported as 39.5% and 72.1%, respectively,45 with 10-year neck pain rates of 28%.48,49 It has been suggested that reduction of postoperative neck pain can be achieved by shorter periods of postoperative immobilization and earlier introduction of range of motion (ROM) exercises.

Transition syndrome Radiographic appearance of adjacent segment degeneration is frequently observed following fusion of the cervical spine (Fig. 70.8). Whether such degeneration occurs more rapidly as a result of increased stress from an adjacent fused segment or whether it represents inevitable progression of underlying spondylosis and disc degeneration remains a subject of debate. Hilibrand et al. reported that symptomatic adjacent segment degeneration occurs at a constant rate of 2.9% per year following anterior cervical fusion with a cumulative risk of 25.6% after 10 years.50 However, in their analysis, the risk of adjacent

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B Fig. 70.7 MRI imaging of 70-year-old female with postlaminectomy cervical kyphosis and recurrent myelopathy. 762

Fig. 70.8 Sixty-year-old female with neck pain 10 years following surgical decompression and anteroposterior C3 through C6 instrumented fusion for spondylotic myelopathy. Advanced disc space collapse and spondylotic degeneration is observed distal to the fused levels.

Section 3: Cervical Spine

segment degeneration was lower following longer fusions, suggesting that the risk of developing symptoms is more strongly related to the location of remaining mobile segments and not necessarily from increased mechanical stresses. Further complicating the issue is the fact that radiographic degeneration correlates poorly with the presence of clinical signs or symptoms. Although avoidance of so-called ‘transition syndrome’ has been widely used to promote motion-sparing surgical techniques, the clinical significance of this entity has not been proven.50,51 Proponents of laminoplasty have suggested that a reduced risk of adjacent segment degeneration represents an advantage of this technique.50,52

OUTCOMES Although well-designed prospective comparative studies are lacking, available clinical evidence suggests there is not much difference in rates of neurological improvement following anterior decompression, laminectomy, and laminoplasty performed for cervical myelopathy.41,53–55 Multiple long-term follow-up studies have suggested clinical improvement rates of approximately 70%.56,57 General health instruments such as the Medical Outcomes Short Form 36 (SF-36) have revealed improvement in approximately 64% of patients, no change in 23%, and deterioration in 14%.58 The most frequently suggested predictors of outcome following surgical treatment of cervical myelopathy includes patient age, duration of symptoms, preoperative neurological status, preoperative and postoperative spinal cord dimensions, cord tissue signal changes on MRI imaging, and longitudinal extent of anatomic cord compression.59 Although a few studies have suggested that advanced patient age is a risk factor for poor outcome following surgical treatment, a majority of recent series has demonstrated no significant difference in complication rate or neurological recovery based on patient age.18,60,61 There is stronger evidence that duration of symptoms is a significant predictor of outcome for severe myelopathy but not necessarily mild to moderate forms.57,62,63 Neurological recovery appears to occur at a higher rate in patients with shorter symptom duration, although some investigators have challenged this finding.64 Severity of preoperative functional deficits has been frequently discussed as a potential predictor of outcome, but studies have been difficult to interpret. Some studies have suggested poorer outcome in patients with more severe myelopathy, while others have examined selected populations of patients with only mild to moderate forms and found better surgical results in patients with more severe involvement.59,65,66 Stronger evidence exists linking preoperative functional status to morbidity and mortality following surgery for myelopathy in patients with rheumatoid arthritis.67 Early postoperative mortality following cervical spine surgery in rheumatoid patients has ranged 3–17%.68 The mortality rate for rheumatoid patients increases to 21% at 5 years and 62–72% at 10 years.69,70 Nonambulatory status has been associated with a doubling of the postoperative complication rate. Despite increased risks, surgery has been shown to extend the life expectancy of rheumatoid patients with myelopathy.69,71,72 The predictive value of MRI findings remains controversial. Poor outcome may be associated with preoperative cross-sectional area of the spinal cord,61,62 although this finding has been rejected in a separate study.65 The significance of MRI signal changes in compressed cord tissue remains a topic of debate (Fig. 70.9). Signal changes appear to reflect various pathological processes from reversible edema to permanent myelomalacia and cavitary necrosis. Studies have found a significant association between the presence of cord parenchyma changes and long-term outcome following surgical intervention. Several researchers have established specific criteria to define signal change characteristics utilizing high-resolution MRI imaging.61,73,74

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B Fig. 70.9 Forty-year-old male with disc herniation at the C5–6 level and cervical myelopathy with increased T2-weighted signal changes in the spinal cord.

Signal changes with sharply demarcated borders have been correlated with poorer neurological recovery and may be associated with regional cord tissue necrosis.75 This finding appears to be more significant in cases of multilevel cord compression.76 On the other hand, postoperative expansion of T2 high-signal intensity areas occurs in 6% of patients following laminoplasty.29 Such expansion is not necessarily related to technical complications during surgery but is often associated with increased postoperative upper extremity weakness. 763

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Animal studies have revealed that multilevel compression leads to more severe tissue degeneration than single-level compression, characteristically affecting cord gray matter as well as both anterior and posterior columns.77 This finding may have a clinical correlation in studies suggesting that neurological outcome is better following surgical decompression of single-level disease as opposed to multilevel compression.78

Anterior decompression Large surgical series have demonstrated generally similar results in terms of neurological improvement and ultimate clinical outcome following both anterior and posterior decompressions in carefully selected patient populations with cervical myelopathy.34 The period of most rapid neurological recovery occurs during the first 3 months following surgery. Continued improvement at a slower rate is typically observed for up to 1 year with little functional change occurring after 1 year. There may be more deterioration of lower extremity function compared with upper extremity function over time, although degenerative conditions of the lumbar spine and arthritis of the hips and knees may play a role.

Anterior reconstruction Sevki et al.7 have reported minimum 2-year follow-up data on 26 patients undergoing multilevel anterior corpectomy and instrumented fusion with and without supplemental posterior instrumented fusion. Mean JOA score improved 10 points while mean Nurick score improved 3.5 points. Normal lordotic alignment was restored and maintained in all patients including three with preoperative kyphosis. Solid fusion by plain radiographic criteria was accomplished at 6 months in all patients without any cases of cage migration or collapse.

Laminectomy and laminoplasty There are several long-term outcome studies following laminectomy for cervical myelopathy.11,79–82 In general, satisfactory results are observed in 75% of patients, with long-term improvement or at least stabilization of neurological status. Without concomitant fusion, subluxation occurs in 26% of patients, and kyphosis in 15%. Short- to mid-term outcomes following laminoplasty are satisfactory, but results often deteriorate with longer periods of follow-up. Ogawa et al. reported minimum 5-year follow-up of 72 patients with OPLL following laminoplasty and observed a recovery rate of 63% using Hirabayashi’s formula:45 ((postop JOA – preop JOA)/ (17 – preop JOA)) × 100 At 10-year follow-up, the recovery rate had decreased to 41%. Although a proposed advantage of laminoplasty over laminectomy and fusion is greater preservation of neck motion following surgery, studies have demonstrated a reduction of neck motion following laminoplasty exceeding 50% at 2-year follow-up. This may occur as a result of soft tissue contracture or spontaneous facet joint fusion.83 Suda et al. reported 2-year mean follow-up results in 15 rheumatoid patients undergoing C3–7 laminoplasty and observed mean range of motion of 14.8° flexion and extension, representing a reduction of 56.3% compared with the preoperative status.84 Even greater loss of motion is observed with longer periods of follow-up. At 5-year follow-up, Ogawa et al. reported ROM 23.9% of preoperative levels in 72 patients with OPLL.45 Spontaneous fusion had occurred in more than one segment in 97% of patients and the mean number of fused segments was 3.2. Reduced ROM following laminoplasty may protect the spinal cord from further injury and contribute to neurological recovery. On the

764

other hand, spontaneous fusion following surgery may leave intermediate unfused segments vulnerable to progression of OPLL and ligamentum flavum thickening, resulting in recurrent cord compression and late neurological deterioration. In general, laminoplasty appears to provide neurological improvement and overall short-term outcomes comparable to anterior decompression and fusion. Wang et al. reported a series of 204 myelopathic patients treated with laminoplasty.18 At average followup of 16 months, 82% were considered to have experienced postoperative ‘functional neurological improvement.’ Sixty-two percent demonstrated improvement in Nurick score, while 1.5% experienced a decline in Nurick score. Twenty percent developed new, persistent, or worsened neck pain. Sakaura et al. reported a long-term outcome study comparing laminoplasty to anterior decompression and fusion and concluded that both approaches result in similar neurological outcomes but that anterior surgery carries a higher risk of surgical complications while laminoplasty carries a higher risk of chronic neck pain.49 Anterior decompression consisted of discectomy or subtotal corpectomy followed by interbody bone graft reconstruction without plating. Outcome in 15 anterior surgery patients with average follow-up of 15 years was compared to 18 laminoplasty patients with average followup of 10 years. Interpretation of these results is difficult due to the small study population, use of older anterior surgical techniques, and use of different follow-up periods.

Ossification of the posterior longitudinal ligament Ossification of the posterior longitudinal ligament (OPLL) has been successfully treated using both anterior and posterior decompression techniques.35,85–91 Although much more prevalent in Asian populations, OPLL is also a frequently observed cause of cervical stenosis and myelopathy among non-Asians. In the United States, many investigators have reported a preference for anterior decompression.35,92 Epstein reported results of surgical treatment for 43 North American patients with OPLL and suggested superior results associated with anterior surgery.35 Thirty-three patients treated with anterior decompression experienced average improvement of 1.6 Ranawat grades, while 10 patients treated with posterior decompression experienced lower average improvement of 0.9 Ranawat grades. Belanger et al.92 reported results in 61 North American patients with OPLL following anterior decompression and fusion. At average follow-up of 4 years, an average improvement of 1.5 Nurick grades was observed. Five of 8 patients who had absent dura identified at the time of surgery developed a postoperative CSF fistula. Fifty-eight of 60 patients experienced successful radiographic fusion. Of 2 patients with pseudoarthrosis, one was asymptomatic while the other was successfully treated with posterior wiring and autograft. Eight of 61 patients experienced new postoperative neurological deficits including three with deltoid weakness and five with upper extremity dysesthesia.

Athetoid cerebral palsy Movement disorders characterized by involuntary motions and posturing can lead to accelerated cervical degeneration, stenosis, and myelopathy, appearing on average a decade earlier than general spondylotic myelopathy. Identical surgical indications and techniques are applicable, but consideration should be given to utilizing stronger stabilization techniques including anteroposterior instrumentation, particularly when malalignment is present.93

Section 3: Cervical Spine

AUTHORS’ PREFERRED TECHNIQUES In general, we consider patients with sagittal cervical canal diameters and moderate or severe myelopathy as candidates for surgical treatment. For patients with cervical stenosis and equivocal or mild myelopathy either early surgical treatment or continued observation is an acceptable option. For anterior compression resulting from disc herniation or disc–osteophyte complexes limited to one or two levels, or for anterior compression extending over the length of a single vertebral body we favor anterior decompression due to the ability to achieve direct access to the compressive pathology. For compression extending over three or more disc spaces in association with significant kyphotic malalignment, anterior decompression and reconstruction should also be performed as a first stage, followed by a supplemental posterior instrumented fusion to reduce the risk of construct failure. If three-level decompression can be performed through a combination of one corpectomy and one discectomy, then a segmentally stabilizing anterior plate can be applied without the need for supplemental posterior fixation. For multilevel stenosis in patients with neutral or lordotic alignment, either laminoplasty or laminectomy and posterior instrumented fusion are our preferred options. For patients with significant preoperative neck pain complaints, laminectomy and fusion is preferred.

CONCLUSION Clinical outcomes following surgical treatment for cervical myelopathy are generally good. If the appropriate surgical technique is applied to appropriately selected indications, most patients will experience neurological improvement. In patients who do not achieve significant recovery of preoperative deficits, most will experience stabilization of their neurological status. The rate of permanent postoperative neurological deterioration is very small. Patients must be carefully instructed prior to surgery that the goal of intervention is to prevent further spinal cord injury and neurological deterioration and not necessarily to restore any function that has been lost, although some degree of recovery often occurs. In patients who understand the nature of their condition and the goals of treatment, satisfaction with surgical results is typically very high.

References

10. Rajshekhar V, Arunkumar M.J, Kumar SS. Changes in cervical spine curvature after uninstrumented one- and two-level corpectomy in patients with spondylotic myelopathy. Neurosurgery 2003; 52(4):799–804; discussion 804–805. 11. Kaptain GJ, et al. Incidence and outcome of kyphotic deformity following laminectomy for cervical spondylotic myelopathy. J Neurosurg 2000; 93(2 Suppl):199–204. 12. Hirabayashi K, et al. Expansive open-door laminoplasty for cervical spinal stenotic myelopathy. Spine 1983; 8(7):693–699. 13. Aita I, et al. Posterior movement and enlargement of the spinal cord after cervical laminoplasty. J Bone Joint Surg [Br] 1988; 80:33–37. 14. Hirabayashi K, et al. Operative results and postoperative progression of ossification among patients with ossification of cervical posterior longitudinal ligament. Spine 1981; 6(4):354–364. 15. Patel CK, Cunningham BJ, Herkowitz HN. Techniques in cervical laminoplasty. Spine J 2002; 2(6):450–455. 16. Ratliff JK, Cooper PR. Cervical laminoplasty: a critical review. J Neurosurg 2003; 98(3 Suppl):230–238. 17. Sakai Y, et al. Postoperative instability after laminoplasty for cervical myelopathy with spondylolisthesis. J Spinal Disord Tech 2005; 18(1):1–5. 18. Wang MY, Shah S, Green BA. Clinical outcomes following cervical laminoplasty for 204 patients with cervical spondylotic myelopathy. Surg Neurol 2004; 62(6):487–492; discussion 492–493. 19. Yabuki S, Kikuchi S. Endoscopic partial laminectomy for cervical myelopathy. J Neurosurg Spine 2005; 2(2):170–174. 20. Ota K, et al. [Outcome of cervical decompressive fenestration for elderly patients with cervical myelopathy without spinal canal stenosis]. Rinsho-seikeigeka 1997; 32:429–433. 21. Epstein NE, et al. Can airway complications following multilevel anterior cervical surgery be avoided? J Neurosurg 2001; 94(2 Suppl):185–188. 22. Terao Y, et al. Increased incidence of emergency airway management after combined anterior-posterior cervical spine surgery. J Neurosurg Anesthesiol 2004; 16(4): 282–286. 23. Emery SE, Smith MD, Bohlman HH. Upper-airway obstruction after multilevel cervical corpectomy for myelopathy. J Bone Joint Surg [Am] 1991; 73(4):544–551. 24. Chiba K, et al. Segmental motor paralysis after expansive open-door laminoplasty. Spine 2002; 27(19):2108–2115. 25. Dai L, et al. Radiculopathy after laminectomy for cervical compression myelopathy. J Bone Joint Surg [Br] 1998; 80(5):846–849. 26. Uematsu Y, Tokuhashi Y, Matsuzaki H. Radiculopathy after laminoplasty of the cervical spine. Spine 1998; 23(19):2057–2062. 27. Komagata M, et al. Prophylaxis of C5 palsy after cervical expansive laminoplasty by bilateral partial foraminotomy. Spine J 2004; 4(6):650–655. 28. Tsuzuki N, et al. Nerve root injury after cervical posterior decompression and pathological analysis of its pathogenesis. J Jpn Orthop Assoc 1987; 61:S652.

1. Teresi LM, et al. Asymptomatic degenerative disc disease and spondylosis of the cervical spine: MR imaging. Radiology 1987; 164(1):83–88.

29. Seichi A, et al. Postoperative expansion of intramedullary high-intensity areas on T2-weighted magnetic resonance imaging after cervical laminoplasty. Spine 2004; 29(13):1478–1482; discussion 1482.

2. Benzel EC, et al. Cervical laminectomy and dentate ligament section for cervical spondylotic myelopathy. J Spinal Disord 1991; 4(3):286–295.

30. Fessler RG, Steck JC, Giovanini MA. Anterior cervical corpectomy for cervical spondylotic myelopathy. Neurosurgery 1998; 43(2):257–265; discussion 265–267.

3. Smith MD, et al. Postoperative cerebrospinal-fluid fistula associated with erosion of the dura. Findings after anterior resection of ossification of the posterior longitudinal ligament in the cervical spine. J Bone Joint Surg [Am] 1992; 74(2): 270–277.

31. Matsunaga S, et al. Dissociated motor loss in the upper extremities. Clinical features and pathophysiology. Spine 1993; 18(14):1964–1967.

4. Epstein NE. Identification of ossification of the posterior longitudinal ligament extending through the dura on preoperative computed tomographic examinations of the cervical spine. Spine 2001; 26(2):182–186. 5. Koc RK, et al. Cervical spondylotic myelopathy and radiculopathy treated by oblique corpectomies without fusion. Neurosurg Rev 2004; 27(4):252–258. 6. George B, Gauthier N, Lot G. Multisegmental cervical spondylotic myelopathy and radiculopathy treated by multilevel oblique corpectomies without fusion. Neurosurgery,1999; 44(1):81–90. 7. Sevki K, et al. Results of surgical treatment for degenerative cervical myelopathy: anterior cervical corpectomy and stabilization. Spine 2004; 29(22):2493–2500. 8. Yonenobu K, et al. Laminoplasty versus subtotal corpectomy. A comparative study of results in multisegmental cervical spondylotic myelopathy. Spine 1992; 17(11):1281–1284. 9. Kanayama M, et al. The effects of rigid spinal instrumentation and solid bony fusion on spinal kinematics. A posterolateral spinal arthrodesis model. Spine 1998; 23(7):767–773.

32. Macdonald RL, et al. Multilevel anterior cervical corpectomy and fibular allograft fusion for cervical myelopathy. J Neurosurg 1997; 86(6):990–997. 33. Saunders RL. On the pathogenesis of the radiculopathy complicating multilevel corpectomy. Neurosurgery 1995; 37(3):408–412; discussion 412–413. 34. Wada E, et al. Subtotal corpectomy versus laminoplasty for multilevel cervical spondylotic myelopathy: a long-term follow-up study over 10 years. Spine 2001; 26(13):1443–1447; discussion 1448. 35. Epstein NE. The surgical management of ossification of the posterior longitudinal ligament in 43 North Americans. Spine 1994; 19(6):664–672. 36. Payne EE, Spillane JD. The cervical spine; an anatomico-pathological study of 70 specimens (using a special technique) with particular reference to the problem of cervical spondylosis. Brain 1957; 80(4):571–596. 37. Zdeblick TA, Ducker TB. The use of freeze-dried allograft bone for anterior cervical fusions. Spine 1991; 16(7):726–729. 38. Rajshekhar V, Arunkumar MJ, Kumar SS. Changes in cervical spine curvature after uninstrumented one- and two-level corpectomy in patients with spondylotic myelopathy. Neurosurgery 2003; 52:799–805.

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Part 3: Specific Disorders 39. Vaccaro AR, et al. Early failure of long segment anterior cervical plate fixation. J Spinal Disord 1998; 11(5):410–415. 40. Epstein NE. Evaluation and treatment of clinical instability associated with pseudoarthrosis after anterior cervical surgery for ossification of the posterior longitudinal ligament. Surg Neurol 1998; 49(3):246–252. 41. Herkowitz H.N. A comparison of anterior cervical fusion, cervical laminectomy, and cervical laminoplasty for the surgical management of multiple level spondylotic radiculopathy. Spine 1988; 13(7):774–780.

68. Nannapaneni R, Behari S, Todd NV. Surgical outcome in rheumatoid Ranawat Class IIIb myelopathy. Neurosurgery 2005; 56(4):706–715; discussion 716. 69. Mori T, et al. 3- to 11-year followup of occipitocervical fusion for rheumatoid arthritis. Clin Orthop Relat Res 1998; (351):169–179.

42. Yonenobu K. et al. Choice of surgical treatment for multisegmental cervical spondylotic myelopathy. Spine 1985; 10(8):710–716.

70. Matsunaga S, Ijiri K, Koga H. Results of a longer than 10-year follow-up of patients with rheumatoid arthritis treated by occipitocervical fusion. Spine 2000; 25(14):1749–1753.

43. Iwasaki M, et al. Expansive laminoplasty for cervical radiculomyelopathy due to soft disc herniation. Spine 1996; 21(1):32–38.

71. Casey AT, et al. Surgery on the rheumatoid cervical spine for the non-ambulant myelopathic patient – too much, too late? Lancet 1996; 347(9007):1004–1007.

44. Yoshida M, et al. Indication and clinical results of laminoplasty for cervical myelopathy caused by disc herniation with developmental canal stenosis. Spine 1998; 23(22):2391–2397.

72. Sunahara N, et al. Clinical course of conservatively managed rheumatoid arthritis patients with myelopathy. Spine 1997; 22(22):2603–2607; discussion 2608.

45. Ogawa Y, et al. Long-term results of expansive open-door laminoplasty for ossification of the posterior longitudinal ligament of the cervical spine. J Neurosurg Spine 2004; 1(2):168–174. 46. Heller JG, et al. Laminoplasty versus laminectomy and fusion for multilevel cervical myelopathy: an independent matched cohort analysis. Spine 2001; 26(12): 1330–1336. 47. Edwards CC 2nd, Heller JG, Murakami H.Corpectomy versus laminoplasty for multilevel cervical myelopathy: an independent matched-cohort analysis. Spine 2002; 27(11):1168–175. 48. Itoh T, Tsuji H. Technical improvements and results of laminoplasty for compressive myelopathy in the cervical spine. Spine 1985; 10(8):729–736. 49. Sakaura, H, et al. Long-term outcome of laminoplasty for cervical myelopathy due to disc herniation: a comparative study of laminoplasty and anterior spinal fusion. Spine 2005; 30(7):756–759.

73. Bucciero A, et al. MR signal enhancement in cervical spondylotic myelopathy. Correlation with surgical results in 35 cases. J Neurosurg Sci 1993; 37(4): 217–222. 74. Okada Y, et al. Magnetic resonance imaging study on the results of surgery for cervical compression myelopathy. Spine 1993; 18(14):2024–2029. 75. Chen CJ, et al. Intramedullary high signal intensity on T2-weighted MR images in cervical spondylotic myelopathy: prediction of prognosis with type of intensity. Radiology 2001; 221(3):789–794. 76. Wada E, et al. Can intramedullary signal change on magnetic resonance imaging predict surgical outcome in cervical spondylotic myelopathy? Spine 1999; 24(5):455–461; discussion 462. 77. Shinomiya K, Mutoh N, Furuya K. Study of experimental cervical spondylotic myelopathy. Spine 1992; 17(10 Suppl):S383–S387. 78. Bohlman HH, Emery SE. The pathophysiology of cervical spondylosis and myelopathy. Spine 1988; 13(7):843–846.

50. Hilibrand AS, et al. Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. J Bone Joint Surg [Am] 1999; 81(4):519–528.

79. Hansen-Schwartz J, Kruse-Larsen C, Nielsen CJ. Follow-up after cervical laminectomy, with special reference to instability and deformity. Br J Neurosurg 2003; 17:301–305.

51. Ghiselli G, et al. Adjacent segment degeneration in the lumbar spine. J Bone Joint Surg [Am] 2004; 86(7):1497–1503.

80. Kumar VG, et al. Cervical spondylotic myelopathy: functional and radiographic long-term outcome after laminectomy and posterior fusion. Neurosurgery 1999; 44:771–777.

52. Hunter LY, Braunstein EM, Bailey RW. Radiographic changes following anterior cervical fusion. Spine 1980; 5(5):399–401. 53. Hirabayashi, H, Bohlman HH. Multilevel cervical spondylosis. Spine 1995; 20: 1732–1734. 54. Kawakami M, et al. A comparative study of surgical approaches for cervical compressive myelopathy. Clin Orthop Relat Res 2000; (381):129–136. 55. Yonenobu K, et al. Laminoplasty versus subtotal corpectomy. Spine 1992; 17: 1281–1284. 56. Phillips DG. Surgical treatment of myelopathy with cervical spondylosis. J Neurol Neurosurg Psychiatry 1973; 36:879–884. 57. Ebersold MJ, Pare MC, Quast LM. Surgical treatment for cervical spondylitic myelopathy. J Neurosurg 1995; 82(5):745–751. 58. Latimer M, et al. Measurement of outcome in patients with cervical spondylotic myelopathy treated surgically. Br J Neurosurg 2002; 16(6):545–549. 59. Kadanka Z, et al. Predictive factors for spondylotic cervical myelopathy treated conservatively or surgically. Eur J Neurol 2005; 12(1):55–63. 60. Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain 1972; 95(1):87–100. 61. Kohno K, et al. Evaluation of prognostic factors following expansive laminoplasty for cervical spinal stenotic myelopathy. Surg Neurol 1997; 48(3):237–245. 62. Fujiwara K, et al. The prognosis of surgery for cervical compression myelopathy. An analysis of the factors involved. J Bone Joint Surg [Br] 1989; 71(3):393–398. 63. Koyanagi T, et al. Predictability of operative results of cervical compression myelopathy based on preoperative computed tomographic myelography. Spine 1993; 18(14):1958–1963. 64. Irvine GB, Strachan WE. The long-term results of localised anterior cervical decompression and fusion in spondylotic myelopathy. Paraplegia 1987; 25(1):18–22. 65. Hamburger C, Buttner A, Uhl E. The cross-sectional area of the cervical spinal canal in patients with cervical spondylotic myelopathy. Correlation of preoperative and postoperative area with clinical symptoms. Spine 1997; 22(17):1990–1994; discussion 1995. 66. Lesoin F, et al. Results of surgical treatment of radiculomyelopathy caused by cervical arthrosis based on 1000 operations. Surg Neurol 1985; 23(4):350–355.

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67. Casey AT, et al. Predictors of outcome in the quadriparetic nonambulatory myelopathic patient with rheumatoid arthritis: a prospective study of 55 surgically treated Ranawat class IIIb patients. J Neurosurg 1996; 85(4):574–581.

81. Mikawa Y, Shikata J, Yamamuro T. Spinal deformity and instability after multilevel cervical laminectomy. Spine 1987; 12:6–11. 82. Herman JM, Sonntag VK. Cervical corpectomy and plate fixation for postlaminectomy kyphosis. J Neurosurg 1994; 80:963–970. 83. Seichi A, et al. Long-term results of double-door laminoplasty for cervical stenotic myelopathy. Spine 2001; 26(5):479–87. 84. Suda Y, et al. Cervical laminoplasty for subaxial lesion in rheumatoid arthritis. J Spinal Disord Tech 2004; 17(2):94–101. 85. McAfee PC, Regan JJ, Bohlman HH. Cervical cord compression from ossification of the posterior longitudinal ligament in non-Orientals. J Bone Joint Surg [Br] 1987; 69(4):569–575. 86. Kojima T, et al. Anterior cervical vertebrectomy and interbody fusion for multi-level spondylosis and ossification of the posterior longitudinal ligament. Neurosurgery 1989; 24(6):864–872. 87. Abe H, et al. Anterior decompression for ossification of the posterior longitudinal ligament of the cervical spine. J Neurosurg 1981; 55(1):108–116. 88. Harsh GR, et al. Cervical spine stenosis secondary to ossification of the posterior longitudinal ligament. J Neurosurg 1987; 67(3):349–357. 89. Onari K, et al. Long-term follow-up results of anterior interbody fusion applied for cervical myelopathy due to ossification of the posterior longitudinal ligament. Spine 2001; 26(5):488–493. 90. Tomita K, et al. Expansive midline T-saw laminoplasty (modified spinous processsplitting) for the management of cervical myelopathy. Spine 1998; 23(1):32–37. 91. Matsuoka T, et al. Long-term results of the anterior floating method for cervical myelopathy caused by ossification of the posterior longitudinal ligament. Spine 2001; 26(3):241–248. 92. Belanger TA, et al. Ossification of the posterior longitudinal ligament. Results of anterior cervical decompression and arthrodesis in sixty-one North American patients. J Bone Joint Surg [Am] 2005; 87(3):610–615. 93. Haro H, et al. Surgical treatment of cervical spondylotic myelopathy associated with athetoid cerebral palsy. J Orthop Sci 2002; 7:629–636.

PART 3

SPECIFIC DISORDERS

Section 4

Biomechanical Disorders of the Thoracic Spine

CHAPTER

Developmental and Functional Anatomy of the Thoracic Spine

71

Venu Akuthota and John Tobey

The thoracic spine has long been treated as the ugly stepsister of the cervical and lumbar spine. It has received little research or review, mostly because thoracic spinal pain syndromes are relatively uncommon or underdiagnosed. The thoracic spine covers more segments than the cervical and lumbar spine, thus making exhaustive research difficult. In addition, the backdrop of rib articulations to the 12 thoracic spinal segments provides inherent stability to this region. Thus, the thoracic spine pain generators are not as susceptible to mechanical forces. Guidelines for the treatment of thoracic spinal pain are nonexistent and are ripe for research.1 However, to develop reasonable guidelines in a field of spine medicine without much research, a thorough understanding of the anatomy and biomechanics of the thoracic spine is needed.

DEVELOPMENTAL ANATOMY Neuralization

with Scheurmann disease such that disc material herniates through the insulted vertebral endplate. Two other posterior primary ossification centers come together to form the neural arch. Rarely, particularly in the setting of poor folate intake, neural arch and tube defects (e.g. spina bifida and hemivertebrae) may arise.

Myotome Myotome cells that migrate toward the posterior aspect, between the developing skin and neural tube, are called epimeres. They transform into the deep muscles of the spine and are all innervated by the dorsal rami of the spinal nerves. These deep muscles include the erector spinae, transversospinalis muscles, and splenius muscles. Myotome cells that migrate ventrally and laterally are referred to as hypomeres. These transform into muscles, such as the intercostals, abdominals, and periscapular muscles, and are innervated by the ventral rami of the spinal nerves.

Neural tube development begins with the formation of the notochord around day 20 of embryogenesis. The neural tube will eventually develop into the spinal cord and brain. The surrounding mesoderm condenses to form somites.2 Somite differentiation in the early part of fetal development separates cells into the dermatome, myotome, and sclerotome cells (Fig. 71.1).

Neural tube

Sclerotome

Postural curves

The vertebrae and associated ligaments are formed by the development of sclerotome cells into a segmental centrum which forms cartilage and then the bony vertebral body.2 Primary and secondary ossification centers provide growth areas to turn cartilage into bone. The secondary ossification centers in the annular epiphysis (apophyseal rings) remain open through adolescence. Scheurmann disease or kyphosis may be caused by an insult to these secondary ossification centers. Eventually, Schmorl’s nodes can develop in these individuals

Sclerotome

The inferior portion of the neural tube differentiates into ependymal (central), mantle (neurons and glia), and marginal layers (axons of tract cells).2 These eventually form the future spinal cord. The neural crest develops into neurons of the peripheral nervous system.

Developmentally, the in utero spine is flexed so that the fetal position is achieved. However, with age and weight bearing, the primary curve of the spine gives way to secondary curves in the cervical and lumbar spine (i.e. lordosis). The thoracic spine remains with the primary curve and, thus, in kyphosis.3 Normal thoracic kyphosis allows for the anterior height of the thoracic vertebral body to be 1.5–2 cm shorter than the posterior height.3 Scoliosis is common in the thoracic spine region. Some have theorized that idiopathic scoliosis may be partly an embryogenesis problem with inadequate development of the junction between the centrum and the neural arch (i.e. neurocentral synchondrosis).

NEURAL ANATOMY

Neural tube

Thoracic spine pain generators

Dermatome

Notochord Aorta

Myotome Yolk sac cavity

Fig. 71.1 Somite differentiation into the dermatome, myotome, and sclerotome cells.2

There have been no comprehensive studies on the innervation schemes of the thoracic spine other than some published descriptions of the dorsal rami of the thoracic spine.4 Innervation schemes must be understood so that pain generators of the thoracic spine can be precisely identified. To date, the thoracic zygapophyseal joints, intervertebral disc, costovertebral joints, and posterior thoracic muscles have been proven to have nerve supply.4 However, other thoracic structures are also likely to be sources of pain (e.g. costotransverse joint, vertebral body) (Table 71.1) In addition, the thoracic spine 767

Part 3: Specific Disorders

Table 71.1: Thoracic Spine Pain Generators Thoracic zygapophyseal joints Thoracic intervertebral disc Costovertebral joints (e.g. synovitis from ankylosing spondylitis) Posterior thoracic muscles (e.g. trigger points) Costotransverse joint

Thoracic spinal cord and its primary divisions

Vertebral body (e.g. compression fractures)

Spinal cord

Dura mater

The spinal cord is housed within the thoracic vertebral canal, which has a relatively small diameter when compared to the cervical and lumbar canal (Fig. 71.2). The lower thoracic vertebral canal and spinal cord are wider to allow for the lumbar segment of the spinal cord. In addition, the vertebral column grows at a faster rate than the spinal cord. Consequently, the newborn spinal cord ends by the L3 vertebral, whereas the adult spinal cord ends between T12 and L2 vertebral bodies.2 Overall, the thoracic spinal cord is smaller in size and has less gray matter relative to the cervical and lumbar spinal cord. There is less relative room in the thoracic vertebral canal and sparse cord vascular supply; thus, the thoracic spinal cord is a precarious area for injury. For those reasons, posterior thoracic decompression (particularly laminectomies) carries a greater relative risk of neural injury.8 In addition, the thoracic spinal cord has an enlargement of the lateral horn due to the incorporation of cell bodies of the preganglionic fibers of the sympathetic nervous system. The spinal cord receives its vascular supply via the anterior spinal artery (ventral two-thirds of the cord) and a pair of posterior spinal arteries (dorsal one-third of the cord). The anterior spinal artery in the thoracic spine is feed by 4–5 radicular arteries. The largest of these radicular arteries is the great radicular artery of Adamkiewicz, which usually courses with a lower thoracic root or upper lumbar root (see Fig. 71.2). It will give vascular supply to the lumbosacral spinal cord segments. The anatomic course and supply of this great radicular artery has become clinically important for spinal injectionists. Inadvertent injection of particulate matter (steroid) into the greater radicular artery while performing a thoracolumbar transforaminal epidural steroid injection may cause paraplegia.9 Other invasive procedures such as lumbar sympathectomy and aortic surgery, or a dissecting aneurysm, may also interrupt supply to the greater radicular artery.2 In addition, the venous plexus about the thoracic spine has been implicated with metastatic cancer. In fact, the thoracic region is the most common location for metastatic spinal spread of many cancers.10

Epidural blood vessels Posterior longitudinal ligament Sympathetic trunk

houses much of the autonomic nervous system of the human body, a well-known modulator of pain syndromes. Ligaments about the thoracic spine, such as the interspinous ligament and posterior longitudinal ligament, may also cause thoracic spine pain.5

Types of thoracic pain Thoracic spine pain conditions can be differentiated by the classifying pain into superficial and deep pain (Table 71.2).6 Superficial pain is sharp pain that is fairly localized and occurs from irritation of the skin or mucosa. The so-called first pain is modulated by the A-delta fibers, followed by second pain modulated by C-fibers. Deep somatic pain may occur from irritation of structures such as periosteum, ligaments, joints, tendons, fascia, and muscles (in order of lower to higher pain threshold). Somatic structures have been shown, by Kellgren’s classic studies, to refer pain distal to the site of irritation.5 On the other hand, radicular pain is fairly precise, shooting, neuropathic pain that is along a two-inch band.7 Many cases of thoracic somatic referred pain are misdiagnosed as thoracic radicular pain. It must be remembered that thoracic disc herniations as causes of thoracic radicular pain are rare. Thoracic somatic referred pain is much more common than thoracic radicular pain. Visceral pain is also a distinct pain classification often presenting as pain in the thoracic or abdominal region. Unless the parietal pleura or viscera is involved, visceral pain is poorly localized. Notably,

Table 71.2: Types of Pain: Somatic vs. Autonomic Nervous System Superficial cutaneous pain Somatic pain Somatic localized pain Somatic referred pain Radicular pain Visceral pain True or localized visceral pain Visceral referred pain Localized parietal pain Referred parietal pain

768

diaphragmatic pain may commonly present as neck pain due to its cervical innervation and embryogenesis. Commonly, kidney disorders will present with pain along the thoracic costovertebral angle. Pancreatic and gallbladder problems can cause dissecting sharp pain into the thoracic spine region. As well, dissecting aortic aneurysms often refer to the interscapular region. All individuals with thoracic spine pain must have visceral sources of pain ruled out.

Branches of the thoracic spinal cord The thoracic spinal cord provides the afferent and efferent contributions to the thoracic dorsal and ventral rootlets, respectively (Fig. 71.3). The rootlets come together to form ventral and dorsal roots. Within the intervertebral foramen, the roots form the short spinal nerve. As the spinal nerve exits the foramen, it enters the thoracic paravertebral space. Within this space, various branches are formed. The large anterior (ventral rami) and posterior (dorsal rami) primary divisions are created and housed within this space. Just before dividing into the rami, the sinuvertebral nerve is formed and returns medially through the intervertebral foramen. Also before the primary divisions are formed, the white and gray rami communicantes branches to the sympathetic trunk (Fig. 71.4). A thoracic paravertebral block will anesthetize all of the above branches.11 The thick anterior primary division is referred to as the ventral rami as well as the segmental nerve. The first 11 thoracic segmental

Section 4: Biomechanical Disorders of the Thoracic Spine

Basilar artery

Brain stem

Vertebral artery

C-1

1

1

2

2

2

Anterior spinal artery

Ventral horn

3

3

4

3

4

5

4

5

6

Dorsal intermediate sulcus

5

7

6 7

6

8

8 T-1

Anterior radicular artery

C

2 3

1

7

2

1

3

2

4

3

T C6 cord segment

5

4

4 6

5 6

8

6

7

9

7

8

10

12

10

Anterior radicular artery

T6 cord segment

9

1

10

2

11

11

3

Ventral horn

4

12 Posterior intercostal artery

8

11

9 Great radicular artery (artery of Adamkiewicz)

Lateral horn

5 7

12

5 1

L-1 3 4 5

2

1

L L4 cord segment

2

Lumbar artery

3 3

4 4

5

5

Lateral artery S-1

2 3 4 5

Coccygeal nerve Filum terminale Fig. 71.2 Posterior view of the spinal cord.

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Part 3: Specific Disorders Medial and lateral branches of posterior primary division

Medial and lateral branches of posterior primary division

Posterior intercostal membrane Subcostal muscles Lateral cutaneous branch

Posterior primary division

Posterior subdivision

Anterior primary division

Anterior primary division Anterior subdivision Collateral branches of intercostal nerve and vessels

Sympathetic ganglion

Pleura Intercostal externus muscle

Intercostal nerve

Intercostal internus muscle

Anterior intercostal membrane

Intercostal intimus muscle

Anterior cutaneous branch

C Costal cartilage Anterior cutaneous branch Lung Pleural cavity Visceral pleura Parietal pleura

A

Serratus anterior muscle

Intercostalis externus muscle Intercostal vein Intercostal artery Intercostal nerve Collateral branches of intercostal nerve and vessels

Intercostalis internus muscle Intercostalis intimus muscle Skin Superficial fascia

B Endothoracic fascia

Fig. 71.3 The nerves of the thoracic spine.

nerves are named the intercostal nerves while the twelfth segmental nerve is named the subcostal nerve. Notably, the anterior primary division of T1 contributes to the brachial plexus. The second and third intercostal nerves also form the intercostobrachial nerve, which provides cutaneous innervation to the axilla and upper medial arm. The intercostobrachial nerve may be injured during axillary surgery and dissection. Thoracotomy incisions may famously cause injury to other levels of intercostal nerves. In fact, up to 61% of individuals may have a degree of post-thoracotomy pain one year after surgery.12

Thoracic posterior primary division (dorsal rami) and its medial branches The posterior primary rami (dorsal rami) further divides into the medial and lateral branches. The posterior primary rami also provide cutaneous innervation to the skin overlying the spinous process, the paravertebral musculature, and the thoracic facet joints. Beginning at the T4 posterior primary rami, each division will travel further and further caudally to provide cutaneous innervation (Fig. 71.5).6 770

The thoracic dorsal rami are formed within 5 mm of the lateral intervertebral foramen. The thoracic transverse process acts as a good landmark for the medial branches of the thoracic dorsal rami. However, it must be remembered that the transverse process of the thoracic spine is a true process, whereas the transverse process of the lumbar spine is actually a costal remnant.13 Thus, the anatomical scheme of the thoracic medial branches will vary slightly as compared to the lumbar medial branches. The opening where the thoracic dorsal rami exits is also referred to as the costotransverse foramen of Cruveilhier.2 The superior border is the transverse process; the medial border is the thoracic facet joint; the inferior border is the inferior rib; and the lateral border is the superior costotransverse ligament. The thoracic medial branches pass within the intertransverse space, i.e. the interval between consecutive transverse processes (Fig. 71.6).13 Depending on the thoracic level, the medial branches pass at different mediolateral points within the intertransverse space.14 After crossing the transverse process, the medial branch will head medially and inferiorly. It will then serve to innervate the zygapophyseal joint at the level of its spinal nerve

Section 4: Biomechanical Disorders of the Thoracic Spine Sympathetic trunk T5

C2 White ramus communicans

3 4 5

T6

T1 2 3

C8

T1 T2

4 Gray ramus communicans

5 6

Sphlanchnic nerve

7

Prevertebral ganglion

9

The thoracic sinuvertebral nerve (SVN or recurrent meningeal nerve) is similar in origin to the lumbar and cervical sinuvertebral nerves. They arise from both a somatic and autonomic root. The origin of the SVN actually begins outside of the neural foramen, and then it proceeds back through the foramen to form its terminal branches (see Fig. 71.3). Contributions of segmental spinal nerve (somatic root) and gray rami communicantes/sympathetic trunk (multiple autonomic roots) to the SVN explain the vast referral pattern of thoracic disc pain. The SVN provides nerve supply to the following: the posterior longitudinal ligament, dural sac, anterior surface of vertebral lamina, and posterior aspect of the vertebral body.4 The thoracic SVN presumably innervates the outer annulus of thoracic discs; however, this is extrapolated from dissection studies of the lumbar spine.4 The

T6 T7

10

Thoracic sinuvertebral nerves

T5

8

Fig. 71.4 The sympathetic trunk and its relation to the thoracic spinal cord.

and the joint below. At T1–3 and T9–10, the medial branches cross the superior and lateral aspect of the transverse process. At T4–8, the medial branches may be suspended within the intertransverse space. At T11– 12, the medial branch has a course akin to the lumbar medial branches such that they pass at the medial aspect of the transverse process, at the root of the superior articular process (Table 71.3). Thoracic medial branch blocks can be performed for the treatment and diagnosis of thoracic facet-mediated spinal pain. The target site for these blocks, based on the above described anatomy, is typically at the superolateral aspect of the thoracic transverse process.14 These blocks are technically easier to perform than thoracic facet intra-articular injections; thus, the medial branch anatomy needs to be well understood. The lateral branches provide innervation to erector spinae muscles and midline skin. Beginning at the T4 posterior primary rami, each division will travel further and further caudally to provide cutaneous innervation.6 The lateral branches may descend up to 4 ribs before providing cutaneous innervation superficial to the spinous process.

T3 T4

T8

11 12 L1 2 3

T9 T10 T12

T11

S1 2

L2

L1

3 S3

A

L3 S1 S2 B

Fig. 71.5 Caudal migration of the thoracic posterior primary rami; innervation of the midline.

thoracic intervertebral disc will be innervated multisegmentally and bilaterally, further explaining its vast referral pattern.

Thoracic sympathetic trunk The autonomic nerve system has an enormous role in the modulation of pain, particularly visceral pain. The thoracic spine houses nearly the entire peripheral sympathetic nervous system. The anatomy of the sympathetic and parasympathetic nerves needs to be wholly understood by pain medicine practioners. The sympathetic division of the autonomic nervous system is also termed the thoracolumbar division because the cell bodies of the preganglionic fibers are typically 771

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Rib

Transverse process

Thoracic facet joint Medial branch of the thoracic dorsal rami

Lateral branch of the thoracic dorsal rami

Fig. 71.6 Anatomy of the thoracic dorsal rami’s medial branches.

Table 71.3: Target Sites for Blocking Thoracic Medial Branches Thoracic Level

MB Description

Target Site

‘Suspended medial branch’

Intertransverse space

T1–3 T4–8

Superolateral TP

T9–10 T11–12

Superolateral TP ‘Lumbar-like’

Junction of the SAP and TP

TP, transverse process; SAP, superior articular process.

housed from T1 to L2 inclusive. These cell bodies are located in the intermediolateral column of the spinal cord (i.e. lateral horn). The preganglionic fibers are incorporated within the anterior root and traverse through the white rami communicantes. The preganglionic fibers end or synapse in the paravertebral sympathetic trunks. Some preganglionic fibers may ascend or descend two levels before synapsing in the sympathetic trunks. Postganglionic fibers have cell bodies in the sympathetic trunks and may pass through the somatic nerves (traversing through the gray rami communicantes) or the visceral nerves. The sympathetic trunk in the thoracic spine lies more posterior.13 In fact, the trunk sits just anterior to the ribs, in close proximity to the pleura and segmental nerve (thoracic ventral rami). Thus, sympathetic nerve blocks are inherently more risky than in the lumbar spine. The thoracic sympathetic trunks form intermittent ganglia at each thoracic vertebral level. The first thoracic ganglion typically fuses with the lower cervical ganglia to form the stellate ganglion. In addition, the first thoracic ganglion is the sole location for the preganglionic sympathetic fibers of the head and neck. Interruption to these fibers will result in Horner’s syndrome (ptosis, miosis, and anhidrosis).6 The upper 4–5 thoracic ganglia form visceral and vascular branches to the thoracic viscera and aorta, respectively. The lower 6–7 thoracic sympathetic ganglia form the splanchnic nerves: the greater, lesser, and least splanchnic nerves. Some of the fibers of the greater splanchnic nerve terminate within the celiac ganglia while some fibers traverse to the medulla of the adrenal gland. The lesser splanchnic nerve terminates in the aorticorenal ganglion and the least splanchnic nerve terminates in the renal ganglion. If spinal cord injury is present above the midthoracic spine, a condition termed autonomic dysreflexia may result from unopposed sympathetic splanchnic outflow after noxious stimulation.

BONE AND JOINT ANATOMY Surface anatomy: bony landmarks The T1 spinous process is easily palpated by identifying the relatively mobile C7 spinous process on top of it. The spine of the scapula is usually located at the level of the T3 spinous process (Fig. 71.7). The

Upper trapezius

Deltoid

T3

Supraspinatus T7

Infraspinatus

Rhomboid Latissimi dorsi

Fig. 71.7 Surface anatomy. 772

Section 4: Biomechanical Disorders of the Thoracic Spine

inferior angle of the scapula corresponds to the level of T6 spinous process in the prone position and T7 in the standing position. The apex of the thoracic kyphosis is usually located at the level from T4 to T6.2

Vertebral column The thoracic bony architecture provides for a stable and compact portion of the vertebral column (Fig. 71.8). Posteriorly, the thoracic laminae are arranged like overlapping shingles on a roof. Anteriorly, each of the 12 thoracic vertebral bodies is cortical bone surrounding cancellous (trabecular) bone. The anterior height of the thoracic vertebral body is normally 1.5–2 cm shorter than the posterior height, creating the thoracic kyphosis.3 A loss of kyphosis, referred to as straight back syndrome, may be associated with a systolic heart murmur.15 The cancellous bone is particularly susceptible to osteoporosis. In particular, the mid and lower thoracic vertebral bodies are common locations of osteoporotic fractures. The attaching ligaments, such as the anterior longitudinal ligament and posterior longitudinal ligament, are arranged similarly to the rest of the spine. The pedicles are stout bones connecting the lamina to the vertebral bodies. Unlike the pedicles of the lumbar spine, which serve as beacons on lumbar anteroposterior (AP) and oblique radiography, the pedicles of the thoracic spine are not easily seen on radiography due to their projections in a posterior and cephalad manner. The thoracic transverse processes are also ‘formidable structures.’13 They serve as useful landmarks for thoracic spinal injections. The direction of the thoracic transverse process is in a cranial and marked posterior manner. They are more easily seen on radiography with a mild contralateral oblique projection.13

Thoracic intervertebral disc Provocation thoracic discography has shown that pain can emanate from the thoracic discs.16 The intervertebral disc is composed of two main structures. The outer component of the disc is the anulus fibrosus, made of concentric lamellae that encapsulate the gelatinous nucleus pulposis. Thoracic discs are thinner than their respective cervical and lumbar counterparts. They also have a greater tendency to calcify. Innervation of the thoracic intervertebral disc (IVD) may come from the sinuvertebral nerve or rami communicantes.17 Disruptions of the thoracic IVD are rare when compared to the lumbar and cervical spine. They account for 0.15–1 .8% of all disc herniations.2,18 Typically, thoracic disc herniations are noted in the mid and lower thoracic spine. Therefore, typical thoracic radicular pain radiates to the abdomen (Table 71.4). Because the thoracic spinal nerves exit at the level below the corresponding vertebral level, a T10–11 lateral disc herniation will affect the T10 spinal nerve. The rarity of thoracic radiculopathy may also be due to the fact that thoracic spinal nerves occupy less relative space (¹⁄¹²) in the intervertebral foramen when compared to the cervical (¹⁄5) and lumbar spine (¹⁄3).2

Thoracic zygapophyseal joints Several distinct synovial joints (discussed below) that exist within the thoracic spine are enveloped by thin capsules.6 The zygapophyseal joints (facet joints) are the major connections between the thoracic segments. Their joint lines lie mostly in the frontal plane to limit flexion and extension. With a normal X-ray of the thoracic spine, the superior and inferior articular processes are indistinguishable.13 They form a wide articular pillar that is located lateral to the vertebral body. Specifically, the lateral aspect of the thoracic facet joint is slightly anterior, and the medial aspect is slightly posterior.19 The

Superior costal facet

Superior articular process

Body

Transverse costal facet

Costocorporeal articulation

Costotransverse articulation

Spinous process Inferior costal facet Rib Inferior articular process A

Spinous process

Posterior longitudinal ligament Costotransverse joint

Lamina

Lateral costotransverse ligament

Articular cartilage

Transverse process

Costotransverse ligament Joint of head of rib Articular capsule

Superior costal facet

Radiate ligament B

Anterior longitudinal ligament

Lateral costotransverse ligament Intertransverse ligament

Radiate ligament of head of rib Intervertebral disc

Cut edge of intraarticular ligament

Superior costotransverse ligament

Rib

C Fig. 71.8 Costovertebral and costotransverse joints.

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Table 71.4: Landmarks of Thoracic Dermatomes T6

Xiphoid

T8

Lower rib cage

T10

Umbilicus

T12

Inguinal line

anterior aspect of the thoracic facet joint is formed by the ligamentum flavum. The posterior aspect of the capsule must be penetrated for an intra-articular injection of the thoracic facet joint. Clinically, the thoracic facet joints have been proven to be sources of pain. Dreyfuss et al. demonstrated that the referral zone for the thoracic facet joints is localized to no more than 2.5 segments inferior to the provoked joint.19 As well, the lower thoracic facet joints have been theorized to refer to the lumbar spine, iliac crest, and buttock (i.e. Maigne’s syndrome).20

Costovertebral and costotransverse joints The costovertebral (CV) joints have been implicated as pain generators in individuals with ankylosing spondylitis and osteoarthritis, yet CV joint pain is extremely rare (see Fig. 71.8).17,21 They are innervated by the sympathetic trunks which lie just anterior to the CV joints.22 Often, they are pictured as a circular shadow in the lateral aspect of the superior vertebral endplate.13 This shadow should not be confused for the thoracic pedicle. The CV joint may have two articulations to the vertebral body yet only one synovial capsule.6 The radiate ligament serves to further secure CV rib articulation to the thoracic spine. Degenerative osteoarthritis is most commonly found in the T1, T6–8, and T11–12 levels but is typically asymptomatic.17 CV pain in patients with ankylosing spondylitis is typically found in individuals who also have other spondyloarthritic features such as sacroiliitis.4 The costotransverse (CT) joints are potential sources of pain that are not easily diagnosed by clinical examination. They have yet to be confirmed as pain generators in any published literature.14 They are absent at T1, T11, and T12 levels. They are innervated by the lateral branches of the thoracic dorsal rami.17 A debate exists whether a single lateral branch or up to three innervate a single CT joint.14

MUSCLE AND FASCIA ANATOMY Surface anatomy The trapezius, latissimus dorsi, and periscapular muscles encompass the superficial muscles of the thoracic spine region (see Fig. 71.7). The trapezius is a diamond-shaped muscle innervated by the accessory nerve. It works as a force couple to provide various scapular triplanar motions. The latissimus dorsi originates from the thoracolumbar fascia and inserts onto the humerus. It is often described as the swimmer’s muscle as it provides for shoulder extension and internal rotation. The other periscapular muscles include the serratus anterior and posterior, rhomboids, levator scapulae, and rotator cuff musculature. All of these muscles are derived from embryogenic hypomeres and thus are innervated by ventral rami. At the lower, lateral portion of the posterior trunk, the quadratus lumborum sits as a quadrangular-shaped muscle that has direct insertions to the thoracic and lumbar spine. McGill states the quadratus lumborum is a major stabilizer of the spine, typically working isometrically.23 774

The thoracolumbar fascia and its muscular attachments The thoracolumbar fascia acts as ‘nature’s back belt.’ It works as a retinacular strap of muscles of the thoracic and lumbar spine. The thoracolumbar fascia consists of three layers: the anterior, middle, and posterior layers. Of these layers, the posterior layer has the most important role in supporting the spine and abdominal musculature. The posterior layer consists of two laminae: a superficial lamina with fibers passing downward and medially and a deep lamina with fibers passing downward and laterally. The transversus abdominis has large attachments to the middle and posterior layers of the thoracolumbar fascia.24 The transversus abdominis fibers run horizontally around the abdomen, allowing for hoop-like stresses with contraction. The internal oblique also has similar fiber orientation to the transversus abdominis, yet receives much less attention with regard to its creation of hoop stresses. Together, the internal oblique, external oblique, and transversus abdominis increase the intra-abdominal pressure from the hoop created via the thoracolumbar fascia, thus imparting functional stability of the thoracolumbar spine. In essence, the thoracolumbar fascia provides a link between the lower limb and the upper limb.25 With contraction of the muscular contents, the thoracolumbar fascia acts as an activated proprioceptor, like a back belt providing feedback in lifting activities.

Paraspinals All paraspinal musculature were originally segmental muscles. But, through the course of ontogenetic and phylogenetic development, the larger superficial muscles became muscle masses that extended the length of the spine.26 There are no paraspinal muscles that are purely confined to the thoracic spine, so a general discussion of all back musculature follows. For example, the splenius muscles originate from the spinous process of the upper thoracic spinous processes and extend into the cervical spine. They act mainly to rotate the head and neck. The paraspinal muscles also have the commonality of being derived from the embryogenic epimeres, and thus, they are all innervated by the dorsal rami. Division of these muscles is purely arbitrary as they work in concert. They act mainly to rotate the head and neck. For the sake of convenience, the paraspinals are further divided into two major groups: (1) the erector spinae (global) muscles and (2) and the transversospinalis (local) muscles. All muscles of the erector spinae have a common tendinous and fleshy origin from pelvis and spinous process of the thoracolumbar region.26 The erector spinae becomes three distinct subgroups of muscles. In the thoracic region, the lateral two subgroups become evident: longissimus system and iliocostalis (lateral) system (Fig. 71.9). These are actually primarily thoracic muscles that act on the lumbar via a long tendon that attaches to the pelvis. This long moment arm is ideal for lumbar spine extension and for creating posterior shear with lumbar flexion.23 Medial to these two systems of muscles lies the slender and poorly developed spinalis thoracis which is also considered an erector spinae muscle. Together the spinalis, longissimus, and iliocostalis form the erector spinae muscles (also termed the SLI muscles). Deep and medial to the erector spinae muscles lay the local transversospinalis muscles. These so-called local ‘fine-tuning’ muscles include the semispinalis, multifidi, rotators, and intertransversi muscles. They do not have a great moment arm and likely represent length transducers or position sensors of a spinal segment by way of their rich composition of muscle spindles. Of this transversospinalis group, the semispinalis crosses the most spine segments (from 5 to 8) while the multifidi pass the fewest segments (2–3 spinal levels).26 The multifidi are theorized to work as segmental stabilizers rather than being involved in gross spinal movement.7 They are well developed in the lumbar spine but

Section 4: Biomechanical Disorders of the Thoracic Spine

and sternum. Rotatory (transverse) motion is the dominant motion. Flexion and extension is limited to about 10 degrees of motion due to the orientation of the facet joints. The lower thoracic spine, without definitive articulations to the ribs and sternum, has the most freedom of movement. The lower thoracic segments, acting as a transition to the lumbar spine, have an increased ability to flex and extend.

SUMMARY

Longissimus thoracis

The thoracic spine has become spine medicine’s elusive frontier. With better understanding of its development and anatomy, perhaps the thoracic spine will move away from its ‘third rail’ position.

References 1. Bogduk N. Thoracic spinal pain: where do we stand. Paper presented at: International Spinal Injection Society 11th Annual Scientific Meeting, 2003; Orlando, Florida.

Iliocostalis lumborum

2. Cramer G, Darby S. Basic and clinical anatomy of the spine, spinal cord, and ANS. St. Louis: Mosby; 1995. 3. Levangie PK, Norkin CC. Joint structure and function. 3rd edn. Philadelphia: FA Davis; 2001. 4. Bogduk N. Innervation and pain patterns of the thoracic spine. In: Grant R, ed. Physical therapy of the cervical and thoracic spine. 3rd edn. New York: Churchill Livingstone; 2002:73–81.

Erector spinae aponeurosis

5. Kellgren J. On the distribution of pain arising from deep somatic structures with charts of segmental pain areas. Clin Sci 1939; 4:35–46. 6. Bonica J, Graney D. General considerations of pain in the chest. In: Loeser J, ed. Bonica’s management of pain. 3rd edn. Philadelphia: Lippincott Williams & Wilkins; 2001:1113–1148. 7. Bogduk N. Clinical anatomy of the lumbar spine and sacrum. 3rd edn. New York: Churchill Livingston; 1997.

Fig. 71.9 Erector spinae muscles of the thoracic spine (Adapted from Bogduk 9-11).

poorly developed in the thoracic spine. The rotatores, on the other hand, are more developed in the thoracic spine and less developed in the lumbar spine.2 The rotatores also have very short muscle fibers and extend 1–2 spinal levels. They act similarly to the multifidi.

8. Leventhal M. Fractures, disclocations, and fracture-dislocations of spine. In: Canale S, ed. Campbell’s operative orthopaedics. St. Louis: Mosby; 2003:1597–1690. 9. Houten JK, Errico TJ. Paraplegia after lumbosacral nerve root block: report of three cases. Spine J 2002; 2(1):70–75. 10. Aebi M. Spinal metastasis in the elderly. European Spine Journal 2003; 12:S202–203. 11. Karmakar MK. Thoracic paravertebral block. Anesthesiology 2001; 95(3):771–780. 12. Perttunen K, Tasmuth T, Kalso E. Chronic pain after thoracic surgery: a follow-up study. Acta Anaesthesiol Scand 1999; 43(5):563–567. 13. Sluijter M. Radiofrequency part 2: thoracic and cervical region, headache, and facial pain. Meggen, Switzerland: FlivoPress; 2003.

BIOMECHANICS Movement of the thoracic spine is minimal. The orientation of the thoracic facet joints in the frontal plane will dictate directions of movement freedom (Fig. 71.10). In general, the thoracic spine is free to move in the transverse plane and somewhat in the frontal plane. Side-bending (frontal plane) motion is prevented by the ribs

14. Chua WH, Bogduk N. The surgical anatomy of thoracic facet denervation. Acta Neurochirurgica 1995; 136(3–4):140–144. 15. Spapen HD, Reynaert H, Debeuckelaere S, et al. The straight back syndrome. Neth J Med 1990; 36(1-2):29–31. 16. Schellhas KP, Pollei SR, Dorwart RH. Thoracic discography. A safe and reliable technique. Spine 1994; 19(18):2103–2109. 17. Chua W. Thoracic spinal pain – a review. Austr Musculoskel Med 1996; 4:280–289. 18. Wood KB, Blair JM, Aepple DM, et al. The natural history of asymptomatic thoracic disc herniations. Spine 1997; 22(5):525–529. 19. Dreyfuss P, Tibiletti C, Dreyer SJ. Thoracic zygapophyseal joint pain patterns. A study in normal volunteers. Spine 1994; 19(7):807–811. 20. Akuthota V, Willick S, Harden R. The adult spine: a practical approach to low back pain. In: Rucker K, Cole A, Weinstein S, eds. Low back pain: a symptom-based approach to diagnosis and treatment. Woburn, MA: Butterworth-Heinemann; 2001:15–42.

20⬚ A

60⬚

B

Fig. 71.10 Orientation of thoracic facet joints.

21. Pascual E, Castellano JA, Lopez E. Costovertebral joint changes in ankylosing spondylitis with thoracic pain. Br J Rheumatol 1992; 31(6):413–415. 22. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes [erratum appears in J Manip Phys Ther 2000; 23(8):530]. J Manip Phys Ther 2000; 23(6):395–403. 23. McGill S. Low back disorders: evidence-based prevention and rehabilitation. Champaign, Illinois: Human Kinetics; 2002.

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Part 3: Specific Disorders 24. Richardson C, Jull G, Hodges P, et al. Therapeutic exercise for spinal segmental stabilization in low back pain. Edinburgh, Scotland: Churchill Livingstone; 1999. 25. Vleeming A, Pool-Goudzwaard AL, Stoeckart R, et al. The posterior layer of the thoracolumbar fascia. Its function in load transfer from spine to legs. Spine 1995; 20(7):753–758.

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26. Jenkins D. Hollinshead’s functional anatomy of the limbs and back. 7th edn. Philadelphia: WB Saunders; 1998.

PART 3

SPECIFIC DISORDERS

Section 4

Biomechanical Disorders of the Thoracic Spine

CHAPTER

Thoracic Spinal Pain

72

Madhuri Are and Allen W. Burton

INTRODUCTION Disorders of the thoracic spine are as disabling as those in the cervical and lumbar spine and therefore deserve wider recognition than they often receive. As a consequence of having a low incidence, diagnosis and treatment often remain a challenge. Thoracic pain accounts for less than 2% of spinal pain.1 Pain may be due to soft tissue, visceral, disc or structural etiologies.2,3 Pain from thoracic spine lesions may present as pain in the anterior and/or posterior thorax, lumbar spine, and extremities.4 In a study by Acre and Dohramm, 57% were found to present with non-specific pain, 24% present with sensory changes, and 17% present with motor changes.5 The thoracic spine is relatively immobile due to the unique anatomy6 and is stabilized and strengthened by the rib cage.7,8

ETIOLOGY There are numerous etiologies for thoracic spinal pain as outlined in Table 72.1. One cause of thoracic pain is thoracic disc disease. The incidence of thoracic disc disease is less than 2%.5,9,10 This low incidence may be due to the orientation of the thoracic facet joints in the coronal plane, restraint of the thoracic spine by the ribs and sternum, and the small size of the thoracic discs. Thoracic spine disc herniations account for only 0.2–5% of all disc herniations and have a male predominance. The lower, more mobile segments (T11–12) are affected with greater frequency.5,11–13 The youngest reported case of thoracic disc herniation was in a child 12 years of age.5 Although trauma may contribute to thoracic disc herniation,12 degenerative changes are the most common cause of thoracic disc herniation.5

Table 72.1: Etiology of Thoracic Spine Pain 1. Disc herniation 2. Spinal stenosis, osteoarthritis 3. Infection: osteomyelitis, tuberculosis, discitis 4. Fractures (traumatic, stress, osteoporotic, tumor (primary, secondary), multiple myeloma 5. Non-disc herniation-related radicular pain: intercostal neuralgia, postherpetic neuralgia, post-thoracotomy pain syndrome 6. Spinal abnormalities: kyphosis, scoliosis 7. Muscular and postural 8. Inflammatory disorders: AS, RA, costochondritis, Tietze’s syndrome 9. Rare causes: CRPS, T4 syndrome, thoracic nerve root dysfunction

Most major thoracic disc lesions occur in the lower thoracic spine, but minor thoracic disc lesions occur in the upper and middle regions. Thoracic disc disease usually affects adults in the fourth through sixth decades of life,5,10 in some cases following spinal trauma. The intervertebral discs of the thoracic spine increase in height and width from cranial to caudal. The spinal canal is relatively small, and the epidural space is narrow. The narrowest point is between T4 and T9. The intradiscal pressure is very high in the ventral segment of the thoracic spine, while dorsally the support is mainly by the vertebral joints. Nevertheless, parts of the intervertebral discs can displace towards the spinal canal.14 Seventy percent of these herniations occur in a posterolateral direction. Onset can be acute, subacute, or chronic.10 Ninety percent of patients have signs of spinal cord compression at the time of diagnosis.5 Another cause of thoracic spinal pain is canal stenosis, often stemming from osteoarthritis with facet hypertrophy combined with hypertrophy of the posterior longitudinal ligament and/or ligamentum flavum with or without facet joint hypertrophy.15–17 Thoracic facet joint disease is most common at the T3–5 segment.4 The incidence of thoracic canal stenosis is approximately 2%.18 Infectious causes of thoracic spinal pain include tuberculosis (Pott’s disease), discitis, or osteomyelitis. This etiology is of particular relevance in the immunocompetent and immunocompromised patient. A retrospective review of 33 patients with tuberculosis of the spine revealed that the majority of the lesions involved the thoracic spine (30%), followed by lumbar spine (27%). Skip lesions were seen in 12% of the patients. Neurological involvement was seen in 50% of patients. The concomitant pulmonary tuberculous rate was 67%.19 In those who are immunocompromised, such as patients with HIV, steroid use, organ transplant, i.v. drug use, or cancer, there may be a delay in diagnosis due to the fact that they may not present with signs and symptoms as evident as in immunocompetent patients.20 Back pain accompanied by fever may be the presenting symptoms of discitis. Septic discitis is inflammation of the intervertebral disc and discovertebral junction. The inflammatory process may extend in to the epidural space, posterior vertebral elements, and paraspinal musculature21 Spondylodiscitis accounts for 2% of all cases of osteomyelitis.22 In a study done by Hopkinson et al., the spectrum of septic discitis was studied. They found that the incidence was 2 per 100 000. Seventy-three percent were 65 years or older; 91% had back pain, with lumbar, thoracic, and then cervical as the most common areas affected. Predisposing factors included cancer, diabetes, and invasive spinal procedures.23 Thoracic spine fractures of various causes may also lead to significant thoracic spinal pain. Thoracic spine fractures are unique due to the anatomy of the thoracic spine and its biomechanics. Fractures can cause neurological compromise because of the small size of the thoracic spinal canal relative to the spinal cord.7,8 Fractures may be due to compression of the vertebral body compounded with or without 777

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compression of neural elements as seen in Figure 72.1. Disorders known to contribute to fractures include osteoporosis, tumor such as primary spinal cord lesions, systemic disease such as multiple myeloma, metastatic disease such as those most commonly found from breast, lung, or prostate cancer, or from trauma itself. Not only do the etiologies differ, they may also have varying physical findings, treatments, and functional outcomes.24 Osteoporosis can lead to significant back pain, kyphosis, impaired respiratory function, and quality of life, as well as morbidity. Fractures due to osteoporosis occur in the spine (especially thoracolumbar), hip, and distal forearm. The lifetime risk of clinically diagnosed vertebral fractures is approximately 15% in Caucasian women.25 Vertebral fractures are the most common skeletal injury from osteoporosis, with an incidence of 700 000 per year in the United States.26 Vertebral body height reduction by 20% or 4 mm can be considered a vertebral compression fracture (Fig. 72.2).27 Three types of vertebral fractures in osteoporosis are described: wedge, crush, and biconcave. Most common are wedge fractures (collapsed anterior border with almost intact posterior border), which occur mostly in the midthoracic and thoracolumbar regions.28 In crush fractures, the entire vertebral body is collapsed. Crush fractures are also usually located in the midthoracic or thoracolumbar areas. Biconcave fractures collapse in the central portion of the vertebral body and are more commonly seen in the lumbar region. Those who have wedge fractures tend to experience severe, sharp pain, which usually gradually decreases over 4–8 weeks, although chronic pain is common in this patient group. Patients with superior endplate discontinuity have progression to complete collapse of the vertebral body and have dull, less severe pain. Those with more severe pain initially and a well-defined wedge fracture may have better functional outcomes with pain management and early mobilization.29 Pain due to vertebral fractures is due to a combination of a reduction in body weight, decreased compressive spinal loading, and decreased bone mass.30 Risk factors include lack

of hormonal replacement in the perimenopausal period, chronic illnesses, smoking, and alcohol use.31,32 Thoracic-region pain in the adolescent or athlete may be due to muscle strain, stress fractures, or costochondritis. Stress fractures occur when there is overloading of the bone. Common areas of stress fractures include the ribs, especially the first rib. Patients usually complain of pain and shoulder discomfort with radiation into the sternum. Costochondritis is an inflammation (without swelling) and Tietze’s syndrome (with swelling) at the costochondral junction where two different tissue types merge, especially in an area stressed by repetitive movement. Costochondritis usually occurs in ribs two through five and is provoked by movement.33 Scoliosis is another abnormality that may also contribute to thoracic pain. Adult scoliosis usually patterns with more rigid deformity than adolescent idiopathic scoliosis.34 Back pain due to metastatic bone disease can lead to fractures, hypercalcemia, and spinal cord compression, all of which can adversely affect a patient’s functional status and quality of life. Metastatic bone disease leads to increased osteoclastic activity and impaired bone metabolism. Patients with neoplastic diseases such as breast, prostate, or lung cancer, and multiple myeloma may experience some of the sequelae of skeletal complications.35 In rare cases, spinal cord compression may be idiopathic. Saito et al. described a 68-year-old female who had chronic midback pain with slowly progressive weakness over 34 years when she became paraplegic. Magnetic resonance imaging (MRI) revealed idiopathic spinal cord herniation at T6–7. She underwent T5–8 laminectomy, and her pain improved although she continued to have some lower extremity weakness.36 Post-thoracotomy pain and postherpetic neuralgia (PHN) are both causes of thoracic pain of radicular origin. In these cases, the pain referral pattern is neuropathic in nature and not usually due to axial pain.37

Fig. 72.1 Sagittal magnetic resonance image revealing large disc herniation at T11–T12. (Courtesy of MD Anderson Cancer Center.)

Fig. 72.2 T8, 9, and 10 compression fractures. (Courtesy of MD Anderson Cancer Center.)

Section 4: Biomechanical Disorders of the Thoracic Spine

Anterior and middle column injuries may contribute to thoracic spinal pain. Posterior column injuries are commonly reported; however, anterior and middle column injuries are often missed and not reported. Katz and Scerpella reviewed seven gymnasts’ reports of back injuries, finding a relatively high incidence of thoracic anterior column pathology in a young patient population. All subjects had tenderness to palpation and were neurologically intact. Two had pain with provocative tests (straight-leg raise or single-leg hyperextension test). Each subject had plain roentgenograms. Three of them were normal. Four subjects had MRIs with findings consistent with disc herniation or degeneration. Of those with abnormal MRI findings, two subjects had vertebral body compression fractures. One subject had a compression fracture of T12 with a 30% loss of height, multiple Schmorl’s nodes, and fractures at L4 and L5. The other one had T11 anterior wedging and T11–12 disc space narrowing. All subjects were treated by physical therapy; two had interventional epidural or facet blocks, and none had surgery. In all cases, practice time was lost. Only one continued to remain competitive. Therefore, anterior and middle column abnormalities from injuries should be included in the differential diagnosis of the thoracic back in athletes.38 Another cause of thoracic back pain may be myofascial pain syndrome. This syndrome is characterized by regional pain, usually in the neck and upper back, with presence of trigger points. The most commonly affected areas of pain and trigger points include the levator scapulae muscles and the upper and lower trapezius.39 Rare causes of thoracic pain may be associated with other pain syndromes such as complex regional pain syndrome-1 (CRPS-1),40 rheumatoid arthritis (RA),41 the T4 syndrome,3 and thoracic nerve root dysfunction (TNRD).42,43 TNRD is most often seen in diabetics who present with chest or abdominal pain, sensory polyneuropathy, or weight loss.42,43 Other causes of TNRD include herpes zoster, scoliosis or osteoarthritis of the thoracic spine, thoracic disc disease, or carcinoma of the thoracic spinal nerve roots.44,45 Rheumatoid arthritis may be associated with thoracic back pain although diffuse joint pain and neck pain may be more prevalent 41 The spinal area most commonly affected is the atlantoaxial region; however, thoracic spinal pain may also be present.46 Ankylosing spondylitis (AS) may also be another cause of thoracic back pain. Back pains with sacroiliitis along with other features of spondyloarthropathy (ethesitis and uveitis) are highly suggestive of AS.47

PHYSICAL EXAM In addition to a thorough history, a general physical exam with a focus on the thoracic spine should be performed. The thorax and back should be examined for any signs of trauma, infection, lesions, or other skin abnormalities. The inspection should also include any overt deformity of the spine such as scoliosis or kyphosis. Abnormalities in posture, biomechanics, and mobility should be noted. The axial spine and ribs should be palpated for any evidence of tenderness. Sensory deficits (hypoesthesia or allodynia) along the back and thorax should be noted. Any abnormalities in the range of motion should be documented. Manual muscle testing in the upper and lower extremities along with reflex testing should be performed.48 The chest should be auscultated to ensure that there are no other physical signs of a systemic disorder. If an infectious etiology is suspected, then examination of lymph nodes and glands may be beneficial. If an inflammatory disease is suspected, then examination of joints and overall musculature is warranted.49 If malignancy is suspected, then the exam should be centered on a systematic approach. Symptoms of thoracic disc disease may be reported as vague and poorly defined.10,11,50,51 The location of the disc herniation may present with different physical findings. For instance, a central disc

herniation may present with pyramidal tract signs, whereas lateral discs may present with radicular pain.6,10–12,52 Common symptoms include motor and sensory deficits with radicular pain or numbness. Bowel and bladder dysfunction may also be present. Examination may reveal upper motor signs such as hyperreflexia, spastic paraparesis, and Babinski signs. If sensory dysfunction is present, it is usually decreased sensation.5,10,12,50,52–54 Symptoms may not present for several years.5,10,12,53 Local pain may be due to distention of the nerve fibers in the anulus fibrosus and posterior longitudinal ligament.10,12 Small disc herniations may also produce spinal cord compression because of the anterior placement of the spinal cord with respect to the thoracic canal.55 Radicular pain may be due to impingement on the short thoracic nerve root by the disc or from traction or stretching of the root by the thecal sac.12 Neurologic symptoms from disorders of the thoracic and lumbar spine can present with upper motor or lower motor findings, cauda equina syndrome, or nerve root lesions.5 In a retrospective review of 26 symptomatic patients, Tokuhashi et al. reviewed different levels of disc herniations and the physical findings for each level. They found that for those with T10–11 and T11–12 disc herniations, the clinical presentation was consistent with upper motor neuron disorders (increased patellar tendon and ankle tendon reflexes), positive Babinski signs, and bowel and bladder dysfunction. In those patients with T12–L1 disc herniations, the physical findings were suggestive of a lower motor neuron disorder (muscle weakness/atrophy, decreased patellar and ankle tendon reflexes, and negative Babinski signs). For the L1–2 disc herniations, mild disorders of cauda equina and sensory disturbance at the anterior or lateral aspect of the thigh were noted. In the L1–3 group, most had severe thigh pain, sensory deficits, and weakness in the quadriceps and tibialis anterior, and decreased or absent patellar tendon reflexes.56 Sometimes, thoracic disc herniations may have unusual presentations or pain referral patterns. Wilke et al. reported a case of thoracic disc herniation that presented with chronic shoulder pain. In this report, a 44-year-old female with shoulder pain underwent acromioplasty. However, symptoms and pain became progressive. She then developed urinary retention. MRI of thoracic spine revealed an extradural space-occupying lesion at T10–11 (sequestered prolapsed intervertebral disc). The patient was treated with costotransversectomy and nucleotomy at T10–11, and her symptoms improved immediately.57 Thoracic disc herniation may also present like acute lumbosacral radiculopathy. Compression of the lumbosacral spinal nerve roots at the lower thoracic level after their exit from the lumbar enlargement may contribute to this physical finding. Lyu et al. reported such a case. A 49-year-old woman was found to have sudden low back pain with radiation into the left buttock and lateral aspect of the left leg and foot. MRI with contrast was consistent with T11–12 midline disc bulge and posterior osteophytes. When she was treated with a laminectomy, her symptoms resolved immediately. A 3-year follow-up revealed normal neurological function with mild low back soreness.58 Thoracic back pain may also present with paresthesias, numbness, or upper extremity pain with or without headaches. DeFranca and Levine described the T4 syndrome where patients presented with upper back stiffness, headaches, and paresthesias without gross neurological deficits. Thoracic joint dysfunction appeared to be the cause of the symptoms.3 For the immunocompromised patient with spinal disease, the most common presenting symptom is back pain (thoracic or lumbar) with radiculopathy, myelopathy, or sensory deficits.20 If discitis is suspected, the patient may have focal back pain, with possible radicular involvement, as well as neurological compromise. The presentation of symptoms may be acute or chronic.21 In the study of septic discitis 779

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in the immunocompetent patient by Hopkinson et al., 45 had neurological symptoms such as weakness, urinary retention, diminished reflexes, and sensory deficits. Therefore, focal back pain in a patient with constitutional symptoms and/or neurological sequelae may be indicative of discitis.23 Although many cases of spondylodiscitis may present acutely, some present after years with the disease. In a case report by Finsterer et al., a 65-year-old female had recurrent, localized thoracic back pain for over 2 years. Approximately 9 months after pain onset, she developed sensory deficit of the left lower extremity. Fourteen months prior to admission, she had recurrent fever, mild weakness, and numbness of the lower extremities.59 In patients with osteoporotic vertebral fractures, the spine may appear kyphotic. These patients become shorter as a consequence of vertebral compression and flexed posture. An exaggerated thoracic kyphosis and a protuberant abdomen may compromise and reduce lung capacity.60 Pain is exacerbated by standing erect or with a change of position or movement. Pain may also be reproduced by palpation of the spinous process at the involved level. Neurological deficits are rare, but should be ruled out by a thorough examination of motor and sensory function.61 Patients who have post-thoracotomy pain syndrome have a history of chest and/or spine surgery several weeks or months prior to development of pain. Examination can reveal muscular tenderness, sensitivity to touch, with either decreased or increased sensation. Tenderness is usually along a dermatome near the incision. Upper extremity range of motion may be decreased due to pain.37 Postherpetic neuralgia (PHN) may have similar physical findings. Pain is usually unilateral. Pain in PHN is a common presenting symptom. Pain from acute herpes zoster may last a few weeks or persist longer.62 Pain in a dermatomal pattern usually presents 7–10 days prior to the rash. Nerves commonly affected include T4–6, cervical, and trigeminal. Pain is produced by inflammation associated with movement of the virus from sensory nerves to skin and subcutaneous tissues.63 Pain may present in 90% of the patients with allodynia

(pain evoked by nonpainful stimuli) or with deafferentation (sensory loss without allodynia).64 Management and treatment should begin immediately after symptoms begin.63 In those patients suspected of having an inflammatory disease such as RA, physical findings in addition to those related to back pain may be beneficial in assisting with the diagnosis. For instance, most patients with RA have symmetrical swelling of small joints and have morning stiffness of at least 1 hour. Extra-articular synovitis along with malaise, fatigue, fever, and weight loss may be seen.41 In patients with AS or suspected AS, there is loss of spinal mobility, especially with restrictions of flexion and extension of the thoracic and lumbar spine, as well as restrictions of chest expansion. Ankylosis along with muscular spasms and limitation of motion may contribute to pain. The spine may be stiff or fused and there may be sacroiliac joint dysfunction along with limitations of bilateral hip involvement, peripheral arthritis, and extra-articular manifestations. Postural abnormalities also contribute to pain. In severe cases, lumbar lordosis is destroyed, the buttocks atrophy, thoracic kyphosis is exaggerated, and the neck is flexed. Thoracic kyphosis may contribute to restricted chest wall motion with concomitant decreased vital capacity.47 If a stress fracture or costochondritis is suspected, patients will experience tenderness with pressure over the affected ribs, especially since the painful area tends to be focal.33 In the myofascial pain syndrome, diagnosis is made by clinical presentation of regional pain, referred pain, taut bands in muscles, tenderness, and restricted range of motion as described by Simons. On examination, pain is due to muscle tension within or over muscles or their attachments. Trigger points are also elicited.65

DIAGNOSIS Laboratory work-up The laboratory work-up for a patient with thoracic back pain can vary based on the history and physical findings. Figure 72.3 summarizes

Diagnosis

Disc herniation CBC, CSF, plain film, CT, MRI, EMG

Rheumatologic CBC, ESR, ANA, HLA, IGA, synovial fluid, plain film, CT/MRI, bone scan

Inflammatory disorders (Tietze’s syndrome/ costochondritis) bone scan, plain film

Spinal infection CBC, CRP, ESR, cultures, MRI, CT, bone scan

DJD/canal stenosis Plain film, CT, MRI

Fractures 1. Trauma – CBC, CMP, plain film, CT/MRI 2. Osteoporosis – CBC, ESR, serum electrophoresis, plain film, MRI 3. Tumors: CBC, CMP, ESR, CRP, tumor markers, urine analyses, electrophoresis, plain film, bone scan, CT/MRI 4. Stress - bone scan

780

Scoliosis/kyphosis Plain film, CT, MRI

Post-herpetic neuralgia and post-thoracotomy pain syndrome Physical exam

Muscle pain syndrome CBC, ESR, CK, TFT

Fig. 72.3 Algorithm for diagnosis of thoracic spinal pain.

Section 4: Biomechanical Disorders of the Thoracic Spine

the diagnostic evaluation of thoracic spinal pain. For instance, if thoracic disc herniation is suspected, complete blood count (CBC) may be normal and cerebrospinal fluid (CSF) analyses usually reveal a normal cell count and clear fluid.12 If tumor or malignancy is suspected, then CBC, complete metabolic profile (CMP), tumor markers, urine analysis, electrophoresis (SPEP, UPEP), and erythrocyte sedimentation rate (ESR) may be beneficial in assisting with the diagnosis. If a rheumatological disorder or connective tissue disorder is suspected, then ESR, ANA, HLA, RF, calcium, alkaline phosphatase, and cultures may be of value. To rule out a source of infection, ESR, C-reactive protein (CRP), CBC, and cultures should be performed. For a spinal infection in an immunocompromised patient, the diagnosis is made by identification of the pathogen since MRI, computer tomography (CT), and bone scan do not aid in the diagnosis unless tuberculosis is suspected.20 In an immunocompetent patient with suspected discitis, MRI is the best imaging study to assist with the diagnosis.21 Hopkinson et al. found that CRP and ESR were elevated in 68% of the patients, and MRI made the diagnosis. The most common pathogen identified was Staphylococcus aureus.23 Findings on imaging studies may also be seen when the symptoms are chronic. For instance, Finsterer et al. found that even after a 2-year presentation of back pain, MRI imaging revealed T11 vertebral body destruction with spondylodiscitis of adjacent discs and epidural abscess from T4–9.59 If a patient is suspected of having back pain and there are other systemic signs, an inflammatory disorder such as RA must be considered in the work-up. Diagnosis may be made with elevated ESR and CRP along with anemia and specific rheumatologic indicators.41 In patients with AS, the HLA-B27 gene is present in 90–95% of patients. Other markers include increased CRP, ESR, raised alkaline phosphatase levels, above normal serum IgA levels, and a mild normochromic normocytic anemia. Synovial fluid analyses are similar to that of other joint diseases.47 In patients suspected of having myofascial pain syndrome, suggested evaluation includes ESR, serum creatine kinase, CBC, and thyroid function tests. These are all normal in myofascial pain syndrome, which is a diagnosis of exclusion.65 Osteoporotic fractures in the upper thoracic spine may be suggestive of an underlying malignancy and a thorough evaluation should be performed. Evaluation with CBC, ESR, and serum electrophoresis can help in identifying an underlying malignancy (including multiple myeloma) in a patient with a high thoracic fracture.66

Radiological work-up In general, the radiological evaluation of patients with thoracic pain includes plain films, CT, and/or MRIs. Plain radiographs may be helpful in determining flexibility of the spine. Techniques commonly used to evaluate flexibility include side bending, fulcrum bending, push-prone, and traction radiographs.67–69 Deviren et al. evaluated potential predictors of flexibility in patients with thoracolumbar and lumbar scoliosis by side-bending radiographs. In this retrospective study of 75 patients with idiopathic thoracolumbar and lumbar scoliosis, preoperative side bending and standing Xrays of thoracolumbar and lumbar curves were taken. Cobb angles, curve flexibility, and axial and radicular pain were noted. Axial and radicular pain were more commonly associated with adult deformity than adolescent idiopathic deformity. Findings revealed that 75 patients had average major curve magnitude of 56° and flexibility of 55%. Both axial and radicular pain was correlated with age but not curve magnitude. Curve magnitude and age are main predictors of structural flexibility. Every 10° increase in curve magnitude over 40° resulted in 10% decrease in flexibility and every 10-year increase in age decreased flexibility of structural curve by 5%. Progressive loss of flexibility with age and curve progression can make surgical correction more challenging.34

Common radiographic findings in thoracic disc herniation include disc space narrowing, osteophyte formation, kyphosis, and calcification.13,52,54 MR can detect spinal cord compression and disc degeneration on T2-weighted sequences.70 Gadolinium enhancement may also detect small and large herniations as seen in Figure 72.1.55 In patients with thoracic canal stenosis, there may be hypertrophy of the facets manifested by increased density overlying the zygapophyseal joints on frontal or lateral radiographs.71–73 Arana et al. found that there may be a relationship between upper thoracic and cervical spine degenerative disc disease. They studied the incidence and evaluated upper thoracic degenerative disc changes on MRI in patients with neck pain. In this study, 156 patients, 19–83 years old, with cervical pain had MRI imaging including thoracic spine. Findings revealed that 13.4% of the patients with cervicalgia had degenerative disc changes in the thoracic spine. The most commonly affected area was in the T2–3 disc.74 Electromyography may also be beneficial in diagnosing patients with thoracic nerve root dysfunction (TNRD). Electromyography may reveal findings suggestive of radiculopathy.75 Such findings include normal nerve conduction studies, decreased recruitment in motor unit action potentials, and the presence of fibrillations or positive sharp waves.76 If a vertebral compression fracture is suspected, radiographs may show osteopenia and a fracture with loss of height, with possible wedging and occasionally retropulsion of osseous fragments into the spinal canal. Most fractures are located in the thoracolumbar area.28 MRI of the spine is most useful in determining fracture age, excluding malignant tumor, and for selecting appropriate treatment. In an acute fracture, MRI shows a geographic pattern of low-intensity signal changes on T1-weighted images and high-intensity signal changes on T2-weighted images, indicating more bone edema in the acute fracture. As the fracture becomes chronic, a linear area of lowintensity signal change replaces the geographic area on T1-weighted images.77 The MRI findings of osteoporotic and metastatic spine fractures are decreased signal intensity on T1-weighted images and increased signal intensity on T2-weighted images. Pedicle involvement or involvement of other posterior elements and presence of lesions in the epidural space or paraspinal regions are suggestive of malignancy rather than osteoporosis.78 Bone scans are sensitive and can be used to identify and discriminate acute from chronic fractures; however, they have low specificity for the diagnosis of the underlying process.79 If a traumatic fracture of the thoracic spine is suspected, it should be treated appropriately. However, many fractures may be occult and missed if no radiological studies are taken. The absence of pain and tenderness does not necessarily exclude significant thoracolumbar trauma.80 For instance, Cooper et al. found that 31% (34 patients) out of 183 patients who had GCS 13–15 in the Maryland Shock Trauma Center had no pain or tenderness, yet all had fractures.81 Thoracolumbar spinal fractures are not uncommon and may be missed. Kirkpatrick and McKevitt recommend clinical clearance (of trauma patients) if patients are clinically responsive, nonintoxicated, and neurologically intact without another spinal injury. Otherwise, they advocate full imaging evaluation to assess for thoracolumbar fractures.80 Patients with inflammatory diseases such as RA and AS may have distinct radiographic presentations. For instance, in RA, radiographic images show juxta-articular osteoporosis.41 In AS, radiological changes reflect the disease process, and sacroiliitis is usually detectable in the early stages of AS. MRI and CT can detect AS lesions earlier than plain radiography. Plain films and MRI also reveal thoracic kyphosis and fused spine in severe cases.47 Reactive changes affect the discovertebral junctions in the thoracolumbar area. On MRI images, inflammatory osteitis of the vertebrae is visualized.82 In patients with 781

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stress fractures, the definitive diagnosis may be made by a bone scan. Bone scans are also helpful in diagnosing Tietze’s syndrome. Plain films may be normal leading to delay in diagnosis with further evaluation only when there is concern that a large bony callus may represent a bone tumor or other pathology.33 Plain films, bone scan, CT, or MRI may evaluate infectious etiologies of the spine.

Differential diagnosis Some patients with thoracic disc disease or pain are thought to have cardiovascular, pulmonary, gastrointestinal, genitourinary, or psychiatric disorders.10,11,50,51 Disc herniation can be confused with esophagitis, nephritis, gastrointestinal ulcers and cholecystitis.83 Some patients with T1 herniation may present with Horner’s syndrome51,84 and T11 herniation with testicular pain.85 Thoracic nerve root dysfunction may be diagnosed as abdominal pain unless a careful history and physical examination are performed.86

TREATMENT In treatment of thoracic disc disease, numerous management strategies, from conservative through aggressive surgical options are available as shown in Figure 72.4.14 The goal of physical therapy is to improve posture, joint and spinal mobility and flexibility, to strengthen musculature such as the trapezius, rhomboids, and latissmus dorsi, and to prevent deconditioning.65 For pain which persists despite conservative treatment, steroid injections can be used in the treatment of pain of spinal origin. These injections can be performed relatively quickly and conveniently with or without radiological guidance, although fluoroscopic guidance may allow more accurate injections to the appropriate anatomic level. The therapeutic effects of corticosteroids are mostly due to their antiinflammatory effects. They may also have local anesthetic-like actions on peripheral nerves. The antiinflammatory effect is through modification of protein

synthesis at a nuclear level. At therapeutic doses corticosteroids up-regulate the production of lipocortin, a protein that inhibits phospholipase A2. This enzyme converts membrane-bound phospholipids into arachidonic acid derivatives, including leukotrienes and prostaglandins that are potent inflammatory mediators. To this date, there are no existing data for epidural steroid injections for the treatment of radicular pain of thoracic origin. Thoracic zygapophyseal joints can be a source of pain and, although steroids and denveration procedures are routinely performed, data currently available do not allow for conclusions to be reached.87 Spinal manipulative therapy is commonly used for treatment of joint dysfunction and pain. Thoracic zygapophyseal joints can be a source of pain.88 A single-blind, randomized, controlled pilot study to investigate the effectiveness of spinal manipulative therapy in the treatment of mechanical thoracic spine pain was performed. Thirty subjects (16–60 years) were split into two groups. All had thoracic spine range of motion tested with BROM II goniometers and pain threshold with algometers. All completed Oswestry Back Pain Disability Index, short-form McGill Pain Questionnaire, and Numerical Pain Rating Scale – 101 Questionnaires. The treatment group received thoracic spinal manipulation, and the placebo group received nonfunctional ultrasound application. The spinal manipulative therapy group showed improvements in both subjective and objective measurements. The ultrasound group, however, showed improvements in subjective measurement only.89 Radiofrequency (RF) ablation of the zygapophyseal joints is a minimally invasive technique used to treat mechanical pain of spinal origin. In a study by Pevsner et al., 122 patients underwent RF of the medial branch nerve for mechanical back pain. The levels included cervical, thoracic, and lumbar segments. Patients were followed at 1, 3, 6, and 12 months after RF. Seventy-five percent of patients had significant pain relief after 1 month; 71% had significant pain relief after 3 months. At 6 months, 66% had pain relief and 34% had no effect. At 12 months, 63% still had good pain relief while 37% had no effect. Complications included transient discomfort and burning pain in 27 patients.90

Treatment

Disc disease NSAIDs, steroids, PT, steroid injections, laser disc decompression nucleotomy discectomy/fusion

Rheumatologic NSAIDs, steroids, disease modifying drugs, bisphosphonates, PT

DJD/canal stenosis NSAIDs, steroids, PT, steroid injections, spinal manipulation, RF

Post-thoractomy Pain syndrome/PHN PT, NSAIDs, steroids, topical anesthetics, anticonvulsants, antidepressants, opioids, muscle relaxants, FIB TENS, intercostal blocks, RF, cryoanalgesia, epidurals

Fractures 1. Trauma – Nonoperative, posterior fixation 2. Osteoporosis – Rest, NSAIDs, opioids, PT, brace, vitamin, calcium, HRT, bisphosphonates, vertebroplasty/kyphoplasty 3. 1⬚ Tumors: Resection, spinal instrumentation 2⬚ Tumors: Chemotherapy, XRT, bisphosphonates, vertebroplasty/kyphoplasty, resection, vertebrectomy/instrumentation Fig. 72.4 Algorithm for treatment of thoracic spinal pain by diagnosis. 782

Spinal infection PT, antibiotics, surgical drainage, debridement, fusion/instrumentation, vertebrectomy/laminectomy

Inflammatory disorders/ stress fractures Rest, NSAIDs, activity modification

Scoliosis/kyphosis Treat underlying cause, fusion/instrumentation

Muscle pain syndrome PT, trigger point injections

Section 4: Biomechanical Disorders of the Thoracic Spine

Another minimally invasive procedure recommended for patients who have no relief with conservative treatment includes nonendoscopic percutaneous laser disc decompression and nucleotomy (PLDN) with Nd-YAG laser 1064 nm.91 Following diagnosis by MRI, this technique may be employed for thoracic discogenic pain. Hellinger et al. recommends Nd-YAG laser 1064 nm with a maximal dose of 15 watts, 1 second per single shot with a total dose of 1000 joules per intervertebral disc. In their practice, regional anesthesia is used and motor function is observed. The procedure is performed with fluoroscopic guidance, as are most minimally invasive procedures. Patients are prescribed a brace for 6 weeks after treatment. In the prospective study by Hellinger et al., aimed at treating 42 patients with thoracic disc protrusions and extrusions, monitored parameters were VAS, subjective condition, neurological findings, and peripheral EMG. At 6 weeks after treatment, success rate was 90%. Complications include one case of spondylodiscitis, one pneumothorax, and one case of pleuritis. Pain relief and decompression of spinal structures was effective and immediate by disc vaporization, shrinkage, and nociceptor destruction.14 When a spinal infection is suspected in an immunocompromised patient based on the appropriate clinical and lab findings, the treatment involves medical management, physical therapy to prevent deconditioning, and immobilization of the affected area. If tuberculosis of the spine is suspected, the mainstay of treatment is antituberculosis chemotherapy, which is highly effective. Additional treatment includes radical anterior debridement and fusion along with anterior or posterior instrumentation.19 Epidural abscesses require surgical drainage if there is neurological compromise. Vertebrectomy may also be indicated if there is evidence of spinal cord impingement or osteomyelitis.20 In the treatment of immunocompetent patients with septic discitis, most without neurological compromise can be treated with i.v. antibiotics. Those with neurological deficits require surgical drainage and laminectomy.23 Even after a 2-year history of back pain and symptoms of epidural abscess, treatment is equivalent to treatment for symptoms that present acutely. For instance, in case study by Finsterer et al. with the diagnosis of an epidural abscess 2 years after the patient had developed symptoms, the abscess was drained and laminectomy was performed. The patient was treated with i.v. antibiotics for S. aureus infection and had full neurological recovery after 10 weeks.59 Patients with thoracic spine fractures due to various causes may present with physical findings and be treated according to their clinical presentation. Dai reviewed thoracic spine fractures in 77 patients. Thirty-seven were compression fractures, 34 were fracturedislocations, 3 burst fractures and 3 burst-dislocations. Twenty-six had complete spinal cord lesions, 14 had incomplete injuries, and 37 were neurologically intact. Approximately 70% were treated nonoperatively and 30% operatively. Those with complete spinal cord lesions had no neurological improvement. One-third of the neurologically intact patients continued to have pain although they retained normal function. Fifty percent of those with incomplete lesions had neurological recovery.24 Thoracic spinal pain due to fractures in the neurologically intact patient may be managed either nonoperatively or with posterior fixation. Surgical treatment usually includes decompression of neural elements and posterior fixation with pedicle screws. This technique provides spinal stability, pain relief, and partial correction of kyphosis. In a prospective study of 80 patients with burst fractures without neurological deficit, patients were randomized into a nonoperative treatment group or a posterior fixation group. All patients were neurologically intact, with burst fractures at T1–L2, had no fracture dislocations or pedicle fractures, had nonpathological cause

of fractures, and had no other musculoskeletal or major organ system injuries. The nonoperative group were allowed activity to pain tolerance while wearing a hyperextension brace. The operative group had a three-level fixation. A 2-year follow-up revealed that the surgical group had less pain only up to 3 months. In the nonoperative group, the kyphosis angle worsened by 4° and retropulsion decreased from 34% to 15%. Therefore, posterior fixation provided partial kyphosis correction and earlier pain relief, but functional outcomes were similar.92 Symptomatic conservative management of osteoporotic fractures includes a short period of bed rest, modification of activity, opioids, antiinflammatory agents, and a brace.26 Appropriate nutrition, calcium and vitamin D, along with cessation of smoking and alcohol plus moderate exercise and physical therapy focused on weight-bearing exercises are recommended. Hormonal replacement in those without contraindications may also be beneficial.93 Other agents commonly prescribed include bisphosphonates and calcitonin.94 The physical therapy regimen includes spinal extension exercises to reduce lumbar lordosis, correction of poor posture, strengthening of abdominal musculature with a focus on weight bearing, and progressive, resistive, and chest expansion exercises. Thoracolumbar orthoses may also be helpful to relieve pain and to promote extension of the spine.65 If an osteoporotic fracture is suspected and patients do not respond to conservative treatment, minimally invasive procedures such as nerve root injections for pain control may be attempted. In a study by Kim et al., 58 patients with osteoporotic vertebral fractures received a nerve root injection with lidocaine, bupivacaine, and DepoMedrol. Pain scores were obtained before treatment, at 1 month and 6 months after treatment (mean of 14 months postfracture follow-up). Six patients reported excellent pain results, 42 reported good results, and 10 reported fair results. Therefore, this study suggests a trial of nerve root injections for reducing symptoms of back pain prior to more invasive procedures.95 Although nerve root injections may help relieve back pain due to osteoporotic vertebral compression fractures, they do not modify the vertebral body causing the pain. Balloon kyphoplasty has been shown to safely reduce and repair vertebral compression fractures and increase independence and quality of life. A retrospective chart review of 96 patients with 133 fractures evaluated functional outcomes of patients at 1 week, 1 month, 3 months, 6 months, and 1 year after balloon kyphoplasty. This procedure increased vertebral body height, decreased acute and chronic back pain, and led to increased independence.96 Both vertebroplasty and kyphoplasty are procedures which percutaneously inject methylmethacrylate into the vertebral body. With kyphoplasty, a balloon ‘tamp’ is inserted into the vertebral body to increase the vertebral body height prior to methylmethacrylate injection. This procedure can correct kyphotic deformity.97 There are no studies directly comparing vertebroplasty and kyphoplasty, but both procedures reduce pain effectively and have low complication rates in numerous cases series.98–100 Benign tumors of the spine that present with back pain are rare and often misdiagnosed. Symptoms can be alleviated with the appropriate management such as excision and debridement of the lesion along with spinal instrumentation and fusion.101 If bony metastases from cancer are suspected, nonsurgical management includes external beam radiotherapy, chemotherapy, as well as bisphosphonates such as zoledronic acid or pamidronate. Bisphosphonates may relieve symptoms of pain from bony metastasis, but the ultimate goal is to prevent and teat osteoporosis in those with cancer.35 Vertebroplasty and kyphoplasty can also be beneficial to patients with painful compression fractures due to metastasis.94 Short-course radiotherapy may lead to significant improvements in symptom control (back pain, weakness) and to improvements in 783

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functional status in patients with metastatic spinal cord compression. In a study by Maranzano et al., they found that early treatment with a short course of radiotherapy for patients had positive clinical outcomes in those with spinal cord compression due to metastatic disease. They studied 53 patients with less radio-responsive primary tumors (non small cell lung, kidney, head and neck, melanoma, sarcomas), and more radio-responsive ones (breast, prostate, lymphoma, and multiple myeloma). All patients received a single fraction of 8 Gy, repeated after 1 week in responders, for a total dose of 16 Gy. All patients also received dexamethasone along with antiemetics. Response was assessed according to back pain, motor function, and bladder function before and after radiotherapy. Findings revealed pain relief in 67% of patients, 63% for motor function, and 98% for improved or preserved bladder function.102 If pain is due to post-thoracotomy pain, which is caused by incisional pain or muscular pain, pleural irritation due to chest tubes, effective analgesia may contribute to improved respiratory function and prevent complications such as infections and atelectasis.38 Treatment of post-thoracotomy pain syndrome includes NSAIDs, steroids, topical local anesthetics, anticonvulsants, opioids, and muscle relaxants. Epidural infusions are frequently used for postoperative pain control.103 Noninvasive and nonpharmacological approaches in the treatment of post-thoracotomy pain include electrical nerve stimulation104 and cryoanalgesia.105 A small preliminary case series showed favorable, short-duration analgesia with the use of focal intense brief transcutaneous electric nerve stimulation (FIBTENS) for the treatment of radicular and post-thoracotomy pain.104 Cryoanalgesia or freezing of intercostal nerves may also offer shortand long-term analgesia.105 In a clinical trial of patients undergoing thoracotomy, 200 patients were randomized to cryoanalgesia versus conventional (parenteral opiates) analgesia groups. Findings revealed that compared to the conventional analgesia group, cryoanalgesia of intercostal nerves led to improvement in postoperative pain scores, decreased opiate analgesia usage, and improvement in respiratory function. Cutaneous sensory changes resolved within 6 months with complete restoration of function.106 If PHN is suspected, there are many treatment options. A few such options include antivirals, antidepressants, corticosteroids, opioids, anticonvulsants, topical agents, nerve blockade (sympathetic nerve blockade, epidural), and spinal cord stimulation.64 In a retrospective study by Rowbotham et al., sympathetic blockade was performed to prevent PHN. Ninety percent of patients were pain free when treatment began within 2 months of zoster onset.107 For treatment of inflammatory disorders such as RA and AS, many options are available. NSAIDs are effective and considered to be firstline treatment although they only provide symptomatic relief without modifying the disease course. Other agents include corticosteroids,47 disease-modifying drugs such as sulfasalazine, methotrexate, thalidomide, and TNF-α.108 Other agents include intravenous bisphosphonates such as pamidronate.109 Nonpharmacological management of AS includes exercises to maintain erect posture, spinal and joint mobility, and chest expansion as well as aerobic exercises.65 However, the spine is susceptible to fractures and dislocation, atlantoaxial and spinal deformity, hip disease, and spinal stenosis, for which surgery may be required.109 Treatment of stress fractures, costochondritis, and Tietze’s syndrome is supportive with NSAIDs, relative rest, and modification of activity.33 For patients with the T4 syndrome as described by DeFranca and Levine, patients were treated with joint manipulation, stretching, and strengthening exercises. The symptoms then resolved.3 If myofascial pain syndrome is suspected based on physical findings, treatment includes correcting poor posture and body mechanics, along with stress management. In addition, prolonged stretching exercises 784

with neuromuscular re-education may be beneficial.65 Localized treatments include spray and stretch technique with vapocoolant spray. Other treatments include trigger point injections with local anesthetics and dry needling.39 Sellman and Mayer studied six patients who had chronic thoracic back pain and were suspected of having TNRD. All patients had pain referred to the abdomen. The main causes of TNRD were osteoarthritis and diabetes. Electromyography revealed acute radiculopathy. All of the patients received treatment with antiinflammatory agents, along with anticonvulsants, tricyclic antidepressants, or local nerve blocks. Symptoms resolved within 6 months of treatment.75 For impairments in posture, joint mobility, muscle performance, and range of motion, along with thoracic intervertebral derangement, an intense physical therapy regimen may lead to more effective thoracic pain control. For example, Austin and Benesky described the biomechanics and alleviation of thoracic pain in a collegiate runner. Examination revealed moderate forward head posture, increased thoracic kyphosis, decreased lumbar lordosis, shoulder depression, decreased thoracic range of motion, and painful trunk rotation. Three weeks of mobilization, high-velocity, low-amplitude manipulation (HVLA), along with multiplanar therapeutic exercise and postural education drastically improved symptoms and function.110 Other muscular causes of thoracic pain such as myofascial pain syndromes may be treated with some similar techniques such as therapeutic exercise, prolonged stretch, and postural and neuromuscular education. In severe cases, additional use of muscle relaxants, trigger point injections, or acupuncture may be helpful.65

SUMMARY Thoracic pain may be due to a variety of causes. It is helpful to categorize the pain into axial and nonaxial components. Etiologies of thoracic axial pain may be due to disc herniation, osteoarthritis and canal stenosis, fractures due to trauma, and primary and secondary tumors as well as osteoporosis. Other culprits include spinal infections such as discitis and osteomyelitis. Deformities of the spine itself such as scoliosis and kyphosis and rheumatologic diseases such as ankylosing spondylitis may also contribute to thoracic axial pain. Nonaxial etiologies can be stress fractures, intercostal neuralgia, post-thoracotomy pain syndrome, postherpetic neuralgia, and inflammatory disorders such as costochondritis and Tietze’s syndrome. Postural abnormalities, muscle strains, and muscle pain syndromes are also in the differential. Each of these entities present with distinct signs and symptoms, which can be differentiated by relevant laboratory studies and radiographic images in addition to a thorough history and physical examination. Based on the diagnosis, appropriate management can lead to more effective pain control and functional improvement.

Acknowledgment The authors would like to thank Ms. Jamie Elaine Frizzell for her assistance in the production of this chapter.

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PART 3

SPECIFIC DISORDERS

Section 4

Biomechanical Disorders of the Thoracic Spine

CHAPTER

Injection Procedures

73

Jan Slezak and Milan P. Stojanovic

INTRODUCTION

Anatomical considerations

Perhaps because of a reduced potential for injury, the prevalence of painful disorders of the thoracic spine is significantly less than disorders of the cervical and lumbar spine. Protection against injury may be due to increased stability afforded by the rib cage1,2 and the steep orientation of the spinous processes that limits excessive extension. Stolker at al.3 reported a 5:2:20 ratio of cervical: thoracic:lumbar complaints of spinal pain in a series of patients seen at a pain clinic. Similarly, Occhipinti et al.4 surveyed factory workers and found a prevalence of thoracic spine symptoms of 5% compared to 24% for cervical and 33% for lumbar. In addition, Linton et al.5 reported the prevalence of spinal pain in Sweden in 35–45-year-olds to be 66.3% and found a 56% incidence of low back pain, a 44% incidence of neck pain, and a 15% incidence of upper back pain. Bogduk6 logically postulated that for any structure to be a cause of back pain it should have a nerve supply, for without access to the nervous system it could not evoke pain. The structure should be capable of causing pain similar to that seen clinically. Ideally, this should be demonstrated in normal volunteers, for inferences drawn from clinical studies may be compromised by observer bias or poor patient reliability. Further, the structure should be susceptible to diseases or injuries that are known to be painful and should have been shown to be a source of pain in patients using diagnostic techniques of known reliability and validity. The potential sources of thoracic pain therefore include intervertebral discs, zygapophyseal joints, costotransverse and costovertebral joints, dura mater, nerve roots, ligaments, and muscles. However, referred pain from visceral sources such as lung, pleura, heart, aorta, gallbladder, esophagus, and mediastinal pathology must not be missed.7,8

Thoracic zygapophyseal joints are true synovial joints. The joints and capsules have nerve plexus formations and some free nerve endings capable of nociceptive transmission. The adventitia of the blood vessels supplying the Z-joints and the cancellous bone of the vertebral bodies contain unmyelinated nerve fiber plexuses that give rise to pain when irritated by various mechanisms. Mechanisms include abnormal postural stress caused by kyphosis and scoliosis, edema from direct trauma or inflammation, direct compression of innervated connective tissues by bone fragments, neoplasms, and acute natural inflammatory response or iatrogenic inflammatory responses secondary to injected hypertonic saline solutions. Nerve fibers converge into medial branch of the primary posterior ramus and relay in dorsal root ganglion prior to entering the spinal cord. Because intersegmental connections in the thoracic spine are not as pronounced as in its cervical and lumbar counterparts, the pain arising in any particular segment of the thoracic spine is more precisely localized than comparable segmental lesions in upper or lower regions of the vertebral column.14 Encapsulated mechanoreceptors and nociceptors in joint capsules of thoracic and lumbar spine have been demonstrated histologically15 and immunohistochemically.16 These mechanoreceptors respond to different states of excursion, provide proprioceptive sense, modulate protective muscular reflexes, and via nociception signal potential tissue damage in the event excessive force is applied. Consistent with neck mobility, need to position the head accurately in space, and the need for coordinated muscle control for protection and posture the cervical spine has more mechanoreceptors than the thoracic spine. In the experimental study of healthy subjects pain was provoked in 72.5% of 40 tested thoracic T3–4 to T10–11 zygapophyseal joints when injected contrast medium distended the joint capsule.17 Referral pain patterns, although overlapping between segmental levels, were more localized compared to patterns obtained by stimulation of lumbar and cervical joints. The most intense pain was reported one segment below and lateral to the injected joint (Fig. 73.1). Precise borders could not be delineated. The largest inferior referral was 2.5 segments while lateral referral did not cross the posterior axillary line. Two subjects reported interesting referral patterns. In one case the T3–4 injection produced pain in the back and subject also stated that ‘pain went into my lung behind my sternum.’ In another case the T3–4 injection produced pain in the back and the subject also reported that pain ‘like a quarter-sized cylinder went toward my breast bone.’ Referral pain patterns from stimulation of zygapophyseal joints C7– T1 through T2–3 and T11–12 were described by Fukui et al. in 1997 (Fig. 73.2).18 A total of 21 joints were injected in 15 patients with previously documented zygapophyseal joint pain. At C7–T1 all patients

THORACIC ZYGAPOPHYSEAL JOINT PAIN Although the thoracic zygapophyseal joint pain is under-reported, the cervical zygapophyseal joints have been extensively studied9–12 and are considered a common cause of spinal pain. There are, however, a few thoracic studies. Manchikanti et al. performed controlled comparative local anesthetic blocks of thoracic medial branches in 46 patients to determine the prevalence of zygapophyseal joint pain.13 Inclusion criteria required failure of conservative management with physical therapy, chiropractic management with physical therapy, absence of radicular pattern of pain, absence of disc herniation, and duration of pain for more than 6 months. Forty-eight percent of patients had positive response to double blocks. Interestingly, a false-positive rate of 58% was seen with single blocks.

787

Part 3: Specific Disorders T4/5

T3/4

T6/7

T5/6

T8/9

T7/8

T10/11

T9/10 T1 T5

T10

Fig. 73.1 Referral pain patterns from stimulation of zygapophyseal joints T3–4 to T10–11 (Adapted from Dreyfuss et al. Thoracic zygapophyseal joint patterns: a study of normal volunteers. Spine 1994; 19(7):807–811).

L5

C7/T1 T1/2 T2/3 T3/4 T1

T5

T10

L5

Fig. 73.2 Referral pain patterns from stimulation of zygapophyseal joints C7–T1 through T2–3 and T11–12 (Adapted from Fukui et al. Regional Anesthesia 1997; 22(4):332–336).

described pain in paravertebral region extending towards the superior angle of scapula, into interscapular region, and to the inferior angle of scapula. Lateral extension toward the shoulder and suprascapular region was described by two patients. T1–2 stimulation referred into interscapular region and to the inferior angle of the scapula. In two subjects referral was reported into the superior angle of the scapula and suprascapular region. Stimulation at T2–3 joint provoked pain laterally toward the interscapular area and caudally toward the inferior angle of the scapula. T11–12 joint injection referred pain into localized area around the injection and one patient described pain over iliac crest. The authors conclude that referral maps from stimulation 788

of joints at levels of C7–T1 to T2–3 provided such a large overlap that their clinical usefulness in tracking the origin of pain is limited. Anatomical dissection confirming the C7 and C8 medial branches traveling to T2 and T3 level17 may explain this observation. Although lumbar facet denervation was introduced in 1974,19 the procedure was not properly performed until Bogduk20 described the anatomical course of the lumbar medial branches in 1979. Percutaneous facet denervation was reported in thoracic Z-joints,3 but the study offered no data on the detailed surgical anatomy of the thoracic medial branches. The targeted points for the thoracic medial branches were at a location that was analogous to the position of the lumbar medial branches proposed previously20 at the junction between the superior articular process and the transverse process. In 1994, Stolker et al. published the data from the anatomical study of two thoracic cadaveric spines, where the cannula was placed under fluoroscopic guidance into a target point at the junction of the base of the superior articular process and the transverse process.21 The specimens were then frozen and sectioned with the heavy-duty cryomicrotome. It was observed that although the cannulas were placed reproducibly onto the osseous targets, the medial branch ‘stem’ was never found within the reach of the electrodes. The authors concluded that if the medial branch ‘stem’ is supposed to be the target, a more anterior, more cranial, and more lateral position would perhaps be more effective. In contrast to the course of the lumbar medial branches, which are at the junction of superior articular process and the transverse process, the medial branch of the thoracic dorsal ramus has a different anatomical location (Figs 73.3, 73.4). Cadaveric dissection of 84 medial branches by Chua and Bogduk revealed the thoracic medial branch arose from the dorsal ramus typically 5 mm lateral to the intervertebral foramen, traversed laterally, dorsally, and inferiorly, and remained posterior to the superior costotransverse ligament.22 After leaving the intertransverse space the medial branch crossed the superolateral corner of the transverse process below (e.g. T3 medial branch and T4 transverse process) and then passed medially and inferiorly across the posterior surface of the transverse process. In its course over the dorsal aspect of the transverse process the nerve was sandwiched between the multifidus muscle anteriorly and the semispinalis thoracis posteriorly. This was the typical course at the levels of T1–4 and T9–10. The T11 medial branch crossed the lateral aspect of base of the superior articular process of T12 vertebra, the transverse process of which is much shorter that other transverse processes. The T12 medial branch had an analogous course to that of the lumbar medial branches at the junction of superior articular and the transverse process of L1. At midthoracic levels (T5–8) the medial branch did not always assume contact with the transverse process and often demonstrated cephalad displacement. The nerve, after making a turn medially in the intertransverse space, descended only slightly inferiorly and remained separated from the transverse process by the fascicles of multifidus muscle.22 Two articular branches were noted to arise from the medial branches. A short ascending branch separated from the medial branch inferior to the Z-joint and innervated the inferior capsule of the joint. A descending articular branch arose from the medial branch at the superolateral border of the transverse process and in its sinuous course through the multifidus muscle reached and innervated the superior capsule of the joint below.22 The medial branches in upper thoracic segments are musculocutaneous, while lower have only muscular distribution.7 Based on these data, the appropriate target for thoracic medial branch block at T1–3 and T9–10 levels is the superolateral corner of the transverse process where the nerve lies against the osseous structure. For radiofrequency denervation the probe, upon contacting the

Section 4: Biomechanical Disorders of the Thoracic Spine T1

T11–12 demonstrated both disc and Z-joint and costovertebral joint degeneration.

Zygapophyseal joint

Diagnostic injections

Transverse process Spinous process

Interspinous ligament

Fig. 73.3 Anatomical location of thoracic medial branches (Adapted from Chua L1 and Bogduk. Acta Neurochir 1995; 136:140–144).

superolateral corner, should be passed over the edge of the transverse process to be in the contact with the medial branch. Targeting of midthoracic medial branches, due to their different positions, would be more challenging and less reliable. T11 and T12 medial branches are blocked in the same fashion as their lumbar counterparts (junction of the transverse process and the superior articular process). Interestingly, multiple interventional textbooks that have recently been published still describe the techniques of thoracic medial branch blocks and denervation not consistent with current knowledge of anatomy.

Thoracic zygapophyseal joint orientation The articular surface of the joint is inclined anteriorly from the frontal plane at approximately 60 degrees to the horizontal plane, making the inferior portion of the joint more posterior and the cephalad pole more anterior. The joint plane is also rotated along the vertical axis about 20 degrees so that the lateral aspect of the joint is more anterior and the medial aspect of the joint is more posterior. This orientation changes in the low thoracic spine, which is the more vulnerable segment of the thoracic spine. While maintaining the frontal orientation at T10–11, the T11–12 level shows considerable variation with transition to sagittal orientation similar to orientation of zygapophyseal joints in lumbar spine.23 In a cadaveric study of 37 male spines by Malmivaara et al.,23 the authors also observed that at T10–11 level pathological changes were mostly disc degeneration, while at the level of T12–L1 level facet and costovertebral joint degeneration were dominant. The level of

Diagnostic blocks used to temporarily denervate the Z-joints are performed using fluoroscopic guidance with local anesthetic injected into the intra-articular space, onto the medial branch, or both. Injecting 0.1–0.2 mL of nonionic water-soluble contrast agent such as iohexol or iopamidol will confirm the proper placement of the needle tip within the joint. False-positive or false-negative findings may result from extracapsular spread into epidural space during intra-articular injection or intravascular uptake during medial branch block. Extravasation of the local anesthetic beyond the intended target will decrease the specificity of the test by blocking the nociceptive transmission via the sinuvertebral nerve, nerve roots, or spinal nerve. Limiting the volume of the anesthetic agent will increase the specificity. Use of volumes larger than 1 mL or even 0.5 mL may be ‘empirically therapeutic,’ but will likely not have a diagnostic value.24 The sensitivity of the diagnostic test is a function of the patient's pain threshold, pain tolerance, pain level prior to the administered test, experience of the injectionist, ease of the procedure, size of the needle and concurrent soft tissue trauma, and psychological profile. Wilson reported the outcome following intra-articular injection of bupivacaine and triamcinolone in 17 patients,25 of which two had thoracic kyphoscoliosis, seven had a history of spine injury, and eight had no apparent precipitating factors. After reproduction of their usual pain, 13 patients reported immediate benefit for the expected duration from the local anesthetic. Nine patients reported significant improvement for more than 1 month. The technique of the intra-articular thoracic zygapophyseal joint injection has been described by Dreyfuss.17 With the monitored patient in a prone position on a fluoroscopy table the appropriate area is routinely prepped with Betadine and draped in a sterile fashion. A true posteroanterior (PA) projection of thoracic spine is obtained. If the T7–8 zygapophyseal joint, for example, is to be injected, the inferior aspect of this joint will be at the superior aspect of the T8 pedicle. A skin mark is then made at the mid to inferior portion of another pedicle below, i.e. T9. A 25-gauge, 3.5 inch needle is inserted in a 60° angle cephalad toward the target joint. Under intermittent fluoroscopic imaging in PA projection, the needle is advanced towards the superior articular process of T8. The needle should remain on the imaginary line connecting the centers of the T8 and T9 pedicles in order to avoid puncturing the pleura laterally or entering the epidural–subarachnoid space medially. Aiming the needle at the inferomedial aspect of the joint may facilitate the joint entry in difficult cases, as this is the most posterior aspect of the joint. As the tip is seen over the mid to superior aspect of the T8 pedicle, the image intensifier is rotated away from the side injected into almost full lateral view until the outline of the joint is clearly visible. The needle is then advanced into the inferior portion of the joint. If the needle is not seen adjacent to osseous structures, manipulation of the needle is performed in the anteroposterior (AP) projection to assure the needle has not strayed lateral or medial. Once the needle is in position, 0.1–0.15 mL of nonionic contrast is administered to confirm the proper placement of the needle. Contrast agent will be observed in superior and inferior recesses of the joint. Local anesthetic (0.5% bupivacaine or 2% lidocaine) with corticosteroid may be injected, but remember that the joint volume is only about 0.5 mL. When firm capsular endpoint is achieved, injection should be stopped to prevent joint capsule rupture. During capsular distension the patient is asked whether concordant pain is reproduced. After the expected onset of anesthesia the patient is asked 789

Part 3: Specific Disorders Articular branches to zygapophyseal joints

Semispinalis thoracis Lateral costotransverse ligament covering costotransverse joint Multifidus Branches of sinuvertebral nerve to epidural vessels Sinuvertebral nerve Spinal nerve

Posterior lamella of the superior costotransverse ligament Costolamellar ligament Anterior lamella of the superior costotransverse ligament Nerve to costotransverse joint

Branches of sinuvertebral nerve to dura mater

Medial branch of dorsal ramus

Sinuvertebral nerve Branches of posterior longitudinal ligament

Lateral branch of dorsal ramus

Radicular artery

Medial and lateral slips of longissimus thoracis

about the pain relief and this is then further observed and recorded in a pain diary for up to 8–24 hours. Dreyfuss reports repeating the joint injection 4 weeks later, up to three times a year if long-term relief is observed. If one can confirm that significant short-duration pain relief consistently occurs after local anesthetic denervation, radiofrequency denervation of the medial branches is the best treatment,17 if one assumes that there is an efficacy similar to that of cervical and lumbar medial branch neurotomies. However, the lack of anatomically based prospective randomized studies evaluating the efficacy of the thoracic medial branch neurolysis precludes the general acceptance of this treatment modality. In summary, the data exist about thoracic facet joint anatomy, referral pain pattern maps in normal volunteers, technique of the procedure, but the studies about therapeutic utility and validity of the procedure are still to come, despite a widespread use of those procedures.

THORACIC DISCOGRAPHY Thoracic provocation discography attempts to confirm or refute the hypothesis that a particular thoracic disc is symptomatic by the concordancy and intensity of pain provoked during disc pressurization with contrast medium. The data obtained are most often used to plan surgical or percutaneous procedures.

Anatomical considerations Thoracic discs and vertebral bodies are innervated by two interconnected nerve plexuses. The ventral nerve plexus is associated with 790

Fig. 73.4 Nerve supply of thoracic spine structures (From Bogduk N. Innervation and pain patterns of the thoracic spine. In: Grant R, ed. Physical therapy of the cervical and thoracic spine, 3rd edn. New York: Churchill Livingstone; 2002:73–81).

the anterior longitudinal ligament and has a bilateral supply from branches of the sympathetic trunk, rami communicantes, and perivascular nerve plexuses of segmental arteries. It is connected to the nerve plexuses of costovertebral joints. The dorsal nerve plexus is made up of the nerve plexus associated with the posterior longitudinal ligament. This nerve plexus is more irregular and receives contributions from the sinuvertebral nerves. Sinuvertebral nerves (recurrent nerves of Luschka) arise as branches from the superior or anterior aspect of the spinal nerves just distal to the dorsal root ganglion after exiting from the intervertebral foramen.8 After 2–3 mm of its course back towards the intervertebral foramen, this somatic root joins with the autonomic root that arises from the gray ramus communicans or sympathetic ganglion at the same segmental level. The sinuvertebral nerve passes through the intervertebral foramen anterior to the spinal nerve and nerve roots. Its branches innervate vertebral lamina, and periosteum of the costal neck. As a part of dorsal plexus it further innervates posterior longitudinal ligament, dura mater, and periosteum of vertebral bodies. Anatomical study of the intervertebral lumbar disc innervation26 also demonstrates distinctive innervation of posterior disc (sinuvertebral nerve) and lateral/anterior disc wall (branches of primary posterior rami and rami communicantes). The assumption that thoracic pain can be generated by thoracic discs is an extrapolation of our knowledge about discogenic lumbar pain. The scientific data are, however, limited and most studies largely describe pain patterns caused by thoracic disc herniations. In a retrospective study of 100 symptomatic patients with magnetic resonance imaging (MRI) documented disc derangement who underwent provocative discography, the authors found discs with annular tears, intrinsic degeneration, and/or associated vertebral

Section 4: Biomechanical Disorders of the Thoracic Spine

endplate infractions to be painful 75% of the time.27 Clinical concordance was about 50%. In this series, the authors observed that in addition to thoracic back pain, extraspinal pain, such as chest wall, intrathoracic and upper abdominal pain, was frequently provoked with thoracic disc injections. They note that location of pain upon provocation appears to relate to the anatomic location of annular tears and may refer to anterior extraspinal sites, such as ribs, chest wall, sternum, and visceral structures within the thorax or upper abdomen. Lateral annular defects often produced radicular-type pain either to visceral or musculoskeletal sites. Posterior annular defects produced back pain either locally or diffusely. The location of provoked sensation was not predictable. The authors stated that the disc with partial annular tears (nonprotruding disc derangements) may be painful and clinically significant, as more than 50% of painful discs fell into this category. The authors did not use antibiotics, and report no incidence of discitis in this series using a thin-needle technique. In this controlled, prospective thoracic discography study, the authors concluded that thoracic discography may demonstrate disc pathology not seen by MRI in asymptomatic individuals and that in truly asymptomatic individual the procedure is not painful. Fiftyfive percent of the discs studied in the symptomatic group were concordant, which, as the authors believe, further establishes thoracic discography as an important tool in investigation of patients with thoracic pain if they are considered candidates for surgical treatment. In addition to history of anaphylaxis to injected agents, pregnancy, inability to communicate the response during the procedure, and concurrent systemic or local infection, the contraindications to the procedure include spinal cord compression with or without myelopathy, bleeding disorder, and anticoagulation therapy. Review of the recent imaging study (MRI, CT, myelography) to evaluate the size of the vertebral canal is necessary prior to the procedure. As described by Schellhas and Pollei27 and complemented by Tibiletti,28 thoracic discography is performed using fluoroscopy with the patient in a prone position. The skin is prepped twice with iodine solution, followed by two rinses with isopropyl alcohol, and sterile drapes are applied. The disc is accessed from the side opposite to patient's clinical pain. If the pain is in the midline, the side of injection is selected based on patient's comfort or individual doctor preferences. A 25-gauge, 3.5 inch spinal needle is advanced through the skin under intermittent fluoroscopic imaging and needle bevel rotation is utilized to control direction. In large patients (over 300 lb) a 5 inch, 22-gauge needle is used. Care is taken to direct the needle lateral to the interpedicular line and medial to costovertebral joints in order to avoid puncture of either the pleura or dura. Needle placement into the upper thoracic discs can be at times technically difficult or even impossible. After annular puncture, the needle is positioned into the center of the disc. Nonionic (e.g. iohexol, iopamidol) contrast agent is injected under fluoroscopic imaging in AP or lateral projection until a firm endpoint is obtained, leakage of contrast medium through annulus is detected, distraction of vertebral bodies occurs, venous opacification is observed, or the patient's pain response prompts the discographer to terminate the injection. The volume of injected contrast and characteristics of the endpoint (firm, gradual, or no endpoint) are recorded. The amount of contrast agent administered is typically 0.6–1.0 mL unless the disc is incompetent and the injectate leaks outside of the disc. In patients with allergy to contrast, sterile saline solution can be injected instead. Spot images are obtained in AP, lateral, and/or oblique projections at each level. The patient's responses are recorded. Provoked sensation is judged concordant versus nonconcordant (familiar versus unfamiliar) relative to clinical pain.

The patient quantifies the pain on a scale 0 to 10 (verbal rating scale or visual analogue scale). Local anesthetic can be injected into painful discs. A positive response is the provocation of 7/10 or higher concordant pain with a negative control disc above and/or below the positive level. Postprocedural care after thoracic discography does not generally differ from care after lumbar or cervical discography with the exception of watching for possible signs and symptoms of pneumothorax. If one stays behind the rib during needle insertion, a pneumothorax should not, however, occur.

COSTOVERTEBRAL JOINT INJECTION T1 and T10–12 vertebral bodies have a single costal facet posterolaterally at the root of the pedicle for articulation with the head of the rib. Occasionally, T10 may share the pattern of T2–T9 levels where the head of the rib articulates with the demifacets at the superior aspect of the ipsisegmental vertebral body and the inferior aspect of the vertebra above.

Anatomical considerations The radiate ligament fans out superiorly, anteriorly, and inferiorly from the head of the rib and attaches the rib to the vertebral body (bodies). The intra-articular ligament bonds the apex of the rib head to the intervertebral disc and divides the synovial cavity into upper and lower halves. Neurohistological documentation of mechanoreceptors and nociceptors has been previously described in the articular tissue of costovertebral joints.29 Innervation of the costovertebral joint is provided by nerve plexuses receiving fibers from the sympathetic trunks and perivascular nerve plexuses in bisegmental fashion, i.e. from the same level and from the adjacent level above.30 Pain referral maps are not available for costovertebral joints. Radiographic changes in CV joints,31 symptomatic CV joint derangement in ankylosing spondylitis, seronegative spondyloarthropathy, rheumatoid arthritis, and functional costovertebral dysfunction was previously suggested in several reports.32–36 Costovertebral joint arthrography was described first in 1988.37 Five cases of CV arthropathy with pain referred into the abdomen and the loin are reported. At T11 and T12 levels, the authors performed costovertebral arthrography, which reproduced concordant pain. Injection of corticosteroid that followed resulted in long-term relief of pain. The joint space is visualized using an oblique discography projection. The needle is advanced dorsomedial to the rib, lateral to the lamina, above the transverse process, and above the superior aspect of the disc, slightly lateral to the discography entry point in the oblique view. Less than 1 mL of solution is injected, including contrast medium, local anesthetic, and corticosteroid. Benhamou et al. studied 28 patients with costovertebral arthropathies who presented with pseudovisceral pain.36 The patients were worked up for chest, abdomen, and flank pain thought to represent the disease of genitourinary, gastrointestinal tract, heart, lung, and pleura. The initial working diagnoses were renal colic, angina pectoris, pulmonary embolism, and spinal tumor. After visceral pathology was ruled out, the musculoskeletal diagnosis was established by clinical examination, reproduction of pain with stressing of the CV joint mechanically, radiological studies, costovertebral arthrography, and anesthetic and corticosteroid injection of the joint. Pathology responsible for costovertebral arthropathy included ankylosing spondylitis, osteoarthritis, diffuse idiopathic skeletal hyperostosis, and degenerative arthropathies other than osteoarthritis. 791

Part 3: Specific Disorders

COSTOTRANSVERSE JOINT INJECTION

10. Barnsley L. Lord S. Bogduk N. Comparative local anaesthetic blocks in the diagnosis of cervical zygapophysial joint pain. Pain 1993; 55(1):99–106.

Anatomical considerations

11. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns I: a study in normal volunteers. Spine 1990; 15:453–547.

Articulation between the facet of the transverse process and the tubercle of the rib forms the costotransverse joint at the levels of T1–10. The lower levels of T11 and T12 lack this joint. T1–5 joint surfaces are reciprocally curved,6 while the lower levels are planar. The joint plane at the rib tubercle is convex and the facet on the transverse process is concave. The costotransverse joint is a synovial articulation and has a thin capsule. The joint is reinforced by the costotransverse, lateral costotransverse, and superior costotransverse ligaments. Innervation is from the articular branches of dorsal ramus and is not strictly segmental.29 Furthermore, each joint is provided with an accessory innervation through twigs derived from the segmentally related intercostal nerves and intramuscular branches of the nerves supplying the multifidus muscle.29 Neither studies in volunteers for the purpose of obtaining referral pain maps nor studies demonstrating pain relief after injecting the painful joint with local anesthetic are available to date. As described by Lau and Littlejohn,38 a needle is directed into the joint using an oblique fluoroscopic imaging at 45–60 degrees ipsilaterally. Due to the high contrast between the spine and lung tissue, coning is recommended to improve visualization. After administration of local anesthesia into skin, a 22-gauge spinal needle is inserted into the joint. The patient is asked to rotate slowly from side to side and the needle tip is observed to be in the same relationship to the joint. After confirmation of proper position of the needle tip in the joint, 0.2 mL of contrast agent with 1 mL of local anesthetic with corticosteroid is administered.

EPIDURAL STEROID INJECTIONS Fluoroscopically guided thoracic epidural injections are often used to decrease middle column inflammation caused by thoracic disc herniations, but publications are few and there is no proof that they are or are not effective compared to placebo. Similarly without proof, thoracic epidural injections may be helpful in decreasing postherpetic neuralgia in the first 2–3 months after onset. Complications are rare but include infection, hematoma, spinal cord injury, pneumothorax, and hiccups.39

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13. Manchikanti L, Singh V, Pampati V, et al. Evaluation of the prevalence of facet joint pain in chronic thoracic pain. Pain Phys 2002; 5:354. 14. Wyke B. The neurological basis of thoracic spinal pain. Rheumatol Phys Med 1970; 10(7):356–367. 15. McLain RF, Pickar JG. Mechanoreceptors endings in human thoracic and lumbar facet joints. Spine 1998; 23:168. 16. Giles LG, Harvey AR. Immunohistochemical demonstration of nociceptors in the capsule and synovial folds of human zygapophyseal joints. Br J Rheumatol 1987; 26(5):362–364. 17. Dreyfuss P. Thoracic zygapophyseal joint patterns: a review and description of an intra-articular block technique. Pain Dig 1994; 4:44–52. 18. Fukui S, Ohseto K, Shiotani M. Patterns of pain induced by distending the thoracic zygapophyseal joints. Reg Anesth 1997; 2(4):332–336. 19. Shealy CN. Facet denervation in the management of back and sciatic pain. Clin Orthopaed Rel Res 1976; 115:157–164. 20. Bogduk N, Long DM. The anatomy of the so-called ‘articular nerves’ and their relationship to facet denervation in the treatment of low-back pain. J Neurosurg 1979; 51(2):172–177. 21. Stolker RJ, Vervest AC, Groen GJ. The management of chronic spinal pain by blockades: a review. Pain 1994; 58(1):1–20. 22. Chua WH, Bogduk N. The surgical anatomy of thoracic facet denervation. Acta Neurochir 1995; 136:140–144. 23. Malmivaara A, Videman T, Kuosma E, et al. Facet joint orientation, facet and costovertebral joint osteoarthrosis, disc degeneration, vertebral body osteophytosis and Schmorl's nodes in the thoracolumbar junctional region of cadaveric spines. Spine 1987; 12:458–463. 24. Raymond J. Intra-articular facet block: diagnostic tests or therapeutic procedure? Radiology 1984; 151:333–336. 25. Wilson PR. Thoracic facet joint syndrome – a clinical entity? Pain Suppl 1987; 4:S87. 26. Bogduk N, Long DM. Percutaneous lumbar medial branch neurotomy: a modification of facet denervation. Spine 1990; 5(2):193–200. 27. Schellhas KP, Pollei SR. The role of discography in the evaluation of patients with spinal deformity. Orthop Clin N Am 1994; 25(2):265–273. 28. Tibiletti C. Practice guidelines: thoracic discography. In: Syllabus of ISIS 11th Annual Scientific Meeting, Orlando, FL, August 8, 2003. 29. Wyke B. Morphological and functional features of the innervation of the costovertebral joints. Folia Morphologica 1975; 23(4):296–305. 30. Groen GJ, Baljet B, Drukker J. Nerves and nerve plexuses of the human vertebral column. Am J Anat 1990; 188(3):282–296. 31. Sanzhang C, Rothschild BM. Zygapophyseal and costovertebral/costotransverse joints: an anatomic assessment of arthritis impact. Br J Rheumatol 1993; 32(12):1066–1071. 32. Le T, Biundo J, Aprill C, et al.. Costovertebral joint erosion in ankylosing spondylitis. Am J Phys Med Rehabil 2001; 80(1):62–64. 33. Ellrodt A, Goldberg D, Oberlin F, et al. Erosive arthritis of the costovertebral joint in seronegative spondyloarthropathy. J Rheumatol 1986; 13(2):452–454. 34. Pascual E, Castellano JA, Lopez E. Costovertebral joint changes in ankylosing spondylitis with thoracic pain. Br J Rheumatol 1992; 31(6):413–415. 35. Arroyo JF, Jolliet P, Junod AF. Costovertebral joint dysfunction: another misdiagnosed cause of atypical chest pain. Postgrad Med J 1992; 68(802):655–659. 36. Benhamou CL, Roux C, Tourliere D, et al. Pseudovisceral pain referred from costovertebral arthropathies. Twenty-eight cases. Spine 1993; 18(6):790–795. 37. Benhamou CL, Roux C, Gervais T, et al. Costovertebral arthropathy. Diagnostic and therapeutic value of arthrography. Clin Rheumatol 1988; 7(2):220–223.

7. Bogduk N. Innervation and pain patterns of the thoracic spine. In: Grant R, ed. Physical therapy of the cervical and thoracic spine, 3rd edn. New York: Churchill Livingstone; 2002:73–81.

38. Lau LS, Littlejohn GO. Costotransverse joint injection: description of technique. Austral Radiol 1987; 31(1):47–49.

8. Wyke B. The neurological basis of thoracic spinal pain. Rheumatol Phys Med 1970; 10(7):356–367.

39. Slipman CW, Shin CH, Patel RK, et al. Persistent hiccup associated with thoracic epidural injection. Am J Phys Med Rehabil 2001; 80(8):618–621.

9. Lord SM, Barnsley L, Bogduk N. The utility of comparative local anesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophysial joint pain. Clin J Pain 1995; 11(3):208–213.

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12. Mooney V, Robertson J. The facet syndrome. Clin Orthop 1976; 115:149–156.

PART 3

SPECIFIC DISORDERS

Section 4

Biomechanical Disorders of the Thoracic Spine

CHAPTER

Thoracic Pain Syndromes

74

Donal F. Harney and Maarten van Kleef

Thoracic pain accounts for approximately 5% of all referrals to the authors’ pain clinic in a University Hospital in the Netherlands,1 which is consistent with that of other clinics.2 Thoracic pain has a varied spectrum of possible etiologies including visceral pain from cardiac and lung pathology to pain from intra-abdominal organs (upper abdominal organs such as gall bladder and pancreas may be referred to the chest). In the lower thoracic regions pain must be differentiated from renal pathology.3 Pain from C5 may be referred over the anterior chest, while pain from C6, C7, and C8 may be referred to the scapular region. Thoracic pain may have an underlying pathology such as disc herniations, aneurysms, tumors,5 postoperative sternal wound infection,6 trauma,7 old fractures, or herpetic infections,8 and stress fractures in athletes.9,10 Chronic postsurgical pain has been described following many different operations, most notably thoracotomy, mastectomy, and coronary artery bypass grafting (CABG) postsurgical pain syndromes.11–15 However, in most cases of thoracic pain there is no specific pathology identified as the cause of the pain and by default the pain is judged to be of spinal origin, emanating from nociceptive nerve endings in the periosteum, ligaments, discs, or joints.16 Diagnostically and clinically, thoracic pain can be divided into thoracic mechanical joint pain and thoracic segmental pain. An appreciation of the intricate anatomy of the thoracic spine is required to understand the various pain syndromes of the thoracic spine. It is somewhat surprising that there is any mechanical pain in the thoracic spines since it is a relatively immobile section of the spine. The range of motion for both flexion and extension is of the order of 10°, and lateral flexion is minimal. Rotation of the thoracic spine provides the only meaningful movement of the thoracic spine. Pain in the thoracic region may come from the articulations with ribs, costovertebral joints between the rib and the vertebral body, and the costotransverse joints between the transverse process and tubercle of the rib. The costotransverse joints are absent at T1, T11, and T12.

THORACIC MECHANICAL PAIN FEATURES Clinical syndrome Thoracic mechanical pain includes pain from both thoracic facet joints and thoracic discs. Pain emanating from thoracic facet joints is usually related to degenerative processes, vertebral collapse, and continuous mechanical straining.16–18 The initial problem can be in the facet joint but may be elsewhere in the spine.19 As with lumbar and cervical facet syndromes there are no specific criteria which have been established whereby facet joint pain could be diagnosed based on patient’s history and/or physical examination. A diagnosis of thoracic facet joint

syndrome can be made based on similarity of symptoms to lumbar and cervical facet syndromes. Extensive examination should be performed to exclude any other pathology as a primary cause for the patient’s signs and symptoms. In 1993, Stolker et al. defined ‘major’ and ‘minor’ criteria for the diagnosis of thoracic facet joint pain.18 Major criteria include: 1

2

Continuous or nearly continuous unilateral or bilateral paravertebral pain in a distinct thoracic area of the back, in the absence of objective neurological signs. Tenderness over paravertebral muscles in the same region by palpating the facet joints. Minor additional diagnostic criteria include:

1 2 3 4 5 6

Exacerbation of all complaints following back movements, most notably hyperextension and rotation. Pain aggravated more in sitting position than in other positions. Localization of radiation (if present) in more than one segment but not extending through a complete segment. Decreased or absent mobility in the painful region of the back Radiological signs (although uncommon) may illustrate slight rotation and curvature of the vertebral column. Related abnormalities may be found in addition to facet joint syndrome – osteoporosis, vertebral collapse, and arthritis.

When thoracic spinal pain becomes chronic and resistant to conservative modalities of treatment such as physical therapy, pharmacological therapy, and transcutaneous electric nerve stimulation (TENS), more aggressive treatment of thoracic pain including radiofrequency ablation of the facet joints can be considered.

Indications for radiofrequency procedures These criteria were the basis for a study by Stolker et al. when they evaluated 40 patients who had a diagnosis of thoracic facet syndrome based on the above-mentioned criteria. These patients underwent percutaneous facet joint denervation (PFD). Included were 24 left sided, 21 right sided and 6 bilateral cases. Seven study patients underwent two sessions and two patients had three PFD sessions. Eighty-two percent of patients had 50–75% pain relief at 2 months. Four patients were lost to long-term follow-up (18–54 months; mean 31 months). Forty-four percent of study patients were pain free while 39% had a 50% or greater reduction in their pain.18 Interestingly, considering that these criteria were non-specific for thoracic facet syndrome, all patients in this study had positive diagnostic blocks performed prior to radiofrequency ablation. Stolker et al. attributed the results to the consistent course that the medial branch of the dorsal rami of the thoracic spinal nerves travel as they leave the intertransverse space; 793

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however, the anatomical target point (junction between the superior articular process and the transverse process) utilized in their study is at variance with the anatomical course of thoracic medial branch described by Chua and Bogduk.20 Chua and Bogduk reported that the medial branch crosses the superolateral corner of the transverse processes and then passes medially and inferiorly along the posterior surfaces of the transverse processes, before entering the multifidus muscle which it supplies.20 Chua and Bogduk have called for the need for a double-blind, controlled clinical trials of Stolker et al.’s approach to thoracic facet nerve denervation or modification of their procedure so as to be consistent with the surgical anatomy of the thoracic medial branches.20 In another study by Tzaan and Tasker in 2000 which evaluated 17 patients with thoracic facet syndrome, 15 patients had satisfactory pain relief at follow-up with 2 patients having their procedure repeated.21 Pevsner et al. evaluated radio frequency ablation in 122 patients with mechanical spinal pain at cervical (20%) and thoracolumbar (80%) levels. At 1-year follow-up 63% had good results (at least 50% decrease in pain levels) and 37% had no effect (<30 % reduction in their pain levels).22

Side effects and complications Spinal thermocoagulation procedures are generally free from side effects other than local contusion and edema at the needle sites. The most common side effect was sensory loss and neuropathic pain in the distribution of the cutaneous branches of the posterior rami.21 Minor complications occurred in 27 patients (22%) who had transient discomfort and burning pain.22 Serious complications of radiofrequency are fortunately rare when optimum target point needle positioning is utilized, i.e. in the lateral facet line on the anteroposterior (AP) projection and posteriorly in the foramen on the transverse projection.

Outcomes While the evidence base is low in the management of thoracic facet pain there is evidence to support the use of percutaneous radiofrequency procedures as therapy.18,21,22

THORACIC DISC LESIONS Clinical syndrome Thoracic disc lesions account for 0.5–2% of all disc lesions.23,24 Symptomatic disc disease is thought to be an uncommon problem with a prevalence of asymptomatic cases of 14.3%.25 Degenerative disc disease is more commonly found in the lower thoracic spine with the upper third (T1–2 to T4–5) being the least affected area.26,27 However, T1–2 is the most common level affected when the upper thoracic spine is involved.28 Recently, Arana et al., in a study of 156 patients with cervical disc pain, reported that 13.4% of these patients had degenerative changes in the upper thoracic spine, most notably at T2–3, with correlation between degenerative disc contour at the C7–T1 level and T1–2, T2–3, T3–4.29 Girard, in another study, evaluated temporal changes in thoracic disc in 40 patients with pain.29a Baseline presence of disc herniation was 10%, degenerative disease 14%, endplate marrow signal alteration 2.3%, Schmorl’s nodes 9.6%; follow-up was 4–149 weeks. Repeat scan revealed a new incidence of disc herniation of 1.5%, degenerative disc disease 2%, all findings predominated in the lower thoracic vertebrae T6–10. Herniations showed the most ability to 794

modify over time with just over one-quarter (27%) showing change. Schmorl nodes showed the least change over time.29 While the majority of prediction indicator studies have been done on lumbar spine, one can infer that a similar clinical picture holds for the thoracic spine. A tissue can only generate pain if it is innervated. In a normal human lumbar disc, nerve endings can only be found in the periphery of the outer anulus at a depth of a few millimeters.30 In highly degenerated discs nerves may even penetrate into the nucleus pulposus.31 Most of these nerve fibers, which are identified by immunohistochemistry, accompany blood vessels relating probably to vasoregulation. Another set of neural fibers has been found in the nucleus of painful discs of those undergoing anterior fusion surgery for low back pain. These neural structures express substance P and have a morphology of nociceptive nerve terminals. These findings emphasize the role of nerve terminals of the degenerated disc in the pathology of back pain and make the distinction between painful disc disease and nonpainful disc disease degeneration more plausible. Discography has been regarded as the gold standard in the diagnosis of discogenic pain. Discographic studies have shown that only annular ruptures extending to the outer anulus reproduce exact or similar pain to that previously described by the patient.32 Discography has been widely used to study and compare to magnetic resonance imaging (MRI) findings of patients with discogenic pain. In addition to annular ruptures, potential discogenic signs on MRI include high intensity zones (HIZs) lesions and endplate degeneration known as modic changes.33 HIZ lesions are not as useful in predicting which individuals will have discogenic pain34 compared with modic changes which are a more reliable imaging predictor of discogenic pain.35 Thoracic discography has been utilized by Schellhas et al. in a study of 100 patients with clinical pain and MRI imaging with morphologically abnormal thoracic disc(s). Abnormal thoracic discs on MRI and at least one control disc adjacent to the abnormal discs were injected with nonionic contrast or normal saline, X-rays were obtained, and pain was rated in intensity from 0 to 10. Discs with annular tears were found to be painful approximately 75% of the time (with a clinical concordance of 50%). Control discs were invariably painless. Schellhas et al. concluded that thoracic discography can be performed safely as a tertiary diagnostic procedure to determine if degenerated discs on MRI studies are related to clinical complaints.36 In another study, the Wood et al. evaluated 10 healthy volunteers using MRI and four-level discography. Provocative responses were graded from 0 to 10. The mean pain response was 2.4/10; however, three discs were intensely painful, on MRI 27 discs of 40 were abnormal with endplate abnormalities, annular tears, and/or herniations. In parallel, they evaluated 10 adults, without pending litigation who had thoracic pain; the mean pain response was 6.3/10 on discography. Twentyfour discs were concordantly painful of the 48 discs studied, and MRI revealed that 21 discs were normal; however, on discography only 10 were judged as normal. Schellhas et al. concluded that thoracic discs with prominent Schmorl’s nodes may be intensely painful even in lifelong asymptomatic individuals but the pain is concordant.37 Thoracic intradiscal pressure has been evaluated as an aid in to understanding the biomechanics of thoracic spine.38 Although discography is the gold standard in the diagnosis of discogenic pain, it is an invasive procedure and not employed for routine diagnosis. Unfortunately, in the chronic low back pain patient population no clinical discriminator has been found that can differentiate discogenic from nondiscogenic back pain.39 The bony vibration test, whereby a small hand-held vibrator is used to produce pain provocation, similar to that in discography, has been tried as a noninvasive pain provocation method to be used in combination with MRI in identifying symptomatic disc pathology.40

Section 4: Biomechanical Disorders of the Thoracic Spine

Genetic variations in collagen IX and aggrecan have been held accountable for lumbar disc disease, it is highly probable that similar variations will be accountable for thoracic disc disease.41

Indications for therapies in discogenic pain Treatment programs for discogenic pain include stabilization of the symptomatic motion segments in order to eliminate painful motion,42 but the external validity of spinal fixation is now being compared with conservative care. The results of randomized, controlled trials do not unequivocally support the use of spinal stabilization procedures.43,44 Video-assisted thorascopic (VAT) surgery has been reported to be successful in thoracic disc herniations. Anand and Regan evaluated 100 patients with a minimum of 2 years’ follow-up after VATs for thoracic disc herniation. They reported an overall 84% satisfaction rate with long-term clinical success rate of 70% in this study population.45 The role of intradiscal electrothermal therapy (IDET) has an exciting prospect as future therapy for the management of discogenic pain as an alternative to spinal fusion in selected patients. To date, IDET has been only described in the management of lumbar disc pain. This may prove especially useful for the young patient with preserved disc height and patients with inoperable multilevel disease.46 However, its effects have been described predominantly in lumbar disc pain to date.47 The long-term benefits of IDET therapy still have to undergo the rigorous of clinical trials,48 but for the present its role is as an antecedent rather than alternative to spinal fusion.

Side effects and complications Spinal stabilization procedures are associated with the usual postoperative complications including blood loss and infection. Neurological complication secondary to vascular compromise is fortunately very rare.49

Outcomes For the present, surgical stabilization procedures and conservative management programs form the mainstay of therapy in treating thoracic discogenic pain. The role of IDET is for the present restricted to lumbar disc pain. However, IDET seems a promising therapy, but scientific data regarding the pathophysiology, biologic effects, and clinical results are relatively scarce. Early biomechanical and histological investigations into the effects of IDET are conflicting. However, in early prospective human trials, IDET seems to provide some benefit with low risk. IDET is a potentially beneficial treatment for internal disc disruption in carefully selected patients as an alternative to spinal fusion. More basic science and clinical research with long-term follow-up evaluation is necessary.48 Emerging therapies with monoclonal antibodies are only at a conceptual stage and it will be many years before they are adopted as meaningful therapeutic options in the management of discogenic pain.

THORACIC SEGMENTAL PAIN SYNDROMES Clinical syndrome Thoracic segmental pain syndromes have many etiologies including disease and/or lesions of ribs, disorders of the thoracic skeletal spine (fractures, arthritis, metabolic disorders, and tumors), or neuropathies originating from spinal roots, spinal nerves, or intercostal nerves.16 Some thoracic segmental pain syndromes are iatrogenic postsurgery, such as post-thoracotomy and postmastectomy syndromes and scar tissue pain after upper gastrointestinal surgery.12–15 Percutaneous thoracic sympathectomy is considered the most efficacious for sympathetic mediated pain, Raynaud’s syndrome, hyper-

hidrosis, and vasculopathy.50 Percutaneous radiofrequency adjacent to the thoracic dorsal root ganglion (DRG) has been described for segmental nerve pain related to intercostal pain, rib tip syndrome, twelfth rib syndrome, vertebral collapse, and segmental peripheral neuralgia.

Indications for percutaneous radiofrequency lesioning Stolker et al.51 evaluated 45 patients with thoracic segmental pain who fulfilled the following criteria: 1 2

3 4 5

Patients had radiating pain in the thoracic region that followed a segmental pattern. No response to conservative therapy including pharmacological, physical therapy, and transcutaneous electrical nerve stimulation. Symptom duration longer than 6 months. No causal therapy was available. Temporary response to an intercostal blockade with lidocaine.

Exclusion criteria included patients with loss of sensation in the painful area, such as postherpetic neuralgia, those with major psychiatric illness, and those awaiting a compensation liability suit in progress. Clinical diagnoses included intercostal neuralgia, post-thoracotomy pain syndrome, postmastectomy pain syndrome, twelfth rib syndrome, rib resection, osteoporosis, vertebral metastasis, and traumatic collapsed vertebra. The 45 patients participating in this study underwent 53 percutaneous radiofrequency procedures adjacent to the dorsal root ganglion, 37 at one level, one patient bilaterally at one level, and seven patients at two levels unilaterally. At first evaluation (using a five-grade evaluation scale) 2 months postprocedure, 66.7% were pain free, 24% obtained more than 50% pain relief, and 9% obtained no pain relief. Four patients were lost to long-term follow up (died from their malignant disease). After a follow-up of 13–46 months (median 24 months) 49% were pain free, 37% had good pain relief, and 14.6% had no pain relief.51 The authors of this study advocate prognostic lidocaine blockade as essential to (1) confirm the diagnosis of segmental pain, (2) determine appropriate level of treatment, and (3) assess potential benefit of percutaneous radiofrequency adjacent to the dorsal root ganglion. In a similar study, van Kleef et al.1 evaluated effects of a singlelevel radiofrequency lesioning adjacent to the dorsal root ganglion in thoracic segmental pain. In this study, 43 patients were evaluated with a minimum of 6 months’ history of unilateral thoracic segmental pain unresponsive to conservative therapies. Twenty-seven of the patients had pain in the distribution of one or two segments (group I) only, while 16 patients had pain in more than two segmental levels (group II). Short-term analysis at 8 weeks postprocedure showed patients in group I were pain free or had good pain relief in 52% of patients, while only 18% of patients in group II were pain free or had good pain relief. Long-term follow-up (36–168 weeks; mean 99 weeks) demonstrated freedom from pain or good pain relief in 37% of patients in group I while only 18% of patients in group II at longterm follow-up (40–160 weeks; mean 128 weeks) were pain free or had good pain relief.

Side effect and complications In the study by Stolker et al., 13% of patients suffered a transient burning pain that subsided within 3 weeks. Four percent of patients suffered a slight sensory loss in the corresponding dermatome, the sensory loss resolved in 3 months. There was no motor loss and 795

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no incidence of pneumothorax.51 In the study by Van Kleef et al., a similar side effect profile was noted with 16% suffering a slight burning pain in the treated dermatome; in addition, 16% of patients had slight hypoesthesia in the treated dermatome at initial follow-up. These side effects had resolved by 12 weeks postprocedure. There was no dysthesias or pneumothorax.1 It is interesting to note in both studies that dorsal root ganglion lesioning above T7 was performed via a hole drilled in the lamina. This was done because the angle of the ribs prevent accurate passage of a needle. A more lateral approach could have been employed in these studies to approach the foramen but, due to the proximity of the pleura, there was a substantial risk of pneumothorax and neither group of authors felt such a technique was justifiable. Complications can occur. Ischemic spinal cord lesions have been reported previously,52 which describe percutaneous radiofrequency lesioning provoking an ischemic lesion on the opposite side to where the lesion was made and one segment lower in two patients. The authors postulated that the lesion was secondary to a ‘steal’ of the local circulation due to the percutaneous radiofrequency spinal lesioning. However, both of these complications were in elderly patients with cardiorespiratory and general vascular disease. Even though radiofrequency is advocated in elderly patients, they are at a higher risk of complication than in the healthy population. When performing radiofrequency procedures, one must be mindful of the blood supply in the thoracic region of the spinal cord. The upper and lower areas are well supplied, but the midthoracic region (T5–8) has poor circulation; the arteries are smaller and less numerous, leaving this region more vulnerable to ischemic lesions.53

Outcomes Radiofrequency lesioning of the dorsal root ganglion is warranted in the management of thoracic segmental pain provided pain is localized to one or two segmental levels only.1

CONCLUSION Thoracic pain syndromes are common in clinical pain practise. Common and uncommon internal diseases should be excluded in this patient group before symptomatic interventions such as radiofrequency (RF) procedures are applied. After careful evaluation by means of diagnostic blocks the longterm outcome of these RF interventions (RF facet and RF-DRG) seems to be acceptable.

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10. Davis BA, Finnoff JT. Diagnosis and management of thoracic and rib pain in rowers. Curr Sports Med Rep 2003; 2:281–287. 11. Kalso E, Perttunen K, Kaasinen S. Pain after thoracic surgery. Acta Anaesthesiol Scand 1992; 36:96–100. 12. Smith WC, Bourne D, Squair J, et al. A retrospective cohort study of post mastectomy pain syndrome. Pain 1999; 83:91–95. 13. Mailis A, Chan J, Basinski A, et al. Chest wall pain after aortocoronary bypass surgery using internal mammary artery graft: a new pain syndrome? Heart Lung 1989; 18:553–558. 14. Bruce J, Drury N, Poobalan AS, et al. The prevalence of chronic chest and leg pain following cardiac surgery: a historical cohort study. Pain 2003; 104:265–273. 15. Kalso E, Mennander S, Tasmuth T, et al. Chronic post-sternotomy pain. Acta Anaesthesiol Scand 2001; 45:935–939. 16. Bonica JJ, Sola AF. Chest pain caused by other disorders. In: Bonica JJ, ed. The management of pain. Philadelphia: Lea & Febiger; 1991:1144–1145. 17. Merskey H, Bogduk N. Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms. 2nd edn. Seattle, WA: IASP Press; 1994. 18. Stolker RJ, Vervest AC, Groen GJ. Percutaneous facet denervation in chronic thoracic spinal pain. Acta Neurochir (Wien) 1993; 122:82–90. 19. Bogduk N, Marsland A. The cervical zygapophyseal joints as a source of neck pain. Spine 1988; 13:610–617. 20. Chua WH, Bogduk N. The surgical anatomy of thoracic facet denervation. Acta Neurochir (Wien) 1995; 136:140–144. 21. Tzaan WC, Tasker RR. Percutaneous radiofrequency facet rhizotomy – experience with 118 procedures and reappraisal of its value. Can J Neurol Sci 2000; 27: 125–130. 22. Pevsner Y, Shabat S, Catz A, et al. The role of radiofrequency in the treatment of mechanical pain of spinal origin. Eur Spine J 2003; 12:602–605. 23. Krämer J. Intervertebral disc disease: Causes, diagnosis, treatment, and prophylaxis. 2nd edn. Stuttgart: Georg Thieme-Verlag; 1990. 24. Vallo MB, Ranshoff RJ. Thoracic disc disease. 2nd edn. Philadelphia: WB Saunders: 1982:500. 25. Matsumoto M, Fujimura Y, Suzuki N, et al. MRI of cervical intervertebral discs in asymptomatic subjects. J Bone Joint Surg [Br] 1998; 80:19–24. 26. Morgan H, Abood C. Disc herniation at T1–2. Report of four cases and literature review. J Neurosurg 1998; 88:148–150. 27. Awwad EE, Martin DS, Smith KR Jr, et al. Asymptomatic versus symptomatic herniated thoracic discs: their frequency and characteristics as detected by computed tomography after myelography. Neurosurgery 1991; 28:180–186. 28. Boutin RD, Steinbach LS, Finnesey K. MR imaging of degenerative diseases in the cervical spine. Magn Reson Imaging Clin N Am 2000; 8:471–490. 29. Arana E, Marti-Bonmati L, Molla E, et al. Upper thoracic-spine disc degeneration in patients with cervical pain. Skeletal Radiol 2004; 33:29–33. 29a. Girard CJ, Schweitzer ME, Morrison WB. Thoracic spine disc-related abnormalities: longitudinal MR imaging assessment. Skeletal Radiol. 2004; 33(4):216–222. 30. Ashton IK, Roberts S, Jaffray DC, et al. Neuropeptides in the human intervertebral disc. J Orthop Res 1994; 12:186–192. 31. Freemont AJ, Peacock TE, Goupille P, et al. Nerve ingrowth into diseased intervertebral disc in chronic back pain. Lancet 1997; 350:178–181. 32. Moneta GB, Videman T, Kaivanto K, et al. Reported pain during lumbar discography as a function of annular ruptures and disc degeneration. A re-analysis of 833 discograms. Spine 1994; 19:1968–1974. 33. Modic MT, Masaryk TJ, Ross JS, et al. Imaging of degenerative disk disease. Radiology 1988; 168:177–186. 34. Carragee EJ, Paragioudakis SJ, Khurana S. 2000 Volvo Award winner in clinical studies: Lumbar high-intensity zone and discography in subjects without low back problems. Spine 2000; 25:2987–2992. 35. Braithwaite I, White J, Saifuddin A, et al. Vertebral end-plate (Modic) changes on lumbar spine MRI: correlation with pain reproduction at lumbar discography. Eur Spine. 1998; 7:363–368. 36. Schellhas KP, Pollei SR, Dorwart RH. Thoracic discography. A safe and reliable technique. Spine 1994; 19:2103–2109. 37. Wood KB, Schellhas KP, Garvey TA, et al. Thoracic discography in healthy individuals. A controlled prospective study of magnetic resonance imaging and discography in asymptomatic and symptomatic individuals. Spine 1999; 24:1548–1555. 38. Polga DJ, Beaubien BP, Kallemeier PM, et al. Measurement of in vivo intradiscal pressure in healthy thoracic intervertebral discs. Spine 2004; 29:1320–1324.

Section 4: Biomechanical Disorders of the Thoracic Spine 39. Schwarzer AC, Wang SC, O’Driscoll D, et al. The ability of computed tomography to identify a painful zygapophyseal joint in patients with chronic low back pain. Spine 1995; 20:907–912. 40. Yrjama M, Tervonen O, Kurunlahti M, et al. Bony vibration stimulation test combined with magnetic resonance imaging. Can discography be replaced? Spine 1997; 22:808–813. 41. Ala-Kokko L. Genetic risk factors for lumbar disc disease. Ann Med 2002; 34: 42–47. 42. Frymoyer JW, Ducker TB, Hadler NM, et al. The adult spine. Principles and practice. Philadelphia, PA: Lippincott; 1997. 43. Fairbank AJ, Frost H, Wilson MacDonald J, et al., The Spine Stabilisation Group. The MRC spine stabilisation trial. A randomized controlled trial to compare surgical stabilisation of the lumbar spine versus an intensive rehabilitation programme on outcome in patients with chronic low back pain. Abstract in the ISSLS meeting, 2004, Porto, Portugal. 44. Fritzell P, Hägg O, Nordwall A, The Swedish Lumbar Spine Study Group. 5–10 years follow up in the Swedish lumbar spine study. Abstract in the ISSLS meeting, 2004, Porto, Portugal. 45. Anand N, Regan JJ. Video-assisted thoracoscopic surgery for thoracic disc disease: Classification and outcome study of 100 consecutive cases with a 2-year minimum follow-up period. Spine 2002; 27:871–879.

46. Saal JA, Saal JS. Intradiscal electrothermal therapy for the treatment of chronic discogenic low back pain. Clin Sports Med 2002; 21:167–187. 47. Pauza KJ, Howell S, Dreyfuss P, et al. A randomized, placebo-controlled trial of intradiscal electrothermal therapy for the treatment of discogenic low back pain. Spine J 2004; 4:27–35. 48. Biyani A, Andersson GB, Chaudhary H, et al. Intradiscal electrothermal therapy: a treatment option in patients with internal disc disruption. Spine 2003; 28:S8–S14. 49. Fessler RG, Sturgill M. Complications of surgery for thoracic disc disease [review]. Surg Neurol 1998; 49:609–618. 50. Wenger CC. Radiofrequency lesions for the treatment of spinal pain. Pain Digest 1998; 8:1–16. 51. Stolker RJ, Vervest AC, Groen GJ. The treatment of chronic thoracic segmental pain by radiofrequency percutaneous partial rhizotomy. J Neurosurg 1994; 80: 986–992. 52. Koning HM, Koster HG, Niemeijer RP. Ischaemic spinal cord lesion following percutaneous radiofrequency spinal rhizotomy. Pain 1991; 45:161–166. 53. Lazorthes G. La vascularisation de la moelle épinière. Rev Neurol 1962; 6: 535–557.

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PART 3

SPECIFIC DISORDERS

Section 4

Biomechanical Disorders of the Thoracic Spine

CHAPTER

Surgery: Thoracic Disc Disease

75

Kirkham Wood

INTRODUCTION Compared with the cervical and lumbar spine, degenerative thoracic disc pathology is relatively uncommon. When present, however, it can produce symptoms of axial or mechanical back pain, radiculopathy, or myelopathy. Surgery is effective for treating many forms of thoracic disc pathology that have failed nonoperative treatment.

INDICATIONS Indications for surgical intervention include myelopathy, progressive neurologic deficit, confirmed radiculopathy, or mechanical axial back pain persisting at an unacceptable level in those who have failed adequate nonsurgical treatment (Fig. 75.1). If surgery is contemplated, it

should be directed at the levels with confirmed pathology as seen on axial diagnostic imaging. Thoracic disc herniations are the most common manifestation of thoracic disc degeneration requiring surgical treatment (Fig. 75.2). With the advent of magnetic resonance imaging (MRI) the frequency with which the diagnosis of a herniated disc is made has increased. It is important to remember, however, that thoracic disc herniations can be seen in an otherwise asymptomatic population. Wood et al.1 found, in their study of asymptomatic individuals, that 37% of those studied had at least one herniation, half of whom had multiple protrusions and many with actual deformation of the spinal cord. In addition, because of the relative paucity of classic clinical findings such as those seen with herniations in the lumbar spine, complaints can often be vague, especially when it is principally axial pain.

Thoracic pain

Non-spinal causes: e.g. gall bladder, retroperitoneal pathology, aortic disease Yes

No Character

Axial (mechanical)

Work-up

Radicular, myelopathic

– Conservative treatment e.g. therapy, NSAIDs Improved

MRI

No improvement

Evaluate costovertebral joints cervical spine + hnp

(–) Continue

MRI

Myelopathy ? +

Yes

Disc degeneration, HNP Discectomy

No

No

Nerve root block Improvement? Yes

Discography Observation + Surgery

– Non-operative treatment

Fig. 75.1 Flow chart diagramming the work-up of a patient presenting with thoracic pain. 799

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Extensive pulmonary scarring such as following previous surgery or radiation, primary or secondary pulmonary diseases precludes the use of video-assisted thoracoscopy for the treatment of degenerated or herniated discs.

TECHNIQUE

Fig. 75.2 Axial MRI image of a thoracic disc herniation.

Historically, a large number of other pathologic conditions including not only lumbar disc disease and neurogenic claudication, but also cardiac, abdominal (e.g. gall bladder), intrathoracic pathologies, and even multiple sclerosis have been mistakenly diagnosed. When myelopathy is found, cervical involvement should be evaluated to rule out concomitant pathology. Making the correct diagnosis begins with MRI, especially for evaluating mechanical back pain. When evaluating spinal cord encroachment, myelography with computed tomography (CT) is another option, but it is invasive, although its sensitivity and specificity are comparable with that of MRI.2,3 CT can also be used to describe calcifications at the disc level, or ossification of the posterior longitudinal ligament or ligamentum flavum. Defining the precise pathology is important, as it will often influence the surgical approach. Many feel that obtaining both an MRI as well as a CT-myelogram is indicated for those scheduled for surgery. In instances where the presentation is less clear – typically mechanical or axial pain – further confirmation of the pathology can be obtained with discographic evaluation. When performed by experienced and skilled technicians, it is a safe and reliable procedure to confirm and locate the site of axial thoracic pain.4,5 It can be especially useful in situations of multiple levels of thoracic pathology with varying grades of disc herniations. A strict contraindication, however, is a large prolapse with spinal cord deformation wherein the instillation of a saline contrast would run the risk of further cord compression. Thus, discography is probably somewhat limited to those situations of smaller or no actual disc protrusion.

CONTRAINDICATIONS Because the presentation of thoracic degenerative pathology can be so vague, and because it can mimic so many other nonspinal conditions, all other possible sources of chest wall pain or myelopathic neurology should be ruled out. It is notable that the presence of any other etiology would be a contraindication to isolated thoracic decompression and/or fusion. Other spinal conditions affecting the cervical spine should be ruled out, especially in the presence of suspected clinical myelopathy. Scoliosis as a cause of thoracic pain, as well as fractures, is a contraindication to isolated thoracic decompression. Infections, tumors, metastasis, skin disorders, and metabolic bone disease are other contraindications to the surgical approach described below. 800

Numerous surgical approaches have been described for the treatment of thoracic disc pathology (Fig. 75.3). In general, a degenerated disc that is believed to be the source of axial back pain can be treated with a subtotal discectomy and interbody fusions. This applies, in the author’s view, to those situations in which the pathology extends over one or two levels. It is the author’s view that for pathology that extends over several levels, a stabilizing posterior instrumented fusion with or without an anterior fusion is an option for axial back pain, in the properly selected individual. Here, discography may well help the decision-making process. For neuropathology due to herniated discs, typically an anterior decompression and fusion is preferred unless the disc is well-confined laterally and accessible posteriorly. Posterior laminectomies are generally regarded as poor approaches for decompression of an anteriorly compromised spinal canal because of a historically high rate of unimproved or worsened neurological status.6 One review of 135 patients treated with laminectomy noted almost one-third being made worse by the procedure.7 It is notable that a compromised spinal cord stands a greater chance of worsening neurological deficits with manipulation than does a healthy one. The other surgical approaches can decompress the thoracic spinal canal without manipulating the spinal cord. Compressive neuropathy from a primarily posteriorly based pathologic process, such as that seen in ossification of the ligamentum flavum, can effectively be treated with a posterior approach. The transthoracic approach is the most straightforward method of decompressing anteriorly based compression of the spinal cord and carries the highest likelihood of achieving neurological improvement with a relatively lower incidence of serious complications.8 The entire disc space can be seen and wide decompression performed without any manipulation of the spinal cord (Fig. 75.4). The chest is entered one or two levels above the herniation via a thoracotomy. The rib head overlying the disc space is removed, followed by removal of the base of the pedicle, allowing visualization of the dura. The posterior third of the adjacent endplates is removed, creating a cavity into which the posterior cortex plus the protruding disc fragment can then be safely pulled and then removed with a curette. If deemed necessary, intervertebral strut grafts and even anterior instrumentation can be facilitated by this approach. Normally, decompressions within the middle and upper thoracic spine are well stabilized by the rib cage, and are not rendered unstable. Large decompressions within the more mobile thoracolumbar region may require arthrodesis to prevent instability. Axial back pain may well be helped by a fusion, but no study yet exists that has compared discectomy with fusion for the surgical treatment of axial thoracic back pain. Disadvantages of this approach include the need for a thoracotomy with the possibility of a diaphragmatic take-down and risk of postoperative complications such as pneumothorax, pulmonary contusion, pneumonia, effusion, and atelectasis. Thoracoscopy is a relatively recent technology which can allow thoracic discectomy,9 fusion with bone graft, if desired, and even instrumentation. Thoracoscopy is best suited for soft (noncalcified) herniations and degenerative discs. It holds the possibility of less morbidity when compared with the traditional transthoracic approach. A thoracic surgeon, well trained in this technique, may be recommended as well as time spent in the training laboratory before beginning. The major advantage of video-assisted thoracoscopic

Section 4: Biomechanical Disorders of the Thoracic Spine HNP?

No?

Yes?

1. Ossification of ligamentum flavum

Posterior, posterolateral?

(Posterior decompression)

No? (far lateral)

Yes?

2. Degenerative spondylosis

Posterior decompression (transpedicular)

Hard (calcified)?

1–2 levels? (discogram positive; no worker’s compensation, litigation, etc.)

No?

No?

Yes?

Thoracoscopy

Transthoracic costotransversetomy

Posterior decompression

Yes? (Transpedicular, costotransversectomy)

Fusion

Discectomy Multiple levels?

No?

Yes?

Consider fusion

Decompression alone

Fig. 75.4 The approach (arrow) and bony resection (hatched lines) in the transthoracic approach.

surgery is that it avoids a large open thoracotomy with its attendant morbidity – chest wall pain, shoulder dysfunction, longer hospitalization – but the learning curve is large and a direct comparison with open procedures is still lacking. Anand and Regan10 described their experience with 100 patients and felt they were able to achieve clinical results similar to open thoracotomy techniques. The costotransversectomy approach may be indicated under certain circumstances such as when a disc herniation is in an extremely posterolateral position or when the pathology is in the uppermost thoracic spine, an area sometimes difficult to reach with a transthoracic approach (Fig. 75.5). One to three rib heads as well as the transverse processes are usually removed with this approach, hence the name. Occasionally, the intercostal neurovascular bundles may need to be sacrificed in order to gain exposure. Once adequate

Fig. 75.3 Flow chart diagramming the various surgical approaches.

Fig. 75.5 The approach (arrow) and bony resection (hatched lines) in the costotransversectomy approach.

visualization is obtained, the technique of decompression and fusion is similar to that of the transthoracic thoracotomy approach. If the herniation is centralized, or intradural, it may be more difficult to visualize across the entire disc with this technique as apposed to the more traditional transthoracic approach. In addition, if the facet is removed during the exposure, one should consider a prophylactic fusion, to prevent possible sagittal plane decompensation. A transpedicular approach is another choice, and although it generally provides less exposure than the transthoracic or costotransversectomy approachs, yet it is suitable for a posterolateral or foraminal herniation (Fig. 75.6). Its advantage is that it avoids a thoracotomy, although the actual access to the disc is still somewhat limited. Finally, performing surgery at the wrong level can be a common error when treating thoracic disc pathology, whether the procedure 801

Part 3: Specific Disorders

Fig. 75.6 The approach (arrow) and bony resection (hatched lines) in the transpedicular approach.

is open or with thoracoscopy. The thoracic anatomy can be more variable than in the lumbar or cervical spines with different numbers of vertebrae and ribs. A chest radiograph is important in the preoperative work-up to be able to count the ribs and verify the correct level. The MRI has to be just as accurate and should, if possible, include sagittal plane images that allow counting down to the sacrum for level verification. A myelogram can be very helpful, identify focal protrusions if present, and also allow counting of ribs to accurately note the pathologic level.

SUMMARY Symptomatic pathology of the thoracic spine is less common than in the cervical and lumbar regions, yet can be a focus of significant illness and can be effectively treated surgically. Herniations are the entity most commonly treated and can usually be approached with simple decompression, typically anteriorly or posterolaterally. Rarely

802

is a concomitant fusion necessary. Thoracoscopy can significantly reduce the morbidity commonly associated with the more traditional transthoracic approach.

References 1. Wood KB, Garvey TA, Gundry C, et al. Magnetic resonance imaging of the thoracic spine: evaluation of asymptomatic individuals. J Bone Joint Surg [Am] 1995; 77:1631–1638. 2. Thornbury JR, Fryback DG, Turski PA, et al. Disk-caused nerve compression in patients with acute low-back pain: diagnosis with MR, CT myelography, and plain CT. Radiology 1993; 186(3):731–738. 3. Anderson RE. Magnetic resonance imaging versus computed tomography – which one? Postgrad Med 1989; 85(3):79–83, 86–87. 4. Wood KB, Schellhas KP, Garvey TA, et al. Thoracic discography in healthy individuals. A controlled prospective study of magnetic resonance imaging and discography in asymptomatic and symptomatic individuals. Spine 1999; 24(15):1548–1555. 5. Schellhas KP, Pollie SR, Dorwat RH. Thoracic discography: a safe and reliable technique. Spine 1994; 19:2103–2109. 6. Bohlman HH, Freehafter A, Dejak J. The results of treatment of acute injuries of the upper thoracic spine with paralysis. J Bone Joint Surg [Am] 1985; 67:360–369. 7. Fessler RG, Sturgill M. Complications of surgery for thoracic disc disease [Review]. Surg Neurol 1998; 49(6):609–618. 8. Bohlman HH, Zdeblick TA. Anterior excision of herniated thoracic discs. J Bone Joint Surg [Am] 1988; 70:1038–1047. 9. Regan JJ, Ben-Yeshay A, Mack M. Video-assisted thorascopic excision of herniated thoracic disc: description of technique and preliminary experience in the first 29 cases. J Spinal Disord 1998; 11(3):183–191. 10. Anand N, Regan JJ. Video-assisted thoracoscopic surgery for thoracic disc disease. Spine 2002; 27(8):871–879.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ i: Physiology and assessment

CHAPTER

Medical Causes of Low Back Pain

76

Stefano Negrini, Donatella Bonaiuti, Marco Monticone and Carlo Trevisan

INTRODUCTION Pain arising in the lumbar region of the spine can be due to many causes and, in as many as 80% of cases, these causes cannot be established with certainty.1 Many terms have been proposed as a label for the condition affecting this vast majority of patients, for example primary, idiopathic, common, or mechanical low back pain, strain, injury, and trouble. Here, we use what is the most common, and probably the correct, definition: low back pain (LBP). LBP is currently recognized by most authors as a bio-psycho-social syndrome2 in which pain constitutes the final common pathway with many possible causes. The course of this complex process begins with the acute onset of pain; in the sub-acute stage, and the interaction of psychological and social factors create the final, individual clinical picture, of chronic pain.1,2 If one accepts this mechanism it becomes clear that we cannot consider only the biological (anatomical) aspects of LBP. Restricting one’s view of its medical causes, at worst to the single painful tissue, and at best to impaired functional mechanisms (a somewhat risky approach given that nobody can categorically state which tissues are most commonly involved in LBP), one will see that the hypotheses are as numerous as the scientists who have advanced them. From an academic point of view, one can divide the medical causes of LBP into three categories: biological, psychological, and social. This approach is entirely consistent with the aforementioned bio-psychosocial model of LBP,2 and with the only currently meaningful classification of the condition, which classifies LBP on the basis of the temporal course of the syndrome: acute (up to 4 weeks of pain), subacute (5 to 12 weeks), and chronic (more than 12 weeks).3,4 This classification differentiates between primary and secondary causes of back pain. The value of this classification is mainly prognostic: the acute phase is benign (spontaneously resolving), whereas resolution of the chronic phase is rare (less than 5–10% of cases).1,5 But this classification could also have etiological significance: whereas the acute phase could be regarded as almost completely biological, and the subacute period to correspond to the gradual evolution toward the complete syndrome, the chronic phase is believed by many authors to be purely psychosocial.1,3 Conversely, there is compelling evidence suggesting that chronic LBP is the expression of a full picture of biological dysfunction.3,6 In view of these considerations, this chapter, before examining the less common secondary causes of pain in the lower back, will explore LBP, including its biological acute causes, its psychosocial components, and the biological (dysfunctional) aspects of chronic LBP.

LOW BACK PAIN Biological causes of acute low back pain Previous studies have focused on the development of the pain sensation and on the tissues in which pain may originate.7 Many researchers

have proposed a single tissue as the main source of LBP even though, in this regard, consensus appears to be lacking.

Pain mechanisms Acute LBP is a nociceptive pain.7 It is initiated by the activation of free nerve endings (pain receptors), which are present in most body tissues (skin, muscles, fasciae, joints, blood vessels). Nerves and nerve stimulation by various chemical substances are an important area of research. Another interesting new field of research concerns the central pain-mediating pathways and the way pain sensation is controlled at different stages.8

Nociception Free nerve endings of C fibers can be found in vertebral body endplates, in the disc anulus, generally in the outer posterior fibers, but not in the inner disc; they are also present in muscles, tendons, capsules, and ligaments (with the exception of the yellow ligaments).7 Nociceptors usually have a high noxious threshold: they do not respond to light pressure, stretching, muscle contractions or joint motion within physiological range, but in certain environmental conditions (inflammation, vibration, etc.) they are sensitized, and their stimulus threshold is reduced. Tissue changes induced by inflammation cause the release of endogenous substances (bradykinin, prostaglandins, histamine, cytokines, and nerve growth factors) most of which sensitize nociceptors. In this way, chronic inflammation and fibrosis are related to LBP. Nociceptor activation in tissue inflammation leads to enhanced activity (dysesthesia) in other receptors, and to a reduced mechanical threshold: consequently, a greater number of receptors are stimulated by lighter mechanical stimuli, such as physiological joint movements. Hypoxia also causes nociceptor sensitization;7 in LBP this phenomenon has been shown during muscular spasm.9 There also exists a withdrawal reflex in acute LBP in which noxious peripheral stimulation, at the joint or ligament level, could activate a motor nerve and its associated muscle. Thus, spasm activates other nociceptors and a cycle is established that results in persistent pain.10 The sympathetic pathway can also be stimulated, causing ischemic or causalgic pain.11

Biochemistry Recent research has shown that cytokines such as matrix metalloproteinase, phospholipase A2, nitric oxide, and tumor necrosis factor-α may contribute to the development of LBP,12 and that mechanical and metabolic factors interact closely to produce nerve damage and pain.13,14 A current hypothesis is that leakage of these agents may produce nociceptor excitation, direct neural injury, nerve inflammation, or increased sensitivity to other pain-producing substances (such as 803

Part 3: Specific Disorders

bradykinin), and lead to nerve root pain. PLA2 and other substances, e.g. substance P, VIP (vasoactive peptide) and calcitonin gene-related peptide,15 are sources of pain. They are released following stimulation, mainly from the dorsal ganglion, where substance P plays an important role in modulating central pain and stimulating the cellular elements of inflammation (mastocytes, histamine, and leukotriene release). The stimulus is often mechanical, such as whole-body vibration.16 The damage produced by mechanical causes and enzymatic processes in outer annular fibers allows PLA2 to enter the epidural space. Damage of the disc and then the motion segment enhances susceptibility to vibrations and extreme loading conditions, establishing a cycle of dorsal ganglion stimulation and neurotransmitter release.

Central pathways and gates The idea that there is cross-interference between skin and pain sensations, due to their convergence on the same medullary neuron, has long been an accepted theory (the gate control theory).17 In recent years, new control mechanisms (gates) have been proposed, mainly involving descending pathways that originate from the emotional centers in the brain and converge on the same neurons.18 Their major contribution seems to be that of opening the gate and keeping it open or in some cases, the reverse. These findings could provide explanations for the cross-interference between pain sensation and emotions and for other psychosocial aspects of pain. Moreover, the recent finding of reduced limb reaction times in chronic LBP patients has induced some authors to suggest the existence of a central nervous system impairment in chronic pain.19

ing of ligaments. Nerve roots exit at different angles: lower roots are more oblique and have a longer path, and thus different exposure to mechanical stress. Continuous stable pressure on a normal nerve usually causes only a brief discharge of impulses, but if the nerve has been injured by demyelinization or inflammation, pressure causes a prolonged discharge.25,26 Experimental studies have revealed the presence of many different bioactive substances in herniated disc tissue. Cytokines, in particular, exert a harmful effect on the nerve root27 and play an important role in LBP. This also provides an explanation for radicular pain in the absence of mechanical nerve root compression.

Dorsal ganglia The dorsal ganglia, which are located in the middle zone of the intervertebral foramina, contain many types of sensory cell bodies and modulate the transmission of pain. They are capable of producing significant quantities of neuropeptides (substance P, enkephalin, and other neuropeptides) following nociceptive and mechanical stimulation.21 Substance P primarily modulates central pain28 and this explains the pain latency following herniated disc pressure. The dorsal ganglion can be a primary source of pain, due to local mechanical pressure from the disc, osteophytosis, stenosis, local neuropeptide production changes due to inflammation or chemical lesion, or ischemic damage produced by root pressure. The nerve root ganglion has an extensive venous plexus which, if obstructed, results in venous hypertension and endoneural edema, which in turn leads to hypoxia, ischemia, and pain.

Facet joints

Painful tissues Discs In the past, discs were not believed to be innervated. Now, however, it has been demonstrated that there are plenty of nerve endings in tissues surrounding the disc: the posterior longitudinal ligament, the outer third of the posterior anulus, the vertebral body, the dura, and the peridural venous and arterial plexuses.20 Innervation is by the sinuvertebral nerve and by the ventral and gray ramus. There are no intradiscal vascular structures, with the closest residing in the nearby endplates; therefore, tissue healing following damage is slow and very limited. In damaged discs, disc chondrocyte activation is directed at type II and type I collagen, which are typical of the outer fibers of the anulus, and the elastin, which is the interface between the disc and vertebral body. The causes of these changes, which remain to be completely defined, may be genetic, mechanical or biochemical. What is certain is that they can trigger a cascade of biochemical processes influencing damage and injuries together with the mechanical forces.21 In spite of this knowledge, the pathogenesis of discogenic pain remains uncertain. Two proposed mechanisms of disc injury suggest the process begins in the outer anulus following an exaggerated motion mainly in flexion and rotation or in the inner fibers and subsequently extends to the peripheral ones. In a study comparing inner annular lesions and disc degeneration, the inner annular lesions were found to be related to LBP.22 Another area of research has been disc oxygenation, nutrition, and catabolic wash out, mainly due to the vessels in the vertebral body and to osmotic mechanisms.23 Movement increases these metabolic changes, as do circadian variations of posture (upright and supine), and even certain exercises. Impairment of these mechanisms has been proposed as a possible source of pain.24

804

In an animal model, posterior joints contain high-threshold mechanosensitive fibers, which function as nociceptors, and low-threshold fibers, which modulate proprioceptive feedback.29 These fibers are also found in joint capsules near the ligamentum flavum and in muscles and tendons. Facet joints have often been suggested as an etiology of LBP following the demonstration of local and distal pain following local injection of 3–8 mL of hypertonic solution.30 However, these results were subsequently refuted by the demonstration that facet joints could hold only 2 mL of solution and therefore the studies were effectively investigating periarticular tissue stimulation, due to the solution leaving the joint.31,32 Although for some authors clinical correlation of facet pathology as a primary cause of LBP remains controversial,1 many studies demonstrate a high prevalence of facet joint pain in low back syndromes and the usefulness of specific interventions.33

Ligaments Most of the vertebral tissues are innervated by the medial ramus of the dorsal nerve. The posterior longitudinal ligament is innervated by the sinuvertebral nerve, which is formed from the union of the ventral branch (somatic) and the gray communicant (sympathetic). A specific relationship between ligamentous injury and spinal pain conditions cannot easily be established but ligaments contribute generically to LBP. In segmental instability, pain is related to ligament disruption and the loss of support. In 1968, Murphey34 demonstrated pain related to the posterior longitudinal ligament and posterior anulus stimulation, called ‘true referred pain,’ different from sciatica secondary to nerve root stimulation. In this study, a central disc protrusion caused severe lumbar pain radiating to both lower limbs, typically increasing with anterior flexion.

Nerve roots

Muscles

Pressure on nerve roots can be due to spondylotic encroachments, disc herniations, foraminal narrowing, venous dilatation, and thicken-

No pathognomonic changes in muscles, tendons, and ligaments are shown by NMR in LBP; nevertheless, some studies35 have shown a

Section 5: Biomechanical Disorders of the Lumbar Spine

unilateral reduction of the muscle mass in chronic LBP, but other studies refuted these findings.36 In any case, there is presumably a difference between chronic and acute LBP. LBP quickly develops after muscular injury following direct trauma or an acute overly rapid or excessive eccentricity. Typically, such pain resolves in 1–3 weeks. Some researchers have also postulated that afferent impulses directly increase muscle tension and affect blood circulation, generating ‘ischemic-like’ pain.37 It also seems that pain from trigger points could have the same mechanism, but a more recent study reported changes of gamma fibers caused by muscular tension.38

Other hypotheses Jayson proposed that most LBP syndromes derive from epidural venous stasis, followed by local chronic inflammation and fibrinous exudation, like a common postphlebitic syndrome of the skin. The usual clinical manifestations are pain that worsens during the night and improves during activity or during maneuvers that usually aggravate disc pain.39 Epidural venous stasis may also directly provoke sciatica by perivenous nervous plexus stimulation.40

The final common pathway In each individual patient, acute LBP can presumably be attributed to a single biological cause, but one does not have any imaging technique, or other examination, history, or clinical findings that allows one to define the majority of cases with accuracy. Acute LBP should be considered as the final common pathway with many different causes.

Psychosocial causes of chronic low back pain Most patients with acute LBP improve naturally, regardless of what specific intervention is instituted,5,41 and 85–90% of these patients derive benefit from analgesics, good advice, and reassurance. Research into the causes of LBP in such cases will presumably lead to the development of new drugs and new ways of accelerating the recovery rate. The remaining 10–15% of patients are at risk of developing chronic LBP, defined as disabling LBP that lasts longer than 3 months and does not resolve spontaneously.1,5 Symptoms and unsatisfactory pain treatments themselves become a source of disability and have a major impact upon patients’ lives, families, and jobs. These LBP sufferers generate the vast majority (90%) of the social costs related to LBP.1,5,42 In these patients, examining the causes of LBP means considering the factors that contribute to the persistence of pain over time, and preclude full recovery, i.e. the so-called risk factors.

Risk factors for chronic low back pain The authors classify the risk factors for LBP reported in the literature into three different categories: individual, physical and biomechanical, and psychosocial.

Individual risk factors 43

The strongest associations are previous LBP and age, while weaker associations were found with gender,44 weight,45 and smoking.46 There was little evidence for an association between level of fitness47 or radiographic abnormalities and chronic LBP (Fig. 76.1).48,49

Physical and biomechanical risk factors Physical and biomechanical risk factors50,51 have been shown to only weakly correlate with LBP. Only a few studies support the possibility that there is a causal relationship between chronic LBP and physical workload in the workplace.52,53 The most frequently reported

variables include heavy lifting,54 motor vehicle driving,55 whole-body vibration,56 excessive spinal loading,57,58 and awkward postures.59

Psychosocial risk factors Psychosocial risk factors,1,60,61 specifically job dissatisfaction, are an important predictor of chronic LBP. Their relative importance when compared to physical factors is unclear, but there is increasing empirical evidence linking LBP with psychosocial risk factors. The main psychosocial predictors are: work characteristics (job satisfaction and level of commitment), disability benefit, previous LBP treatment and patient satisfaction, and level of education. In particular, job satisfaction and social aspects were the factors found to be the most significant with respect to the development of severe LBP. Psychosocial problems are likely more significant than biological factors in the development of persistent low back pain rather than its onset.1,2,48 Patients who say that they are in poor health, describe general symptoms, and say that they always feel ill (illness behavior) are more likely to have chronic pain, despite receiving the usual pain treatments. The symptoms they report seem to reflect a psychological condition more than a biological aspect of their original LBP. Most authors reported that, after only 1 year, the severity of initial LBP no longer shows a relationship with disability status.62,63 This underscores how psychosocial variables play an important role in pain perception and its evolution, once the chronic phase has been entered. There seems to be a significant, and predominant, psychosocial component underpinning prolonged disability secondary to LBP. Early identification of psychosocial problems is fundamental to understanding and hopefully prevent the development of LBP. It now appears that persisting symptoms of LBP, particularly when there is a previous history of LBP, is more likely a function of psychological influences than medical factors. There is good reason to think that a reduction in the number of non-specific LBP patients progressing to a chronic state may be obtained by early interventions designed to encourage positive coping strategies and reduce illness behavior patterns. As indicated by Waddel in 1987,2,64,65 chronic LBP is a complex psycho-socio-economic phenomenon. Psychosocial factors do not only play a significant role in determining which injured workers will develop chronic LBP and any disability, but they also interact closely with physical/dysfunctional factors in determining the very onset of disability. Chronic LBP disability is multidimensional and challenging not only the familiar paradigms of illness and health, but also social and medical decision-making structures. In the best interests of all patients involved, one needs to dismiss the usual pain-related therapeutic approaches to LBP in favor of a more thoughtful approach.

What comes first in low back pain: physical or psychosocial problems? There is now no doubt that psychosocial factors including illness behavior, fear/avoidance behavior, and work dissatisfaction are closely involved in the vicious circle that is chronic LBP. Nevertheless, acute LBP starts as a physical problem with physical causes, whereas psychosocial factors become more important and influential as it evolves to the chronic stage. These results have led some authors to propose that chronic LBP is mainly psychological, and that psychic and social disorders are responsible for the development of chronic symptoms.63 After all, evolution is not the same as onset. No study has found a clear association between psychosocial factors and LBP onset, although high rates of psychopathology have been shown in chronic LBP.62 On the other hand, one cannot ignore the likelihood 805

Part 3: Specific Disorders Mechanical factors

Chemical factors

Disc damage Disc herniation Anular fissure PLA2 release and activation

Arachidonic acid

Prostaglandin G2

Leukotrienes Prostaglandin H2

Nerve compression

Tissue-specific isomerases Prostacyclin THX A2 PGD2 PGE2 PGF2α Perineural inflammation Neural damage Pain Weakness Sensory loss Reduction of reflex

that constant pain, lasting for months and leading to physical and social limitations, can undoubtedly create psychosocial problems. Fear/avoidance behavior, physical distress, and depression may be concomitant with and/or the final result of a long-lasting back problem, while the origin of chronic LBP may also lie in other, more biological or dysfunctional factors.

Biological and dysfunctional aspects of chronic low back pain A review of the biological aspects of the development of chronic LBP provides an example of how scientific thought can change in just a few years. In the 1970s and early 1980s, most authors considered the following biological factors as major predictors of chronic lumbar spine disabilities: gradual onset of pain, pain referring to the legs, impaired straight leg raising test, spinal root irritation, and muscle weakness. These studies reported that the evolution of patients with nerve root involvement was worse in terms of chronicity and disability than that of patients with simple LBP in the absence of root disease.66,67 In other studies, the most important predictors of recurrent or persistent LBP were for males: intermittent claudication, restlessness, or other discomfort in the lower limbs, frequent headache, and living alone; and for females: rumbling of the ‘stomach’ or a feeling of fatigue.68,69 According to these studies, biological factors 806

Fig. 76.1 Mechanisms of nerve injury in lumbar disc disease.16.

were considered very important not only in LBP onset, but also for predicting an evolution of the picture into chronic LBP. Most clinicians firmly believed in the biological nature of LBP onset and evolution, and only few attached any significance to psychosocial factors. In the 1980s, the intensity and severity of pain were considered as major predictors of developing chronic LBP. Pain severity after 3–6 months was found to be related to severe chronic pain, but also to reduced work capacity and increased absenteeism. However, in the 1990s these beliefs were altered as pain perception was found to be less important in the development of chronic pain than in the acute phase of LBP.70 The authors of these latter studies, however, failed to show pain intensity and mechanical or neurological signs as predictors of chronic LBP.71,72 Currently there is unequivocal evidence of the role played by biological risk factors in the onset of LBP, but the evidence for their role in the progression to chronic pain is disputed. Furthermore, many spine scientists have studied and advocate the importance of dysfunctional aspects as cocausative factors in chronic LBP.73 Dysfunction is a new field of research potentially full of interesting answers and new questions. As time passes, research into biological risk factors is becoming less important as compared to the investigation of the dysfunctional characteristics of chronic LBP patients. A number of issues have been raised as a consequence of a focus on these dysfunctional characteristics:6,73,74

Section 5: Biomechanical Disorders of the Lumbar Spine

Spinal motor control deficits Chronic LBP patients have been shown to have many different types of spinal motor control deficits resulting in impaired movement, decreased kinesthesia, spinal repositioning error, and lack of peripheral feedback.75,76

Pain Sensitization Behavioral changes

Spinal protective behavior Fear/avoidance behavior leads to illness behavior. Chronic LBP patients try to protect themselves by restricting more and more their usage of their spine, and thus also their lumbar range of motion, strength, resistance, and coordination. This behavior is the result of a passive coping strategy in which the patient focuses only on avoiding pain.77,78

Postural control abnormalities and difficulties Chronic LBP is frequent in the presence of abnormalities of postural control; chronic LBP is clearly associated with postural imbalance.79

Inefficient control of spinal stability The electromyogram (EMG) activity of abdominal (mainly trasversus abdominis) and spinal (mainly lumbar multifidus) muscles was found to be significantly delayed in chronic LBP patients. According to these authors, the result of this abnormal contraction is a lack of spinal protection and the generation of increased loads associated with everyday movements.80

Low reaction times Chronic LBP patients have low reaction times compared with control subjects. Reaction times provide important clues regarding chronic LBP onset, and they show the nature of the involvement of the central nervous system.79

Selective muscle weakness and fatigue Spinal weakness is a common finding in chronic LBP patients. Difficulty maintaining a contraction in a given position is associated with increased risk of spinal lesions. Early fatigue results in a high risk of spinal repositioning error, and a lack of proprioceptive protective control, with abnormal movement and dangerous loading of the spine.81,82

Absence of the lumbar flexion relaxation phenomenon In healthy subjects, the paraspinal muscles are electrically silent (EMG) during full lumbar flexion, demonstrating a relaxation effect. This effect is rarely present in chronic LBP patients. It is probable that fear/avoidance behavior leads to the creation of a vicious cycle in which lumbar flexion is gradually limited and muscle relaxation is impeded.83–86 While these aforementioned concepts are important, they do not represent all of the factors that are intertwined in the disability process. Recent efforts have focused upon the relationship between psychosocial factors and biological reactions.87,88 A group of biomechanical scientists, coordinated by Marras,87,88 replicated in healthy subjects several possible mechanisms of lumbar spine injury development as a consequence of psychosocial abnormalities. They showed that in situations characterized by emotional distress and poor human relationships, people react with anomalous movement control causing increased mechanical loading of the spine. It is hypothesized that these situations, once chronic, could easily give rise to LBP, despite the absence of an acute or specific injury to the spine. More

Psychosocial factors

Dysfunction

Deconditioning

Fig. 76.2 The vicious cycle of chronic low back pain may explain the self-perpetuating nature of this pain, in which psychosocial and physical factors play a role. Over time, pain induces behavioral changes, favored by individual psychosocial risk factors. Behavioral changes cause: (1) a central sensitization; (2) deconditioning through fear/avoidance behaviour; and (3) dysfunction, which directly increases pain through both deconditioning and sensitization. Sensitization, deconditioning, and dysfunction contribute to behavioral changes and interact with each other, thus perpetuating the problem.

importantly, if the causative ‘pathological’ psychosocial situation is left untreated, the risk of pain will not be reduced and presumably chronic LBP will evolve. Given this construct, it is reasonable to state that in this circumstance the biological and psychosocial factors seem to be intertwined in the development of chronic LBP. As the differences between pain and disability become more evident it has become clear that dysfunction and psychosocial problems are all key elements in the syndrome of chronic LBP, but at having varying impact at different stages. Psychosocial aspects undoubtedly play a decisive role in the evolution to chronic LBP. The findings of dysfunction in LBP patients suggest that there exists a physical basis, presumably created as a consequence of psychosocial problems, with the potential to give rise to and to perpetuate pain (Fig. 76.2). This explains why it may be impossible to find a precise source of the pain in a large proportion chronic LBP patients. Indeed, the initial injury may have long since resolved.. The solution to the LBP puzzle is probably even more complex if one considers the broader dysfunctional and psychosocial factors.3

The full syndrome and individual predominance As previously stated, chronic LBP represents a bio-psycho-social syndrome. Today, one is almost certain that the onset of pain is biological, while the causes of its persistence are in most cases psychosocial, mediated through physical factors (deconditioning and dysfunction). But one cannot ignore the fact that in specific individuals different factors interact in unique ways. Whatever the original acute cause of pain or the subacute cause of the persistence of pain, the final picture is, without doubt, the chronic bio-psycho-social syndrome of LBP. In each individual case, before proposing a treatment, it is imperative to look at the whole picture and to determine its predominant aspects.

SECONDARY LOW BACK PAIN Pain in the low back is a frequent complaint, second only to upper respiratory diseases among the symptom-related reasons for consulting a physician.89 Nearly 80% of the patients with pain in the low back seen by primary care practitioners are affected by simple, non-specific LBP. That is low back or leg pain associated with an anatomical or functional abnormality, in the absence of an underlying malignant, neoplastic, infectious, or inflammatory disease.41 As already stated, LBP has a benign natural course, with two-thirds of affected patients showing improvements at 7 weeks;90,91 and only a 807

Part 3: Specific Disorders

small percentage of patients developing chronic pain which is not a life-threatening condition. An exhaustive classification of LBP, which includes causes of non-specific (idiopathic) LBP and secondary LBP, and which may be useful for differential diagnosis, has been suggested by Deyo and Weinstein.41 They divide LBP into three different categories: mechanical LBP or leg pain, nonmechanical spinal conditions, and visceral diseases (Table 76.1) Mechanical LBP or leg pain as defined by this classification may account for about 97% of LBP cases in the primary care setting. This group includes conditions of spinal origin with distinctive mechanical characteristics of pain, such as non-specific LBP, which accounts for over 80% of cases. In this group, the second most frequent condition is osteoporotic compression fracture, which is particularly frequent in older women, having a lifetime prevalence of 25% in postmenopausal women.92,93 Nonmechanical spinal conditions account for 1% of LBP cases in primary care settings.94 They include all neoplastic, infectious, and inflammatory conditions that originate in the spine, whose symptoms are not related to loading of the spine, not responding to rest. Tumors, of which metastatic carcinoma is the most frequent form, may account for less than 1% of cases of LBP. Another neoplastic condition that should be in the differential diagnosis, due to its relative frequency, is multiple myeloma. The most common symptom of multiple myeloma is bone pain, present in nearly 70% of cases and usually involving the back and the ribs.95 Spinal infections are less common than tumors, affecting only around 1 in 10 000

LBP patients.41 In some cases, the diagnosis is difficult; the condition may have a subtle course, characterized by only occasional slight raises of body temperature, loss of body weight, and asthenia. The most frequent inflammatory condition of the spine is ankylosing spondylitis, which usually begins in the second or third decade of life with insidious, dull pain in the lower lumbar or gluteal region. Ankylosing spondylitis is three times more frequent in males than females.96 Visceral diseases may be observed in 2% of patients. These diseases generally present with their characteristic features and only occasionally is the diagnosis uncertain. Deriving an accurate differential diagnosis can be difficult in the following diseases in which LBP may be the only symptom: gastrointestinal perforation secondary to an ulcer, chronic pancreatitis, slowly increasing aortic aneurysm, and gastrointestinal infiltrating tumors. Judging whether the symptoms of LBP are due to one of the myriad of nonmechanical spinal conditions such as neoplastic, infectious, or inflammatory disease and visceral diseases is the first challenge confronting the interventional spine specialist. Each of these pathologic entities requires specific treatment, carries different prognostic possibilities, and may even be life-threatening. Therefore, it is imperative that the interventionist strive to identify the rare patient with an underlying malignancy or infection even if this task can be likened to looking for the proverbial needle in a haystack. History and physical examination are the first steps to take when seeking to rule out the possibility of serious underlying systemic diseases and to establish the need for further diagnostic investigations. In various guidelines for LBP, systematic reviews of the problem

Table 76.1: LBP-related conditions: proposed diagram for differential diagnosis30 Mechanical back or leg pain

Nonmechanical spinal conditions

Non-specific LBP

Neoplasia

Disease of pelvic organs

Lumbar strain, sprain

Multiple myeloma

Prostatitis

Degenerative processes of discs and facets

Metastatic carcinoma

Endometriosis

Discogenic LBP

Lymphoma and leukemia

Chronic pelvic inflammatory diseases

Presumed instability

Spinal cord tumor Retroperitoneal tumor

Renal disease

Primary vertebral tumor

Nephrolithiasis

Herniated disc

Perinephric abscess

Spinal stenosis

Infections

Pyelonephritis

Osteoporotic compression fractures

Osteomyelitis

Aortic aneurysm

Spondylolisthesis

Discitis

Traumatic fractures

Paraspinal abscess

Gastrointestinal disease

Congenital diseases

Epidural abscess

Pancreatitis

Severe scoliosis

Shingles

Cholecystitis

Severe kyphosis Transitional vertebrae

Perforated ulcer Inflammatory arthritis Ankylosing spondylitis

Spondylolysis

Psoriatic spondylitis Reiter’s syndrome Inflammatory bowel disease Scheuermann’s disease Paget’s disease of bone

808

Visceral diseases

Section 5: Biomechanical Disorders of the Lumbar Spine

Table 76.2: Red flags: warning signs that generate suspicion of a serious underlying disease in the diagnostic process of patients with a chief complaint of LBP Age at onset of LBP <20 years old or >55 years old Violent trauma Constant, increasing, nonmechanical pain Thoracic pain

Finally, LBP is a symptom of several conditions which differ considerably in terms of their etiology, management, and prognosis. The majority of cases of LBP are benign and require mainly education and reassurance. Of the remaining 25%, only a small percentage will be a potentially fatal condition. This makes the process of formulating an accurate hierarchal differential diagnosis a crucial and critical mandatory first step in the management of LBP patients. The clinician must always keep in mind the less common and potentially fatal causes of LBP so that they are not missed.

CONCLUSION

History of tumor Systemic steroids Drug abuse, HIV Systematically unwell, e.g. fevers, chills Weight loss Severe persistent reduction of lumbar range of motion Diffuse neurological deficit Structural deformity Pain duration >6 weeks

have led to the compilation of a list of general warning signs, or ‘red flags,’ which efficiently guide the physician through the screening process (Table 76.2).4 Their systematic use reduces the risk of missing serious diseases. Another important aspect of the diagnostic process is awareness of the sensitivity of various historical and clinical factors in the diagnosis of different conditions (Table 76.3).93 If a factor known to have high diagnostic sensitivity for a certain condition is absent, this means that there is a high probability that that diagnosis can be excluded. Conversely, its presence increases the likelihood that the patient is affected by the condition in question.

Identifying specific causes of LBP will facilitate the development of new hypotheses which will enable clinicians to formulate new therapies tailored to the needs of individual patients. In today’s climate of uncertainty over the biological causes of acute LBP, an evidence-based clinical approach should carefully consider the data on the efficacy of analgesics, NSAIDs, activity in general, including the continuation of activities of daily living, and the enormous value of reassurance. Obviously, according to individual needs, specific therapeutic approaches must be developed. The growing understanding of the physical, psychological, and social factors that contribute to the evolution of an acute episode of LBP, through the subacute stage, to the chronic persistence of LBP, impose new, fully rehabilitative treatments,3 even though not forgetting the need to identify carefully any specific pathology whose primary treatment is mandatory. In the meantime, one cannot ignore the physical characteristics of chronic LBP patients, including deconditioning and dysfunction, which are the direct causes of a vicious cycle that can be difficult to resolve. The goal for these patients should be full physical recovery in the context of the psychosocial approach.97 Last, but by no means least, every time one examines a patient one must always bear in mind the full spectrum of known causes of pain in the low back. Even if LBP has no recognized causes, its diagnosis must be reached by a process of exclusion of all the known and dangerous causes of secondary LBP.

Table 76.3: Accuracy of history for the diagnosis of secondary LBP33 Related disease

History

Sensitivity

Specificity

Cancer

Age >50 years old

0.77

0.71

History of cancer

0.31

0.98

Unexplained weight loss

0.15

0.94

No improvement after 1 month of therapy

0.31

0.90

No improvement with bed rest

0.90

0.46

Pain duration >1 month

0.50

0.81

Spinal infection

Drug abuse or urinary infection

0.40

na

Vertebral fracture

Age 50 years old

0.84

0.61

Age 70 years old

0.22

0.96

Trauma

0.30

0.85

Ankylosing spondylitis

Systemic steroids

0.06

0.99

Age at onset under 40 years old

1.00

0.07

Pain not improved in the supine position

0.80

0.49

Morning lumbar rigidity

0.64

0.59

Pain duration >3 months

0.71

0.54

na: not available.

809

Part 3: Specific Disorders

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66. Pedersen PA. Prognostic indicators in LBP. J Roy Coll Genl Practition 1981; 31:209– 216.

86. Kaigle AM, et al. Muscular and kinematic behaviour of the lumbar spine during flexion–extension. J Spinal Disord 1998; 11(2):163–174.

67. Roland MO, et al. Can general practitioners predict the outcome of episodes of back pain? Br Med J 1983; 286:523–525.

87. Marras WS, Davis KG, Heaney CA, et al. The influence of psychosocial stress, gender, and personality on mechanical loading of the lumbar spine. Spine 2000; 25(23):3045–3054.

68. Lloyd DCEF, Troup JDG. Recurrent back pain and its prediction. J Social Occup Med 1983; 33:66–74. 69. Chavannes AW, et al. Acute LBP: patient’s perceptions of pain four weeks after initial diagnosis and treatment in general practice. J Roy Coll Genl Practition 1986; 36:271–273. 70. Frank JW, et al. Disability resulting from occupational low back pain. Spine 1996; 21:2908–2929. 71. Gatchel RJ, et al. The dominant role of psychosocial risk factors in the development of chronic low back disability. Spine 1995; 20:2702–2709. 72. Burton AK et al. Psychosocial predictors of outcome in acute and subchronic low back trouble. Spine 1995; 20:722–728. 73. Kermond W, Gatchel RJ, Mayer TG. Functional restoration treatment for chronic spinal disorder or failed back surgery. In: Mayer TG MV, Gatchel R, eds. Contemporary conservative care of painful spinal disorders. Philadelphia: Lea & Febiger; 1991:473–481. 74. Luoto S, Taimela S, Hurri H, et al. Mechanisms explaining the association between low back trouble and deficits in information processing. A controlled study with follow-up. Spine 1999; 24(3):255–261. 75. Rothwell J. Control of human voluntary movement, 2nd edn. Cambridge: Cambridge University Press; 1994. 76. Schmidt RA. Motor control and learning. A behavioural emphasis, 2nd edn. Champaign, Illinois: Human Kinetics; 1988. 77. Croft PR, et al. Psychologic distress and low back pain. Evidence from a prospective study in the general population. Spine 1995; 20(24):2731–2737. 78. Estlander AM, et al. Do psychological factors predict changes in muscoloskeletal pain? A prospective, two-year follow-up study of a working population. J Occup Environ Med 1998; 40(5):445–453.

88. Davis KG, Marras WS, Heaney CA, et al. The impact of mental processing and pacing on spine loading: 2002 Volvo Award in biomechanics. Spine 2002; 27(23): 2645–2653. 89. Deyo RA, Phillips WR. Low back pain. A primary care challenge. Spine 1996; 21(24):2826–2832. 90. Cherkin DC, Deyo RA, Street JH, et al. Predicting poor outcomes for back pain seen in primary care using patients’ own criteria. Spine 1996; 21(24):2900–2907. 91. Croft PR, Macfarlane GJ, Papageorgiou AC, et al. Outcome of low back pain in general practice: a prospective study. Br Med J 1998; 316(7141):1356–1359. 92. Wasnich RD. Epidemiology of osteoporosis. In: Favus MJ, ed. Primer on metabolic bone diseases and disorders of mineral metabolism, 4th edn. Philadelphia: Lippincott, Williams & Wilkins; 1999:257–259. 93. Deyo RA. Accuracy of diagnostic tests. In: Weinstein JN, Rydevik BL, Sonntag VKH, eds. Essentials of the spine. New York: Raven Press; 1995: 43–56. 94. Slipman CW, Patel RK, Botwin KP, et al. Epidemiology of spine tumors presenting in musculoskeletal physiatrists. Arch Phys Med Rehabil 2003; 84(4):492–495. 95. Longo DL. Plasma cell disorders. In: Wilson JD, Braunwald E, Isselbacher KJ, et al., eds. Harrison’s principles of internal medicine. New York: McGraw-Hill; 1991:1410–1417. 96. Taurog JD, Lipsky PE. Ankylosing spondylitis and reactive arthritis. In: Wilson JD, Braunwald E, Isselbacher KJ, et al., eds. Harrison’s principles of internal medicine. New York: McGraw-Hill; 1991:1451–1453. 97. Guzman J, Esmail R, Karjalainen K, et al. Multidisciplinary bio-psycho-social rehabilitation for chronic low back pain. Cochrane Database Syst Rev 2002(1): CD000963

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SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ i: Physiology and assessment

CHAPTER

The Lumbar Degenerative Disc

77

Christopher T. Plastaras, Gwendolyn A. Sowa and Brad Sorosky

INTRODUCTION AND EPIDEMIOLOGY Lumbar degenerative disc disease is an ubiquitous process that occurs in most humans. In this chapter, the degenerative disc process will be outlined, discussing pathoanatomy, biochemical findings, radiographic correlations, and clinical correlations. Low back pain is a pervasive symptom, affecting the majority of the adult population at some point in life. Despite the high prevalence of this disorder, the etiology remains controversial. The main diagnostic challenge lies in identification of the pain generator. It has been shown that the intervertebral disc is capable of acting as a pain generator, and degenerative discs are believed to be involved in the pathogenesis of low back pain. Degeneration of the intervertebral discs is common among patients with disc-related pain, and it has been suggested that degeneration of the disc is a prerequisite for disc herniation.1 The L4–5 and L5–S1 levels are most frequently affected and usually show degenerative changes earlier than upper lumbar segments. This correlates with the higher incidence of pain in these distributions. Intervertebral disc degeneration increases with age, and is present radiographically in nearly all spines by age 50.2–4 In fact, the intervertebral disc shows degenerative changes earlier than other cartilaginous structures. In a radiographic study of people aged 55–64 years, 83% of men and 72% of women showed disc degeneration. Many studies have confirmed the association of age and radiographic disc degeneration. Although radiographic changes are evident, the clinical significance of these changes is unclear. Symptoms and physical examination findings frequently do not correlate with the appearance of the intervertebral disc. This complicates not only diagnosis, but also treatment. Because the distribution of the patient’s pain may not correspond to the main site of radiographic pathology, targeting a particular level for intervention may be difficult. This discrepancy between the radiographic abnormality and the ‘real pain generator’ may account for the variable effectiveness of specific treatments directed toward degenerative discs. In addition, surgical outcomes are often less than expected, based on anatomic preoperative findings.5 Nevertheless, the increased incidence of degenerative changes and low back pain with aging suggests an important role for disc degeneration in the pathogenesis of low back pain. The question that remains is which changes are related to normal aging and which changes represent pathologic degeneration.

THE DISC AS PAIN GENERATOR The belief that the intervertebral disc itself could be a potential pain generator originated in 1947 when Inman showed that the disc had its own nerve supply.6 Subsequent studies then reported that there

were no nerve endings within the disc7,8 and, consequently, a debate emerged as to whether the disc itself could be painful. This controversy was resolved with the findings published by Malinsky and others demonstrating a variety of free and complex nerve endings within the outer third of the anulus fibrosus.9–11 Currently, it is believed that the disc is innervated and therefore can act as a source of pain. According to Bogduk, the current data regarding the pathology of disc pain, though incomplete, lead to three distinct diagnoses. These include discitis, torsion injuries, and internal disc disruption.12 Discitis, an infection of the disc, is associated with extreme pain. While this diagnosis is rare, its existence demonstrates that pain can arise from isolated pathology in the disc itself. Discitis can be identified with elevated serum chemistries such as sedimentation rate and C-reactive protein13 as well as imaging including bone scan and magnetic resonance imaging (MRI) with and without contrast.14 The second diagnosis, torsion injury, remains a clinical diagnosis. The underlying mechanism involves forcible rotation of the intervertebral joint, resulting in disc torsion and lateral shear which together lead to painful circumferential tears in the outer anulus. Coupled with flexion which stresses the anulus, torsion can lead to even greater injury. While a patient may present with a similar mechanism of injury and exacerbation of pain with flexion and rotation, confirmation of this diagnosis cannot be made with any current imaging because the nucleus pulposus is not involved. However, with advances in imaging it may become a more concrete entity in the future.12 Finally, internal disc disruption (IDD), the third diagnosis accounting for discogenic pain, is believed to be the most common cause of disc-mediated chronic low back pain that can be confirmed objectively. Here, compression of the disc is hypothesized to result in vertebral endplate fracture which may alter nuclear homeostasis. Degradation of the nucleus pulposus ensues and, over time, extends peripherally to the anulus fibrosus creating radial fissures. Pain is proposed to occur via chemical and mechanical stimulation of nerve fibers in the outer third of the anulus. As opposed to the clinical diagnosis of torsion injury, IDD cannot be diagnosed by history and physical examination; however, it can be demonstrated with specific radiographic and interventional techniques. While MRI may demonstrate high-intensity signal in the anulus (see below), the current diagnostic criteria for IDD include disc stimulation reproducing pain and postdiscography CT revealing a grade 3 or greater annular fissure12 In summary, several studies have proven that discs are in fact innervated. The specific finding of nerve fibers within the outer third of the anulus fibrosus leads to the belief that the disc has the potential to create pain. Whether it is discitis, torsion injury, or internal disc disruption, the disc has proven to be a common cause of back pain.

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THE DEGENERATIVE CASCADE: DYSFUNCTION, INSTABILITY, AND STABILITY In order to understand the progression from an anatomically normal spine to a painful, degenerative spine, it is useful to walk through this process step by step as a person ages (Fig. 77.1). Kirkaldy-Willis coined the term ‘degenerative cascade’ to describe changes that occur over time consequent to recurrent compressive forces coupled with lumbar spinal flexion, extension, axial rotation, and side bending. This process can be conceptualized as occurring in three phases: the dysfunctional phase, the unstable phase, and the stabilization phase. In considering these phases, it is important to recall the notion of three-joint complex proffered by Kirkaldy-Willis, which refers to the functional unit at each spinal level comprised of the disc and the two zygapophyseal joints. Because the three joints at a given level are interconnected, forces and anatomic changes occurring in one component not only affect its function, but also affect the function of the other two components.15 The first phase, dysfunction, refers to the abnormal functioning of the components of the three-joint complex. A patient typically presents with an acute to subacute history of low back pain following a minor episode of trauma or unusual activity. The pain is usually localized to a specific area on one side of the low back; while the pain may refer, it rarely does so below the knee. Movement tends to make the pain worse, while rest makes it better. On examination, spinal muscles may be tender and spastic at that level. Testing of spinal range of motion may reveal painful, decreased movement in all planes, especially with extension and lateral bending. The patient’s neurologic examination is usually normal.15 Radiographs are normal for the most part or reveal only very mild abnormalities, such as misaligned spinous processes, irregular facets, early disc height changes, and asymmetric decreased movement on lateral bending views. MRI findings may show early disc desiccation with decreased signal within the nucleus pulposus and annular changes. Early zygapophyseal joint synovial changes may be noted on T2-weighted imaging.16 The mechanism underlying this phase involves minor trauma or unusual activity resulting in small tears in the zygapophyseal joint capsule and anulus; this damage leads to minor zygapophyseal joint subluxation and synovitis. In order to minimize the subluxation and protect the joint, the posterior segmental muscles contract continuously, become locally ischemic, and thereby create pain. Early on, these changes are minor and may even be reversible with simple conservative measures. However, with each traumatic episode, healing of the tears is not as complete as before. As a result, the patient is likely to progress to the second phase.15 The unstable phase, the second phase of the degenerative cascade, is labeled as such because of the abnormal movement present in the three-joint complex. The patient presents either with or without an inciting episode of minor trauma or unusual activity. Characteristic symptoms include back pain similar to that of the severe dysfunction phase, sometimes with the sensation of giving way or ‘catching’ in the back upon rising from a forward flexed position. Pain may be experienced with transitional movements such as from prolonged sitting to standing transfer or from prolonged standing to the sitting position. Examination may reveal abnormal movement between adjacent spinal levels at rest or during range of motion testing. As the patient comes to a standing position after bending forward, a ‘catch’ or lean towards one side may be appreciated. On lateral bending radiographs, successive vertebrae may appear to be laterally shifted, rotated, or abnormally tilted. On oblique films, facets may be open and misaligned. Flexion and extension films may reveal translation, increased foraminal narrowing, abnormal disc opening, and abrupt change in interpedicular height. The mechanism in this phase involves further 814

trauma and/or continuing stress leading to increased dysfunction in the disc and zygapophyseal joints. In the disc, small fissures will form within the anulus. As the fissures unite, concentric tears appear parallel to the circular-shaped annular lamellae. Additional concentric tears occurring at different depths of the anulus enable these concentric tears to coalesce together to form radial tears perpendicular to the annular lamellae. Depending on the location and severity of these tears, this may manifest in internal disruption, annular bulging, or loss of nucleus pulposus material into the subannular space, extra-annular but subposterior longitudinal ligament, or even beyond the posterior longitudinal ligament.16 Rauschning’s cryoplane anatomic analysis of 83 degenerated frozen human cadaver lumbar spines nicely details these degenerative findings in the disc. He found clefts through the anulus on the periphery, with the lamellae frequently detached from the apophyseal rim and the vertebral body periosteum. Sometimes these fissures were filled with granulation tissue and small blood vessels dividing the more peripheral layers of the lamellae. With internal disc disruption, a 1–2 mm thick darkened ‘annular capsule’ was identified in the outermost layer of the anulus. This caused circumferential bulging and occlusion of the retrodiscal space.17 Increased concentrations of inflammatory mediators and proteolytic enzymes have been found in association with annular tears. In addition, annular tears may subject the previously immunoprotected nucleus pulposus to autoimmune attack, resulting in further inflammation and chemically mediated pain.18–20 Regarding the zygapophyseal joint, the intra-articular facet cartilage degenerates leading to attenuation and then laxity of the capsule. Recurrent inflammation and effusions occur within a weakened joint capsule. Synovial fluid-filled cysts, or outpouchings, can form, extending into the nearby neural canal causing radicular pain.21–23 Small rents in the weakened facet capsule may represent one avenue of inflammatory synovial fluid leaking into the neural foramen, causing radicular symptoms as a result of chemical spinal nerve irritation.17 As the zygapophyseal joint experiences this laxity, the articular processes progressively override, causing subluxation of the joint24 and intervertebral disc narrowing accompanied by buckling or infolding of the ligamentum flavum.17 The ligamentum flavum can form cysts,25 fray, partially rupture, and ossify. Even though it does not represent hypertrophy of tissue, this buckling or redundancy of tissue is frequently referred to as ‘ligamentum flavum hypertrophy,’ which is a term that may not actually reflect the pathologic process.17 This degeneration further compromises the three-joint complex leading to increased instability. Krismer’s demonstration that fissured discs have increased axial rotation and lateral translation after torque supports this observation.26 During this phase, microinstability occurs at a specific segment, increasing stresses and loads in the zygapophyseal joint and disc complex. Further overload of these structures contributes to further annular tearing which frequently culminates in a path through the lamellae of the anulus fibrosus through which the nucleus pulposus can pass. It is at this point that a disc protrusion develops. This mass effect of the protruding anulus extends into the lumbar vertebral canal, the lateral recess, or more rarely, the foramen. Traversing nerve roots can be chemically irritated and/or mechanically compressed, causing radicular leg symptoms. As the protruding disc resorbs spontaneously or is iatrogenically removed with a surgical procedure, leg symptoms will commonly abate. The disc, however, is still left with a weakened anulus with compromised structural integrity accompanied by disc space narrowing. This newly weakened anulus in combination with laxity of the two zygapophyseal joint capsules creates a relatively unstable segment. The vertebral bodies just above and below this segment may shift and supercede the prior physiologic anterior–posterior translation, axial rotation, and/or flexion–extension bending. Thus, this superphysiologic motion creates instability at thesegment in question, sometimes

L5

L4

L3

Nucleus pulposus

Invertebral disc

Vertebral body

L5

L4

L3

S1

S1

L5

L4

L3

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L1 L2

‘High intensity zone’ annular tear

Disc dessication

Anulus fibrosus

Cauda equina

Disc dessication

Spinous process

Thecal sac

Lamina

Sacral nerves

S1 nerve

L5 nerve root in lateral recess

Anulus fibrosus

Axial

Left L4–5 3-joint

L4–5 3-joint with early osteophytic changes

IAP

SAP

‘High intensity zone’ annular tear

Inferior articular process

Superior articular process

Exiting L4 spinal nerve

Nucleus pulposus

Sagittal Axial

Fig. 77.1 The degeneration of the L4–5 segment (Part d [MRI scans]. From Jinkins JR, Rivista di Neuroradiologia 2002; 15:343 figures d and c.139)

Segmental dysfunction and early zygapophyseal joint degenration

Annular tear

Normal

Sagittal

Section 5: Biomechanical Disorders of the Lumbar Spine

815

816

Fig. 77.1 Cont’d

Joint cyst causing left L5 lateral recess stenosis, central stenosis and left radiolar symptoms

Microinstability causing joint fluid

Microinstability (MRI images reproduced from Jinkins JR, Rivista di Neuroradiologia 15:343, with permission)

L5

L4

L3

L5

L4

L3

S1

L5

L4

L3

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Upright flexion

Sagittal

S1

3-joint cyst

L4–5 zygapophyseal joint fluid

Disc morphology change in dynamic-kinetic MRI with flexion and extension

L5

L4

L3

Upright extension

Microinstability stretching 3-joint capsule

3-joint cyst causing left lateral recess and central stenosis

3-joint fluid

Axial

3-joint osteophytes

L5 spinal nerve root

L4 spinal nerve

3-joint osteophytes and degenerative changes

Sagittal

Axial

Part 3: Specific Disorders

Fig. 77.1 Cont’d

Disc extrusion

Disc protrusion

Diffuse disc bulging and disc dessication

L5

L4

L3

L5

L4

L3

L5

L4

L3

Sagittal

S1

S1

S1

Disc extrusion

Disc protrusion

Disc dessication and diffuse bulging

Axial

Disc protrusion

Disc dessication and diffuse bulging

Sagittal

Axial

Section 5: Biomechanical Disorders of the Lumbar Spine

817

818

Fig. 77.1 Cont’d

Central spinal stenosis

L5 degenerative spondylolisthesis

Disc bulge

Sagittal

L5

L5

L4

L3

L4

L3

S1

S1

Central spinal stenosis

Ligamentum flavum buckling

Central stenosis

Lateral recess narrowing (stenosis)

L4

L5

Axial

3-joint arthropathy

Diffuse disc bulging and degeneration

Foraminal narrowing (stenosis)

Sagittal

Axial

Part 3: Specific Disorders

Section 5: Biomechanical Disorders of the Lumbar Spine

causing degenerative spondylolisthesis. Degenerative spondylolisthesis most frequently occurs at the L4–5 segment, commonly accompanied by vertebral canal, lateral recess, and foraminal narrowing with the shifted vertebral bodies.16 Over time, with repetitive loading and progression of laxity and instability, the bone responds with osteophyte formation and may ultimately reach the third phase of the degenerative cascade as described below. The previously unstable spine becomes increasingly stiff in the stabilization phase, the third stage of the degenerative cascade. A patient may present with a long history of axial low back pain now with predominating leg pain. During the examination, range of motion is typically reduced in all directions, particularly with extension. There may also be tenderness over the paraspinal musculature as well as scoliotic curves. Notably, sustained lumbar extension may elicit radicular signs. Radiographs typically show uni- or multilevel spondylosis including hypertrophic osteophytic zygapophyseal joints, significant loss of disc height, extensive vertebral body osteophytes, narrowed foramina, and degenerative scoliosis. Reduced movement may also be present on lateral bending or flexion and extension films. During the mechanism of ‘stabilization’ further changes in the zygapophyseal joint and the disc are observed. In the zygapophyseal joint, cartilage destruction leads to joint fibrosis and enlargement, locking facets, and finally periarticular fibrosis. Concurrently, in the disc, nuclear loss leads to vertebral body approximation, endplate destruction, disc fibrosis, and finally osteophyte formation identified at the vertebral body ring apophysis. Circumferential osteophytic ridges form posterolaterally around extending laterally and anteriorly. These vertebral body rims consistently appear sclerotic, peaking posteriorly and lipping up superiorly at the tip, thus creating deep, oblique grooves.17 Osteophyte formation from the inferior articular process contributes to vertebral canal stenosis, and osteophyte formation extending from the superior articular process can contribute to narrowing of the neural foramen.27 The combination of disc height loss and bulging, ligamentum flavum buckling, and zygapophyseal joint osteophytic changes all combine to narrow the central spinal canal,28 the lateral recesses,29,30 and the neural foramina, compressing the traversing nerve and creating dynamic radicular leg pain. The end result of all of these changes is increased stiffness of the spine, eventually culminating in near-complete spondylosis and ‘autofusion.’ While it is tempting to make clear separations between each of the three phases of the degenerative cascade, the lines of distinction are in fact blurred. Thus, over a person’s lifetime, the spine transitions from excellent flexibility and disc hydration and pliability as a teenager moving to intermittent episodes of low back pain and muscle spasm as a young adult. This reflects the initial phase of the degenerative cascade, the dysfunctional phase. The patient usually experiences the instability phase next. These intermittent flares of axial low back pain lasting several days start to become more frequent, with episodes lasting for longer periods of time, reflecting progressive intervertebral disc annular tears. As the intervertebral disc anulus weakens and disc protrusions and extrusions develop, the patient has episodes of axial low back pain and/or leg pain usually lasting several weeks to months. With progression of osteophyte formation, the patient transitions from middle adulthood into late adulthood with the stability phase. Constant axial low back pain may become less constant as the spine autofuses, with some patients noting that their back pain has just melted away. If significant stenosis has developed as a result of this stabilizing spondylotic process, intermittent episodes of radicular pain may occur. In addition, while a patient has a tendency over time to sequentially pass from dysfunction to the unstable phase and then to stabilization, this might not always be the case. For example, one patient may bypass the second phase and pass

directly from dysfunction to stabilization, while another may pass back from the unstable phase to dysfunction, perhaps as a result of treatment. Finally, one must keep in mind that different levels may predominate at adjacent spinal levels. In summary, people of all ages may present with low back pain and spine pathology; an individual assessment at each episode will help guide noninterventional and interventional treatment algorithms to maintain patient function. Frequently, by communicating the natural history of spinal aging, the clinician can allay some of the patient’s fears and provide hope for maintained age-appropriate function.

PREDISPOSING ANATOMY AND ACTIVITIES The intervertebral disc is subjected to significant load during normal daily activities. Standing erect places approximately 500 N of compressive force on the spine, with an additional 1500 N caused by bending forward to lift 10 kg.31 Loading of the spine results in decreased disc height. Similarly, with enough force applied, traction has reproducibly been shown to increase the intervertebral height; however, consistent clinical effectiveness of lumbar traction has not been shown. Approximately 1.13% of body height is lost through normal daily activity, and this difference increases with advancing age and increasing body weight. The ability of the nucleus to displace under asymmetrical loading decreases with age,32 and traction can cause more intervertebral height in younger individuals. It appears that compressive forces contribute to disc degeneration, and the altered physical response of the aged disc may facilitate this response. The clinical correlate to these observed changes resulting from load lies in the findings of increased incidence of disc degeneration among persons involved in heavy physical work.33–35 It has been shown that benign spine pathology is associated with moderate work levels, while painful spine pathology correlated to the highest and lowest degrees of physical activity.36 Other studies have shown earlier onset of disc degeneration in men than women, possibly a result of men being more commonly involved in occupations involving heavy manual labor. Because compressive forces applied to the disc cause biomechanical changes, it would be expected that obesity, with the resulting increased load, would be involved in the acceleration of degenerative discs. However, studies on the effects of obesity on the prevalence and severity of degenerative discs have yielded conflicting results.34–38 Further evidence for excessive load as causative of disc degeneration is found in examination of persons involved in athletics. A small study of elite athletes demonstrated more severe disc degeneration than nonathletes, which was most commonly observed at the L5–S1 level. However, evaluation of elite athletes revealed no increased incidence of low back pain,39 again raising the question of the clinical significance of radiographic findings. The extreme physical loading experienced with weight lifting has been shown to correlate with only about 10% of the disc degeneration found.40 A study of elite gymnasts showed an increased incidence of radiographic disc degeneration (75%) compared to nonathletes (31%), and was able to demonstrate a correlation with back pain.41 At the opposite end of the spectrum, a sedentary life style and occupations such as motor vehicle driving have shown an increased incidence of disc degeneration.42 There is evidence to show that exercise can be beneficial in the treatment of low back pain.43–49 It is believed that this beneficial effect is primarily through early activation after onset of pain, maintenance of aerobic exercise, directional preference exercises, and possibly increased strength of the muscular corset surrounding the spine. The types of forces that are destructive and result in 819

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pathology versus those which facilitate repair and protection of the disc from further damage remain unknown. Altered forces may also be created by the spinal anatomy. Spinal disorders such as spondylolisthesis and scoliosis have been associated with an increased incidence of degenerative disc disease.50 This effect is most likely a result of abnormal forces imposed on the disc by the altered anatomy. In addition, excessive motion of an unstable bony framework results in internal disc disruption, tears, and annular bulging. This corresponds to the instability phase, the second phase of the degenerative cascade.15 Spine anomalies such as ‘transitional vertebra’ can lead to a similar alteration in biomechanical forces in the spine, thus affecting disc degeneration. To keep nomenclature consistent, especially for interventional procedures, effort should be made to label transitional vertebra as a sacralized lumbar segment or a lumbarized first sacral segment. In order to do this, the spinal segments should be labeled by counting down from the cranium and/or the ribs. The prevalence of transitional vertebra has been noted to be 7–30%, depending on the groups sampled and the criteria and methods used. Luoma studied a group of men without active complaints of low back pain. There were 138 working men (age range of 40–45) and 25 others aged 18–20 years. On MRI, transitional vertebrae were found 30% of the time with increased frequency of degenerative changes in the disc above the transitional segment among the younger men. In the middle-aged men there was decreased risk of degenerative changes in the disc below the transitional vertebra, presumably lending a protective effect on the lower disc. Interestingly, in this group of volunteers, when questioned about their low back pain history over the previous 4 years, there was no association of increased low back pain in those individuals with a transitional vertebra.51 Bertolotti’s syndrome depicts low back pain in association with an anomalous transitional lumbosacral segment. Elster revisited Bertolotti’s syndrome in a study of radiographic findings in 2000 patients with back pain who had lumbar spine X-rays and computed tomography (CT) or MRI scans. Transitional segments were found in 7% of subjects, who had disc pathology at the level immediately above the transitional segment nine times more often. Stenosis was also noted at an increased rate at the level above. Again, disc preservation at the level immediately below was observed.52 The hypothesized reason that early disc degeneration occurs in the segment above the transitional level is that more motion is forced in the segment immediately adjacent to the fixed segment, concentrating torsional biomechanical stresses. By the same token, postsurgical fusion is frequently associated with hastened adjacent level disc degeneration.53 In addition to the mechanical effects of load, compressive, torsional, and strain forces have been demonstrated to alter the biosynthetic activity of intervertebral discs.54 This may contribute to early degenerative changes through alterations in the supporting matrix. Clinically, flexion and torsional stress have been identified as risk factors for degenerative disc disease.42,55 Torsional stresses on the lumbar discs can be magnified by relative inflexibilities or weakness of parts of the body above and below the lumbar spine. If a hip joint capsule is relatively tight and restricts internal rotation during a functional activity such as walking, this requires segments above to accommodate the need for the pelvis to rotate in the transverse plane. If the pelvis cannot get the necessary axial motion to get proper pelvic rotation from the hip, the next joint complex to be asked for rotational motion will be the lumbar spine. Thus, increased rotational forces could develop in the lumbar discs and zygapophyseal joints. By the same token, it is easy to see how a transverse plane dominant activity such as golf and racket sports can introduce increased forces in the lumbar spine. If the hip joint and/or the thoracic spine/shoulder complex do not have the available range of motion, forces are quickly transmitted into the lumbar spine 820

structures. Although lower limb flexibility is not a predictor of low back pain, hamstring flexibility is strongly correlated to motion in subjects with a history of low back pain.56 Hip joint restriction can be a contributing factor that predisposes an individual to advanced lumbar disc degeneration. Hip inflexibility can increase forces seen in the lumbar spine zygapophyseal joints and thereby be associated with lumbar disc degeneration.57 If the iliopsoas muscle, tendon, and anterior hip joint capsule unit are restricted, this puts the pelvis in an anterior pelvic tilt. In other words, the anterior superior iliac spines are more inferior relative to the posterior superior iliac spines. In an individual with such restriction in the anterior hip structures, compensatory spinal extension must occur for a person to remain fully erect in the sagittal plane. Without this compensatory spinal extension motion, the person would have to walk looking toward the ground. These extension-type forces can increase the biomechanical stress in the zygapophyseal joints,12 creating inflammation and laxity, and thereby creating abnormal strain forces and degeneration in the lumbar discs. Iliopsoas and anterior hip capsule flexibility again becomes an important factor in later stages of the lumbar degenerative disc cascade as the spine matures developing osteophytes that narrow the vertebral canal, lateral recesses, and the foramina. This frequently becomes problematic during spine extension as the spinal canal narrows and the traversing nerve structures are constricted.27,58,59 When the spinal canal is already narrowed by degenerative changes, activities requiring relative lumbar extension such as walking are associated with compression on these neural structures, causing neuropathic-type radicular symptoms in one or both legs. To reduce the symptoms and the degree of flexion in the spine, the compensatory postural change is frequently to bend forward at the waist. This compensatory posture puts the iliopsoas muscles in a shortened position. After a period of time, the hip flexors become shortened, weakened, and tight. This hip flexor tightness adds to the lumbar extension moment forces, leading to further compression of neural structures as they pass through a tightened neural canal. Therefore, assessing iliopsoas flexibility and hip joint capsule mobility is clinically important whether the patient is in the earliest or the latest stages of the lumbar degenerative cascade. Vad et al. found a significant correlation between low back pain and decreased hip internal rotation in the lead hip in professional tennis players (mean age of 25.4 years)60 and golfers (mean age of 30.7 years).61 This important kinetic chain link between the hip and the spine has also been clinically demonstrated in small case series of hip osteoarthritis and lumbar spinal stenosis. Surin reported that 5 of 15 subjects who had severe spinal stenosis also had severe hip osteoarthritis; excellent results were noted in 4 patients who underwent a decompressive laminectomy followed by a total hip replacement.62 Similarly, lumbar spinal stenosis has been associated with patients who have undergone a hip joint replacement, but have continued leg pain. Six of 8 patients with disabling posterior buttock pain after hip arthroplasty underwent a lumbar decompressive procedure with complete relief of their symptoms.63 McNamara reported on 14 patients with both symptomatic lumbar spinal stenosis and lower limb degenerative joint disease. Nine of the patients had persistent symptoms attributed to spinal stenosis over 9 months after joint arthroplasty, seven of whom subsequently required lumbar decompressive surgery.64 Therefore, because of the relationship between the hip and the lumbar spine, it is important to address hip inflexibility in the rehabilitation program. Specifically, manual mobilization and functional flexibility exercises of the hip joint have been shown to decrease pain and disability in a series of patients with lumbar spinal stenosis.65 Not only proper flexibility of the lower limb is required to normalize lumbar spine forces, but also strength of the ‘core musculature.’

Section 5: Biomechanical Disorders of the Lumbar Spine

These core muscles include the abdominals (rectus abdominis, obliques, transversus abdominis),66 lumbar paraspinal muscles (erector spinae, multifidi), quadratus lumborum,67 pelvic floor muscles,68 the diaphragm,69 and the hip girdle musculature.70 If these core muscles exhibit weak muscular control, this may cause excessive external loads on the disc.57 The strength and firing patterns of the quadratus lumborum67 and the transversus abdominis,66 gluteus maximus, and gluteus medius,70,71 have received particular attention as important spine stabilizers in low back pain. Multifidi muscle atrophy has been associated with low back pain.72 Pelvic floor muscles have been observed to be co-activated with the contraction of the transversus abdominis.68 It also seems that endurance of the core muscles is even more important than strength.73 It remains to be seen if improving core muscle strength and endurance will prevent symptomatic degenerative discs, but early data do suggest that a core muscle strengthening program trends toward decreasing the incidence of low back pain.74,75 Core stabilization exercises for treatment of low back pain have seen some success.47,76,77 More randomized controlled studies need be performed to further document the utility of core strengthening programs in the prevention and treatment of lumbar degenerative discs.

HISTOLOGY The biomechanical function of the disc is determined by the structure. The histology of normal and degenerative discs has been extensively examined in attempt to provide a more thorough understanding of the structural changes which predispose the disc to mechanical failure. Changes have been observed in the anulus, nucleus, cellular layout, and protein composition of the matrix. A normal young anulus fibrosus consists of a complex system of fibers in a circular course, with lamellae of differing thickness. The lamellae of collagen fibers run obliquely, separated by layers of ground substance. By the fifth decade, gaps and fissures are observed between the collagen fiber bundles. Fragmentation and loss of individual collagen fibers is observed by age 65, and increased appearance of chondroid tissue is present by 70 years of age.78 Clinically, three different types of annular tears have been described. Rim lesions are tears in the periphery of the anulus, which occur more predominantly anteriorly. Concentric tears represent rupture between the collagen lamellae in a circumferential pattern. Radial tears divide the lamellae and are perpendicular to the endplate. Radial tears occur more commonly in the posterior aspect of the anulus. These annular tears may be sufficient to cause low back symptoms and certainly predispose the disc to herniation. Unfortunately, a uniform classification system has not been universally accepted for disc herniation. Disc bulging typically refers to appearance of diffuse bulging without focal prominence associated with loss of disc space. An isolated disc bulge is generally not sufficient to cause canal or foraminal stenosis unless accompanied by hypertrophic degenerative changes of the vertebral body endplates and superior articular processes or from congenitally short pedicles. Protrusion represents a focal lesion of the nucleus through a defect in the internal annular fibers. However, the nucleus remains contained within the anulus. Extrusion represents a full disruption of annular fibers through which the nucleus migrates, but communication is maintained with the parent disc. Sequestration represents complete separation of a nuclear fragment from the disc, which may migrate cranially or caudally. This fragment has separated from the disc of origin. Although it would be preferred that all clinicians follow the same ‘rules’ to describe disc pathology, it is even more important for a clinician to be internally consistent in the way in which he or she describes the anatomic abnormalities on MRI

scan.79 As such, with all clinicians not adhering to the same terminology,80 it is essential to view the actual images of each patient for whom the clinician is providing care. In the end, only the healthcare provider that has obtained a careful history and physical examination can clinically correlate properly the findings on radiographic imaging with the patient’s symptoms. Not only does the histology of the anulus change, but so do the biomechanical properties. Healthy intervertebral discs show decreasing tensile strain of the anulus fibrosus from inner to outer layers when placed under compressive loads. Compression alone, as described above, is not sufficient to cause herniation. Disc degenerative changes coupled with sagittal and transverse plane motions lead to annular tears, which allow the nucleus to herniate under load. The integrity of the annular fibers is critical to maintaining normal disc structure. In healthy discs, annular fibers are responsible for restricting axial rotation to a greater degree than facet joints.81 However, a change in loading pattern appears to exist in degenerative disc anulus fibrosus,82 and the mechanical properties of the anulus have been shown to change with age. The tensile behavior is related to the composition of the tissue. Therefore, increased degeneration results in altered biomechanics, which predisposes the disc to further degeneration. Further evidence for this cycle can be found in modeling studies which have demonstrated that annular tears may have a role in further accelerating degenerative changes.83 In fact, in animal models, degenerative discs can be created which closely mimic human histology by introducing an annular laceration.84 Further evidence for a pivotal role of the anulus is the finding that disc degeneration appears to occur before facet osteoarthritis.85 Changes are also observed in the character of the nucleus. The homogenous, gelatinous central disc changes to dry, fibrous tissue with advancing age. The water content of the nucleus decreases from 90% to 74% throughout the first eight decades.32 However, this loss of water appears to be related to aging and not degeneration as it has been shown that degenerative and normal discs from the same spine have the same water content.86 This again raises the concern over distinguishing between normal aging changes seen radiographically and true symptomatic pathology. Severely degenerative discs have also been found to contain granulation tissue and the boundary between the nucleus pulposus and anulus fibrosus becomes more diffuse, with the two tissues becoming less distinguishable. These changes are associated with loss of endplate cartilage and osteophyte formation, as well as formation of fissures and cavities in the anulus and nucleus. A morphologic grading system has been proposed by Thompson et al. which scores degenerative discs on the basis of changes in the nucleus, anulus, endplate, and vertebral body. This system is based on the gross appearance of pathologic sections. Grade I represents a bulging nucleus, an anulus with discrete fibrous lamellae, uniformly thickened endplates, and vertebral bodies with rounded margins. Grade II has white fibrous tissue on the periphery of the nucleus, mucinous material between lamellae of the anulus, irregular endplates, and pointed margins of the vertebral body. Grade III describes a nucleus with consolidated fibrous tissue, extensive mucinous infiltration of the anulus with loss of the annular–nuclear demarcation, focal defects in endplate cartilage, and early osteophytes. Grade IV represents a nucleus with horizontal clefts, focal disruption of the anulus, irregularity and focal sclerosis of subchondral bone, and osteophytes of less than 2 mm. Finally, grade V represents clefts extending through the nucleus and anulus, diffuse sclerosis, and large osteophytes. 87 Degeneration and aging also affect the cellular layout. Young human discs show cells within small lacunar spaces within the matrix, 821

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whereas degenerative disc specimens show cells clustered amidst decreased or architecturally modified matrix.88 In addition, fibroblasts are the predominant cell type in young anulus, with increasing populations of chondrocytic phenotypes with advancing age.78 Changes have been observed at the molecular level, which helps explain the altered matrix arrangement and water content. The biochemical composition of the disc is crucial to the osmotic balance and therefore mechanical behavior of the disc.89 The major structural proteoglycan in the intervertebral disc is aggrecan, which acts to attract water into the disc. Nucleus pulposus cells from degenerative discs show decreased expression of aggrecan, and a similar decrease in water content.90 The collagen network creates the matrix of the disc, within which fibroblasts or chondrocytes are imbedded. Degenerative discs have a low proteoglycan to collagen ratio. Cells of the anulus fibrosus exhibit decreased collagen expression following degeneration. Whereas the growth and development phase shows active synthesis of aggrecan and procollagen type I and II, the degeneration phase is associated with increase in the denaturation of type II collagen without an increase in type II procollagen or aggrecan synthesis. Specifically, type II procollagen synthesis is decreased, and type II collagen denaturation is increased. Type I collagen expression has also been shown to increase and contribute to abnormal matrix synthesis.91 In addition to the changes in structural protein synthesis that occur with degeneration, the degenerative disc is also characterized by an increase in catabolic activity. Proteases capable of producing degradation of extracellular matrix are normally kept in check by tissue inhibitors. However, this balance is altered in disc degeneration, with cytokines, in particular interleukin (IL)-1, implicated in activating the active degradation process. In addition, there is a net increase in matrix degrading enzyme activity, such as matrix metalloproteinases, which act to cleave aggrecan.92 Compounded on the changes observed with age, the physical environment of the disc may alter the balance between matrix synthesis and breakdown. Altered metabolism of disc cells has been shown to occur in response to mechanical loads. This response may be due to changes in systemic factors, disc fluid shifts, and resultant changes in osmolality, blood flow, altered nutrition, mechanosignaling, or a combination of these factors.93 Compressive forces in vivo in animal models have demonstrated an increase in collagen type I and decrease in proteoglycans, chondroitin sulfate, and collagen type II in the nucleus.54 This may contribute to early degenerative changes through alteration in the supporting matrix. In turn, these changes at the biochemical level appear to have profound impact on the mechanical behavior of the disc. The decrease in aggrecan parallels the decreased water content observed in disc degeneration, which leads to increased deformation under compressive and torsional loads. The deformation results in increased strain experienced by disc fibrochondrocytes, and may alter the synthesis and homeostasis of reparative and degenerative enzymes, leading to further disruption of the matrix. The clinical importance of changes in the matrix is underscored by the finding that the components of the matrix from discs of the same degenerative grade do not differ with lumbar level, age, or sex, suggesting that the differences are in fact a result of degeneration.87 The net effect of all of these changes is a cascade of degeneration. Age and degeneration result in an altered histological composition of the disc. In addition, altered biomechanics of the disc, which also occur with aging and degeneration, lead to abnormal distribution of forces and result in altered biosynthesis. In turn, these changes at the molecular level result in a decreased ability of the disc to accept normal physiologic loads and motion, further contributing to the degenerative cascade. As a result, a cycle of degeneration and maladaptive responses to stress occurs. 822

CHEMICAL INFLAMMATORY PROPERTIES OF THE DEGENERATIVE DISC Mechanically compressive disc protrusions are not the only causes of radicular pain. For this reason, chemical markers from the disc have been implicated in the inflammatory response. Saal found phospholipase A2 in human disc samples resected for lumbar degenerative disc-related radiculopathy.94 IL-1 has been implicated in chemical radiculitis in rats.95 Matrix metalloproteinases, nitric oxide, IL-6, and prostaglandin E2 have also been implicated in intervertebral disc protrusions.96,97 Glutamate has been detected in higher levels in herniated discs compared to nonherniated discs.98 In addition, different types of disc herniations seem to have different biochemical traits. Leukotriene B4 and thromboxane B2 are seen in higher levels in noncontained disc herniations compared to contained disc herniations.99 Higher concentrations of prostaglandin E2 have been found in sequestered disc fragments and in those individuals with a positive straight leg raise.100 Furthermore, prostaglandin E2 seems to be upregulated by IL-1α and decreased by tumor necrosis factor-alpha and betamethasone.101

MEDICAL AND GENETIC RISK FACTORS As persons with similar anatomy and predisposing activities have differing incidence of degenerative disc disease, a number of environmental, medical, and genetic factors have been investigated as potential risk factors. In addition, there is evidence for familial trends in degenerative disc disease.102,103 In particular, two collagen IX alleles have been associated with lumbar disc herniation,104 as well as aggrecan, vitamin D receptor, and matrix metalloproteinase-3 gene polymorphisms.42 Specific vitamin D receptor alleles have also been associated with radiographic disc degeneration.105 In a study of metalloproteinase polymorphisms, the 5A/6A polymorphism was associated with radiographically identified degenerative changes in elderly subjects, suggesting this as a possible risk factor. The study did not show any evidence of accelerated degenerative changes in young persons carrying this genotype.106 However, a case-control study of radiographic changes did demonstrate an association of degenerative changes associated with an aggrecan allele subtype in young subjects.107 There is also evidence for synergistic effects of genetic and environmental factors. A cross-sectional study of the COL9A3 gene polymorphism, obesity, and the incidence of radiographic degenerative disease demonstrated that the effect of obesity on lumbar disc degeneration was modified by this polymorphism.108 This may help to explain the inconsistencies found in studying the effect of obesity on disc degeneration as discussed above. However, most of the studies investigating genetic predispositions focused on radiographic criteria for the definition of degenerative disease, and did not assess clinical symptoms. Future studies are needed to evaluate the incidence of clinically significant, symptomatic disease among patients believed to be at increased risk. Ischemia is believed to play an important pathogenic role in initiating disc degeneration. Decreased oxygen tension with resulting decrease in synthesis of proteoglycans and collagen may be responsible for this effect. The association of several medical conditions with increased incidence of degenerative disease further supports the role of ischemia. Calcific deposits on the posterior aortic wall, indicative of advanced aortic atherosclerosis, have been associated with increased incidence of radiographic disc degeneration as well as low back pain.109,110 The rationale for this association comes from the fact that the feeding arteries of the lumbar spine originate from

Section 5: Biomechanical Disorders of the Lumbar Spine

the posterior aorta, and atherosclerosis would cause decreased blood flow and ischemia of the lumbar spine. Further evidence of the deleterious effect of ischemia comes from identical twin studies that have demonstrated that smoking is associated with an 18% increased incidence of disc degeneration in the lumbar spine.111 It has also been established that smokers are more likely to complain of back pain.112 Infection may also act as a precipitating factor and has clinically been associated with discogenic radiculitis. A study of 36 disc samples from patients undergoing discectomy demonstrated positive isolates of Propionibacterium acnes, coagulase negative staphylococcus, or corynebacterium in 53% of samples. No isolates were recovered from control samples taken at the time of surgical fusion.113 Therefore, this study links infectious bacteria to symptomatic discs but does not establish an association of infection with histological disc degeneration. Interestingly, clinical associations have been noted with degenerative changes and osteoporosis,114,115 and Scheuermann’s disease.116 The increased incidence of both degenerative disc disease and osteoporosis among sedentary individuals suggests that the effect may not be causative. Heithoff et al.116 found degenerative lumbar discs in younger patients who also had findings of thoracolumbar Scheuermann’s disease. In a group of 1419 patients referred for lumbar spine MRIs, there was an incidence of this interesting link in 9% of patients. Eighty-one percent of the subjects were younger than 40 years old and 9% under 21 years old. This association was hypothesized to be an expression of an intrinsic disc defect and/or cartilaginous endplates that compromises nutrition and results in structural weakness and early degeneration.116 This association may represent a clinical subpopulation as opposed to a distinct pathologic mechanism.

RADIOGRAPHIC FINDINGS The incidence of radiographic degenerative disc disease is known to increase with age. However, radiographic changes do not directly correlate with symptoms. Asymptomatic subjects show abnormal findings in the disc in 24% of lumbar myelograms, 36% of CT scans, and 38% of discograms.117–119 In young, asymptomatic women aged 21–40, 33% showed MRI evidence of disc degeneration.120 Boden et al. found that one-third of 67 asymptomatic subjects (average age 42, range 20–80 years old) had abnormalities on lumbar spine imaging. For subjects younger than 60 years old, 20% had herniated disc. In individuals over age 60, 57% were abnormal – 36% with a disc herniation and 21% with spinal stenosis.121 Jensen et al. also studied MRI findings in asymptomatic individuals with 98 subjects of mean age of 42.3 years (range 20–80 years old). He noted 52% had a bulge at least at one level, 27% had a disc protrusion, 1% had a disc extrusion, 19% had a Schmorl’s node, 14% had annular defects, and 8% had zygapophyseal joint arthropathy. Only 36% of discs were completely normal at all levels.122 In a study of working males aged 20–58, 32% of asymptomatic subjects had abnormal imaging on MRI, and 47% of subjects with low back pain had normal MRI findings.123 In addition, abnormal MRI findings in asymptomatic persons have not been shown to be predictive of development of low back pain in the future.124 Therefore, the key is to use the imaging studies to complement the clinical picture. Clinical correlation is required to determine the significance of abnormalities observed on MRI. To this end, obtaining imaging studies too early could lead to inappropriate treatment if not used in the context of patient symptoms. If these aforementioned studies have clearly shown that lumbar discs degenerate both with and without symptoms, perhaps we should be challenged to reconsider the label of ‘lumbar degenerative disc disease.’

The term ‘disease’ usually is used to describe a pathologic state of illness, and patients frequently become alarmed when they learn that they have acquired a new ‘disease.’ How can so many people be walking around without symptoms and have ‘lumbar degenerative disc disease’ on MRI? Therefore, as spine healthcare providers, it is necessary to be cautious in the word choice we use to describe our patients’ intervertebral discs as well as the diagnoses with which we label them. Many patients can be relieved to know that the normal spine commonly changes with age in a similar manner to gray hair appearing on their head. With this caveat, magnetic resonance imaging can be a useful tool for assessing disc degeneration. Annular bulging or tears and decreased signal intensity of the nucleus pulposus on T2-weighted images can be observed. In addition, these changes of the disc are frequently accompanied by adjacent marrow changes. Modic et al. defined these changes as types I–III, with type I representing decreased intensity on T1-weighted, increased intensity on T2-weighted, type II with increased intensity on T1-weighted and isointense signal on T2weighted, and type III with hypointense signal on both T1- and T2-weighted images.125 Diurnal changes have been observed on T2weighted MRI among younger individuals (age < 35), reflecting the alteration in water content throughout the day. This diurnal variation does not appear to be present radiographically in individuals over the age of 35 or among patients with degenerative discs,126 consistent with the observed loss of water content in these populations. As the saying goes, ‘the bigger they are, the harder they fall,’ so it goes for lumbar disc herniations. The larger the disc herniation, the more the disc tends to resorb.127 Disc extrusions seem to have a better chance of ‘shrinking’ spontaneously.94,128 Ahn et al. studied 36 subjects with a herniated disc (18 subligamentous, 14 transligamentous, and 4 sequestered). Overall, 25 of the 36 (69%) decreased in size. The further the disc material traveled beyond the posterior longitudinal ligament, the more the material disappeared. Fifty-six percent of the subligamentous herniations, 79% of the transligamentous herniations, and 100% of the sequestered herniations decreased in size.129 The mechanism of disc material resorption is presumably from immune system-mediated phagocytic response. This proposed mechanism is supported by the finding of inflammatory products, including cell infiltration, neovascularization, and granulation, which were observed in 100% of transligamentously extruded discs, 81.8% of subligamentously extruded discs, and only 16.9% of contained protruded discs.130 Antigen–antibody complexes are likely implicated as well.131 As mentioned, although MRI is able to demonstrate anatomic changes, these findings do not always correlate with the clinical picture and affect the patient symptomatically or functionally. High-intensity zones on MRI have frequently been associated with discogenic pain. However, there is also a high prevalence of this finding among asymptomatic persons.132 To date, the only imaging method for symptomatic assessment of low back pain remains provocation lumbar discography. The distinction between these imaging modalities is demonstrated by the observation that among patients with discography-proven discogenic pain, no specific abnormality found on MRI can be used as a predictor of pain. Discography may be superior to MRI for the identification of annular tears,133 and discography has the ability to provoke the patient’s symptoms. Reproduction of a patient’s typical back pain upon injection, with a negative pain response in at least one control level, represents a positive discogram. Discography findings in disc degeneration include loss of disc height with complex or multiple annular fissures with or without leakage of contrast agent. A bulging anulus is also often observed. A diffuse pattern of annular tearing suggests the chronic nature of degeneration. The modified Dallas scale, introduced by Bogduk and April, grades 823

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discs at 0–4. Grade 0 represents contrast remaining entirely within a normal nucleus pulposus. Grade 1 represents contrast extending radially along a fissure involving the inner third of the anulus. Grade 2 lesions show contrast extending into the middle third, and grade 3 extending into the outer third. Grade 4 represents a grade 3 tear dissecting radially to involve more than 30° of the disc circumference.134 Other authors have added grade 5 (full-thickness tear), grade 6 (disc sequestration), and grade 7 (diffuse annular tear).135,136 Please refer to Chapter 94 on the clinical utility of lumbar discography and how it is used in the algorithmic assessment of a low back pain. Investigations are currently underway with ultrasound to locate specific pathologic defects in intervertebral discs. Previous studies have shown utility in screening for disc degeneration,137 and the use of a vibrating probe for pain provocation has been suggested as a useful screen prior to discography.138

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81. Krismer M, Haid C, Rabl W. The contribution of annulus fibers to torque resistance. Spine 1996; 21(22):2551–2557.

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82. Shiraz-Adl SA, Suresh CS, Ahmed AM. Stress analysis of the lumbar disc-body unit in compression. Spine 1984; 9:120–134.

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56. Esola MA, McClure PW, Fitzgerald GK, et al. Analysis of lumbar spine and hip motion during forward bending in subjects with and without a history of low back pain. Spine 1996; 21(1):71–78. 57. Akuthota V, Nadler SF. Core strengthening. Arch Phys Med Rehabil 2004; 85(Suppl 1):S86–S92. 58. Dai LY, Yu YK, Zhang WM, et al. The effect of flexion–extension motion of the lumbar spine on the capacity of the spinal canal. An experimental study. Spine1989; 14:523–525. 59. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al. Lumbar spinal nerve lateral entrapment. Clin Orthop 1982; 169:171–178. 60. Vad VB, Gebeh A, Dines D, et al. Hip and shoulder internal rotation range of motion deficits in professional tennis players. J Sci Med Sport 2003; 6(1): 71–75. 61. Vad VB, Bhat AL, Basrai D, et al. Low back pain in professional golfers. The role of associated hip and low back range of motion deficits. Am J Sports Med 2004; 32(2):494–497. 62. Surin V, Hedelin E, Smith L. Degenerative lumbar spinal stenosis: results of operative treatment. Acta Orthop Scand 1982; 53(1):79–85. 63. Bohl WR, Steffee AD. Lumbar spinal stenosis. A cause of continued pain and disability in patients after total hip arthroplasty. Spine 1979; 4:168–173. 64. McNamara MJ, Barrett KG, Christie MJ, et al. Lumbar spinal stenosis and lower extremity arthroplasty. J Arthroplasty 1993; 8(3):273–277. 65. Whitman JM, Flynn TW, Fritz JM. Nonsurgical management of patients with lumbar spinal stenosis: a literature review and a case series of three patients managed with physical therapy (Review). Phys Med Rehabil Clin N Am 2003; 14(1): 77–101, vi–vi.i 66. Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain. A motor control evaluation of transversus abdominis. Spine 1996; 21:2640–2650. 67. McGill SM. Low back stability: from formal description to issues for performance and rehabilitation. Exerc Sport Sci Rev 2001; 29:26–31. 68. Sapsford RR, Hodges PW. Contraction of the pelvic floor muscles during abdominal maneuvers. Arch Phys Med Rehabil 2001; 82:1081–1088. 69. Hodges P, Kaigle Holm A, Holm S, et al. Intervertebral stiffness of the spine is increased by evoked contraction of transversus abdominis and the diaphragm: in vivo porcine studies. Spine 2003; 28(23):2594–2601. 70. Nadler SF, Malanga GA, Feinberg JH, et al. Relationship between hip muscle imbalance and occurrence of low back pain in collegiate athletes: a prospective study. Am J Phys Med Rehabil 2001; 80:572–577. 71. Nadler SF, Malanga GA, DePrince M, et al. The relationship between lower extremity injury, low back pain, and hip muscle strength in male and female collegiate athletes. Clin J Sport Med 2000; 10(2):89–97. 72. Hides JA, Richardson CA, Jull GA. Multifidus muscle recovery is not automatic after resolution of acute, first-episode low back pain. Spine 1996; 21:2763–2769. 73. Taimela S, Kankaanpaa M, Luoto S. The effect of lumbar fatigue on the ability to sense a change in lumbar position. A controlled study. Spine 1999; 24:1322–1377. 74. Nadler SF, Malanga GA, Bartoli LA, et al. Hip muscle imbalance and low back pain in athletes: influence of core strengthening. Med Sci Sports Exerc 2002; 34:9–16.

84. Anderson DG, Izzo MW, Hall DJ, et al. Comparative gene expression profiling of normal and degenerative discs: analysis of a rabbit annular laceration model. Spine 2002; 27(12):1291–1296. 85. Butler D, Trafimow JH, Andersson GB, et al. Discs degenerate before facets. Spine 1990; 15(2):111–113. 86. Pearce RH, Grimmer BJ, Adams ME. Degeneration and the chemical composition of the human lumbar intervertebral disc. J Orthop Res 1987; 5:198–205. 87. Thompson JP, Pearce RH, Schechter MT, et al. Preliminary evaluation of a scheme for grading the gross morphology of the human intervertebral disc. Spine 1990; 15(5):411–415. 88. Gruber HE, Hanley E. Analysis of aging and degeneration of the human intervertebral disc: comparison of surgical specimens with normal controls. Spine 1998; 23(7):751–757. 89. Urban JP, McMullin JF. Swelling pressure of the intervertebral disc: influence of proteoglycan and collagen contents. Biorheology 1985; 22:145–157. 90. Sive JI, Jeziorsk M, Watkins A, et al. Expression of chondrocyte markers by cells of normal and degenerate intervertebral discs. Molec Pathol 2002; 55:91–97. 91. Antoniou J, Steffen T, Nelson F, et al. The human lumbar intervertebral disc: evidence for changes in the biosynthesis and denaturation of the extracellular matrix with growth, maturation, ageing, and degneration. J Clin Invest 1996; 98(4): 996–1003. 92. Freemont AJ, Watkins A, Le Maitre C, et al. Current understanding of cellular and molecular events in intervertebral disc degeneration: implications for therapy. J Pathol 2002; 196:374–379. 93. Urban JP. The effect of physical factors on disk cell metabolism. In: Buckwalter JA, Goldberg VM, Woo S.L-Y, eds. Musckuloskeletal soft tissue aging impact on mobility. Rosemont, IL: Am Acad Orthopaed Surgeons; 1993:391–412. 94. Saal JA, Saal JS, Herzog RJ. The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine 1990; 15(7):683–686. 95. Wehling P, Cleveland SJ, Heininger K, et al. Neurophysiologic changes in lumbar nerve root inflammation in the rat after treatment with cytokine inhibitor. Evidence for a role of interleukin-1. Spine 1996; 21(8):931–935. 96. Kang JD, Georgescu HI, McIntyre-Larkin L, et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 1996; 21(3):271–277. 97. Kang JD, Stefanovic-Racic M, McIntyre LA, et al. Toward a biochemical understanding of human intervertebral disc degeneration and herniation. Contributions of nitric oxide, interleukins, prostaglandin E2, and matrix metalloproteinases. Spine 1997; 22(10):1065–1073. 98. Harrington JF, Messier AA, Berelter D, et al. Herniated lumbar disc material as a source of free glutamate available to affect pain signals through the dorsal root ganglion. Spine 2000; 25(8):929–936. 99. Nygaard OP, Mellgren SI, Osterud B. The inflammatory properties of contained and noncontained lumbar disc herniation. Spine 1997; 22(21):2484–2488. 100. O’Donnell JL, O’Donnell AL. Prostaglandin E2 content in herniated lumbar disc disease. Spine 1996; 21(4):1653–1655. 101. Takahashi H, Suguro T, Okazima Y, et al. Inflammatory cytokines in the herniated disc of the lumbar spine. Spine 1996; 21(2):218–224.

75. Leetun DT, Ireland ML, Willson JD, et al. Core stability measures as risk factors for lower extremity injury in athletes. Med Sci Sports Exer 2004; 36(6):926–934.

102. Matsui H, Kanamori M, Ishihara H, et al. Familial predisposition for lumbar degenerative disc disease. A case-control study. Spine 1998; 23(9): 1029–1034.

76. Manniche C, Lundberg E, Christensen I, et al. Intensive dynamic back exercises for chronic low back pain: a clinical trial. Pain 1991; 47:53–63.

103. Simmons ED Jr, Guntupalli M, Kowalski JM, et al. Familial predisposition for degenerative disc disease. A case-control study. Spine 1996; 21(13):1527–1529.

77. Saal JA, Saal JS. Nonoperative treatment of herniated lumbar intervertebral disc with radiculopathy. An outcome study. Spine 1989; 14:431–437.

104. Annunen S, Paassilta P, Lohiniva J, et al. An allele of COL9A2 associated with intervertebral disc disease. Science 1999; 285(5426):409–412.

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123. Savage RA, Whitehouse GH, Roberts N. The relationship between the magnetic resonance imaging appearance of the lumbar spine and low back pain, age, and occupation in males. Eur Spine J 1997; 6(2):106–114.

106. Takahashi M, Haro H, Wakabayashi Y, et al. The association of degeneration of the intervertebral disc with 5a/6a polymorphism in the promoter of the human matrix metalloproteinase-3 gene. J Bone Joint Surg [Br] 2001; 83(4):491–495.

124. Borenstein DG, O’Mara JW, Boden SD, et al. The value of magnetic resonance imaging of the lumbar spine to predict low-back pain in asymptomatic subjects: a seven-year follow-up study. J Bone Joint Surg [Am] 2001; 83A(9): 1206–1211.

107. Kawaguchi Y, Osada R, Kanamori M, et al. Association between an aggrecan gene polymorphism and lumbar disc degeneration. Spine 1999; 24(23):2456–2460. 108. Solovieva, S, Lohiniva J, Leino-Arjas P, et al. COL9A3 gene polymorphism and obesity in intervertebral disc degeneration of the lumbar spine: evidence of gene–environmental interaction. Spine 2002; 27(23):2691–2696. 109. Kauppila LI, McAlindon T, Evans S, et al. Disc degeneration/back pain and calcification of the abdominal aorta. A 25-year follow-up study in Framingham. Spine 1997; 22(14):1642–1649. 110. Kurunlahti ML Tervonen O, Vanharanta H, et al. Association of atherosclerosis with low back pain and the degree of disc degeneration. Spine 1999; 24(20): 2080–2084. 111. Battie MC, Videman T, Gill K, et al. Smoking and lumbar intervertebral disc degeneration: an MRI study of identical twins. Spine 1991; 16(9):1015–1021. 112. Miranda H, Viikari-Juntura E, Martikainen R, et al. Individual factors, occupational loading, and physical exercise as predictors of sciatic pain. Spine 2002; 27(10):1102–1109. 113. Stirling A, Worthington T, Rafiq M, et al. Association between sciatica and Propionibacterium acnes. Lancet 2001; 357:2024–2025.

126. Karakida O, Ueda H, Ueda M, et al. Diurnal T2 value changes in the lumbar intervertebral discs. Clin Radiol 2003; 58(5):389–392. 127. Matsubara Y, Kato F, Mimatsu K, et al. Serial changes on MRI in lumbar disc herniations treated conservatively. Neuroradiology 1995; 37(5):378–383. 128. Yukawa Y, Kato F, Matsubara Y, et al. Serial magnetic resonance imaging followup study of lumbar disc herniation conservatively treated for average 30 months: relation between reduction of herniation and degeneration of disc. J Spinal Disord 1996; 9(3):251–256. 129. Ahn SH, Ahn MW, Byun WM. Effect of the transligamentous extension of lumbar disc herniations on their regression and the clinical outcome of sciatica. Spine 2000; 25(4):475–480. 130. Ikeda T, Nakamura T, Kikuchi T, et al. Pathomechanism of spontaneous regression of the herniated lumbar disc: histologic and immunohistochemical study. J Spinal Disord 1996; 9(2):136–140.

114. Harada A, Okuizumi H, Miyagi N, et al. Correlation between bone mineral density and intervertebral disc degeneration. Spine 1998; 23(8):857–861.

131. Satoh K, Konno S, Nishiyama K, et al. Presence and distribution of antigen– antibody complexes in the herniated nucleus pulposus. Spine 1999; 24(19): 1980–1984.

115. Margulies JY, Payzer A, Nyska M, et al. The relationship between degenerative changes and osteoporosis in the lumbar spine. Clin Orthop 1996; 324:145–152.

132. Carragee EJ, Paragioudakis SJ, Khurana S. Lumbar high intensity zone and discography in subjects without low back problems. Spine 2000; 25(23):2987–2992.

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133. Boden SD. The use of radiographic imaging studies in the evaluation of patients who have degenerative disorders of the lumbar spine. J Bone Joint Surg [Am] 1996; 78A(1):114–125.

117. Hitselberger WE, Witten RM. Abnormal myelograms in asymptomatic patients. J Neurosurg 1968; 28:204–206. 118. Holt EP. The question of lumbar discography. J Bone Joint Surg [Am] 1968; 50:720–726. 119. Wiesel SW, Tsourmas N, Feffer HL, et al. A study of computer assisted tomography. I. The incidence of positive CAT scans in an asymptomatic group of patients. Spine 1984; 9:549–551.

134. April C, Bogduk N. High intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. Br J Radiol 1992; 65:361–369. 135. Bernard TN. Lumbar discography followed by computed tomography refining the diagnosis of low back pain. Spine 1990; 15:690–707. 136. Schellhas KP, Pollei SR, Gundry CR, et al. Lumbar disc high intensity zone: correlation of magnetic resonance imaging and discography. Spine 1996; 21(1): 79–86.

120. Powell MC, Wilson M, Szypryt P, et al. Prevalence of lumbar disc degeneration observed by magnetic resonance in symptomless women. Lancet 1986; 2(8520):1366–1367.

137. Tervonen O, Lahde S, Vanharanta H. Ultrasound diagnosis of lumbar disc degeneration. Spine 1991; 16:951–954.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disk Disorders ■ i: Physiology and Assessment

CHAPTER

78

Biomechanics of the Intervertebral Disc Dawn M. Elliott, Chandra S. Yerramalli and Joshua D. Auerbach

INTRODUCTION: STRUCTURE AND FUNCTION OF DISC The intervertebral disc separates the rigid vertebral bodies and allows for large, complex, three-dimensional motion of the spine. The disc, therefore, must be soft enough to permit spinal motions of axial compression, flexion–extension, lateral bending, and axial rotation, all of which subject the disc to compressive, bending, shear, and torsional forces, respectively (Fig. 78.1). At the same time, the disc must be stiff enough to maintain stability and withstand the large loads encountered as the lumbar spine progresses through the physiologic motions required by daily living. This is accomplished in part by the disc’s unique ability to absorb and dissipate energy that is generated during these activities. Clearly, the primary function of the disc is mechanical. Therefore, an appreciation of normal and degenerative disc biomechanics is critical to understanding the etiology and sequelae of disc disease, as well as the consequences of intervention. The disc is composed of substructures which are themselves distinct tissues: the nucleus pulposus, anulus fibrosus, and cartilaginous M

M

Fcompression

Tensile region

Compressive region

A

Fcompression Compression

B

Bending

endplates (Fig. 78.2).1 The composition and structure of these disc components are summarized briefly below. NUCLEUS PULPOSUS: This gelatinous semisolid structure is comprised of a loose meshwork of randomly distributed collagen fibrils in a hydrated extrafibrillar matrix. In younger, nondegenerate discs, water constitutes about 70–80% of the nucleus pulposus, while collagens account for approximately 20% of the dry weight of the central nucleus. Collagen type II predominates, with minor contributions from collagen types V, VI, IX, and XII. Proteoglycans comprise about 50% of the dry weight of the nucleus in a nondegenerate disc. ANULUS FIBROSUS: This fibrocartilage surrounds the nucleus pulposus and consists of 15–40 concentric layers of collagen fibers that are oriented at approximately 30° from the horizontal plane and alternate above and below the plane in adjacent layers. Water comprises about 65% of the anulus. While the dense, fibrous outer anulus is comprised mainly of type I collagen, the composition shifts towards a higher concentration of type II collagen at the less-dense region of the inner anulus. ENDPLATE: The cartilaginous endplate is comprised of thin hyaline cartilage located at the superior and inferior aspects of the vertebral body. Like hyaline cartilage found elsewhere in the body, the predominant collagen in the endplate is type II. When the disc degenerates, its biochemical, cellular, structural, and mechanical functions are compromised. Some of these changes include anulus fibrosus fissures and tears, nucleus pulposus loss of proteoglycan and depressurization, endplate calcification and failure, and cell senescence and death.2 Despite the widely accepted notion that disc degeneration is an important potential source of back pain, a clear link between disc pathology and back pain has not yet been established. Further, a clear distinction between physiologic aging of the disc and disc degeneration has not been delineated. Nevertheless,

Ttorque

Fshear

Endplate (EP) Annulus fibrosus (AF) Fshear C

Shear

Ttorque D

Torque

Fig. 78.1 Spine loading configurations. (A) Compression. (B) Bending. (C) Shear. (D) Torsion.

Nucleus pulposus (NP) Fig. 78.2 Schematic of intervertebral disc substructures. 827

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while the precise mechanisms by which the disc may produce back pain have yet to be identified, disc degeneration is considered an important potential source of pain and the subject of continued intense investigation.3,4 The overall goal of understanding the biomechanics of the disc are to aid in the treatments of disc disorders. Throughout this chapter the authors will describe how basic science studies (performed in vivo, as cadaveric experiments, as animal models, or using computational models) contribute to one’s understanding of disc biomechanics. Such studies of the nondegenerate and degenerate disc are necessary for determining mechanisms of degeneration that are related to mechanical loading of the spine, and for quantifying the mechanical function for design and evaluation of treatment therapies. The authors will begin by defining the basics of biomechanical terminology and principles. The authors will then describe how these biomechanical principles apply to the individual substructures of both the nondegenerate and degenerate discs, and finally present the biomechanics of the entire motion segment (bone–disc–bone), how the applied loads are distributed, and how the mechanics change with degeneration.

M F

d

Force acting on distance of ‘d’, from the centre of disc causing a lateral bending moment A T d

F

BASIC BIOMECHANICS Basic biomechanics terminology Biomechanics deals with the study of forces and displacements acting on biological materials and their resulting effects. In this section, basic biomechanical terminology and principles are defined and applied to the disc. A more detailed explanation of these biomechanical concepts can be found in two excellent texts written for nonengineers by Low and Read5 and Panjabi and White.6 FORCE: Force is an action that moves or deforms a body – a push or a pull. It is a vector quantity often depicted using an arrow which indicates a magnitude, direction, and a point of application. Figure 78.3 demonstrates these actions applied to a spinal motion segment. The unit of force is a Newton. Complex forces are usually broken down into their ‘components.’ For example, the generic applied force in Figure 78.3A is broken down into its components of normal force and shear force as shown in Figure 78.3B. BENDING MOMENT OR TORQUE: When a force is applied at some distance from the center of an object it may cause a bending or turning effect, which is known as a moment or a torque (Fig. 78.4). Moment and torque are both defined as the magnitude of the force times the lever arm (the perpendicular distance between the force and the chosen center of rotation). The units for bending and torque are N-mm or N-m, depending on the scale of the objects considered. Bending moment and torque are the same except that generally in bending the force and lever arm are in the plane parallel to the axis of the structure (Fig. 78.4A), while for a torque they are perpendicular to the axis of the structure (Fig. 78.4B). An example of a

F Fnormal Fshear

A

828

B

Fig. 78.3 Force vector acting on the motion segment. (A) Generic direction. (B) Components for force in normal (compression) and shear loading.

Force acting on distance of ‘d’, from the centre of disc causing an axial torsion torque B

Fig. 78.4 Moments and torques acting on the motion segment. (A) Bending. (B) Torsion.

bending moment is forward flexion, where the weight of the upper body times its distance from the spine is the applied bending moment. An example of torque is the torso twisting along the long axis of the body. Another example is when a screwdriver is turned; in this case, the force applied to the handle times the diameter of the handle is the torque. The clinical application of moments and torques in the spine explains how seemingly small forces may generate significant moments as a result of large lever arms. STRESS: Force is generally not applied at a single point, but is distributed over a contact area. This distribution of force, or load intensity, is defined as stress. Stress is the ratio of force divided by the area of application and usually has the units of N/mm2 (MPa or Megapascals) or N/m2 (Pascals), depending on the size scale. Stress is sometimes defined in Imperial units as pounds per square inch (psi). Stress can be broken down into its components, as is done for force. The force components shown in Figure 78.3B, when divided by the disc surface area, can be used to calculate the applied compressive and shear stress. Externally applied stresses on an object give rise to internal stresses. PRESSURE: There are two types of pressures: contact pressure and fluid pressure (Fig. 78.5). Contact pressure occurs in solids and is an applied compressive stress. For example, the contact of the two facet joint surfaces imposes a compressive stress that is sometimes called a contact pressure. Importantly, fluid pressure, also known as hydrostatic pressure, occurs in contained fluids and should not be confused with solid stress or contact stress, even though it has the same units. Fluid pressure is the intensity of loading within a contained fluid. The fluid pressure is generated by the interactions of the fluid molecules with the surface of its container. Hydrostatic pressure is isotropic, which means that it is the same in all directions. The nucleus pulposus of the disc is considered to be a fluid (or fluid-like)

Section 5: Biomechanical Disorders of the Lumbar Spine

Contact pressure

Endplate Hydrostatic pressure

HP

Endplate

DISPLACEMENT AND STRAIN: Displacement refers to the motion of particles within an object. Similar to force, displacement is a vector quantity and therefore has both a magnitude and a direction. The units of displacement are millimeters (mm) or meters (m), depending on the size of the object, and are sometimes further decreased to micrometers. Like force, displacement is often broken down into its components. The application of force to a body usually causes a displacement of the body. Strain is defined as the ratio of displacement of the object to its original length and, therefore, is unitless. Strain is sometimes multiplied by 100 and given as a percent strain. Externally applied displacements lead to internal displacements and strains.

Soft tissue mechanical behaviors Fig. 78.5 Nucleus pulposus hydrostatic pressure and facet joint contact.

substance and therefore generates a hydrostatic pressure when the disc is loaded. This pressure is the same in all directions: vertically against the endplates and radially against the containing walls of the anulus fibrosus, as shown in Figure 78.5.

LOADING CONFIGURATIONS: There are three standard mechanical testing configurations for soft tissues: tension, compression, and shear. For tension and compression experiments the specimen ends are pulled away from each other (tension) or pushed towards each other (compression). In a tension test, the specimen is generally long and thin (Fig. 78.6A) and is held in the testing machine at both ends. The specimen ends are pulled apart leading to an increase in the length and decrease in width. In a compression test, the sample

A

B

C

Fig. 78.6 Standard loading configurations in tension, compression, and shear. (A) Tension. (B) Compression. (C) Shear.

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is generally a short cylinder, and the two ends of the specimen are pushed towards each other resulting in a decrease in the height of the specimen (Fig. 78.6B). For shear loading tests, a sample may be either rectangular or cylindrical and the load is applied parallel to the surface (Fig. 78.6C). The sample then changes its shape without undergoing either compression or tension. Compression tests can have three distinct loading configurations because more complex experiments are used to quantify the loading mechanisms that resist the applied load: hydrostatic pressure in the interstitial fluid and the solid matrix stress. These mechanisms are quantified by considering the tissue as a multiphase material consisting of a solid, a fluid, and sometimes an ionic charge phase. Compression tests are performed in either an unconfined manner, where the boundaries of the cylinder expand upon loading, or in a confining chamber. In the confined compression experiment, a cylindrical sample bathed in a fluid is constrained within a chamber of the same diameter, above which a porous platen is placed. While the sample is held in this position, a swelling pressure is generated within the tissue. Next, stepwise increases in compressive displacements are applied to confined samples and the resultant force is recorded. Each displacement is held for several minutes or hours until equilibrium and a steady state is reached. The force, displacement, and time data are analyzed. Confined compression mechanical tests are typically analyzed using a biphasic model and the material properties of solid matrix modulus and permeability are determined from the experiment. The solid matrix modulus is the normalized stiffness of the material and has units of MPa. The permeability is defined as the ease by which the fluid phase flows through the solid phase and has units of m4/Ns. Another type of compression test is ‘indentation’ where a probe is compressed against any flat surface and the amount of indentation is recorded. One advantage of this technique is that it can be applied to the tissue sample in situ (without excising and precisely preparing a test sample). A disadvantage, however, is that sophisticated numerical analyses are needed to calculate material properties from the measured data. STRUCTURAL AND MATERIAL PROPERTIES: A biomechanical study typically involves experimentation and curve-fitting to a mathematical equation to determine the relationship between the force and displacement. However, for specimens of the same material with different dimensions, the force–displacement curves will be different, as shown in Figure 78.7A. This is because both force and displacement are ‘as measured’ quantities and not normalized with respect to the specimen geometry (e.g. cross-sectional area and height). Thus, it is important that the data for force and displacement be normalized to enable comparisons among different-sized samples. These principles have led to the development of normalized quantities such as stress and strain. The stress–strain response of the same material prepared into samples of different sizes is the same (Fig. 78.7B). The slope of this curve is defined as the modulus of the material and has the units of MPa or N/mm2. Similarly, the slope of the force versus

A

B

Fig. 78.7 Representative response for structural and material properties. (A) Force–displacement. (B) Stress–strain response.

830

displacement curve is defined as the stiffness and has the units of N/ mm. For tension and compression testing, Poisson’s ratio is defined as the negative of the lateral contraction strain divided by the applied longitudinal strain. In shear testing, the shear modulus is calculated as the slope of the shear stress (applied parallel to the sample surface) versus the angle of displacement. NONLINEARITY: A material is nonlinear if the force–displacement or stress–strain response does not have constant slope. While many materials are linear, most biological materials are nonlinear. Consequently, a single stiffness or modulus cannot describe the tissue’s behavior over all loading levels. In motion segment mechanics, this nonlinearity is exemplified by the dramatically different behavior in the low-stiffness neutral zone compared to the high-stiffness loading zones (Fig.78.8A). In soft tissue mechanics, nonlinearity is observed by the low ‘toe region’ modulus and the larger ‘linear region’ modulus (Fig. 78.8B). The large differences in compressive and tensile properties are another form of material nonlinearity. Nonlinearity in a spine motion segment is observed as the very large changes in stiffness as the motion segment is moved through the range of motion in any single loading direction. This is an important mechanical behavior because it contributes to the overall range of motion and because an increase in the neutral zone length is consistently observed in degenerated discs.7 A typical cyclic load response of an intervertebral disc is shown in Figure 78.8A. The curve is characterized by high stiffness regions at the extreme ends of loading and by a low stiffness region at low loads. The region of the response in the low load (or moment) and low deformation (or rotation) region is called the ‘neutral zone.’ The neutral zone is defined as the region on either side of the neutral position where there is little or no resistance to motion.7,8 The neutral zone mechanical properties are used to understand the stability of the disc motion segment. Although early studies reported the neutral zone as simply the displacement (rotation) over which loads (moments) are negligible, recent studies have focused on quantifying this important region of disc mechanical function.9,10

A

B Fig. 78.8 Nonlinearity (A) Nonlinear motion segment response showing neutral zone. (B) Nonlinear stress–strain response.

Section 5: Biomechanical Disorders of the Lumbar Spine

VISCOELASTICITY: All biological tissues, including disc, bone, cartilage, muscle, tendon, and ligaments, exhibit viscoelastic behaviors. A material is viscoelastic if it has time-dependent mechanical behaviors. For example, if a constant compression load (load-control) is applied to a spine segment it will immediately deform (the elastic response) and it will slowly continue to deform over the next several minutes and hours (the viscous response). The most commonly used test to evaluate tissue viscoelasticity in the spine is called a creep test (Fig. 78. 9A). The analogous test applied under a constant displacement (displacement-control) is called a stress-relaxation test (Fig. 78.9B). In this case, a constant displacement is applied to the spine segment which immediately experiences a stress (the elastic response). Over the next few minutes or hours, the segment relaxes to a lower stress value (the viscous response). In a viscoelastic experiment, the stress (relaxation) or strain (creep) data are applied to a best-fit curve, the constants from which permit comparisons among different specimens. Another viscoelastic response is hysteresis, which describes a difference of cyclic loading in the load-displacement curve in the loading and unloading phases. The intervening area in this curve is described as the hysteresis area, and represents energy lost as heat due to viscous effects (see Fig. 78.8A). ANISOTROPY: A material is anisotropic if its mechanical behaviors vary under different directions of loading. Most soft tissues, including the anulus fibrosus, are highly anisotropic due to their collagen fiber structure. The stiffness and modulus when the material is stretched along the fiber direction is much larger than when stretched in any other direction. The nucleus pulposus is generally considered isotropic because its mechanical behaviors are the same in all directions. This is likely a result of the random orientation of the collagen fibers and because hydrostatic pressure dominates its mechanical response. INHOMOGENEITY: A material is inhomogeneous if its mechanical behaviors vary with location within the tissue. The anulus fibro-

A

B Fig. 78.9 Viscoelastic response of soft tissues. (A) Creep. (B) Stress– relaxation.

sus and most other soft tissues are inhomogeneous. Variations in the underlying structure and composition of soft tissues generate inhomogeneous mechanical properties. Consequently, when measurements of tissue properties are performed, it is necessary to specify the location from which the samples were obtained.

TISSUE MECHANICS OF DISC SUBSTRUCTURES The nucleus pulposus, anulus fibrosus, and endplate comprise the intervertebral disc substructures. In healthy discs, each component works together to provide a balance between stability and mobility of the disc. The process of disc aging and degeneration alters the composition and mechanical function of each of the substructures. Therefore, no discussion on intervertebral disc or spine biomechanics can be complete without a thorough description of the individual contributions from the substructures which, taken together, regulate nondegenerate and degenerate disc mechanics. The focus of this section is on mechanics of the individual disc substructures, while the following section will describe the mechanics of the entire disc and motion segment.

Nucleus pulposus mechanics The nucleus pulposus is a highly hydrated gel with important material properties that include swelling pressure, compression modulus, permeability, and shear modulus. The nucleus has a large water and proteoglycan content. Proteoglycans have negatively charged glycosaminoglycans attached, which attract positive ions and generate high osmotic pressures. If the nucleus pulposus is removed and placed in a hydrating solution it swells to at least two times its volume. The nucleus swelling pressure has been measured using a pressure transducer in vivo and in excised cadaveric spines under mechanical loading. The swelling pressure of a healthy nucleus is 0.1–0.2 MPa in a recumbent position and may reach as high as 1–3 MPa when standing or lifting.11,12 Similarly high pressures have been measured in cadaveric motion segments under externally applied loads.13,14 The swelling pressure has also been measured using osmometry methods15 and in confined compression,16 producing values consistent with in vivo measurements. The nucleus pulposus swelling pressure has been shown to be correlated with the glycosaminoglycans content.15,16 The large propensity of the nucleus pulposus to swell makes it difficult to prepare test samples and to measure its mechanical properties. As a result, there is a paucity of studies in the literature which have examined these properties. This dearth of mechanical data has made it difficult to properly model the nucleus pulposus in finite element studies of the spine. Lack of mechanical data has also hampered the development of tissue-engineered and artificial disc replacements because clear targets for mechanical function are needed. Fortunately, recent studies have provided measures of the tissue properties and their changes with degeneration. The equilibrium shear modulus of nondegenerate human nucleus pulposus is 0.2 kPa and increases to 0.6–0.8 kPa with degeneration.17 The high water content of the nucleus pulposus contributes to the large viscoelastic effects observed. Further, the dynamic shear modulus is almost two orders of magnitude larger than the equilibrium modulus, ranging 5–60 kPa17 and increases with degeneration. When dynamic loading is applied in shear, the nucleus behaves like a viscoelastic solid, suggesting that finite element models that describe the nucleus as a fluid may miss important behaviors.18 The compression modulus measured at equilibrium in a confined compression test is three orders of magnitude higher than the shear modulus at 0.5 MPa for nondegenerate human tissue.16 The viscoelastic behavior, as measured by the hydraulic permeability, was calculated to be 3 × 10–16 m4/Ns.16 831

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The nucleus pulposus is the first disc substructure to exhibit degenerative changes: the shear stiffness increases,18 the pressure decreases,15 the compression stiffness increases,16 the permeability decreases,16 and its compositional changes lead to a shift from a fluidlike behavior to a solid-like behavior.17 When the nucleus is degenerated, the swelling pressure decreases dramatically to 0.03 MPa or less.11,12,16,19 While stiffness increases with degeneration and the behaviors become more solid-like, osmometry and mechanical compression tests show that even with degeneration the overall behavior of the nucleus pulposus is still dominated by the swelling component.16,20 These biochemical changes observed in the degenerating nucleus pulposus and their biomechanical consequences may be key factors in further progression of degeneration.

Anulus fibrosus mechanics The anulus fibrosus surrounds the nucleus pulposus and has a highly organized fibrocartilagenous structure. Although compression is considered the primary loading configuration of the anulus, it is also loaded under tension, compression, and shear, and its structural organization and biochemical composition reflect these complex loading configurations. COMPRESSION: The anulus fibrosus undergoes large compression loads during the activities of daily living due to both axial loading and as a result of bending and torsional loading. The primary directions for compression loading in the anulus are in the axial direction, due to body weight, and in the radial direction, due to nucleus pulposus swelling. The swelling pressure represents the pressure generated when the anulus is held at the in situ displacement. Swelling pressure correlates with the biochemical content of glycosaminoglycan due to the osmotic pressures generated by balancing their negative charges. Since the glycosaminoglycan content is high in the anulus fibrosus (and nucleus pulposus), the swelling pressure is an important material parameter. Confined compression experiments and biphasic analyses have revealed the material properties of solid matrix modulus and permeability. The anulus compressive modulus is 0.6 MPa and the permeability is 2 × 10–16 m4/Ns.21,22 The anulus behavior in compression is nonlinear and inhomogenous. Nonlinearity is observed by the increase in the compressive modulus and the decrease in permeability with increasing amounts of applied compressive strain.21 The nonlinear properties of the anulus are more dramatic for the compressive stiffness than for the permeability.23 Inhomogeneity is demonstrated by regional and radial variations in both material properties and biochemical composition.21,23 Unlike the tensile material properties, the compression properties are not strongly anisotropic.21 Very little compression anisotropy is observed for samples oriented in the axial and radial direction. This suggests that the collagen alignment does not strongly influence the anulus behavior in compression. That is, this loading configuration is primarily supported by the fluid pressurization mechanism. In contrast, the anulus fibrosus permeability is direction dependent, with the highest permeability in the radial direction.24 Anisotropic swelling of the anulus has been observed, where the tissue swells more in the radial direction than in the axial direction.25 Similarly, anisotropy in the swelling behavior under confined compression for radial and axial tissue samples has been observed.21,26 With disc degeneration, the swelling pressure of the anulus fibrosus decreases dramatically from 0.13 MPa to 0.05 MPa.21,23 The permeability also changes with degeneration: the radial permeability decreases and the axial and circumferential permeabilities increase.24 The combination of an inability to generate hydrostatic pressure when loaded in compression and altered permeability transfers more of the compressive load onto the anulus solid matrix. When this 832

occurs, the anulus is likely to accelerate degeneration due to both mechanical fatigue and altered cell response to this altered loading. Interestingly, the loss of swelling pressure is partially compensated for by an increase in stiffness of the solid matrix from 0.5 MPa in nondegenerated anulus to 1.1 MPa in degenerated anulus.21,23 This increased modulus is likely due to a combination of increased matrix density following loss of water, to increased collagen cross-linking, and to cellular remodeling in response to altered load. TENSION: While the components of the intervertebral disc act in unison to withstand significant loads and to resist excessive intervertebral motion, it is the anulus fibrosus that is primarily responsible for resisting the large tensile forces to which the disc is subjected. When compression loads are applied to the disc, the nucleus pulposus is pressurized causing circumferential tensile stresses in the anulus. Tensile loads in the circumferential direction are also generated when the anulus is compressed axially by the resistance of the collagen fibers to stretch in the circumferential direction. The classic studies of Galante showed that the material properties of the anulus are nonlinear, anisotropic, inhomogeneous, and viscoelastic.27 These material behaviors, defined in the previous section, give the anulus its special functional properties and delineate the complexity of a biological tissue from most synthetic materials such as plastic, rubber, or metal. The nonlinear nature of the stress–strain curve observed for the anulus under tensile stress is similar to the material behavior of other soft collagenous tissues, namely articular cartilage, tendon, and ligament. Studies using both single layer and multilayer anulus fibrosus samples have demonstrated that, in response to axial deformation, there exists a nonlinear portion of the stress–strain curve called the ‘toe’ region which represents a low force observed for small tensile strains. This is then followed by a ‘linear’ region, and then failure of the tissue at highest strains (see Fig. 78.8B).28–30 The modulus in the toe region is 2 MPa and in the linear region is 20 MPa for circumferentially aligned samples. This 10-fold increase in modulus with increasing applied strain demonstrates very large nonlinearity.28–31 Anisotropy is a key material behavior for the anulus fibrosus because it provides the functionality to support the large and complex loads encountered by the disc. Anisotropy is demonstrated by the near 1000-fold increase in tensile modulus for annular samples tested along the collagen fibril direction when compared with across the fibrils. A single lamella or layer of the anulus, when loaded parallel to the collagen fiber direction, has a modulus of 136 MPa at the anterior outer site.32 The circumferential modulus, as noted in the previous paragraph, is 20 MPa. The axial modulus is 0.8 MPa30 and the radial modulus is 0.2 MPa.33 Thus, there is a high degree of anisotropy in the anulus tensile properties which is due to the structural contribution of the aligned collagen fibers. Mathematical models of anulus material behavior have shown how fiber alignment contributes to anisotropy.34–38 The inhomogeneous nature of the anulus fibrosus is due to the spatial variation in structure and composition. Biochemical composition studies have revealed significant spatial variations of water, collagen, and proteoglycan content from outer to inner sites (radial variation) and from anterior to posterior sites (circumferential variation).39,40 The fiber-aligned and circumferential tensile properties of the anulus reflect this variability with site in the tissue.28–30,32 However, little inhomogeneity is observed in the radial or axial tensile properties.30,33 This is probably due to the relatively small contribution of the collagen fibers in these orientations.38 For the circumferential orientation, it has been shown that the anterior anulus is stiffer than the posterior, and that the outer anulus is stiffer than the inner.28–30 In some cases, these differences can be as large as an order of magnitude. The relative mechanical inferiority at the posterolateral region

Section 5: Biomechanical Disorders of the Lumbar Spine

of the disc may be due to structural differences there. The posterolateral region is characterized by incomplete lamellar layers, increased fiber-interlacing angles, and ‘loose’ interconnections of fibers.41,42 These regional variations in composition and tensile properties of the posterolateral anulus fibrosus may represent potential areas for compromise of structural integrity, and may predispose to annular tears, fissures, and herniations. The composite layered structure of the anulus makes it resistant to mechanical failure.43 However, under damaging fatigue loading or extremely high loads, anulus fibrosus delamination and failure occur.44,45 The tensile properties of the anulus fibrosus change with aging and degeneration; however, the magnitude of these changes are relatively small in light of the dramatic gross morphologic alterations which have been shown to occur with degeneration. The properties of failure stress, strain energy density, and Poisson’s ratio are significantly lower in the degenerate anulus.28 This means that the degenerate anulus is more likely to fail at lower stresses when compared with the nondegenerate anulus. The toe region modulus and the reorientation of collagen fibers are also significantly altered with degeneration.31 These alterations will cause increased stresses throughout the disc under the loads of daily living and may contribute to annular injury. SHEAR: The anulus fibrosus has also been shown to be nonlinear, viscoelastic, and anisotropic in shear loading.46,47 The equilibrium shear modulus of the anulus measured in these experiments is quite small at 0.1 MPa. However, analysis of motion segment torsion experiments and fiber-reinforced modeling studies predict the anulus shear modulus to be two orders of magnitude larger at 20 MPa.38,48,49 The shear modulus increases with degeneration, but not significantly.46 Additional information regarding the anulus function in shear is still needed.

Endplate mechanics The endplates are thin layers of hyaline cartilage between the intervertebral disc and the bony vertebra. The cartilaginous endplates represent the interface between the vertebral body and the disc and play a very important role in supporting and distributing the load from the disc to the vertebra.50 As the nucleus, hydrostatic pressure increases, and the endplate tends to experience large pressures and bulge into the vertebra. For quite large axial loads, the endplate is the substructure that generally fails first.51,52 Endplate damage leads to reduced nucleus pulposus hydrostatic pressure and increased stresses within the anulus fibrosus. A key function of the endplate, apart from load bearing, is to facilitate the diffusion of nutrients into the intervertebral disc.53,54 Relatively little is know about the mechanical properties of the endplate, especially in comparison to the more widely studied nucleus pulposus and anulus fibrosus. The endplate has been studied mechanically using confined compression,55 indentation,56–58 and for resistance to fluid diffusion or flow.53,59,60 Additional studies on the mechanics of endplate under compression, tension, and torsional shear would help in developing a better understanding of the mechanical role of the cartilaginous endplate and its changes in degeneration. The only study of the compressive properties of the cartilaginous endplates is in the baboon lumbar spine.55 The results indicated that the cartilaginous endplate has a hydraulic permeability associated with rapid transport and pressurization of the interstitial fluid in response to loading and an increased emphasis on flow-independent viscoelastic effects.55 The study results suggested that the fluid pressurization in the cartilaginous endplate may be important in the maintenance of a uniform stress distribution across the boundary between vertebral body and the intervertebral disc.

The endplate exhibits a spatial variation in its strength and stiffness according to indentation studies.56,57 In his classic studies, Perey noted three major failure patterns in the endplate: central, peripheral, and the complete endplate.56 During central failure, observed in the case of nondegenerate discs, the nucleus hydrostatic pressure increased under compressive loads and caused excessive loading and failure in the endplate. In the peripheral failure pattern, observed in degenerate discs, the nucleus loses its hydrostatic pressure and most of the load under compression is transmitted through the anulus fibrosus. Thus, the endplate is loaded in the periphery and fails by fracture of the endplate. The central part of the endplate is weaker than the peripheral regions.56,57 In addition, the superior endplate is weaker than the inferior endplate.57 Increased degeneration is associated with decreased failure properties in the bony endplate, but stiffness is not affected.58 Resistance of the endplate to fluid flow, necessary for disc nutrition, has been studied and shown to be direction dependent.60 With aging and degeneration the cartilaginous endplate calcifies, thins, and fissures occur.61,62 Since the porous endplates act to regulate the diffusion of molecules and the fluid flow to and from the nucleus and the vertebra, changes in the bone–endplate region can limit solute transport required for nutrition and are associated with disc degeneration.59,63 However, the mechanisms by which endplate calcification and degeneration contribute to disc degeneration are unknown. The mechanical response of the endplate to the changes induced by aging and degeneration has not yet been fully quantified.

STRUCTURAL MECHANICS OF THE DISC MOTION SEGMENT The disc, composed of the substructures described in Tissue Mechanics of Disc substructures above, undergoes large and complex loading. It is the unique material behaviors and arrangement of the substructures in the disc, together with the other components of the spine (e.g., vertebral bodies, facet joints, ligaments, and muscles), that permit the spine to function as well as it does under the rigorous loading that physiologic activities impose. The loads exerted on the spine arise from external forces (gravity) and internal forces (abdomen and back muscles, ligaments, and intra-abdominal pressure).43,64 One’s understanding of spine mechanics comes from wideranging studies including in vivo measurements, ex vivo mechanical experiments in human and animal cadavers, in vivo animal models, and mathematical models. Together, these studies have formed the foundation for understanding how the disc works and its alterations with degeneration. In vivo mechanical measurements include pressure, muscle activity, and disc height. Mathematical modeling and cadaveric testing are used to calibrate and to interpret these measurements into mechanical behaviors. Disc pressure measurements are performed by inserting a needle pressure sensor into the center of the disc. The pressure has been measured in vivo,11,12 providing estimates of the compression load on the spine. The amount of compression load may also be estimated by the time-course of loss in disc height, or creep, under an applied load such as lifting or simply standing.65,66 The role of muscle forces on spine loading has been estimated using mathematical models and electromyography measurements of muscle activity.67–70 Determination of muscle force is very difficult due to the large number and size of muscles, antagonistic muscle activity, variability in the relationship between electromyography value and muscle force, and the variable moment arm generated by the muscle due to uncertainty in insertion site and moving body position.64 Ex vivo mechanical experiments in human cadaver and animal motion segments provide much more quantitative information than can be obtained in vivo. Furthermore, the mechanisms of 833

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disc degeneration can be studied by performing these experiments in spines with natural degeneration or in animal models where the disc is altered surgically or chemically to resemble degeneration. Cadaveric mechanical tests are performed by dissecting out one or more bone–disc–bone motion segments and attaching it to a testing rig. The ends of the segments are usually potted in bone cement to obtain a rigid structure with which to interface with the testing rig. Loads, moments, displacements, or angles are imposed according to the study design. Several cycles through the entire range of motion in an orientation of interest (e.g., axial compression–tension, flexion–extension, or left–right torsion) are typically repeated so that consistent datasets are obtained. The individual experimental results across motion segment studies vary widely due to differences in technique, instrumentation, gripping, boundary conditions, hydration, and inherent complexity of the motion segment itself (e.g. nonlinearity, viscoelasticity, coupled motions). Furthermore, the tissue substructures’ complex properties, their interactions, and their changes with aging and degeneration contribute to the wide ranges in experimental data. Nonetheless, some conclusions can be made regarding changes in the disc structural mechanics with degeneration and age including: decreased stiffness, decreased nucleus pulposus pressure, decreased fatigue life and failure properties, and decreased viscoelastic energy dissipation.2,52,71–75 In vitro cadaveric testing has shown that, like the underlying substructures, the motion segment has mechanical behaviors that are viscoelastic and nonlinear. An additional feature of motion segment mechanics is the observed ‘coupled motion’, where loading in one orientation simultaneously induces loads and deformations in other orientations.76–78 Abnormal coupled motion has been associated with low back pain.76 In vivo and cadaveric studies provide the disc’s overall response to mechanical loads. However, they do not give crucial information regarding the internal stresses and strains within the disc substructures. Mathematical models are thus important tools, together with experiments, to understand disc function and mechanisms of degeneration. Mathematical models provide the ability to model the complex geometry and material properties under various physiologically relevant loads, and to alter these factors to determine their role in disc function.79–83 While spinal motion is complex, just as force vector was broken down into components in the first section, spine loading can generally be considered by its components in the major directions of axial compression–tension, flexion–extension, lateral bending, axial torsion, and shear. Disc function and changes with degeneration will be discussed in light of the above-mentioned spinal motion in vivo studies, ex vivo cadaveric and animal studies, and mathematical models. Primary focus is on the lumbar bone–disc–bone structural unit; however, in some cases the more complete structural unit that also includes the facet joints will be described.

Axial compression and tension The intervertebral disc experiences large loads in compression, so understanding the mechanical response of the disc to compressive loads is essential to one’s understanding of disc biomechanics. Compressive forces in the lumbar spine arise from several sources including gravity, inertial effects, contraction of muscles, and increased intra-abdominal pressure. The spine can experience compressive loads of 500–1000 N, in excess of twice the body weight, from common daily activities such as relaxed standing and sitting.11,12 Lifting and other activities can increase the compression load to 5000 N, which is approximately 50% of the ultimate compression failure load.12,84,85 While these peak loads may not cause the disc to 834

fail, they are likely to contribute to fatigue damage over time.52,86,87 Factors that affect the peak compressive load include inertial forces, stabilizing muscle activity, amount of spine flexion and asymmetry, speed of lifting, position of load to be lifted, amount of control, and anticipation of subject.64,88,89 Muscle forces are required to stabilize the spine during standing, lifting, and bending activities and generate large compression loads.11,12,90,91 Large compression forces are similarly required to stabilize the spine in quadruped animals, so that even though they do not stand upright, large compression loads are applied across the lumbar spine, making the animals potentially appropriate models for the human spine.92 The spine experiences large compressive loads which are supported by the disc’s anulus fibrosus and nucleus pulposus, and to a lesser extent by the facet joints.93,94 The load-sharing mechanisms between nucleus hydrostatic pressure, anulus tension, and endplate bulging have been quantified in motion segment cadaveric testing51,95–97 and by mathematical modeling.98–100 The disc can be considered as a pressurized, thick cylinder as shown in Figure 78.1A.50,101 Axial compression forces applied to the anulus induce tensile stresses in the circumferential (hoop) direction. The fibrous, laminated structure of the anulus resists these circumferential tensile loads and provide the large stiffness necessary to support compression.38,102 In addition, compression loads generate large hydrostatic pressures in the nucleus pulposus. These pressures can cause the vertebral end plates to bulge outward into the vertebral bodies, the anulus fibrosus to bulge outward radially, and also generate circumferential tensile stresses in the anulus. Recent motion segment studies suggest that the nucleus pulposus pressurization is largely responsible for the neutral zone, low load, region of the axial loading regimen, and the anulus fibrosus supports a larger proportion at the higher loads where larger stiffness is needed.97,103 Viscoelastic creep, whether applied via a static compression load or by repeated cyclic loads, plays a significant role in disc mechanical function. Creep is evident as part of the diurnal height loss phenomena where fluid is exuded from the disc and outward bulging increases.74,104 When unloaded overnight the fluid returns through a passive osmotic pressure mechanism.105 Creep loading alters viscoelastic behaviors, decreases the fluid content within the disc, and decreases the disc height. Finite element models suggest that creep loading is associated with decreased permeability and stiffness in the anulus fibrosus and decreasing fluid loss from the nucleus pulposus as the creep time increases.100,106 Cadaveric studies have associated these creep alterations with increased anulus fibrosus loading, resulting in anulus fibrosus fissures and delaminations. At very high compression loads the anulus is unable to maintain its structure and failure occurs first in the endplate and vertebral body.52,56,86,87,107 Endplate failure may increase the shear loads on the anulus, predisposing it to fissures and delaminations, further advancing the degenerative process.45,108 Disc degeneration, with loss of nucleus pulposus proteoglycan content, decreased hydrostatic pressure, and decreased disc height,11,14 has several effects on axial compression loading. The nucleus pulposus absorbs less of the compressive stress and transfers more of the axial load onto the anulus fibrosus. As a result, disc stress distributions are altered: large peak stresses occur within the outer anulus, more of the axial compression stress is supported by the inner anulus, which then bulges inward, and shear stresses increase.14,102,108–110 Such altered loading may play a role in the progression of degeneration due to cellular responses to the altered loading or due to mechanical fatigue. Additionally, in a degenerated disc, where the disc height is already decreased, the relative proportion of load carried by the facet joint increases up to 70%.111 At these higher facet load levels, the facet joint cartilage may be damaged and osteoarthritic changes may develop.

Section 5: Biomechanical Disorders of the Lumbar Spine

Flexion–extension bending and lateral bending

Torsion

Bending motion due to changes in spine loading or body position has been measured in vivo using three-dimensional tracking devices, stereo-radiographs, videofluoroscopy and, more recently, dynamic computed tomography.112–116 The amount of motion, or rotation, in an individual level is 8–12° in flexion, 1–5° in extension, and 1–6° in lateral bending.116,117 In general, the lower levels tend to have less bending motion than the upper lumber levels. The range of motion for both flexion–extension and lateral bending decrease with age.118–120 Several factors affect the bending motion, including age, measurement duration (due to creep, deformation increases the bending angle), time of day (due to fluid loss in the disc), posture and position of other spinal structures, physical training, and muscle flexibility.64 Bending moments (force × distance) have not been directly measured in vivo. The in vivo moments, however, can be estimated from the measurements in cadaveric studies. A bending moment of 10–20 Nm is generated while lifting a 10 kg mass, which is well below a damaging level.113 Bending moments may be affected by the mobility of the subject, mass of the object being lifted, rate of the motion, muscle fatigue, ligamentous creep, and hydration level of the disc.64 The mechanisms for load support in bending is complex and depends upon the amount of motion and the rate of movement.50,94,121–123 For small flexion angles, in the neutral zone where stiffness is low, the disc and the ligamentum flavum are the primary contributors to bending load support. As the flexion angle increases, the disc supports most of the loading via compression in the anterior anulus and tension in the posterior anulus. At very high flexion angle the capsule ligaments of the facet joints and other ligaments support a larger proportion of the load. Bending stiffness increases when there is a compression preload applied.78,121,124 Bending loads induce simultaneous compression and tension on the opposing faces of the intervertebral disc with maximum tensile or compressive stresses at the outermost layer of the anulus, outward bulge on the compression side, and stretching on the tensile side (see Fig. 78.1B).117,125,126 For example, in forward flexion, the anterior anulus is compressed to a 30% reduction in disc height (up to 80% reduction in a degenerated disc) and bulges, while the posterior anulus is stretched by 50–90%. Similarly, under extension motion the height of the disc is decreased posteriorly and the disc bulges out posteriorly. Lateral bending is not as well studied as flexion–extension and generally occurs in combination with flexion while reaching to the side for an object. Lateral bending is resisted by both the disc and the facet joints. Direct measurements of surface strain during bending indicates that large fiber strains occur such that the anulus must deform and fibers reorient to prevent failure.127 In early degeneration the motion segment bending stiffness is reduced and the range of motion is increased.126,128,129 Most of the change occurs within the neutral zone portion of the load– displacement response. This increase in motion is described as instability. With increasing degeneration and loss of disc height, however, the load experienced by the facets increases, bony osteophytes form, range of motion decreases, and the stiffness of the motion segment increases again, thereby restoring stability.130 The anisotropic and laminated structure of the anulus fibrosus leads to the development of shear stresses between the adjacent layers of the anulus under bending forces. Interlaminar shear stresses are highest at the inner anulus, which is consistent with the sites of clinical tears. When radial or circumferential anulus tears are present, interlamelar stresses increase,108,131 potentially accelerating the degenerative cascade. Finite element models to evaluate mechanical failure mechanisms show small discrete peripheral tears in the anulus which may have a role in forming circumferential tears.132

The disc is subjected to torsional loading whenever the adjacent vertebrae are subjected to opposing rotations about their own longitudinal axis. The physiologic range of axial rotation is small at 1–2° but increases to 8° with degeneration, likely due to changes to the facet joints.117,120,126,133 At approximately 20° of axial rotation disc failure occurs.134 Although the in vivo torsion loads are not known, torsion damage occurs in cadavers at 15–30 Nm.64,135 Cadaveric testing in torsion shows that 6° of rotational motion corresponds to 15 Nm of torsion load and 7% tensile strain in the collagen fibers.127 The relative rotation between the vertebrae induce torsional shear stresses in the intervertebral disc. During torsion motion half of the anulus fibers are loaded in tension and the other half remain relatively unloaded. The combination of shear stresses and the lamellar structure of the disc can lead to delaminations in the anulus fibrosus under torsional shear forces. Coupled loading is important in torsion as the rotational motion simultaneously induces axial compression, and the compression causes the nucleus pulposus pressure to increase.136 As in bending, compression loads increase the torsional stiffness of the motion segment.78,124 Resistance to axial rotation stems from a combination of anulus fibers and compression in the facet joints.122,133,136 Within physiological ranges of 1–2°, torsion finite elemental models and cadaveric studies show that the facet joints support between 10% and 50% of the torsional moments.98,126,133,136 The center of rotation of the disc lies in the posterior anulus.137 As such, axial rotation tends to place more stress on the anterior annular fibers due to the longer moment arm acting upon the anterior aspect of the disc and has been proposed as a mechanism of disc injury. Because the torsional load-sharing is so strong between the disc and the facet joints, it remains unclear which structure – the disc or the facet joints – are damaged first in torsional loading. Evidence for facet degeneration to occur first lies in the observation that facet tropism is associated with high rates of degeneration,138 and some cadaver and finite element studies suggest that facet joints would be injured in torsion before the anulus failed.139,140 However, other evidence suggests that disc degeneration precedes facet degeneration. For example, cadaveric experimental torsional loading causes annular fissures and circumferential tears that are similar to those seen in vivo,134 and an increase in concentric tears and rim lesions correspond with a decrease in torsional stiffness.141 Further support stems from a study which found that in nondegenerate discs, compared with facet joints, the anulus fibrosus fibers are more capable of restricting axial rotation and torsion-induced changes, such as peripheral rim lesions and circumferential lesions. These disruptions may contribute to early disc injury and degeneration.142 The presence of annular tears and the associated disc degeneration decreases the stiffness in torsion.143 With degeneration, stiffness changes in torsion follow the same pattern as in bending: early decreases in stiffness, followed by late-stage increases in stiffness.73,126,128,129 Degenerate discs have a 25% lower load to failure when compared with normal, healthy discs.134

CONCLUSIONS This chapter provided an overview of the biomechanical principles that underlie intervertebral disc mechanical behavior. In the first section basic terminology and definitions were outlined. In the second section a detailed description of the application of these principles to the disc substructures was described. In the third section, the biomechanics of normal and pathological spinal motion segments were discussed. The goal of this approach was to provide an appreciation for the interplay between disc structure and the mechanical function of the healthy disc, as well as how alterations are associated with disc 835

Part 3: Specific Disorders

degeneration. A basic understanding of disc biomechanical principles facilitates not only further understanding of the etiology of disc disease and current treatment options, but also promotes the continued development of biomechanically sound interventions.

References

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33. Fujita Y, Duncan NA, Lotz J. Radial tensile properties of the lumbar anulus fibrosus are site and degeneration dependent. J Orthopaed Res 1997; 15:814–819.

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37. Eberlein R, Holzapfel GA, Schulze-Bauer CAJ. An anisotropic model for anulus tissue and enhanced finite element analyses of intact lumbar disc bodies. Computer Methods Appl Mech Eng 2001; 4:209–229.

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39. Eyre DR, Muir H. Types I and II collagens in intervertebral disc. Interchanging radial distributions in anulus fibrosus. Biochem J 1976; 157(1):267–270.

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14. McNally DS, Adams MA. Internal intervertebral disc mechanics as revealed by stress profilometry. Spine 1992; 17(1):66–73.

41. Marchand F, Ahmed AM. Investigation of the laminate structure of lumbar disc anulus fibrosus. Spine 1990; 15(5):402–410.

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42. Tsuji H, Hirano N, Ohshima H, et al. Structural variation of the anterior and posterior anulus fibrosus in the development of human lumbar intervertebral disc. Spine 1993; 18(2):204–210.

16. Johannessen W, Elliott DM. Swelling dominates function of human nucleus pulposus even with degeneration. Spine 2005; 30(24):E724–729.

43. Stokes IA, Iatridis JC. Mechanical conditions that accelerate intervertebral disc degeneration: overload versus immobilization. Spine 2004; 29(23): 2724–2732.

17. Iatridis JC, Setton LA, Weidenbaum M, et al. Alterations in the mechanical behavior of the human lumbar nucleus pulposus with degeneration and aging. J Orthopaed Res 1997; 15:318–322. 18. Iatridis JC, Weidenbaum M, Setton LA, et al. Is the nucleus pulposus a solid or a fluid? Mechanical behaviors of the nucleus pulposus of the human intervertebral disc. Spine 1996; 21(10):1174–1184. 19. Sato K, Kikuchi S, Yonezawa T. In vivo intradiscal pressure measurement in healthy individuals and in patients with ongoing back problems. Spine 1999; 24(23): 2468–2474. 20. Urban JPG, McMullin JF. Swelling pressure of the intervertebral disc: influence of proteoglycan and collagen contents. Biorheology 1985; 22:145–157. 21. Iatridis JC, Setton LA, Foster RJ, et al. Degeneration affects the anisotropic and nonlinear behaviors of human anulus fibrosus in compression. J Biomechanics 1998; 31:535–544. 22. Yao H, Justiz MA, Flagler D, et al. Effects of swelling pressure and hydraulic permeability on dynamic compressive behavior of lumbar anulus fibrosus. Ann Biomed Eng 2002; 30(10):1234–1241.

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44. Green TP, Adams MA, Dolan P. Tensile properties of the anulus fibrosus; II. Ultimate tensile strength and fatigue life. Eur Spine J 1993; 2:209–214. 45. Iatridis JC, ap Gwynn I. Mechanisms for mechanical damage in the intervertebral disc anulus fibrosus. J Biomech 2004; 37(8):1165–1175. 46. Iatridis JC, Kumar S, Foster RJ, et al. Shear mechanical properties of human lumbar anulus fibrosus. J Orthop Res 1999; 17(5):732–737. 47. Fujita Y, Wagner DR, Biviji AA, et al. Anisotropic shear behavior of the anulus fibrosus: effect of harvest site and tissue prestrain. Med Eng Phys 2000; 22(5): 349–357. 48. Spilker RL, Jakobs DM, Schultz AB. Material constants for a finite element model of the intervertebral disc with a fiber composite anulus. J Biomech Eng 1986; 108:1–11. 49. Elliott DM, Sarver JJ. Young investigator award winner: validation of the mouse and rat disc as mechanical models of the human lumbar disc. Spine 2004; 29(7): 713–722. 50. Broberg KB. On the mechanical behavior of intervertebral discs. Spine 1983; 8(2):151–165.

23. Best BA, Guilak F, Setton LA, et al. Compressive mechanical properties of the human anulus fibrosus and their relationship to biochemical composition. Spine 1994; 19(2):212–221.

51. Brinkmann P, Frobin W, Hierholzer E, et al. Deformation of the vertebral end-plate under axial loading of the spine. Spine 1983; 8(8):851–856.

24. Gu WY, Mao XG, Foster RJ, et al. The anisotropic hydraulic permeability of human lumbar anulus fibrosus. Influence of age, degeneration, direction, and water content. Spine 1999; 24(23):2449–2455.

52. Hansson TH, Keller TS, Spengler DM. Mechanical behavior of the human lumbar spine. II. Fatigue strength during dynamic compressive loading. J Orthop Res 1987; 5(4):479–487.

Section 5: Biomechanical Disorders of the Lumbar Spine 53. Maroudas A, Stockwell RA, Nachemson A, et al. Factors involved in the nutrition of the human lumbar intervertebral disc: cellularity and diffusion of glucose in vitro. J Anat 1975; 120(1):113–130.

80. Spilker RL, Daugirda DM, Schultz AB. Mechanical response of a simple finite element model of the intervertebral disc under complex loading. J Biomechanics 1984; 17(2):103–112.

54. Roberts S, Menage J, Urban JPG. Biochemical and structural properties of the cartilage end-plate and its relation to the intervertebral disc. Spine 1989; 14(2): 166–174.

81. Shirazi-Adl A, Ahmed AM, Shrivastava SC. Finite element study of a lumbar motion segment subjected to pure sagittal plane moments. J Biomechanics 1986; 19(4):331–350.

55. Setton LA, Zhu W, Weidenbaum M, et al. Compressive properties of the cartilaginous end-plate of the baboon lumbar spine. J Orthop Res 1993; 11(2):228–239.

82. Gilbertson LG, Goel VK, Kong WZ, et al. Finite element methods in spine biomechanics research. Crit Rev Biomed Engineer 1995; 23:411–473.

56. Perey O. Fracture of the vertebral endplate in the lumbar spine: an experimental biomechanical investigation. Acta Orthopaed Scand Suppl 1957; 25:1–101.

83. Natarajan RN, Williams JR, Andersson GB. Recent advances in analytical modeling of lumbar disc degeneration. Spine 2004; 29(23):2733–2741.

57. Grant JP, Oxland TR, Dvorak MF. Mapping the structural properties of the lumbosacral vertebral endplates. Spine 2001; 26(8):889–896.

84. Potvin JR, McGill SM, Norman RW. Trunk muscle and lumbar ligament contributions to dynamic lifts with varying degrees of trunk flexion. Spine 1991; 16(9):1099–1107.

58. Grant JP, Oxland TR, Dvorak MF, et al. The effects of bone density and disc degeneration on the structural property distributions in the lower lumbar vertebral endplates. J Orthop Res 2002; 20(5):1115–1120. 59. Nachemson A, Lewin T, Maroudas A, et al. In vitro diffusion of dye through the endplates and the anulus fibrosus of human lumbar intervertebral discs. Acta Orthopaed Scand 1970; 41:589–607. 60. Ayotte DC, Ito K, Tepic S. Direction-dependent resistance to flow in the endplate of the intervertebral disc: an ex vivo study. J Orthop Res 2001; 19(6):1073–1077. 61. Bernick S, Cailliet R. Vertebral end-plate changes with aging of human vertebrae. Spine 1982; 7(2):97–102. 62. Modic MT, Steinberg PM, Ross JS, et al. Degenerative disk disease: assessment of changes in vertebral body marrow with MR imaging. Radiology 1988; 166(1 Pt 1):193–199. 63. Urban JPG, Holm S, Maroudas A, et al. Nutrition of the intervertebral disc: Effect of fluid flow on solute transport. Clin Orthopaed Related Res 1982; 170: 296–302. 64. Adams MA, Bogduk N, Burton K, et al. The biomechanics of back pain. Edinburgh: Churchill Livingstone; 2002. 65. Althoff I, Brinckmann P, Frobin W, et al. An improved method of stature measurement for quantitative determination of spinal loading. Application to sitting postures and whole body vibration. Spine 1992; 17(6):682–693. 66. de Looze MP, Visser B, Houting I, et al. Weight and frequency effect on spinal loading in a bricklaying task. J Biomech 1996; 29(11):1425–1433. 67. Schultz AB, Andersson GB, Haderspeck K, et al. Analysis and measurement of lumbar trunk loads in tasks involving bends and twists. J Biomech 1982; 15(9): 669–675. 68. McGill SM, Norman RW. Partitioning of the L4–L5 dynamic moment into disc, ligamentous, and muscular components during lifting. Spine 1986; 11(7):666–678. 69. Granata KP, Marras WS, Davis KG. Variation in spinal load and trunk dynamics during repeated lifting exertions. Clin Biomech (Bristol, Avon) 1999; 14(6): 367–375. 70. Callaghan JP, McGill SM. Low back joint loading and kinematics during standing and unsupported sitting. Ergonomics 2001; 44(3):280–294.

85. Dolan P, Earley M, Adams MA. Bending and compressive stresses acting on the lumbar spine during lifting activities. J Biomech 1994; 27(10):1237–1248. 86. Liu YK, Njus G, Buckwalter J, et al. Fatigue response of lumbar intervertebral joints under axial cyclic loading. Spine 1983; 8(8):857–865. 87. Brinckmann P, Biggemann M, Hilweg D. Fatigue fracture of human lumbar vertebrae. Clin Biomech 1988; 3S:S1–S23. 88. Lavender SA, Tsuang YH, Hafezi A, et al. Coactivation of the trunk muscles during asymmetric loading of the torso. Hum Factors 1992; 34(2):239–247. 89. Fathallah FA, Marras WS, Parnianpour M. An assessment of complex spinal loads during dynamic lifting tasks. Spine 1998; 23(6):706–716. 90. Anderson CK, Chaffin DB, Herrin GD, et al. A biomechanical model of the lumbosacral joint during lifting activities. J Biomech 1985; 18(8):571–584. 91. McGill SM, Norman RW. Dynamically and statically determined low back moments during lifting. J Biomech 1985; 18(12):877–885. 92. Smit TH. The use of a quadruped as an in vivo model for the study of the spine – biomechanical considerations. Eur Spine J 2002; 11(2):137–144. 93. Adams MA, Hutton WC. The effect of posture on the role of the apophysial joints in resisting intervertebral compressive forces. J Bone Joint Surg [Br] 1980; 62(3):358–362. 94. McGlashen KM, Miller JA, Schultz AB, et al. Load displacement behavior of the human lumbo-sacral joint. J Orthop Res 1987; 5(4):488–496. 95. Reuber M, Schultz A, Denis F, et al. Bulging of lumbar intervertebral discs. J Biomech Eng 1982; 104:187–192. 96. Ohshima H, Tsuji H, Hirano N, et al. Water diffusion pathway, swelling pressure, and biomechanical properties of the intervertebral disc during compression load. Spine 1989; 14(11):1234–1244. 97. Johannessen W, Cloyd JM, O’Connell, et al. Trans-endplate nucleotomy increases deformation and creep response in axial loading. Ann Biomech Eng 2006; 34(4): 687–696. 98. Shirazi-Adl A. Finite-element evaluation of contact loads on facets of an L2–L3 lumbar segment in complex loads. Spine 1991; 16(5):533–541.

71. Virgin WJ. Experimental investigations into the physical properties of the intervertebral disc. J Bone Joint Surg 1951; 33B(4):607–611.

99. Shirazi-Adl A, Parnianpour M. Nonlinear response analysis of the human ligamentous lumbar spine in compression on mechanisms affecting the postural stability. Spine 1993; 18(1):147–158.

72. Hirsch C, Nachemson A. New observations on the mechanical behavior of lumbar discs. Acta Orthop Scand 1954; 23(4):254–283.

100. Argoubi M, Shirazi-Adl A. Poroelastic creep response analysis of a lumbar motion segment in compression. J Biomechanics 1996; 29(10):1331–1339.

73. Nachemson AL, Schultz AB, Berkson MH. Mechanical properties of human lumbar spine motion segments. Influence of age, sex, disc level, and degeneration. Spine 1979; 4(1):1–8.

101. Schultz AB, Aston-Miller JA. Biomechanics of the human spine. In: Mow VC, Hayes WC, eds. Basic orthopaedic biomechanics. New York: Raven Press; 1991:337–374.

74. Keller TS, Spengler DM, Hansson TH. Mechanical behavior of the human lumbar spine. I. Creep analysis during static compressive loading. J Orthop Res 1987; 5(4):467–478.

102. Kulak RF, Belytschko TB, Schultz AB. Nonlinear behavior of the human intervertebral disc under axial load. J Biomechanics 1976; 9:377–386.

75. Adams MA, McNally DS, Dolan P. ‘Stress’ distributions inside intervertebral discs. The effects of age and degeneration. J Bone Joint Surg [Br] 1996; 78(6):965–972. 76. Cholewicki J, Crisco JJ 3rd, Oxland TR, et al. Effects of posture and structure on three-dimensional coupled rotations in the lumbar spine. A biomechanical analysis. Spine 1996; 21(21):2421–2428. 77. Ogon M, Bender BR, Hooper DM, et al. A dynamic approach to spinal instability. Part I: Sensitization of intersegmental motion profiles to motion direction and load condition by instability. Spine 1997; 22(24):2841–2858.

103. Yerramalli C, Chin K, Elliott D. Disc mechanical function following altered loading in the nucleus pulposus: potential use of crosslinking as a treatment therapy for degeneration. Biomech Model Mechanobiol, 2006. 104. Adams MA, McMillan DW, Green TP, et al. Sustained loading generates stress concentrations in lumbar intervertebral discs. Spine 1996; 21(4):434–438. 105. Johannessen W, Vresilovic EJ, Wright AC, et al. Intervertebral disc mechanics are restored following cyclic loading and unloaded recovery. Ann Biomedl Eng 2004; 32:70–76.

78. Gardner-Morse MG, Stokes IA. Structural behavior of human lumbar spinal motion segments. J Biomech 2004; 37(2):205–212.

106. Simon BR, Wu JSS, Carlton MW, et al. Structural models for human spinal motion segments based on a poroelastic view of the intervertebral disc. J Biomechan Eng 1985; 107:327–335.

79. Belytschko T, Kulak RF, Schultz AB. Finite element stress analysis of an intervertebral disc. J Biomechanics 1974; 7:277–285.

107. Yoganandan N, Cusick JF, Pintar FA, et al. Cyclic compression–flexion loading of the human lumbar spine. Spine 1994; 19(7):784–790; discussion 791.

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126. Oxland TR, Lund T, Jost B, et al. The relative importance of vertebral bone density and disc degeneration in spinal flexibility and interbody implant performance. An in vitro study. Spine 1996; 21(22):2558–2569.

109. Seroussi RE, Krag MH, Muller DL, et al Internal deformations of intact and denucleated human lumbar discs subjected to compression, flexion, and extension loads. J Orthopaed Res 1989; 7:122–131.

127. Stokes IA. Surface strain on human intervertebral discs. J Orthop Res 1987; 5(3):348–355.

110. Gunzburg R, Fraser RD, Moore R, et al. An experimental study comparing percutaneous discectomy with chemonucleolysis. Spine 1993; 18(2):218–226. 111. Dunlop RB, Adams MA, Hutton WC. Disc space narrowing and the lumbar facet joints. J Bone Joint Surg [Br] 1984; 66(5):706–710. 112. Gregersen GG, Lucas DB. An in vivo study of the axial rotation of the human thoracolumbar spine. J Bone Joint Surg [Am] 1967; 49(2):247–262.

129. Fujiwara A, Lim TH, An HS, et al. The effect of disc degeneration and facet joint osteoarthritis on the segmental flexibility of the lumbar spine. Spine 2000; 25(23):3036–3044.

113. Adams MA, Dolan P. Technique for quantifying the bending moment acting on the lumbar spine in vivo. J Biomechanics 1991; 24(2):117–126.

130. Natarajan RN, Andersson GB. The influence of lumbar disc height and cross-sectional area on the mechanical response of the disc to physiologic loading. Spine 1999; 24(18):1873–1881.

114. Axelsson P, Johnsson R, Stromqvist B. Mechanics of the external fixation test in the lumbar spine. A roentgen stereophotogrammetric analysis. Spine 1996; 21(3):330–333.

131. Kim Y. Prediction of peripheral tears in the anulus of the intervertebral disc. Spine 2000; 25(14):1771–1774.

115. Haughton VM, Rogers B, Meyerand ME, et al. Measuring the axial rotation of lumbar vertebrae in vivo with MR imaging. Am J Neuroradiol 2002; 23(7):1110–1116.

132. Natarajan RN, Ke JH, Andersson GBJ. A model to study the disc degeneration process. Spine 1994; 19(3):259–265.

116. Wong KW, Leong JC, Chan MK, et al. The flexion-extension profile of lumbar spine in 100 healthy volunteers. Spine 2004; 29(15):1636–1641.

133. Adams MA, Hutton WC. The relevance of torsion to the mechanical derangement of the lumbar spine. Spine 1981; 6(3):241–248.

117. Pearcy M, Portek I, Shepherd J. Three-dimensional x-ray analysis of normal movement in the lumbar spine. Spine 1984; 9(3):294–297.

134. Farfan HF, Cossette JW, Robertson GH, et al. The effects of torsion on the lumbar intervertebral joints: the role of torsion in the production of disc degeneration. J Bone Joint Surg [Am] 1970; 52(3):468–497.

118. Sullivan MS, Dickinson CE, Troup JD. The influence of age and gender on lumbar spine sagittal plane range of motion. A study of 1126 healthy subjects. Spine 1994; 19(6):682–686.

135. Pearcy MJ. Twisting mobility of the human back in flexed postures. Spine 1993; 18(1):114–119.

119. Dvorak J, Vajda EG, Grob D, et al. Normal motion of the lumbar spine as related to age and gender. Eur Spine J 1995; 4(1):18–23.

136. Ueno K, Liu YK. A three-dimensional nonlinear finite element model of lumbar intervertebral joint in torsion. J Biomech Eng 1987; 109(3):200–209.

120. McGill SM, Yingling VR, Peach JP. Three-dimensional kinematics and trunk muscle myoelectric activity in the elderly spine – a database compared to young people. Clin Biomech (Bristol, Avon) 1999; 14(6):389–395.

137. Cossette JW, Farfan HF, Robertson GH, et al. The instantaneous center of rotation of the third lumbar intervertebral joint. J Biomech 1971; 4(2): 149–153.

121. Adams MA, Hutton WC, Stott JR. The resistance to flexion of the lumbar intervertebral joint. Spine 1980; 5(3):245–253.

138. Noren R, Trafimow J, Andersson GB, et al. The role of facet joint tropism and facet angle in disc degeneration. Spine 1991; 16(5):530–532.

122. Schendel MJ, Wood KB, Buttermann GR, et al. Experimental measurement of ligament force, facet force, and segment motion in the human lumbar spine. J Biomech 1993; 26(4–5):427–438.

139. Liu YK, Goel VK, Dejong A, et al. Torsional fatigue of the lumbar intervertebral joints. Spine 1985; 10(10):894–900.

123. Wang JL, Parnianpour M, Shirazi-Adl A, et al. Viscoelastic finite-element analysis of a lumbar motion segment in combined compression and sagittal flexion. Effect of loading rate. Spine 2000; 25(3):310–318.

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128. Mimura M, Panjabi MM, Oxland TR, et al. Disc degeneration affects the multi-directional flexibility of the lumbar spine. Spine 1994; 19(12): 1371–1380.

140. Shirazi-Adl A. Nonlinear stress analysis of the whole lumbar spine in torsion – mechanics of facet articulation. J Biomechanics 1994; 27(3):289–299. 141. Thompson RE, Pearcy MJ, Downing KJ, et al. Disc lesions and the mechanics of the intervertebral joint complex. Spine 2000; 25(23):3026–3035.

124. Janevic J, Ashton-Miller JA, Schultz AB. Large compressive preloads decrease lumbar motion segment flexibility. J Orthop Res 1991; 9(2):228–236.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ i: Physiology and Assessment

CHAPTER

79

Physical Examination of the Lumbar Spine Scott F. Nadler*

INTRODUCTION Low back pain (LBP) is one of the most common disorders in the industrialized world1–4 and it is a frequent complaint in patients with musculoskeletal disorder.5 Lifetime incidence of LBP in the general population in the United States is 50–80%.1 LBP is the most frequent cause of work-related disability in workers younger than 45 years old, and second only to arthritis in people 45–65 years old.4 A detailed history and physical examination of the lumbar spine should be completed in all patients with low back pain. A systematic approach to the physical examination is crucial to the correct diagnosis and treatment of the patient and could significantly affect the potential outcome. A complete examination of the lumbar spine should include the following: inspection, palpation, range of motion, flexibility, muscle strength, sensory examination, reflexes, provocative maneuvers, as well as examination of gait. One must remember that the physical examination should be always be used as an adjunct to a patient’s history, and together they should guide the development of a differential diagnosis and treatment plan.

INSPECTION Inspection of the patient should begin the moment the clinician encounters the patient. While taking a patient’s history, the clinician often makes observations that will enhance the physical examination. Observation begins as the patient walks into the office with the gait providing many clues. Patients with low back pain generally ambulate in a slow, and sometimes antalgic gait. Depending on the nature of back pain, certain patients ambulate in a forward flexed position for pain relief, where others ambulate in a rigid posture to avoid motion of the lumbar spine. Patients with back pain located on one side usually lean to the unaffected side for pain relief while, depending on the location of a herniated disc, the patient’s pelvis may shift more medially for a lateral herniation and laterally for a herniation medial to the exiting nerve root. Full examination should begin with the patient standing upright. The patient’s back and legs need to be fully exposed. The examiner should assess the skin for signs of echymosis, erythema, rash, infection, skin lesions, or muscle atrophy. Echymosis would indicate trauma. Erythema can be a sign of infection. Skin lesions are also important, such as scars from a previous surgery. Muscle atrophy can be due to nerve root or peripheral nerve injury. To ensure a complete examination, inspection should be performed from head to toe. A systematic approach to inspection includes the anterior, posterior, and lateral planes.

shoulders are usually equal in height; although in many people, especially overhead athletes, the dominant shoulder is slightly lower.6 The anterior superior iliac spine, the iliac crest and the greater trochanter should be equal in height. The patellas should also be equal in height and face anteriorly. Examiner should identify genu valgus/varus. The medial malleoli should also be equal in height. The clinician should look for varus/valgus deformity of the forefoot and prone/supine position of the feet and note the foot arch.

Posterior inspection Posterior observation is the most crucial aspect of inspection in patients with LBP. Symmetry of the head and shoulder height should be reexamined in this plane (Fig. 79.1). Scapular symmetry is assessed. The spine of scapula is normally at the T3 level. Inferior angle of scapula is at the level of T8. The clinician should assess symmetry of the scapula at these levels. The distance of inferior angle of scapula from the spine is also noteworthy. With inspection of the spine, the clinician should search for tissue asymmetry, signs of edema, or erythema. The spinal column should be evaluated for signs of scoliosis. Asymmetrical paraspinal fullness is also clinically significant and should be noted. The waist lines should be equal in height. Iliac crests should be symmetrical (Fig. 79.2). Gluteal folds, popliteal

Anterior inspection With the anterior inspection, the examiner must begin with the head. The position of the head should be symmetrical on the shoulders. The *Arjang Abbasi assisted in the preparation of this chapter.

Fig. 79.1 Assessment of shoulder height. 839

Part 3: Specific Disorders

Fig. 79.2 Assessment of iliac crest height.

creases and medial malleoli should also be symmetrical bilaterally. The Achilles tendons and the heels should be midline.

Lateral inspection With examination of the patient in the coronal plane, alignment of the ear, the shoulder and the peak of the iliac crest are assessed. The lumbar spine is generally in lordosis. An increased lumbar lordosis could be a sign of spondylolisthesis, weak hip extensors, or a hip flexor contracture. A flattened lumbar lordosis could be a sign of disc herniation or acute low back pain.

RANGE OF MOTION Assessment of range of motion (ROM) of the lumbar spine is a critical aspect of lumbar spine examination. It is an important tool in evaluation of recovery in a patient with low back pain. Abnormal spinal motion is associated with abnormal spinal mechanics.7 Motion of the lumbar spine must be assessed in all planes including flexion, extension, side bending, and rotation. ROM can be done actively or passively. If passive ROM is performed, caution should be made not to put too much pressure on a person who expresses discomfort at a certain angle. Key findings that the examiner should look for are endrange pain and side-to-side asymmetry. Examiners should be aware that lumbar flexion is composed of lumbar ROM as well as pelvic motion.8,9 Lumbar motion occurs prior to pelvic movement. This is very important, especially in a subgroup of patients who are flexible enough to bend forward and touch their toes using only hip motion.10 For this reason, when asking a patient to flex fully, one should also look for reversal of lumbar lordosis. Caillet has shown that the first 45 degrees of flexion consists of reversal of the lumbar lordosis with the remainder of motion secondary to pelvic rotation.11,12 Generally, the first 60 degrees of flexion are attributed to the lumbar spine. However, there have not been any accurate measures to confirm this observation.13 The most accurate method to measure the movement of the vertebrae is through radiologic studies. However, use of long-term radiography is not realistic due to risk of radiation and cost.10,14 Various 840

methods have been utilized in measurement of the lumbar spine. Burdett et al.15 and Portek et al.16 both performed studies comparing plain radiographs with various external measurements. However, the findings were inconsistent. Mayer et al.10 compared flexion and extension measured by an inclinometer to radiographic films and found no statistical significance between the two measurements. Saur et al.14 also compared lumbar ROM in flexion and extension with and without radiologic determination using an inclinometer. The results showed that flexion alone demonstrated a strong correlation (r=0.95) while extension showed a more moderate though good correlation (r=0.82). Ng et al.17 measured normative values in 35 healthy men in all three planes using pelvic restraint as well as lumbar lordosis. They found good reliability in all measurements. The ICC and Pearson’s r values were greater than 0.9. Their normative values in degrees are shown in Table 79.1. The examiner should also be aware of variables affecting lumbar range of motion. McGregor et al. studied spinal motion in 203 normal subjects and concluded that range of motion is affected by age and sex. They also found that occupation and body mass index have little or no effect on spinal range of motion.18 Mellin determined that age had a significant, though indirect relation with spinal ROM.19 Sullivan et al.20 demonstrated a significant difference between flexion and extension angle of men and women, but a small difference between genders for total lumbar sagittal ROM; they also showed total sagittal ROM, flexion and extension angle to decrease with an increase in age. The examiner must be able to eliminate sources of error in measurement, such as improper technique and poor standardization. Studies have shown total lumbar range of motion to be variable in the afternoon as compared to the morning.21 The clinician should also bear in mind that decreased lumbar ROM in a patient who is asymptomatic is not predictive of low back pain.

Fingertip to floor test Measurement of fingertip to the floor is a simple test which is commonly used in clinical practice. The patient is asked to stand erect and bend forward as far as possible with the knees fully extended and heel on the floor. The distance between the tip of the middle finger and the floor is then measured. This test, however, can only be used as a crude method of measuring lumbar function because it does not take into account the contribution of pelvic movement and tightness of the hamstrings.22 Merritt et al.23 found the mean coefficient of

Table 79.1: Lumbar range of movement in 35 healthy men Type of motion

Degrees of motion

Flexion

52 + 9

Extension

19 + 9

Flexion & extension (sagittal plane)

71 + 12

Right lateral flexion

31 + 6

Left lateral flexion

30 + 6

Lateral flexion (coronal plane)

60 + 11

Right axial rotation

32 + 9

Left axial rotation

33 + 9

Axial rotation (transverse plane)

65 + 17

Lumbar lordosis

24 + 8

17

From Ng et al.

Section 5: Biomechanical Disorders of the Lumbar Spine

variation for this test to have an inter-examiner reproducibility of 83% and an intra-examiner reproducibility of 76.4%. Gill et al.24 found the intra-examiner coefficient of variation to be 14%. Thomas et al.25 performed fingertip to floor on 344 patients with new-onset low back pain and 118 individuals without any history of back pain and found the test to have a sensitivity of 45.3% with a specificity of 88.8%. Fingertip to floor distance is also used in lateral flexion. The patient is asked to stand with the head and buttock pressed firmly against the wall and bend sideways as far as possible without bending the knees. Flexion is measured as the distance covered by the fingertips on the lateral thigh. Thomas et al. showed right lateral flexion to have a sensitivity of 23.1% and a specificity of 94.1%. Left lateral flexion had a sensitivity of 26.1% and a specificity of 92.4%.25

Schober test The Schober test was first described by Schober in 1937 to measure segmental motion of the lumbar spine. The examiner marks the S1 spinous process and measures and marks 10 cm above the first mark. Patient is then asked to flex forward as far as possible. The increased distance is then measured. In absence of any pathology, the distance should increase by 4–5 cm.26 This test, however, is only utilized to measure lumbar flexion. The intra-tester variation with this test is reported as 4.8%.27

Modified, modified Schober test

Modified Schober test Macrae and Wright modified the Schober test in 1971.28 The examiner draws a line between the posterior superior iliac spines with the patient standing erect. The distance 10 cm above and 5 cm below is measured. The patient is then asked to fully forward flex. The distance between the two marks is re-measured.24,28 Normal values are consistent with a greater than 5 cm increase in distance between the two marks when measured in full flexion (Fig. 79.3). Thomas et al. compared standing extension, lateral flexion, modified Schober test, finger to floor, and knee extension in a study comparing 344 patients with back pain to 118 patients with no

A

history of back pain and found modified Schober test to be the most specific: 94.9%. However, they found the sensitivity of the test to be only 25.3%.25 Gill et al.24 compared this test to fingertip to floor test, the two-inclinometer method, and photometric technique. They found modified Schober test to have the best repeatability and good intra-tester reliability. They found the coefficient of variation of this test to be 0.9% in flexion and 2.8% in extension. Meritt et al.23 found inter-examiner reproducibility to be 6.3% and intra-examiner reproducibility to be 6.6% with the modified Schober test in flexion and suggested that it be added to a routine lumbar spine examination.23 Reynolds29 found the coefficient of variation to be 11.65% in flexion and 21.57% in extension. He found the test to have good reliability with Pearson coefficients of 0.59 for lumbar flexion and 0.75 for extension. Fitzgerald et al. showed the Pearson coefficient to be 1.0 in lumbar flexion and 0.88 in lumbar extension.30 Miller et al.31 also noted a good inter-rater reliability of the modified Schober method, while Stankovic et al. showed this test to have an intra-rater and inter-rater correlation coefficient of 0.95 and 0.94, respectively.32 The modified Schober test is a simple procedure which can easily be performed in the office setting. It is specific but not sensitive when comparing patients with and without low back pain.33 It is also fairly reproducible.

B

This test was described by Van Adrichem and van der Korst. The patient stands erect with feet 15 cm apart. A horizontal line is made across the posterior superior iliac spine. Another horizontal line is drawn 15 cm superior to the first line. Patient is then asked to flex or extend as far as possible. The new distance between the two lines is measured and the distance is recorded.34 No studies to date have evaluated sensitivity and specificity of the modified, modified Schober test. Van Adrichem and van der Korst reported the Pearson correlation coefficient of this test to be 0.78–0.89 in lumbar flexion and 0.69–0.91 in lumbar extension. The inter-rater reliability was 0.72 in flexion and 0.76 in extension.

Fig. 79.3 Range of motion. (A) Modified Schober technique (neutral standing). (B) Modified Schober technique (full flexion). 841

Part 3: Specific Disorders

Inclinometer This technique requires the use of more advanced equipment for measurement of motion. An inclinometer is a handheld, circular, fluidfilled disc that has a weighted gravity pendulum attached to it that is maintained in the vertical direction. It is graduated by 0.5 degree intervals over 360 degrees. Various studies have described the use of this device using a single inclinometer and dual inclinometers. The use of dual inclinometer has shown to have superior results. The American Medical Association has recommended the dual inclinometer technique.35 This method is attributed to Loebl and Troup.36,37 Mayer later modified the test in 1984.10 One inclinometer is placed over the sacrum with the patient in the erect position. The second inclinometer is placed on the T12–L1 spinous process. These areas are marked. The patient is then asked to fully forward flex while the readings of the two inclinometers are recorded. The difference between the readings in the inclinometer in the T12–L1 area measures the rotation of the torso, whereas the difference between the readings in the sacral area measures the rotation of the pelvis. Range of motion in lumbar flexion is then calculated by subtraction of the sacral rotation from the torso rotation (Fig. 79.4). This process can also be done in extension.10,24 Mayer et al. reported results using single and double inclinometry and found no difference between the two techniques.10,24 However, Nattrass et al.,38 comparing goniometry and dual inclinometry, found intra-rater reliability to be poor, with a Pearson correlation coefficient ranging 0.38–0.54. The measurement of error for thoracolumbar and lumbar movements ranged from 9 degrees to 30 degrees.38 A review of inter- and intra-tester reliability using single and dual inclinometer technique shows varying results. Using a standard goniometer, Reynolds29 found the test to have an inter-tester reliability of 0.75 in flexion and 0.87 in extension. Burdett et al.15 used a parallelogram

goniometer and found inter-tester reliability to be 0.73 in flexion and 0.27 in extension. Saur et al.14 demonstrated high reliability using a standard inclinometer with an inter-tester reliability of 0.88 and 0.94 in flexion and extension, respectively. They also showed a very close correlation (r=0.93) between the measurements taken with radiographic studies as compared to the ones taken without. Merritt et al.23 found intra-tester coefficient of variation to be 9.6 in flexion and 65.4 in extension and inter-tester coefficient of variation to be 13.4 in flexion and 50.7 in extension. Using a dual inclinometer technique, Dillard et al.39 found a high inter-examiner reliability in flexion (r=0.78) with a poor interexaminer reliability in extension (r=0.27). Nattrass et al.38 established an intra-tester reliability of 0.90 in flexion and 0.70 in extension. Williams et al.40 concluded inter-tester reliability to be 0.60 in flexion and 0.48 in extension compared to 0.72 and 0.76, respectively, in flexion and extension for the modified, modified Schober test. They also found intra-tester reliability to be poor with the reliability ranging 0.13–0.87 in flexion and 0.28–0.66 in extension. Mellin19,41,42 used dual inclinometers and found inter-tester reliability to be 0.86 in flexion and 0.93 in extension. Gill et al.24 looked at the range of motion of the lumbar spine comparing dual inclinometer, fingertip to floor, and modified Schober test. They found the modified Schober test to be the most repeatable test. Intra-tester coefficient of variation (COV) of dual inclinometer was 9.3–33.9 in flexion and 3.6–4.7 in extension as opposed to modified Schober test with COV of 0.9 and 2.8, respectively, in flexion and extension. Other studies have used different versions of goniometers. A computerized goniometer (CA 6000) was used by Dopf et al. who found inter-examiner correlation coefficient to be 0.76 and intra-examiner correlation coefficient to be 0.936.43 Ng et al.17 utilized a modified inclinometer with a pelvic restraint. Their data showed intra-tester reliability to be 0.87 in flexion and 0.92 in extension. The inclinometer is also used in lateral rotation. The placement of the inclinometer is identical to the spots used in flexion and extension. The first inclinometer is placed over the sacrum with a second inclinometer being place over the T12–L1 spinous process. The patient is then asked to bend laterally. The degree of lumbar lateral flexion is obtained by subtracting the values from the sacral goniometer from the one over the T12–L1 interspace.44 Dillard et al.39 found the intra-tester reliability in lateral flexion to be 0.66 using a double inclinometer. Using the same device, Nattrass et al.38 found that lateral flexion intra-tester reliability ranged 0.89–0.90. Ng et al.17 showed an intra-tester reliability of 0.96 in right lateral flexion and 0.94 in left lateral flexion using a modified inclinometer with pelvic restraint. Overall, the inclinometer is moderately reliable, though it is very inconsistent in patients with low back pain and has been found to be less reliable in extension than flexion.

PALPATION

Fig. 79.4 Range of motion: inclinometer technique.

842

Palpation of the lumbar spine should be performed both in the standing and in the prone position. It is crucial to know certain landmarks in order to better isolate the symptomatic level. An imaginary horizontal line through the peak level of iliac crests crosses the lumbar spine at the L4 spinous process and through the tubercles of the iliac crests is the L5 spinous process. As the fingers move inferiorly from the L5 spinous process, the posterior superior iliac spine (PSIS) is palpated. The simplest way to find the PSIS is by placing the fingers on the iliac crest and moving them posteriorly until they rest on the two small dimples located at the base of the sacrum. The PSIS is at the level of the second sacral vertebra. The upper margin of the greater sciatic notch is at the level of the third sacral vertebra. Moving

Section 5: Biomechanical Disorders of the Lumbar Spine

caudally from the PSIS, the ischial tuberosity (IT) is palpated, the origin of the hamstring muscles. Drawing a line from the PSIS to IT, the posterior inferior iliac spine (PIIS) is located 5 cm distally with the ischial spine 10 cm caudal. The ischial spine is opposite the first portion of the coccyx. In the standing position, a horizontal line can be drawn joining the pubic tubercle to the top of the greater trochanter; at the midline, the acetabulum and the head of the femur are located. In the standing position, the clinician also palpates the spinous processes to look for any evidence of a step-off deformity, which may indicate spondylolisthesis. Landmarks are obtained by the abovementioned techniques. Usually, palpation of the lumbar spine begins by placing the fingers on the iliac crests to palpate the L4–5 spinous processes. At that point, the examiner may also recheck iliac crest, greater trochanter, scapular, and shoulder height. In the prone position, the spinous processes are palpated along the midline with the transverse processes palpated approximately 4 cm laterally in the same fashion. In a patient with lumbar spine dysfunction, the clinician must palpate above and below the lumbar area to assess the etiology of patient’s discomfort. In the prone position, other structures to be palpated include the PSIS, iliac crests, greater trochanters, ischial tuberosities, along with various muscle groups including the paraspinals, tensor fascia lata, gluteus maximus, gluteus medius, and piriformis. The examiner should look for tissue texture changes from side to side, tender points, and trigger points. A trigger point is a tender muscle area that, when palpated, has a band-like quality and causes radiation of pain to an area distant to the area palpated. Deyo et al.45 described spine and paraspinal tenderness as having low specificity and poor reproducibility. Importantly, they described vertebral tenderness to be suggestive of spinal infection (sensitivity 0.86).

A

FLEXIBILITY Assessment of flexibility of the muscles attached to the pelvic girdle is a very important and often overlooked aspect of the examination of the lumbar spine. The rectus femoris and iliopsoas are attached to the anterior aspect of the pelvis. Tightness of these muscles causes an anterior pelvic tilt, resulting in an increased lumbar lordosis. By the same principle, the hamstrings and gluteus maximus, which are attached posteriorly to the pelvic girdle, cause a decrease in lumbar lordosis if they are tight. Any change in the lumbar lordosis may increase force distribution to the lumbar spine, and may additionally affect the function of the sacroiliac joint. It also causes postural changes in the thoracic and cervical spines. Tightness of any of the above muscles could be either the cause of back pain or a contributing factor to exacerbation of the pain. This knowledge can also aid the examiner in providing a more optimal rehabilitation regimen for the patient.

Thomas test This maneuver examines the flexibility of the iliopsoas. The test is performed with the patient in the supine position. The patient is asked to flex the hip to the chest (Fig. 79.5). Elevation of the opposite hip off the table would indicate hip flexure tightness. Kujala et al.46 studied factors associated with low back pain in 138 adolescents (100 athletes and 38 non-athletes). They found tightness of the hip flexors to be the one factor associated with incidence of low back pain.

Ely’s test Ely’s test assesses rectus femoris flexibility. The patient lies prone on the examining table. The clinician passively flexes the knee maximally,

B Fig. 79.5 Flexibility. (A) Normal Thomas test (flexibility of iliopsoas). (B) Positive Thomas test.

approximating the ankle to the buttock (Fig. 79.6). Elevation of the buttocks from the table is indicative of rectus femoris tightness. Another sign is inability of the heel to contact the buttocks. The distance from the heel to the buttocks can be measured to assess side-to-side differences.

Popliteal angle The hamstrings are tested via measurement of the popliteal angle or passive straight leg raise. Popliteal angle is measured by having the patient lie supine. The examiner flexes the patient’s hip to 90 degrees. The knee is then extended. Popliteal angle is defined as the line formed by a perpendicular line drawn around the axis of the knee and the knee at end range (Fig. 79.7). Esola et al.47 found a high correlation between hamstring flexibility and low back pain. They also concluded that improving hamstring flexibility in subjects with a history of low back pain may decrease the stress on the lumbar spine during flexion by allowing a greater hip range of motion. 843

Part 3: Specific Disorders

ASSESSMENT FOR LEG LENGTH DISCREPANCY

A

Leg length discrepancy can be a cause of low back pain. In assessment of leg length discrepancy, the clinician needs to place the patient’s legs in precisely comparable positions and measure the distance from the anterior superior iliac spines to the medial malleoli of the ankles. In a supine position, the examiner will ask the patient to raise the pelvis off the examining table and place it back on the table with the knees flexed at 90 degrees, with the feet flat on the table. If there is a height discrepancy between the knees, the tibia is longer on the side where the knee lies superiorly. If one knee is more anterior with respect to the other knee, it indicates that the femur of that extremity is longer. If the knees are fully aligned, the next step is for the examiner to fully extend the patient’s knees passively. Leg length discrepancy is assessed by comparing the position of the medial malleoli. For another useful measurement, the examiner can measure distance between the umbilicus and each medial malleolus. Unequal distances signify an apparent leg length discrepancy, usually due to pelvic obliquity or from adduction or flexion deformity in the hip joint. Nadler et al.48 demonstrated no association between leg length discrepancy and the development of low back pain in college athletes.

NEUROLOGICAL EXAMINATION Neurological examination is one of the most important aspects of examination of lumbar spine. We will discuss the sensory, motor, and reflex examination in detail to gain a better understanding of the various components.

B Fig. 79.6 Flexibility. (A) Normal Ely test (flexibility of rectus femoris). (B) Positive Ely test.

Motor examination Strength in the lower extremities is generally assessed by manual muscle testing (MMT). Manual muscle testing was first utilized in 1912 by Robert Lovett to examine patients with poliomyelitis during the epidemic. Since that time, MMT has become the standard of force production evaluation. Classifications of MMT utilize a 6-point scale.49–51 The scale is shown in Table 79.2. The examiner needs to have a systematic approach to performing this test. The examination should include the hip flexors (L1–3), quadriceps (L2–4), tibialis anterior (L4–5), extensor hallucis longus (L5), and the gastrocnemius/soleus complex (S1). Hip extensor and hip abductor strength also need to be assessed. Hip extensors are examined by placing the patient prone and asking him or her to extend the lower extremity. The examiner will apply a downward force and the patient is instructed to resist the examiner’s force. Hip abductor strength is tested by having the patient lie on the table on his or her side. The patient is then asked to raise the leg that is upward and resist a downward force by the examiner. Hip abductor weakness can

Table 79.2: Classification of manual muscle testing 0 = no palpable muscle contraction 1 = palpable or visible contraction 2 = full range of motion with gravity eliminated 3 = full range of motion against gravity 4 = full range of motion against moderate resistance Fig. 79.7 Flexibility. Assessment of popliteal angle (flexibility of hamstrings). 844

5 = full range of motion against full resistance

Section 5: Biomechanical Disorders of the Lumbar Spine

also be detected by the Trendelenburg test. The patient is instructed to stand on one leg; with a weak hip abductor, the patient leans the trunk toward the weak side or the pelvis drops to the contralateral side. Varus deviation of the proximal lower extremity while performing one-legged squats further confirms this finding. To assess the strength of each muscle correctly, two things need to be done: the muscle should be tested in the midrange motion and just proximal to the next distal joint. For instance, the quadriceps strength should be examined with resistance applied just proximal to the ankle. The examiner also needs to place the patient in a position that will specifically isolate each muscle and eliminate the antagonist muscles. Manual muscle testing is subjective and is reliant on the patient. Factors such as motivation, cooperation, pain, and fatigue strongly affect the outcomes of this test. Also, patient’s age, comprehension skills, and ability to follow commands can affect the usefulness of MMT. Barr et al.52 showed increased variability among older and younger patients. Escolar et al. also showed increased variability in children.53 Due to the subjectivity of manual muscle testing, there may be a need for specialized equipment to quantify the amount of force produced. Quantitative muscle testing produces data demonstrating the amount of force produced. It is composed of isokinetic and isometric muscle testing. Isokinetic muscle testing measures maximum torque and work across a joint throughout the range of motion. Reliability of isokinetic muscle testing has been confirmed in many studies. In 1996, Li et al. determined the reliability of the Cybex 6000 isokinetic dynamometer in knee flexors and extensors using 30 subjects with no previous history significant of knee injuries. They found the dynamometer to be highly reliable with the intra-class correlation coefficient (ICC) ranging 0.82–0.91 for peak torque, 0.76–0.89 for total work, and 0.71–0.88 for average power. The average variability for the three tests was 9–14%.54 Pincivero et al. utilized a Biodex System 2 isokinetic dynamometer to assess test/re-test reliability for concentric quadriceps and hamstring strength. The results showed high ICC values ranging 0.88–0.97 at 60 degrees/second and 0.82–0.96 at 180 degrees/ second.55 Emery et al. used a Cybex Norm isokinetic dynamometer to evaluate reliability of eccentric hip flexor and adductor peak torque. Nineteen male volunteers participated in this study. ICC was measured to be >0.84 with eccentric measurement of peak hip adductor torque.56 Callaghan et al. looked at the reliability of isokinetic testing in 20 healthy subjects and 16 patients with patellofemoral pain syndrome. In the healthy population, ICC estimates were >0.75 for isokinetic peak torque and >0.83 for average power and total work. In the patients with patellofemoral syndrome, intraclass correlation coefficient estimates were >0.82 for isokinetic peak torque and >0.75 for average power and total work.57 Isokinetic testing has been proven to be highly reliable in all of the above studies. However, the equipment needed to perform this test is large and expensive. Isometric testing measures the maximum amount of force produced at a specific joint angle. Handheld dynamometers (HHD) are generally used for isometric testing. Compared to the equipment needed for isokinetic testing, the HHD is much less expensive and is portable. Numerous studies have been done on intra-tester and inter-tester reliability of manual muscle testing. Results demonstrating a correlation coefficient of ≥0.75 have been shown to demonstrate good reliability. Results in the same grade or within one grade are thought to be reliable. Isolating the muscle being tested and minimizing substitutions from other muscles allow more-consistent results. In general, training individuals prior to performing manual muscle testing will improve intra-tester reliability.

Many studies comparing MMT with quantitative muscle testing have shown MMT to falsely overestimate a muscle as having full strength, whereas quantitative muscle testing is able to detect subtle differences. Comparing MMT to a handheld dynamometer, Beasley demonstrated that 50% of quadriceps strength needs to be lost before manual muscle testing can identify knee extensor weakness.58 Bohannon, studied knee extension force in 50 patients comparing MMT to a HHD. He found the two tests to be significantly correlated (p=0.001). However, he also found the two test scores to be significantly different (p<0.001). He concluded that MMT may overestimate knee extensor strength.59 Several studies have examined the sensitivity and specificity of muscle strength in patients with lumbar radiculopathy. In 1961, Knutsson showed great toe extensor weakness to have a sensitivity of 76% and a specificity of 52% in patients with an L5 root involvement.60 Spangfort looked at 2504 patients with a confirmed lumbar radiculopathy and found that 70–90% of patients with a weak ankle dorsiflexor had a herniated disc at L4–5 level. Ankle dorsiflexor weakness showed an overall sensitivity of 49% and a specificity of 54%.61 In a study of 1986 patients with lumbar disc herniation, Hakelius et al. demonstrated quadriceps weakness to have a sensitivity of <1% with a specificity of 99%. Reduced ankle dorsiflexor strength had a sensitivity of 49% and a specificity of 54%. Great toe extensor strength was 37% sensitive and 71% specific. Ankle plantar weakness only had a sensitivity of 6% and a specificity of 95%.62,63 Kerr et al. showed ankle dorsiflexion weakness in 54% and ankle plantar flexion weakness in 13% of the patients with L4–S1 disc herniations. The overall specificity was 89%.64 Lauder compared MMT to electrodiagnostic findings in 170 patients with radiculopathy. In this study, 40% of the patients with an L3–4 radiculopathy had weak knee extensors (specificity = 89%). In patients with an L5 radiculopathy, she found toe extensor weakness to be 61% sensitive and 55% specific. In patients with a documented S1 radiculopathy, ankle plantar flexion strength had a sensitivity of 47% with a specificity of 76%.65

Sensory examination A detailed sensory examination of bilateral lower extremities should be performed. Light touch, pinprick, temperature, vibration, and proprioception can be assessed during this evaluation. In most clinical settings, sensory testing is performed assessing light touch and pinprick sensation. When evaluating sensation, the examiner must delineate a true dermatomal versus a more diffuse stocking distribution sensory loss seen in peripheral neuropathies. A dermatome is defined as an area of the skin that is innervated by a single nerve root. The regions of the lower extremity tested should include the medial distal thigh area (L3), medial leg (L4), lateral leg (L5) and calf (S1). A consistent pattern should be assessed in the foot area. In the feet, the medial malleolus is in the L4 dermatomal distribution, the dorsum of the foot is L5, and lateral heel is of S1 distribution.66 Several studies have looked at the sensitivity and specificity of sensory loss in patients with lumbar radiculopathy. Kosteljanetz et al.67 found the sensitivity of sensory loss to be 66% with a specificity of 51%. Knutsson60 recorded a sensitivity of 29% and a specificity of 67%. Kortelainen et al.68 performed a prospective study of the neurological symptoms and sign in patients with sciatica, compared with myelographic and operative findings in 403 patients. They found sensory deficits to be associated with 38% of the disc ruptures.

Muscle stretch reflexes Reflexes are involuntary contractions of muscle that are caused by stimulus. Rene Descartes first established the concept of reflex 845

Part 3: Specific Disorders

action in the early seventeenth century.69,70 In the early nineteenth century, Marshall Hall, an English physician, discussed the concept of an anatomically and physiologically distinct sensorimotor reflex arc in animals after removal of their brain.70,71 Around the same time, Erb also noted the importance of the muscle stretch reflexes and correctly termed the phenomenon as a true reflex arc.70 In 1883, Erno Jendrassik reported what is known as the Jendrassik maneuver. In this maneuver, the subject is asked to flex the fingers of both hands and then instructed to hook the fingers together and pull them apart as strongly as they can.72 This maneuver will aid the clinician in eliciting a reflex in patients with hypoexcitability of the ventral motor neurons.73–75 The maneuver is thought to have a direct excitatory effect on the alpha motor neurons.76,77 Tendon reflex activity and muscle tone depend on the status of the alpha motor neurons, the muscle spindle and their afferent fibers, and the small gamma neurons whose axons terminate on the small intrafusal muscle fibers within the spindles. A tap on the tendon stretches the spindles and activates the fibers. The afferent fibers then synapse with the alpha motor neurons and send impulses to the skeletal muscle fibers. This results in a brief muscle contraction, which is termed a monophasic stretch reflex. Muscle stretch reflexes are also known as deep tendon reflexes. However, this is a misnomer because the only function of the tendon being tested is in mechanically transmitting the sudden stretch from the reflex hammer to the muscle spindle. Otherwise, they have little to do with this response. In addition, some muscles with stretch reflexes such as the jaw jerk do not have any tendon.73 The common stretch reflexes being tested in the lower extremity are the patellar or quadriceps reflex (L3–4) and the Achilles or ankle reflex (S1). Additionally, the medial hamstring reflex is mainly innervated by the L5 and S1 nerve root (Fig. 79.8). The presence of symmetrically active gastrocsoleus reflexes, asymmetry of the medial hamstring reflexes indicates an L5 nerve root lesion.78 Jensen performed a study of medial hamstring reflex in 52 hospitalized patients with a suspected lumbar nerve root compression. He concluded that an abnormal medial hamstring reflex is a sign of L4–5 disc herniation, with an L5 nerve root compression. The results showed a predictive value of 85–89% and the negative predictive value was 51–61%. He recommended a medial hamstring reflex to be included in the general neurological examination of patients with suspected lumbar disc herniation.79 Muscle stretch reflexes are elicited by a quick, sharp tap to the tendon with a reflex hammer. It is difficult to elicit a reflex in a person if the muscles are contracted, as in an anxious patient. Absence of muscle stretch reflexes or brisk reflexes does not necessarily signify a neurologic disease. In the elderly, 6–50% lack Achilles reflexes bilaterally.72 In addition, in some normal individuals, it is normal to get hyperreflexia with a few beats of clonus.73,80 The absent reflex is only significant when there are other lower motor neuron findings such as weakness, atrophy, or the reflexes are asymmetric. An exaggerated response is significant only if there are other upper motor neuron findings, such as a positive Babinski, Hoffman’s sign, signs of weakness or spasticity, or if there is a side-to-side asymmetry.73 There is no universally accepted grading system for reflexes. The most popular muscle stretch reflex test is the National Institute of Neurological Disorders and Stroke (NINDS) scale. It has a five point scaling system. Zero is an absent reflex, 1 is less than normal (includes trace response or a response only brought out with reinforcement), 2 is a reflex in the lower half of normal, 3 is in the upper half of normal, 4 is an enhanced reflex, more than normal and includes clonus if present.72,81,82 A study done on the NINDS by Litvan et al.81 showed a moderate inter-observer reliability with a kappa correlation coefficient of 0.50–0.64. Manschot et al.82 performed a study to establish the inter-examiner reliability of NINDS. However, they 846

A

B Fig. 79.8 Sensory evaluation. (A) Medial hamstring reflex. (B) Alternative method to elicit Achilles reflex.

found a kappa correlation coefficient to be 0.35. They concluded that NINDS scale does not give an acceptable reliability in the performance of different clinicians. In regards to the sensitivity and specificity of the muscle stretch reflexes in the lower extremities in patients with lumbar disc herniation, several studies have been performed. Aronson et al.83 found the sensitivity of the patellar reflex to be 0.50. Spangfort61 showed similar results with a sensitivity of 50% and a specificity of 62% in a study of 2504 patients. Hakelius et al.63 studied 1986 patients with lumbar disc herniation and found ankle reflex to be 52% sensitive

Section 5: Biomechanical Disorders of the Lumbar Spine

and 63% specific. Vucetic and Svensson84 examined physical signs in patients with lumbar disc herniations. They found 11% to have patellar arreflexia and 29% to have Achilles arreflexia. In similar studies, Jönsson and Strömqvist85,86 found 11% of the patients to have an absent patellar reflex and 49% to have an absent Achilles reflex while Kortelainen et al.68 found 7% of patients with an absent patellar and 52% with an absent Achilles reflex. The muscle stretch reflexes are an important component of the physical examination. However, an absent or an exaggerated muscle stretch reflex in isolation is of questionable value.

PROVOCATIVE MANEUVERS Many provocative maneuvers have been devised to complement the information obtained in the physical examination. As with every other test, these maneuvers are best utilized in conjunction with all other findings.

Straight leg raising test Ernst Charles Laségue initially described the concept of pain of the sciatic nerve in 1864.87 J.J. Forst, a student of Laségue, described the straight leg raising (SLR) test in 1881, and named it Laségue sign, giving the credit to his mentor. Forst hypothesized that pain elicited during this maneuver was caused by pressure on the nerve by the hamstring.88 In his description, the patient’s leg is passively lifted in the supine position while maintaining it extended via pressure on the knee.88 Laza K. Lazarevic had already described a similar phenomenon in Belgrade in 1880. He had published an article in which he described six of his patients who suffered from sciatic pain. He described his patients experiencing increased pain with stretching or increased tension in the sciatic nerve. He devised an examination containing three steps. In the first step, the patient is asked to forward flex in a standing position, keeping the knees straight. The second step entailed the patient lying supine with the examiner passively bringing the patient into a sitting position, keeping the knees extended. In the third step, the patient was in a supine position while the leg was passively raised with the knee extended. All three steps were noted to reproduce pain in the sciatic nerve distribution.89 Lazarevic also measured the distance between his own PSIS and heel and concluded that when the leg was maximally stretched, the distance of 103 cm was increased to 111 cm. Lucien de Beurmann, in 1884, explained that pain produced by lifting of a stretched leg is caused by stretching of the sciatic nerve, not by compression from the muscle.88 In 1942, Inman and Saunders showed a distal migration of 2–7 mm of the spinal nerve roots with SLR testing.90 Falconer et al.91 noted a 2–6 mm caudal movement while performing the test in 1948. Goddard et al. studied the movement induced by SLR in the lumbosacral roots and found a motion of 3 mm in the L5 roots and 4–5 mm in the S1 root.92 The SLR test is thus performed with the patient in a supine position. The examiner then passively raises the patient’s leg. The SLR test is positive when pain is produced in the posterior leg below the knee between 30 and 70 degrees (Fig. 79.9).93,94 Pain below 30 degrees is deemed to be nonphysiologic and pain above 70 degrees is felt to be due to hamstring tightness, gluteal muscle tightness, or sacroiliac dysfunction.93–95 In a prospective study of 55 patients with unilateral sciatica, Kosteljanetz et al.96 noted that no ‘typical Laségue’ sign – defined by ‘pain in the leg ipsilateral with the sciatica elicited on SLR’ – was seen at an angle greater than 70 degrees. Various studies have looked at the sensitivity and specificity of SLR test by comparing preoperative results with results confirmed at surgery. Charnley looked at sensitivity and specificity of SLR testing in detecting lumbar disc hernias in 88 patients and found 74 patients

Fig. 79.9 Provocative maneuver: straight leg raise, positive at 30–70 degrees.

to have a herniated lumbar disc. The sensitivity of the SLR test was found to be 0.85 with a specificity of 0.57.97 In a study of 182 patients, Knutsson found SLR to have a sensitivity of 0.95 with a specificity of 0.10.60 Gurdjian analyzed lumbar disc herniations in 1176 patients and concluded SLR testing to have a sensitivity and specificity of 0.81 and 0.52 respectively.98 In a study of 232 patients, Hirsch and Nachemson noted that 91% of the patients had a positive SLR test. The specificity of the test was found to be 32%.99 Hakelius looked at reliability of preoperative diagnostic methods in lumbar disc surgery in 1986 patients. Eighty-eight percent of the patients were found to have a herniated disc. The SLR test in this study had a sensitivity of 0.96 and a specificity of 0.14.63 Spangfort studied 2504 lumbar disc herniation operations and noted that 96.8% of the patients with a lumbar disc herniation confirmed with surgery had a positive straight leg raising test. The specificity of the test was found to be 0.11. Positive SLR was noted in 96–98% of the patients with L4–S1 herniations, and in 73% of patients with L1–2 and L3–4 herniations.61 Kosteljanetz looked at the predictive values of clinical and surgical findings in 100 patients with unilateral sciatica. Fifty-eight patients were found to have a lumbar disc herniation. Sensitivity and specificity of the test were 0.78 and 0.48, respectively.67 In another study in 1988, Kosteljanetz found SLR test to be present in 49/55 patients with unilateral sciatica with 43 of the patients found to have disc pathology at surgery. The SLR test had a sensitivity of 0.89 and a specificity of 0.14.96 Kerr et al. looked at 136 patients, 100 of whom had lumbar disc protrusions and found SLR to be the most frequent sign in the patients with a disc protrusion (98%). However, 55% of the controls exhibited the same sign.64 Jönsson et al. graded SLR depending on the degree, dividing the patients into four areas: positive at 0–30 degrees, 30–60 degrees, greater than 60 degrees, or negative. Of patients, 86% had a positive SLR test preoperatively. When broken down into groups, 42% of those were 0–30 degrees, 26% were 30–60 degrees, and 18% were above 60 degrees. The results showed an overall sensitivity of 0.87 and a specificity of 0.22.85 Albeck looked at SLR test in 80 patients with monoradicular sciatica and found the maneuver to have a good sensitivity (0.82) with a specificity of only 0.21.100 Andersson and Deyo determined the positive predictive value of SLR test with a high probability of having a herniated disc to be 67%. The negative predictive value in these patients was 57%. However, 847

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the positive predictive value in patients with a low probability, which included patients with no sciatica or neurological sign, was only 4% with a negative predictive value of 99%.101 Deville et al. performed a literature review up to 1997 and found 17 diagnostic publications evaluating the SLR test with surgery as a reference standard. Out of the 17 studies, 11 were selected and a statistical analysis was done looking at the sensitivity and specificity of the studies.60,61,63,64,67,96–100 The pooled sensitivity for SLR test was 91% (95% CI 0.82–0.94) with a pooled specificity of 26% (95% CI 0.16–0.38). Also, positive predictive value was 89% at the average prevalence of 86% with a negative predictive value of 33%.102 They concluded the straight leg raising test is very sensitive, but not specific. In addition, they concluded that the high predictive value of the SLR testing in the patients was due to the fact that all studies were surgical case series. The patients included in the studies that were used all had severe symptoms and required surgery. Flaws in the study included interpretation and verification bias along with retrospective design.102

Deville et al. also evaluated the CSLR test within a literature review. Six studies were used for meta-analysis.60,61,63,64,85,96 The pooled sensitivity was calculated to be 0.29 (95% CI 0.24–0.34) with a pooled specificity of 0.88 (95% CI 0.86–0.90).102 They also found the positive predictive value to be 0.92 at a prevalence of 0.82, and the negative predictive value to be 0.22.102

Braggard’s sign/ankle dorsiflexion test This test is a modification of the straight leg raise test. The examiner passively elevates the patient’s leg to the point of pain provocation. At that point, the examiner drops the leg down to a nonpainful range and dorsiflexes the ipsilateral ankle, thereby increasing the tension in the sciatic nerve distribution (Fig. 79.10).93 Studies have shown the test to have a sensitivity of 71%.107

Crossed straight leg raising test In 1901, Fajersztajn described the concept of the ‘well’ leg elevation producing contralateral leg pain. He found in a cadaver study that SLR not only stretches the ipsilateral root, but also the contralateral root.103 Woodhall and Hayes found the crossed straight leg raising (CSLR) test to be highly predictive of disc herniation. They showed the test to be positive in 97% of patients with a large disc herniation. They also noted that 32% of the patients with a positive test required surgical intervention.104 Similarly, Edgar and Park found 44% of the patients with a positive CSLR test to need surgery.105 Khuffash and Porter examined CSLR testing on 113 patients presenting with root tension signs from lumbar disc lesions. They found crossed leg pain to be present in 30% of these patients. In addition, 59% of those patients required surgery. They concluded that a positive CSLR test is a sign of poor prognosis, indicating that conservative management will fail.106 Numerous studies have looked at sensitivity and specificity of this maneuver by comparing preoperative results with result confirmed by surgery. Knutsson found the test to be 25% sensitive and 93% specific when looking at a total of 182 patients.60 Spangfort looked at 2504 lumbar disc herniation operations. He concluded that only 23% of the patients with a surgically confirmed disc herniation had a positive CSLR test. However, 88% of the patients with a positive CSLR test were confirmed to have a disc herniation at surgery.61 Hakelius performed a similar study looking for reliability of CSLR test in patients with lumbar disc herniation. He found the test to have a sensitivity of 0.28 with a specificity of 0.88.62 Kosteljanetz et al. found 11/11 patients with a positive CSLR to have disc herniations at surgery. When including an atypical CSLR test, defined as only back and possible hip pain elicited by the maneuver, the results showed a specificity of 95% (19 out of 20 patients). They found the test to have a low sensitivity.96 Kerr et al. also looked at a total of 136 patients, 100 of whom were found to have a lumbar disc protrusion, with 93% having a positive CSLR also found to have a disc protrusion. The sensitivity of the test was calculated as 43%.64 Andersson and Deyo examined the prevalence, sensitivity, and specificity of CSLR test.101 They found the test to have a sensitivity of 23–42% with a specificity of 85–100%. They concluded that CSLR test is less sensitive, but much more specific than SLR test. The results showed the positive predictive value to be 79% and the negative predictive value to be 44% in a patient with a positive CSLR test. In patients with a low probability, including people with no sciatica or neurological signs, the positive predictive value was 7% with a negative predictive value of 98%.101 848

A

B Fig. 79.10 Provocative maneuvers. (A) Ankle dorsiflexion test. (B) Linder maneuver.

Section 5: Biomechanical Disorders of the Lumbar Spine

Bowstring sign/posterior tibial nerve sign Bowstring sign was originally described by Gower in 1888, and later on reintroduced by Cram in 1953. This test is another modification of the straight leg raising test in which the patient’s leg is passively raised until patient experiences pain in the leg; then the examiner slightly flexes the patient’s leg and applies pressure to the tibial nerve in the popliteal fossa. Popliteal space compression is noted to cause stretching of the sciatic nerve and cause pain.108 Supik and Broom107 compared the sensitivities of several provocative maneuvers associated with lumbar nerve root compression due to a disc. They found the bowstring sign to be positive 69% of the time compared with straight leg raising test which was positive 96% of the time and crossed straight leg raising test which was positive 21% of the time.107

Slump test Cyriax initially described the slump test in 1942.109 In this maneuver, the patient is asked to sit in the edge of the examining table with the posterior part of the knee supported against the edge of the table. The patient will then ‘slump’ his spine into thoracic and lumbar flexion. The patient is asked to flex his/her head. The examiner then uses over-pressure to affirm that the neck is in full flexion. At this point, the examiner asks the patient to extend the knee while the examiner maximally dorsiflexes the foot. The test is repeated with the other leg, and the distances are compared. If the patient experiences pain with knee extension and is unable to fully extend the knee, the examiner then releases the neck flexion, and the patient extends the neck to neutral. If the patient is able to raise the knee further with the neck in neutral position or if the symptoms decrease with neck in neutral, the test is positive and is a sign of increased neural tension.93,109 Stankovic et al. performed a prospective study comparing validity of various clinical tests to findings on CT and/or MRI scans. All 105 patients were seen and examined by the senior author. Based on the radiological findings, the patients were divided into 52 patients with herniated discs, 41 patients with bulging discs, and 12 patients without positive findings. The study showed that 94.2% of the patients with a frank disc herniation had pain reproduction with the slump test. In patients with disc bulges, 78% had pain reproduction, while 75% of the patients with no positive radiological findings also had a positive test.32

Femoral nerve stretch test Wassermann first published femoral nerve stretch test, also known as reverse straight leg raising test, in 1918. He described this maneuver in soldiers complaining of anterior thigh and shin pain, with an absent straight leg raising sign. The patient is prone on the examining table. The clinician places the palm at the popliteal fossa and fully flexes the knee. The test is positive if the patient experiences excruciating pain in the back, anterior thigh, or groin.110 The pain is caused by stretching of an irritable femoral nerve in a patient with an L2, L3, or L4 herniated disc.111 Unlike lower lumbar radiculopathies, high lumbar disc herniations are less common and not as well known by many clinicians. Therefore, they are more challenging to diagnose. The reverse straight leg raise test is probably the best screening tool to diagnose a high lumbar radiculopathy. This test has been shown to be positive in 84–95% of the patients with high lumbar disc herniations.112–114 Estridge et al. showed the femoral nerve stretch test to be invaluable in patients with L3–4 disc herniations.115 They observed traction forces, resulting in a 2 mm movement of the L4 root. Christodoulides demonstrated pain to be induced with cross femoral nerve test in 95% of the patients with lateral L4–5 disc protrusions causing L4 nerve root pain.113

Penning and Wilmink studied the biomechanics of the lumbar dural sac using myelography. They showed that the dural sac moves anteriorly with the spine in extension with indentation, especially at the L3–4 and L4–5 levels.116 Geraci and Alleva117 added hip extension to the femoral nerve stretch test in 1996 and showed the modified test to be more sensitive. The findings by Penning and Wilmink116 help explain the added benefit of extension during the reverse straight leg raising test (Fig. 79.11). The clinician needs to be aware that many other conditions may reproduce these symptoms. These may be a tight iliopsoas, rectus femorus, hip pathologies, femoral neuropathy, or diabetic amyotrophy. In order to reduce the false positives, it would help to perform this test bilaterally.8,9

Crossed femoral nerve stretching test The crossed femoral nerve stretching test was first illustrated by Cyriax in 1948.118 The maneuver is performed in the same manner as the femoral nerve stretching test. However, in this maneuver, the patient experiences pain with the femoral nerve stretching test being performed on the uninvolved extremity producing pain on the affected extremity. This test can essentially be thought of as a reverse straight leg raising test for the femoral nerve. No publications were done on this test until 1976, when Dyck published a case report on this test.111 He suggested that stretching of the psoas and quadriceps places traction on the L3 and L4 nerve roots, referred to as crossed femoral stretch test.111 In 1996, Kreitz et al. published a case on a 73-year-old male with a lateral L3–4 disc herniation in whom the test was positive.118 Nadler et al. published another case report on two patients diagnosed electrodiagnostically with an L4 radiculopathy who had a positive femoral nerve stretching test and crossed femoral nerve stretching test.9 They suggested that the femoral nerve stretching test is a valuable tool in the diagnosis of high lumbar disc herniations; however, because of the many confounding issues, its specificity is drawn into question. They suggest that the addition of the crossed femoral nerve stretching test helps to improve the specificity of this often confusing diagnosis.9

Nonorganic signs Waddell’s signs In 1980, Gordon Waddell et al. described a relatively simple technique to assess nonorganic signs in patients presenting with a complaint of

Fig. 79.11 Provocative maneuver: reverse straight leg test. 849

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low back pain. They suggested that this test be used on a regular basis to screen patients that require more in-depth psychological evaluation.119 Five physical signs were developed and studied: tenderness, simulation, distraction, regional disturbances, and overreaction. The acronyms DORST or DOReST are used to remember these signs. 1. Distraction test: The examiner performs a routine test and obtains a positive test. He/she then repeats the test while the patient is distracted. If the findings are only positive when a formal examination is done and negative at other times, it may indicate a nonorganic component. An example for this would be obtaining a positive supine straight leg raising test and a negative seated straight leg raising test. 2. Overreaction means a disproportionate reaction during the examination. This could translate into verbalization, facial expression, muscle tenderness, tremor, sweating, or collapsing. 3. Regional disturbances involve a motor or a sensory exam where the deficits expressed by the patient do not follow a true myotomal or dermatomal pattern. For example, a herniated disc usually affects one or two roots at the most. If a patient expresses hemisensory or stocking/glove sensory loss on one extremity, that would raise a red flag. 4. Simulation tests are performed to give the patient the impression that a test is being carried out, but it is not. An example for this is axial loading, which can be done in a seated position. The test is considered positive if patient complains of pain radiating down the lumbar spine to the legs with performance of this test. 5. Tenderness can be superficial or nonanatomic. Superficial tenderness entails tenderness to light pinch over a large area on the lumbar skin. Nonanatomic tenderness is when the patient complains of deep tenderness to palpation, which is not localized to one area or structure. These steps help identify patients who have nonorganic symptoms. A total of three or more of the five steps suggests that the patient has a significant psychological overlay.119–121 The clinician needs to be careful in labeling patients as having organic signs. Geraci stated that the seated straight leg raising test in not equivalent to supine straight leg raising test and suggested substituting the seated straight leg raising test with the slump test.122 In axial loading, neck pain should be considered normal. Also, in sensory evaluation, the clinician must be aware of other possibilities such as peripheral neuropathy or spinal stenosis causing multiroot involvement.119 These signs combined were found to have a reproducibility of more than 80% with a kappa coefficient of 0.55–0.71.119–121 This test has often been misinterpreted. Main and Waddell published a reappraisal of the interpretation of Waddell’s sign.123 They stated multiple signs suggest that the patient does not have a straightforward physical problem, but that one needs to also consider psychological factors. However, they mentioned that having nonorganic signs does not mean that the patient does not require medical treatment. It merely suggests that the patient may need a psychological assessment in addition to more standard medical treatment.58 In addition, positive results do not indicate malingering.101,123

Hoover test The Hoover test is performed to assess a patient’s effort during a physical examination. The patient is in the supine position on the examining table. The examiner cups the heels and asks the patient to raise each leg individually. If the patient provides a true effort, it will cause contralateral leg extension to stabilize the pelvis. This will result in the examiner feeling increased pressure in the untested heel.

850

CONCLUSION Physical examination of the lumbar spine is crucial in assessing the nature and severity of low back pain. The knowledge of the proper techniques, the sensitivity, specificity, and reliability of the maneuvers is beneficial in formulating a differential diagnosis and plan of treatment or further evaluation. In conclusion, although it is important to know how a test is performed, the most important art is the ability to utilize those findings in the context of the history and the physical examination. There are a multitude of examination maneuvers and special tests used in the evaluation of patients with low back pain. Unfortunately, some have yet to be systematically evaluated for their clinical value. By careful examination, combining multiple techniques and awareness of the limitations of each maneuver, a scientific approach to clinical diagnosis is possible. In the future, we have the responsibility to move the evidence-based knowledge forward with respect to the examination of the patient with lumbar pain. This will help streamline patient evaluation and the subsequent differential diagnosis.

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44. Mooney V. Physical measurement of the lumbar spine. Phys Med Rehabil Clin N Am 1998; 9(2):391–410.

73. McGee S. Evidence-based physical diagnosis. Philaelphia: WB Saunders; 2001: 772–777.

71. Hall M. Synopsis of the distatic nervous system. London: Joseph Mallett; 1850.

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Part 3: Specific Disorders 74. Jendrassik E. Beitrage zur Lehre von den Sehnenreflexen. Deutches Archiv Fur Klinische Medizin 1883; 33:177–199.

105. Edgar MA, Park WM. Induced pain patterns on passive straight leg raising in lower lumbar disc protrusion. J Bone Joint Surg [Br] 1974; 56:658–666.

75. Schiller F. The reflex hammer: In memoriam Robert Wartenberg (1887–1956). Med Hist 1967; 11:75–85.

106. Khuffash B, Porter RW. Cross leg pain and trunk list. Spine 1989; 14(6):602–603.

76. Burke D, McKeon B, Skuse NF. Dependence of the Achilles tendon reflex on the excitability of spinal reflex pathways. Ann Neurol 1981; 10:551–556. 77. Bussel B, Morin C, Pierrot-Deseilligny E. Mechanism of monosynaptic reflex reinforcement during Jendrassik Maneuvre in man. J Neurol Neurosurg Psychiatry 1978; 41:40–44.

108. Cram RH. A sign of the sciatic nerve root pressure. J Bone Joint Surg [Br] 1953; 35:192–195. 109. Cyriax J. Perineuritis. Br Med J 1942; 1:578–580.

78. Felsenthal G, Reischer MA. Asymmetric hamstring reflexes indicative of L5 radicular lesion. Arch Phys Med Rehabil 1982; 63(8):377–378.

110. Wassermann S. Ueber ein neues Schenkelnersymptom nebstr Bemerkungen zur Diagnostik der Schenkelnerverkrankungen. Dtsch Z Nervenbeilk 1918/1919; 43:140–143.

79. Jensen OH. The medial hamstring reflex in the level-diagnosis of a lumbar disc herniation. Clin Rheumatol 1987; 6(4):570.

111. Dyck P. The femoral nerve traction test with lumbar disc protrusions. Surg Neurol 1976; 6:163–166.

80. Dick JP. The deep tendon and the abdominal reflexes. J Neurol Neurosurg Psychiatry 2003; 74(2):150–153.

112. Abdullah AF, Wolber PG, Warfield JR, et al. Surgical management of extreme lateral lumbar disc herniations. Neurosurgery 1988; 22:648–653.

81. Litvan I, Mangone CA, Werden W, et al. Reliability of the NINDS myotatic reflex scale. Neurology 1996; 53:1187–1189.

113. Christodoulides AN. Ipsilateral sciatica on the femoral nerve stretch test is pathognomonic of an L4/5 disc protrusion. J Bone Joint Surg [Br] 1989; 71:88–89.

82. Manschot S, van Passel L, Buskens E, et al. Mayo and NINDS scales for assessment of tendon reflexes: between observer agreement and implications for communication. J Neurol Neurosurg Psychiatry 1998; 64:253–255.

114. Porchet F, Frankhauser H, de Tribolet N. Extreme lateral lumbar disc herniation: a clinical presentation of 178 patients. Acta Neurochir (Wien) 1994; 127:203–209.

83. Aronson HA, et al. Herniated upper lumbar discs. J Bone Joint Surg [Am] 1963; 45:311–317.

115. Estridge MN, Rothe SA, Johnson NG. The femoral stretching test: A valuable sign in diagnosing upper lumbar disc herniation. J Neurosurg 1982; 57:813–817.

84. Vucetic N, Svensson O. Physical signs in lumbar disc hernia. Clin Orthop 1996; 333:192–201.

116. Penning L, Wilmink JT. Biomechanics of lumbosacral dural sac. A study of flexion–extension myelography. Spine 1981; 6:398–408.

85. Jönsson B, Strömqvist B. The straight leg raising test and the severity of symptoms in lumbar disc herniation. Spine 1995; 20(1):27–30.

117. Geraci MC, Alleva JT. Physical examination of the spine and its functional kinetic chain. In: Cole AJ, Herrring SA, eds. The low back pain handbook. Philadelphia: Hanley & Belfus; 1996:60.

86. Jönsson B, Strömqvist B. Symptoms and signs in degeneration of the lumbar spine. A prospective, consecutive study of 300 operated patients. J Bone Joint Surg [Br] 1993; 75:381–385. 87. Laségue C. Considerations sur la sciatique. Arch Gen Med 1864/II; 6:558–580. 88. Karbowski K, Radanov BP. Historical perspective: The history of the discovery of the sciatica stretching phenomenon. Spine 1995; 20(11):1315–1317. 89. Lazarevic LK. Ischias postica cotunnii. Archivum Serbicum Pro Universa Scientia et Arte Medica Recipienda 1880; 7:23–35. 90. Inman VT, Saunders JB. The clinico-anatomical aspects of the lumbosacral region. Radiology 1942; 38:669–678. 91. Falconer MA, McGeorge M, Begg AC. Observations on the cause and mechanism of symptom production in sciatica and low back pain. J Neurol Neurosurg Psychiatry 1948; 11:13–26. 92. Goddard MD, Reid JD. Movements induced by straight leg raising in the lumbosacral roots, nerves and plexus and in the intrapelvic section of the sciatic nerve. J Neurol Neurosurg Psychiatry 1965; 28:12–18. 93. Magee DJ. Orthopedic physical assessment. Philadelphia: WB Saunders; 1992. 94. Shiqing X, Quanzhi Z, Dehao F. Significance of the straight leg raising test in the diagnosis and clinical evaluation of lower lumbar intervertebral disc protrusion. J Bone Joint Surg [Am] 1987; 69(4):517–522. 95. Fahrni WH. Observation on straight leg raising with special reference to nerve root adhesions. Can J Surg 1966; 9:44–48. 96. Kosteljanetz M, Bang F, Schmidt-Olsen S. The clinical significance of straight leg raising (Laségue’s sign) in the diagnosis of prolapsed lumbar disc: interobserver variation and correlation with surgical finding. Spine 1988; 13(4):393–395.

118. Kreitz BG, Cote P, Yong-Hing K. Crossed femoral stretching test. A case report. Spine 1996; 21(13):1584–1586. 119. Waddell G, McCulloch JA, Kummel E, et al. Nonorganic physical signs in low-back pain. Spine 1980; 5(2):117–125. 120. Waddell G, et al. Normality and reliability in the clinical assessment of backache. Br Med J (Clin Res Ed) 1982; 284(6328):1519–1523. 121. Waddell G, et al. Objective clinical evaluation of physical impairment in chronic low back pain. Spine 1992; 17:617–628. 122. Geraci MC. Validation of physical examination: cervical and lumbar spine. Assoc Acad Phys Prog 1997; 254–265. 123. Main CJ, Waddell G. Spine update: behavioral responses to examination. A reappraisal of the interpretation of ‘nonorganic signs.’ Spine 1998; 23(21): 2367–2371.

Further Reading Forst JJ. Contribution a l’etude clinique de la sciatique. Paris: These No. 33 Faculte de Medecine: 1881. Gonnella C, et al. Reliability in evaluating passive intervertebral motion. Phys Ther 1982; 62:436–444. Hoehler FK, Tobis JS. Low back pain and its treatment by spinal manipulation: measures of flexibility and asymmetry. Rhematol Rehabil 1982; 21:21–26. Hseih CY, et al. Straight leg raising test: compression of three instruments. Phys Ther 1983; 63:1429–1432.

97. Charnley J. Orthopaedic signs in the diagnosis of disc protrusion. With special reference to the straight leg raising test. Lancet 1951; 260:186–192.

Hsu K, Zucherman J, Shea W, et al. High lumbar disc degeneration: incidence and etiology. Spine 1990; 15:679–682.

98. Gurdjian ES, Webster JE, Ostrowski AZ, et al. Herniated lumbar intervertebral discs: An analysis of 1176 operated cases. J Trauma 1961; 1:158–176.

Hudgins WR. The crossed straight leg raising test: A diagnostic sign of herniated disc. J Occup Med 1979; 21(6):407–408.

99. Hirsch C, Nachemson A. The reliability of lumbar disk surgery. Clin Orthop 1963; 29:189–195.

Keely J, et al. Quantification of lumbar function: Part 5. Reliability of range-of-motion measures in the sagittal plane and in vivo torso rotation measurement technique. Spine 1986; 11:31–35.

100. Albeck MJ. A critical assessment of clinical diagnosis of disc herniation in patients with monoradicular sciatica. Acta Neurochir (Wien) 1996; 138:40–44. 101. Andersson GB, Deyo RA. History and physical examination in patients with herniated lumbar discs. Spine 1996; 21(24 Suppl):10S–18S. 102. Deville WL, van der Windt DA, Dzaferagic A, et al. The test of Laségue: systematic review of the accuracy in diagnosing herniated discs. Spine 2000; 25(9):1140–1147.

Kummel BM. Nonorganic signs of significance in low back pain. Spine 1996; 21(9): 1077–1081. Lindblom K, Hultqvist G. Absorption of protruded disc tissue. J Bone Joint Surg [Am] 1950; 32:557–560.

Klinische

McCombe PF, Fairbank JCT, Cockersole BC, et al. 1989 Volvo Award in clinical sciences. Reproducibility of physical signs in low-back. Spine 1989; 14(9):908–918.

104. Woodhall B, Hayes G. The well leg raising test of Fajersztajn in the diagnosis of ruptured lumbar intervertebral disc. J Bone Joint Surg [Am] 1950; 32:786–792.

McGregor AH, McCarthy ID, Dore CJ, et al, Quantitative assessment of the motion of the lumbar spine in the low back pain population and the effect of different spinal pathologies of this motion. Eur Spine J 1997; 6(5):308–315.

103. Fajersztajn J. Ueber das gekreutzte Wochenschrift 1901; 14:41–47.

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107. Supik LF, Broom MJ. Sciatic tension signs and lumbar disc herniation. Spine 1994; 19(9):1066–1069.

ischiaphanomen.

Wiener

Section 5: Biomechanical Disorders of the Lumbar Spine Mayer TG, Kondraske G, Beals SB, et al. Spinal range of motion. Accuracy and sources of error with inclinometric measurement. Spine 1997; 22(17):1976–1984.

Pearcy MJ, Tibrewal SB. Axial rotation and lateral bending in the normal lumbar spine measured by three-dimensional radiography. Spine 1984; 9:582.

Moll JMH, Wright V. Normal range of spinal mobility: an objective clinical study. Ann Rheum Dis 1971; 30:381–386.

Spengler DM, Ouellette AE, Battie M, et al. Elective discectomy for herniation of lumbar disc. J Bone Joint Surg [Am] 1990; 72:230–237.

Nadler SF, Malanga GA, Feinberg JH, et al. Relationship between hip muscle imbalance and occurrence of low back pain in collegiate athletes: a prospective study. Am J Phys Med Rehabil 2001; 80(8):572–577.

Thomas M, et al. Surgical treatment of low backache and sciatica. Lancet 1983; 2: 1437–1439.

Nelson MA, et al. Reliability and reproducibility of clinical findings in low-back pain. Spine 1979; 4(2):97–110.

Troup JDG. Straight leg raising (SLR) and the qualifying tests for increased root tension. Their predictive value after back and sciatic pain. Spine 1981; 6(5): 526–527.

Ohlen C, et al. Measurement of spinal configuration and mobility with Debrunner’s Kyphometer. Spine 1989; 14:580–583.

White AA, Panjabi MM. Clinical biomechanics of the spine. Philadelphia: J.B. Lipinncott; 1978.

O’Keeffe ST, Smith T, Valacio R, et al. A comparison of two techniques for ankle jerk assessment in elderly subjects. Lancet 1994; 344(8937):1619–1620.

Yuen EC, Olney RK, So YT. Sciatic neuropathy: clinical and prognostic features of 73 patients. Neurology 1994; 44:1669–1674.

Pearcy MJ, Portek, J, Shepherd J. Three-dimensional x-ray analysis of normal measurement in the lumbar spine. Spine 1984; 9:294.

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SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ i: Physiology and Assessment

CHAPTER

80

Developmental and Functional Anatomy of the Lumbar Spine Russell V. Gilchrist

INTRODUCTION A thorough knowledge of human anatomy continues to be the cornerstone for all diagnosis and treatment planning. This awareness allows spinal physicians to rise above mediocrity and arm themselves for the complex issues involved in spine care. Unlike peripheral joints, spinal anatomy involves many joints interacting in conjunction to bring about complex, multiplanar motions. These motions have physiological restrictions and weaknesses based upon this anatomy. These weaknesses allow for the unfortunate consequences resulting in axial and radicular pain syndromes that spinal physicians know so well. This chapter will hopefully provide the reader with a basic understanding of both the developmental and functional anatomy of the lumbar spine.1 Since the lumbar and cervical vertebrae develop embryologically in a similar manner, it will only be reiterated here from Chapter 46. The aspects specifically pertaining to the cervical spine will be deleted. Specific differences concerning ossification centers and growth pattern will also be discussed.

EMBRYOLOGIC DEVELOPMENT In order to give a more temporal flow to the embryologic development of the spine we will use the general staging scale devised originally by Streeter.2 This scale consists of 23 stages of growth that starts with fertilization and runs to the sixtieth day of growth.3 Each stage typically has duration of 2–3 days in length.4 Growth and differentiation of the neurospinal axis begins in embryonic stage 6. These cells typically originate from the primitive streak and node at the thirteenth to fifteenth day from fertilization. In the following stage the cells that will form the notochord travel rostrally from the primitive node. The notochordal cells’ growth cause abutment to the overlying ectoderm, which thickens and becomes the neural plate.5,6 This neural plate serves as the primordium for all nervous system evolution.7 This stage occurs at the 17–19 day mark (stage 8) and marks the first stage of nervous system development. The superior notochord promulgates growth of neuroectodermal structures, while the inferior notochord stimulates growth of mesodermal structures.8 In stage 9 the neural plate molds itself into a neural fold/groove.6 This stage is also notable as the first three somites are formed during this 19–21 day period. The somites represent paired, block-like masses of mesoderm lying alongside the neural tube. The human embryo develops 42–44 paired somites: 4 occipital, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 8–10 coccygeal somites. They consist of two cell collections; the ventromedially placed sclerotomal cells and dorsolaterally situated dermo-myotomes.9 The sclerotomal structures are responsible for the formation of the vertebral column, and the dermo-myotomal

cells form the segmental skin and musculature.10 It is postulated that early vertebral segmentation occurs during this stage, most notably is the formation of the first two cervical vertebrae and cranial vertebral junction.6 These bony structures are formed by the first eight occipital somites. Spinal cord primordium is also present during this stage with continuing growth occurring through stage 12. In this stage the inferior neuropore closes and 21–29 somite pairs have formed. At this point vertebral differentiation has occurred through the lumbar segments. Stage 13 (28–32 days) marks completion of pontine and cervical flexures of the spine and continuing neurulation caudal to closure of the posterior neuropore.11 Concluding contouring of the caudal neural tube and adjacent vertebrae begins in this stage and progresses through gestation and into early infancy.6,11 Structures such as the conus medullaris, ventricular terminalis, and filum terminale originate from this caudal neural tube.12 Specific vertebral development occurs through three stages: membrane, cartilage, and bone formation.13 Membrane formation occurs as the notochord encounters the neural tube dorsally and the foregut ventrally. As growth progresses, cavities are formed between the notochordal and neural tube/foregut interface. Sclerotomic cells then infiltrate these cavities. Dorsal migration of sclerotomic cells also occurs during this period. These migrating cells settle in regions that ultimately will become the neural arches.13 This occurs through stages 10 through 12 of embryologic growth. Anterolateral movement of sclerotomal cells occurs in stage 13. These pockets provide primordium for future growth of the ribs. Stages 15 and 16 are characterized by fissuring and flexures of the notochord alongside vertebral body and intervertebral disc primordium.6 The period of cartilage formation in vertebral development takes place through embryonic stages 17 through 23. This chondrification begins in the vertebral bodies and subsequently migrates dorsally into the neural arches.6 During the latter part of stage 23 the dorsal aspect of the neural arches begins to deviate medially. Bone formation starts in the early fetal stage of growth with ossification of the cervical and thoracic regions followed by lumbar and sacral vertebral segments. This final period continues into infancy and adolescence.14 Growth of spinal nerves begins with formation of the spinal cord. This initial differentiation involves clumping of neural crest cells in embryologic stage 12.15 Over the next three stages of development the neural crest cells form spinal ganglia that expand and move ventrally. The first ventral root fibers occur during stage 13. The primordium of the cervical and brachial plexuses also forms during this stage. Stage 14 is marked by complete development of all motor roots from C1 to S2 and growth of intersegmental anastomoses between these motor roots.16 Shortly after this stage the motor nerve roots move

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away from the spinal ganglia and toward their respective intervertebral foramen. Formation of the spinal nerve by mingling of motor and sensory root fibers occurs in stage 15. The roots enter the medial aspect of the foramen during stage 18, and progress completely into the foramen by stage 23. Other motor nerve developments worth noting are the following: the end of stage 14 marks the motor nerve fibers from the L2–4 segments moving a short distance into the leg.17 Creation of the brachial plexus begins in stage 16 and progresses through stage 23. At this point, the major motor subdivisions of the brachial plexus resemble those of the adult.15 Stage 16 also heralds formation of the lumbar plexus and the individual femoral, obturator, tibial, and peroneal nerves, and stage 17 marks development of the hypogastric, pudendal, genitofemoral, and ilioinguinal nerves.15 The sensory nerves develop in a similar manner as their neighboring motor fiber counterparts. As discussed above, the formation of sensory spinal ganglia anlage begins in stage 12 of embryologic development.18 Sensory root fibers grow out first centrally from the ganglia to make connections with the spinal cord in stage 14. In the following stage the fibers move peripherally to blend with the motor root fibers to form the spinal nerve. Entrance to the intervertebral foramen is gained by the end of embryologic stage 16, and complete access to the foramen by all sensory nerve roots is gained by stage 23.19 The autonomic system also begins its formation during the middle embryologic stages of development. Unlike the motor and sensory nerve roots, the autonomic nerve differentiation begins with primordium formation in the lower thoracic, esophageal, and upper abdominal regions rather than in the cephalocaudal growth of the vertebra and nerve roots.20 This occurs at embryologic stage 13. This primordium continues differentiation in the lower cervical to sacral region in stage 14. The first white communicantes fibers can be identified in the T2–9 level at this stage.15 Anlage of the autonomic pelvic plexus begins in stage 15.21 Stage 16 is marked by continued growth of the white rami communicantes through the L3 spinal level. The sympathetic chain also has a cephalad movement from the thoracic to upper cervical segments during this stage. The first gray rami communicantes begin to appear at the C8–T1 level around this time (37–42 days).22 Auerbach’s plexus begins differentiation in embryologic stage 17. Continued growth of gray rami communicantes occurs through stage 23 with formation of autonomic nerve fibers to the S5 spinal level.16 The development of the meninges originates from a thin cellular network that exists between the somites, notochord, and neural tube.6 Its early formation is termed the ‘meninx primitiva.’ It serves as a host site for the migration of cells and eventual development of the meninges. This meninx primitiva generation occurs in embryologic stage 15, and grows to surround the complete neural tube in stage 16. In the following stage, the denticulate ligaments begin to form. By stage 18 the spinal canal has started to take shape with cavitation of the meninx primitiva quickly following in embryologic stage 19. Evidence of pia mater structure formation also occurs during this time. It consists primarily of meninx primitiva cells with a small contribution from neural crest cells. Formation of the dura mater in the cervical and thoracic regions follows pia mater growth in stage 20. It consists of mesodermal cells from sclerotomal and meninx primitiva origins. It initiates growth anterior to the spinal cord with progression longitudinally and circumferentially around the cord. Dura mater growth reaches the lumbar region by stage 22, and completely surrounds the spinal cord end to end at stage 23. Constructs of the epidural space also begin during this last stage. Arachnoid mater development continues to be poorly understood at this time. It is believed to be the last of the meninges to form. This occurs after completion of the embryologic stages, i.e. post 60 days fertilization. 856

FETAL DEVELOPMENT All major structures of the spine are clearly distinguishable by the end of the embryologic period of spinal growth. The next stage of development occurs during the fetal period. Its temporal boundaries include the termination of stage 23 of the embryologic period to birth. As discussed above, chondrification of the vertebra begins in the embryological period. It can be identified in the pedicles, lamina, and transverse processes of vertebrae prior to the fetal period. Early into the fetal period these chondrification centers enlarge and migrate into the posterior arches and vertebral bodies. Fusion of the posterior vertebral structures and dorsal growth of the spinous processes occur at the end of the first trimester (twelfth week).23 This period is also marked by the onset of ossification anteriorly in the body and posteriorly in the lamina of the vertebra (Fig. 80.1). These two bony growth centers progress in a dissimilar manner. Ossification of the vertebral body first occurs in the thoracic region and spreads bi-directionally towards the cervical and lumbar segments. The laminar bony growth takes place in a more typical cephalocaudal pattern from cervical to coccygeal segments.24 In addition, one sees a longitudinal growth of the spinal structures during this fetal period. This growth is demonstrated by measurement of the vertex–coccyx segment over this period. At 3 months, this segment measures about 10 cm long, and reaches to roughly 34 cm at birth.25 The intervertebral disc undergoes changes during this fetal period. The end of the embryologic stage and beginning of the fetal period see the notochord expand into the center of the disc. This cell ingrowth to the disc forms a strand-like appearance that is implanted into an amorphous mucoid substance called chorda reticulum.26 The embryologic cartilage surrounding the expanding notochordal cells begins to have collagen fibers formed within it around the tenth week of gestation.27 Interestingly, their growth patterns are identical to those in the adult.28 Their formation is well established by the sixth month of fetal growth. In addition, the neighboring anterior and posterior longitudinal ligaments begin to develop around the same time as the annular fibers. They grow from perivertebral mesenchymal cells.29 As the fetal period continues, the chorda reticulum enlarges and radially expands. During the terminal stage of this period the chorda reticular cells bordering the annular cartilage themselves begin a transition to fibrocartilage cells. These cells arrange themselves into patterns similar to those seen in the collagen fibers of the adult anulus fibrosus.26,30

Spinous process Superior articular process

Transverse process

Lamina

Pedicle

Vertebral body

Fig. 80.1 Three primary ossification Ossification centers of lumbar center spine.

Section 5: Biomechanical Disorders of the Lumbar Spine

POSTNATAL DEVELOPMENT This final stage of development takes place from birth to adulthood. It is by far the longest of the three stages in duration. In contrast, this stage involves minimal plastic changes in the spinal tissues. This period primarily involves tissue maturation and longitudinal growth of the spine.25 The spinal maturation process involves continued ossification of the vertebrae. This is a continuation from its onset in the fetal period. As discussed above, the vertebrae typically have three primary centers of ossification: one in the ventral vertebral body and one in each of the lamina. The cervical and thoracic vertebrae typically have two secondary centers of ossification, whereas the lumbar spine is unique as it has two additional secondary centers of ossification. This gives the lumbar spine a total of seven ossification centers (Fig. 80.2).48 At birth, approximately 30% of the spine is ossified, primarily from these ossification centers. The articular processes, transverse processes, spinous processes, and the last few sacral and coccygeal segments still demonstrate a cartilaginous pattern at birth.31 Hyaline cartilage also still persists in the superior, inferior, and peripheral portions of the vertebral body. A striking feature at birth is that all pars interarticularis of the cervical, thoracic, and lumbar spine are ossified at birth. Failure of this pars ossification at birth has clinical implications for development of spondylolysis and spondylolisthesis in adulthood.32 The atlas and axis are unique as to their ossification centers number and placement. The reader is referred to the cervical spine anatomy chapter for a more detailed discussion regarding these two vertebrae. The remaining cervical, thoracic, and lumbar segments all develop in a more traditional pattern. As noted above, they have three main primary ossification centers: one located in the vertebral body, and one in each lamina (see Fig. 80.1). The vertebral body is almost entirely ossified by 6 years of age, and the neural arches approximate posteriorly at around 2–3 years of age.31 The epiphyseal plates of the vertebral bodies do not undergo ossification until completion of growth. This occurs around the twentieth year of life. This bony growth progresses in a radial pattern from a peripheral to central direction. However, this inward growth is arrested to leave a central cartilaginous portion that becomes the end-plate zone in the adult. The pedicles remain cartilaginous until the sixth year of life when their ossification process is complete and they fuse with their respective vertebral bodies.37 Secondary ossification sites occur at the transverse processes and spinous processes around the fifteenth to sixteenth year of life. As mentioned earlier, the lumbar vertebrae have two more secondary ossification sites than the thoracic and cervical vertebrae (see Fig. 80.2). These additional sites are found in the dorsal aspect of the bilateral superior articular processes.49

Ossification centers

Spinous process Transverse process Superior articular process

Vertebral body

Fig. 80.2 Five secondary ossification centers of lumbar spine.

These areas usually fuse in the second to third decade of life. An accessory secondary ossification site may occur in the transverse process of the seventh cervical vertebrae.32 If this accessory center fails to fuse with the main secondary center in the transverse process, the accessory site may progress to formation of a cervical rib.33 The intervertebral disc also undergoes changes during the postnatal period. There is a progressive decline in the notochordal mesenchymal cells at birth. This is accompanied by a steady increase in the mucoid substance of the nucleus pulposus. A fibrocartilage capsule surrounds these diminishing notochordal cells and increasing mucoid substance. This change is typically evident by the fifth month of growth.38 By 4 years of age there are no active notochordal cells within the nucleus.39 After this point the nucleus pulposus halts any further growth. Future growth of the disc thereafter occurs through the anulus fibrosus. This growth involves primarily production of fibrous elements. As years advance there is ingrowth of fibrous tissue into the nucleus pulposus with resultant progressive loss of its liquid content.40 Intervertebral disc shape in the newborn has a relatively wedge-shaped appearance with the nucleus located posteriorly in the disc.41 The nucleus reverses position and is primarily anteriorly placed by 2 years of age.41 As the child assumes a more upright posture and gait, the nucleus takes on a more central position in the disc. This occurs around the fourth to the eighth year of life.30,41 A significant horizontal and longitudinal growth phase occurs in the disc after birth. This growth progresses late into adolescence. A more generalized discussion on growth after birth and to adulthood will be summarized to demonstrate the developmental requirements of the spine. It is marked by two main growth spurts: one occurring after birth and the second during puberty.42 The early growth spurt takes place from birth through the age of 5 years. Almost half of this initial growth occurs through the first year of life.41 As mentioned above, at birth the sitting height measures around 35 cm. After the first year of growth this sitting height increases to about 47cm2. In the following 4 years of growth the sitting height increases from 47 cm to 62 cm. So by the time the normal infant reaches 5 years age they have increased their height 27 cm. Over the next 5 years the truncal growth slows dramatically in comparison to the prior 5 years. It increases about 10 cm over this period. The pubertal, or adolescent, phase marks the last stage of linear spinal growth. This commonly occurs at the tenth through eighteenth years of life. During this final stage is when the second growth spurt occurs. Its onset is slightly different for each gender. In females it usually begins slightly earlier than in males. Most commonly, it occurs around the age of 11. There is an initial period of rapid growth over the first 2 years that is followed by a slower growth phase over the remainder of the pubertal stage. The early phase increases sitting height approximately 7 cm, while the slower second stage increases height by another 5 cm. In males, the pubertal stage usually has its onset around age 13 years. The male growth pattern is similar to that of the female’s. However, there is a slight increase in height versus the female growth during the first phase of this growth spurt.41 By the time one reaches from birth to adulthood the spine has nearly tripled in size. This longitudinal growth is accomplished primarily through growth of the vertebral bodies. As discussed earlier, this growth occurs at the superior and inferior surfaces of the bodies.42 These regions persist as cartilaginous zones for continued growth and ossification of the vertebral body.43 The cartilage cells in these regions are arranged in a perpendicular-like pattern to the body. Thus, the longitudinal growth of the vertebral body is much the same as the growth of the metaphyses of long bones in the human body.25,44 Whereas the cells closest to the vertebral body undergo ossification and unite with the vertebral body, other cartilaginous cells moving toward the vertebral body then replace these ossifying cells.45 857

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Hence, the vertebral body continues its longitudinal growth through this ossifying process.44 This growth terminates between the ages of 18 and 25.46 The growth plate then thins and calcifies. However, there remains a fibrocartilaginous region neighboring the disc. This area becomes the adult vertebral end-plate. Each level (i.e. cervical, thoracic, lumbar, and sacral) increases their vertebral height to different degrees. The average cervical and thoracic vertebral body height triples from birth to adulthood.23 The lumbar vertebral segments quadruple their longitudinal size by adulthood.23 At birth, the vertical length of the cervical spine measures about 3.7 cm. It doubles in length by 6 years of growth, during the first growth spurt, and nearly doubles its length again at the pubertal growth spurt. By the end of the pubertal growth spurt the cervical spine constitutes about 22% of the total spine length, and 15 to 16% of the sitting height.23 A lumbar vertebra can increase its height anywhere from 5 to 18 mm from birth to the age of 5.47,50,51 From the age of 5 to adulthood, the lumbar spine almost doubles in size to a height of 25 to 34 mm.47,51 In addition to vertical growth, the vertebral body also expands in a radial pattern.45 From birth to 7 years of age the lumbar vertebral body expands in a dorsoventral diameter from 3 to an average of 27 mm.50 During this 7-year period the lumbar lateral diameter also increases in size. On average, the lumbar body can increase by 29 mm through these years.50 At adulthood, the dorsoventral diameter measures approximately 34 mm.47 Periosteal ossification is primarily responsible for this horizontal growth. Most expansion, similar to vertical growth, occurs during the two main growth spurts.47

FUNCTIONAL ANATOMY Bony structures The lumbar spine is composed of five similar bony vertebral segments. They each contain a vertebral body, two laminas, two transverse processes, two pedicles, one spinous process, and two superior and inferior articular processes (Figs 80.3–80.8). The vertebral body occupies the ventral portion of the lumbar vertebrae. Its cranial appearance is that of a kidney, with the concavity facing dorsally. The lateral appearance of the vertebral body is that of a rectangular block (see Fig. 80.3). Its dorsal aspect serves as the anterior boundary of the spinal canal. Small elevations can be seen in the posterior rim of the superior surface of the body. Two small indentations can be seen on the posterior rim of the inferior surface of the vertebral body. The elevations on the superior surface are remnants of the uncinate processes that are prominently seen in the cervical spine.53 This rudimentary uncinate process allows for the commonly seen posterolateral disc protrusions in the lumbar spine. Foramens can be seen on the

Spinous process Transverse process Superior articular process

Lamina

Vertebral canal

Pedicle

Fig. 80.4 Axial view of the lumbar spine vertebrae.

Vertebral body

dorsal and anterolateral surfaces of the vertebral body. These holes serve as passageways for nutrient arteries and basivertebral veins.52 The lumbar vertebral body’s lateral diameter is typically larger than its anteroposterior diameter. The anterior height of the body is also larger than the dorsal height of the vertebral body. This configuration of the bodies is responsible for creating the normal lordotic curve that is seen in the lumbar spine.49 The pedicles are short cylindrical bones that project from the superolateral portion of the dorsal aspect of the vertebral body (see Figs 80.3 and 80.4). Their medial border helps form the anterolateral aspect of the spinal canal. Its caudal edge forms the roof of the segmental neural foramens.54 As the pedicle is the sole bony connection to the vertebra, it must be responsible for transmitting all the forces from the posterior bony structures to the vertebral body. In essence, the pedicle acts as a bridge between the anterior vertebral body and the posteriorly positioned facet joints and lamina. This functional

Spinous process

Pedicle

Intervertebral foramen Transverse process Superior articular process Inferior articular process

Pedicle Intervertebral disc

Superior articular facet

Sacrum Vertebral body Intervertebral disc

Vertebral body Intervertebral disc Inferior articular facet

858

Spinous process

Fig. 80.3 Lateral view of the lumbar vertebrae.

Fig. 80.5 Lateral view of the anterior vertebral canal.

Section 5: Biomechanical Disorders of the Lumbar Spine

eral direction to allow the articular processes to smoothly articulate and form a lumbar facet joint. The orientation of the superior articular processes alters as one moves from a superior to inferior direction. The upper lumbar segments tend to have a more sagittalyl oriented superior articular process, whereas the L5 and S1 superior articular processes tend to have a more coronal orientation. Physicians performing lumbar facet joint injections commonly observe this phenomenon, as they need to progressively rotate the C-arm as they target lower lumbar facet joints.55

Transverse process Superior articular process Spinous process

Ligaments

Intervertebal discs Inferior articular process

Fig. 80.6 Posterior view of the lumbar spine.

importance is seen in the presence of thickened cortical walls and a trabecular bone pattern designed to support this load transference. The lamina is a broad and thick bone that has a sheet-like appearance (see Fig. 80.4). It connects ventrally to the pedicle and projects posteriorly in a medially directed plane. The dorsal portions of the lamina merge to form the posterolateral portion of the spinal canal.54 The medial and inferior portion of the lamina has an irregular or roughened appearance due to it being the attachment site of the ligamentum flavum. The superomedial surface of the lamina is smooth with a slight curve in it.55 The ventroinferior aspect of the lamina has a bony mass which projects caudally and is called the inferior articular process. This process articulates with the corresponding superior articular facet from the vertebra below to form a facet joint. A linear posterior projection of bone called the spinous process occurs at the dorsal junction of the lamina (see Fig. 80.4). The spinous process is the easiest of the lumbar vertebral bones to palpate, as it lies most dorsal in the spine.54 From a lateral perspective, the spinous process has a rectangular shape. Its dorsal end is roughened secondarily, and this area serving as attachment sites to numerous muscles and ligaments of the lumbar spine. Its anterior surface helps form the dorsal aspect of the spinal canal. At the junction of the pedicle and lamina a bony process projects out laterally. This flat and rectangular bone is called the transverse process (see Fig. 80.4). It is positioned just ventral to the superior articular process and posterior to the intervertebral foramen.49 In contrast to their cervical counterparts, they do not contain a transverse foramen. The anteroposterior diameter of these bones tends to be short, making them rather thin in comparison to the lamina and pedicles. Their width narrows from a superior to inferior direction. These lateral bony processes are designed to serve as fulcrums through which muscles may exert their actions.56 A superior directed bony projection occurs at the junction of the lamina and pedicle. This bony projection is called the superior articular process (Figs 80.4–80.9). The medial surface of this articular process is lined by hyaline cartilage. This cartilage is also present on the lateral surface of each of the inferior articular processes. The cartilaginous zones of the superior and inferior articulating processes are referred to as the articular facet of each articular process.54 All lumbar superior articular processes face in a medial and dorsal direction. Their inferior articular process counterparts face in a ventrolat-

The two longest ligaments in the lumbar spine are the anterior and posterior longitudinal ligaments. They are both present throughout the entire length of the vertebral column. The anterior longitudinal ligament extends from the sacrum to the cervical region (Fig. 80.7). It lies on the anterolateral aspect of the lumbar vertebral bodies. In contrast to its cervical and thoracic divisions, its lumbar portion is more developed and wider in dimension.57 It consists of superficial and deep fibers. The deep fibers are short and extend a distance of no greater than one intervertebral joint. They commonly insert into the margins of the vertebral bodies. The superficial fibers can cross up to five intervertebral segments before attaching to either the superior or inferior margins of the vertebral body. In contrast to the posterior longitudinal ligament, the anterior longitudinal ligament maintains only a loose connection to the anterior portion of the intervertebral disc and ventral portion of the vertebral bodies.58 The primary function of the anterior longitudinal ligament is to resist vertical and extension forces through the lumbar spine. The posterior longitudinal ligament is also present from the sacrum, extending proximally to the cervical region where it becomes the tectorial ligament (see Fig. 80.8). Its fiber composition is similar

Anterior longitudinal ligament Posterior longitudinal ligament

Fig. 80.7 Lateral view of the lumbar spine. 859

Part 3: Specific Disorders Ligamentum flavum

Pedicle sectioned Posterior longitudinal ligament

Intervertebral disc

Lumbar vertebral body Fig. 80.9 Posterior view of the lumbar spine

Spinous process Ligamentum flavum

Fig. 80.8 Posterior coronal view of the lumbar spine.

to the anterior longitudinal ligament. As the name implies, it lies on the posterior aspect of the vertebral bodies and intervertebral discs. On visual inspection the ligament has a saw-toothed, or denticulated, appearance in the lumbar spine. It forms a narrow band as it crosses each lumbar vertebral body, and widens laterally as it overlies the intervertebral disc (see Fig. 80.8).59 This ligament also contains both superficial and deep fibers. The superficial fibers can span anywhere from 3 to 5 vertebral bodies in length before inserting into the margin of the vertebral body. The deep fibers typically span a distance of two intervertebral discs before inserting into either the superior or inferior vertebral body margin. Unlike the loose association of the anterior longitudinal ligament, the posterior longitudinal ligament maintains an intimate connection with the intervertebral discs’ posterior anulus fibrosus. This merging of fibers is so prevalent that gross dissection of the ligament from the posterior anulus fibrosus is extremely difficult.59 The function of the posterior longitudinal ligament is to oppose vertical distraction forces from the dorsal aspect of the vertebral bodies and to resist flexion moments to the lumbar vertebral column.56,59 The ligamentum flavum is a paired ligament that attaches between consecutive lumbar lamina (see Figs. 80.9, 10).60 It is the thickest and strongest of the spinal ligaments. It inserts inferiorly into a medial and lateral attachment site of the distal lamina. The lateral portion inserts into the anterior aspect of the superior and inferior articular processes. The medial attachment occurs on the dorsal aspect of the upper lamina. It should be noted that the lateral portion of the inferior ligamentum flavum contributes to the formation of the anterior capsule of the neighboring facet joint.61 Far lateral fibers also can insert into the pedicle at the same level.49 These anterior and lateral fibers of the ligamentum flavum help to form the posterior boundary of the intervertebral foramen.62 The superior insertion site of the ligamentum flavum is into the inferior portion of the ventral aspect of the lamina and dorsoinferior pedicle one level above the inferior insertion site. The function of this ligament is to resist excessive distracting forces through the posterior aspect of the lumbar spine.63 860

Interspinous ligament Spinous process

Fig. 80.10 Lateral view of the lumbar spine.

It also aids in preventing excessive flexion moments through the lumbar spinal column. Buckling of the ligamentum into the spinal canal during extension of the spine could potentially create compression on the neurovascular structures within the canal. This buckling phenomenon is minimized by the elastic nature of this ligament. In contrast to other spinal ligaments, the ligamentum flavum is comprised of 70–80% elastic fibers.64 These fibers have the special ability to undergo deforming forces (i.e. stretch) and return to their original resting length after the stretch has concluded.65 The interspinous ligaments run between contiguous spinous processes. It is typically absent or rudimentary in the cervical spine and membranous in the thoracic spine. However, it is a well-developed ligament in the lumbar spine.67 The lumbar interspinous ligaments have been described as existing in three different parts: anterior, middle, and posterior.59,66 The anterior part of this ligament is paired (right and left) and has its superior attachment into the ventral portion of the upper spinous process. The inferior insertion of the anterior portion occurs into the ligamentum flavum at the level of the lower spinous process.59,66 The middle part of the interspinous ligament is the largest of the three portions. It inserts into the middle third of consecutive spinous processes. The posterior portion of the interspinous ligament

Section 5: Biomechanical Disorders of the Lumbar Spine

inserts inferiorly into the dorsal half of the superior spinous process. As it courses superiorly it moves dorsally to pass posteriorly to the spinous process above the inferior insertion site. On passing the superior spinous process it merges with the supraspinous ligament.59 It functions as a weak resistor to lumbar flexion and distraction forces.67 Some authors consider these ligaments the first to undergo tearing during a hyperflexion moment through the spine.68 The supraspinous ligament travels just dorsally to the spinous processes in the lumbar spine where it is the strongest (Fig. 80.11). Its intersegmental presence in the lumbar spine can be variable. It can terminate at the L4 spinous process in about 73% of individuals, the L3 spinous process in about 22%, and is only seen bridging the L4–5 interspace in about 5% of individuals. It is rarely seen at the L5–S1 level.69,70 Some authors believe the fibers of the lumbar erector spinae musculature and thoracolumbar fascia replace the supraspinous ligament fibers distal to the L4 level.49 Other authors have postulated that the supraspinous ligament is not a true individual ligament, but is composed of ligamental fibers of the thoracolumbar fascia and neighboring fibers of the multifidis and longissimus thoracis muscles.49,59 It functions as a weak resistor to distraction forces through the spinous processes.67 The iliolumbar ligaments are paired ligaments whose attachments provide a support to the lumbosacral junction area. Their proximal insertion site is into the L5 transverse process. Upon leaving the transverse process, the iliolumbar ligament can divide into 2–5 bands. These bands insert distally into iliac crest, sacral ala, and anterior sacroiliac joint capsule (Fig. 80.12). The two most commonly seen of the bands are the superior and inferior bands. The inferior band is also known as the lumbosacral ligament. It specifically inserts distally into the anterosuperior aspect of the sacral ala and joins the ventral sacroiliac ligament.71 The superior band inserts distally into the iliac crest just ventral to the sacroiliac joint. Its primary function is to restrict forward displacement of the L5 vertebra on the sacrum. Secondary functions include restriction of abnormal forward, backward, lateral bending, and rotation of the L5 vertebra.72

Vascular supply Arterial The abdominal aorta gives rise to four paired lumbar arteries. These lumbar arteries provide blood supply to the first four lumbar vertebral bodies. They are closely related to the midportion of the anterior and lateral aspects of the vertebral body.73 They continue to curve around the vertebral body until they meet the intervertebral foramen. The L5 vertebral body receives its arterial supply from the mid-

Supraspinous ligament

Fig. 80.11 Lateral view of the lumbar spine.

L5 vertebra Sacrum Iliolumbar ligament Iliac crest

Fig. 80.12 Posterior view of the lumbar spine.

dle sacral artery and branches of the iliolumbar arteries.74,75 Similar to the lumbar arteries, the middle sacral artery also originates from the posterior wall of the abdominal aorta. Each lumbar artery gives off two branches to the vertebral body. The first branch of the lumbar artery is the short centrum branch.76 They penetrate the vascular foramina of the vertebral body at regular intervals, subjacent to the lumbar artery. The second set of vessels are the longer ascending and descending branches that form dense arterial plexuses on the anterior and lateral aspects of the vertebral bodies. Their terminal branches enter the bone in the area neighboring each vertebral endplate, while other branches form fine vertical networks on the surfaces of the anterior longitudinal ligament and anulus fibrosus.77 The small segmental arteries supplying the fifth lumbar vertebra, sacrum, and coccyx arise from the median sacral artery. This is a branch of variable caliber originating from the back of the aorta just above its bifurcation and ending in the coccygeal body.73 At the level of the intervertebral foramina, but just lateral to the exit zone, each lumbar artery separates into a series of major branches. These include the anterior, intermediate, and posterior branches.77 The anterior branches lie medial to and then behind the psoas muscles anterior to the lumbar plexus. They give off neural branches to the dorsal rami and parallel with each lumbar nerve.78 The intermediate branch of the lumbar artery divides into three subdivisions: the anterior spinal branches, nervous system branches, and posterior spinal branches. The anterior spinal canal branch divides into an ascending and descending branch immediately after entering the spinal canal. They anastomose with corresponding ascending and descending branches from above and below to form a dense network of vessels on the ventral wall of the spinal canal. The nervous system branches from the intermediate artery travel both proximal and distally with nerves within the canal. The posterior branches of the intermediate artery form a closely woven plexus on the anterior surface of the lamina and ligamentum flavum giving them a blood supply. A laminar branch arises from the posterior spinal canal arterial network on each side. This laminar branch enters the lamina and travels toward the facet joints giving a blood supply to both.77 861

Part 3: Specific Disorders

The posterior branches of the lumbar artery pass dorsally away from the foramina to lie on the outer surface of the lamina and cross the pars interarticularis. As these arteries pass the zygapophyseal joints they give branches to supply the posterior aspects of this joint.77 They continue to travel dorsally on the middle surface of each spinous process. They give ascending and descending branches at this point to supply the paraspinal muscles, and penetrating branches to give a blood supply to the spinous processes.73 Direct branches from the lumbar arteries supply the internal aspect of the vertebral body and corresponding superior and inferior endplates anteriorly and posteriorly by branches from the anterior division of the lumbar artery. These vessels penetrate the vertebral body in a horizontal plane to form a dense arterial complex. From this complex they send vertical branches superiorly and inferiorly to supply the vertebral body and endplate.73,77 Blood supply to the lumbar spinal nerves occurs centrally from branches of the longitudinal vessels of the conus medullaris. These vessels only travel a few centimeters along the rootlets before terminating.79 The dorsal nerve roots obtain vascular supply from the dorsolateral longitudinal spinal arterial system. This arterial structure is a direct extension of the vasa corona. It forms an interrupted plexiform network of arterial vessels that maintains intimate contact with the dorsal rootlets. The ventral rootlets each receive direct branches from the closest vasa corona.79 The remaining proximal portions of the nerve roots receive blood supply via the dorsal and ventral proximal radicular arteries.80 These blood vessels are derived from the dorsal longitudinal spinal artery and accessory anterolateral artery, respectively. These proximal radicular arteries enter the nerve root and follow the length of the nerve distally to merge with the distal radicular artery.80 Their entrance into the proximal nerve roots occurs just after the rootlets exit the spinal cord. The delay in contact of the proximal radicular artery is to eliminate redundancy in the vascular supply pattern. As mentioned earlier, the dorsal and anterior longitudinal vessels are already supplying the most proximal portion of the rootlets. The distal radicular artery branches from the lumbar artery at the level of the intervertebral foramen. It then divides into two branches, one entering each dorsal and ventral root. They then both travel proximal and distally along the length of the nerve roots giving it a blood supply.81 The vascular pattern for venous drainage closely resembles its arterial supply.82 The vertebral body has two main venous collection systems. The vertebral body contains a horizontal articular collecting system, which receives vascular drainage from most of the interior portion of the vertebral body.83 The outer anterolateral portions of the vertebral bodies drain directly into either an anterior internal or external vertebral venous plexus. A second venous drainage network is seen at the vertebral endplate. This complex is termed the subchondral postcapillary venous network of the vertebral bodies. It is smaller and runs a relatively horizontal and parallel course to the articular collecting vein system. This postcapillary network drains into adjacent veins on the surface of the vertebral bodies or sends branches to the articular collecting system.73,83 From these two internal venous complexes, venules drain into a large venous plexus from which the basivertebral veins begin.82 The basivertebral vein then proceeds dorsally to exit at the midpoint of posterior aspect of the vertebral body. At this point it merges with the anterior internal vertebral plexus. This anterior internal venous plexus runs along the ventral and dorsal walls of the spinal canal. It merges with the external venous plexus at the lumbar intervertebral foramen to form the lumbar veins. These lumbar veins also accept drainage from the anterolateral surface of the vertebral bodies by a network of veins called the external vertebral venous plexus. The lumbar veins subsequently drain into the 862

vena cava and left common iliac vein. Posterior elements of the lumbar vertebral canal receive venous drainage from vessels traveling in a similar distribution to the posterior arterial branches of the lumbar artery. They empty into the lumbar vein at the level of the intervertebral foramen. There are two venous systems involved in drainage of lumbar nerve roots. They are separated into proximal and distal radicular venous systems. The distal radicular veins empty into the lumbar vein at the level of the intervertebral foramen. The proximal radicular veins drain into the spinal cord venous plexuses.79 The proximal venous complex has been shown to return through the vasa corona plexus and drain proximally into the anterior and posterior longitudinal veins of the spinal cord.73,84 Veins that drain the nerve roots have shown similarity to the arteries of the nerve root in that they are highly variable in their number and location.80 The nerve root veins structure and distribution emulate more the veins of the central nervous system. Their walls are thin and lack a tunica media. They also differ from peripheral nerve veins as they are usually smaller in number and tend toward a more spiraling (i.e. tortuous) course through the deeper parts of the nerve root.84

Lumbar muscles There are multiple muscles that have insertions into the lumbar spine. These will be separated into four different groups based upon their action on the lumbar spine: the forward flexors, lateral flexors, extensors, and rotators. All muscles of the spine will have multiple actions on the spine, but have been grouped into these four areas based upon their principal actions.56 The forward flexors of the lumbar spine are divided into two groups, the extrinsic and intrinsic muscles. The extrinsic flexors of the lumbar spine consist of the abdominal wall muscles: the rectus abdominis, external and internal obliquus. These muscles serve as the primary forward flexors of the spine. The external oblique also serves as a lateral flexor and rotates the spine to turn the anterior trunk to the opposite side. The internal abdominal oblique has the added function of lateral flexion and rotates the spine to turn the anterior trunk to the same side.52 The psoas major and iliacus muscles function as weak, if any, forward flexors of the lumbar spine. The superior attachment of the psoas major is to the anteromedial surface of the T12–L5 transverse processes, intervertebral disc, and neighboring vertebral bodies to the intervertebral disc. It inserts inferiorly into the lesser trochanter of the femur.85 When the lower limb is fixed, the psoas major may function as a lateral flexor and a rotator of the anterior trunk to the opposite side.52 The iliacus muscle attaches proximally into the iliac fossa and inferiorly into the lesser trochanter. The primary action of these two muscles is to flex the thigh. It also serves as a weak flexor of the lower lumbar spinal segments.56,85 There also exists a psoas minor muscle that is present in approximately 60% of the population. It inserts superiorly into the T12 and L1 vertebral bodies. It connects inferiorly to the pectin pubis and iliopubic eminence. It functions as a weak flexor of the lumbar spine.57 The extensors of the lumbar spine consist of three muscle layers. The superficial group being the erector spinae muscles. They consist of the longissimus and iliocostalis muscles (Fig. 80.13).86 The longissimus muscle attaches proximally to lumbar transverse processes and ribs and transverse processes of T2–L2. The longissimus muscle is both the longest and thickest part of the erector spinae. It inserts distally into the medial aspect of the posterosuperior iliac spine and spinous processes of the lumbar spine.86 The iliocostalis muscle lies lateral to the longissimus muscle. Its proximal attachments include the transverse processes of the lumbar spine and lower eight ribs. Distally, it inserts to the iliac crest and sacrum.87 These erector

Section 5: Biomechanical Disorders of the Lumbar Spine Iliocostalis muscle Longissimus muscle

Interspinalis muscle

Intertransversarius muscle

Interspinalis muscle

Fig. 80.15 Posterior view of the lumbar spine. Fig. 80.13 Posterior view of the lumbar spine.

spinae muscles extend the spine and laterally bend the spine to the ipsilateral side, and most parts rotate the front of the trunk of the ipsilateral spine.56,87 Just deep and medial to the erector spinae lay the multifidus muscles (Fig. 80.14). They are a series of muscle fibers that attach proximally to the lamina and spinous processes in the lumbar spine. The short fibers of this muscle insert distally into the mammillary process of vertebral bodies two segments distally.56 The larger fibers of the multifidus muscle insert into the lower lumbar mammillary processes and posterior superior iliac spine and sacrum.87 The deeper fibers of this muscle can also attach to the facet joint neighboring the lumbar mammillary processes.88 Even though these muscles’ primary action is extension, they also serve as stabilizers in intersegmental axial rotation, lateral flexion of the spine to the ipsilateral side, and rotators of the front of the trunk to the opposite side.56,89 The deepest layer of the extensor group includes the interspinalis and intertransversarius muscles (Fig. 80.15). The interspinalis muscle connects the adjacent spinous processes of lumbar vertebra. These

Mammillary process

Short fibers multifidus muscle

Long fibers multifidus muscle

Fig. 80.14 Posterior view of the lumbar spine.

paired muscles function as weak segmental extensors. The intertransversarius muscle connects neighboring transverse processes of the lumbar spine. Its proximal attachment is into the accessory and mammillary processes.56 The inferior insertion is into the mammillary process of the vertebra below. It functions as a weak extensor and lateral flexor of the lumbar spine.90 It has been also theorized that these small segmental muscles may act more in a proprioceptive capacity than as weak spinal movers.90,91 Lateral flexion of the lumbar spine is usually found in coordination with rotation. Pure lateral flexion can only be achieved if antagonist muscles neutralize the rotatory component. Most commonly, the ipsilateral actions of the internal and external oblique and the quadratus lumborum muscles cause lateral flexion.82,91 The quadratus lumborum muscle has attachments to the posterior iliac crest and lower lumbar spinous processes. It inserts into the last rib and upper lumbar spinous processes.92 The rotators of the lumbar spine consist of a number of muscles that function as primary extensors and lateral flexors that follow a sloping course. This oblique orientation produces rotation when antagonist muscle groups neutralize their primary action.91

Innervation of lumbar spine The adult spinal cord typically terminates at the L1–2 vertebral level.93 However, the spinal canal continues distally to protect the nerve roots of the lumbar spine and sacrum. These nerve roots travel distally and exit at their respective lumbosacral foraminal levels.94 For instance, the L5 nerve roots exit at the L5 foramen. Each foramen is numbered according to the vertebra beneath which it lies (Fig. 80.16). As the nerve roots enter the intervertebral foramen they merge to become the spinal nerve. Each spinal nerve has a dorsal and ventral root. The dorsal root transmits sensory fibers from the spinal nerve to the spinal cord. The ventral root primarily contains motor fibers, but may also contain sensory fibers.94 These fibers run from the cord to the spinal nerve. Preganglionic sympathetic fibers are also found in the L1 and L2 ventral roots. While in the lumbar vertebral canal, the lower lumbar and sacral nerve roots travel within the dural sac. The conglomeration of these nerve roots is referred to as the cauda equina, because its appearance is similar to a horse’s tail on myelography. Each pair of roots exits the thecal sac just proximal to their respective intervertebral foramen. Dura mater and arachnoid mater continue to surround each nerve root as it proceeds toward the intervertebral foramen. At the level of the intervertebral foramen the dura and arachnoid sleeves become the epineurium of the spinal nerve.56,94 863

Part 3: Specific Disorders

Pedicle of L 3

L 3 vertebra

L 3 spinal nerve

Vertebral body Ventral root

Intervertebral disc L 4 vertebra

Ventral ramus Spinal nerve

Intervertebral foramen

Dorsal ramus

Dura mater

Dorsal root ganglion

Lamina

L 4 spinal nerve L 5 spinal nerve

L 5 vertebra

Sacrum

Dorsal root

Nerve rootlets Spinous process

S 1 foramen S 2 foramen

Fig. 80.17 Axial view of the lumbar spine.

S 3 foramen S 4 foramen S 5 foramen Fig. 80.16 View of spinal canal with posterior elements removed.

The spinal nerve exists within the intervertebral foramen (Fig. 80.17). It consists of the merging of both ventral and dorsal roots. Just proximal to the formation of the spinal nerve, the dorsal root expands into a segment called the dorsal root ganglion. This segment is unique in that it contains the cell bodies of sensory fibers in the dorsal root.95 As the spinal nerve leaves the intervertebral foramen it separates into a dorsal and ventral rami. Each L1–4 lumbar dorsal rami take a sharp turn posteriorly to pass through the intertransverse space.96 The L5 dorsal ramus’ path is longer than the other lumbar dorsal rami due to its extensive course over the sacral ala.97 As the dorsal rami approach their subjacent transverse process they commonly divide into three branches: the medial, intermediate, and lateral branches.96,97 The L5 dorsal ramus is unique in that it forms only medial and intermediate branches.56,97 The lateral branches of the lumbar dorsal rami innervate the iliocostalis muscle. The first three lateral branches exit from the dorsolateral border of the iliocostalis and proceed superficially to give cutaneous innervation to the skin.98 The area of skin receiving innervation encompasses the iliac crest to the greater trochanter.98 The intermediate branches of the dorsal rami give innervation only to the longissimus muscle. They terminate within this muscle and form a series of intersegmental connections.56,96,97 The medial branch of the first four dorsal rami travels across the junction of the transverse process and superior articular process. At this point it curves around the superior articular process, passing under the mammilloaccessory ligament.89 It then travels across the lamina to innervate the multifidus muscle. The medial branch then 864

terminates by giving innervation to the interspinous ligament and muscle, and facet joints above and below the medial branch.99 The medial branch of the L5 dorsal ramus takes a slightly different route. It crosses the junction of the ala and superior articular process of the sacrum. The medial branch then turns medially around the L5–S1 facet joint before giving it innervation. It finally terminates in the L5–S1 level multifidus muscle.94 The ventral ramus of the lumbar spinal nerves leave the intervertebral foramen and immediately penetrate the psoas major muscle to form lumbar and lumbosacral plexuses.94 Just prior to entering the psoas muscle the ventral ramus gives off branches to the psoas major, psoas minor, quadratus lumborum muscles, and a somatic branch. This somatic branch is joined with the gray rami communicantes, a branch from the lumbar sympathetic trunks, at the level of the intervertebral foramen. The joining of these somatic and autonomic branches forms the sinuvertebral nerve.56,99 The sinuvertebral nerve immediately re-enters the intervertebral foramen, passing just below the pedicle. It then makes a path along the middle of the posterior vertebral body. At this point the nerve sends ascending and descending branches along the spinal canal. These ascending and descending branches combine to form a posterior plexus on the dorsal aspect of the posterior longitudinal ligament.100 This plexus gives innervation to the posterior longitudinal ligament, posterolateral aspect of the intervertebral disc, periosteum of the vertebral bodies, and blood vessels of the spinal canal and vertebral bodies.56,94,99,101 Thick meningeal branches from the sinuvertebral nerve, thin branches from the nerve plexus of the dorsal posterior ligament, and small branches of perivascular nerve plexuses of the radicular rami of segmental arteries all join to form an anterior nerve plexus on the ventral aspect of the dura mater.102,103 This anterior nerve plexus consists of a rich, overlapping network of nerves, which give both nociceptive and autonomic innervation to the anterior dura mater.102,103 However, most studies regarding the innervation of the posterolateral portion of the dura mater have shown minimal innervation with nociceptive and autonomic fibers.56,103–105 Immunohistochemical studies have demonstrated that the majority of these nerve fibers in the ventral aspect of

Section 5: Biomechanical Disorders of the Lumbar Spine

the dura are autonomic in origin, with only a few nociceptor nerve fibers noted.104,106,107 More studies directed at identifying nociceptive fibers in the dura mater need to be performed before one can discount the dura mater as a potential pain generator in the lumbar spine.56 Branches from the lumbar sympathetic trunks and gray rami communicantes innervate the anterolateral aspect of the lumbar vertebral bodies and intervertebral discs. These autonomic fibers form a nerve plexus along the surface of the anterior longitudinal ligament.100 These nerve fibers are primarily sympathetic in origin, but nociceptive fibers have been noted in this area. Based upon current findings, the anterolateral aspect of the vertebral bodies and intervertebral discs also need more investigation before they can be discounted as a potential source of low back pain.56,100

Anatomy of intervertebral foramen Since the nerve root is one of the most frequent areas for nerve impingement and injury, a more detailed look will be taken at this specific area. The boundaries of the intervertebral foramen contain both osseous and ligamentous structures. Two joints also contribute to defining the foramens boundaries. These joints give a dynamic quality to the lumbar foramens to allow for a change in its configuration according to the movements of the trunk. There have been no generally accepted boundaries for the intervertebral foramens. Different authors have chosen separate and distinct classifications to describe the foramen.108–110 Crock108 described the intervertebral foramen as a single sagittal slice through the narrowest portion of the nerve root canal. Lee et al.109 separated the foramen into three zones: lateral recess, midzone, and an exit zone. The foramen will be discussed below in a more generalized approach.111 When observing the intervertebral foramen from the inside outward it takes on the appearance of an oval, round, or inverted teardrop-shaped window.112 The roof of the foramen is the caudal aspect of the vertebral notch of the pedicle of the superior vertebra, the ligamentum flavum at its outer free edge, and posteriorly lies the pars interarticularis and the facet joint.108,113 The floor of the intervertebral foramen is composed of the superior vertebral notch of the pedicle of the inferior vertebra, posteroinferior margin of the superior vertebral body, the intervertebral disc, and the posterosuperior margin of the inferior vertebral body.108,113 Structures bounding the anterior aspect of the foramen include the posterior aspect of adjacent vertebral bodies, the intervertebral disc, the lateral expansion of the posterior longitudinal ligament, and the anterior longitudinal venous sinus.111 The posterior boundaries of the foramen include the lateral prolongation of the ligamentum flavum, and the superior and inferior articular process of the facet joint at the same level as the foramen. The medial foramen is composed of the dural sleeve, while the lateral boundary of the foramen is composed of a fascial sheet and overlying psoas major muscle.113 Two oval perforations are seen in the fascia: a distal and proximal perforation. The smaller proximal perforation houses blood vessels traversing the canal. The larger distal perforation contains the nerve roots.113 The height of the neural foramen is dependent upon the height of the intervertebral disc. Any decrease in intervertebral disc height has direct implications for the available area for neurovascular elements to pass through the canal. Direct cadaveric measurements of lumbar foraminal heights have varied from 11 to 19 mm. One cadaveric study has reported foraminal width to average about 7 mm.111,114,115 Lumbar foraminal height measurements have also been studied in healthy subjects by using magnetic resonance imaging (MRI). One study recorded the following average foraminal heights of the L1–2 through the L4–5 levels: L1–2, 17.1±2 mm; L2–3, 18.4±1.7 mm; L3–4, 18.1±1.5 mm; and L4–5, 17.1±3.6 mm.116

The true anatomic nerve root canal initially arises from the lateral aspect of the dural sac and travels through the lumbar foramen. At each level, two to six anterior and posterior roots converge in the thecal sac to form anterior and posterior roots.117 The nerve roots of the lumbar spine exit the thecal sac approximately one segmental level above their respective foraminal canal. Extensions of the dural sac encase the nerve roots as they leave the thecal sac.99 As they exit the dural sac, the nerve roots take a sloping direction downwards and laterally toward the intervertebral foramen. The upper lumbar nerve roots take a more acute angle toward the foramen than the lower lumbar roots.118 This acute angle in the upper lumbar nerve roots renders the intraspinal portion of the nerve roots extremely short. Essentially, the upper lumbar nerve roots exit the intervertebral foramen and immediately enter the lumbar intervertebral foramen.108 Epidural fat surrounds each nerve root throughout their course to the intervertebral foramen. Just prior to the nerve root’s entrance into the neural foramen it enters an osseous groove at the medial base of the pedicle.117 This groove may be more pronounced at the level of the fifth lumbar foramen due to its more trefoil configuration.119 The term lateral recess has been used to describe this area where the nerve root travels through the osseous groove of the pedicle. The nerve root then slides under the medial edge of the pedicle and takes a caudal and oblique direction away from the pedicle.117 At this point, the nerve roots are located within the foramen. They combine to form the spinal nerve at this point. The dorsal root ganglion is an enlargement of the dorsal root seen just prior to merging of the ventral and dorsal roots. The dorsal root ganglion is most commonly seen within the anatomic boundaries of the intervertebral foramen.116,120,121 The exception to this rule is the S1 dorsal root ganglion. Studies have demonstrated that the S1 dorsal root ganglia are located within the intraspinal canal 80% of the time.116,122 This position of the S1 dorsal root ganglia within the spinal canal increases the risk for injury by disc herniations or degenerative changes from the L5–S1 disc or facet joints.116 Within the foramen, nerve roots typically occupy approximately 30% of the available foraminal space,122 but percentages as high as 50% have been recorded in some studies.111,123 When the spinal nerve reaches the foraminal outlet it turns around the base of the subjacent pedicle and transverse process. At this exit zone of the foramen the spinal nerve divides into primary anterior and posterior rami. These primary rami run between the deep layers of the psoas muscle and the vertebral column.111,117 As the ventral rami penetrate the psoas muscle, they merge together to form large trunks that travel caudally along the surface of the junctional area between the body and the pedicle of the lumbar spine.124 The lumbar nerve roots are attached to two of their surrounding structures. The proximal area of fixation occurs at the neck of the nerve root sheath as it exits the dural sac. Fibrous bands serve to attach the neck of the nerve root sheath to the periosteum of the subjacent pedicle. The second area of fixation occurs at the lateral aspect of the foramen. Fibrous bands connect from the nerve root and travel in cranial and caudal directions to attach to the superior and inferior pedicles. Avulsions are commonly seen to occur at these two areas of fixation. The average rupture force in one study for the roots of the L1–4 levels was 7.25 kg, 13 kg for the L5, and 11.5 kg for the S1 nerve root.125

Anatomy of the intervertebral disc Between each vertebral body is located an intervertebral disc. These discs have three main components: the cartilage endplates adjacent to the vertebral bodies above and below, a central nucleus pulposus, and a surrounding anulus fibrosus.52,126 While no distinct bound865

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ary exists between the interfaces of these structures, the peripheral aspect of anulus and the central aspect of the nucleus maintain a unique appearance and structure.56 The nucleus pulposus is a semifluid mass of mucoid material, eccentrically located such that it is more oriented toward the posterior aspect of the disc. It consists of proteoglycans and collagen fibers spread in a medium of ground substance.126 These collagen fibers and proteoglycans are synthesized by chondrocytes and fibroblasts of the nucleus. Approximately 70–90% of the nucleus pulposus is comprised of water.127 Proteoglycans constitute roughly 65% of the dry weight of the nucleus,128 and are responsible for fastening and containing the water in the disc. Collagen contributes approximately 20% of the dry weight to the nucleus with type II collagen predominating.129 It serves to stabilize the proteoglycan molecules so that they may bind water. The mixture of proteoglycan units, aggregates, and collagen fibers within the nucleus pulposus is referred to as the matrix of the nucleus.56,126 As the disc ages, the glycosaminoglycans degenerate and are subsequently decreased in concentration. This loss in glycosaminoglycan content results in replacement with fibrocartilaginous tissue. Ultimately, each disc is destined to contain lower water content with resultant increased viscosity within the disc. An increase of intradiscal viscosity leads to a decrease in the compliance of the disc. Morphologically, these alterations minimize the distinction between the nucleus and anulus fibrosus. As these changes progress, the nucleus becomes more dry and granular and the nucleus is less able to transmit weight and exert pressure on the anulus fibrosus.52 The anulus then becomes the primary loadbearing agent of the spine. Unfortunately, the anulus fibrosus is not equipped to handle these increased stresses, and degenerative changes result.56,130 The nucleus also contains proteolytic enzymes. These enzymes are known as matrix metalloproteinases and function to remove dysfunctional matrix and allow new components to be constructed in their place.130 Collagenase and streptomelysin are the primary agents responsible for the removal of aging and dysfunctional matrix.130 The functional activity of these metalloproteinases is highly dependent upon the ability of nutrients to diffuse across the disc space. Disruption of this nutrient flow causes derangement in the production and elimination of the basic properties of the nucleus, thereby inhibiting proper biomechanical function of the disc. This cascade of events may ultimately lead to pathological changes in the disc resulting in the manifestation of low back pain.56,126,130 The principal component of the anulus fibrosus is water, accounting for approximately 60% of its weight.131 Collagen constitutes 50% of the dry weight of the annulus.132 The annular fibers are arranged in a highly ordered pattern, and are grouped into 10–20 sheets called lamellae. The collagen fibers in each lamella lie parallel to one another, and insert into the hyaline cartilage plates and bony ring epiphyses that cover the ends of the vertebral bodies above and below the disc. All fibers in each lamella measure approximately 30–70° from the vertical.133 While the angle of each lamella remains unchanged, the direction of inclination alternates with each lamella. For instance, if the first lamella is 65° to the right, then the next lamella will be angled at 65° to the left, and so forth.134 In cross-section, this gives the anulus the appearance of the rings of a cut tree trunk. One also notices in transverse section that the posterior aspect of the anulus is thinner than lateral and anterior segments. This asymmetry is the result of the posterior placement of the nucleus in the adult intervertebral disc. The vertically oriented lamellae fibers function to resist flexion, extension, and lateral bending moments of the spine. The horizontal collagen fibers in each lamella serve to resist rotation moments of the spine.52,56,126 866

Chronic degeneration and fissuring of the anulus fibrosus can put the disc at risk for herniation of the nucleus pulposus. These herniations most commonly occur through the posterolateral aspects of the anulus fibrosus. This is due to a number of factors. Firstly, the intervertebral discs of the lumbar spine have a wedge-shaped appearance with the height of the disc being greater anteriorly than posteriorly. For any length of displacement, the shorter posterior fibers will be placed under greater strain than the anterior collagen fibers.52,56,126 As mentioned above, the nucleus is situated more dorsally in the disc space. This causes the dorsal portion of the anulus to have a decreased radial dimension, thereby offering less support to the posterior aspect of the disc. The most common motion of the lumbar spine is flexion. Unfortunately, this motion causes strain through the posterior anulus, thus speeding degenerative changes. Most herniations occur dorsolaterally due to the anterior and dorsomedial portions of the disc receiving support from the anterior and posterior longitudinal ligaments, respectively. The dorsolateral aspect of the intervertebral disc doesn’t receive any support from surrounding ligaments.52,56,126 The vertebral endplates are positioned along the superior and inferior aspect of the vertebral bodies. They measure about 0.6–1 mm thick and rest on a flat subchondral bone plate supported by the spongiosa of the vertebral body.135 The endplates of each disc cover the entire nucleus pulposus and a portion of the anulus fibrosus. The endplate receives its blood supply from contact with small vascular buds through small openings of the bony endplate.77 It is composed of both hyaline cartilage and fibrocartilage fibers.136 The hyaline cartilage is located toward the vertebral body, while the fibrocartilage is concentrated toward the nucleus pulposus. As the patient ages, the endplate changes entirely to fibrocartilage. Due to the attachment of the lamellae of the anulus fibrosus, the endplate is strongly bound to the intervertebral disc. In contrast, it is weakly attached to the vertebral bodies.52,56,126,136 The vertebral endplate functions as the primary nutritional pathway for the intervertebral disc. Nutrients must diffuse from blood vessel contacts through cartilage to reach the cells of the endplate. These nutrients must then pass through several millimeters of disc matrix before reaching the center of the disc. Transport properties of the endplate are similar to that of the anulus and nucleus. However, since the endplate is such a thin structure it does not restrict flow of nutrients through its substance. Decreased nutrient flow can occur as a result of calcification of the cartilage of the endplate.136 This calcified cartilage serves as an impermeable barrier to nutrient transport. The number and size of blood vessels abutting the endplate also serves as a determinant of nutrient flow.136 Marrow contacts with the endplate also serve as a secondary means of providing nutrient flow to the disc via the endplate.52,56,126,136

Innervation of the intervertebral disc There has been a large amount of research dedicated to establishing the presence of nociceptive nerve fibers within the anulus fibrosus and posterior longitudinal ligament. Absence of these fibers would negate the disc from being responsible as a pain generating structure within the lumbar spine.56 The first studies to report the presence of nerve endings in the intervertebral discs and adjacent posterior longitudinal ligament were published in the early 1940s.137–139 They noted nerve fibers in the posterior longitudinal ligament and on the superficial aspect of the intervertebral disc. In 1959, Malinsky139 demonstrated the presence of encapsulated and nonencapsulated nerve endings in the outer third of the anulus fibrosus. The greatest number of fibers was noted to occur in the lateral region of the disc, with the anterior and pos-

Section 5: Biomechanical Disorders of the Lumbar Spine

terior regions demonstrating few nerve fibers.139 These findings were later confirmed by Rabischong et al.140 in 1978 and Yoshizawa et al.141 in 1980. In Yoshizawa et al.’s study, they demonstrated the presence of an abundant axonal network in the posterior ligament and outer half of the anulus fibrosus, with abundant free-lying terminals, often arranged in complex, branched-spray formations. These free-lying nerve fibers were primarily found in the lateral aspect of the disc, and had similar morphology to pain receptors reported elsewhere.142 Histologic studies performed by Bogduk also supported Malinsky’s findings, where he noted nerve fibers up to a depth of one-third the total thickness of the anulus fibrosus.143 Bogduk has also reported additional innervation of the disc through pathways other than direct branches from the sinuvertebral nerve. These included direct branches from the ventral rami and two types of branches from the rami communicantes. All of these branches enter the postero-lateral aspect of the intervertebral disc. Branches from the rami communicantes were also noted to travel caudally and overlay the subjacent disc.52,56,94,126,143 Current immunohistochemical studies in human discs have also demonstrated the presence of sensory nerve fibers in the anulus fibrosus.56,144,145 Palmgren et al.146 performed histochemical analysis using substance P- and C-flanking peptide of neuropeptide Y (CPON) as nerve markers for sensory and autonomic nerve fibers, respectively.56 Synaptophysin (SYN) served as a general neuronal marker for the study. Nine normal nondegenerated lumbar intervertebral disc tissue specimens were stained and underwent microscopic analysis. Substance P immunoreactivity was seen in 50% of the posterior anulus specimens. SYN fibers were seen in 75% of posterior annular specimens, and CPON-reactive fibers were seen in 75% of the posterior anulus specimens. Interestingly, all anterior anulus specimens demonstrated the presence of substance P and CPON fibers. The depth of penetration of immunoreactive fibers was also recorded using a morphometric scale attached to the microscope. A maximum depth of 0.50 mm was seen for substance P, 0.45 mm for CPON, and 3.5 mm for SYN. Using this technique, Palmgren et al. were able to document ingrowth of nerve endings into annular tissue to a maximal depth of 3.5 mm. In 1994, Ashton et al.144 performed immunohistochemical analysis of 12 human intervertebral discs. These discs were obtained from patients undergoing anterior lumbar fusion secondary to intractable low back pain. Protein gene product (PGP 9.5) served as a general nerve marker, and CPON as a marker for autonomic fibers. CGRP, VIP, and substance P acted as primary sensory markers. Immunoreactivity to CGRP, substance P, CPON, and VIP were seen throughout the outer 3 mm of the anulus fibrosus. No immunoreactive fibers were noted penetrating the deep fibers of the anulus or in the nucleus pulposus. Substance P fibers were the sparsest fibers seen on microscopic analysis. Only a small number of these fibers were detected in the periphery of the disc. CPON fibers were exclusively noted traveling in association with blood vessels. All of the above studies have also documented a profuse network of nerve fibers innervating the posterior longitudinal ligament.56 A number of animal studies have also acknowledged the presence of nerve fibers in the posterior longitudinal ligament and lateral annular fibers.56,147–151 Those studies using immunohistochemical techniques have specifically been able to identify the presence of sensory afferent fibers in the posterior longitudinal ligament and superficial annular fibers.56,147,149 Comparable to most human studies, animal studies have been unable to reveal the presence of afferent nerve fibers within the inner aspects of the anulus fibrosus and nucleus pulposus. In 1995, Imai et al.147 were able to demonstrate a dual innervation to the posterior longitudinal ligaments in rats. A superficial network on the dorsal aspect of the posterior longitudinal ligament was seen to contain both nociceptive and sympathetic fibers. This dorsal plexus

formed a polysegmental innervating system by anastamoses from adjacent upper and lower branches. A deeper network ventral to the posterior longitudinal ligament was seen to contain only nociceptive fibers. This deeper network did not form connections with adjacent levels at the level of the intervertebral disc, thereby making this anterior arrangement unisegmental in innervation. A different study has promulgated a possible alternate pathway for return of annular sensory nerve fibers through the sinuvertebral nerve, rami communicantes, and the lumbar sympathetic trunks.56,151 This is in contrast to traditional belief that sensory nerve fibers only traveled afferently through the ventral rami, instead of rami communicantes and lumbar sympathetic trunk.56,151 This study has identified afferent nociceptor fibers, via immunohistochemical techniques, traveling along with sympathetic fibers in the sympathetic trunk to re-enter the spinal cord level with the gray rami communicantes at the L2 level.56,150 Based on current data, the intervertebral disc has a rich nerve supply in its posterolateral portion. These nerve fibers cover the superficial aspect of the disc and penetrate the anulus to a minimal extent. Thick networks of nerve fibers are seen innervating the posterior longitudinal ligament. This network probably involves a large amount of cross-innervation between neighboring levels. This complex network would then give each disc a diffuse, polysegmental innervation. In addition, there exist polysegmental pathways in which these fibers may return to the spinal cord.56

CONCLUSION The lumbar spine is composed of numerous musculoskeletal and neurovascular structures. Many of these structures possess nociceptor innervation. The presence of this innervation identifies these structures as potential pain generators in the lumbar spine. A thorough understanding of the anatomical relationships of the lumbar spine allows for an accurate diagnosis and treatment program for the patient. Hopefully, this chapter has given the reader the basic anatomic knowledge to enable better treatment for their patients.

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116. Hasegawa T, Mikawa Y, Watanabe R, et al. Morphometric analysis of the lumbosacral nerve roots and dorsal root ganglia by magnetic resonance imaging. Spine 1996; 21:1005–1009.

85. Louis R. Topographic relationships of the vertebral column, spinal cord, and nerve roots. Anat Clin 1978; 1:3–12.

117. Rauschning W. Normal and pathologic anatomy of the lumbar root canals. Spine 1987; 12:1008–1019.

86. Luk KDK, Ho HC, Leong JCY. The iliolumbar ligament. J Bone Joint Surgery [Br] 1986; 68B:197–200.

118. Epstein JA, Epstein BS, Lavine L. Nerve root compression associated with narrowing of the lumbar spinal canal. J Neurol Neurosurg Psychiat 1962; 25:165–176.

87. Macintosh JE, Valencia F, Bogduk N, et al. The morphology of the lumbar multifidus muscles. Clin Biomechanics 1986; 1:196–204. 88. Donisch EW, Basmajian JV. Electromyography of deep back muscles in man. Am J Anat 1972; 133:25–36. 89. Bogduk N. The lumbar mamillo-accessory ligament. Spine 1981; 6:162–167. 90. Nitz H, Peck D. Comparison of muscle spindle concentrations in large and small human epaxial muscles acting in parallel combinations. Am Surg 1986; 52: 273–277. 91. Bogduk N. The lumbar muscles and their fascia. In: Bogduk N. Clinical anatomy of the lumbar spine and sacrum. London: Churchill Livingstone; 1997:101–126. 92. Bogduk N, Pearcy M, Hadfield G. Anatomy and biomechanics of psoas major. Clin Biomech 1992; 7:109–119. 93. Louis R. Topographic relationships of the vertebral column, spinal cord, and nerve roots. Anat Clin 1978; 1:3–12. 94. Bogduk N. Nerves of the lumbar spine. In: Bogduk N. Clinical anatomy of the lumbar spine and sacrum. London: Churchill Livingstone; 1997:127–144. 95. Moore KL. Anatomy. Baltimore, MD: Williams and Wilkins; 1992:323–369. 96. Bradley KC. The anatomy of backache. Aust NZ J Surg 1974; 44:227–232. 97. Bogduk N, Wilson AS, Tynan W. The human lumbar dorsal rami. J Anat 1982; 134:383–397. 98. Johnston HM. The cutaneous branches of the posterior primary divisions of the spinal nerves, and their distribution in the skin. J Anat Physiol 1908; 43:80–91. 99. Bogduk N. The innervation of the lumbar spine. Spine 1983; 8:286–293. 100. Groen G, Baljet B, Druckker J. The nerves and nerve plexuses of the human vertebral column. Am J Anat 1990; 188:282–296. 101. Bogduk N, Tynan W, Wilson AS. The innervation of the human lumbar intervertebral discs. J Anat 1981; 132:39–56. 102. Kimmel DL. Innervation of spinal dura mater and dura mater of the posterior cranial fossa. Neurology 1960; 10:800–809. 103. Edgar MA, Nundy S. Innervation of the spinal dura mater. J Neurol Neurosurg Psych 1964; 29:530–534. 104. Groen G, Baljet B, Drukker J. The innervation of the spinal dura mater. Acta Neurochir 1988; 92:39–46. 105. Kallakuri S, Cavanaugh JM, Blagoev DC. An immunohistochemical study of innervation of lumbar spinal dura and longitudinal ligaments. Spine 1998; 23: 403–411.

119. Dommisse GF. Morphological aspects of the lumbar spine lumbosacral region. Orthop Clin North Am 1975; 6:163–175. 120. Bose K, Balasubramaniam P. Nerve root canals of the lumbar spine. Spine 1984; 9:16–18. 121. Cohen MS, Wall EJ, Brown RA, et al. Cauda equina anatomy: extrathecal nerve roots and dorsal root ganglia. Spine 1990; 15:1248–1251. 122. Hasue M, Kunogi J, Konno S, et al. Classification by position of dorsal root ganglia in the lumbosacral region. Spine 1989; 14:1261–1264. 123. Rauschning W. Correlative multiplanar computed tomographic anatomy of the normal spine. In: Rauschning W. Computed tomograghy of the spine. Baltimore; Williams and Wilkins; 1984:1–57. 124. Bae HG, Choi SK, Joo KS, et al. Morphometric aspects of extraforaminal lumbar nerve roots. Neurosurgery 1999; 44:841–846. 125. Peretti F, Micalef JP, Bourgeon A, et al. Biomechanics of the lumbar spinal nerve roots and the first sacral root within the intervertebral foramina. Surg Radiol Anat 1989; 11:221–225. 126. Bogduk N. The inter-body joint and the intervertebral disc. In: Bogduk N. Clinical anatomy of the lumbar spine and sacrum. London: Churchill Livingstone; 1997:13–32. 127. Beard HK, Stevens RC. Biochemical changes in the intervertebral disc: In: Jayson MI, ed. The lumbar spine and backache. London: Pitman; 1980:407–436. 128. Gower WE, Pedrini V. Age related variation in protein polysaccharides from human nucleus pulposus, annulus fibrosis and costal cartilage. J Bone Joint Surg [Am] 1969; 51A:1154–1162. 129. Bushell GR, Ghosh P, Taylor TKF. Proteoglycan chemistry of the intervertebral discs. Clin Orthop 1977; 129:115–123. 130. Sedowfia KA, Tomlinson IW, Weiss JB, et al. Collagenolytic enzyme systems in human intervertebral disc. Spine 1982; 7:213–222. 131. Naylor A. The biochemical changes in the human intervertebral disc in degeneration and nuclear prolapse. Orthop Clin North America 1971; 2:343–358. 132. Adams P, Eyre DR, Muir H. Biochemical aspects of development and ageing of human lumbar intervertebral discs. Rheum Rehab 1977; 16:22–29. 133. Hickey DS, Hukins SW. X-ray diffraction studies of the arrangement of collagen fibers in human fetal intervertebral discs. J Anatomy 1980; 131:81–90. 134. Marchand F, Ahmed AM. Investigation of the laminate structure of lumbar disc annulus fibrosus. Spine 1990; 15:402–410.

106. Kumar R, Berger RJ, Dunsker SB, et al. Innervation of the spinal dura. Spine 1996; 21:18–26.

135. Eyring EJ. The biochemistry and physiology of the intervertebral disk. Clin Orthop 1969; 67:16–28.

107. Ahmed M, Bjurholm A, Kriecbergs A, et al. Neuropeptide Y, tyrosine hydroxylase, and VIP-immunoreactive fibers in the vertebral bodies, discs, dura mater, and spinal ligaments of the rat lumbar spine. Spine 1993; 18:268–273.

136. Roberts S, Menage J, Urban PG. Biochemical and structural properties of the cartilage end-plate and its relation to the intervertebral disc. Spine 1989; 14: 166–174.

108. Crock HV. Normal and pathological anatomy of the lumbar spinal nerve root canals. J Bone Joint Surg [Br] 1981; 63B:487–490.

137. Roofe PG. Innervation of annulus fibrosus and posterior longitudinal ligament. Arch Neurol Psyc 1940; 44:110–103.

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145. Cavanaugh JM, Kallakuri S, Ozaktay AC. Innervation of rabbit lumbar intervertebral disc and PLL. Spine 1995; 20:2080–2085.

139. Malinsky J. The ontogenetic development of nerve terminations in the intervertebral discs of man. Acta Anat 1959; 38:96–113.

146. Palmgren T, Gronblad M, Virri J, et al. An immunohistochemical study of nerve structures in the annulus fibrosus of human normal lumbar intervertebral discs. Spine 1999; 24:2075–2079.

140. Rabischong P, Louis R, Vignaud J, et al. The intervertebral disc. Anat Clin 1978; 1:55–64. 141. Yoshizawa H, O’Brien JP, Smith WT, et al. The neuropathology of intervertebral discs removed for low back pain. J Pathology 1980; 132:95–104. 142. Palmgren T, Gronblad M, Virri J, et al. An immunohistochemical study of nerve structures in the annulus fibrosus of human normal lumbar intervertebral discs. Spine 1999; 24:2075–2079.

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147. Imai S, Hukuda S, Maeda T. Dually innervating nociceptive networks in the rat lumbar PLL. Spine 1995; 20:2086–2091. 148. Gronblad M, Korkala O, Konttinen YT, et al. Immunohistochemical observations on spinal tissue innervation. Acta Orthop Scand 1991; 62:614–622. 149. Ohtori S, Takahashi K, Chiba T, et al. Sensory innervation of the dorsal portion of the lumbar intervertebral discs in rats. Spine 2001; 26:946–950.

143. Kimmel DL. Innervation of spinal dura mater and dura mater of the posterior cranial fossa. Neurology 1960; 10:800–809.

150. Suseki K, Takahashi Y, Takahashi K, et al. Sensory nerve fibers from lumbar intervertebral discs pass through rami communicans. J Bone Joint Surg [Br] 1998; 80B:737–742.

144. Ashton IH, Roberts S, Jaffray DC, et al. Neuropeptides in the human intervertebral disc. J Orthop Res 1994; 12:186–92.

151. Wiberg G. Back pain in relation to the nerve supply of the intervertebral disc. Acta Orthop Scand 1949; 19:211–221.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ ii: Lumbar Radicular Pain

CHAPTER

Medical Rehabilitation

81

Howard Liss, Donald Liss and Steven Helper

INTRODUCTION This chapter will provide the reader with a strategy for treating radicular pain and radiculopathy caused by lumbar disc herniations, stenosis, synovial cysts, and spondylolisthesis. These strategies rely on identifying the cause of nerve root irritation and tailoring the treatment algorithms based on the specific causes. The methods are based on the evidence-based literature and our groups' collective experience. Because there is little or no evidence that commonly used treatments for radicular pain are either effective or not effective, our approach emphasizes the history and physical examination rather than imaging and electrodiagnostic studies. We will argue that the ultimate patient outcome is best predicted by the clinical presentation and early response to treatment. The main reason why we base our prescription on the history and presentation is because the history and presentation are the best indicators of what prescription will work. The art of treating a patient with lumbar radiculopathy involves considering many factors before deciding on or changing a course of action (Table 81.1). Blanket statements such as, ‘A patient should have physical therapy for 6 weeks before considering imaging,’ fail to take into account many and varied factors. For example, the patient's medical conditions, emotional state, magnitude of pain, and personal and/or social situation must be considered before treatment recommendations are made. Ideally, the risks and benefits of any considered treatment, including the absence of any treatment, should be carefully explained so that the patient can contribute as much as possible to the decision as to how to proceed. In the ideal world, as long as we can measure an ongoing positive response to treatment which is better than the expected natural course of the condition, continued treatment is appropriate. On the other hand, if the rate of recovery is not acceptable to the patient, or if there is no measurable response to treatment, then other treatment options should be explored. Unfortunately, this ideal is seldom achieved because third-party payers often put limits on continued therapy and may not authorize changes in therapy or further diagnostic tests By far the most common cause of lumbar radicular pain is a paramedian herniated nucleus pulposus (HNP) and the treatment for this specific cause will be described in detail. How treatment differs when caused by a lateral or foraminal HNP, sequestered HNP, lumbar stenosis, synovial cysts, and spondylolisthesis will be described in each specific case.

THE MANAGEMENT OF LUMBAR RADICULOPATHY SECONDARY TO A PARAMEDIAN HERNIATED NUCLEUS PULPOSUS Natural history A paramedian herniated disc presents with a characteristic history and physical examination. Imaging studies and electrodiagnostic testing will help confirm the diagnosis and help rule out other etiologies of pain or neurological deficits. Most patients with a paramedian HNP report a history that includes both low back and lower extremity pain. The pain is often worse in the morning, is usually aggravated by sitting more than standing or walking, or upon arising after a sustained period of sitting. Valsalva maneuvers, such as coughing, sneezing, or straining, may also aggravate the patient's symptoms. The physical examination usually reveals positive straight leg raising. When a positive crossed straight leg raising sign is present, there is a very high correlation with an extruded HNP, although the location is not necessarily paramedian. In a review article, Benoist reported that approximately 60% of patients with a symptomatic herniated disc will report a marked decrease in back and leg pain during the first 2 months, while 20–30% will still complain of back and/or leg pain at 1 year.1 Most studies indicate that most patients with a paramedian HNP can be satisfactorily treated with conservative measures.2–6 Komori et al. report: ‘Several well-designed studies of patients with HNP have revealed the satisfactory results of conservative treatment, although some authors have reported that about 20% of all patients had to be treated surgically during follow-up because of prolonged or aggravated leg pain.’7 Saal and Saal performed a retrospective cohort study on the success of nonoperative treatment of herniated lumbar discs with radicular pain and radiculopathy without associated spinal stenosis. All patients had a chief complaint of leg pain, positive straight leg raising of less than 60 degrees, herniated discs on computed tomography (CT) scan, and a positive electromyogram (EMG). The average follow-up time was 31.1 months. The patients underwent aggressive physical rehabilitation, including back school and stabilization training. Ninety percent reported a good or excellent outcome, and 92% returned to work after an average sick leave of 15.2 weeks.3–5,8

871

872 L5 deficit ↓ Dorsiflexion ↓ Hip abduction Upper lumbar knee instability Lumbar cushions/ ergonomic seating Use universally

Continue if patient is responsive Most effective for paramedian HNP

Lumbar traction

Vary degree of lumbar extension

Manipulation (high thrust) If pain cannot be centralized and contraindications not present

Advice re: sports and recreation At completion of treatment

Spine, hip and/or SI as directed by exam

Neural mobilization

Gradual increased stretching beginning approximately 2 weeks after onset of radicular complaints

Modify body mechanics walker/cane

PLO, boot cane

Mobilization

Caution if osteoporosis

Gapping – effective for list/foraminal HNP

Supine or prone

S1 deficit ↓ Push off

Begin immediately

Rocker bottom flexible PLO

Address functional deficits

Centralization

Table 81.1: Medical treatment of lumbar radiculopathy – overview

To prevent recurrences and maximize self-care must be able to tolerate sitting for class

Back school

Stretching as tolerated: iliopsoas, hip rotators, hamstrings, quadriceps, gastrocs Strengthening as tolerated: stabilization/ core strengthening

Day 1 – centralize

Therapeutic exercise

Day 1 – bed to chair, with progress – education in high-level ADL

Modify body mechanics in ADL

HNP: reduce sitting, lifting, bending, twisting.

Stay active as tolerated for paramedian

Activity modification

Occasional help when acute

Taping, corsets, bracing

- Early on – when trigger points are impressive - When myofascial release, acupressure, spray and stretch fail

Trigger point injection

Soft tissue Rx early on, as directed by history and exam

Myofascial release, acupressure, spray and stretch

TENS Acupuncture

Meds

Analgesic options

Part 3: Specific Disorders

Section 5: Biomechanical Disorders of the Lumbar Spine

The patient's history and examination not only are critical in making a diagnosis, but also allow us to forecast the likelihood of a patient's responding to therapy alone as opposed to requiring epidural steroid injections or surgery.

Early indications for surgery Although only 0.0004% of patients have a cauda equina syndrome, symptomatic compression of the cauda equina must be ruled out before proceeding with conservative care. Cauda equina compression usually presents with urinary retention. In addition, patients will infrequently have bowel incontinence, and may note sexual dysfunction. There is often diminished perineal sensation, bilateral lower extremity complaints, and absent bilateral Achilles reflexes. When any of these symptoms are present, magnetic resonance imaging (MRI) must be immediately performed, and if significant compression is shown patients must undergo immediate surgical decompression. Other patients who are usually candidates for prompt surgical decompression are those who have progressive neurological deficits despite conservative care. There are, however, two situations where surgery is probably not the next step. If patients have multiple medical comorbidities or advanced age that make the risk–benefit ratio of surgical intervention questionable, one may treat the neurological deficit with an orthotic device to support weakness and ambulation aids rather than performing surgery. In the early stages after the onset of radicular pain, patients may present with severe pain, positive mechanical signs, and mild or no neurological deficits. These patients may demonstrate worsening of neurological deficits within the next 3–7 days but a lessening of radicular pain and improving mechanical signs. In this case, the patients probably had significant compression of the nerve root causing evolving neurological deficits. Unless the deficit is profound, these patients usually will improve neurologically as well and will not require surgery. Since no literature is available to predict outcomes in patients with radicular pain and radiculopathy, it is very difficult to advise them with confidence. Nonetheless, our anecdotal experience treating many patients with radicular pain and radiculopathy who refuse surgical intervention has shown that the vast majority of these patients will reach full or nearly full neurological resolution. Review of the surgical literature reveals an interesting paradox. The results from surgical studies suggest that patients who do require surgery face a greater likelihood of successful outcome if they are operated on relatively soon after the onset of radicular pain. One study reported a worse overall prognosis for patients whose surgery takes place 12 months or more after the initial onset of radicular symptoms.9 Only with a clear understanding of both the natural history and effective conservative interventions for paramedian disc herniations can informed decisions be made regarding surgical consultation. There are several studies that help predict which patients will respond best to nonoperative care. Patients who present with negative crossed straight leg raising, and the ability to extend the lumbar spine without associated radicular pain, usually respond well to conservative management.10 Patients with normal or very mild neurological deficits also have a better chance of responding to nonoperative care. We also feel that outcome is better when the onset of discogenic radicular symptoms was acute rather than insidious. There are numerous reports of significant shrinkage, or even disappearance, of extruded herniations that usually occurs over a 3–6-month period.1,11–14 Subligamentous disc herniations, however, are often more stubborn and resolve more slowly than extruded herniations.

Treatment goals The primary goal of conservative treatment of lumbar radiculopathy is to accelerate the recovery process and educate patients on methods to help prevent or reduce the intensity of future occurrences. We discuss their chances of recovery with conservative care as opposed to requiring spinal injections or surgery. They should be carefully informed as to their chances of recovery from each course of treatment, and should understand the risk of complications and any other negative aspects associated with each approach, including time of recovery. Conservative treatment seeks to help improve nerve root inflammation, reduce the further expansion of the outer anulus or extrusion of material into the epidural space, and to help the patient compensate for reduced mobility and reduced neurological function.

Functional deficits Patients occasionally present with significant neurological deficits that may be concerning or disabling. Many of these patients may not require surgery, but until adequate neurological recovery occurs they will need assistance in compensating for these deficits and minimizing the risk of falls. Patients with motor deficits may require lower extremity support. Patients with S1 deficits have poor push-off and a rocker-bottom shoe can improve the cosmesis of the gait, and a flexible posterior leaf orthosis may help compensate for a patient's lack of push-off. Patients with L5 deficits may have significant dorsiflexion weakness and may benefit from wearing boots that fit firmly above the ankle. They may also benefit from ankle–foot orthoses such as a lightweight, flexible posterior leaf orthosis. If there is substantial mediolateral weakness of the ankle, more rigidity must be incorporated into the orthosis. Often overlooked, patients with L5 radiculopathies infrequently have significant weakness of hip abduction with a Trendelenburg gait abnormality and may require the use of a cane on the contralateral side in addition to specific strengthening exercises. Patients with significant quadriceps weakness from upper lumbar deficits are at risk of falling, particularly when they step off curbs, go down stairs, or walk downhill. These patients should be instructed in compensatory mechanisms that minimize the risk of the knee buckling. On occasion, a knee extension orthosis is advisable. Patients with significant sensory deficits face the risk of ankle sprains and may benefit from mediolateral ankle support. Patients with disc disease should also be selectively counseled regarding various assistive devices, such as reachers, as well as on reorganizing and relocating their personal items in order to make the activities of daily living easier while also reducing the strain on their lumbar discs.

Activity modification Activity modification is one of the least studied areas of treatment, but a particularly important component of our practice. In a review of ten trials of bed rest and eight trials of advice to stay active, Waddell et al. reported consistent findings showing that bed rest is not an effective treatment for acute low back pain, and in fact may delay recovery.15 Although these patients were not carefully separated into those with axial back pain as opposed to those with radicular pain, the authors concluded that patients should be advised to remain active. In a trial comparing 2 days of bed rest with 7 days of bed rest for patients with mechanical low back pain without neurological deficits, Deyo et al. reached a similar conclusion: the group with the shorter period of bed rest missed fewer days of work.16 No other difference was noted between the two groups in terms of their functional, physiological, or perceived outcomes. 873

Part 3: Specific Disorders

In fact, there is no evidence that bed rest hastens recovery or improves outcome in patients with radicular pain and radiculopathy. On the contrary, numerous studies demonstrate the deterioration of many physiological systems as a result of bed rest. Abnormalities that develop include, but are not limited to, decreased cardiac output, atelectasis, orthostatic hypotension, decreased aerobic capacity, diffuse muscular atrophy, constipation, renal lithiasis, osteopenia, and depression. On the other hand, Wiesel et al. conducted a study on military recruits with nonradiating back pain and found that those who were on brief periods of bed rest had a faster return to full duty than those who remained ambulatory.17 Despite numerous studies indicating that continued activity is preferable to bed rest, many patients have too much pain to get out of bed and will require a short period of bed rest until the severe pain lessens. Pain can often be reduced by the following: lying supine with hips and knees both in significant flexion, supported by pillows underneath the calves; lying on either side in a fetal position with the pillow between the knees; and short periods of lying prone with a pillow under the mid-abdomen. In addition, patients are advised to use firmer mattresses, with a soft, thin surface layer.18 Patients with radiculopathy caused by paramedian herniated discs should keep sitting to an absolute minimum. To encourage them to limit time spent sitting, we instruct patients to imagine a nail coming out of their buttock, and to envision it being driven in further if they sit. We also advise them to limit their commute to work and, if possible, being driven in a reclined position as opposed to driving themselves. If they must drive, patients are instructed to tilt up the front of the seat and recline the back, with the use of a lumbar support. Walking, on the other hand, places fairly minimal pressure on the discs and is well tolerated by the vast majority of patients with paramedian disc herniations. Patients should also be cautioned to keep bending, twisting, and lifting to a minimum.

Clinical use of medications There is no evidence that any oral medication will change the course of lumbar radiculopathy due to a herniated disc. On the other hand, medication can help control symptoms. Patients are, however, warned to avoid activities that they know would be painful or inadvisable when not taking their medications because such activity could ultimately exacerbate rather than alleviate their symptoms (Table 81.2).

Nonnarcotic analgesics Acetaminophen, in doses of 500–1000 mg every 4–6 hours, up to a maximum of 4000 mg per day provides mild but relatively safe analgesia. Side effects are rare and there is no gastrointestinal toxicity and no sedation. There is no impact on bleeding time and organ toxicity is rare if the dosage is limited to less than 4000 mg per day. Tramadol (Ultram) is a weak opioid agonist with analgesic properties equal to acetaminophen/codeine combination preparations that is well tolerated by most, including the elderly. Tramadol is often prescribed as 50 mg to a maximum of 100 mg every 6 hours. It is also available in a combination tablet, which includes 37.5 mg of tramadol and 325 mg of acetaminophen (Ultracet). Tramadol has the advantage of causing less sleepiness and constipation than narcotics, with a similar analgesic benefit to mild narcotics. Uncommon side effects include sleepiness, dizziness, and nausea. Tramadol may decrease the seizure threshold in patients with epilepsy.19 Practitioners must be cautious when treating concomitantly with tramadol and other drugs that increase serotonin activity, such as monoamine oxidase inhibitors (MAOIs), tricyclic antidepres874

sants, Paxil, and Effexor. Patients taking significant doses of Ultram in combination with these medications can develop a ‘serotonin syndrome,’ which includes various autonomic, neuromotor, and cognitive–behavioral symptoms. Symptoms may include diaphoresis, hyperthermia, nausea, diarrhea, shivering, hyperreflexia, myoclonus, muscular rigidity, tremor, and ataxia. There have been reports of agitation, mania, hallucinations, and even seizures and death.

Narcotic analgesics Narcotics are a mainstay in the treatment of severe pain and when used appropriately in patients without a prior history of addiction present a low risk of addiction. Side effects include somnolence, nausea, pruritus, and constipation. Constipation is of particular concern in patients with disc herniation, since straining not only causes pain, but could also cause worsening of symptoms. Time-released preparations of oxycodone, morphine, or fentanyl should be considered for those patients who are unable to sleep due to severe pain.

Nonsteroidal antiinflammatory drugs No studies show that nonsteroidal antiinflammatory drugs (NSAIDs) improve either the objective signs or the long-term outcome in patients with lumbar radiculopathy. There is, however, some evidence that NSAIDs are effective for short-term symptomatic relief in patients with acute low back pain, but no specific type appears to be more effective than the others.20 There is evidence that antiinflammatories can reduce inflammatory mediators in animal studies.21 A comparison of indomethacin with placebo did not demonstrate a difference in objective neurological signs or subjective reports of pain relief.22 One study revealed a symptomatic improvement with meloxicam in acute sciatica when compared with placebo and diclofenac in a doubleblinded trial.23 Neverthless, NSAIDs are frequently used to treat patients with lumbar radiculopathy. Although the course of the condition is not changed, there is probably a role for these drugs in many patients. At the time that this book was going to press, rofecoxib (Vioxx) and valdecoxib (Bextra) had been withdrawn from the market, and other selective COX-2 inhibitors, such as celecoxib (Celebrex), were under investigation in the wake of studies indicating an increased risk of adverse cardiovascular events. NSAIDs have several advantages when used for pain relief in lumbar radiculopathy, including lack of sedation and the ability to reduce the demand for narcotics. Side effects include gastrointestinal (GI) toxicity and some alteration in bleeding time. Under investigation are NSAIDs that do not appreciably increase bleeding time, including meloxicam (Mobic) and salsalate (Disalcid). However, the prolonged use of all NSAIDs and, in particular the COX-2 inhibitors, may increase the risk of heart attacks and stroke. The first concern about the cardiovascular safety of rofecoxib emerged with the VIGOR study, reported in 2000. It involved a fivefold increase in myocardial infarction and a twofold increase in stroke, or cardiovascular death among 8076 rheumatoid arthritis patients treated for a median of 9 months with rofecoxib compared with naproxen.24–27 Further questions about the cardiovascular safety of rofecoxib were raised in 2001 by an overview of the clinical trial data.28 These data prompted the FDA to initiate a label change in 2002, highlighting the potential cardiovascular risks of rofecoxib. Despite more recent observational studies also suggesting an increased early (within the first 30 days of treatment) and late (beyond 30 days) risk of acute myocardial infarction or sudden cardiac death with rofecoxib,29,30 conclusive evidence of increased cardiovascular risk from adequately powered randomized trials was lacking.31

Oral corticosteroids Theoretically decrease root inflammation Not proven to alter course Caution: AVN, multiple side effects

Anti-TNF Experimental Anti-inflammatory – disease modifying

Long acting – for hours, for chronic pain Caution: sedation – add provigil, constipation – add laxatives, nausea, pruritus, addictive potential

Muscle relaxants

Variably sedating Role when diffuse muscular tenderness Some with anticholinergic effect Some with addictive potential

Selective COX-2 inhibitors, meloxicam Salsalate – ↓GI toxicity, normal bleeding time Caution: fluid retention, GI toxicity – add PPI, misoprostol, ↑ bleeding time, ↑ vascular events

Tamadol – max 100 g every 6 h Caution: interaction with serotonergic drugs

Analgesic effect only Short acting

Analgesic effect primarily Disease altering for: synovial cyst, Facet syndrome

Analgesic effect only Acetaminophen – max 4 g per day

Narcotic analgesics

NSAIDs

Non-narcotic analgesics

Table 81. 2: Medications for lumbar radiculopathy – summary

For pain with neuropathic quality Lidocaine patch, capsaicin

Topical agents

Effexor, Paxil, duloxetine – theoretical benefit of increasing both central serotonin and neuroepinephrine

SSRIs – not well studied

For pain with neuropathic quality Tricyclics – most common is amitriptyline, variable sedation, variable anticholinergic

Antidepressants

Caution: somnolence, dizziness, nausea

For pain with neuropathic quality, ???, burning Most common: gabapentin, titrate up to 1800 mg per day for most, max. 3600 mg per day

Anticonvulsants

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Part 3: Specific Disorders

The decision by Merck to withdraw rofecoxib worldwide was prompted by an unexpected source. APPROVe (Adenomatous Polyp Prevention On Vioxx) was a multicenter, placebo-controlled trial of 2600 patients designed to examine the effects of treatment with rofecoxib on the recurrence of neoplastic polyps of the large bowel in patients with a history of colorectal adenoma.27 An interim analysis of this trial demonstrated an almost twofold increase in cardiovascular events in patients treated with rofecoxib (25 mg daily) compared with placebo. When these data are extrapolated to the Australian population, the increased risk of 16 events per 1000 patients treated for up to 3 years equates to a potential excess of several thousand cardiovascular events caused by rofecoxib. This may represent an underestimate of the number of events caused by rofecoxib, because patients with inflammatory arthritis are likely to be at higher baseline risk of cardiovascular events than the ‘low-risk’ population included in APPROVe.27 Selection of a particular NSAID type is primarily based upon pharmacokinetics. Prior tolerance of a drug and a low incidence of GI toxicity, as well as minor effects on bleeding time, are all significant factors to consider in choosing the appropriate NSAID. Proton pump inhibitors and misoprostol (Cytotec) are well tolerated and can significantly reduce the incidence of gastrointestinal bleeding and other gastrointestinal side effects. NSAID types that must only be taken once or twice daily are better tolerated than a three-times-a-day schedule.

Muscle relaxants Some studies support a weak benefit of muscle relaxants over placebo for the treatment of axial back and neck pain,32–35 but we are not aware of any trials on the use of muscle relaxants for lumbar radiculopathy. Muscle relaxants do affect the musculature, as well as the central nervous system. All relaxants are sedating and therefore are useful when sedation is desired. Muscle relaxant drugs can cause addiction and some are associated with a withdrawal syndrome. Serious toxicity is rare if one keeps within the prescribed dosage range. Lioresal (baclofen) facilitates gamma-aminobutyric acid (GABA) transmission, and has been demonstrated to be effective in trigeminal neuralgia and may reduce neuropathic pain. Tizanedine (Zanaflex) is a centrally acting alpha2-adrenergic agonist and effects an inhibition of spinal reflexes. Zanaflex may be useful in patients with diffuse muscular tenderness. Cyclobenzaprine (Flexeril) is chemically similar to amitriptyline (Elavil) and, because of the anticholinergic effects, may not be suitable for patients with close-angle glaucoma or benign prostatic hypertrophy.

Antidepressants Tricyclic antidepressants are known to reduce neuropathic pain, but no known studies are specific to lumbar radiculopathy. Although amitriptyline is the best-studied and most accepted drug for the treatment of neuropathic pain, it is also the most sedating of the tricyclic antidepressant medication. All tricyclic drugs have anticholinergic side effects. The use of selective serotonin reuptake inhibitors (SSRIs) in the treatment of radicular pain is largely unsupported. In studies comparing tricyclic antidepressants with SSRIs for chronic pain syndromes, tricyclics were found to be more effective in every case.36 On the other hand, venlafaxine (Effexor) shares similarities with the tricyclic antidepressants but lacks their most troublesome side effects. In addition, venlafaxine has a similar structure to tramadol. There are case reports, open trials, and preclinical work that support the efficacy of venlafaxine for both nociceptive and neurogenic pain. 876

In addition, paroxetine (Paxil) has been found to inhibit the reuptake of both norepinephrine and serotonin. Therefore, theoretically, it should be a more effective analgesic than the other SSRIs. Duloxetine (Cymbalta), a selective serotonin and norepinephrine reuptake inhibitor (SSNRI), is available in doses of between 20 mg and 120 mg per day, administered either once or twice daily. Efficacy has been demonstrated in diabetic peripheral neuropathy in two randomized, double-blind, 12-week, placebo-controlled studies in which patients were followed for at least 6 months.37,38 Improvements were seen as early as 1 week after initiating the drug. Doses above 60 mg per day did not offer greater improvement. The drug is contraindicated in patients with narrow-angle glaucoma, as well as in patients with end-stage renal disease or hepatic insufficiency. Most commonly observed adverse effects include nausea, dry mouth, constipation, fatigue, decreased appetite, somnolence, and increased sweating. The overall discontinuation rate due to adverse events was 14%, compared with 7% for placebo.

Anticonvulsants Most anticonvulsant agents have shown effectiveness in the reduction of neuropathic pain, and may be useful in reducing pain caused by lumbar radiculopathy. Three relatively newer antiepileptic agents – gabapentin (Neurontin), lamotrigine (Lamictal), and topiramate (Topamax) – have become drugs of choice for neuropathic pain syndromes. Gabapentin is the most often prescribed medication for the symptomatic control of neuropathic radicular pain both because it has the most favorable side effect profile and, due to its low incidence of organ toxicity, because blood levels are not required.. To help avoid side effects, treatment is usually started at 100–200 mg b.i.d. and 200–300 mg h.s. and slowly titrated upward, by 100 mg per dose. Side effects can include sedation, dizziness, ataxia, and gastrointestinal distress. Maximum daily dosage is 3600 mg per day. Gabapentin is usually tolerated in dosages up to 1800 mg per day, and is generally taken three times per day. The drug can also be used only at bedtime to reduce nocturnal pain. The antiepileptic drug lamotrigine (Lamictal) has recently been studied in the management of intractable sciatica.39 The study demonstrated improvements in lumbar range of motion, straight leg raising, and a short form of the McGill pain questionnaire. Newer promising anticonvulsant drugs include tiagabine (Gabitril), oxcarbazepine (Trileptal), zonisamide (Zonegran), felbamate (Felbatol), and levetiracetam (Keppra).

Oral corticosteroids Although short courses of corticosteroids are often prescribed for radicular pain, there are no double-blind, placebo-controlled trials supporting or not supporting the use of corticosteroids for the treatment of radicular pain caused by a herniated disc or spinal stenosis.40 Because of the risk of avascular necrosis of joints with the intake of 60 mg doses of dexamethasone,41 we only occasionally treat radicular pain with oral corticosteroids.

Antitumor necrosis factor medications Several recent studies show that tumor necrosis factor TNF-α may be a significant pain mediator in radicular pain.42,43 According to Murata et al.,43 TNF-α is produced and released from chondrocyte-like cells of the nucleus pulposus and acts to reduce nerve conduction velocity, induce intraneural edema and intravascular coagulation, reduce blood flow, and cause myelin splitting. Murata treated rats with intraperitoneal infliximab (Remicade), a selective inhibitor of TNF-α and showed

Section 5: Biomechanical Disorders of the Lumbar Spine

that injected rats produced a significant reduction in histologic changes in the dorsal root ganglion. Korhonen et al. demonstrated the beneficial effect of a single infusion of infliximab, 3 mg per kg, for herniation-induced sciatica.44 Eight of the 10 patients treated with infliximab remained pain-free 1 year after injection, and no ill effects were reported in any of the 10 patients. Six of the 10 had achieved pain-free status at 2 weeks, seven at 4 weeks, and nine at 3 months. All had severe sciatic pain below the knee, positive straight leg raising at less than or equal to 60 degrees, and a disc herniation concordant with symptoms on MRI. By comparison, only 43% of the 62 control patients, who also had disc herniation-induced sciatica, were pain free at 12 months.

Heat (thermotherapy) Heat can be used as a temporary analgesic,48 and can be administered by hydrocollator packs, heating pads, hydrotherapy, or thin wraps that can be placed on the skin for a prolonged application. In fact, heat wraps have been demonstrated to be more effective than ibuprofen and acetaminophen for acute low back pain,49 and are helpful for relieving overnight pain.50 Diathermy and ultrasound are usually ineffective in reducing radicular pain. Heat should not be used in patients with inadequate or altered sensation of pain, and should not be applied to regions of acute trauma, anesthetic skin, or compromised circulation.

Electrotherapy Topical agents Lidocaine 5% patch reduces pain associated with postherpetic neuralgia without toxicity. The only side effect is an occasional local rash. Lidoderm patches have been tried in various conditions associated with neuropathic pain. Although the drug's insert instructs that the use should be an on-and-off 12-hour schedule, there does not appear to be any physiological risk to 24-hour use of the patch. There are, however, no studies demonstrating efficacy in lumbar radiculopathy.45 Topical capsaicin (Zostrix), applied three times a day, has been shown to reduce neuropathic pain in concentrations of both 0.025% and 0.075%. Effectiveness is generally unappreciated for at least 2 weeks, and some patients have significant discomfort due to an initial local burning sensation. There is no evidence that this agent is effective in lumbar radiculopathy. Considering the long onset of action and questionable efficacy, we rarely use capsaicin in patients with acute lumbar radiculopathy.

Physical therapy It is critical for the treating physician and therapist to work closely together and agree on the details of ongoing treatment. The most important role of the physical therapist is to educate patients in proper body mechanics, as well as to guide them through centralization exercises. Several physical therapy modalities can benefit patients with lumbar radiculopathy. Some patients may respond to lumbar traction and some may benefit from soft tissue modalities. Transcutaneous electrical nerve stimulation (TENS) has an occasional role as an analgesic modality. Selected patients may respond to spinal and neural mobilization techniques. Stabilization and core strengthening exercises are theoretically beneficial, particularly in the prevention of future discogenic episodes. Thermotherapy, electrotherapy, and cryotherapy can temporary relieve pain and are often combined with stretching techniques to reduce soft tissue pain.

Superficial cold (cryotherapy) Application of cold packs placed in wet towels or ice massage can afford temporary analgesia.46 Cold causes vasoconstriction of superficial vessels, indirectly resulting in vasodilatation of deeper vessels. Contraindications to cryotherapy include cold hypersensitivity and urticaria, Raynaud's phenomenon, cryoglobulinemia, and paroxysmal cold hemoglobinuria. In addition, cryotherapy should not be applied to areas of skin anesthesia or decreased circulation. Vapo-coolant spray and stretching (spray and stretch) can also be used for the management of myofascial pain. This is often used in combination with trigger point injections as described by Travell and Simons.47

Various forms of electrical stimulation, such as high-voltage pulsed galvanic stimulation or interferential electric stimulation, can be applied in the office setting, either in isolation or in conjunction with heat or cold. These modalities seem to contribute to relaxation and temporary analgesia, perhaps through decreasing spasm. Electrical stimulation should not be applied to patients with cardiac pacemakers or defibrillators, or to anesthetic areas or incompletely healed wounds.51 TENS uses a small pulse generator clipped to the skin connected to one to four variously placed transcutaneous electrodes. The pulse frequency, amplitude, and wave form are adjusted to achieve maximal effect. TENS can provide analgesia,52 but there are no specific trials evaluating the efficacy for treating lumbar radiculopathy. In general, TENS has an occasional role and may be most useful in decreasing night pain. Percutaneous electrical nerve stimulation (PENS) uses needle probes similar to those used in acupuncture to deliver electrical pulses to peripheral sensory nerves at dermatomal levels.53 In a trial comparing PENS, sham PENS, TENS, and exercise, both PENS and TENS were effective in reducing sciatic pain. Although PENS was more effective, because it is a tedious in-office procedure, supported by only a few studies, and does not help structurally, PENS has not been used in our management of radicular pain

Lumbar traction Lumbar traction is an old procedure and in the past low-poundage continuous traction was a standard hospital treatment for lumbar radiculopathy. No longer practiced, continuous in-bed traction is only effective in forcing a patient to remain in bed.. The following are the current spinal traction techniques: 1. Intermittent mechanical traction, employing a mechanical device and a split table that can administer up to 200 pounds of traction, usually for 40–50 seconds with 10 seconds of rest each cycle. 2. Sustained traction, which is the same as the above but without periods of rest. 3. Manual traction applied by steadily pulling on the patient's limbs. 4. Autotraction in which the patient lies with flexed hips and knees and pulls on a railing to generate force while the pelvis is held by a harness and encircling belt. 5. Gravity lumbar (inversion traction) in which the patient is suspended upside down, either with the knees flexed over the top of the device or by the use of ankle boots. Because inversion may be associated with an elevated systolic and diastolic blood pressure, decreased heart rate, periorbital and pharyngeal petechiae, blurred vision, and headache, many healthcare practitioners are reluctant to provide inversion traction within their facilities The evidence supporting traction remains inconclusive, but may in part be due to poor study design. A review article found no conclusive 877

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evidence that any form of traction is efficacious in the treatment of low back pain, with or without radicular involvement.54 However, several studies have revealed a reduced size of herniation following traction.55,56 Nachemson and Elstrom demonstrated a 20–30% reduction in intradiscal pressure with traction.57 Fifteen minutes of sustained traction will cause increased height.58 Despite the lack of clinical evidence, many of our otherwise unresponsive patients have a lessening of symptoms following lumbar traction. When treating patients with lumbar radicular pain and radiculopathy, we use traction if symptoms are not promptly responsive to centralization techniques. Our protocol uses approximately 15 minutes of intermittent traction alternating a 40–50-second pull with 10–15second rest period. If necessary in larger patients, we will use up to 150 pounds of traction and in smaller or elderly patients as little as 60 pounds of traction. When treating patients with paramedian disc herniations, we have often initiated traction with the lumbar spine in flexion, and have attempted to gradually modify the traction so that the lumbar spine is more in extension, in accordance with the principle of the centralization phenomenon as introduced by Robin McKenzie (see Centralization below). In fact, traction is administered in a prone position in patients that centralize in extension (Fig. 81.1). When radicular pain is persistent, we have used a gapping technique so that the pull is angulated somewhat toward the asymptomatic side (Fig. 81.2). About 5% of our patients with paramedian HNPs undergoing traction complain of a transient increase in axial pain. Very rarely does this pain last more than a few hours. In the last 15-year period, we have never knowingly caused a vertebral fracture, even though we are certain that many patients with osteoporosis received traction during the initial years of our practice. More recently, however, we avoid traction in patients at risk for osteoporosis, but when other conservative therapy fails, we will administer lower-poundage traction, to a maximum of 80 pounds.

Back schools and patient education Patient education may be the most important factor in the prevention of recurrent episodes of discogenic pain, and back schools are an excellent forum for providing this education. In existence since 1977, back schools in Sweden, Canada, and California boast validated success in reducing the incidence of back pain.59–61 Most back schools have four to eight patients in a class that meets for two to four sessions, with a total education time of approximately 4–6

Fig. 81.2 Gapped traction in side-lying.

hours. Patients are educated regarding anatomy, epidemiology, and biomechanics that pertain to low back pain. They are generally tested on their knowledge, and taken through an ‘obstacle course’ to determine how sound their body mechanics are when performing activities of daily living. Classroom education is supplemented with literature and audiovisual materials, and patients benefit from each other's questions. At the conclusion of back school, patients are retested on what they have learned. Patients also complete the obstacle course again, to demonstrate their ability to incorporate a sound understanding of body mechanics into their daily lives. Patients are also educated in self-care in the event of recurrent back pain, given an exercise program, and advised as to the dos and don'ts of recreational exercise. In addition, back schools teach patients stabilization and exercises to increase core strength. Because the success rate is better when a specific and appropriate population is targeted, our back school is limited to patients who have either axial or radicular pain caused by paramedian disc herniations. By limiting the participants to this subset, education in body mechanics and exercises applies to all participants. Back school theory is primarily based on the effects of body posture on disc pressure published by Dr. Alf Nachemson62 and the Robin McKenzie approach.63 Dr. Nachemson measured the intradiscal pressure in volunteers in numerous positions, while performing activities of daily living, and performing various exercises (Fig. 81.3). From these studies, he found lower intradiscal pressures when standing compared to sitting. Bending forward in either the sitting or standing position increased intradiscal pressure above sitting pressures. Coughing and straining caused significant rises in intradiscal pressure. Lifting weights further from the body raises pressure more than lifting weights closer to the body. These increases in pressure are often reflected in patients increased pain during positions and activities that increase intradiscal pressure. Robin McKenzie, a New Zealand physical therapist, has pioneered the conservative management of low back pain. He theorizes that centralization of pain or when pain moves from a more distal to a more proximal location, reflects a structural improvement. His exercise protocol emphasizes passive lumbar extension and performing activities of daily living in a lordotic posture.

Centralization Fig. 81.1 Prone traction. 878

Many physicians and physical therapists use the McKenzie method in both assessment and treatment of lumbar spine patients, including

Section 5: Biomechanical Disorders of the Lumbar Spine % 275 % 220 150

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those with radiculopathy. In 1972, McKenzie first presented favorable outcomes of 500 consecutive patients treated according to his centralization protocol.64 McKenzie and his disciples categorize patients with back pain, leg pain, or both based on whether their pain ‘centralizes’ in response to spinal movement. Centralization is defined as a change in the location of pain from a distal or peripheral location to a more proximal or central position. McKenzie classifies patients' presentations as either ‘mechanical’ when symptoms change in response to spinal movement, or ‘nonmechanical,’ when symptoms are unchanged. Patients with mechanical presentations are further classified into the three following syndromes: postural, which implies prolonged end-range stress of normal structures; dysfunction, implying end-range stress of shortened structures; and derangement, implying anatomical disruption or displacement within the motion segment. Each syndrome has further subsets. Assessment and management of patients with an intact contiguous nucleus pulposus using the McKenzie Method® assumes that movement will effect the position of the nucleus pulposus within the anulus fibrosus. Although an assumption, many studies support his belief,65–68 and in addition one study shows a good inter-tester reliability.69 The McKenzie approach examines the patient during repeated end-range movements when standing, forward bending, back bending, and side bending. Similar repeated end-range movements are performed while the patient is recumbent, including knees to chest while supine, passive extension while prone, and prone lateral shifting

of hips off the midline. As the patient performs each of these maneuvers, the clinician records whether there is a directional preference or centralization, as opposed to peripheralization, of pain (Fig. 81.4). Based on the results, the patient is categorized and a treatment plan is suggested. Patients who do not show a directional preference are not candidates for centralization exercises and may have a cause of pain other than disc pathology. Patients with a directional preference are given exercises and postural advice based on the preference. In addition, practitioners can use the McKenzie Method® to determine which patients are candidates for manual techniques that can accelerate their recovery. These techniques may include correction of a sciatic list or ‘shift,’ as well as mobilization techniques to improve lumbar extension. Most patients with mechanical pain have extension as their directional preference which may be a positive prognostic sign. Kopp et al.10 studied 67 patients that required hospital admission for lumbar pain with radiation to the calf or foot. These patients had positive root tension signs, and were determined to have lumbar disc disease with all other etiologies of lumbar radiculopathy ruled out. The McKenzie approach was used on these 67 patients. Of the 35 patients who were able to be treated without surgery, 97% were able to achieve normal lumbar extension within 3 days of admission to the hospital. Only 6% of the 32 surgically treated patients were able to achieve normal lumbar extension preoperatively. In 1990, Donelson et al. reviewed 87 patients with back and radiating leg pain.70 Centralization occurred in 76 (87%) and in the majority 879

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Fig. 81.4 Elements of the McKenzie examination. (A) Side gliding while standing. (B) Flexion while lying. (C) Extension while lying. (D) Side gliding with overpressure. (E) Extension while standing. (F) Flexion while standing.

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Section 5: Biomechanical Disorders of the Lumbar Spine

centralization occurred within 2 days of the initial visit. All of the 59 patients who had an excellent outcome experienced centralization of pain during the initial evaluation. In the 13 patients with good results, 10 had centralization, 4 of 7 patients with fair results centralized; and only 3 or 8 patients with poor results centralized. A review of the literature by Wetzel and Donelson concluded that McKenzie centralization protocol benefited patients with lumbar radiculopathy who were able to centralize. The authors advised that surgery should not be considered until these patients had an adequate trial of the centralization technique.71 Snook et al. also demonstrated benefit in low back pain when patients restricted flexion activities during early morning hours when discs are fully hydrated and thus more susceptible to intra-anular prolapse.72 Donelson and Aprill et al. demonstrated a correlation between the McKenzie assessment and results of discography and showed that a significant number of patients who centralize have an intact outer anulus.73 Sixty-three patients with back and lower extremity pain based on disc disease were studied. The majority of these patients had pain below the knee. None had neurological deficits and all had at least one MRI study and none required surgery. Fifty of the patients were able to centralize their referred pain, and in this group 74% had positive discograms and 91% of those had an intact anulus. In the 25% of patients who peripheralized their pain during McKenzie assessment, 69% had positive discograms, but only 54% of those had an intact anulus. Twenty-five percent of patients did not centralize or peripheralize their pain in response to testing maneuvers and only 12.5% of these patients had positive discograms. Many studies74–79 have shown that centralization is a better predictor of outcome than the location of the initial pain. For this reason, our practice uses centralization to predict outcome and guide treatment. The ability of a patient with lumbar radicular pain and radiculopathy to centralize is assessed as soon as possible. We find that a high percentage of these patients are able to centralize and will respond to the appropriate exercises and biomechanical advice. Most centralize with extension, and respond to passive extension exercise programs. We have, however, found that patients who routinely perform multiple repetitions of prone lying press-ups often develop or exacerbate prior musculoskeletal conditions. These include facet pain caused by increased stress on posterior lumbar elements, increased cervical pain caused by strain on the cervical spine, acromioclavicular joint inflammation, and medial epicondylitis. We do, however, modify the passive extension exercises to avoid these problems. For instance, one can insert pillows underneath the head and chest to create passive extension, instead of relying wholly on the upper extremities. The patient can also move the hands caudally to allow a traction force to the lumbosacral spine with less stress on the posterior element.

Therapeutic exercises Stretching Reducing lumbar strain requires maximally stretched iliopsoas musculature and maximal internal and external rotation flexibility of the hip. Individuals who run also need good flexibility of the hamstrings, quadriceps, and gastroc/soleus musculature. If a patient has an acute disc herniation, specific stretches should only be added when safe.

Strengthening Treating back disorders with strengthening has been prescribed for at least three-quarters of a century. Strengthening of the flexion musculature is an important part of the Williams flexion exercises.80 Patients have been given flexion, extension, or mixed exercise

programs in an effort to strengthen trunk musculature and unload the lumbar spine. In 1989, the Saal brothers formalized their stabilization/strengthening program.3,81 This program, which consists of gradually more challenging trunk strengthening exercises, quickly became incorporated into rehabilitation programs throughout the United States (Figs 81.5, 81.6). Within the past several years, ‘core strengthening’ has rapidly become a catchphrase in rehabilitation programs, gyms, and fitness centers throughout the country. A core strengthening program incorporates more functional movements of the body as a whole, while maintaining contracted trunk musculature. Improved clinical outcomes following core strengthening have not been proven. In a review of core strengthening, Akuthota and Nadler wrote, ‘To our knowledge, no randomized controlled trial exists on the efficacy of core strengthening. Most studies are prospective, uncontrolled case studies.’82 A 2002 study by Nadler et al. evaluated the incidence of low back pain before and after incorporation of a core strengthening program for athletes. This study was unable to demonstrate a significant change in overall incidence of low back pain.83 Nonetheless, numerous models demonstrate why stronger trunk musculature should afford greater stability to the lumbar spine.84 Studies have demonstrated that many muscles contract during stabilization exercises.85 Other studies have demonstrated that increased abdominal pressure stabilizes the lumbar spine. Such increased pressure can occur either as a result of antagonistic muscle co-activation or abdominal muscle contraction.86,87 It has also been shown that simply stimulating paraspinal musculature stabilizes the lumbar spine.88 Furthermore, investigators have demonstrated various trunk muscle abnormalities in the population of patients who have back problems. The latency for lumbar muscle contraction is longer in patients with sciatica.89 Patients who were 5 years post-laminectomy demonstrated persistent atrophy of the multfidi, but to a much lesser extent than in patients that had good outcomes from surgery.90 Multifidus muscles were noted by Hides to be weak 10 weeks after a low back pain episode.91 Arendt-Nielsen noted active paralumbar muscles on EMG during gait in chronic low back pain patients, but silent lumbar paraspinal musculature during gait in controls.92 Hodges found a late onset of transversus abdominus contraction in patients with low back pain while performing upper extremity activities.93 In 1997, Cholewicki et al. studied trunk flexor–extensor musculature in healthy individuals, and performed a number of calculations with the use of a model.94 They concluded that average antagonistic flexor–extensor muscle co-activation levels were 1.7% of maximum voluntary contraction when there was no load added, and 2.9% when a 32 kg mass was added to the torso. They further calculated that an individual with spine injury and stiffness would exert 3.4% of maximum voluntary contraction of antagonist muscle co-activation for no extra load, and 5.5% when 32 kg were added. The authors stated that, ‘It seems reasonable to expect that the requirements of spine stability in a neutral posture should not demand more than 5% maximum voluntary contraction of muscle co-activation, because that could lead to muscle fatigue during the entire day.’ Although we prescribe trunk strengthening exercises in our practice, these exercises are not emphasized more that other treatment options. In addition, many of these exercises increase intradiscal pressure. Exercises that might exacerbate symptoms of patients with disc herniations include hyperextension exercises, isotonic truck flexion exercises such as sit-ups, and exercises involving trunk torsion. In this respect, the literature does not support a correlation between strength of core muscles and the reduced incidence of lumbar disc disease. No studies specifically demonstrate that individuals with weaker trunk musculature are at higher risk for disc problems. In 881

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D Fig. 81.5 Examples of basic stabilization exercises. (A) Abdominal crunch. (B) Hook lying bent leg lift. (C) Hook lying combination. (D) Hook lying extremity flexion. (E) Bridging.

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fact, the greatest incidence of first-time disc herniations is between the age of 25 and 29, when one can only assume that the trunk musculature is stronger than in older individuals. Nevertheless, we do prescribe some trunk strengthening and usually include only isometric exercises. We advise strengthening of back musculature, but avoiding hyperextension. We strongly advocate maintaining a neutral spine and isometrically co-contracting trunk musculature while performing such activities as bending and lifting. The strengthening exercises are provided in a graduated fashion. A greater emphasis is placed on strengthening exercises for those patients returning to demanding recreational and athletic activities. 882

Mobilization Mobilization techniques performed by physical therapists can be a useful treatment modality in patients with lumbar radiculopathy caused by a paramedian HNP. There are many schools of mobilization, and it is best to have training in multiple methods, since individuals at times will respond to one manual technique and not another. It is important that a patient have good mobility of the adjacent spinal segments which should theoretically reduce the stress at the level of the herniated disc. Good hip mobility is also important, because increased torsional lumbar spine forces occur in patients who have

Section 5: Biomechanical Disorders of the Lumbar Spine

contractured hips. Normal sacroiliac alignment and mobility should also reduce forces on the lumbar spine. Clinicians must approach mobilization of the involved disc segment with great caution, particularly when the patient is acute. If the involved segment is determined to be hypomobile, then low-grade posteroanterior (PA) mobilizations of the involved segment, without torsion, may have a role very early on in treatment to promote increased passive extension.

Myofascial release Many patients with lumbar radiculopathy develop localized areas of tenderness within the lumbar and gluteal musculature, and occasionally in the lower extremity muscles. These tender areas are usually trigger points. It is unclear why or how these areas of muscle tenderness occur, but many physicians, including ourselves, feel that trigger points contribute to pain.95

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Fig. 81.6 Examples of advanced stabilization exercises. (A) Bridging on ball. (B) Sitting opposite arm and leg raise. (C) Prone opposite arm and leg raise. (D) Squatted arms outstretched. (Continued) 883

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E

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Fig. 81.6 Cont’d (E) Forward lunge. (F) Advanced abdominal crunch.

Travell and Simons have detailed maps of trigger point pain referral zones for trigger points for almost every muscle (Fig. 81.7).96 Although there are no double-blind, controlled studies validating any type of trigger point treatment, we believe that treating trigger points may reduce pain, particularly when palpation of a trigger point generates radiating pain. According to Travell and Simons, the goal of treating trigger points is to restore pain-free stretch to the involved muscle. This can often be accomplished through physical therapy alone, but trigger point treatments including acupressure, myofascial release, and spray and stretch will often improve outcome. The patient should be educated in specific stretches for the involved musculature, assuming that these movements are not contraindicated because of the patient's primary condition.

Neural mobilization In the 1980s, physical therapists began using sophisticated tension tests to assess adhesions and nervous system injury.97 These new diagnostic procedures led to passive mobilizing treatment techniques called neural mobilization. In part, neural mobilization is the result of studies showing increased tension in lumbar nerve roots as a result of passive neck flexion.98,99 Similarly, altered neck and arm pain may be demonstrated by the addition of ankle dorsiflexion to a straight leg raising maneuver. Neural mobilization advocates view the nervous system as a continuous organ that stretches from the brain to the feet. In 1987, Butler introduced the term ‘adverse mechanical tension in the nervous system,’ and discussed how to diagnose and treat neurogenic pain and neurological symptoms.99 Tension tests not only produce an increase in tension within the nerve, but also between the nerve and surrounding tissues. In 1976, Sunderland demonstrated that inflammatory changes around the nerve could lead to changes in the connective tissues within the nerves, with a resultant intraneural fibrosis.100 As a result of this fibrosis, nerves lose elasticity, and tension tests are altered. The ‘slump test,’ which includes neck and thoracolumbar flexion, links neural and connective tissue components of the nervous system from the pons to the termination of the sciatic nerve in the foot. Deviation toward the affected limb during lumbar–sacral flexion is also indicative of adverse neural tension. 884

An acutely herniated paramedian disc causes acute inflammation of the traversing root resulting in extraneural fibrosis and often resulting in dysesthesia and weakness in the distribution of the affected root. Extraneural symptoms are more effectively tested by positions that cause movement of the nerve rather than direct neural stretching. When pain and radiculopathy are caused by a herniated lumbar disc, neural mobilization may be gradually introduced when positive neural tension signs remain and the acute inflammation is judged to be diminished. Specific techniques are used for each peripheral nerve. For example, ankle dorsiflexion stresses the tibial component of the sciatic nerve, whereas ankle plantar flexion combined with inversion stresses the common peroneal portion of the sciatic nerve. Neck flexion, medial hip rotation, and hip adduction can also be added, and the velocity and amplitude of the stretching maneuvers can be varied. The common goal is to free intraneural and extraneural adhesions. We will often use neural mobilization treatment in all patients with persistent positive neural tension signs, and we apply them more aggressively in subacute and chronic cases.

Manipulation Manipulation involves the application of passive, controlled forces and moment loads to alter the mechanical behavior of the functional spinal unit and internal stress distributions.101 Although manipulation procedures encompass an extremely broad array of treatments that cause passive movement to a portion of the body, we will restrict our discussion of manipulation in this chapter to rapid, high-thrust maneuvers. Several studies of manipulation demonstrate short-term efficacy.102–104 Practitioners who believe in the McKenzie approach to radicular pain and radiculopathy also probably believe that patients can improve more rapidly by adding spinal manipulation. High-thrust manipulation is rarely indicated in the treatment of radicular pain caused by a lumbar disc herniation. If the patient centralizes his or her pain with McKenzie treatments, then manipulation is not needed, and when the patients do not centralize, high-thrust manipulation has a low success rate and an increased complication rate. Contraindications to manipulation include cauda equina syndrome, undiagnosed loss of bowel or bladder control, undiagnosed progressive neurological deficit, severe osteoporosis, primary

Section 5: Biomechanical Disorders of the Lumbar Spine

Acupuncture TrP2 TrP1

Our review of the acupuncture literature revealed no controlled studies supporting its use in the treatment of lumbar disc herniations. Most studies have major methodological flaws, and rarely was the treated population well described.106 Acupuncture may, however, provide temporary analgesia, and practitioners may decide to pursue this treatment based on expense and ease of access. We use acupuncture on occasion for analgesia for the treatment of lumbar radiculopathy.

Taping, corsets and braces, and ergonomic aids

Gluteus medius

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Fig. 81.7 Common lumbar and gluteal trigger points. (Adapted from Travell JG, Simons DG, Simons LS. Myofascial pain and dysfunction: the trigger point manual, Vols 1 and 2. Baltimore: Williams & Wilkins; 1999 and 1992, with permission.)

or metastatic tumors, or conditions containing unstable motion. Cauda equina syndrome is, however, a rare complication and only 26 cases are reported in the world literature. Local, transient discomfort is not uncommon and is probably underreported. High-thrust manipulation in patients with disc herniations may result in increased radicular pain and rarely minor radicular neurological deficits.

Most patients with radicular pain and radiculopathy secondary to a paramedian lumbar HNP are encouraged to maintain lumbar lordosis during their activities of daily living. When patients are not progressing and have poor postural awareness, tape can be applied to the thoracolumbar area to encourage a mild lordosis. The tape is generally applied for a period of 12–48 hours and although studies do not exist to confirm or refute this treatment strategy, we feel that this technique often reduces patient symptoms. Lumbar orthotics and braces will variably restrict range of motion by operating through a three-point pressure system. They may increase postural awareness and might possibly reduce disc pressure by supporting weak abdominal muscles and increasing intra-abdominal pressure. Nachemson and Morris determined that an inflatable corset was able to decrease intradiscal pressure by 25–30%.107 Several types of lumbar orthoses are available.108 Flexible lumbosacral corsets are constructed from fabric, such as Neoprene, canvas, or elastic, and encircle the lumbosacral area. These devices provide postural feedback while mildly restricting range of motion, and may slightly increase intra-abdominal pressure. Corset closure is achieved with laces, buckles, or Velcro. Lumbar belts are made of elastic fabric, with or without pockets for removable plastic inserts. The inserts can be heated and custom-molded to the patient's lumbar region. The belts provide a mild reduction in lumbar range of motion, are generally fairly comfortable, and remind the patient to maintain the desired posture. They may increase intra-abdominal pressure, and may also protect individuals from work-related injuries. There are many rigid orthoses, and because all these devices are more cumbersome than the flexible corsets and belts they are less comfortable to wear. These braces restrict range of motion much more than flexible braces, but most do not make contact circumferentially and therefore do not increase intra-abdominal pressure. Because these braces are uncomfortable to wear, we infrequently prescribe them. There are, however, two rigid hyperextension braces that may be useful to the patient with lumbar radiculopathy caused by paramedian HNP. The first is the Cash orthosis (Fig. 81.8) that consists of anterior horizontal and vertical bars forming a large cross. The vertical bar extends from the sternum to the pubic bone. The brace fastens with straps in the back, and is lightweight and easy to put on and take off. It accommodates large breasts, but is difficult to fit on patients with protuberant abdomens. It certainly discourages thoracolumbar flexion, since any flexion is met by rigid pressure over the patient's sternum or pubic bone. There are, however, no controlled studies to validate the effectiveness of this brace. The second is the Jewitt hyperextension brace (Fig. 81.9) that consists of an anterior frame that is attached to sternal, suprapubic, and thoracolumbar pads and will also maintain the patient in a hyperextended posture. We utilize corsets and braces in approximately 5–10% of patients with paramedian disc herniations. Braces are particularly appropriate for patients who must sit for hours in poorly supportive seating, 885

Part 3: Specific Disorders Fig. 81.8 Cash orthosis. (Adapted from Cole A, Herring S. The low back pain handbook: a guide for the practicing clinician, 2nd edn. Philadelphia: Hanley & Belfus; 2003:453–457.)

A

B

Fig. 81.9 Jewitt hypertension brace. (Adapted from Cole A, Herring S. The low back pain handbook: a guide for the practicing clinician, 2nd edn. Philadelphia: Hanley & Belfus; 2003:453–457.)

a seat, are also available for the car and offer both a firmer surface to sit on and added lumbar support. These devices can also be used in chairs with backs at home, in the office, in restaurants, and at the theater. There is a cushion called a Night Roll, a long cylindrical pillow about 5–6 inches in diameter that wraps around the waist with a Velcro closure. On occasion, this cushion can help reduce trunk side-bending or gliding when used during sleep.

Trigger point injections

patients who are making slow progress and demonstrate poor postural support, patients who are returning to work or athletics, and patients whose symptoms are particularly sensitive to lumbar flexion and extension and who are not progressing in the rehabilitation program. Numerous pillows and cushions of varying size and density, which can be placed at the mid-lumbar level in chairs and cars, offer lumbar support by encouraging a lumbar lordosis. Patients usually choose a specific device based on their natural lumbar curve and overall comfort. Ergonomic devices, including those that have both a back and 886

Although there are no randomized, controlled studies supporting the use of trigger point injections, the technique is used by many and there is copious literature describing trigger point injection techniques. Trigger points are localized intramuscular areas of tenderness that usually feel nodular when palpated. These trigger points are thought to have a characteristic referral pattern when palpated. Authors have described taut bands within trigger points that, after palpation, will cause referral of pain into a location that is typical for that muscle.96 We consider trigger points as a primary cause of myofascial pain and as such are part of the differential diagnosis. If the location of a patient's pain can be explained by trigger points that are found during examination, we feel treatment is appropriate. These trigger points often respond to physical therapy techniques but if resistant to physical therapy, and particularly if there is very significant tenderness and palpation causes radiation of pain, we treat the trigger points with localized injections Although techniques, needle size, and injectates vary, trigger point injections are most successful when the injection reproduces the patient's pain and the best results are predicted when the muscle twitches when the needle enters the trigger point (jump sign). In our experience, there is a much higher success rate when physical therapy immediately follows an injection, and myofascial techniques are used to help regain painless stretch of the involved muscle. We use 25-gauge needles and inject approximately 2 cc of 0.5% lidocaine into each trigger point. We will add small doses of corticosteroid, such as 1 mg of Decadron, only if the patient had persistent

Section 5: Biomechanical Disorders of the Lumbar Spine

soreness after previous trigger point injections. When the patient's pain is reproduced during needle entry, we usually ‘dry needle’ the trigger point several times. Trigger points that commonly accompany lumbar radiculopathy are found in the quadratus lumborum muscle, paralumbar muscles, gluteus medius and maximus, and piriformis musculature. On occasion, trigger points can also be found in the lower extremity musculature. Only a few trigger point injection sessions are needed in more acute patients who are responding to treatment, but more chronic pain unresponsive to treatment may require more sessions.

Advice on recreation As patients' radicular symptoms resolve, we advise patients to return to their usual recreational activities. Walking is generally well tolerated and permitted very early on in the course of recovery. Swimming using the crawl and breast stroke is also usually tolerated. The side stroke is not recommended until full recovery because if improperly done the stroke cause significant lumbar torque forces. The butterfly is a flexion–extension movement and therefore we encourage patients to avoid this stroke until they are asymptomatic for at least 3 weeks. As patients recover, we are cautious about their return to hightorque sports such as golf, squash, batting in baseball, and tennis, particularly if they play at a high level with a two-handed backhand. Bowling also probably involves significant levels of disc pressure. We often suggest that individuals ease their way back into these sports and consider wearing a soft corset at least during the early weeks or months of their return. Patients should generally be asymptomatic for at least 3 weeks before participating in the above sports. We generally advise that patients should be asymptomatic for at least 6 weeks before participating in sports such as basketball, soccer, and hockey. Jogging and running are usually well tolerated once straight leg raising has become negative. We caution weight trainers to avoid Valsalva maneuvers, lifting weights in front, isotonic abdominal strengthening exercises that involve trunk torsion, and deep squats or leg presses. We also advise against performing knee extension strengthening with both legs simultaneously. Patients are also advised to lift smaller weights with a greater number of repetitions to reduce the injury rate. When individuals perform flexibility exercises, we warn them not to stretch both hamstrings simultaneously, since this is likely to place the lumbar spine in a good deal of flexion. Skiers should be cautioned to avoid skiing moguls and to avoid skiing at a level that is challenging enough to pose a significant risk of falling. Patients can gradually increase their activities as their pain-free intervals increase. Maximal improvement is likely to be reached 3 months after full resolution and at that time patients can resume their regular exercise and work-related activities..

Travel We advise patients who have travel plans to choose two small suitcases, rather than one large one. Every effort should be made to minimize bending, twisting, and lifting during the packing process. If they are traveling by car, patients should reduce the amount of time that they drive. While being driven, they should sit reclined at 45 degrees or more, with frequent stops to stand up and extend the back for a few minutes. Patients traveling by plane should stand as long as possible before takeoff, and get up and walk about frequently during the course of the flight. For those who can afford it, traveling first or business class so that they can recline is advisable.

INDICATIONS FOR SPINAL INJECTIONS OR SURGERY A patient who has or develops a cauda equina syndrome needs emergency decompression. A patient that has a significant worsening of neurological signs should be strongly encouraged to undergo surgical decompression. If, however, mild neurological deterioration is accompanied by significantly improved mechanical signs, nonoperative care can continue. If after a week of conservative care, significant radicular pain remains and mechanical signs are persistent, further progress with conservative care will probably be slow. Patients with a positive straight leg raising at 35 degrees or less, positive cross straight leg raising at 50 degrees, and inability to centralize should be offered a transforaminal epidural steroid injection to help relieve middle column inflammation. If there is no improvement after 2 weeks of treatment, other rehabilitation measures such as taping, gap traction, and further activity modification could be considered. But if unresponsive, the patient should be advised to consider an epidural injection. Even if the patient is improving, but the progress is slow and the level of pain is severe despite medication and rehabilitative care, an epidural injection should be offered. In all cases, however, patients should be advised fully of the risks and benefits of spinal injections.

VARIATIONS IN TREATMENT FOR OTHER MECHANICAL CAUSES OF LUMBAR RADICULOPATHY See Table 81.3 for a summary.

Lateral or foraminal herniated nucleus pulposus Patients presenting with foraminal or lateral herniated discs are usually older, averaging about 55 compared to patients presenting with paramedian herniated discs, whose average age is about 40 years. These patients primarily have leg pain aggravated by postures of standing, walking, and lying down, and are most comfortable in a sitting position. Often, unable to find a comfortable position in bed, they sleep in recliners. Symptoms often begin without any clear precipitating factor. The herniation often consists of fragments of endplate and anulus fibrosus within the lateral or foraminal canal. The physical examination typically reveals a flexed forward posture and an intolerance to weight bearing. However, these physical findings are often unimpressive relative to the magnitude of the patient's pain. Reproduction of lower extremity pain with side bending is the most sensitive finding. Root tension signs are often negative. Neurological deficits, when present, are in a monoradicular distribution. L4 radiculopathy is the most common finding. The diagnosis is made clinically, without imaging, unless neurological deficits are significant or progressive, or the intensity of pain is such that the patient elects to undergo epidural injections or surgery. Some of these herniations may not be apparent even with a high-resolution MRI. On the other hand, it is not uncommon to find incidental foraminal HNPs that have no correlation with present or past symptoms. Although over 90% of these patients can be successfully treated without surgery, a significant percentage, between 40% and 70%, will require epidural injections. Although patients are advised to avoid prolonged sitting, it is impractical to tell this patient population not to sit since that is often their only comfortable position. These 887

888 2b 2b 2b 1c 3b

Trigger point injections Corsets/braces Ergonomic aides Back school Manipulation

a – early Rx b – mid period Rx c – late Rx

2b

Therapeutic exercise

1 – strong role 2 – moderate role 3 – minimal or no role

2b 2b

Mobilization – spinal and neural Traction

2b

Address function deficits Myofascial release

1a 1a

ADL education

3b

2c

3b

3b

2b

2b

1a

2b

3b

1a

2a

1a

3a

1a 1a

Centralization

Lateral or sequestered HNP

Paramedics HNP

Analgesia (meds/modalities)

Treatment options

3-

2c

2b

2b

2b

2b

2b

2b

2b

1a

1a

1a

1a

Lumbar stenosis

Table 81.3: Algorithm for benign mechanical causes of lumbar radiculopathy

2b

3-

3-

3-

2b

2b

2b

2b

1a

1a

2a

1a

3a

Synovic cysts

3b

2c

2b

1b

2b

2b

2b

2b

1b

1a

1a

1a

1a

Spondylolisthesis

Part 3: Specific Disorders

Section 5: Biomechanical Disorders of the Lumbar Spine

patients often require more frequent and stronger analgesics and neural modulating agents than patients with a paramedian disc herniation. Due to the more frequent occurrence of intense nocturnal pain, a trial of TENS and topical agents is more often attempted. Patients with lateral or foraminal HNP often fail both centralization techniques and traditional education in body mechanics. Nevertheless, at least a brief attempt should be made at centralizing their pain. Manipulation is contraindicated. Acupuncture may help with analgesia if it can be obtained without a great deal of travel. Traction, and especially traction with gapping, is often beneficial in these patients. In our experience it is one of the only physical therapy techniques that has a reasonably high success rate. On the other hand, approximately 5–10% of these patients will have short-term increased pain from traction.

Sequestered herniated nucleus pulposus Sequestered herniated discs usually have similar clinical findings to those patients with lateral or foraminal herniated discs. Making the diagnosis based on clinical presentation alone is therefore unlikely. Occasionally patients with sequestered discs will have pain in all positions, but Valsalva maneuvers should not cause radiating pain. Classically, the patient will report that the pain had initially involved the back and leg and worsened with sitting and with Valsalva maneuvers. Suddenly, the back pain lessened or resolved, but the leg pain significantly increased and was now aggravated by standing and walking, while sitting and Valsalva maneuvers were no longer painful. Treatment of a sequestered herniated disc is essentially the same as treatment for a lateral or foraminal herniated disc.

Stenosis: central, lateral, and foraminal Stenosis is a narrowing of the spinal canal caused by bone, ligaments, disc, or soft tissue. The prevalence of lumbar stenosis increases with age. There is no evidence that medication or physical therapy will enlarge the spinal canal and treatment with medication is used only to control pain. In some cases, we will provide a corset or brace that maintains the lumbar spine in slight flexion. Patients with central spinal stenosis usually experience the insidious onset of gradually increasing pseudoclaudication, which may be unilateral or bilateral. Examination may demonstrate a positive spinal Phalen's (sustained extension) maneuver, and there may be neurological deficits, but other mechanical signs are usually absent. Foraminal or lateral recess stenosis usually causes radicular pain that is worse with walking and standing, and is reproduced by extension. The diagnosis is confirmed by an MRI scan that shows significant central, lateral recess, or foraminal stenosis. Radicular pain can also be caused by spinal stenosis secondary to a disc protrusion narrowing the lateral recess or foramen, or both. Patients who have radicular pain caused by a disc protrusion may have a more acute onset of radicular pain which is increased with Valsalva maneuver and pain that is better rather than worse while walking. Some have leg pain provoked by a straight leg raising test. It the patient's pain can be reduced by repeated extension movement, the patient’s pain is probably caused by a disc protrusion rather then stenosis. Although most consider flexion exercises, we gently test for centralization in the initial work-up. If the patient does not have significant osteoporosis we will utilize up to 150 pounds of traction. Trigger point injections are administered if the physical examination reveals myofascial trigger points. We find that most of these patients will require spinal injections and many may eventually need surgical decompression. If neurological deficits are present, reversal is less likely and therefore we will obtain early surgical consultation.

Synovial cysts Patients with radicular pain caused by a synovial cyst have symptoms that are hard to distinguish from a lateral or paramedian disc herniation. Although the patients are usually older, the patients usually seek medical consultation because of the gradual or acute onset of buttock and leg pain caused by compression of the traversing or exiting roots at either the L4–5 or L5–SI levels. The diagnosis, however, may only be considered when patients fail to respond to a discogenic protocol. A synovial cyst is best identified on an MRI scan. Once identified, we first treat the radicular pain with NSAIDs, but transforaminal epidurals and facet injections with corticosteroids are usually required. In some cases the facet cysts can be decompressed by aspirating through the facet joint. If the cyst is large and pushing the dura centrally, the cysts can also be decompressed by directing a needle into the cyst using a translaminar approach. Some interventionist will poke many holes in the cyst in an attempt to decompress the cyst, and in some cases the cyst can be ruptured by high-volume injection. In many cases, however, the cyst is filled with thick granular debris which cannot be aspirated. Surgical excision is, however, relatively straightforward.

Spondylolisthesis Symptomatic isthmic spondylolisthesis often presents in early adulthood and is most common at L5–S1. Degenerative spondylolisthesis usually occurs at an older age and is most common at the L4–5, level. Patients present with variable histories that are not necessarily indicative of a spondylolisthesis. Physical examination is only helpful when there is a significant degree of instability, by which we mean at least a 20% slip in a thin individual or a greater slip in a heavier individual. The majority of spondylolistheses at L4–5 and L5–S1 are not unstable, as judged by lumbar flexion, neutral, and extension films while standing. When a spondylolisthesis is discovered, we usually obtain flexion–extension films, because the results may influence the physical therapy exercise regimen and instruction in body mechanics. Instability is defined as anteroposterior translation of 3 mm or greater, or tilt of one vertebra of 5 degrees or greater, on flexion–extension films. Even smaller amounts of movement, however, might influence the approach in physical therapy. When unstable, L4–5 often demonstrates increased slippage in flexion, whereas L5–S1 often demonstrates increased slippage in extension. In the absence of instability, this patient population is treated identically to the paramedian disc herniation population, with one exception. When back pain is present, particularly when there is localized tenderness on thrusting of spinous processes or palpation in the facet region, we believe there is an indication for full-dose antiinflammatory medication. When back pain is a significant symptom, we often encourage these patients to undergo facet joint injections if NSAIDs have not been successful. When there is instability on flexion–extension films, we emphasize stabilization exercises and body mechanics with a ‘neutral spine.’

SUMMARY The patient's clinical presentation and response to treatment are the most important guides to establishing diagnosis, prognosis, and treatment plan. Testing and treatment should be individualized, based on a patient's medical status, emotional state, magnitude of pain, and social circumstances, in addition to clinical presentation and response to treatment. 889

Part 3: Specific Disorders

Patients with a cauda equina syndrome or progressive neurological deficits should be emergently studied and referred to a spine surgeon if the results of studies indicate a compressive lesion. Activity modification is important in the management of paramedian HNP. The patient should avoiding sitting, bending, lifting, and twisting. There are no oral or systemic medications that have been demonstrated to alter the course of lumbar radiculopathy. Many medications can reduce pain through various mechanisms. Selective inhibitors of TNF-α may prove to be a weapon of the future that will alter the course of lumbar radiculopathy. Heat, cold, and electricity serve as adjuncts to physical therapy through their analgesic and relaxation effects. Lumbar traction is supported in physiological studies, but has not been proven to be effective in clinical trials. We are convinced that it plays a role in lumbar radiculopathy. The McKenzie approach is useful on day 1 to assist in diagnosis, establishing a prognosis, and as an initial guide for treatment. Back schools are effective in reducing the incidence of recurrence of low back pain. Trunk strengthening exercises are addressed in abundant literature in terms of their theoretical role and the evidence of trunk muscular dysfunction in patients with back disorders. There is yet no evidence attesting to the effectiveness of a specific exercise regimen in reducing lumbar radicular pain, low back pain, or preventing future disc herniations. Manual therapy may play an adjunctive role in the mobilization of spinal, sacroiliac, or hip joints, in addressing myofascial involvement, or in mobilizing adherent neural tissue. High-thrust manipulation is rarely indicated in the management of lumbar radiculopathy. Acupuncture provides temporary analgesia for some patients with lumbar radiculopathy. Taping, corsets, braces, and ergonomic aids appear to reduce symptoms in selected patients with lumbar radiculopathy. We have found trigger point injections to be effective in reducing associated myofascial pain, when physical therapy follows immediately after injections. As the patient nears completion of treatment, he or she should be counseled regarding activity modifications for work, recreation, and travel. Rehabilitation approaches and expectations vary for different specific etiologies of lumbar radiculopathy.

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81. Saal JA. The new back school prescription: stabilization training part II. Occup Med: State of the Art Reviews 1992; 7(1):33–42.

53. Ghoname E, et al. Percutaneous electrical nerve stimulation: an alternative to TENS in the management of sciatica. Pain 1999; 83:193–199. 54. Harte A, et al. The efficacy of traction for back pain: a systematic review of randomized controlled trials. Arch Phys Med Rehabil 2003; 84:1542–1553. 55. Matthews JA. Dynamic discography: a study of lumbar traction. Ann Phys Med 1968; 9:275–279. 56. Onel D, et al. Computed tomographic investigation of the effect of traction on lumbar disc herniations. Spine 1989; 14(1):82–90. 57. Nachemson A, Elstrom G. Intravital dynamic pressure measurements in lumbar disc swelling: a study of common movements, maneuvers and exercises. Scand J Rehabil Med (Suppl) 1970; 1:1–40. 58. Bridger RS, et al. Effect of lumbar traction on stature. Spine 1990; 15:522–524. 59. Berquist-Ullman M, Larsson U. Acute low back pain in industry. Acta Orthop Scand (Suppl) 1977; 170:73. 60. Hall H, Iceton JA. Back school. Clin Orthop 1983; 179:10. 61. White AH. Low back injury prevention programs at Southern Pacific Railroads. Presented to the International Society for the Study of the Lumbar Spine. Paris, France; 1981.

82. Akuthota V, Nadler S. Core strengthening. Arch Phys Med Rehabil 2004; 85(1): S86–S92. 83. Nadler SF, et al. Hip muscle and balance in low back pain in athletes: influence of core strengthening. Med Sci Sport Exerc 2002; 34:9–16. 84. Fritz JM, Erhard RE, Hagen BF. Segmental instability of the lumbar spine. Phys Ther 1998; 78:889–896. 85. Kavcic N, et al. Determining the stabilizing role of individual torso muscles during rehabilitation exercises. Spine 2004; 29(11):1254–1265. 86. Cholewicki J, et al. Intra-abdominal pressure mechanism for stabilizing the lumbar spine. J Biomech 1999; 32:13–17. 87. Gardner-Morse MG, Stokes I. The effects of abdominal muscle co-activation on lumbar spine stability. Spine 1998; 23(1):86–91. 88. Kaigle A, et al. Experimental instability in the lumbar spine. Spine 1995; 20(4):421–430. 89. Leinonen V, et al. Disc herniation-related back pain impairs feed-forward control of paraspinal muscles. Spine 2001; 26(16)E367–E372. 90. Rantanen J, et al. The lumbar multifidus muscle five years after surgery for a lumbar intervertebral disc herniation. Spine 1993; 18(5)568–574.

62. Nachemson A. The lumbar spine: an orthopedic challenge. Spine 1976; 1:59.

91. Hides J, et al. Multifidus muscle recovery is not automatic after resolution of acute, first-episode low back pain. Spine 1996; 21:2763–2769.

63. McKenzie R. The lumbar spine: mechanical diagnosis and therapy. Waikanae, NZ: Spinal Publication Ltd; 1981.

92. Arendt-Nielsen L, et al. The influence of low back pain on muscle activity and coordination during gait: a clinical and experimental study. Pain 1995; 64:231–240.

64. McKenzie RA. Manual correction of sciatic scoliosis. NZ Med J 1972; 76(484): 194–199.

93. Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain: a motor controlled evaluation of transversus abdominus. Spine 1996; 21(22):2640–2650.

65. Krag M, et al. Internal displacement and distribution from in vitro loading of human thoracic and lumbar spinal motion segments: experimental results and theoretical predictions. Spine 1987; 12(10):1001–1007. 66. Shah JS, et al. The distribution of surface strain in the cadaveric lumbar spine. J Bone Joint Surg [Br] 1979; 60(2):246–251.

94. Cholewicki J, et al. Stabilizing function of trunk flexor–extensor muscles around a neutral spine posture. Spine 1997; 22(19):2207–2212. 95. Cole A, Herring S. The low back pain handbook: a guide for the practicing clinician, 2nd edn. Philadelphia: Hanley & Belfus; 2003:453–457.

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Part 3: Specific Disorders 96. Travell JG, Simons DG. Myofascial pain and dysfunction: the trigger point manual, volume II. The lower extremities. Baltimore: Williams and Wilkins; 1992. 97. Butler D, Gifford L. The concept of adverse mechanical tension in the nervous system. Physiotherapy 1989; 75(11):622–636. 98. Brieg A, Marions O. Biomechanics of the lumbosacral nerve roots. Acta Radiologica 1963; 1:1141–1161. 99. Butler DS. The sensitive nervous system. Australia: Noigroup Publications; 2000. 100. Sunderland S. The nerve lesion in carpal tunnel syndrome. J Neurol Neurosurg Psychiatry 1976; 39:615–626.

105. Weitling J, Andary M, Holmes T, et al. Manipulation, massage and traction. In: Physical medicine and rehabilitation; principles and practice 4th edn. Philadelphia: Lippincott; 2005. 106. Longworth W, McCarthy PW. A review of research on acupuncture for the treatment of lumbar disc protrusions and associated neurological symptomatology. J Alternat Complemet Med 1997; 3(1):55–76.

101. Cole AJ, Herring SA. Low back pain: a guide for the practicing clinician. Philadelphia: Hanley & Belfus; 2003.

107. Nachemson A, Morris JM. In vivo measurement of intradiscal pressure: discometry, a method for the determination of pressure in the lower lumbar discs. J Bone Joint Surg [Am] 1964; 46:107.

102. Matthews JA, et al. Back pain and sciatica: controlled trials of manipulation, traction, sclerosant, and epidural injections. Br J Rheumatol 1987; 26:416–423.

108. Stillo JV, Stein AB, Ragnarsson KT. Low back orthoses. Phys Med Rehabil Clin N Am 1992; 3:57–94.

103. Crawford CM, Hannan RF. Management of acute lumbar disc herniation initially presenting as mechanical low back pain. J Manipul Physiol Ther 1999; 22(4): 235–244.

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104. Troyanovich SJ, et al. Low back pain in the lumbar intervertebral disc: clinical considerations for the doctor of chiropractic. J Manipul Physiol Ther 1999; 22(2): 96–104.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ ii: Lumbar Radicular Pain

CHAPTER

An Algorithmic Methodology

82

Michael J. DePalma and Curtis W. Slipman

Lumbosacral radiculopathy is defined as the neurophysiologic dysfunction of the nerve roots affecting both motor and sensory fibers in varying proportions. Signs and symptoms of motor fiber involvement include paresis and atrophy, hyporeflexia, fatigue, cramps, or fasciculations. Sensory abnormalities can range from mild distal paresthesias to anesthesia, dysesthesias, or severe pain. These painful symptoms may be the sole complaint of the patient, while in other instances motor deficits may predominate.1 Nerve root pain can appear in any anatomical area subserved by that nerve root. Hence, any region between the midline spinous processes and lower extremity digits, may be perceived as painful to the patient due to nerve root irritation. Although radicular pain can occur in the absence of overt weakness, it can be quite impairing for the patient, and can represent a challenge to the treating spine care specialist. Lumbosacral (L/S) nerve root injury can occur anywhere along its long subarachnoid course through the cauda equina within the spinal canal. Clinical clues for segmental localization are less reliable than in the cervical spine.1 The L/S nerve roots exit from the intervertebral disc space below their respective vertebral body. Hence, in the lower limb, sensory deficits may be a more reliable discriminator of the involved level than motor impairments.1 Accurate localization allows for an accurate diagnosis, and both are necessary for successful treatment.

THE ETIOLOGIES AND IMITATORS OF LUMBOSACRAL RADICULOPATHY The chief complaint of limb pain greater than axial pain typifies radicular symptomatology, but can also be present in other conditions. Sacroiliac joint dysfunction can present with gluteal and proximal lower limb pain.2–4 Piriformis syndrome, as described by Yeoman in 1928,5 represents a constellation of symptoms including limb pain and/or paresthesias with or without gluteal or lumbar pain.6–8 Intrinsic hip joint pathology, such as osteoarthritis, will present with gluteal, groin, or anteromedial thigh pain.9 Strain injuries to the hamstring musculature will cause complaints of soreness and pain in the posterior thigh. Pain in the region of the greater femoral trochanter, buttock, or lateral thigh depicts greater trochanteric pain syndrome, has a 20% prevalence in patients referred to surgical spine specialists,10 and can mimic symptoms of lumbar radiculopathy.11 Lumbosacral plexopathy or peripheral nerve entrapment, such as meralgia paresthetica, can also approximate radicular symptoms. Various spinal structures such as the intervertebral disc, dura, ligaments, or zygapophyseal joints may refer pain distally. However, the primary complaint in these instances is axial pain sometimes associated with less severe lower limb symptomatology. Since Mixter and Barr’s seminal paper in 1934,12 the intervertebral disc has widely been recognized as a cause of L/S radiculopathy. However, several other etiologies of L/S radiculopathy have been

annotated. Central or lateral canal stenosis13,14 can arise due to an array of causes: congenitally short pedicles, ligamentum flavum buckling, facet joint arthropathy, vertebral body hyperostosis, spondylolisthesis, spinal tumors, or spinal cysts. Intraspinal cysts may evolve as a consequence of the degeneration of the zygapophyseal joint,15 ligamentum flavum,16 posterior longitudinal ligament,17 dura mater,18 or chronic spondylolysis,19 and can arise from the root sheath itself.20 Diabetic patients are prone to thoracic radiculopathy,21 perhaps due to intraneural absorption of sorbitol while confined by a nonexpansile dural sheath. Extraforaminal compression by the L/S ligaments may also result in lumbar radiculopathy.22 Analyzing the various culprits responsible for L/S radicular symptoms exposes the intricate nature of the pathophysiology of L/S radiculopathy, and the difficulty in accurately diagnosing and successfully treating these painful conditions.

PATHOPHYSIOLOGY OF LUMBOSACRAL RADICULOPATHY Mixter and Barr’s landmark description in 193412 had led many spine care practitioners to suspect intervertebral disc (IVD) herniation to be causative in a variety of lumbar radicular pain syndromes. The implicit premise has been that biomechanical compression of neural elements was the sole etiologic factor leading to the manifestation of signs and symptoms.23 However, there is evidence that mechanical influence is not the sole etiologic factor.24–33 There is little correlation between the severity of radiculopathy and the size of the disc herniation.25,28,29 Resolution of symptoms after conservative treatment has been observed without a concurrent reduction in disc herniation volume.28,29 Mixter and Ayer, a year after Mixter and Barr’s hallmark paper, demonstrated that radicular pain could occur without significant disc herniation.30 However, it was not conclusive if this ‘radicular pain’ was nerve-root mediated or somatically referred from another spinal structure. It is probable that, in most instances, biomechanical injury is not the singular cause for the expression of lumbar radicular symptoms related to lumbar intervertebral disc herniation. Early observations by Lindahl and Rexed32 in 1951 established the presence of pathologic changes including inflammatory cells in nerve roots of patients suffering from sciatica. Subsequent animal studies have demonstrated autoimmune and inflammatory reactions to autogenous nucleus pulposus.34,35 The human intervertebral disc has been shown to be a potent source of phospholipase A2,31 a regulator of the inflammatory cascade which causes perineural inflammation, conduction block, axonal injury,36 and dorsal root demyelination and mechanically induced ectopic discharges in the rat animal model.37 Herniated lumbar intervertebral discs have been observed to spontaneously produce increased amounts of other potentially neurotoxic inflammatory mediators.38 A rapid transport route may exist, bridging

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the epidural space and intraneural capillaries, providing quick access for this nuclear material to spinal nerve axons.39,40 In stark contrast to the peripheral nerve, the nerve root lacks a perineurium, which provides tensile strength and a diffusion barrier.41,42 Consequently, the nerve root possesses less resilience to tension forces and chemical irritants.42 Furthermore, the epineurium, which provides mechanical cushion to resist compression, is less abundant or developed in the nerve root.42 Within the nerve root itself the fasciculi do not branch to form a plexiform pattern; instead, they run in parallel, loosely held together by connective tissue.41,42 Hence, the nerve root is not as well suited to withstand either mechanical or chemical insult as compared to a peripheral nerve. Furthermore, once the inflammatory cascade is initiated, the nerve root lymphatic system is poorly equipped to adequately clear the inflammatory mediators.42 An inflamed nerve root is thus predisposed to a chronic inflammatory reaction with invasion by fibroblasts with eventual development of intraneural fibrosis.42 Cadaveric studies have discovered a functional tethering of the nerve root to the intervertebral foramen.42,43 When an intervertebral disc herniates in a posterior or posterolateral fashion, the exiting nerve root is placed under tension and not always compressed.42 The ensuing inflammatory response sensitizes the involved nerve root, decreasing its resilience to biomechanical influences. An inflamed nerve will fire repetitively with just minor perturbations; whereas a nonirritated nerve will tolerate more vigorous manipulation without prolonged firing patterns.41,44 The length to which a nerve root must be stretched for it to incur neurophysiologic dysfunction is believed to be 10–15% of resting length.45,46 Clinically, nerve root irritability can be appreciated by elevating the involved lower limb with the knee extended, straight leg raising (SLR). Goddard and Reid43 demonstrated stretch without displacement of the nerve root upon raising the affected limb 20–30° to 70°. Since no nerve root motion is occurring, the radicular pain elicited by this maneuver is a consequence of nerve root tension.43 In asymptomatic patients this movement is nonpainful despite the same amount of tension placed on the neural elements. However, intraforaminal disc herniation or herniation in the presence of spinal stenosis may inflict a biomechanical compromise to the nerve root that may have implications for successful treatment. The ramification of this growing body of evidence supporting a biochemical paradigm is an evolution of minimally invasive therapeutic interventions. Less than 15% of L/S radiculopathies will eventually require surgical correction.47 Thus, a large proportion of cases can be successfully managed conservatively.25 Conservative care includes physical therapy, oral antiinflammatory medications, and precision intraspinal injections; yet, as interventional spine care continues to evolve, further minimally invasive interventions are being offered. Directing a successful plan of care hinges on accurately diagnosing the patient’s condition. Diagnosing L/S radiculopathy does not always create a mystery for the spine clinician. However, proficiently maneuvering through the list of differential diagnoses, utilizing evidence-based medicine, and accounting for the pharmacologic effects of injected medications requires an appropriate algorithmic approach. This systematic evaluation relies upon thorough history acquisition and physical examination, the accurate assessment of imaging studies, astute electrodiagnostic examinations, and the appropriate use of diagnostic block injections.

THE CLINICAL APPROACH TO LUMBOSACRAL RADICULOPATHY Although radicular pain is categorically defined as limb pain greater than axial pain, occasionally, a patient might report paramedian lum894

bar pain that could be perceived as back pain. However, this region of discomfort may very well represent the sole region exhibiting painful nerve root symptoms. Yet, the spine clinician must recognize the overlap of referral patterns of pain emanating from nerve root, zygapophyseal joint, intraspinal ligament, intervertebral disc, sacroiliac joint, trochanteric bursa, or the piriformis muscle, and then perform a probability analysis of which structure, or segmental level, is likely generating the symptomatology. Lumbosacral radicular symptoms commonly arise in conjunction with focal intervertebral disc pathology12 or spinal stenosis.13 Disc herniations can lead to functional stenosis and a clinical picture of neurogenic claudication. However, symptom onset associated with disc herniation commonly occurs explosively after a short stint of axial pain or symptoms, and are exacerbated by prolonged sitting or Valsalva maneuvers. Neurogenic claudication due to spinal stenosis progresses more insidiously and its symptoms are exacerbated by prolonged standing and walking. Typically, patients will report bilateral or unilateral lower limb paresthesias, weakness, fatigue, or heaviness that is absent at rest and precipitated by walking that eventually persuades them to stop and rest.48 The patient’s walking tolerance, the point at which pain forces the patient to stop and rest, is usually twice the distance at which discomfort is first felt.48 Assuming a forward stooping posture may dissipate some of the symptoms, and the capability to walk further while traveling uphill, in contrast to downhill, can discriminate between neurogenic and vascular claudication. No clinical features characteristically identify sacroiliac jointmediated pain.49 However, a history of a direct fall onto the buttock, rear-end motor vehicle accident (with the ipsilateral foot on the brake), and a fall into a hole (with one foot in the hole and the other extended outside) provides a potential mechanism of injury.49 Patients suffering from greater trochanteric pain syndrome have difficulty sleeping on the affected side,10 and may experience worsening symptoms during ambulation or squatting. Piriformis syndrome is most commonly due to overuse or trauma.8 Magnetic resonance imaging studies have suggested the presence of effacement of the fatty sciatic foramen in elite athletes diagnosed with piriformis syndrome.8 Lumbosacral plexopathy can be due to pelvic trauma, hip arthroplasty, pelvic or gastrointestinal neoplasms, and autoimmune or vascular disorders.1 Meralgia paresthetica, lateral femoral cutaneous neuropathy, can be due to compression by tight belts, corsets, seatbelts, psoas muscle tumor, or prolonged hip flexion.1 Physical examination findings can be helpful in formulating a differential diagnosis, and help guide the diagnostic work-up. Yet, the distribution of radicular pain in radiculopathy appears to be the only sensitive, thus useful, sign indicating the segmental level of disc herniation.50 In the authors’ experience at the Penn Spine Center, upper buttock radicular pain has proven to be a manifestation of L4 nerve root-mediated pain, midgluteal pain a representation of L5 root pain, and lower gluteal pain an expression of S1 root pain. Limb pain referred from the L4 nerve root may trigger painful symptoms solely in the anterior knee and/or medial ankle, while L5 nerve root pain may masquerade as isolated lateral knee and/or dorsal foot symptomatology (Fig. 82.1). Although lateral thigh and lateral calf pain characterizes L5 nerve root involvement, posterolateral thigh and posterolateral calf pain implicates S1, or L5 and S1 fiber alterations. Meticulously differentiating between lumbar pain and buttock pain is imperative as patients may refer to both synonymously, but to the interventional spine clinician each indicates different potential pain generators. Employing various dural tension maneuvers will help illuminate the pattern of pain referral into the lower limb. Straight leg raising (SLR), reproducing radicular pain between 20–30° and 70°,43 seems to be sensitive, while crossed SLR is more specific for the level of disc herniation.50 Reverse SLR with the patient prone, will assess

Section 5: Biomechanical Disorders of the Lumbar Spine

A

B

= L4 = L5 = S1

C

Fig. 82.1 Schematic representation of isolated areas of lower lumbar radicular pain. (A) Lateral view. (B) Dorsal view. (C) Ventral view.

upper lumbar nerve root fibers. Sensory impairments are less reliable and the diagnostic value of historical findings remains unclear.50 Vibratory sensation abnormalities in dermatomal distributions may be the most reliable measure of sensory disturbances.51 Repetitive motor examination maneuvers such as repetitive calf raises, will elicit subtle motor weakness not detected on static manual muscle testing. When assessing strength statically, the examiner should place the muscle at a biomechanical disadvantage to completely reveal a deficit. Typically, L2 myotomal strength is assessed by hip flexion, L3 by knee extension, L4 by ankle dorsiflexion, L5 by great toe extension, and S1 by ankle plantar flexion. Yet, an astute spine clinician must be aware of anomalous innervation patterns in transitional spinal segments. In instances of sacralization of L5, myotomal innervation patterns overlap so that an L5 radiculopathy may present clinically as L5, S1, or both. Conversely, in lumbarization of S1, innervation patterns are more discrete and clinical findings correlate more closely with the expected compromised nerve root.52

nerve conduction studies (EDX). Anesthetizing injections have been termed functional tests because patient participation is essential to identify the abolition of their typical pain complaints (see Chs 16, 17, 18, 19).53 Although these diagnostic tools have been thoroughly discussed, the following will highlight their clinical utility in evaluating L/S radiculopathy.

DIAGNOSTIC EVALUATION

Plain films of the L/S spine detail the osseous structures of the vertebral column. However, radiographs have a limited capacity to identify soft tissue abnormalities within the spinal canal. Lumbar flexion– extension views can identify gross segmental instability, which may cause L/S radiculopathy due to central or foraminal stenosis. The identification of anomalous segmentation, spondylolysis, or spondylolisthesis on plain films may increase one’s suspicion of these entities as the etiology of the spinal pain. However, further diagnostic testing is required to confirm this suspicion because these conditions are commonly encountered in the asymptomatic population. Yet, the presence of anomalous segmentation should alert the spine clinician to the possibility of atypical nerve root pain due to altered innervation patterns.52 Except for these entities or when the presence of fracture, malignancy, or infection are suggested by history, plain films are of little value in the investigation of L/S radiculopathy. At the Penn Spine Center, for the most part, the authors utilize plain films

Treatment failure may reflect an inaccurate diagnosis, ineffective treatment, or misguided intervention. Lumbosacral radicular symptoms that have not responded to conservative care or are incapacitating for the patient warrant further diagnostic studies to clarify the diagnosis and redirect treatment strategies. Accurately diagnosing the etiology of lower limb pain requires astute and thorough history gathering and physical examination, and the appropriate prescription of imaging studies, electrodiagnostic evaluation, and precision diagnostic injections. These diagnostic evaluations are appropriately divided into visual anatomic, neurophysiologic, and functional diagnostic assessments.53 Plain radiography, radionuclide imaging, myelography, computed tomography, and magnetic resonance imaging constitute the visual anatomic studies. Neurophysiologic tests include electromyography (EMG) and

Visual anatomic tests Visual anatomic tests categorically provide information about anatomy and the structural relationships among the osseous, soft tissue, and neural elements. Imaging studies help define morphology that may be causal in pain generation, but do not distinctly identify which abnormality is responsible for symptomatology in the absence of clinical information.

Plain radiography

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to assess for gross segmental instability (excessive sagittal translation, rotation, or sagittal angulation), segmentation anamolies, spondylolysis, spondylolisthesis, compression fracture, and disc height when considering percutaneous discectomy.

Myelography Myelography’s utility in diagnosing clinically significant spinal abnormalities was first investigated in 1967. Hitselberger and Witten24 observed a lumbar myelographic abnormality in 24% of 71 examinations in adults 18–76 years of age (mean, 51) without complaints of lumbar or L/S radicular pain. Although myelography has been highly sensitive in detecting a posterolateral disc protrusion in the nonoperated lumbar spine,54 its ability to reveal a central protrusion at the L5–S1 level is impaired due to this segment’s large epidural space.55 In addition, myelography is incapable of detecting a lateral disc herniation, beyond the spread of the contrast column ending at the neural foramen (termination of the dura),56 and relatively incapable of demonstrating foraminal stenosis. Myelography cannot differentiate epidural fibrosis from recurrent disc herniation or other extradural lesions in the postoperative patient, and its accuracy in this patient population has been demonstrated to be as low as 24%.57 Currently, myelography is rarely used as the sole imaging study in the work-up of L/S radiculopathy, due its limitations, except in extenuating circumstances such as severe scoliosis or metallic implants that would cause artifact on both magnetic resonance imaging (MRI) and computed tomography (CT).

Computed tomography Computed tomography is useful to delineate bony detail, which can be helpful in preoperative planning. Wiesel et al.26 found a falsepositive rate of 35.4% in 52 asymptomatic individuals undergoing computed axial tomography. In subjects less than 40 years of age, disc herniation was identified in 19.5%. In subjects over 40 years of age, 26.9% demonstrated herniated discs, 10.4% facet joint disease, and 3.4% stenosis.26 The sensitivity of CT images in identifying neurocompressive lesions has been reported to be 91%.58 In patients with L/S radiculopathy who have not undergone surgery, CT images adequately resolve disc abnormalities such as lateral and far lateral herniations, bulging annuli, ligamentum flavum hypertrophy, vacuum disc phenomenon, facet arthrosis, endplate sclerosis, and foraminal or central canal stenosis. Sagittal and coronal reconstructed sequences improve the diagnostic accuracy and should be utilized in all instances. However, the sensitivity of CT in evaluating the postoperative patient decreases to 71%.59 Hence, CT is a useful assessment tool in the evaluation of the spine patient, without previous history of spine surgery, with signs and symptoms of L/S radiculopathy, and its sensitivity approaches that of MRI, especially when performed after myelography. Contrast enhanced MRI remains the anatomic test of choice in the postoperative spine. The authors rely on CT to evaluate for etiologies of L/S radiculopathy in two circumstances. When MRI is contraindicated, such as with pacemakers, or to assess boney stenosis, multiplanar reformatted CT scan is used. In patients who have hardware in place, image artifact often impairs the ability to visualize the discs that are of concern with MRI.

Magnetic resonance imaging The sensitivity of MRI for the detection of lumbar spinal abnormalities approaches 100% and has been reported to be as high as 96% in the postoperative patient.60 Although MRI is highly sensitive, its clinical, not radiologic, specificity is lacking. Boden et al.27 found abnormalities on MRI scans of lumbar spines in 28% of asymptomatic subjects, 24% demonstrated herniated nucleus pulposus (HNP), 896

and 4% stenosis. In subjects less than 60 years old, 20% had HNP, while 57% of those over 60 years of age demonstrated HNP and stenosis, and the proportion of degenerative discs increased with advancing age.27 However, no study attempted to differentiate disc protrusions from disc extrusions until the 1994 publication by Jensen et al.33 Their work showed that 64% of 98 asymptomatic subjects had an intervertebral disc abnormality, 52% of which had a bulge at one level, 27% a protrusion, and 1% an extrusion.33 The presence of intervertebral disc extrusion may be significant and causally related to nerve root injury.25,29,61 Determining the clinical significance of abnormalities discovered on MR imaging has led to the increased use of diagnostic injection procedures in this patient population.53,62–68 The authors’ algorithmic approach to L/S radiculopathy involves the judicious use of precision, fluoroscopically guided diagnostic spinal injections when necessary to better elucidate the level of clinically relevant pathology.

Neurophysiologic evaluation Electrodiagnostic medicine allows the physician to assess the neurophysiologic correlate of anatomical findings, and is an extension of the physical examination.69 If imaging studies corroborate the physician’s clinical impression, accurate treatment can be instituted. If imaging studies are equivocal, or the clinical findings are nondiagnostic, electrodiagnostic evaluations are pursued. Motor nerve conduction studies provide prognostic information regarding the recovery of motor function. The differential diagnosis for foot drop includes L5 radiculopathy, peroneal neuropathy at the fibular head, sciatic neuropathy involving the peroneal division, and alpha motor neuron disease. Although a thorough physical examination will typically detect a myotomal pattern rather than peripheral nerve pattern of weakness, the needle electrode examination can verify the diagnosis. For example, a physiatrist was consulted to evaluate an inpatient psychiatric patient with a chief complaint of isolated lateral ankle pain seemingly confined to the lateral malleolus. Plain radiography and a subsequent MRI of the foot and ankle were negative for osseous or soft tissue injury. Physical examination revealed subtle ankle inversion and great toe dorsiflexion weakness. Nerve conduction studies were normal, but electromyography revealed mild muscle membrane irritability in the lower lumbar paraspinals, and increased recruitment frequencies in the tibialis anterior, extensor hallicus longus, and tensor fascia lata of normal-appearing motor unit potentials. A follow-up lumbar spine MRI demonstrated a focal disc protrusion at L4–5 dorsally displacing the traversing L5 nerve root. The patient responded to conservative treatment, comprised of L/S stabilization, core conditioning, and oral antiinflammatory medications, once it was correctly directed at the accurate diagnosis. Similarly, in diabetic patients with preexisting peripheral neuropathy and a new complaint of anterior thigh pain, an electrodiagnostic study can detect a superimposed radiculopathy versus diabetic amyotrophy or mononeuropathy1 Needle electrode examination will characteristically detect acute membrane irritability in proximal limb muscles of a myotomal distribution or in the muscles innervated by the femoral nerve, respectively, in addition to the more chronic membrane irritability and motor unit potential changes in the distally sampled muscles due to the underlying metabolic peripheral neuropathy. Information gathered during the electrodiagnostic evaluation is indispensable in shaping an effective treatment plan. In a diabetic patient, a femoral mononeuropathy will respond to tighter glycemic control,1 which differs from the treatment protocol already mentioned, directed at an L5 radiculopathy. Many clinicians do not appreciate the value of electrodiagnostic medicine in evaluating and treating L/S radiculopathy. A variety of subtle abnormalities can be detected by the astute electrodiagnostician from the onset of nerve root pain. If weakness is clinically

Section 5: Biomechanical Disorders of the Lumbar Spine

apparent, an increased recruitment frequency will be noticed in the affected muscles upon minimal contraction.70 Within 1–3 weeks, early polyphasic motor unit potentials can be present and may represent ephaptic activation of neighboring axons adjacent to volitionally activated axons.71 Seven to eight days after the onset of radicular symptoms, positive sharp waves can be evoked in the corresponding deep paraspinal musculature,72,73 and these may be the only observed abnormal findings in 30% L/S radiculopathy cases.72 If so, the Hreflex measurement, the electrical correlate of the Achilles muscle stretch reflex, can differentiate between an L5 and an S1 radiculopathy.74 An asymmetry of 1 msec or greater is significant for sideto-side difference,75 and can be present from the onset of symptoms. By 2 weeks after symptom onset, fibrillation potentials may be present in the paraspinal muscles and positive sharp waves in the affected proximal limb muscles.72 Closer to 3 weeks after symptom onset, proximal and distal muscles of the affected myotome will show abnormalities to varying degrees.72 The value of electrodiagnostic medicine in diagnosing L/S radiculopathy has been well established in the literature since 1950.72,76 More recently, its prognostic value has been well validated.72,73 In 1971, Johnson and Melvin’s work was published addressing the clinical management of L/S radiculopathy.72 In a review of 314 cases, 170 electrodiagnostic studies were normal and 111 abnormal in patients presenting with L/S radicular signs and symptoms. After 3 days, only neurapraxic fibers will conduct distal to the affected nerve root. In contrast, wallerian degeneration due to axonotmesis will result in a decrement of the evoked compound muscle action potential (CMAP) amplitude.72,73 The area of this CMAP amplitude can be compared to that of the identical contralateral muscle. If the affected CMAP amplitude of the evoked potential is greater than 50% of the contralateral muscle, motor function recovers with conservative care.72,73 After 14 days, if little spontaneous activity is noticed compared to the amount of clinical weakness and there is less than 10–15% decrement in the CMAP amplitude, an accurate conclusion is that the motor fibers are neurapraxic and recoverable rather than irreversibly damaged.72,73 Johnson and Melvin also witnessed the improvement in SLR concurrent with the reduction in limb pain, and cautioned against using pain alone to guide treatment differently from that supported by the electromyography findings.72 Seventy-five percent of 100 patients treated conservatively with L/S stabilization, oral antiinflammatory medications (four with oral steroids), and restricted bed rest achieved significant reduction in their symptoms allowing return to light duty by 3 months from onset of treatment.73 Twenty-five of these patients returned to this level of activity by 1 month, and all patients were treated within 3 weeks of onset of their symptoms.73 Concurrent with their clinical improvement was the resolution of the electrodiagnostic abnormalities.73 Johnson and Melvin’s conclusion was that electrodiagnostic evaluations help diagnose L/S radiculopathy, and then semiquantitatively assess the degree of reversible motor axonal injury.72 If L/S radiculopathy is diagnosed early and effectively treated with conservative measures, 95% of patients will adequately heal.73 Between 45% and 54%72,77 of L/S radiculopathies may not demonstrate electrodiagnostic abnormalities, and this proportion varies depending on the skill of the electrodiagnostician. In a study of both cervical and L/S radiculopathy, Nardin et al.77 found that electrodiagnostic and MRI findings agree in 60% of patients with a clinical presentation of radiculopathy; however, only one study was positive in 40% of patients. The probability of at least one abnormal study is positively correlated with the presence of neurologic signs on physical examination.77 The authors concluded that their results suggest a complementary relationship exists between MRI and electrodiagnostic studies in diagnosing L/S radiculopathy.77 It is possible that this

60% is an underestimation if subtle electromyographic findings are not detected. In a study of 170 L/S radiculopathy patients, Lauder et al.69 found that 15–18% of subjects had abnormal electrodiagnostic examinations despite normal physical examinations, and the latter was better than symptomatology at predicting abnormalities in the former. If clinical weakness is present, and this may only be appreciated on repetitive testing as an endurance deficit, motor unit recruitment changes will be present despite the chronology of symptoms. Early polyphasic motor unit potentials and H-reflex asymmetry can also be relied upon before the appearance of membrane irritability to confirm clinical suspicion of L/S radiculopathy. Consequently, electrodiagnostic data can be invaluable to better elucidate the significance of anatomical abnormality on advanced imaging, and is a reasonable and appropriate diagnostic test subsequent to equivocal imaging and clinical findings.

Functional diagnostic tests If the electrodiagnostic testing is inconclusive, advanced imaging demonstrates multiple abnormalities or no corroborative abnormality, fluoroscopically guided, diagnostic selective nerve blocks are performed to elucidate the level of pain generation, and to direct invasive therapeutic measures, whether they are interventional or surgical.53

Diagnostic selective nerve root block The rudimentary conviction supporting the role of a diagnostic block is that anesthetizing a structure will relieve symptoms if that structure is responsible for those symptoms.53 The accuracy of diagnostic selective nerve root blocks (SNRBs) depends upon the selective anesthetization of the targeted nerve root. In achieving nerve root block, neighboring structures must be avoided to prevent a false-positive response. As already mentioned, structures other than the lumbar nerve root can be responsible for painful lower limb symptoms. Other structures such as the intervertebral disc, posterior longitudinal ligament, dura, zygapophyseal joint, and sacroiliac joint are known to cause lower limb symptoms mimicking radiculopathy. Kellegren78 was first to establish pain referral patterns from non-neural spinal structures when he observed lower limb symptoms upon stimulation of the axial and limb muscle, tendon, fascia, and periosteum. Although Kellegren demonstrated a dermatomal referral pattern with stimulation of spinous process periosteum, Kuslich et al.79 found that stimulation of the intervertebral disc anulus, longitudinal ligament, and zygapophyseal joint provoked a nondermatomal referral pattern. Subtle similarity between nerve root-mediated pain and the somatic referral from a non-neural structure has significant clinical ramifications. The astute spine interventionist will be able to discern between the two scenarios to enact a successful treatment regimen. The literature does not provide evidence of pathognomonic historical features, or physical examination or radiologic findings to identify the intervertebral disc,80 facet joint, or sacroiliac joint48,81–84 as the etiology of pain referred to the lower limb. Rather, there is support48,82–85 for the use of anesthetic block of the suspected joint as a valid diagnostic tool. If a diagnostic SNRB is negative in a patient with atypical radicular symptoms or in a patient without a corroborative lesion on visual anatomic studies, an alternate sclerotomal referral source ought to be pursued.53 Nerve root involvement itself may refer pain in an atypical, nondermatomal pattern. Slipman et al.86 demonstrated that mechanical stimulation of a cervical nerve root frequently produced symptoms outside of the classic dermatome, in a dynatomal pattern, for that nerve root. Similar referral patterns may arise from the lumbar spine. For example, the furcal nerve is a separate nerve root with its own 897

Part 3: Specific Disorders

Specificity of a test is the ratio of true negatives divided by the sum of true negatives and false positives, and reflects the probability of a test screening negative in the absence of disease. The specificity of diagnostic SNRBs relies upon the instillation of an anesthetic agent selectively adjacent to the appropriate nerve root without overflow onto neighboring structures or neural elements. The medial branch of the dorsal primary ramus, which provides afferent sensory information to the central nervous system, travels within a few millimeters of the nerve root exiting its foramen.89 The sinuvertebral nerve is a recurrent sensory nerve that innervates the dura and posterior longitudinal ligament traveling back through the foramen after branching from the spinal nerve.89 The inadvertent anesthetization of these sensory nerves can result in a false-positive SNRB in the presence of a painful dural sheath, posterior longitudinal ligament, or zygapophyseal joint. Precise and accurate technique is, therefore, indispensable in achieving adequate specificity (Figs 82.2, 82.3). The specificity of diagnostic SNRBs ranges 87–100%.57,65,67,68,90,91 In 1973, Schutz and colleagues found that 13 of 15 patients (87%) with a positive diagnostic SNRB had a corroborative lesion revealed

during surgery.91 However, this retrospective study did not provide information regarding postsurgical outcomes. A year later, Krempen and Smith90 reported the surgical results of 16 failed back surgery patients who had both a positive diagnostic SNRB and a corroborative lesion. All 16 patients had previous laminectomies or laminectomies and fusions, and all experienced good or excellent relief of their lower limb pain. In 1985, Haueisen and coworkers57 retrospectively analyzed SNRB, electromyography, and myelography results in 55 (57% failed back surgery patients) patients who had positive diagnostic SNRBs. Surgical confirmation of a corroborative lesion was demonstrated in 94% of patients. Dooley et al., in 1988, retrospectively evaluated the responses to diagnostic SNRB and surgical outcomes in 46 patients (51.6% failed back surgery patients).65 Forty-four of 46 patients in whom the diagnostic SNRB initially provoked concordant lower limb pain with subsequent, complete relief after the instillation of local anesthetic, had surgical confirmation of corroborative pathology (one patient did not undergo surgery). Interestingly, 9 of 9 patients (100%) with herniated discs experienced complete relief of limb pain, 14 of 17 (82%) with stenosis described complete symptom resolution, the remaining 19 patients had either arachnoiditis or epidural fibrosis, with 8% of the former and 71% of the latter obtaining postsurgical symptom relief. In 1990, Stanley et al.68 conducted a prospective study in which 50 consecutive radiculopathy patients underwent diagnostic SNRB. Nineteen of 20 patients who experienced concordant limb pain during nerve root stimulation and subsequent relief following local anesthetic infiltration underwent surgical intervention. Eighteen (95%) had corroborative lesions identified intraoperatively, of which lateral canal stenosis was the predominant abnormality. The authors did not comment on surgical outcomes. In 1993, van Akkerveeken67 recorded positive diagnostic SNRBs after symptom provocation with eventual relief after injection of local anesthetic. Of those patients with complete relief of limb pain, surgery confirmed a lesion in 100%. Van Akkerveeken observed a specificity of 90% when negative diagnostic SNRBs were performed at levels free of radiologic evidence of neurocompressive lesions, and a positive predictive value of 95%. However, the positive predictive value may actually fall anywhere from 70% to 95% due to a number of his patients refusing surgical intervention.

Fig. 82.2 Fluoroscopic image of a right L5 diagnostic SNRB. Notice the thin and precise outline of the exiting right L5 nerve root. This contrast pattern was obtained by positioning the needle tip inferior and lateral to the midpoint of the L5 pedicle as the exiting nerve obliquely traverses the L5 foramen.

Fig. 82.3 Fluoroscopic image of a right L5 transforaminal epidural steroid injection. In contrast to Fig. 82.2, more epidural spread of contrast was achieved in this injection. A more ventral placement of the needle tip into the neural foramen introduced the contrast medium more superiorly and medially into the epidural space.

dorsal root ganglion, and most commonly travels with the L4 nerve root at the L4–5 level. However, it may also accompany the L3 and L5 nerve roots through their respective foramina.53 After exiting the foramen, this anomalous root merges with the lumbosacral plexus, the obturator nerve, or the femoral nerve. Moriishi et al. observed intersegmental anastomoses in the lumbar spine in 20% and 5% of the dorsal and ventral nerve roots, respectively.87 However, extradural anomalous nerve roots may have greater clinical significance.88 For example, in the instance of a type 2B nerve root anomaly, two roots exit via one foramen, decreasing their resilience to withstand a mass lesion, and obscuring their clinical expression.88 Hence, L/S radicular pain may present with dynatomal patterns in a similar fashion as the patients studied by Slipman. Consequently, radicular involvement at one level may manifest as unusual distribution of symptomatology. Nonetheless, a diagnostic SNRB can reliably detect the level of pathology despite an atypical symptom complex.53,62–68

Utility of diagnostic selective nerve root block

898

Section 5: Biomechanical Disorders of the Lumbar Spine

The probability of a true-positive test result in the presence of disease reflects the test’s sensitivity. The sensitivity of diagnostic SNRBs has not been as rigorously studied. The diagnostic utility of a clinical test requires that this test be capable of detecting disease at a rate equal to or higher than other available tests.53 Van Akkerveeken67 recorded a sensitivity of 100% for diagnostic SNRBs. Haueisen and colleagues’57 retrospective study compared the sensitivity of diagnostic SNRB to myelography and electromyography, and observed 99% sensitivity for diagnostic SNRBs in contrast to a rate of correct identification of 24% and 38% for myelography and electromyography, respectively. However, the article did not disclose the authors’ criteria for a positive (or negative) electrodiagnostic study. Regardless, if the sensory afferent axon fibers are primarily affected, an EMG study may not be able to indicate the segment involved. However, in the case of S1 involvement, H-reflexes will reflect sensory fiber dysfunction in the absence of motor fiber injury. Since the inception of MRI, this diagnostic modality has proven to be very sensitive in depicting spinal abnormalities.27,33 Yet, determining the clinical significance of these imaged abnormalities requires a complementary diagnostic test of high specificity. Diagnostic SNRBs have great value in verifying a given MRI abnormality as the pain generator when the patient’s symptoms are in conflict with the MRI findings, or in the presence of more than one MRI abnormality.66,67 Although most available studies antedate the routine use of MRI, several studies have investigated the role of diagnostic SNRB in complex spine cases. As early as 1971, Macnab62 demonstrated the value of diagnostic SNRBs in the preoperative evaluation of patients with negative imaging studies despite clinical signs of nerve root irritation. In 1988, Kikuchi and Hasue92 correlated the results of myelography and SNRB with surgical findings and outcomes. Eighty-six out of 119 treated patients underwent surgery and experienced complete resolution of their limb symptoms. Although myelography illustrated the involved segment, contrast patterns during SNRB more accurately localized the abnormal area. Thus, SNRB was capable of identifying a single level of symptomatic root compression in light of imaging and symptoms suggesting multilevel pathology. Decompressive surgical intervention was then limited to the level involved. White93 briefly discussed the utility of preoperative diagnostic SNRB in his 1983 article on diagnostic injections. He supported presurgical diagnostic SNRB as a more precise technique than caudal or interlaminar approaches, and useful in patients with equivocal visual anatomic findings. Herron,66 in his 1989 article, retrospectively examined the utility of diagnostic SNRB in selecting patients for surgery after other diagnostic testing – myelography, CT, EMG, and MRI – were found to be equivocal. He found diagnostic SNRBs to be useful in identifying previously undetected disc herniations, the symptomatic level in multilevel disc herniations, the primary pain generator in ‘spine hip syndrome,’ root irritation in spondylolisthesis, the symptomatic level in multilevel stenosis, and the symptomatic root in patients with postoperative fibrosis. However, Herron did not use contrast media to confirm needle location; rather, he relied on concordant symptom provocation during needle placement and 75% postinjection reduction of the patients typical pain. This technique has more important ramifications regarding specificity as compared to sensitivity, however. Stanley et al.68 proposed that diagnostic SNRB is also useful in identifying the symptomatic level in patients with anomalous spinal segmentation. When performed by well-trained interventional spine physicians, major complications are extremely rare. Major complications related to lumbar SNRB including respiratory and cardiac arrest, seizure, infection, nerve root trauma with permanent injury, dural puncture, perforation of viscous and/or vascular structures, broken needles, and

even death have rarely been reported. The potential benefit to the patient must be weighed against these known risks. The incidence of both major and minor complications has been extensively studied. Two large studies94,95 found the incidence of major complications, related to transforaminal epidural steroid injections, to be zero, and the incidence of minor complications (transient nonpositional headache, increased lumbar or limb pain, or vasovagal reaction) was 9.6% per injection.95 Diagnostic SNRBs play an integral role in evaluating patients who present with painful L/S radicular symptoms. In trained hands, these minimally invasive procedures are safe, and provide valuable information that may not be available from other diagnostic tests. The evidence supporting this conviction, however, is not definitive. All the above-mentioned studies were retrospective, except for Stanley’s, which was prospective, but did not report outcomes. The authors’ experience at the Penn Spine Center, however, has been that diagnostic SNRBs, when performed meticulously, are safe, reliable, and useful to determine which specific nerve root is, or is not, involved.

Extraspinal axial diagnostic injections Minimally invasive diagnostic injections can also be utilized to evaluate other etiologies of lower limb pain in the differential diagnosis for lumbar radicular pain. Lower limb pain referred from the sacroiliac joint can be confirmed by diagnostic intra-articular anesthetic injections.84,96 Schwarzer et al. diagnosed sacroiliac joint (SIJ) pain with single intra-articular injections of anesthetic and found an incidence ranging from 13% to 30% in low back pain sufferers.96 Maigne et al. observed a 35% prevalence rate in 54 subjects of SIJ pain employing a single block of short-acting anesthetic.84 However, only 10 (18.5% of the cohort) of these 19 responders had a positive response to a longer-acting anesthetic. Thus, SIJ-mediated pain must be part of the differential diagnosis in a patient complaining of gluteal and lower limb pain with negative spinal imaging and electrodiagnostic testing. More importantly, a false-positive response of up to 47.4% may dilute the sensitivity of single diagnostic SIJ blocks. Therefore, a double block paradigm may be necessary to produce accurate information to diagnose SIJ-mediated pain. However, further prospective studies are required to uphold this presumption. The diagnosis of piriformis syndrome is one of exclusion. Only after negative spinal imaging and electrodiagnostic evaluation for radiculopathy, reproduction of concordant limb symptoms with percutaneous, intrarectal, or intrapelvic pressure should the spine clinician suspect piriformis syndrome.7 The modified H-reflex, as described by Fishman and Zybert6 may not be a reliable electrodiagnostic tool to evaluate for piriformis syndrome. Slipman et al.7 calculated a positive predictive value of 33% in a small study with stringent inclusion criteria. Symptom relief with injection of the piriformis muscle is considered to be diagnostic of this disorder,7,98,98 and these authors use a symptom reduction of 80% to define a positive injection. Intrinsic hip pathology can mimic upper lumbar radicular pain or somatically referred pain from the lumbar intervertebral discs.99 Faraj et al. retrospectively evaluated responses to diagnostic intra-articular hip injections in 47 patients with radiographically confirmed hip osteoarthritis.9 Twenty-four patients had a positive diagnostic block response and subsequently experienced pain relief after total hip replacement. Three out of the 23 nonresponders eventually gained pain relief after total hip arthroplasty 2 years after diagnostic injection. The authors concluded that intra-articular hip injections of local anesthetic are valuable diagnostic aids, and calculated a sensitivity of 88% and a specificity of 100%. Diagnostic intra-articular hip injections can be employed reliably to differentiate intrinsic hip joint pain from spinal pain. Intra-articular 899

Part 3: Specific Disorders

diagnostic SIJ, and intramuscular diagnostic piriformis injections are probably useful in evaluating these structures as the source of referred lower limb pain. Yet, these functional diagnostic tests must be appropriately pursued to confirm one’s clinical suspicion and not relied upon solely to determine the source of a patient’s pain.

AN ALGORITHMIC APPROACH The spine clinician’s methodology to accurately diagnose and treat a patient presenting with L/S radiculopathy should rely upon evidencebased medicine. At the Penn Spine Center, the authors’ algorithmic approach to L/S radicular symptoms utilizes available evidence to properly diagnose and direct an appropriate plan of care to expeditiously return the patient to his or her prior level of function. If clinical and advanced imaging findings do not correlate, or if the clinical impression is not specific for monosegmental involvement, an electrodiagnostic evaluation is performed. Electrodiagnostic studies are completed as a functional correlate to the anatomic studies, and to aid in prognosis, as previously outlined. Nerve conduction studies can confirm the presence of an underlying peripheral neuropathy, as well as a peripheral entrapment neuropathy including meralgica paresthetica, and peroneal neuropathy at the fibular head, L/S plexopathy, S1 radiculopathy (H-reflex), and piriformis syndrome (modified H-reflex). The CMAP amplitude of the weakest muscle will reflect the remaining viable axons, help differentiate neurapraxia from axonotmesis, and aid in prognosis. Electromyography assesses the integrity of the motor unit fibers and will help differentiate whether plexopathy, alpha motor neuron disease, diabetic amyotrophy, peripheral neuropathy, entrapment neuropathy, and radiculopathy-provided motor fiber axons are involved. Subsequent nerve conduction and electromyography studies can be performed to semiquantitatively assess the progression or improvement of the neurologic condition. If the electrodiagnostic evaluation conclusively demonstrates L/S radiculopathy at the segmental level of structural disease indicated by advanced imaging, therapeutic interventions are prescribed. Alternate diagnoses are similarly treated if diagnosed by electrodiagnostic examination. If the electrodiagnostic testing is negative or inconclusive, diagnostic blocks are employed to confirm the clinical impression, and to maximize therapeutic interventions. A diagnostic SNRB is performed at the level of suspicion substantiated by the history and physical examination. However, if advanced imaging and electrodiagnostics are negative, and history and physical examination are supportive, diagnostic blocks of other structures are performed such as the sacroiliac joint, piriformis muscle, hip joint, or trochanteric bursa. In performing a diagnostic SNRB at the Penn Spine Center, the authors use 2% preservative-free xylocaine and define a positive block as an 80% reduction of the preinjection visual analog scale (VAS) rating. A reduction of less than 80% may require the patient to undergo a second diagnostic SNRB with 4% xylocaine if radiculopathy is a firm clinical impression. Since 4% xylocaine does not come preservative free, the authors are particularly cautious about the pattern of contrast spread. If there is any suspicion the injected agents could reach the epidural space, the needle is repositioned until a safe flow is assured. Relying on precision spinal injections to verify the pain generator is appropriate as therapeutic injections probably have distant systemic effects. Thus, if a selective nerve root glucocorticoid injection is moderately successful for a short period of time, the question still remains unanswered: was this effect due to systemic absorption after inaccurate deposition, or did the pathology simply not respond to the appropriately placed anti-inflammatory agent? This decision-making process is more crucial when evaluating the postsurgical patient suffering from recurrent symptomatology. Utilizing this algorithmic approach 900

(Fig. 82.4) at the Penn Spine Center, the authors have been able to accurately diagnose 94.4% of patients presenting with recurrent lumbar and/or radicular symptoms after lumbar surgery.100 Patients presenting with signs or symptoms of L/S radiculopathy undergo a thorough patient–physician interview and physical examination. Important historical cues include the onset and duration of symptomatology, as well as exacerbating and alleviating factors. Acute onset of explosive limb pain is suggestive of an acute intervertebral disc herniation, and often may be preceded by a short period of midline, axial lumbar pain. In contrast, gradual onset of limb pain may be secondary to nerve root irritation due to degenerative disc disease, intraspinal cysts, facet joint arthopathy/synovitis, tumor, infection, or, in some cases, acute disc herniation. A shorter duration of symptoms, less than 4–6 weeks, may suggest a relatively acute to subacute inflammatory process that may be amenable to antiinflammatory medications. More chronic symptoms, longer than 3–6 months, may still respond to such measures, or may reflect those cases that were destined to fail conservative care, thus requiring surgical correction. Assessing the exact location of limb pain can be difficult as it requires effective communication, and the patient may not be able to articulate this precise information. Evoking referred pain patterns during dural tension maneuvers can be an effective measure to verify a patient’s exact complaint. Eliciting the exacerbating and alleviating factors can also be difficult but must be obtained to better validate advanced imaging findings when multiple abnormalities are discovered, and to better treat the patient’s condition. Activities that increase subarachnoid pressure such as sitting, squatting, coughing, sneezing, Valsalva, lifting, and bending forward will precipitate symptoms due to a disc herniation. In such instances, symptoms can be eased by lying supine or in the lateral decubitus position, changing positions, and ambulation. In contrast, stenosis-related L/S radiculopathy, neurogenic claudication, is triggered by standing, walking (especially downhill), lying supine, and can be reduced by leaning forward or sitting, but prolonged sitting can separately aggravate the symptoms. Vascular claudication should be differentiated from stenosis-related symptoms, as treatment obviously varies. Lower limb pain precipitated by exercise and not relieved by forward flexion, sometimes associated with resting foot pain, warrants a vascular work-up. Red flags such as nocturnal pain worse with recumbency, recent weight loss, history of prior cancer, and immunosuppression must alert the spine care professional to the possibility of tumor or infection. Typifying the behavior of the patient’s L/S radicular symptoms helps categorize a diagnosis allowing the extraction of more useful information from imaging studies, appropriately direct electrodiagnostic studies, and more effective treatment of the patient’s ailment. Examination of the patient serves several purposes: to exclude long-tract signs, assess weakness patterns, evaluate propensity for consequential injury due to weakness, record provocative maneuvers, gauge legitimacy of complaints, and focus the differential diagnoses. Upper motor neuron signs indicate central nervous system involvement, thus redirecting imaging studies toward the remaining neural axis as deemed by other examination findings. For example, cervical and perhaps intracranial imaging might be indicated in the presence of upper limb motor neuron signs. Myotomal deficits should be discerned from the weakness patterns of plexopathy, neuropathy, myopathy, or myelopathy. Again, such findings will result in different imaging studies. If a myotomal deficit is identified, its functional ramifications must be considered parallel to diagnostic and treatment interventions. A patient with a significant foot drop, for example, may require an ankle–foot orthosis to restore safe and effective gait, and prevent soft tissue injury or a fall. Recording dural tension signs such as the angle at which straight leg raising is positive, provides a baseline for comparison to follow clinical improvement. Subsequent

Section 5: Biomechanical Disorders of the Lumbar Spine Radiculopathy 2° HNP SXs = Signs and symptoms Th = Therapeutic SNRB = Selective Nerve Root Block PD = Percutaneous Discectomy D/C = Discharge

MRI (CT if MRI contraindicated)

C) Corroborative IVD extrusion/ sequestration

B) Corroborative IVD protrusion

pain incapacitating, work, ADLs disrupted

PD/Th SNRB

pain moderate w/o disrupting work ADLs

SXs incapacitating

SXs moderate

Th SNRB × 3–4

PT, NSAID

Physical therapy, NSAIDs, monitor progress

PT, NSAID

SXs SXs improve persist/progress SXs improve

SXs SXs improve progress

Electrodiagnostic evaluation

Conclusive of radiculopathy

Physical therapy, NSAIDs

SXs persist

D) Negative for corroborative HNP

SXs persist/ progress

Th SNRB x 3-4

SXs improve

SXs persist/ progress

D/C

Th SNRB × 3–4

Surgery

SXs incapacitating

SXs moderate

Th SNRB, PT, NSAID

PT, NSAID

Inconclusive for radiculopathy

DX SNRB clinically affected level

positive

negative

D/C PD SXs persist Repeat SNRB × 2

D/C

Surgery

Surgery

D/C

Surgery

SXs persist

Improvement

Th SNRB Corroborative IVD injury = IVD injury @ segmental level suggested by pain distribution, myotomal deficit, or reflex changes

Re-evaluate MRI +/– new imaging to evaluate missed diagnosis

MRI pelvis

Positive pursue W/V

Repeat DX SNRB 4%

D/C

Negative

A

Negative

Positive

Somatically referred

Fig. 82.4 A set of diagnostic algorithms to guide the clinical approach to the patient with a chief complaint of lower limb pain. (A) Algorithm for radiculopathy due to disc herniation. (B,C) Algorithms for central spinal canal stenosis, congenital and acquired, related root injury. (D) Algorithm for radiculopathy due to lateral canal, foraminal, and extraforaminal stenosis. (E) Algorithm for postoperative radiculopathy.

901

Part 3: Specific Disorders Radiculopathy 2° central spinal stenosis (neurogenic claudication)

MRI (CT if MRI contraindicated)

A) Congenital

Acquired

Multiple segments stenotic

Corroborative segment stenotic

EDX* evaluation Pain lessens minimally when sitting and is incapacitating

Pain mild− moderate, but patient co’s lower limb fatigue, cramping w/ambulation

Pain relieved by sitting

Negative for nerve root injury

PT, NSAID, avoid extension activities

Surgery EDX evaluation

One segment involved [refer to #]

Surgery

DX SNRB @ indicated level

Evidence of chronic, remote denervation

Improvement Evidence of acute or chronic changes (ongoing injury) D/C

Th SNRB × 4 @ involved levels

Improvement

SXs persist

D/C

Surgery

SXs persist Negative

Th SNRB × 4 @ indicated levels bilaterally starting on more painful side

Surgery

Superimposed central Consider somatic HNP by MRI referral PD/Th SNRB @ this level

Improvement

SXs persist SXs persist

D/C

Improvement

Surgery D/C

Corroborative stenotic segment B Fig. 82.4—Cont’d

902

=

Stenosis @ segment clinically indicated by distribution of pain, myotomal deficit, or reflex changes

Multiple roots involved

Repeat Th SNRB x 3

Positive (relieves all limb pain) [refer to #]

Consider alternate level

Section 5: Biomechanical Disorders of the Lumbar Spine Acquired

Facet joint hypertrophy/ Ligamentum flavum Hypertrophy

Degenerative spondylolisthesis

Flexion/extension L/S X-rays

Instability (>4.5 mm translation, >15° angulation)

Flexion/extension X-rays

No gross movement

Flexion-biased L/S stabilization, core conditioning, NSAID

Surgery

Instability

No gross movement [refer to A)]

Surgery

SXs persist

SXs improve

D/C Involved segment not clearly indicated clinically

Th SNRB @ level indicated by pain distribution, myotomal deficit, or reflex change

EDX evaluation [refer to *] Improvement

C

D/C

examinations must verify this angle, and that the weakness is stable or improving. If weakness continues to progress, surgery may be indicated. If pain is minimal, and the patient’s chief complaint is weakness and sensory changes, a neurocompressive lesion might be illuminated by advanced imaging. Under such circumstances, decompressive surgical intervention may be necessary to successfully treat the condition. As has already been detailed, magnetic resonance imaging is very sensitive in detecting spinal abnormalities. Plain radiography can be useful to evaluate osseous alignment. Thus, the authors routinely order both imaging modalities to initiate the work-up of the L/S radiculopathy patient. Lateral flexion–extension views evaluate for segmental instability of levels of degenerative facet joint disease. If gross instability, >4.5 mm of translation at L5–S1 or >4 mm at higher lumber levels; or >15 degrees of sagittal angulation; or >2 degress of rotation is present, surgical care is prescribed. Intervertebral disc

SXs persist

Surgery

Fig. 82.4—Cont’d

height can be assessed prior to performing intradiscal procedures, such as percutaneous discectomy. If MRI displays a corroborative lesion such as HNP, or central or lateral canal stenosis, affecting the clinically suspected nerve root, therapeutic interventions are initiated. The authors employ a tiered treatment approach when addressing L/S radiculopathy. The initial step involves prescribing physical therapy (PT) with passive modalities for pain relief and graduated exercises that do not increase extremity complaints, oral nonsteroidal antiinflammatory medications (COX-2-specific agents with celebrex 100 mg b.i.d. as drug of choice), avoidance of aggravating activities, and a soft L/S corset if needed. Passive modalities such as cryotherapy, heat, and transcutaneous electrical nerve stimulation help modulate the patient’s pain to allow participation in PT. Lumbosacral stabilization and core conditioning exercises are prescribed in PT to stabilize the L/S spine. William’s flexion-biased L/S stabilization is utilized in 903

Part 3: Specific Disorders Radialopathy 2°

Lateral recess stenosis

Foraminal stenosis

Extraforaminal stenosis

Explosive onset

Gradual onset

MRI

MRI

$ Corroborative IVD extrusion/ sequestration

Corroborative IVD protrusion

Intraspinal cyst No evidence [may present with decreased of HNP sitting or standing tolerance]

[refer to C]

Emanating from chronic spondylolysis

Flex/Ext. X-rays

Emanating from posterior longitudinal ligament, duramater, IVD

[ refer to D ]

No instability

SXs moderate

SXs severe

Improvement

Compression by lumbosacral ligaments [refer to $]

SXs persist

D/C SXs moderate and not disruptive

SXs severe & disruptive

L/S stabilization, NSAID

Improvement L/S stabilization, NSAID D/C

SXs improve

SXs persist

D/C

Th SNRB × 3–4, PT, NSAID

SXs Th SNRB × 3–4, improve PT, NSAID

SXs persist

DC

Surgery

SXs persist

Th SNRB x 3-4, PT, NSAID

Surgery Improvement

SXs persist

D/C

Cyst aspiration

D Fig. 82.4—Cont’d

Surgery

Cyst puncture

Surgery

Apposition of transverse process to sacral ala [refer to $]

Th SNRB × 3–4, PT, NSAID

Surgery

904

Exit-zone stenosis d/t hyperostosis of vertebral body endplates [refer to $]

SXs severe

SXs moderate and do not disrupt work/ ADL’s

Flexion-biased L/S stabilisation, core conditioning, NSAID Instability

Loss of intervertebral canal fat, compression of exiting root, loss of disc height [refer to $]

EDX evaluation

[ refer to B ]

Emanating from arthritic facet joint

FJA/ Ligamentum flavum hypertrophy

May or may not present as neurogenic claudication

Section 5: Biomechanical Disorders of the Lumbar Spine Postoperative radiculopathy

MRI

Epidural hematoma

E) Pseudomeningocele compressing involved root

Central/peripheral clumping of nerve roots c/w arachnoiditis

Seroma

refer to E) (refer to E) Doesn’t corroborate clinical findings

EDX evaluation

Corroborates clinical SXs

Corroborative

Non-corroborative

Surgery

EDX evaluation

Anti-epileptic medications (AED), NSAID, PT

Conclusive for clinically involved root

Non-conclusive

Conclusive for radialopathy

Refer to stenosis flow-chart

Inconclusive

DX SNRB Surgery

DX SNRB

Positive Positive

E

Unaffected lateral recess, foraminal, or extra-foraminal stenosis

Negative

Negative

AEDs, NSAID, Repeat D×L SNRB PT @ alternate level

Repeat DX SNRB @ alternative level Somatic referral

cases of stenosis; McKenzie evaluation and treatment is employed in cases of disc herniation. If the patient does not improve over 1–3 weeks, or the patient presents with disruption of the ADLs, insomnia, inability to perform work-related duties due to severe pain, the authors will offer fluoroscopically guided therapeutic injections once the diagnosis has been confirmed. These minimally invasive injection procedures in addition to the aforementioned conservative measures constitute the second tier. The third treatment tier is defined by the use of percutaneous discectomy using the Dekompressor, coblation technology (nucleoplasty) or automated percutaneous discectomy (APLD), in addition to the measures offered in the first two tiers. The authors typically perform percutaneous discectomy in conjunction with a selective nerve root corticosteroid injection to address both the biomechanical and biochemical insults. Percutaneous disc decompression offers a minimally invasive percutaneous treatment, short of surgery, that has been shown to effectively treat L/S radiculopathy.101 In certain cases, however, nucleoplasty102 may be offered earlier in the treatment algorithm. APLD is preferred when there is a need to extract a larger volume of tissue or in cases of recurrent disc herniation.

Fig. 82.4—Cont’d

If a patient presents with unilateral or bilateral neurogenic claudication after acute onset, and MRI reveals a central focal disc protrusion causing functional stenosis, as can occur in a congenitally small canal due to short pedicles, the authors will incorporate both biomechanical and biochemical treatment pathways. In the authors’ experience, percutaneous disc decompression combined with therapeutic SNRB has been successful in treating such stenosis cases, and if not, the patient is referred to a surgical colleague. In instances of a more gradual onset of claudicating symptoms due to spinal stenosis, its etiology helps guide treatment. Amundsen et al. advocated bracing and physical therapy as initial treatment of stenosis patients presenting with unilateral or bilateral neurogenic claudication.103 The authors found that moderate pain would satisfactorily decrease in 50% of the patients after 3 months of conservative care. The other 50% nonresponders and those with severe pain benefited from surgical decompression; however, their treatment algorithm did not encompass therapeutic SNRBs. Botwin et al. documented a 50% reduction in visual analog scale scores in 75% of elderly stenosis patients who underwent therapeutic SNRBs 12 months prior, to treat unilateral neurogenic claudication, in addition to therapy and oral antiinflammatory medications.104 The Penn Spine 905

Part 3: Specific Disorders

Center approach blends the findings of both of these studies. The first tier offers PT, oral antiinflammatory medications, bracing, and activity modification. If symptoms do not abate, therapeutic SNRBs are offered unless there is a superimposed disc protrusion in a tight canal, and a subsequent surgical referral if improvement is unsatisfactory. If, however, a patient complains of lower limb fatigue, cramping, or heaviness with ambulation, or pain not alleviated by sitting, the threshold for a surgical referral is lowered. Spinal stenosis due to degenerative facet joint cysts may require percutaneous aspiration or puncture. Therapeutic SNRBs can be effective because an inflammatory process is probably present. The authors have observed perineural enhancement on fat-suppression sagittal MRI with gadolinium consistent with perineural venous engorgement and/or inflammation in cases of facet joint cystmediated radiculopathy (Fig. 82.5). The third treatment tier in facet joint cyst-related radiculopathy involves attempted aspiration of the cyst via an intra-articular approach through the joint. Involution of the cyst wall can be achieved via suction through a 20-gauge needle with a 10 cc syringe.105 If aspiration proves unsuccessful, cyst puncture can be attempted, again utilizing an intra-articular approach. As many as 50% of successfully treated facet joint cyst-related radiculopathies may require aspiration or puncture.106 In disc herniation-induced radiculopathy, treatment options again follow the tiered protocol, incorporating minimally invasive procedures, if necessary. Regardless of whether the herniation is a protrusion, extrusion, or sequestration, therapeutic SNRBs are offered if more conservative efforts fail. If therapeutic SNRBs are not curative, nucleoplasty, Dekompressor, or APLD can be employed to treat contained herniations. The authors have used the Dekompressor and APLD for disc extrusions with excellent outcomes, but those results have not been published as of yet. Nucleoplasty ought not be performed in the setting of a disc extrusion. If the patient’s pain improves but his or her weakness persists, as has been witnessed in cases of disc sequestration, surgical decompression has often been necessary. Seventy percent of patients will experience significant reduction in pain at 12 months after undergoing 1–4 therapeutic SNRBs107,108 A smaller proportion, who have disc sequestrations, will experience a similar outcome.25

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CASE REPORT The following case report exemplifying the Penn Spine Center approach to a complicated L/S radiculopathy case. A 59-year-old female presented with a 6-month history of right paramidline lumbosacral pain referring to her superior buttock and posterior thigh to her midcalf. Her symptoms started gradually, were sharp, burning, and achy in nature, and her VAS rating was a 5 out of 10. Exacerbating factors included sitting, bending forward, driving, sneezing, and coughing. Ambulation consistently alleviated her symptoms. Her pain had not lessened despite physical therapy and Bextra 20 mg b.i.d. Physical examination revealed a mildly obese female ambulating with a nonantalgic gait pattern without demonstration of Trendelenburg gait or truncal list. Lumbosacral range of motion was full but painful in flexion. Mild tenderness to palpation was noted over the right paraspinal region. Straight leg raising to 50° produced right lumbar and gluteal pain. Sustained bilateral hip flexion reproduced her lumbar and gluteal pain. Manual muscle testing did not detect weakness, and muscle stretch reflexes were intact and symmetric. Sensory examination for light touch, pin-prick, and proprioception were intact. Upper motor neuron signs were absent. Magnetic resonance imaging revealed intra-articular fluid and joint gapping in the right L4–5 zygapophyseal joint (Fig. 82.6). Subarticular stenosis was noted on the right at this level, and a small central focal protrusion was observed at L5–S1. Flexion–extension plain radiography did not reveal gross instability. An electrodiagnostic evaluation demonstrated normal sural sensory and peroneal motor nerve conduction studies. However, the H-reflex latencies were asymmetric with the right latency 1.45 ms longer than the left. The differential diagnoses included right S1 versus L5 radicular pain, L4–5 versus L5–S1 Z-joint synovitis, and lumbosacral internal disc disruption syndrome with somatic pain referral. Advanced imaging revealed evidence to support each of these conditions. However, the electrodiagnostic findings suggested a right S1 radiculopathy. The authors’ algorithmic approach employed an initial right S1 diagnostic selective nerve root injection. An L5 diagnostic block followed by diagnostic intra-articular injections of the Z-joints would ensue.

Fig. 82.5 (A) Sagittal view of T1-weighted fat suppressed images illustrating increased perineural signal around the L5 nerve root due to edema or venous congestion (white arrow). In contrast, the nonenhanced L4 nerve root exits its foramen one segment above (gray arrow). (B) Axial T2-weighted image of the same segment demonstrating the cyst emanating from the right L5–S1 zygapophyseal joint (gray arrow).

Section 5: Biomechanical Disorders of the Lumbar Spine

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B

However, the S1 diagnostic root injection was positive, and she subsequently underwent two therapeutic right S1 selective nerve injections with complete resolution of her pain. Purposely withheld from this case report was the history of an ineffective intra-articular steroid injection into the right L4–5 Z-joint months prior to the evaluation of this patient. Increasing the volume within this joint would not be expected to relieve this patient’s symptoms. Although intra-articular injection of antiinflammatory medication might be expected to alleviate the symptoms, the S1 nerve root was the inflamed structure both clinically and electrodiagnostically. Hence, the most appropriate target for treatment was the S1 nerve root, rather than the Z-joint or intervertebral disc.

Fig. 82.6 (A) Sagittal T2-weighted view of the right paramidline lumbosacral spine demonstrating increased signal (black arrow) within the right L4–5 Z-joint. (B) The corresponding axial segment displays intraarticular gapping and increased signal (black arrow).

4. Fortin JD, Washington WJ, Falco FJE. Three pathways between the sacroiliac joint and neural structures. Am J Neuroradiol 1999; 20(Sept):1429–1434. 5. Yeoman W. The relation of arthritis of the sacro-iliac joint to sciatica with an analysis of 100 cases. Lancet 1928; 2:1177–1180. 6. Fishman LM, Zybert PA. Electrophysiologic evidence of piriformis syndrome. Arch Phys Med Rehabil 1992; 73:359–364. 7. Slipman CW, Vresilovic EJ, Palmer MA, et al. Piriformis muscle syndrome: a diagnostic dilemma. J Muscul Pain 1999; 7(4):73–83. 8. Fishman LM, Dombi GW, Michaelsen C, et al. Piriformis syndrome: diagnosis, treatment, and outcome – a 10-year study. Arch Phys Med Rehabil 2002; 83: 295–301. 9. Faraj AA, Kumaraguru P, Kosygan K. Intra-articular bupivacaine hip injection in differentiation of coxarthrosis from referred thigh pain: a 10-year study. Acta Orthop Belg 2003; 69(6):518–521.

CONCLUSION

10. Tortolani PJ, Carbone JJ, Quartararo LG. Greater trochanteric pain syndrome in patients referred to orthopedic spine specialists. Spine J 2002; 2(4):251–254.

Lumbosacral radiculopathy is most commonly managed successfully by conservative treatment measures.25,47,56,67,68 Among these tools are therapeutic SNRBs or transforaminal epidural steroid injections. The mechanism of action of these interventions is not completely understood but it appears to involve both local (W. D. Chow, personal communication, San Francisco, 2003) and systemic effects.109 Thus, clinical improvement may occur after the instillation of steroids at the incorrect nerve root level or inaccurate site of pathology due to a nonspecific systemic steroid effect. Maximizing the therapeutic benefits of axial steroid injections requires accurate placement of these medications. Therefore, appropriate diagnosis is requisite, and warrants the judicious use of visual anatomic, electrophysiologic, and functional diagnostic testing guided by a sound algorithm.

11. Swezey RL. Pseudo-radiculopathy in subacute trochanteric bursitis of the subgluteus maximus bursa. Arch Phys Med Rehabil 1976; 57:387–390.

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12. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934; 211(5):210–215. 13. Verbiest H. A radicular syndrome from developmental narrowing of the lumbar vertebral canal. J Bone Joint Surg [Br] 1954; 36;230–237. 14. Porter RW. Spinal stenosis and neurogenic claudication. Spine 1996; 21(17): 2046–2052. 15. Kao C, Uihlein A, Bickel W, et al. Lumbar intraspinal extradural ganglion cyst. J Neurosurg 1968; 29:168–172. 16. Abdullah AF, Chambers RW, Daut DP. Lumbar nerve root compression by synovial cysts of the ligamentum flavum: report of four cases. J Neurosurg Psychiatry 1984; 60:617–620. 17. Lin R, Wey K, Tzeng C. Gas-containing ganglion cyst of lumbar posterior longitudinal ligament at L3. Spine 1995; 18:2528–2532. 18. Schreiber F, Nielson A. Lumbar spinal extradural cysts. Am J Surg 1950; 80: 124–126. 19. DePalma MJ, Strakowski JA, Mandelker EM, et al. An instance of an atypical intraspinal cyst presenting as an S1 radiculopathy. A case report and brief review of pathophysiology. Arch Phys Med Rehabil 2004; 85(6):1021–1025.

2. Fortin JD, Dwyer AP, West S, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique. Part I: asymptomatic volunteers. Spine 1994; 19(13):1475–1482.

20. Tarlov IM. Perineural cysts of the spinal nerve roots. Arch Neurol Psychiatry 1938; 40:1067–1074.

3. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37.

21. Kikta DG, Breuer AC, Wilbourn AJ. Thoracic root pain in diabetics: the spectrum of clinical and electromyographic findings. Ann Neurol 1982; 11;80–85.

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Part 3: Specific Disorders 22. Olsewski JM, Simmons EH, Kallen FC, et al. Evidence from cadavers suggestive of entrapment of fifth lumbar spinal nerves by lumbosacral ligaments. Spine 1991; 16:336–347. 23. Howe JF, Loeser JD, Calvin WH. Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pain of nerve root compression. Pain 1977; 3:25–41.

50. Vroomen PC, de Krom MC, Knotterus JA. Diagnostic value of history and physical examination in patients suspected of sciatica due to disc herniation: a systematic review. J Neurol 1999; 246:899–906.

24. Hitselberger WE, Witten RM. Abnormal myelograms in asymptomatic patients. J Neurosurg 1968; 28:204–206.

51. Nasseri K, Strijers RL, Dekhuijzen LS, et al. Reproducibility of different methods for diagnosing and monitoring diabetic neuropathy. Electromyog Clin Neurophysiol. 1998; 38(5):295–299.

25. Saal JA, Saal JS. The nonoperative treatment of herniated nucleus pulposus with radiculopathy: an outcome study. Spine 1989; 14:431–437.

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53. Slipman CW, Palmitier RA. Diagnostic selective nerve root blocks. Crit Rev Phys Med Rehabil Med 1998; 10(2):123–146.

27. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects: a prospective investigation. J Bone Joint Surg 1990; 72A(3):403–408.

54. Modic MT, Masaryk T, Boumphrey F, et al. Lumbar herniated disk disease and canal stenosis: prospective evaluation by surface coil MR, CT, and myelography. AJNR 1986; 7:710–717. 55. Ross JS, Glicklich M, Buchesneau PM. Imaging of the lumbar spine. In: Hardy RW, ed. Lumbar disc disease. 2nd edn. New York, NY: Raven Press; 1993.

28. Maigne JY, Rime B, Delinge B. Computed tomographic follow-up study of fortyeight cases of nonoperatively treated lumbar intervertebral disc herniation. Spine 1992; 17:1071–1074.

56. Williams AL, Haughton VM, Daniels DL, et al. CT recognition of lateral lumbar disc herniation. AJNR 1982; 3:211–213.

29. Delauche-Cavallier MC, Budet C, Laredo JD, et al. Lumbar disc herniation: computed tomography scan changes after conservative treatment of nerve root compression. Spine 1992; 17:927–933.

57. Haueisen C, Smith B, Myers SR, et al. The diagnostic accuracy of spinal nerve injection studies. Their role in the evaluation of recurrent sciatica. Clin Orthop 1985; 198:179–183.

30. Mixter WJ, Ayer JB. Herniation or rupture of the intervertebral disc into the spinal canal. N Engl J Med 1935; 213:385–395.

58. Anand AK, Lee BCP. Pain and metrizamide CT of lumbar disc disease: comparison with myelography. AJNR 1982; 3:567–571.

31. Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990; 15(7):674–678.

59. Sotiropoulos S, Chafetz NI, Lang P, et al. Differentiation between postoperative scar and recurrent disc herniation: prospective comparison of MR, CT, and contrast enhanced CT. AJNR 1989; 10:639–643.

32. Lindahl O, Rexed B. Histologic changes in spinal nerve roots of operated cases of sciatica. Acta Orthop Scand 1951; 20:215–225. 33. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 331(2):69–73.

60. Ross JS, Masaryk TJ, Schrader M, et al. MR imaging of the postoperative spine: assessment with gadopentate dimeglumine. AJNR 1990; 11:771–776. 61. Saal JA, Saal JS, Herzog RJ. The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine 1990; 15(7):683–686.

34. Bobechko WP, Hirsch C. Auto-immune response to nucleus pulposus in the rabbit. J Bone Joint Surg 1965; 47B(3):574–580.

62. Mcnab I. Negative disc exploration: an analysis of the causes of nerve-root involvement in sixty-eight patients. J Bone Joint Surg 1971; 53:891–903.

35. McCarron RF, Wimpee MW, Hudkins PG, et al. The inflammatory effects of nucleus pulposus: a possible element in the pathogenesis of low back pain. Spine 1987; 12:760–764.

63. Tajima T, Furukawa K, Kuramochi E. Selective lumbosacral radiculopathy and block. Spine 1980: 5:68–77.

36. Saal JS, Franson R, Myers R, et al. Human disc PLA2 induces neural injury: a histolomorphometric study. Presented at the International Society for the Study of the Lumbar Spine, Annual Meeting, May 20–24, 1992. 37. Chen C, Cavanaugh JM, Ozaktay C, et al. Effects of phospholipase A2 on lumbar nerve root structure and function. Spine 1997; 22:1057–1064.

64. Kikuchi S, Hasue M, Nishiyama K. Anatomic and clinical studies of radicular symptoms. Spine 1984; 9:23–30. 65. Dooley JF, McBroom RJ, Taguchi T, et al. Nerve root infiltration in the diagnosis of radicular pain. Spine 1988; 13:79–83. 66. Herron LD. Selective nerve root blocks in patient selection for lumbar surgery – surgical results. J Spinal Disord 1989; 2:75–79.

38. Kang JD, Georgescu HI, McIntyre-Larkin L, et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 1996; 21(3):271–277.

67. van Akkerveeken PF. The diagnostic value of nerve sheath infiltration. Acta Orthop Scand 1993; 64:61–63.

39. Byrod G, Olmarker K, Konno S, et al. A rapid transport route between the epidural space and the intraneural capillaries of the nerve roots. Spine 1995; 20:138–143.

68. Stanley D, McLoren MI, Evinton HA, et al. A prospective study of nerve root infiltration in the diagnosis of sciatica. A comparison with radiculopathy, computed tomography and operative findings. Spine 1990; 15:540–543.

40. Slipman CW, Chow DW. Therapeutic spinal corticosteroid injections for the management of radiculopathies. Phys Med Rehabil Clin N Am 2002; 13:697–711. 41. Rydevik B, Brown MD, Lundborg G. Pathoanatomy and pathophysiology of nerve root compression. Spine 1984; 9:7–15. 42. Murphy RW. Nerve roots and spinal nerves in degenerative disk disease. Clin Orthop Rel Res 1977; 129:46–60. 43. Goddard MD, Reid JD. Movements induced by straight leg raising in the lumbosacral roots, nerves and plexus, and in the intrapelvic section of the sciatic nerve. J Neurol Neurosurg Psychiatr 1965; 28:12. 44. Howe JF, Loeser JD, Calvin WH. Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pain of nerve root compression. Pain 1977; 3:25–41. 45. Bradley KE. Stress–strain phenomena in human spinal nerve roots. Brain 1961; 84:120. 46. Bora FW, Pleasure DE, Didizian NA. A study of nerve regeneration and neuroma formation after nerve suture by various techniques. J Hand Surg 1976; 1: 138–143.

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49. Fortin JD. Sacroiliac joint dysfunction. A new perspective. J Back Musculoskel Rehabil 1993; 3(3):31–43.

69. Lauder TD, Dillingham TR, Andary M, et al. Effect of history and exam in predicting electrodiagnostic outcome among patients with suspected lumbosacral radiculopathy. Am J Phys Med Rehabil 2000; 79(1):60–68. 70. Pease WS, Johnson EW, Charles M. Recruitment interval in L5 radiculopathy: a preliminary report. Arch Phys Med Rehabil 1984; 65:654. 71. Colachis SC, Pease WS, Johnson EW. Polyphasic motor unit action potentials in early radiculopathy: their presence and ephaptic transmission as an hypothesis. Electromyogr Clin Neurophysiol 1992; 32:27–33. 72. Johnson EW, Melvin JL. Value of electromyography in lumbar radiculopathy. Arch Phyl Med Rehabil 1971; 52(6):239–243. 73. Johnson EW, Fletcher FR. Lumbosacral radiculopathy: review of 100 consecutive cases. Arch Phys Med Rehabil 1981; 62(7):321–323. 74. Braddom RI, Johnson EW. Standardization of H-reflex and diagnostic uses in S1 radiculopathy. Arch Phys Med Rehabil 1974; 55:161–166. 75. Strakowski JA, Redd DD, Johnson EW, et al. H-reflex and F-wave latencies to soleus normal values and side-to-side differences. Am J Phys Med Rehabil 2001; 80(7):491–493.

47. Bush K, Cowan N, Katz DE. The natural history of sciatica with associated disc pathology: a prospective study with clinical and independent radiologic follow-up. Spine 1992; 17:1205–1212.

76. Shea PA, Woods WW, Werden DH. Electromyography in diagnosis of nerve root compression syndrome. Arch Neurol Psychiat 1950; 64:93–104.

48. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical examination in diagnosing sacroiliac joint pain. Spine 1996; 21(22):2594–2602.

77. Nardin RA, Patel MR, Gudas TF, et al. Electromyography and magnetic resonance imaging in the evaluation of radiculopathy. Muscle Nerve 1999; 22:151–155.

Section 5: Biomechanical Disorders of the Lumbar Spine 78. Kellegren JH. On the distribution of pain arising from deep somatic structures with charts of segmental pain. Clin Sci 1939; 3:35–46. 79. Kuslich SD, Ulstrom CL, Michael CL. The tissue origin of low back pain and sciatica: a report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia. Ortho Clin N Am 1991; 22(2):181–187. 80. Schwarzer AC, Aprill CN, Derbry R, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995; 20(17):1878–1883. 81. Kokmeyer DJ, Van der Wurff P, Aufdemkampe G, et al. The reliability of multitest regimens with sacroiliac pain provocation tests. J Manip Phsiol Ther 2002; 25(1):42–48. 82. Slipman CW, Sterenfeld EB, Chou LH, et al. The value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehabil 1998; 79:288–292. 83. Slipman CW, Sterenfeld EB, Chou LH, et al. The value of radionuclide imaging in the diagnosis of sacroiliac joint syndrome. Spine 1996; 21(19):2251–2254. 84. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21(16):1889–1892. 85. Revel M, Poiraudeau S, Auleley GR, et al. Capacity of the clinical picture to characterize low back pain relieved by facet joint anesthesia: proposed criteria to identify patients with painful facet joints. Spine 1998; 23(18):1972–1977. 86. Slipman CW, Plastaras C, Palmitier RA, et al. Symptom provocation of fluoroscopically guided cervical nerve root stimulation: are dynatomal maps identical to dermatomal maps? Spine 1998; 23(20):2235–2242. 87. Moriishi J, Otani K, Tanaka K, et al. The intersegmental anastomoses between spinal nerve roots. Anat Rec 1989; 224(1):110–116. 88. Neidre A, MacNab I. Anomalies of the lumbosacral nerve roots. Spine 1983; 8:294–299. 89. Bogduk N. Nerves of the lumbar spine. In: Bogduk N, ed. Clinical anatomy of the lumbar spine and sacrum. 3rd edn. London: Elsevier Science; 2002. 90. Krempen JD, Smith B. Nerve root injection: a method for evaluating the etiology of sciatica. J Bone Joint Surg 1974: 56A:1435–1444. 91. Schutz H, Lougheed WM, Wortzman G, et al. Intervertebral nerve-root in the investigation of chronic lumbar disc disease. Can J Surg 1973; 16:217–221. 92. Kikuchi S, Hasue M. Combined contrast studies in lumbar spine diseases: myelography (peridurography) and nerve root infiltration. Spine 1988; 13:1327–1331. 93. White A. Injection techniques for the diagnosis and treatment of low back pain. Orthop Clin N Am 1983; 14:553–567.

94. Huston CW, Slipman CW, Garvin, C. Complications and side effects of cervical and lumbosacral selective nerve root injections. Arch Phys Med Rehabil 2005; 86(2):277–283. 95. Botwin KP, Gruber RD, Bouchlas CG, et al. Complications of fluoroscopically guided transforaminal lumbar injections. Arch Phys Med Rehabil 2000; 81(8):1045–1050. 96. Schwarzer AC, Aprill CN, Bogduk M. The sacroiliac joint in chronic low back pain. Spine 1995; 20(1):31–37. 97. Durranti A, Winnie AP. Piriformis muscle syndrome: an underdiagnosed cause of sciatica. J Pain Symp Manage 1991; 6:374–371. 98. Solheim LF, Siewers P, Paus B. The piriformis muscle syndrome. Acta Orthop Scand 1981; 52:73–75. 99. Slipman CW, El Abd OH, Brandys EB, et al. The prevalence of referred abdominal and inguinal pain in patients with lumbar internal disruption syndrome. In press. 100. Alo KM, Wright RE, Sutcliffe J, et al. Percutaneous lumbar discectomy: clinical response in an initial cohort of fifty consecutive patients with radicular pain. Pain Pract 2004; 4(1)19–29. 101. Slipman CW, Shin CH, Patel RK, et al. Etiologies of failed back surgery syndrome. Pain Medicine 2002; 3(3):200–207. 102. Maillefert JF, Aho S, Huguenin MC, et al. Systemic effects of epidural dexamethasone injections. Rev Rhum [Engl Edn] 1995; 62(6):429–432. 103. Sharps LS, Isaac Z. Percutaneous disc decompression using nucleoplasty. Pain Phys 2002; 5(2):121–126. 104. Amudsen T, Weber H, Nordal HJ, et al. Lumbar spinal stenosis: conservative or surgical management?: a prospective 10-year study. Spine 2000; 25(11): 1424–1436. 105. Botwin KP, Gruber RD, Bouchlas CG, et al. Fluoroscopically guided lumbar transforaminal epidural steroid injection in degenerative lumbar stenosis: an outcome study. Am J Phys Med Rehabil 2002; 81(12):898–905. 106. Lutz GE, Shen T. Fluoroscopically guided aspiration of a symptomatic lumbar zygapophyseal joint cyst: a case report. Arch Phys Med Rehabil 2002; 83(12): 1789–1791. 107. Slipman CW, Lipetz JS, Yusuke W, et al. Nonsurgical treatment of zygapophyseal joint cyst-induced radicular pain. Arch Phys Med Rehabil 2000; 81(8):973–977. 108. Lutz GE, Vad VB, Wisneski RJ. Fluoroscopic transforaminal lumbar epidural steroids: an outcome study. Arch Phys Med Rehabil 1998; 79:1362–1366. 109. Riew KD, Yin Y, Gilula L, et al. The effect of nerve-root injections on the need for operative treatment of lumbar radicular pain. J Bone Joint Surg 2000; 82A: 1589–1593.

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SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ ii: Lumbar Radicular Pain

CHAPTER

Injection Procedures

83

Jaro Karppinen and Jukka-Pekka Kouri

PATHOPHYSIOLOGY OF RADICULAR LUMBAR PAIN Lumbar radicular pain, i.e. sciatica, in this context is defined as pain referred from the back into the dermatome of the affected nerve root along the femoral or sciatic nerve trunk. This has to be differentiated from nonradicular pain, which refers symptoms into the leg in a nondermatomal pattern.1 Radicular pain is shooting and bandlike, whereas somatic referred pain is usually constant in position but poorly localized and diffuse, and is aching in quality. True radiculopathy is defined as radicular pain in the presence of a neurological deficit.2 The prevalence of lumbar disc syndrome (herniated disc or typical sciatica) was studied as part of the Mini-Finland Health Survey.3 A diagnosis of lumbar disc syndrome was made for 5.1% of men and 3.7% of women aged 30 years or over. In a Finnish longitudinal birth cohort study, symptomatic lumbar disc disease (herniated nucleus pulposus or sciatica) appeared around the age of 15 years, and the incidence rose more sharply from the age of 19 years.4

Tissue origin of lumbar radicular pain The tissue origin of sciatic pain has been studied during decompression operations performed with local anesthesia. In these studies, sciatic pain could be produced only by pressure on the compressed, swollen nerve root, or on the dorsal root ganglion (DRG). Pressure on normal nerve roots or on other tissue did not produce sciatica.5,6

Intervertebral disc Disc herniation is the single most common cause of radicular pain.2 Mixter and Barr7 discovered that soft tissue ‘tumours’ were actually derived from the intervertebral discs, and that their surgical removal relieved sciatica symptoms. The causal link between herniated nucleus pulposus (HNP) and radicular pain is, however, not so straightforward since (1) HNP can be found in 20–36%, depending on the age, of asymptomatic subjects,8–11 and (2) internal disc ruptures (without HNP) may also induce disabling radicular pain,12,13 indicating the existence of an alternative mechanism to neural compression. Even though this chapter does not cover the clinical diagnosis of lumbar radicular pain, the authors stress that nerve root tension signs, assessed by the straight leg-raising test, can be positive in sciatica patients without HNP in MRI.14

Central and lateral stenosis Spinal stenosis is a condition associated with degenerative changes of the disc and zygapophyseal joints at multiple levels, which may include degenerative spondylolisthesis.15 Spinal stenosis has both structural and dynamic components. When the spinal canal is

structurally narrowed, slight extension can cause compression of the nerves.16,17 Extension can also cause an increase in epidural pressure.18 Flexion has the reverse effect, widening the spinal canal and foramina and reducing the epidural pressure. These typical features can be used in the practical clinical diagnosis of spinal stenosis and also in the algorithm of radicular pain. Lateral lumbar spinal stenosis due to osteoarthritis can be divided into entrance zone, midzone and exit zone stenosis.19 When a nerve root is laterally entrapped, it gives unilateral pain that is worse on walking. When central canal is narrow, pain radiates to one or both legs while walking and is relieved with flexion postures.20,21 Midzone stenosis is clinically the most relevant entity, because the DRG occupies a large part of the midzone.19 Recent experimental data also support the critical role played by the DRG in the pathophysiology of painful stenosis.22 The authors found that neither demyelinization nor axonal degeneration in the cauda equina induced mechanical allodynia, i.e. neuropathic pain, whereas lesions distal or immediately proximal to it are painful. They concluded that DRG apoptosis may be important for the production and maintenance of mechanical allodynia.22

Pathophysiological mechanisms of radicular pain Evidence of other mechanisms that can elicit lumbar radicular pain other than nerve root compression comes from many directions. We have already cited the findings of experimental surgery in anesthesia, existence of HNP in asymptomatics, and on the other hand, sciatica syndromes in those without an HNP. Additional evidence comes from animal experiments. McCarron et al.23 demonstrated that nuclear material of the intervertebral disc is chemically inflammatory and neurotoxic. Olmarker et al. showed that nuclear material – without any compression – can induce structural and functional changes in porcine nerve roots.24 The functional changes included focal degeneration of myelinated fibers and focal Schwann cell damage in nondegenerated axons. The damage to the Schwann cells resulted in a disintegration of Schmidt-Lantermann incisures, which represent connections of Schwann cell cytoplasm inside and outside the myelin sheath.25 Additional evidence supporting inflammation comes from the finding that nucleus pulposus is chemotactic, attracting leukocytes, and it may also induce macromolecular leakage and spontaneous firing of axons in vitro.26 Inflammation-induced capillary leakage increases endoneural pressure and reduces blood flow, thereby causing a ‘compartment syndrome’ in the DRG.27 A similar decrease in blood flow has been observed also in the canine nerve root. This reduction correlated with decrease in nerve conduction velocity, and was maximal within 1 week and recovered within 1 month. The pattern of nucleus-exposed DRG was, however, different, showing no clear recovery.28 These findings suggest that DRG irritation may lead into 911

Part 3: Specific Disorders

a different – perhaps more conservative treatment-resistant – radicular pain entity than nerve root involvement only. An additional, important landmark study is that of Kawakami et al.29 They nicely showed that leukocytes are essential in experimental radicular pain. In a rat model of mechanical hyperalgesia induced by application of nucleus pulposus to nerve roots, depletion of leukocytes with nitrogen mustard inhibited the generation of hyperalgesia. This indicated that the leukocytes are important in the production of pain-related behavior. The cells first appearing in and around the HNP on nerve–nuclear interface were polymorphonuclear leukocytes. Macrophages, originating from monocytes, did predominate a few days later and then remain in the affected region until the inflammation subsided.29 The implication of the observations is that lumbar radicular pain is a systemic disease, at least in the early stages of the disease. What is the leukotactic signal(s) of extruded nuclear material? Many substances, including hydrogen ions and glycoproteins, have been suspected of causing chemical radiculitis.30–32 A crucial finding was the one reported by Olmarker et al.33 They noted that the neurotoxicity of the nucleus seems to be associated with disc cells, as freezing prevented the neuronal damage. This observation limited the number of possible inflammatory candidates, but several were still ‘without alibi.’ Phospholipase A2 (PLA2) was a promising suspect, as it is the ratelimiting enzyme in the synthesis of proinflammatory lipid mediators (prostaglandins, leukotrienes, lipoxenies, and platelet-activating factor). It is calcium-dependent, adsorbing tightly to plasma membranes and intact cells. PLA2 liberates arachidonic acid from the membrane phospholipids, and is secreted extracellularly by activated phagocytes in response to cytokines.34 Additionally, it is released from rabbit chondrocytes in response to interleukin (IL)-1.35 It was found in extraordinarily high concentrations in herniated and painful discs,36 although this finding has since been questioned.37 It is also itself inflammatory38 and neurotoxic.39 When PLA2 was injected epidurally, motor weakness, demyelinization, and increased sensitivity of dorsal roots to mechanical stimulation were observed 3 days after the injection, but not beyond 3 weeks.40 Tumor necrosis factor alpha (TNF-α) is another potential candidate in HNP-induced nerve root irritation. TNF-α is a cytokine produced mainly by activated macrophages and T cells in response to inflammation, and by mast cells and Schwann cells in response to peripheral nerve injury.41,42 It activates the transcription factors NF-κB and AP-1 by binding to its p55 TNF-receptor (TNFR1), thereby inducing the production of proinflammatory and immunomodulatory genes.43 Endoneurial TNF-α causes demyelinization, axonal degeneration, and hyperalgesic pain states.44 In thermal hyperalgesia, two peaks have been associated with Wallerian degeneration, and can be reproduced in chronic injury to peripheral nerves.45 These peaks are also related to changes in TNF-α expression. It seems that the first peak, 6 hours after the nerve injury, is due to the local expression of the cytotoxic transmembrane 26 kDa TNF-α protein released by the resident Schwann cells. The second peak occurs 5 days after the injury, and may represent TNF-α protein released by hematogenously recruited macrophages.45 It has been shown immunohistochemically that TNF-α is expressed in the porcine nucleus pulposus.46 In a rat model, the concentration of TNF-α was found to be approximately 0.5 ng per herniated rat disc.47 Moreover, exogenous TNF-α produced neuropathological and behavioral changes (Wallerian degeneration of nerve fibers, macrophage recruitment to phagocytoze the debris, splitting of the myelin sheath) that mimicked those of the nucleus pulposus.47 Application of TNF-α on porcine nerve roots induced a reduction of the nerve conduction velocity that was even more pronounced than for nucleus pulposus, whereas application of IL-1β and IFNδ induced slight reductions of conduction velocity compared with fat, 912

but they were not statistically significant.48 Additional evidence for a crucial role of TNF-α comes from an animal study in which soluble TNF-α receptor (etanercept, Enbrel™) reversed nucleus pulposusinduced nerve conduction block and nerve root edema.49 However, TNF-α is not just a ‘bad guy’ as it also has an important role in the resorption of disc herniations. Macrophages secrete matrix metalloproteinase (MMP)-7 (=matrilysin) enzyme, which liberates soluble TNF-α from macrophage cell membranes. Soluble TNF-α induces disc chondrocytes to secrete MMP-3 (stromelysin), required for the release of a macrophage chemoattractant and subsequent macrophage infiltration of the disc.50,51 In addition to TNF-α, other inflammatory mediators may take part in the inflammatory component of radicular pain. These mediators could be either proximal to TNF-α, i.e. increase the expression of TNF-α, or distal to TNF-α, i.e. they are upregulated by TNF-α. Kang et al.52 observed increased matrix metalloproteinase activity, and increased levels of nitric oxide, prostaglandin E2, and IL-6 in HNP culture media compared with the control discs. Similarly, Burke et al.53 also detected increased levels of IL-6 in disc extracts from patients undergoing fusion for discogenic pain. They found additionally increased levels of a chemokine, IL-8. Interleukin-6 is an interesting interleukin, as it regulates to a large extent the hepatic acute phase and cachectic responses to an acute inflammatory stimulus.54 Recently, it was found that sciatica patients have an elevated acute phase response.55 Mean sensitized C-reactive protein (CRP) levels were significantly higher in sciatica patients compared to age- and sex-matched controls (1.68 versus 0.74 mg/L; p=0.002). We have genotyped sciatica patients with regard to some inflammatory genes and compared these patients to asymptomatic subjects. A genotype leading to increased production of IL-6 was overexpressed in sciatica patients.56 Additionally, in the HNP homogenates IL-1α, IL-1β and granulocyte-macrophage colony stimulating factor are detectable.57 The exact role of IL-1 in HNP-induced radicular pain is not known but it may have separate activity as it has in experimental arthritis.58

Natural course of lumbar radicular pain The long-term prognosis of lumbar radicular pain is considered to be good59 although in one study only one-third of sciatica patients recovered fully within 1 year, whereas one-third underwent surgery and one-third had residual symptoms.60 This study by Balague60 is in concordance with a systematic review on the long-term course of low back pain (LBP).61 Sixty-two percent of LBP patients still experienced pain at 12 months, 16% were sick-listed 6 months after inclusion into the study, and 60% experienced relapses of pain. A cohort of primary care patients with sciatica was followed in the Netherlands.62 An unfavorable outcome was predicted by a disease duration of more than 30 days, increased pain on sitting, pain upon coughing, and straight leg raising restriction. Magnetic resonance imaging (MRI) follow-up examinations have shown that HNP tends to regress over time, with partial to complete resolution after 6 months in two-thirds of people.63 We have recently rescanned 21 patients with HNP-induced severe sciatica at 2 weeks, 3 months, and 6 months in an intervention trial. Significant resorption seemed to occur already as early as 3 months in most patients.64 There is a predilection for large extrusions to resorb well.65,66 The resorption process seems to associate with HNP-encircling rim enhancement,67 which is thought to represent a neovascularized zone with macrophage infiltration.68 Neovascularization probably remains high in extrusions, as these have ruptured the posterior longitudinal ligament and entered the epidural space, allowing small vessels to penetrate the disc tissue more easily, whereas subligamentous herniations are more or less immunoprivileged.69 This is supported

Section 5: Biomechanical Disorders of the Lumbar Spine

by the higher resorption rate for extrusion-type disc herniations.70 We have recently analyzed determinants of HNP resorption.71 In the final model, the only significant determinants for resorption were thickness of rim enhancement and Komor classification, i.e. herniation extending above or below 67% of the adjacent vertebra.72

INTERVENTIONAL TREATMENT OPTIONS FOR LUMBAR RADICULAR PAIN Evidence on substantiating the best method to achieve successful treatment of lumbar radicular pain is still sparse. A recent systematic review found only 19 randomized, controlled trials (RCTs), of which eight met the three major requirements (comparability of groups, observer blinding, and intention-to-treat analysis).73 From the perspective of this review, no significant effect was demonstrated for nonsteroidal antiinflammatory agents (NSAIDs), traction, or intramuscular steroids. Considering the, at least partial, inflammatory nature of lumbar radicular pain, blocking of the cytokine cascade by local or systematic corticosteroids might, however, be effective. It is known from animal experiments that methylprednisolone injected within 2 days after the application of the nucleus pulposus inhibits the nucleus-induced vascular permeability and functional impairment, i.e. decrease of nerve conduction velocity.74 Any clinically useful intervention for radicular pain should be (1) effective in pain alleviation, (2) safe (i.e. no harmful complications), and (3) the technical details of the procedure or the equipment used should not be too complicated so that the intervention can be used widely in clinical practice. Moreover, if two different interventions are found equally effective and safe on radicular pain, the more cost-effective procedure should be chosen. When designing and using interventions for radicular pain, one should not tamper with the benign natural course of sciatica. In the ensuing, epidural injections, selective nerve root blocks, and anticytokine therapy are discussed in more extensive detail.

Epidural injections Epidural injections in the cervical, thoracic, and lumbosacral spine have been used for both diagnostic and therapeutic purposes in modern interventional spine practice. Epidural injections should preferably be combined with other therapeutic modalities, e.g. physical training and musculoskeletal rehabilitation. Epidural injection of medication allows a concentrated amount of the treatment agents (i.e. mostly corticosteroids) to be deposited and retained, thereby exposing the nerve roots to the medication for a prolonged period of time. The ability of steroids injected through an epidural route to reach their target in the anterior or anterolateral epidural compartment has been questioned. Indeed, even in experienced hands 25–45% of blind interlaminar or caudal epidural needle placements may be incorrect.75–77

Technical procedure There are two different routes to perform epidural injections: a caudal route through the sacral hiatus, and a lumbar interlaminar route. Epidural injection can be done with fluoroscopy or without it. Many specialists recommend fluoroscopy, because without fluoroscopy the needle is not always placed in the epidural space. Additionally, fluoroscopy prevents accidental intravascular injection. The incidence of intravascular uptake during lumbar spinal injection procedures was found to be approximately 8.5%. Absence of flashback of blood upon preinjection aspiration did not predict extravascular needle placement.78 Recently, fluoroscopic guidance has evolved into the standard approach in the US, although some clinicians stubbornly perform blind injections (Curtis Slipman, personal communication). Typically, blind injections are reserved for pregnant women and heavy patients who exceed the weight limits of the fluoros-

copy table. It is easiest and safest to insert the needle at L2–3 or L3–4, close to the superior spinous process. The standard technique used in epidural injections is the loss of resistance technique, where a controlled and well-defined loss of resistance occurs upon entering the epidural space through the ligamentum flavum. One study found that in the non-obese patient, lumbar interlaminar injections can be accurately placed without X-ray screening, in contrast to caudal injections, which require X-ray screening independent of the weight of the patient.79 In the caudal epidural injection, the quantity of corticosteroid that is possible to apply near to the inflamed nerve root is usually small. As well, the precise application is always uncertain, because anatomical structures such as septas may interfere with the flow of the injectate. However, caudal epidural route is useful in cases when the lesion is at L5–S1, but the interspinous route is preferable if the lesion is located at L4–5 or above.

Efficacy Epidural steroid injections are found to have a high success rate when evaluated in terms of long-term alleviation of radicular symptoms due to lumbar HNP.80,81 One published meta-analysis concluded that epidural corticosteroids are effective in both the short and long term in low back pain and sciatica.82 In contrast, the systematic review by Koes et al. that included higher-quality trials, found at most a shortterm effect on sciatica.83 To further complicate the matter, the systematic review by Vroomen et al. on treatment of sciatica concluded that epidural steroids may produce a short-term benefit for lumbar radicular pain.73 Following these aforementioned studies, two RCTs on epidural steroids for sciatica have been published. In the trial of Buchner et al.,84 patients with lumbar radicular pain consequent to a confirmed HNP were randomized into the epidural group (3 injections of 100 mg methylprednisolone in 0.25% bupivacaine; n=17) and control group (n=19). At 2 weeks, patients receiving methylprednisolone injection showed a significant improvement in straight leg raising test results and a tendency for a greater pain relief. At 6 weeks and 6 months, no significant differences were observed in any of the outcomes. In the trial of Valat and colleagues,85 three epidural injections of 50 mg prednisolone acetate (n = 43) were compared to epidural saline injections (n = 42) in HNP-induced sciatica. A significant improvement was observed in both groups, but epidural steroid injections provided no additional benefit over saline. Our conclusion, which stems from the reviews and subsequent RCTs, is that epidural steroids may have, at best, a short-term beneficial effect on lumbar radicular pain. Additionally, cost minimization analysis suggests that epidural injections under fluoroscopy may not be justified on the basis of the current literature.86 The authors’ personal preference is to use selective nerve root blocks (SNRB) in lieu of interlaminar epidurals for lesions at L4–5 or above. At L5–S1, our present view is to prefer computed tomography (CT)-guided SNRBs over caudal epidurals, and caudal epidurals over fluoroscopy-guided SNRBs. We do acknowledge that there is no uniform consensus regarding the approach at L5–S1.

Safety A major concern when administrating anesthetics into the epidural space is systemic toxicity. There is the theoretical risk of cardiovascular toxicity and central nervous system (CNS) effects. These complications can be avoided by adhering to careful technique and using lower doses of less concentrated anesthetics as discussed in the spinal injections technique chapter (Ch. 23). The maximum epidural dose recommended for a single injection is 500 mg for lidocaine and 225 mg for bupivacaine. The amount of local anesthetic agent used for SNRBs is much less. Epidural injections are usually considered to be extremely safe when performed with the proper technique.87 Nevertheless, the interlaminar 913

Part 3: Specific Disorders

route may be prone to complications, which include dural puncturecaused spinal headache, transient hypotension, Cushing’s syndrome, bacterial meningitis, chemical meningitis, epidural abscess, sinus arrhythmia, respiratory distress from spinal anesthesia, transiently increasing back or leg pain, numbness, transient dizziness, and cardiopulmonary arrest.88 In the meta-analysis of Watts and Silagy, which was based on seven trials with 431 patients, 2.5% suffered from dural taps, 2.3% transient headache, 1.9% transient increase in pain, and 0.2% irregular menstrual cycle.82 Long-term complications were not covered in the original reports, but, according to data from the American Society of Anesthesiologists Closed Claims Project database (1970– 1999), epidural steroid injections accounted for 40% of all chronic pain management claims. Serious injuries, involving brain damage or death, occurred, especially with local anesthetics and/or opioids.89

Selective nerve root blocks Derby et al.90 have postulated that the transforaminal approach may get corticosteroid more reliably in the anterior epidural space, where most of the pain-sensitive structures are located. In the procedure, the pharmaceutical agents are injected between the nerve root and the epidural sheath, depicting the nerve root in tubular fashion.91 Hereafter, we use the term selective nerve root block (SNRB), but synonymous terms

include selective nerve root injection, periradicular infiltration, transforaminal injection, and perineural injection. The mechanism of therapeutic effect is postulated to rely on mainly on the antiinflammatory effect of corticosteroid, which blocks the afferent impulses from the periphery.91 However, the anesthetic component may have an effect on its own, as lidocaine has been shown to increase intraradicular blood flow identical to the responses of a sympathetic ganglion block.92 SNRBs are useful in the diagnosis of radicular pain in atypical presentations. They have an accuracy of 85–94% in identifying a single symptomatic root, sensitivity of 100%, and a positive predictive value of 93–95% has been presented for root blocks.1,91,93,94 Indications are: (1) atypical extremity pain; (2) when imaging studies and clinical presentation do not correlate; (3) when electromyography and MRI do not correlate; (4) anomalous innervations, such as conjoint nerve roots or furcal nerves; (5) failed back surgery syndrome with atypical extremity pain; and (6) transitional vertebrae.88 A diagnostic SNRB is usually done without any antiinflammatory drug such as steroid in order to confirm the identity of the affected nerve root, whereas in therapeutic injections the ultimate goal is a therapeutic effect (typically achieved with a corticosteroid with or without local anesthetic). See the algorithm on diagnostic SNRBs and treatment of lumbar radicular pain, Figures 83.1A and 83.1B, respectively.

−

Positive SLR

SNRB

+

Pain worsened with extension and better when sitting

Pain below the knee Radicular pain: Back pain:

Radicular pain: Back pain: no influence

No influence on radicular pain nor on back pain

Possible HNP or disc rupture

Repeat 2–4 times if necessary

Facet or SI-joint injections

+

Severe symptoms, duration 0–2 wks Active noninvasive pain therapy, activity modifications, conservative therapy

Sympathetic blockade

A

−

+

+

SNRB of L2 nerve root

Pain radiating mainly above the gluteal fold

Unilateral pain

Bilateral pain, pain mainly proximally

Confirm with CT or MRI

− +

+

Possible spinal stenosis

Possible lateral stenosis

Confirm with CT or MRI

Confirm with CT or MRI

+ Possible SIor facet joint pathology + SI- or facet joint injection

+

+

SNRB irrespective of symptom duration

Mild symptoms Conservative therapy

+

+ Severe symptoms, >2 wks

Severe or persisting symptoms

SNRB +

− Refer to surgery

B Fig. 83.1 Algorithms for diagnosis (A) and treatment (B) of lumbar radicular pain. 914

+ Repeat 2 or more times

+ −

Repeat 2–4 times

SNRB

Refer to foraminotomy

Epidural injection

−

Mild but persisting symptoms

−

Refer to surgery anticytokine therapy??

Repeat SNRB 1 or more times

Repeat 1–2 times

Refer to decompressive surgery

Section 5: Biomechanical Disorders of the Lumbar Spine

Technical procedure Fluoroscopy-guided SNRB is typically the simplest, most rapid, and cost-effective technique. The details of this procedure have been thoroughly explained in Chapter 23. There are, however, two other techniques to confirm the proper needle insertion and placement: CT and MRI guidance.

CT guidance During CT-guided SNRBs, patients are in prone position on the scanner table. Axial slides are taken and analyzed before the procedure. The safe triangle described within the numerous technique chapters is the targeted area. The trajectory of the injection can be preplanned according to the information obtained from the CT scans. The entry point is marked on the skin with ink and can be controlled with a new CT scan (Fig. 83.2). Injection angle and the distance between skin and target area can be measured accurately. The interventionalist can check the correct angle of the injection needle with an angle measurement device and thus guide the clinician throughout the procedure. The correct injection site can also be controlled with contrastenhanced CT scans when needed. For postoperative radicular pain, CT-guided injection seems to be superior to fluoroscope-assisted injection for both its visualization and a longer-lasting effect.95

MRI guidance MRI guidance is another method, though it has not gained wide popularity because of the expensive MRI equipment required. The technical details of the MRI imaging system include an openconfiguration c-arm magnet, an MR-compatible in-room console, large screen display unit, and optical navigator.96 An MRI-guided procedure lacks the disadvantages of the other two methods. There is no ionizing radiation risk, and because of its ability to provide superior soft tissue contrast detail, contrast agent is not required. MRI guidance offers three-dimensional information during the nerve root injection, which is particularly advantageous for S1 infiltrations,96 which tend to produce unsatisfactory results by fluoroscopy.97

Efficacy It was observed in diagnostic studies that patients with lumbar spinal stenosis due to spondylosis or degenerative spondylolisthesis had

Fig. 83.2 An axial view of a CT-guided SNRB. The red line indicates the correct angle of the injection needle.

experienced a better therapeutic benefit from SNRBs than those with radicular symptoms referable to a disc herniation or to spondylolytic spondylolisthesis.91,98 Several uncontrolled follow-up studies confirmed these observations of a therapeutic effect.99,100 In HNPinduced radiculopathy, there was a 75% long-term recovery after an average of 1.8 transforaminal injections per patient of betamethasone acetate combined with Xylocaine. The outcome was better for symptom duration of less than 36 weeks.100 Weiner and Fraser used fluoroscopy-guided SNRB for patients with severe lumbar radiculopathy secondary to foraminal and extraforaminal disc herniation, which had not resolved with rest and nonsteroidal antiinflammatory agents. They observed a considerable and sustained pain relief in 22 out of 28 (79%) patients.99 Derby and colleagues observed that a successful SNRB is a good prognostic sign for a positive surgical result for those with symptomatology of at least 1-year duration.101 Fluoroscopically guided transforaminal steroid injections seem to be beneficial in radicular pain due to lumbar spinal stenosis in terms of both pain reduction and improved walking tolerance.102 However, a prospective cohort study involving radicular patients with a disc herniation or spinal stenosis indicated that the response was significantly better in patients with a HNP.103 So far, only 6 RCTs comparing perineural corticosteroid injection to a nonsteroid regimen have been published. Kraemer et al.104 used an interlaminar injection of triamcinolone and lidocaine (n=47), which was compared to paravertebral local anesthetic (n=46). Actually, they did not use SNRB but an oblique interlaminar method. This injection method, however, is somewhat similar to the SNRB precision technique and therefore it is reviewed in this context. Three injections were given with 1-week intervals. They used a composite score and prevention of back surgery in the assessments. Their results indicated that epidural perineural injections were more effective than conventional posterior epidural injections. Devulder et al.105 used transforaminal injections for failed back surgery. The combination of methylprednisolone, bupivacaine, and hyaluronidase (n=20) was compared to a combination of saline, bupivacaine, and hyaluronidase (n=20). Their main outcome measure was at least 50% reduction in leg pain. No statistical differences were found between the treatment groups, although it is unlikely that SNRBs are effective in postoperative radicular syndromes with a high probability of neuropathic pain component. Riew et al.106 used transforaminal injections for degenerative lumbar radicular pain in patients indicated for surgery. Patients had either a disc herniation or central or lateral stenosis confirmed in MRI and/or CT. Patients were randomized to a selective nerve root injection with either bupivacaine alone or bupivacaine with betamethasone. Nineteen patients received multiple injections. Eighteen out of 27 patients in the control group underwent back surgery, as compared to 8 out of 28 patients in the active group. The difference in the operative rates between the two groups was statistically and clinically significant (p<0.004). In the Finnish RCT,107 transforaminal injection was given to nonoperated patients with radicular pain extending below the knee. Eighty-two percent of all randomized patients had an MRI-confirmed HNP. In the study, a single injection of methylprednisolone (80–120 mg) with bupivacaine (n=80) was compared to isotonic transforaminal saline (n=80). A short-term effect was observed in favor of the steroid injection, but at later follow-up assessments the treatments were of equal efficacy. In a later subgroup analysis, it was found that the effect of steroid was greater at L3–4 or L4–5 level and in case of contained, i.e. subligamentous, herniations.108 Vad et al.109 used transforaminal injection of betamethasone with Xylocaine (n=25), which was compared to lumbar paraspinal trigger-point injections with saline (n=25) for nonoperated sciatica patients. The active group had a success rate of 84% in the long term, as compared to with 48% in the control group. 915

Part 3: Specific Disorders

The effect estimate may be, however, biased because patients were not blinded to treatment allocation. An additional factor, which may increase treatment effect is the fact that patients did not undergo a trial of conservative care before the SNRB. Ng et al.110 compared 0.25% bupivacaine and 40 mg methylprednisolone to 0.25% bupivacaine only for chronic leg pain. Patients had MRI-verified root compromise due to herniation or lateral stenosis with a mean symptom duration of more than 12 months. The final study population included 43 patients in both groups. At 3 months, there was no statistically significant difference in the outcome measures between the groups (Oswestry Disability Index, visual analogue scores for back and leg pain, change in walking distance). A recent systematic review found moderate evidence in support of SNRBs in treating painful radicular symptoms.111 The authors of the review concluded that current studies support use of SNRBs as a safe and minimally invasive adjunct treatment for lumbar radicular symptoms. However, conclusive evidence is still lacking.111 The current authors agree with the conclusion of the review – SNRB is a safe intervention for lumbar radicular pain in experienced hands. In clinical practice most patients with HNP- or lateral stenosisinduced lumbar radicular pain seem to improve permanently (from the current episode) with a single SNRB. In the subanalysis of our RCT on SNRB, injection with steroid was cost-effective in case of subligamentous, i.e. contained, herniations, whereas saline was cost-effective in case of large herniations, i.e. extrusions and sequestrations.108 The difference in the cost-effectiveness was due to different surgery rates in these subgroups; the steroid injection patients with large HNP tended to undergo surgery more commonly in comparison to the saline injection and vice versa in the subgroup of contained herniations. This led us to suspect the existence of a negative effect of steroids on the resorption process as described by Minamide et al. in rabbits.112 Yet, in our analyses we did not observe such an effect exerted by SNRBs when using steroids.113 Readers are invited to view the algorithm constructed by the authors for the treatment of lumbar radicular pain (see Fig. 83.1B).

Safety In a retrospective evaluation of 322 SNRB injections, complications included transient nonpositional headache (3.1%), increased back pain (2.4%), increased leg pain (0.6%), facial flushing (1.2%), vasovagal reactions (0.3%), increased blood sugar in a insulin-dependent diabetic (0.3%), and intraoperative hypertension (0.3%). No dural punctures occurred and all reactions resolved without morbidity.114 Intravascular injections have been encountered in 11.2% of SNRBs, the rate being higher at S1.115 Serious complications of SNRBs have also been encountered, and include epidural abscess, arachnoiditis, epidural hematoma, cerebrospinal fluid fistula, hypersensitivity reaction to injectate, and even persisting paraplegia.116 However, in a recent prospective 3-month follow-up study of cervical and lumbosacral SNRBs (with complications as the primary outcome) no major complications were encountered.117 Minor complications of lumbosacral procedures included increased pain at the injection site (17.1% of 306 injections performed), increased radicular pain (8.8%), lightheadedness (6.5%), increased spine pain (5.1%), nonspecific headache (1.4%), and vomiting (0.5%).117

Practical considerations The authors use SNRBs only for lumbar radicular pain regardless of the presence of motor and/or sensory defects. Those who experience a partial or total muscle paresis without concurrent pain represent a unique challenge. We have observed that moderate motor weakness improves with a SNRB, whereas sensory defect and abnormal tendon 916

reflexes mainly do not. The differential recovery rate of sensory and motor fibers has been verified also in animal studies.117 We try to encourage patients that the prognosis of motor paresis is benign, and although sensory disturbances are likely to remain they do not result in any functional limitation (of course, there must be an awareness about the possibility of a burn or other tissue injury because of the anesthetic skin). Basically, we use SNBRs only for patients with radicular pain but some painless patients might benefit from the procedure. However, we try an SNRB only once in these cases and refer them to surgery in case motor weakness does not improve following this intervention. Recently published long-term results of lumbar discectomy showed that preoperative foot drops recovered almost completely irrespective the cause (HNP or lumbar spinal stenosis).118 Our patients with lumbar radicular pain typically demonstrate an HNP that clinically corroborates with the distribution of the pain. We do not consider surgery the initial management step. Patients must be apprised of the benign natural course of the symptom manifestation of disc herniations and the variety of treatment options for the radicular component. Invariably, we supplement the performance of SNRBs with physical therapy that emphasizes the McKenzie approach.119 Centralization of pain is a good prognostic sign.120,121 For more chronic patients with intermittent radicular symptoms we use additional therapies that involve physical conditioning and a cognitive behavioral approach.122 One of these approaches is the DBC method, which is an active outpatient therapy using specific devices to enhance lumbar spine function in combination with a behavioral approach.123,124 A combination of an SNRB and exercise is usually effective for patients with HNP to avoid surgery, as indicated in the trial of Riew et al.106

Anticytokine therapy Animal studies indicate that TNF-α assumes a crucial role in the pathophysiology of radicular pain. Either intervertebral disc-contained TNF-α or another molecule, acting through the upregulation of TNF-α expression, causes hematogenously recruited leukocytes and macrophages to accumulate in the environment of the nerve root and/or DRG. This leads to increased capillary permeability and endoneural pressure, and ultimately to endoneural ischemia. Thus, a strong theoretical rationale exists for the use of anti-TNFα therapy in lumbar radicular pain. Other cytokines may also be involved,53 but so far anticytokine therapy other than anti-TNF-α or anti-IL-1 has not been exploited for radicular pain. Several new anti-TNF-α preparations, including an orally administered one, will be commercially available shortly. The different preparations may differ in the safety profile and the efficacy for lumbar radicular pain. Therefore, before a wide-scale clinical implementation of the various anticytokine preparations both proof of concept trials and phase IV studies are needed to elucidate the clinical effectiveness and safety issues.

Technical procedure Currently, four commercial anticytokine preparations are available: chimaeric, mouse/human monoclonal antibody against TNF-α (infliximab, Remicade™) is infused intravenously over 2 hours; soluble TNF-α receptor (etanercept, Enbrel™) is injected subcutaneously; humanized monoclonal antibody against TNF-α (adalimumab, Humera™) can be delivered subcutaneously; and a recombinant IL-1 receptor antagonist (Anakinra™) is injected subcutaneously. The elimination half-life of infliximab is 10 days compared to 3–9 hours for the IL-1 receptor antagonist Anakinra, which therefore requires daily subcutaneous injection. Prior to the infusion, patients must be screened for serious infections, hepatitis B or hepatitis C, human immunodeficiency virus (HIV),

Section 5: Biomechanical Disorders of the Lumbar Spine

opportunistic infections, malignancies, latent or active tuberculosis, lymphoproliferative disease, pregnancy, and severe progressive or uncontrolled renal, hepatic, hematologic, gastrointestinal, endocrine, pulmonary, cardiac (e.g. congestive heart failure), neurologic or cerebral diseases including demyelinating diseases such as multiple sclerosis. All of these cytokine inhibitors may cause anaphylactic reactions. Therefore, patients have to be followed carefully after the injection for hypotension or other symptoms of anaphylaxis. In order to treat anaphylaxis, should it occur, the appropriate personnel, medication (epinephrine, inhaled beta agonists [e.g. albuterol], antihistamines and corticosteroids) and other equipment to treat such a response should be available before the infusion is started. If symptoms of an allergic response (e.g. urticaria, itching, hives) appear, the patient should be observed carefully and, when necessary, the infusion should be slowed down or stopped. If signs of anaphylaxis (e.g. generalized urticaria, bronchospasm, hypotension, etc.) appear, the infusion should be stopped immediately and appropriate treatment given.

Efficacy An open-label study indicated that a single infusion of infliximab 3 mg/kg is efficacious for the treatment of HNP-induced acute sciatica. The curative effect occurred within 3 hours after infusion initiation and was sustained throughout the 3-month follow-up period.125 In the 1-year follow-up of the open-label study, the effect was sustained in all but one patient over the follow-up period as evidenced by the outcomes reported for both leg pain and disability measured with the Oswestry scale. The nonresponder was operated on shortly before the 1-year assessment.126 The dose of 1 mg/kg was given to two patients. One of them had a rapid and complete relief of radicular pain, but the other had no benefit from the infusion. Furthermore, a single infusion of infliximab did not interfere with the spontaneous resorption of disc herniations. The observation of a nondeleterious effect on herniation resorption was later confirmed in a randomized setting.64 Recently, we finished a 3-month follow-up of an RCT where intravenous infliximab 5 mg/kg was compared to intravenous saline.127 Unfortunately, the positive results of the openlabel study125,126 could not be replicated. Patients in both groups had a similarly good response, with approximately two-thirds responding well (i.e., at least 75% reduction in leg pain). Seven patients in both groups had discectomy by 3 months. The pronounced placebo effect could be best observed in the straight leg raising test as 3 hours after the i.v. saline infusion this test had improved by 15 degrees. Our conclusion is therefore that routine clinical use of infliximab is not recommended until efficacy is established. In addition to infliximab, etanercept has also been used for lumbar radicular pain. In a Swiss study,128 five consecutive patients with acute severe sciatica received three injections of etanercept (25 mg every 3 days). They were compared to seven consecutive patients who received 3 intravenous injections of methylprednisolone (250 mg every 3 days). At 10 days, patients treated with etanercept exhibited a significant improvement in both leg pain and disability. Further improvement was observed at 6 week. In the steroid group, significant improvement was noted at 10 days, but at 6 weeks symptoms reoccurred. Tobinick and Britschgi-Davoodifar129 have documented their experiences on etanercept for discogenic pain. Most of their patients had a rapid and sustained benefit after a single subcutaneous injection of 25 mg etanercept. They had 14 patients with clear-cut lumbar or cervical radiculopathy, and five patients with suspected lumbar radicular pain. In a case of lumbar radicular pain, the author administered etanercept by a perispinal subcutaneous injection to the lower lumbar region Wehling et al.130 compared steroid injections to IL-1 receptor antagonist injections in experimental allergic radiculitis. Prednisolone

appeared to be somewhat more effective than IL-1 receptor antagonist but a causative role for IL-1 in sciatica was speculated.

Safety All of the anti-TNF-α drugs are prone to potentially serious adverse effects. At the moment, clinical safety data are available for infliximab and etanercept, as both of these drugs have been used in clinical practice for several years. Both are contraindicated in patients with severe infection, anemia, neutropenia, lymphoma, demyelinating disease, or who have active or latent tuberculosis.131 Infliximab and etanercept should not be used in patients with moderate or severe heart failure. A potential problem with all biological medicines is immunogenicity. Antibodies against all of the anti-TNF-α drugs may develop and may cause serious allergic reactions. A possible acute infusion reaction is defined as any adverse event that occurs during or within 1 hour after the administration of the infusion. A possible delayed hypersensitivity reaction consists of myalgia and/or arthralgia with fever and/or rash (that does not represent signs and symptoms of other recognized clinical syndromes) occurring 3–12 days after an infusion of study drug. These may be accompanied by other events including pruritus, facial, hand, or lip edema, dysphagia, urticaria, sore throat and/or headache. Delayed hypersensitivity reactions may occur in patients retreated with these agents following a period of several years without any exposure to the drug in question. In the open-label study, we have treated 12 patients with a single infusion of infliximab (10 with a 3 mg/kg dose and 2 with 1 mg/ kg dose), but no immediate or delayed adverse effects have been encountered.126 In the RCT,127 three mild adverse effects (rhinitis, diarrhea, otitis media with sinusitis maxillaris) were encountered.

ALGORITHM FOR DIAGNOSIS AND TREATMENT OF RADICULAR PAIN To establish the diagnosis of radicular pain, we always prefer SNRBs (see Fig. 83.1A). Our preference is to use CT guidance, especially in case of S1 injections, and with a minimal injectate volume in order to minimize or prevent caudal spreading. If there is a positive response in both radicular and low back pain, diagnosis of the affected level is confirmed. SNRB can be repeated if necessary (see also Fig. 83.1B on treatment of radicular pain). If the SNRB relieves radicular pain but LBP remains, a facet joint or SI joint injection may need to be performed. If the SNRB does not have effect on radicular pain nor on LBP, SNRB can be performed at the L2 level, as it is hypothesized that discogenic pain is transmitted mainly by sympathetic afferent fibers in the L2 nerve root.132 It may be that L2 SNRB is not very effective for the radicular component but it seems to alleviate the local pain component effectively.132 There is, so far, no hard scientific evidence to justify any intervention for treatment of lumbar radicular pain. This does not mean that such interventions should not be useful in clinical practice because uncontrolled studies suggest that a variety of interventions are useful in radicular pain. One specific intervention is, however, unlikely to benefit all patients with radicular pain. Therefore, we need more information on prognostic factors, which may increase treatment effect of different therapeutic interventions. Lumbar radicular pain may not be as homogeneous an entity as we have thought. Time since onset of symptoms is one prognostic factor that ought to be considered. In clinical practice, patients who have more acute radicular pain (less than 3 months) respond better to epidural and transforaminal injections than those with long-lasting radicular symptoms (longer than 1 year). In animal experiments, methylprednisolone reversed the nucleus pulposus-induced nerve root injury but steroid was 917

Part 3: Specific Disorders

injected within 2 days of the experimental lesion.74 Acute symptoms could thus be more susceptible to treatment and, on the contrary, it is unlikely that local steroids would be beneficial in case of neuropathic radicular pain. Other prognostic factors to be considered are DRG involvement,28 the level of the lesion,108 type of symptomatic herniation (subligamentous versus transligamentous),108 having workers’ compensation, and work requiring lifting.133 In Figure 83.1B, an algorithm for treatment of lumbar radicular pain is presented. If SLR is positive and pain extends below the knee, an HNP or disc rupture should be suspected. MRI can also visualize disc ruptures, whereas CT is useful only in the case of HNP. When symptoms have only been present for a short interval, regardless of their severity, noninvasive active pain therapy including NSAIDs and opiates, activity modifications and conservative therapy (see Practical considerations, above) is preferred. Unfortunately, NSAIDs may often not be sufficient to alleviate radicular pain. Patients with indications for emergency surgery (cauda equine, progressive muscle paresis, or rapidly increasing pain) are, of course, referred for surgery, as these are considered the sole indications for immediate/emergency surgery. Patients should avoid bed rest134 and stay active. Transforaminal steroids is the option to be chosen for continuing disabling radicular pain but usually patients should have demonstrated a failure to improve with less invasive treatment options (rehabilitation techniques). Transforaminal steroids are preferred and repeated as necessary as they may prevent surgery.106 SNRBs are usually repeated 2–4 times. In case of severe short-term pain not responding to SNRBs, consideration of a more aggressive approach should be entertained, such as open surgery. The exact indications for different invasive techniques are reviewed elsewhere in this book. It has been our observation that patients with an L4–5 HNP and major trunk list do not respond well with SNRBs and typically require surgery. Anticytokine therapy may be indicated for the more severe cases but so far we have no evidence based on randomized, controlled trials to justify its use. Therefore, we strongly discourage off-label use, despite some optimistic commentaries,135 because anticytokine therapies may potentially produce serious adverse effects. At present, evidence has been demonstrated only for surgery in herniation-induced sciatica.136 However, the conclusion drawn from this classic by Weber has been questioned, as a recent Finnish trial could not replicate his findings.137 Interestingly, a subanalysis of this intention-to-treat trial found evidence that surgery may be effective at L4–5. When the SLR test is negative but radicular pain is worsened with extension and walking and better with sitting, a stenotic process should be suspected. When there are bilateral symptoms, central spinal stenosis is the probable cause. In case of central stenosis, we prefer epidural injections, which can be repeated 1–2 times. In case of mild symptoms, conservative rehabilitation methods are always the initial treatment intervention, which may be followed by more invasive procedures. If symptoms persist or the intensity of pain or bothersomeness increases, epidural injections are indicated. Surgery should be reserved only for patients with severe symptoms.138 In case of lateral stenosis, we prefer SNRBs always, regardless of symptom duration. If pain is relieved, but only temporarily, patients may be referred for other more aggressive treatments ranging from percutaneous disc decompression to decompressive foraminotomy (see Fig. 83.1B). Indications and techniques for SI joint and facet joint injections are discussed elsewhere in this book.

CONCLUSIONS In view of the recent findings about the inflammatory component of lumbar radicular pain, treatments aiming to block the cytokine cascade seem to be justified. When lumbar radicular symptoms have only been present for a short interval, regardless of their severity,

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noninvasive active pain therapy is preferred. Patients should avoid bed rest and stay active. SNRB is the option to be chosen for continuing, disabling radicular pain caused by HNP or intervertebral disc rupture. In case of severe short-term HNP-induced pain not responding to SNRBs, consideration of a more aggressive approach should be considered. Anticytokine therapy may be indicated for the more severe cases but so far we have no evidence based on randomized, controlled trials to justify its use. In case of mild central lumbar spinal stenosis symptoms, conservative rehabilitation methods are always the initial treatment intervention. If symptoms persist or the intensity of pain or bothersomeness increases, epidural injections are indicated. Surgery should be reserved only for patients with severe symptoms. In case of lateral stenosis we always prefer SNRBs, regardless of symptom duration. If pain is relieved, but only temporarily, patients may be referred for other more aggressive treatments. Although hard scientific evidence is sparse, the authors’ personal feeling is to favor SNRBs in disabling, persisting lumbar radicular symptoms. Our preference is to use CT-guided SNRB, especially in case of S1 injections, and with a minimal injectate volume in order to minimize or prevent caudal spreading. SNRB can be repeated if necessary. The authors strongly wish to see more information on prognostic factors, which may increase treatment effect of different therapeutic interventions.

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94. Dooley JF, McBroom RJ, Taguchi T, et al. Nerve root infiltration in the diagnosis of radicular pain. Spine 1988; 13:79–83. 95. Lutze M, Stendel R, Vesper J, et al. Periradicular therapy in lumbar radicular syndromes: methodology and results. Acta Neurochirurgica 1997; 139:719–724. 96. Ojala R, Vähälä E, Karppinen J, et al. Nerve root infiltration of the first sacral root with MRI guidance. J Magn Reson Imaging 2000; 12:556–561. 97. Viton JM, Rubino T, Peretti-Viton P, et al. Short-term evaluation of periradicular corticosteroid injections in the treatment of lumbar radiculopathy associated with disc disease. Revue Du Rhumatisme, English Edition 1998; 65:195–200.

121. Long A, Donelson R, Fung T. Does it matter which exercise? A randomized control trial of exercise for low back pain. Spine 2004; 29:2593–2602. 122. Schonstein E, Kenny D, Keating J, et al. Physical conditioning programs for workers with back and neck pain: a Cochrane Systematic Review. Spine 2003; 28: E391–E395. 123. Kankaanpää M, Taimela S, Airaksinen O, et al. The efficacy of active rehabilitation in chronic low back pain. Effect on pain intensity, self-experienced disability, and lumbar fatigability. Spine 1999; 24:1034–1042.

98. Kikuchi S, Hasue M, Nishiyama K, et al. Anatomic and clinical studies of radicular symptoms. Spine 1984; 9:23–30.

124. Taimela S, Diederich C, Hubsch M, et al. The role of physical exercise and inactivity in pain recurrence and absenteeism from work after active outpatient rehabilitation for recurrent or chronic low back pain: a follow-up study. Spine 2000; 25:1809–1816.

99. Weiner BK, Fraser RD. Foraminal injection for lateral lumbar disc herniation. J Bone Joint Surg [Br] 1997; 79:804–807.

125. Karppinen J, Korhonen T, Malmivaara A, et al. Tumor necrosis factor-alpha monoclonal antibody, infliximab, used to manage severe sciatica. Spine 2003; 28:750–753.

100. Lutz GE, Vad VB, Wisneski RJ. Fluoroscopic transforaminal lumbar epidural steroids: an outcome study. Arch Phys Med Rehabil 1998; 79:1362–1366.

126. Korhonen T, Karppinen J, Malmivaara A, et al. Efficacy of infliximab for disc herniation-induced sciatica. One-year follow-up. Spine 2004; 29:2115–2119.

101. Derby R, Kine G, Saal JA, et al. Response to steroid and duration of radicular pain as predictors of surgical outcome. Spine 1992; 17:S176–S183.

127. Korhonen T, Karppinen J, Paimela L, et al. The treatment of disc herniation-induced sciatica with infliximab. Results of a randomized, controlled, 3-month follow-up study. Spine 2005; 30:2724–2728.

102. Botwin KP, Gruber RD, Bouchlas CG, et al. Fluoroscopically guided lumbar transformational epidural steroid injections in degenerative lumbar stenosis: an outcome study. Am J Phys Med Rehabil 2002; 81:898–905.

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103. Ng LC, Sell P. Outcomes of a prospective cohort study on peri-radicular infiltration for radicular pain in patients with lumbar disc herniation and spinal stenosis. Eur Spine J 2004; 13:325–329.

128. Genevay S, Stingelin S, Gabay C. Efficacy of etanercept in the treatment of acute and severe sciatica. A pilot study. Ann Rheum Dis 2004; 63:1120–1123.

Section 5: Biomechanical Disorders of the Lumbar Spine 129. Tobinick EL, Britschgi-Davoodifar S. Perispinal TNF-alpha inhibition for discogenic pain. Swiss Med Wkly 2003; 133:170–177.

134. Vroomen PC, de Krom MC, Wilmink JT, et al. Lack of effectiveness of bed rest for sciatica. N Engl J Med 1999; 340:418–423.

130. Wehling P, Cleveland SJ, Heininger K, et al. Neurophysiologic changes in lumbar nerve root inflammation in the rat after treatment with cytokine inhibitors. Evidence for a role of interleukin-1. Spine 1996; 21:931–935.

135. Cooper RG, Freemont AJ. TNF-alpha blockade for herniated intervertebral discinduced sciatica: a way forward at last? Rheumatology (Oxford) 2004; 43:119–121.

131. Bencsath M, Blaskovits A, Borvendeg J. Biomolecular cytokine therapy. Pathol Oncol Res 2003; 9:24–29. 132. Nakamura SI, Takahashi K, Takahashi Y, et al. The afferent pathways of discogenic low-back pain. Evaluation of L2 spinal nerve infiltration. J Bone Joint Surg [Br] 1996; 78:606–612. 133. Tong HC, Williams JC, Haig AJ, et al. Predicting outcomes of transforaminal epidural injections for sciatica. Spine J 2003; 3:430–434.

136. Weber H. Lumbar disc herniation. A controlled, prospective study with ten years of observation. Spine 1983; 8:131–140. 137. Österman H, Seitsalo S, Karppinen J, et al. Effectiveness of microdiscectomy for lumbar disc herniation. A randomised controlled trial with two years of follow-up. Spine. 2006; 31:2409–2414. 138. Herno A, Airaksinen O, Saari T, et al. Lumbar spinal stenosis: a matched-pair study of operated and non-operated patients. Br J Neurosurg 1996; 10:461–465.

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Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ ii: Lumbar Radicular Pain

CHAPTER

Percutaneous Discectomy

84

Conor W. O’Neill, John Carrino and Cynthia Chin

INTRODUCTION Percutaneous discectomy is a method for treating disc herniations. There are two basic types of percutaneous discectomy: selective and nonselective.1 The goal of a selective percutaneous discectomy is to remove disc from the posterior third of the disc space, where herniations reside.1 This is typically accomplished with surgical instruments and/or lasers which can be placed in the disc with an endoscope and then directed to the area of the herniation under direct vision. As such, it is a true surgical procedure, and will not be discussed further in this chapter. The goal of a nonselective discectomy is to remove nucleus from the center of the disc, relying on the accompanying changes in disc mechanics to effect a change in the herniation (Fig. 84.1). The original device used to perform a nonselective percutaneous discectomy was the nucleotome (Fig. 84.2). This device functions as a mechanical shaver which is placed into the center of the disc under fluoroscopic guidance, and nucleus is then aspirated. While other devices have largely supplanted the nucleotome, the objective of the procedure remains nonselective removal of nucleus from the disc. As all the devices used for nonselective discectomy are placed using fluoroscopy, without incisions or surgical instruments (Fig. 84.3), in

Non-selective discectomy

contemporary practice the procedure is commonly done by interventional spine physicians and radiologists as well as by surgeons.

EVOLUTION OF PERCUTANEOUS DISCECTOMY The driving force behind the development of percutaneous discectomy was the series of neurological catastrophes that occurred with the use of chymopapain in the United States in the 1970s.1 Chemonucleolysis with chymopapain was introduced into clinical practice in 1964 by Lyman Smith.2 In the years since, it has been demonstrated in randomized controlled trials to be an effective treatment for sciatica due to disc herniation.3 Unfortunately, due to technical errors by some practitioners, chymopapain was injected into the subarachnoid space of a number of patients who developed severe neurological deficits, leading it to be removed from the US market in 1985, although it continued to be available in other parts of the world. The prevailing theory on the mechanism of action of chymopapain at the time was that it relieved nerve root pressure due to disc herniation by ‘internally decompressing’ the disc; that is, by decreasing intradiscal pressure it reduced mechanical tension on a bulging anulus and relieved nerve root compression.4 Onik, who introduced the nucleotome, postulated that decreasing intradiscal pressure by mechanical means would have the same therapeutic effect as chymopapain, while avoiding the dangers associated with chymopapain.5 Subsequent biomechanical studies confirmed that percutaneous discectomy resulted in a decrease in intradiscal pressure.6 Percutaneous discectomy with the nucleotome, which became known as automated percutaneous lumbar discectomy (APLD), was adopted with considerable enthusiasm. This enthusiasm seemed justified by early, nonrandomized studies, which yielded 70–75% success rates in treating patients with sciatica due to a disc herniation with very low complication rates.7,8 However, controlled studies, one comparing APLD to chemonucleolysis and the other to

Selective discetomy

Fig. 84.1 Illustration of goals of selective and nonselective percutaneous discectomy.

Fig. 84.2 Illustration of nucleotome. 923

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B

A

Fig. 84.3 (A) AP and (B) lateral radiographs of Arthrocare spine wand in disc (change highlighted).

microdiscectomy, demonstrated considerably lower success rates of 29–37%.9,10 By the latter part of the 1990s, APLD had fallen out of favor in much of the world, although there continue to be areas, most notably Italy, where it is still commonly performed.

Recently, there has been a resurgence of interest in percutaneous discectomy, coinciding with the introduction of new devices for doing the procedure (Fig. 84.4). These devices are all considerably smaller than the nucleotome and are therefore easier to insert. The

A

B

Image fiber Illumination fiber

Laser Irrigation fiber C

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Fig. 84.4 (A) Dekompressor, (B) Arthrocare spine wand, (C) LASE devices.

Section 5: Biomechanical Disorders of the Lumbar Spine

Dekompressor device is similar to the nucleotome in that it removes tissue mechanically, while both the Lase device and the Arthrocare spine wand vaporize tissue, the Lase device with laser and the Arthrocare device with a low-temperature process known as coblation. As there are no controlled studies available on the efficacy of these devices, at this point it is not possible to determine whether they represent an advance over percutaneous discectomy done with the nucleotome.

INDICATIONS Defining the indications for a procedure requires determining the effects of various clinical variables on outcome. The original indication for percutaneous discectomy, patients with sciatica due to a contained disc herniation, was based on a logical analysis of the effects of the procedure on the disc. Early clinical studies showed good results in that patient population as well as high failure rates in patients with noncontained disc herniations,8 stenosis, or loss of more than 25% of disc height.11 While these observational studies supported the proposed indication for percutaneous discectomy, subsequent comparative studies did not. The comparative study that is most relevant is from Chatterjee et al., who compared the results from percutaneous discectomy against microdiscectomy, which has become the gold standard treatment for disc herniations.10 All patients in that study had a primary complaint of radicular pain and a contained HNP at a single level, the height of which was less than 30% of the sagittal canal size. Patients were randomized to either microdiscectomy or APLD, with the results demonstrating 80% good or excellent outcomes in the microdiscectomy group and 29% in the APLD group. Based upon these results, at present there is no evidence-based justification for the use of APLD over microdiscectomy for the treatment of contained disc herniations. Despite this, there may be a subpopulation of patients with contained disc herniations that will do better with percutaneous discectomy than surgery. Chatterjee et al. noted that the success rate from surgery in their patients, while much better than APLD, was worse than studies on noncontained disc herniations, which have success rates in 90% range.10 They speculated that patients with small contained disc protrusions are different from the overall population of patients with herniated discs, that inflammatory changes may be particularly important in those discs, and that nonsurgical remedies should be sought.10 More recently, Carragee et al. demonstrated that, based on intraoperative findings, contained disc herniations could be classified into two types: those with an associated subanular fragment and those without.12 Furthermore, surgical outcomes differed considerably between the two kinds. Those patients who had a subanular fragment had outcomes comparable to uncomplicated noncontained herniations, while those without a fragment did poorly, including 38% with recurrent or persistent sciatica. Of the types of contained disc herniation defined by Carragee, the one without a fragment would seem to be the most likely to respond to percutaneous discectomy. If there is a fragment of nucleus trapped in the outer annular fibers it would not be expected to shift towards the center in response to a debulking procedure in the center of the disc.1 Debulking the center of the disc may, however, lead to a reduction in the size of a herniation, if pressure equilibrates between the center of the disc and the herniated portion. This latter contention is supported by Castro et al., who found an 80% success rate with percutaneous discectomy when a broad-based protrusion was identified on CT-discography and a 53% success rate with a narrow based herniation.6 In contrast, Dullerud and Johansen did not find any correlation between outcomes following percutaneous discec-

tomy and CT-discography findings.11 Although appealing on theoretical grounds, additional study is needed to determine if the specific subset of contained disc herniation without a subanular fragment constitutes an appropriate indication for percutaneous discectomy.

FUTURE DIRECTIONS The therapeutic effect associated with percutaneous discectomy may be a result of changes in pressure on the nerve that accompany removal of disc tissue. However, clinical studies suggest that there may be other therapeutic mechanisms, as outcome following percutaneous discectomy is independent of changes in disc height and removed disc volume.13 It has been postulated that percutaneous discectomy may lead to pain relief by drainage of inflammatory substances from the disc.14,15 Another potential mechanism is alterations in expression of inflammatory cytokines associated with pain and tissue healing. This latter hypothesis is supported by findings from a large animal model demonstrating that percutaneous discectomy using coblation technology led to significant changes in interleukin-1 and interleukin-8 in degenerated discs.16 Better understanding of the therapeutic effects of percutaneous discectomy may lead to more valid indications for the procedure, as well as optimized treatment protocols, potentially including co-interventions such as pharmacologic manipulation of cytokine networks.16 A particularly intriguing question raised by the results from this animal study is whether percutaneous discectomy may have a role in treating contained disc herniations in patients with a primary complaint of low back pain, rather than sciatica. If percutaneous discectomy affects levels of inflammatory mediators in the disc, then it may be effective in relieving low back pain, in addition to whatever effect it may have on nerve root compression. At present, the gold standard surgical treatment for patients with low back pain secondary to a contained disc herniation is a spinal fusion, which has a considerably lower success rate than a microdiscectomy for sciatica. A number of observational studies have examined the effect of percutaneous discectomy on patients with a primary complaint of low back pain,8,11,14 with success rates ranging from 0%14 to 70%.11 Given the limited options available to patients with discogenic pain, the existing evidence would seem to suggest that a controlled trial is indicated.

SUMMARY The concept behind percutaneous discectomy, minimally invasive treatment of sciatica due to a contained disc herniation, is appealing, particularly given the new, small-profile devices that can be used to perform the procedure. Despite its appeal, the current evidence does not support the use of this procedure over microdiscectomy. However, as all the evidence against percutaneous discectomy is derived from studies using the nucleotome, studies to determine the efficacy of the newer devices are needed. Particular attention should be focused on identifying those contained disc herniations that respond poorly to surgery (i.e. those without a subanular fragment), and determining if percutaneous discectomy will lead to better outcomes.

References 1. Mayer HM. Spine update. Percutaneous lumbar disc surgery. Spine 1994; 19(23):2719–2723. 2. Smith L. Preliminary communication: enzyme dissolution of the nucleus pulposus in humans. 1964; JAMA 187(2):177–180. 3. Gibson JN, Grant IC, et al. The Cochrane review of surgery for lumbar disc prolapse and degenerative lumbar spondylosis [In process citation]. Spine 1999; 24(17):1820–1832).

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Part 3: Specific Disorders 4. Spencer DL, Miller JA, et al. The effect of intervertebral disc space narrowing on the contact force between the nerve root and a simulated disc protrusion. Spine 1984; 9(4):422–426. 5. Onik G, Helms CA, et al. Percutaneous lumbar diskectomy using a new aspiration probe: porcine and cadaver model. Radiology 1985; 155(1):251–252. 6. Castro WH, Jerosch J, et al. Restriction of indication for automated percutaneous lumbar discectomy based on computed tomographic discography. Spine 1992; 17(10):1239–1243. 7. Grevitt MP, McLaren A, et al. Automated percutaneous lumbar discectomy. An outcome study. J Bone Joint Surg [Br] 1995; 77(4):626–629. 8. Onik G, Mooney V, et al. Automated percutaneous discectomy: a prospective multiinstitutional study. Neurosurgery 1990; 26(2):228–232; discussion 232–233. 9. Revel M, Payan C, et al. Automated percutaneous lumbar discectomy versus chemonucleolysis in the treatment of sciatica. A randomized multicenter trial. Spine 1993; 18(1):1–7. 10. Chatterjee S, Foy PM, et al. Report of a controlled clinical trial comparing automated percutaneous lumbar discectomy and microdiscectomy in the treatment of contained lumbar disc herniation. Spine 1995; 20(6):734–738.

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11. Dullerud R Johansen JG. CT-diskography in patients with sciatica. Comparison with plain CT and MR imaging. Acta Radiol 1995; 36(5):497–504. 12. Carragee E J, Han MY, et al. Clinical outcomes after lumbar discectomy for sciatica: the effects of fragment type and annular competence. J Bone Joint Surg [Am] 2003; 85A(1):102–108. 13. Dullerud R, Amundsen T, et al. Clinical results after percutaneous automated lumbar nucleotomy. A follow-up study. Acta Radiol 1995; 36(4):418–424. 14. Kornberg M. Automated percutaneous lumbar discectomy as treatment for lumbar disc disruption. Spine 1993; 18(3):395–397. 15. Gunzburg R, Fraser RD, et al. An experimental study comparing percutaneous discectomy with chemonucleolysis. Spine 1993; 18(2):218–226. 16. O’Neill CW, Liu JJ, et al. Percutaneous plasma decompression alters cytokine expression in injured porcine intervertebral discs. Spine J 2004; 4(1):88–98.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ ii: Lumbar Radicular Pain

CHAPTER

Percutaneous Disc Decompression

85

Curtis W. Slipman, Klaus Birnbaum and Victor W. Isaac

INTRODUCTION An increase in intradiscal pressure resulting from age, disease, or injury may alter the balance between the mechanical, physical, chemical, and pharmacological factors that maintain the cellular activity and tissue morphology of the intervertebral disc resulting in disc protrusion, herniation, and eventual disc degeneration.1 Surgical treatment of intervertebral disc herniation such as open discectomy, microdiscectomy, and laminectomy are often targeted for patients with herniated, extruded, or sequestered discs. In contrast, patients presenting with a contained herniated disc, which has not responded to conservative, noninvasive treatment, are often not considered as surgical candidates. For such herniations, percutaneous disc decompression has been performed using a variety of chemical and mechanical techniques Different concepts of how these methods work have been proposed, including mechanical, chemical, and a mere placebo effect.2,3 The mechanical concept is based on reduction of the intradiscal pressure with successive relief of the pressure of the nerve root or the pain receptors around the disc. Chemonucleolysis, percutaneous nucleotomy, percutaneous discectomy, and laser treatments incorporate this approach, and all have been shown to reduce intradiscal pressure. However, each treatment has its limitations, and success rates vary considerably. The indications for each of these technologies is identical. The ideal patient for percutaneous disc decompression should describe leg pain greater than back pain, provided the diagnosis indicates that pain is caused by a contained disc herniation. Ideal inclusion criteria for patients include: ● ● ● ●

● ● ● ●

Radicular symptoms Leg pain > back pain Physical examination providing objective corroborative evidence If physical examination is not corroborative then objective evidence is obtained with electrodiagnostic testing and/or diagnostic selective nerve root block Magnetic resonance imaging (MRI) or computed tomography (CT) evidence of a corroborative disc protrusion or extrusion If there is evidence of a disc extrusion, coblation technology should be avoided At least 50% of disc height remaining for the involved disc Intensive conservative therapy for 2–3 months that has failed to provide substantial symptom relief. This program should includes active physical therapy, oral antiinflammatory agents, activity modification, patient education, and at least one epidural space steroid instillation

Absolute contraindications include systemic infection, cellulitis, discitis, osteomyelitis, collapse of disc space, sequestered herniations, cauda equina syndrome, uncorrectable bleeding diathesis, and gross instability. One the other hand, relative contraindications include noncontained disc herniation, disc extrusion, and spinal stenosis. FDA approval of the techniques to perform disc decompression has been

for contained disc protrusions at the exclusion of noncontained disc herniations or extrusions. Our experience, as well as that of some leaders in the technique of percutaneous disc decompression, disputes that notion (Personal communications: Guiseppe Bonaldi; Mark Brown). In the instance of spinal stenosis, narrowing of the canal is a multifactorial process, representing a combination of disc protrusion, ligamentum flavum buckling, and zygapophyseal joint hypertrophy. In cases where the disc appears to be the predominant contributor to the stenosis, it may be an effective intervention, whereas it is less likely to be successful in cases of bony or ligamentous causes of stenosis. There has been no reported permanent nerve injury or great vessel damage with these techniques. In contrast, open surgical procedures have a small yet palpable risk of a major adverse event. Ramirez and Thisted4 reported that in 28 000 open discectomies, there was a major complication in 1 in 64 patients, neurological complication in 1 in 334 patients, and 1 in 1700 patients died from the procedure. Pappas et al.5 reported outcome analysis in 654 surgically treated lumbar disc herniations; there were two major vascular injuries, one of which resulted in death. It seems that the safety profile of percutaneous disc decompression is superior to that of open surgery.6

CHEMONUCLEOLYSIS Introduction Chemonucleolysis is a medical procedure that involves the dissolving of the gelatinous cushioning material in an intervertebral disc by the injection of an enzyme such as chymopapain. In 1956, Thomas7 injected papain into the vein of a rabbit’s ear, observed the floppiness of that ear (compared with the erect state of the control ear), and confirmed softening of the cartilage attributable to papain. Chemonucleolysis with chymopapain was introduced by Smith and Brown8,9 in 1964 as an effective therapy for some types of intervertebral disc herniation. However, because of the protein nature of chymopapain, anaphylactic reactions and neurotoxicity have limited the use of this therapy. Although it has demonstrated long-term success rates between 66% and 88%,10,11 a controlled study initiated by the US Food and Drug Administration12 (FDA) found chymopapain no more effective than placebo. Though it has become commercially unavailable in the US, it is still widely used outside of the US. Two enzymes have been described as effective when used in vivo: chymopapain, which catalyzes the hydrolytic cleavage of glycosaminoglycans from proteoglycan aggregates in the disc, and collagenase, which splits the type 2 collagen fibers with relative particularity. The basic collagenase enzyme synthesized by Clostridium histolyticum consists of varied subenzymes that split the collagen fibers at different locations. The purified collagenase is relatively specific for type 2 collagen, seen mainly in the nucleus pulposus, which consists of 15–20% collagen in its dry weight. Wittenberg et al.13 did a 5-year 927

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clinical follow-up assessment of a prospective, randomized study of chemonucleolysis using chymopapain (4000 IU) or collagenase (400 ABC units). At 5 years, good and excellent results were observed in 72% of the chymopapain group and 52% of the collagenase group. If conservative treatment in patients with recurrent disc herniation after chemonucleolysis fails, surgery is usually recommended. Historically, a second injection was considered contraindicated because of the fear of allergic or anaphylactic reactions. Schweigel and Berezowskyj14 suggested a second injection of chymopapain generally is contraindicated. They observed five major anaphylactic reactions in a review of 35 patients. Due to the high incidence of anaphylaxis, they considered repeat use of chymopapain to be an unacceptable alternative to surgery until a definitive test for chymopapain sensitivity is available. Sutton15 did not observe an anaphylactic reaction when patients were premedicated with histamine receptor blockers. The effect of histamine, released by the immunoglobulin E mediated mast cells, will be blocked. Van de Belt et al.16 reviewed 85 patients who received a second injection of chymopapain because of a recurrent disc herniation between 1980 and 1996. All patients were pretreated for 3 days with H1 and H2 receptor blockers. Immediate sensitivity reactions were not seen. Four type 1 and one type 2 reactions were seen after the second injection, and no other complications were seen. Age can be a factor in choosing patients for chemonucleolysis. Patients older than 60 years may lack sufficient mucoprotein in the offending disc to be hydrolyzed. Patients younger than 20 years have not been studied as frequently as older patients, but 80–90% satisfactory results are reported even though stiffness of the back may persist for a year or more. Single-level involvement with leg pain greater than back pain, corroborative physical findings, and imaging studies represent the ideal chemonucleolysis candidate.17 A successful intervention depends on the chymopapain reaching the mucoprotein of the herniated nucleus pulposus to hydrolyze it, so there must not be a sequestrated fragment surrounded by fibrosis or a posterior ligament defect closed by fibrosis to prevent the enzyme reaching an extrusion. If the offending herniation is primarily composed of annular tissue, its collagenous content will not be reduced by chymopapain. Spinal stenosis, whether central or lateral, may be exacerbated by chemonucleolysis rather than helped. Deburge et al.18 reported lateral recess stenosis in 16 patients and two cases of sequestrated discs in 38 patients who had not been successfully treated with chymopapain. For the diagnosis of disc abnormalities, MRI is superior to CT scan However, MRI is not as effective in the diagnosis of bony lesions, which makes CT scan essential in the preoperative evaluation of chemonucleolysis. With CT scan, information regarding chronic degenerative disc abnormalities, such as lateral recess stenosis and facet hypertrophy, as well as bony spurs and calcified discs, may be obtained. If a soft protrusion is demonstrated without spinal stenosis on CT scan, the success rate is expected to be better (Table 85.1).19

Complications Between 1982 and 1991, 121 adverse events in 135 000 patients were reported to the FDA and investigated. Seven cases of fatal anaphylaxis, 24 infections, 32 bleeding problems, 32 neurological events, and 15 miscellaneous occurrences were found. The overall mortality rate was 0.019%.17 A major disadvantage of chemonucleolysis is the occurrence of back spasm, which can be quite severe in approximately 10% of patients.17 Comparing the complications of laminectomy reported by Ramirez and Thisted.4 in 1989 with those of chemonucleolysis, Nordby et al.17 reported that he found anaphylaxis to be unique to chemonucleolysis; infection occurred 17 times as often with laminectomy as with chemonucleolysis, neurologic and hemorrhagic events 928

Table 85.1: Contraindications for chemonucleolysis ABSOLUTE Allergy to chymopapain or papaya derivatives Central/lateral spinal stenosis Cauda equina syndrome Sequestered disc fragment Fibrosis due to prior surgery Failed back surgery syndrome Arachnoiditis Multiple sclerosis Pregnancy Profound or rapidly progressive neurological deficit Severe spondylolisthesis Spinal cord tumor Spinal instability RELATIVE Polyneuritis of diabetes Hypertension Morbid obesity Stroke Patients on beta blockers are at increased risk, should anaphylaxis occur, because beta blockade inhibits the effects of epinephrine

six times as often with laminectomy, and mortality rates incidental to the procedures occurred three times as frequently with laminectomy. Other potential complications include overdecompression, disc collapse, or instability of the motion segment. These side effects can result from excess ‘digestion’ of disc material. More serious complications have been reported, including lumbar subarachnoid hemorrhage and paraplegia. When chymopapain is inadvertently injected into the subarachnoid space, a cauda equina syndrome results.20 Wittenberg et al.13 reported cauda equina syndrome in two patients using collagenase. A case of acute transverse myelitis (ATM) was observed 21 days after an injection in 1982, and an additional five cases were subsequently reported to the FDA.21 Since no case of ATM has occurred in nearly 60 000 cases since 1984, an association between ATM and chemonucleolysis probably does not exist. Consequently, as of 1992, the FDA approved removing even the mention of ATM from the detailed chymopapain package Full Prescribing Information.21

Long-term results Following chemonucleolysis, relief of leg pain is immediate; however, in up to 30% of patients, maximal relief of symptoms may take up to 6 weeks. There are some specific measures that can be utilized during chemonucleolysis to reduce the incidence of low back pain which includes infiltrating the needle track with local anesthetic and the use of antiinflammatory medications after the procedure.22 A prospective, placebo-controlled, double-blind, multicenter, crossover trial of 88 patients demonstrated a 73% success rate in the

Section 5: Biomechanical Disorders of the Lumbar Spine

chemonucleolysis group and a 42% success rate in the placebo group The failures in the placebo group later underwent chemonucleolysis and had a 90% success rate.23 The primary end point for considering a patient a failure was if the patient had pain severe enough to consider another intervention for treatment. Nordby et al.17 reported that in a 7–10-year follow-up of 3130 patients with chemonucleolysis, overall satisfactory results were reported from 71–93% among the 13 contributors for an average of 77%. The use of chymopapain has been greater in Europe and Australia than in the United States since the acute transverse myelitis scare, and intrathecal complications have been rare there. A combined long-term report of 1736 patients in 1992 from the United Kingdom, France, and Germany showed good to excellent results of 66–84%, with an overall average of 75.3%. A prospective, randomized, controlled trial comparing automated percutaneous lumbar discectomy (APLD) to chemonucleolysis for the treatment of sciatic pain reported a 1-year outcome of 66% success in the chemonucleolysis group and 37% in the APLD group.24 The most compelling evidence that chemonucleolysis is a safe and effective treatment for herniation of the nucleus pulposus is found in well-designed and conducted prospective, randomized, double-blind studies in the United States and Australia.25 One of these double-blind studies has been carried through for 10 years without code break or loss of follow-up. Success persisted in 77% of patients with chemonucleolysis compared with only 38% for the placebo group (p=0.004). Only six of the patients with chemonucleolysis had required laminectomy compared with 14 in the placebo group (p=0.028). Launois et al.26 reported the success rate at 1 year for chemonucleolysis at 88% and for laminectomy at 76%. Chemonucleolysis continued to be superior to surgery after an additional year. In a 9–11-year prospective, randomized study comparing patients with these two methods, Wilson et al.27 concluded that ‘surgically treated patients that had done well initially deteriorated with time, whereas those who did well following chemonucleolysis maintained a successful outcome in the long-term cost savings.’ A major consideration in cost savings is the absence of epidural scarring or adhesive arachnoiditis with chemonucleolysis, thus avoiding the frequent ‘failed back syndrome’ seen with laminectomy, which has become an ever-increasing health and economic burden.28 When the results of surgery after chemonucleolysis failure were compared with the results from microdiscectomies performed without prior injections, slightly more good and excellent results were observed in the primary surgery patients.29 Other authors such as McCulloch and MacNab30 stated that open surgery was easier after prior chemonucleolysis. Norton31 obtained very poor results in patients treated either surgically or with chymopapain. All of his patients were claiming workmen’s compensation. Others have shown that on treatment with chymopapain such patients do not respond as well as those who are more highly motivated and covered by private insurance. Nordby and Wright32 reported that 45 studies were analyzed, some including comparisons of chemonucleolysis to open laminectomy/discectomy and others to percutaneous discectomy. Individual success rates exceeded 60%, whereas cohort total averaged 76%. In studies comparing chemonucleolysis with open discectomy, success rate averaged 76.2% as compared with 88% for open surgery. In two other studies, percutaneous discectomy was less successful than chemonucleolysis. Where included, duration of hospitalization showed less time and thus less costs for chemonucleolysis. Return to work compilations showed time off slightly less for chemonucleolysis than for laminectomy. Wittenberg et al.13 reported a 5-year clinical follow-up assessment of a prospective, randomized study of chemonucleolysis using chymopapain (4000 IU) or collagenase (400 ABC units); patients in the chymopapain group started work in the same job an average of

8 weeks after injection, whereas patients in the collagenase group returned to work after an average of 11 weeks. Kim et al.19 reported that three thousand patients with herniated lumbar disc were treated with chemonucleolysis between 1984 and 1999 and found that the clinical success rate in their series was 85%. The patient group with the chief complaint of leg pain achieved a better clinical outcome than the patient group with low back pain (88% versus 59%), and a positive straight leg raising test was strongly correlated with good clinical outcome. Patients manifesting a soft, protruded disc had a better outcome than those manifesting diffuse bulging disc. Other prognostic factors favoring a good outcome were young age, short duration of symptoms, and no bony spur or calcification on radiological study. Revel et al.33 conducted a randomized clinical trial to compare the results of automated percutaneous discectomy with those of chemonucleolysis in 141 patients with sciatica caused by a disc herniation; 69 underwent automated percutaneous discectomy and 72 were subjected to chemonucleolysis. The principal outcome was the overall assessment of the patient 6 months after treatment. Treatment was considered to be successful by 61% of the patients in the chemonucleolysis group compared with 44% in the automated percutaneous discectomy group. At 1-year follow-up, overall success rates were 66% in the chemonucleolysis group and 37% in the automated percutaneous group. Within 6 months of treatment, 7% of the patients in the chemonucleolysis group and 33% in the discectomy group underwent subsequent open surgery. The complication rates of both treatment groups were low, with the exception of a high rate of low back pain in the chemonucleolysis group (42%). In another prospective study, 22 patients with painful disc herniations were randomized either to chemonucleolysis or APLD; at 2 years the chemonucleolysis-treated patients were significantly better, based upon outcomes as measure with the Oswestry Disability Index, back pain and leg pain recurrence.34 The combination of low-dose chemonucleolysis with 500 IU chymopapain followed by an automated percutaneous nucleotomy of the cervical spine has been performed. A follow-up of at least 1 year of the first 22 patients showed in 19 patients good or excellent results. In one patient a fair result was obtained and in two patients the symptoms were unchanged.35

AUTOMATED PERCUTANEOUS LUMBAR DISCECTOMY Introduction In 1975, Hijikata et al.2 performed the first percutaneous discectomy using modified pituitary rongeurs. A decade later in 1985, Onik and colleagues24 developed the nucleotome, an automated suction shaver that allows for the performance of an automated percutaneous lumbar discectomy (APLD). The shaver functioned by drawing the nucleus pulposus into a small cutting port and eliminated a portion of the nucleus via a reciprocating ‘guillotine-like’ blade. APLD utilized a 20.3 cm needle inserted through a 2.8 mm diameter cannula. Onik and Helms36 reported an 85% success rate independent of the amount of disc material removed. It is believed that the removal of nuclear material from the center of the disc results in disc decompression. Ultimately, it is believed this decreases pressure transmitted through the rent in the anulus to the herniation. This results in decreased pressure on the affected nerve.

Indications Different morphological and pathophysiological parameters are used to define criteria for selecting candidates for APLD. Some clinicians 929

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stress the value of CT discography. Mochida and Arima37 demand the absence of perforation of the posterior longitudinal ligament and degenerative canal stenosis detected by CT or MRI along with other clinical guidelines including age and disturbance of innervated muscles. APLD is efficacious for patients whose herniations are still contained by the anulus or the posterior longitudinal ligament. Patients with sequestered fragments are not candidates because there is no biomechanical mechanism by which that fragments would be resorbed. MRI can be extremely helpful in excluding obviously migrated fragments and large disc extrusions.36 An absolute contraindication of APLD is the migration of a disc fragment. When small degrees of migration are present (3 mm or less) the possibility of a good result from APLD is not precluded. The success rate for APLD is about 43% in those patients who had fragments that migrated more than 3 mm from the disc space. In a study by Carragee and Kim examining outcomes of open discectomy, it had been shown that herniations larger than 6 mm generally did well with discectomy, whereas smaller herniations were associated with a poor outcome (26% success).38 These studies suggest that patients with smaller herniations are ideal candidates for APLD and probably with other techniques that effect percutaneous disc decompression. A CT discogram is the most definitive procedure for selecting patients for APLD which demonstrate complete tears of the anulus and posterior longitudinal ligament. A CT discogram also allows the assessment of the size of the rent in the anulus that is communicating with the herniation. Besides the characterization of the herniation on imaging studies, patients should clinically have the symptoms of radiculopathy.36 APLD is not a procedure for those patients with vague or equivocal symptoms or simply a bulging disc. APLD can be an excellent procedure for patient who has had a reherniation at the site level of previous disc surgery. These patients who are reoperated at the same level obtain lower success rates, as well as being exposed to a much higher morbidity due to lack of tissue planes caused by epidural fibrosis. APLD takes a posterolateral course that avoids the epidural space and does not create epidural fibrosis. Mirovsky and Neuwirth39 reported 10 patients with lumbar disc reherniation at the same level as a previously open operation with follow-up of 2.5 years They report that 70% of their patients showed complete or significant pain relief avoiding reoperation. Sixty percent showed motor deficit improvement. Failure was primarily relegated to those with spinal stenosis or segmental instability. Onik et al.40 reported that patients whose herniations occur in the lateral location beyond the intervertebral foramen are candidates for APLD. Such patients are difficult to treat with the traditional interlaminar approach of microdiscectomy, which requires the removal of all or a large portion of the facet. APLD showed excellent results in those patients because the percutaneous discectomy instrumentation drives over the herniation itself. The poor results occurred in patients with concomitant stenosis.41 ALPD can be the procedure of choice for those patients suspected of infectious discitis. The first principles of treatment for disc space infection are to make the diagnosis and isolate the organism. Diagnosis may be delayed because patient’s complaints are relatively non-specific. Imaging studies may direct one to the diagnosis, but tissue must be obtained for the confirmation and isolation of the organism. APLD biopsy is a minimally invasive procedure for obtaining sufficient material for histological analysis and culture. The rate of secondary surgical intervention may be reduced if infected disc material is removed by percutaneous biopsy; however, surgical treatment is indicated in all patients who develop neurological deficits as well as in the presence of epidural or retroperitoneal abscess.42 930

Gebhard and Brugman43 reported a case in which nucleotome was used to remove 5 ml of disc material and the disc space was irrigated with 75 ml of normal saline containing cefazolin, the patient reported immediate relief of his back and thigh pain. Fouquet et al.44 obtained bacteriologic diagnosis in only nine of 25 patients biopsied with a Mazabraud trocar. Krodel et al.45 reported seven positive cultures of 15 patients who underwent needle biopsy. Yu et al.46 described two cases in which automated biopsy was used to diagnose unusual infections include Candida discitis and tuberculosis. Percutaneous discectomy has been used also in the treatment of cervical disorders. Theron et al.,47 in 1992, reported preliminary experience in 23 cases. All patients complained of neck pain or brachialgia due to single, soft herniated disc at a single level; the success rate was 80%. They later reported 78 treated cases, including 68 with follow-up of at least 6 months and overall success rate of 70.6%, and no complication was reported (Table 85.2).

Complications Complications result from periprocedural issues or from the technique. Periprocedural complications may involve adverse reactions to anesthetic, sedative/analgesic medications, perioperative antibiotic prophylaxis, or intravenous fluid management. Technique-related complications include nerve root injury, discitis, osteomyelitis, cellulitis, uncontrolled bleeding, dural puncture, annular injury, and vertebral endplate injury. Matsui et al.48 reported a rare complication of a case of lateral disc herniation which occurred soon after percutaneous discectomy. In that case, it appeared that the extrusion occurred through the hole in the anulus made during the procedure.

Long-term results Mochida and Arima37 reported that the postoperative pain relief and patient satisfaction that can be achieved by APLD is related to patient age, motor function of the lower limbs, and the length of preoperative

Table 85.2: Contraindications for APLD ABSOLUTE Cauda equina syndrome Sequestered disc fragment Arachnoiditis Pregnancy Profound or rapidly progressive neurological deficit Severe spondylolisthesis Bleeding dyscrasia Spinal instability or fracture Spinal tumor RELATIVE Previous open surgery at proposed treatment level Central stenosis Significant bony spurs that could block percutaneous entry into the disc space

Section 5: Biomechanical Disorders of the Lumbar Spine

conservative treatment. Hijikata49 reported poorer results at the level L5–S1. Others reported that the only significant predictive factor for a positive outcome with respect to pain relief and satisfaction was age. Outcome is also influenced by physical activity. Patients who are active in sports are significantly more satisfied compared to patients who are not, but sporting activity is not in itself a predictive factor for a positive outcome.50 Sahlstrand and Lonntoft51 evaluated the size of the disc herniation with MRI before, on the day, and 6 weeks after APLD and compared the MRI findings with the early clinical outcome. The development of pain, nerve root tension sign, and neurological findings were analyzed and no significant difference in the maximum protrusion of the disc herniation among the three measurements was reported. The sciatic pain improved significantly on the first day after the procedure, but not at 1 week or 6 weeks after the procedure. There was no correlation between the MRI findings and the early clinical outcome. It has been reported that with APLD approximately 2–7 g of human disc has been removed. The amount of disc material retrieved is superior to any the other methods of percutaneous discectomy. In a study by Chatterjee et al.52 comparing APLD with microdiscectomy for contained herniations, the microdiscectomy group had an 80% success rate. The risk of reoperation was reported by Bernd et al.50 to be 25% while Nachemson53 reports that 6.6% of patients in his study required reoperation. Stevenson et al.54 did a cost-effectiveness study of APLD versus microdiscectomy in the treatment of contained lumbar herniation in a randomized, controlled trial and found that APLD is less cost-effective than microdiscectomy. In summary, APLD has a positive effect in patients suffering from pain related to disc herniation. Outcome is influenced by the natural course, patient age, the extent of nerve involvement, and physical activity.

PERCUTANEOUS LASER DISCECTOMY Introduction In 1984, percutaneous laser disc decompression was pioneered in America by Choy et al.,55,56 who were intrigued by the principle that a small change in volume in a contained area results in a large change in pressure. This pressure reduction was demonstrated by Choy and coworkers in 18 cadavers. They measured intradiscal pressure using a pressure transducer that was inserted into the lumbar discs. Afterwards, 1000 J from an Nd:YAG, 1.32-ym laser was delivered through a quartz fiber. The mean intradiscal pressure after loading (pre-treatment) was 2419 mmHg. After laser treatment, the mean pressure decreased by 1073 mmHg, a decrement of 44%. The laser (Light Amplification by Stimulated Emission of Radiation) transmits energy in the form of light. This light is transformed into heat, which can simultaneously cut, coagulate, and vaporize tissue. The primary advantage of laser energy is its ability to focus at a single point. Several types of laser are available. The most commonly used are the KTP laser (potassium-titanyl-phosphate), Nd:YAG (neodymium:yttrium-aluminum-garnet) and Ho:YAG (holmium:YAG). The choice of laser type is dependent on the ability of energy to be delivered through a fiberoptics system, tissue absorption/ablation properties, and the amount of thermal generation and spread.57 Hellinger et al.58 reported that percutaneous laser discectomy with the Nd:YAG laser (1064 nm) markedly reduces the postoperative density by 20% in protrusion and extrusion of the intervertebral discs. Percutaneous laser discectomy of the cervical disc herniation spine can be done under X-ray fluoroscopy. CT-guided technique also provides safe and accurate position of the needle tip during puncture of the needle on axial images, permitting accurate laser ablation of the

intervertebral disc. The use of CT also avoids damage to adjacent and visceral structures since it is superior in spatial and soft tissue resolution to X-ray fluoroscopy (Table 85.3).59 Ohnmeiss et al.57 found that patients who met the following criteria, which included leg pain, positive physical examination finding, discographic confirmation of contained disc herniation, and no stenosis or spondylolisthesis, found that the success rate was 70.7% and the success rate was only 28.6% among patients who did not meet all the criteria. The advantage of performing discography immediately before laser disc discectomy is that it could be performed through the same needle placement to be used for the laser discectomy. The advantage of performing discography 1 or more days prior the laser discectomy that it allows more time to evaluate the discogram results and increases the allotted time for a patient to consider alternative treatments. The contraindications of this procedure are paralysis, hemorrhagic diathesis, spondylolisthesis, spinal stenosis, previous surgery at the indicated level, significant psychological disorders, significant narrowing of disc space, and industrial injuries with monetary gain. For 2 weeks after the procedure, any position that could induce hyperkyphosis as well as athletic activities should be restricted.61 The use of percutaneous laser disc decompression for the treatment of erectile dysfunction caused by herniated disc disease has been reported in two patients.62 In addition to the early return of the erectile function in both patients, immediate pain relief was achieved in the second case. Follow-up visits confirmed continued normal sexual function and lack of pain.62

Complications Choy et al. reported one case of discitis. Bosacco et al.63 reported one minor complication involving a single patient, who had acute urinary retension and reflex ileus, out of 63 patients who underwent laser disc decompression with KTP 532 laser. There were no complications involving infection, hematoma, neurological injury, myelitis, or great vessel disease. Nerubay et al.64 reported complications with symptoms and signs of root irritation in 4 of 50 patients who underwent CO2 laser discectomy which were probably caused by thermal damage to the root caused by warming the cannula. Ohnmeiss et al.57 reported

Table 85.3: Contraindications for percutaneous laser discectomy ABSOLUTE Central stenosis Significant bony spurs that could block percutaneous entry into the disc space Facet hypertrophy Sequestrated disc fragment. Ruptured posterior longitudinal ligament ( epidural leak of contrast medium in discography) RELATIVE Progressive neurological deficit Involvement in workers’ compensation cases Previous surgery at the same disc level

931

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one case of reflex sympathetic dystrophy and 12 cases of postoperative dysesthesia among 164 patients who underwent leaser disc discectomy. Hellinger65 reported bowel necrosis, subsequently requiring resection, resulting from inadvertent perforation of the anterior anulus and two cervical cases of infections with succeeding neurological deficits. In one case there was a reversible paresis of the arm and in the other case there was paraplegia. Hellinger and Hellinger describe their outcomes and complications in greater detail in Chapter 29.

Long-term results Percutaneous laser discectomy has been performed on both cervical and thoracic disc but the numbers are so small as to make their reporting anecdotal. The advantages of laser discectomy include short recovery time, it is performed under local anesthesia, it reduces the soft tissue and bone injury, there is no epidural fibrosis, lessened chance of creating instability since only a small amount of tissue is removed, and reduced missed time from work.57 Disadvantages include the relative expense of the procedure and inadequate temperature control causing nerve root, vertebral body, and endplate damage.73 Choy et al.67 reported the results of 333 patients in whom they performed laser discectomy with the Nd:YAG laser and obtained 78.4% good results and poor responses for 21.6%. One hundred and sixty patients experienced immediate pain relief during the procedure. Choy also reported in another study that there is no association between outcome and sex, age, duration of symptoms, or disc level.74 Liebler60 reported that the success rate of the KTP laser based on 2 years’ follow-up was 72% and the success rate with the Nd:YAG laser was very similar, at 70%. For all patients, the average overall pain index declined immediately after the procedure. Pain intensity had a tendency to decrease as the duration of the follow-up continued, but this was not the case for the neurological findings. There were no statistical differences noted in knee jerk, ankle jerk, pin prick and Lasague’s sign as a function of disc level and follow-up for all patients. Nerubay et al.66 reported the results of 50 patients in whom they performed laser discectomy with the carbon dioxide laser and obtained 74% good results. Chronic effects of laser discectomy have been evaluated in animals. Using a CO2 laser for cervical discectomies in a canine model, Gropper et al.69 found that the disc, easily and safely ablated, was replaced by dense, fibrous tissue in 10 weeks. Using Ho:YAG laser, Black et al.70 noted a similar effect in pigs. Laser discectomy yields results comparable to those of manual or automated percutaneous discectomy,47 but is considerably more expensive. Percutaneous laser nucleolysis can damage endplates from excess thermal energy,66 and also has been shown to be significantly less effective than chemonucleolysis.71 Dangaria72 reported 15 cases where laser was used as a second attempt to relieve the symptoms of lumbar disc herniation in patients having undergone prior percutaneous discectomy with unsuccessful outcome. He found that only three out of 15 patients had good results, while none had excellent results. Chiu et al.73 reported that cervical discectomy with laser thermodiscoplasty is safe and effective for the treatment of cervical disc herniation. A 94.5% success rate was obtained in 200 patients selected through diagnostic MRI, CT, and electromyogram (EMG) correlated with signs and symptoms. Knight et al.74 also reported that cervical laser disc decompression produces sustained and significant clinical benefit in over 51% of patients observed for a mean period of 43 months. In a further 25%, functional benefit was achieved. Paresis, sensory deficits, neck pain, brachialgia, and headache improved considerably in most patients. 932

NUCLEOPLASTY (COBLATION) Introduction Coblation is a new minimally invasive procedure, using radiofrequency (RF) energy to remove nucleus material and create small channels within the disc. With coblation technology, RF energy is applied to a conductive medium, causing a highly focused plasma field to form around the energized electrodes. The plasma field is composed of highly ionized particles. These ionized particles have sufficient energy to break organic molecular bonds within tissue and form a channel. The by-products of this non-heat-driven process are elementary molecules and low molecular weight inert gases, which are removed from the disc via the needle. On withdrawal of the Perc-DC® Spine Wand, the newly created channel is thermally treated, producing a zone of thermal coagulation. Thus, nucleoplasty combines coagulation and tissue ablation to form channels in the nucleus and decompress the herniated disc. The temperature is kept below 70°C to minimize tissue damage. Unlike chemonucleolysis, nucleoplasty is not dose dependent, and pressure changes seem to occur quicker. Chen et al.75 assessed the intradiscal pressure change after disc decompression with nucleoplasty in human cadavers, and found that intradiscal pressure was markedly reduced in the younger, healthy disc cadaver. In the older, degenerative disc cadavers, the change in intradiscal pressure after nucleoplasty was very small. There was an inverse correlation between the degree of disc degeneration and the change in intradiscal pressure. The limitation of this study was that pressure measurements were performed on cadavers and not in vivo. Chen et al.76 also reported that after histological examination of disc and neural tissue in two pigs that underwent coblation there was no evidence of direct mechanical or thermal damage to the surrounding tissues and there were clear evidence of coblation channels with clear coagulation borders of the nucleus pulposus. Normal histological findings of the anulus and endplate with normal neural elements of the spinal cord and nerve roots at the level of the procedure were observed. Since its first application in July 2000, the DISC Nucleoplasty procedure has been used to treat over 55 000 patients in the USA and around the world. Other techniques used for percutaneous disc decompression have suffered from the following limitations: Removal of too much tissue – Decompressing the disc in most cases requires the removal of only a small amount of tissue. Excessive tissue removal can cause the disc to lose height, possibly leading to disc degeneration. DISC Nucleoplasty allows controlled removal of a precise amount of tissue by the surgeon. Indiscriminate removal of tissue – removing tissue beyond a small, targeted area can cause injury to the anulus of the disc, or to other surrounding structures in the spine. DISC Nucleoplasty provides the surgeon with full control over which tissue is removed. Thermal injury to the disc – high temperature (>100°C) tissue removal systems (including laser) remove tissue by exploding molecules with extreme temperatures, but with the result that remaining tissue can be severely burned or charred. This is particularly of concern in the disc where there are no blood vessels to allow necrotic tissue to be resorbed into the body. DISC Nucleoplasty does not rely on heat for tissue removal, and does not introduce excessive heat to cause such tissue damage in the disc. Aggressive access into the disc – introduction of large instruments into the nucleus of the disc can cause irreparable damage to the anulus. Such damage has been shown to lead to the onset or acceleration of disc degeneration. DISC Nucleoplasty uses a small 17-gauge needle to access the disc; no technique uses a narrower needle to decompress the disc.

Section 5: Biomechanical Disorders of the Lumbar Spine

Coblation can be performed from either side of the affected disc, not just from the ipsilateral, symptomatic side. Thus, treatment approaches are not limited to one site only.

Indications The inclusion criteria for cervical or lumbar coblation are leg and back pain with MRI evidence of contained disc protrusion with a disc height >50%, after failed medical rehabilitation, and interventional spine therapy for 4 weeks. The exclusion criteria are disc height <50%, complete annular disruption revealed by discography, and moderate to severe bony and/or ligamentous spinal stenosis. Spinal stenosis caused by a large central disc protrusion is not a contraindication for this technique.

Operative procedure using Perc-DC® for the cervical spine Technique At first, the surgeon has to find the right position of the introducer needle by an anterolateral (AP) approach. It will be in the lateral border of the disc with an approach from the right side of the patient, who is supine. The esophagus and trachea are displaced to the left and the internal carotid artery to the right. Within this newly created artificial, plane the introducer needle is advanced into the disc space. The introducer needle has a sharp stylet tip and a luer lock. In contrast, the catheter for the cervical disc (Perc-DC® Wand) has a looped tip with a small profile. Typically, the needle is advanced until it reaches the midpoint of the disc as viewed in lateral and AP images. Once that position is reached, the stylet is gradually removed while the needle is simultaneously and incrementally advanced. In this fashion the needle tip will now be in the middle of the disc. This is an important step, as the initial placement of the introducer needle insures that the edge of the stylet, which protrudes 2 mm from the introducer needle, is in the center of the disc and not the needle tip. If this step is not pursued, the needle may have very little purchase in the nucleus and/or annulus, leading to the needle migrating out of the disc. Proper needle position is reconfirmed by viewing in at least two planes. Then, using real-time imaging, the coblation wand is advanced into the introducer needle and then into the disc. If the tip of the wand begins to bend, repositioning of the introducer needle is required. The Perc-DC device is locked on to the needle hub through a screw mechanism during the procedure. Once the device is locked in placed, an electrical cord is attached to the wand and the RF machinery. Application of the coagulation mode for 5–10 seconds and querying the patients regarding the presence of extremity symptoms prevents any catastrophic neural injury. The percutaneous decompression will then be done by coblation mode. Tissue ablation is accomplished by rotating the wand 360 degrees. The wand is rotated over a 10-second interval. This is repeated once or twice, after slightly withdrawing the needle/wand complex such that is resides in a different portion of the nucleus. Of course, proper position is checked visually and then coagulation mode is used to determine if neural stimulation has occurred. If proper position is confirmed and no extremity pain is perceived, another ablation mode is completed. The authors typically use a power setting of 2, but at times have used a power of 3. At the conclusion of the procedure the catheter is withdrawn into the introducer needle and then both are simultaneously removed.

Postoperative procedure Typically, the patient can return to light work after 1 week. In the lumbar spine, postoperative bracing for 1–2 weeks after the operative

procedure may be needed. Lifting is limited to 5–10 pounds for 2 weeks after the lumbar spine procedure. After the cervical procedure, we recommend wearing of a soft collar for 2–7 days postoperatively. Gentle exercise should start after 1 week postoperatively.

Complications The potential complications following cervical coblation include laceration of the ipsilateral internal carotid artery, vertebral artery, or jugular vein. The spinal cord can be impaled, or the trachea or esophagus can be pierced. If the esophageal wall is breached, there is a dramatic increase in the risk of discitis unless a new introducer needle is used. A common event is passage through the thyroid and the development of a hematoma. This side effect is invariably transient provided repeated prodding of the thyroid did not occur. Firm external compression for 5 minutes following the completion of the coblation procedure is recommended if concern about thyroid injury arises. One of the simplest ways to minimize these potential complications is to perform this technique only from the right side because the esophagus and trachea tend to rest slightly left of the midline. Using a sterile marking pen to outline the internal carotid may be helpful; however, we do not routinely do this. At the C2–3 and less commonly the C3–4 level, the esophagus may overlie or rest very close to the anticipated path for the introducer needle. In cases in which the margins of the esophagus are not clear we have the prospective candidate swallow a barium paste to outline the margins of the esophagus, thereby allowing us to avoid this bacterial reservoir. There are instances in which the introducer needle will back up after proper positioning has been accomplished. It is therefore strongly recommended that the introducer needle and catheter position be checked prior to stimulating with coagulation. Prospective data on complications and side effects of lumbar nucleoplasty reported soreness at the injection site as the most common side effect, which dropped rapidly after the first 72 hours postprocedure. Numbness and tingling were the next most commonly reported side effects.77 Finally, it cannot be overemphasized that the most important issue to avoid serious postprocedure sequelae is physician experience. Cervical coblation is not for novices or those who have not performed in excess of 100 cervical discograms.

Long-term results Slipman et al.78 reported their initial experience using nucleoplasty in five patients with cervical radiculopathy. All subjects showed 75% reduction in the Visual Analogue Scale (VAS) score at all follow-up intervals. Of five patients, four returned to full-time work within 2 weeks postprocedure. In another pilot study by the author,78a 20 consecutive patients with a mean age of 43.4 years were prospectively enrolled. All patients underwent cervical combined percutaneous plasma field discectomy and nerve root glucocorticoid injection. The average symptom duration preprocedure was 35.9 weeks. Each patient was deemed an appropriate operable candidate by the spine surgeon. The mean size of the focal protrusion was 3.6 mm and the mean size of the canal was 11.7 mm. There was a statistically significant VAS rating reduction at each follow-up ( p<0.001), which transpired at 2 weeks, 4 weeks, 3 months, 6 months, and 1 year. The preprocedure VAS rating for the cohort was 7.0 and at each of the follow-ups it was 2.9, 2.1, 1.7, 1.2, 1.3, and 1.4. No significant early-term side effects were noted. Five patients experienced minor bleeding, which resolved by 72 hours. All patients experienced self-limited soreness at the procedure site. One patient underwent surgical intervention between 8 and 12 weeks, and returned to work pain free. 933

Part 3: Specific Disorders

Derby et al.79 reported greater than 50% VAS improvement at 3 months’ follow-up in nine patients with neck or upper axial back pain who underwent nucleoplasty. The results in controlled trials are total resolution of leg pain in 70% of cases and patient satisfaction after 6 months in around 80%.80,81 Nardi et al.82 reported the results of his prospective study in which 50 patients underwent cervical coblation. There results were compared to 20 controls. Unfortunately, the average follow-up interval was only 3.8 months (range 2–9 months). The coblation group achieved 80% success, while the controls 15%. Since there is only one reported, and as of yet not published, longterm study, it is difficult to distinguish between the treatment effect and the natural history of the disease. As well, we want to determine whether the benefits of this procedure are sustained beyond 12 months, thereby subjecting this technology to the same criteria as used for determining whether open surgery is effective.

Percutaneous discectomy using the Dekompressor The Dekompressor is a single-use disposable lumbar discectomy probe that passes through and works in conjunction with a 15 mm introducer cannula to remove intervertebral disc nucleus pulposus material (Fig. 85.1) It is manufactured by the Stryker Corporation and has been available for clinical use since 2004. Devices made for cervical and lumbar access vary by the length and/or width of the probe. The cervical device is 3.5 inches in length and is placed within a 19-gauge introducer needle The three lumbar dekompressors are 6 inches in length and inserted through a 17-gauge or 19-gauge introducer needle and the third is 9 inches in length and inserted into a 17-gauge needle, This array of lumbar devices allows for the treatment of thin through obese patients.

Technique The Dekompressor is introduced into the disc in a similar fashion to performing nucleoplasty. A point of entry is established that allows the working device to traverse the longest possible length of the disc through an extrapedicular approach. The patient is placed in a left lateral decubitus position with a slight obliquity on a fluoroscopy table. As in all decompression techniques the patient is prepped and draped in sterile fashion. Conscious sedation is administered intravenously. Disc access via an extrapedicular approach is then gained using a 1.5 mm (17-gauge) Dekompressor cannula with stylet under fluoroscopic guidance. Once the cannula is in place, the stylet is removed and the probe (titanium auger) is introduced through the cannula into the disc (Figs 85.2–85.4). As part of the construction of the probe, the auger has been connected to a disposable rotational motor, which spins the probe. The rotational motion of this probe creates

suction and removal of nucleus pulposus through the cannula using the Archimedes pump principle. The nuclear material collects along the length of the probe and in some instances reaches the collection chamber at the base of the probe. We perform two or three passes of the probe/introducer needle complex and then withdraw the probe. This allows us to check the amount of nuclear material removed. If there has not been sufficient material removed, the stylet is replaced into the introducer needle and placed in new position within the disc. Once sufficient nuclear material has been removed, the introducer needle/probe complex is gradually withdrawn and then discarded. Typically, we perform a therapeutic selective nerve root block at the affected nerve root.

Indications Patients with lumbar radiculopathy due to contained focal disc protrusion or diffuse disc bulge/central focal protrusion causing spinal stenosis may be candidates for this procedure. In our experience, patients with disc extrusions are candidates as well.83

Contraindications Contraindications include the following: ● ● ● ● ● ● ● ● ● ●

Less than 50% disc height preservation; Spinal instability or fracture; Spinal tumor; Cauda equina syndrome; Arachnoiditis Pregnancy; Profound or rapidly progressive neurological deficit; Severe spondylolisthesis; Bleeding diatheses; and Sequestered disc fragment.

Complications Complications with the Dekompressor include the risk of infection, bleeding, nerve damage, endplate injury, increased pain, discitis, paralysis, anaphylaxis, device malfunction, and death. Thus far, there are no case reports in the literature describing any of these potential complications with this novel device.

Outcomes To date, only two articles have been published reporting outcomes.84,85 Amoretti et al.85 reported on 10 cases where 8 of 10 patients described 70% drop in VAS scores in follow-up ranging from 6 to 10 months. Alo et al.84 published a study in 2005 describing a cohort of 50 patients with lumbar radicular pain with 1-year follow-up data. Patients included in this study had to have history and

Activation switch Moveable depth marker 1.5 mm cannula

Removeable collection chamber

Probe tip

934

Fig. 85.1 Lumbar Dekompressor and blow-up of probe tip.

Section 5: Biomechanical Disorders of the Lumbar Spine

Fig. 85.2 Introducer needle inserted into affected disc using an extrapedicular approach.

examination, and MRI findings. If the examination did not provide objective correlative data, an electrodiagnostic study was performed. If that was negative, a diagnostic selective nerve root block was completed. If each of these criteria was met and there was failure of proper medical rehabilitation and interventional spine treatment, the patient was selected to be in the study. Preliminary results show that 41 of 47 patients remain in the study at 6 months. Of the six who have failed percutaneous discectomy with the Dekompressor, four patients went onto surgery, one to acupuncture, and one was successfully treated with pregabelin. One of the 41 patients had not been treated for radicular pain, but for weakness. This patient described a marked improvement in strength (3/5 preprocedure and 4+/5 postprocedure). For the remaining 40, the Oswestry Disability Index dropped from 47.2% before percutaneous discectomy to 23% at 6 months, representing a change in one full category of disability. The average preprocedure VAS was 7.3, and at 6 months it was 1.7. Seventy-five percent had a VAS of 2 or less. Medication usage diminished as well. The reduction in VAS, Oswestry, and medication usage was statistically and clinically significant for each.82 One-year data are in the process of being collected and it appears the results are stable.

CONCLUSION

Fig. 85.3 Advancement of Dekompressor into introducer needle after removal of stylet.

There has been a gradual evolution of minimally invasive techniques in the management of painful spinal disorders. The pace of technological advancement has increased rapidly, which leads to promising option for symptomatic patients with contained herniated discs. Percutaneous disc decompression procedures should not be thought of as procedures that are equivalent to surgery, but rather a therapeutic tool that can avoid open surgery. As such, it should be integrated into a conservative treatment algorithm for patients with discogenic arm or leg pain.

References 1. Hutton WC, Elmer WA, Boden SD, et al. The effect of hydrostatic pressure on intervertebral disc metabolism. Spine 1999; 24:1507–1515. 2. Hijikata S, Yamagishi M, Nakayama T, et al. Percutaneous nucleotomy: a new treatment method for lumbar herniation. J Toden Hosp 1975; 5:39–44. 3. Delamarter R, Howard M, Goldstein T, et al. Percutaneous lumbar discectomy. preoperative and postoperative magnetic resonance imaging. J Bone Joint Surg [Am] 1995; 77:578–584. 4. Ramirez LF, Thisted R. Complication and demographic characteristics of patients undergoing lumbar discectomy in community hospitals. Neurosurgery 1989; 25:226–231.

Fig. 85.4 Locking of needle hub onto Dekompressor probe just prior to advancement of needle/probe complex.

5. Pappas CTE, Harrington T, Sonntag VKH. Outcome analysis in 654 surgically treated lumbar disc herniations. Neurosurgery 1992; 30:862–866. 6. Onik GM, Mooney V, Maroon JC, et al. Automated percutaneous discectomy: a prospective multi-institutional study. Neurosurgery 1990; 26:228–233. 7. Thomas L. Reversible collapse of rabbit ears after intravenous papain and prevention of recovery by cortisone. J Exp Med 1956; 104:245–252. 8. Smith L. Enzyme dissolution of nucleus pulposus in humans. JAMA 1964; 187: 137–140.

physical examination evidence of lumbar radicular involvement with confirmation in the form of MRI or discography and diagnostic selective nerve root blocks. Eight of 50 patients were lost to follow-up. Of the remaining 42 patients, VAS (Visual Analogue Scale) scores dropped from an average of 79 before percutaneous discectomy to an average of 2.8 at 12 months. Reported patient satisfaction was 88.1% with patients reporting improved function and decreased medication usage. Slipman et al.83 is conducting a study using outcome measures of VAS, medication usage, and Oswestry Disability Index in patients with lumbar radiculopathy due to diffuse disc bulging causing central stenosis, contained focal protrusion, or disc extrusion. Inclusion criteria for this pilot study required corroborative history, physical

9. Smith L, Brown JE. Treatment of lumbar intervertebral disc lesions by direct injection of chymopapain. J Bone Joint Surg [Br] 1967; 49(3):502–519. 10. Mansfield F, Polivy K, Boyd R, et al. Long-term results of chymopapain injections. Clin Orthop 1986; 206:67–69. 11. Gogan WJ, Fraser RD. Chymopapain. A ten-year, double-blind study. Spine 1992; 1:388–394. 12. Poynton AR, O’Farrell DA, Mulcahy D. Chymopapain chemonucleolysis: a review of 105 cases. J Roy Coll Surg Edinb 1998; 43:407–409. 13. Wittenberg RH, Oppel S, Rubenthaler FA, et al. Five-year results from chemonucleolysis with chymopapain or collagenase a prospective randomized study. Spine 2001; 26(17):1835–1841. 14. Schweigel JF, Berezowskyj J. Repeat chymopapain injections. Spine 1987; 12: 800–802.

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Part 3: Specific Disorders 15. Sutton JC. Repeat chemonucleolysis. Clin Orthop 1986; 206:45–49. 16. van de Belt H, Franssen S, Deutman R. Repeat chemonucleolysis is safe and effective. Clin Orthoped Rel Res 1999; 1(363):121–125. 17. Nordby E J, Fraser R, Javid MJ. Spine update. Chemonucleolysis. Spine 1996; 21(9):1102–1105. 18. Deburge A, Rocolle J, Benoist M. Surgical findings and results of surgery after failure of chemonucleolysis. Spine 1985; 10:812–815. 19. Kim YS, Chin DK, Choy D. Predictors of successful outcome for lumbar chemonucleolysis: analysis of 3000 cases during the past 14 years. Neurosurgery 2002; 51(2):123–128. 20. Agre K, Wilson RR, Brim M, et al. Chymodiactin postmarketing surveillance: demographic and adverse experience data. Spine 1984; 9:479–486.

48. Matsui H, Aoki M, Kanamori M. Lateral disc herniation following percutaneous lumbar discectomy. A case report. Internat Orthoped 1997; 21:169–171. 49. Hijikata S. Percutaneous nucleotomy. A new concept technique and 12 years experience. Clin Orthop 1989; 238:9–23. 50. Bernd L, Schiltenwolf M, Mau H, et al. No indications for percutaneous lumbar discectomy. Internat Orthoped 1997; 21(3):164–168. 51. Sahlstrand T, Lonntoft M. A prospective study of preoperative and postoperative sequential magnetic resonance imaging and early clinical outcome in automated percutaneous lumbar discectomy. J Spinal Disord 1999; 12(5):368–374.

21. Javid MJ, Nordby EJ. Current status of chymopapain for herniated nucleus pulposus. Neurosurg Q 1994; 4:92–101.

52. Chatterjee S, Foy PM, Findlay GF. Report of a controlled clinical trial comparing automated percutaneous lumbar discectomy and microdiscectomy in the treatment of contained lumbar disc herniation. Spine 1995; 20:734–738.

22. Alexander AH. Chymopapain chemonucleolysis. In: Chapman MW, ed.. Operative orthopedics. Philadelphia: JB Lippincott; 1993:2787–2794.

53. Nachemson A. Lumbar disc herniation – conclusions. Acta Orthop Scand 1993; 64(Suppl 251):49–50.

23. Scwetschenau PR, Ramirez A, Johnson J. Double blind evaluations of intradiscal chymopapain for herniated lumbar discs: early results. J Neurosurg 1976; 45:622.

54. Stevenson RC, McCabe CJ, Findlay AM. An economic evaluation of a clinical trial to compare APLD with microdiscectomy in the treatment of contained lumbar disc herniation. Spine 1995; 20(6):739–742.

24. Onik G, Maroon J, Helms C, et al. Automated percutaneous discectomy: initial patient experience, work in progress. Radiology 1987; 162:129–132. 25. Gogan W, Fraser RD. Chymopapain. A 10 year double-blind study. Spine 1992; 17:388–394. 26. Launois R, Rebous-Marty J, Henrey B, et al. Cost-utility analysis after seven years of treatment of lumbar discal hernia. J Econ Med 1992; 10:307–325. 27. Wilson LF, Chell J, Mulholland RC. The long-term results of chemonucleolysis. Presented at the annual meeting of the European Spine Society, Cambridge, England, September 1992. 28. Javid MJ. Chemonucleolysis versus laminectomy: a cohort comparison of effectiveness and cost. Spine 1995; 20:2016–2022. 29. Krämer J, Wittenberg RH. Microdiscectomy for lumbar disc herniation. Orthop Traumatol 1993; 2:10–18. 30. McCulloch JA, MacNab I. Sciatica and chymopapain. Baltimore: Williams and Wilkins; 1983. 31. Norton WL. Chemonucleolysis versus surgical discectomy: comparison of cost and results in worker’s compensation claimants. Spine 1986; 11:440–443. 32. Nordby EJ, Wright PH. Efficacy of chymopapain in chemonucleolysis. Spine 1994; 19(22):2578–2583. 33. Revel M, Payan C, Vallee C, et al. Automated percutaneous lumbar discectomy versus chemonucleolysis in the treatment of sciatica. A randomized multicenter trial. Spine. 1993; 18(1):1–7.

55. Choy DSJ, Altman PA, Case RB, et al. Interaction of laser radiation with human intervertebral discs at wavelengths of 193 nm, 488 nm, 514 nm, 1064 nm, 1318 nm, 2150 nm, 2940 nm, 10600 nm. Clin Orthop 1990; 267:245–250. 56. Choy DSJ, Altman P. Fall of intradiscal pressure with laser ablation. Spine State Art Rev 1993; 7:23–29. 57. Ohnmeiss DD, Guyer RD, Hochschuler SH. Laser disc decompression: the importance of proper patient selection. Spine 1994; 19:2054–2058; discussion 2059. 58. Hellinger J, Linke R, Heller H. A biophysical explanation for Nd:YAG percutaneous laser disc decompression success. J Clin Laser Med Surg 2001; 5(19): 235–238. 59. Harada J, Dohi M, Fukuda K, et al. CT- guided percutaneous laser disk decompression for cervical disk hernia. Radiation Med 2001; 5(19):263–266. 60. Liebler WA. Percutaneous laser disc nucleotomy. Clin Orthop Rel Res 1995; 310:58–66. 61. Gangi A, Dietemann JL, Casser B. Interventional radiology with laser in bone and joint. Rad Clin North Am 1998; 36(3):547–557. 62. Choy D. Early relief of erectile dysfunction after laser decompression of herniated lumbar disc. J Clinical Laser Med Surg 1999; 1(17):25–27. 63. Bosacco SJ, Bosacco DN, Berman AT. Functional results of percutaneous laser discectomy. Am J Orthoped 1996; 25(12):825–828. 64. Nerubay J, Casi I, Levinkopf M. Percutaneous carbon dioxide laser nucleolysis with 2–5 years follow-up. Clin Orthop Rel Res 1997; 337:45–48.

34. Krugluger J, Knahr K. Chemonucleolysis and automated percutaneous discectomy – a prospective randomized comparison. Internat Orthoped 2000; 24:167–169.

65. Hellinger J. Technical aspects of the percutaneous cervical and lumbar laser disc decompression and nucleotomy. Neurol Res 1999; 21:99–102.

35. Hoogland T, Scheckenbach C. Low-dose chemonucleolysis combined with percutaneous nucleotomy in herniated cervical disks. J Spinal Disord 1995; 8(3):228–232.

66. Nerubay J, Caspi I, Levinkopf M, et al. Percutaneous laser nucleolysis of the intervertebral lumbar disc: an experimental study. Clin Orthop Rel Res1997; 337:42–44.

36. Onik GM, Helms C. Nuances in percutaneous discectomy. Radiol Clin North Am 1998; 36:523–532.

67. Choy DSJ, Asher PW, Saddekni S, et al. Percutaneous laser decompression. Spine 1992; 17:949–956.

37. Mochida J, Arima T. Percutaneous nucleotomy in lumbar disc herniation. Spine 1993; 18:2063–2068.

68. Choy DS. Percutaneous laser disc decompression: twelve years’ experience with 752 procedures in 518 patients. J Clin Laser Med Surg 1998; 16(6):325–331.

38. Carragee EJ, Kim DH. A prospective analysis of magnetic resonance imaging findings in patients with sciatica and lumbar disc herniation: correlation of outcomes with disc fragment and canal morphology. Spine 1997; 22:1650–1660.

69. Gropper GR, Robertson JH, McClellan G. Comparative histological and radiographic effects of CO2 laser versus standard surgical anterior discectomy in the dog. Neurosurgery 1984; 14:42–47.

39. Mirovsky Y, Neuwirth MG, et al. Automated percutaneous discectomy for reherniations of lumbar discs. J Spinal Disord 1994; 7:181–184.

70. Black J, Rhodes A, Lane GJ, et al. The chronic effects of anterior cervical and percutaneous lumbar discectomy using the holmium: YAG laser: an animal model. State of the Art Reviews (Spine) 1993; 7:31–36.

40. Onik G, Maroon J, Shang Y. Far lateral disc herniation: treatment by automated percutaneous discectomy. Am J Neuroradiol 1990; 11:865–868, 41. Onik G. Automated percutaneous lumbar discectomy. Mt Sina J Med 1991; 58:151. 42. Haaker R, Senkal M, Kielich, et alk. Percutaneous lumbar discectomy in the treatment of lumbar discitis. Euro Spine J 1997; 6:98–101. 43. Gebhard JS, Brugman JL. Percutaneous discectomy for the treatment of bacterial discitis. Spine 1994; 19:855–857. 44. Fouquet B, Goudpille P, Jattiot F, et al. Discitis after lumbar disc surgery: features of aseptic and septic forms. Spine 1992; 17:356–358. 45. Krodel A, Sturz H, Siebert CH. Indications for and results of operative treatment of spondylitis and spondylodiscitis. Arch Orthop Trauma Surg 1991; 110:78–82. 46. Yu W, Diu C, Wing P, et al. Percutaneous suction aspiration for osteomyelitis: report of two cases. Spine 1991; 16:198–202.

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47. Theron J, Huet H, Courtheoux F Percutaneous automated cervical discectomy. Rachis 1992; 4:93–105.

71. Reinhard SWR, Kraemer J. Chemonucleolysis versus laser disc decompression: a prospective randomized trial. J Bone Joint Surg [Br] 1997; 79:247. 72. Dangaria T. Result of laser-assistant disc ablation after unsuccessful percutaneous discectomy. J Clin Laser Med Surg 1998; 16(6):321–323. 73. Chiu JC, Clifford TJ, Greenspan M, et al. Percutaneous microdecompressive endoscopic cervical discectomy with laser thermodiskoplasty. Mt Sinai J Med 2000; 67:278–282. 74. Knight M, Goswami A, Patko J. Cervical percutaneous laser disc decompression: preliminary results of an ongoing prospective outcome study. J Clin Laser Med Surg 2001; 1(19):3–8 75. Chen Y, Sang-heon L, Chen D. Intradiscal pressure study of percutaneous disc decompression with nucleoplasty in human cadavers. Spine 2003; 28(7): 661–665.

Section 5: Biomechanical Disorders of the Lumbar Spine 76. Chen Y, Sang-Heon L, Saenz Y, et al. Histological findings of disc, endplate and neural elements after coblation of nucleus pulposus: an experimental nucleoplasty study. Spine 2003; 6(3):466–470. 77. Bhagia SM, Slipman CW, Nirschl M, et al. Side effects and complications after percutaneous disc decompression using coblation technology. Am J Phys Med Rehabil 2006; 85(1):6–13. 78. Slipman CW, Bhagia SM, Frey ME, et al. Nucleoplasty procedure for cervical radicular pain – initial case series. In: Proceedings of interventional Spinal Injection Society. Orlando, FL; 2003:104–105. 78a. Slipman CW, Frey ME, Bhargava et al. Outcomes and side effects following percutaneous cervical disc decompression using coblation technology: a pilot study. The Spine Journal 2004; 4:71S 79. Derby R, Chen Y, Lee SH, et al. Non-surgical interventional treatment of cervical and thoracic radiculopathies. Pain Phys 2004; 7:389–394.

of The American Academy of Physical Medicine and Rehabilitation. Hawaii, Nov 9–12, 2005. 84. Alo K, et al. Percutaneous lumbar discectomy: one year follow up in an initial cohort of fifty consecutive patients with chronic radicular pain. Pain Practice 2005; 5(2):116–124. 85. Amoretti N, et al. Decompression probe (Dekompressor) in percutaneous discectomy. Ten case reports. J Clin Imaging 2005; 29:98–101.

Further Reading Côté P, Cassidy D, Corroll L. The Saskatchewan Health and Back Pain Survey. The prevalence of neck pain and related disability in Saskatchewan adults. Spine 1998; 23:1689–1698.

80. Vijay Singh, et al. Percutaneous disc decompression using coblation (Nucleoplasty™) in the treatment of chronic discogenic pain. Pain Phys 2002; 5(3):250–259.

Linton SJ, Hellsing AL, Hallden K. A population-based study of spinal pain among 35–45 year old individuals. Prevalence, sick leave and health care use. Spine 1998; 23:1457– 1463.

81. Sharp L. Percutaneous disc decompression using nucleoplasty. Pain Phys 2002; 5(2):121–126.

Borghouts JAJ, Koes BW, Bouter LM. Cost-of-illness in neck pain in the Netherlands in 1996. Pain 1999; 80:629–636.

82. Nardi PV, Cabezas D, Cesaroni A. Percutaneous cervical nucleoplasty using coblation technology. Clinical results in fifty consecutive cases. Acta Neurochiir Suppl 2005; 92:73–74.

Deyo RA, Bass JE. Lifestyle and low back pain. Spine 1989; 14:501.

83. Slipman CW, Bender F, Menkin S, et al. Percutaneous lumbar disc decompression using the Dekompressor: A Pilot Study. Procedings of the 67th Annual Meeting

Schwarzer A, Aprill C, Derby R, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995; 20:1878–1883.

Bigos SJ, Battie MC. The impact of spinal disorders in industry. In: Frymoyer JW, ed. The adult spine. New York: Raven Press; 1991.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ ii: Lumbar Radicular Pain

CHAPTER

86

Surgical Decompression for Herniated Nucleus Pulposus Rick B. Delamarter and Ben B. Pradhan

INTRODUCTION Lumbar herniated nucleus pulposus (HNP) falls within the spectrum of degenerative spinal conditions, and can occur with little or no trauma. Lumbar disc abnormalities increase with age.1,2 The actual incidence of lumbar disc herniations is unknown, as many people with herniations are asymptomatic.1,3,4 Ninety percent of lumbar herniations occur at the L4–5 and L5–S1 levels.5,6 More than 200 000 discectomies are performed in the United States each year.7 The success of this procedure, as with all surgical procedures, depends vastly on proper patient selection and to a lesser extent on surgical technique. However, it is incumbent on the spinal surgeon to be absolutely meticulous with intraoperative technique once the decision for surgery is made. To this end, The authors recommend the use of a microscope for lumbar discectomy. The authors believe that once the learning curve has been traveled, the microscope not only offers advantages over loupes, it forces one to think at a much higher level of clarity about what and where root encroachment pathology is present.8 More importantly, the patient has less morbidity and an earlier hospital discharge compared to standard or limited discectomy.6,9–14

PATHOPHYSIOLOGY Intervertebral discs cushion and tether the vertebrae, providing both flexibility and stability. The normally gelatinous nucleus pulposus is surrounded by the ligamentous anulus fibrosus. In the young and healthy disc, the nucleus and anulus blend. Degenerative or pathologic changes can cause separation of the two entities, as well as compromise the integrity of the anulus, such that a sufficient load can cause nuclear fragments to migrate and impinge on neural elements.15 Lumbar disc herniations may occur with little or no trauma, although patients frequently report a bending or twisting motion as the inciting event, causing the onset of symptoms. Common causes of lumbar herniations include falls, car accidents, repetitive heavy lifting, and sports injuries of all types. Lumbar disc herniations are commonly described according to the type of annular/nuclear disruption. Lumbar disc herniation implies an annular bulge or tear along with nucleus pulposus displacement. Extrusion implies nuclear material coming completely through the anulus into the canal. Sequestration suggests the nuclear free fragment in the canal separated from the disc space. A bulging disc infers the anulus is still intact although bulging into the canal. Disc herniations are also described by size (millimeters), or location (central, paracentral, intraforaminal, and extraforaminal).

is frequently straightforward as well. A patient with a lumbar herniation generally presents with some element of low back pain with radiation into the buttocks, thigh, leg, and foot. The leg radiation almost always follows a dermatomal distribution. Patients frequently complain of numbness, tingling, or weakness in the affected dermatome. Lying down may relieve the symptoms, whereas sitting, walking, and standing may exacerbate symptoms. Complaints of bowel and bladder dysfunction may signal a cauda equina syndrome, and should be emergently evaluated.

Physical examination Visual inspection may reveal lumbar muscle spasm, fasciculations, and postural changes, including listing to the side and a forward flexed position. Gait observation can reveal a listing antalgic walk. Patients will list towards the side of an axillary disc herniation and away from a herniation lateral to the nerve root. Weakness can give a dropped foot type of gait (anterior tibialis) or buckling of the leg (quadriceps). Range of motion testing may be limited secondary to pain. Neurologic testing is extremely important and should include motor, sensory, and reflex testing. Lumbar herniations may cause varying degrees of dermatomal weakness, sensory deficits, and reflex changes. Straight leg raises are a good indicator of nerve root impingement in lower lumbar herniations, and a positive femoral stretch can indicate an upper lumbar herniation.

Imaging and other tests Magnetic resonance imaging (MRI) is the imaging study of choice to diagnose a lumbar disc herniation (Fig. 86.1). Plain radiographs should always be obtained. Patients who cannot obtain an MRI can be diagnosed using computed tomography (CT), CT myelogram, or CT discogram. These imaging tests are so sensitive that discectomy is not indicated if a disc is not found to be herniated by one of these techniques. Other tests can include an electromyogram (EMG) or nerve conduction study (NCS).

Differential diagnosis Low back pain with radiating lower extremity complaints can be caused by a number of conditions: ● ● ● ●

DIAGNOSIS The radiographic diagnosis of lumbar disc herniation has been made rather simple with magnetic resonance imaging. The clinical diagnosis

● ● ●

Herniated disc; Intraspinal pathology proximal to herniated disc; Spinal stenosis; Degenerative disc disease; Vascular claudication; Tumors (retroperitoneal, pelvic, or sciatic with neural impingement); Infection with neural impingement, or herpes zoster; 939

Part 3: Specific Disorders

A

● ● ● ● ● ●

B

Inflammation: arachnoiditis; Sprain/strain; Aortic aneurysm; Hip or sacroiliac joint disease; Neuropathy (secondary to diabetes, alcohol, tumor, etc.); and Gynecologic conditions.

MANAGEMENT It is important to understand that most patients with symptomatic herniated lumbar discs will get better over time regardless of the type of treatment. Weber’s classic study16 reported that sciatica from herniated nucleus pulposus (HNP) would improve 60% of the time with nonsurgical methods, and 92% of the time with surgery at 1 year. By 4 years out, he reported no statistical difference between the two groups, and no difference at 10-year follow up. In the absence of cauda equina syndrome, progressive or significant neurologic deficits, most practitioners attempt at least 4–8 weeks of conservative care before suggesting surgical intervention.

Medical rehabilitation and interventional spine treatment Conservative treatment may include: ● ● ● ● ●

940

Fig. 86.1 T2-weighted sagittal (A) and axial (B) MRI images of a herniated nucleus pulposus. The arrowhead denotes the herniation at the L4–5 level, and the axial cut reveals a large left-sided paracentral herniation into the canal, causing significant stenosis in the left lateral recess.

Modified activity; Modified bed rest for 2–3 days (prolonged bed rest should be avoided);17–19 Analgesic and/or antiinflammatory medication (e.g. NSAIDs, steroids); Physical therapy (as tolerated) or external support (e.g. corset, brace); and Epidural steroid injections (the authors recommend up to 3).

● ● ● ● ●

Failure of conservative treatment; Unbearable and/or recurrent episodes of radicular pain; Significant neurologic deficit; Increasing neurologic deficit (absolute indication); or Cauda equina syndrome (absolute indication).

Conservative treatment consists of medical rehabilitation and interventional spine management and careful observation for at least 4–8 weeks. Some may benefit from a short trial of conservative treatment even after 8 weeks if no prior care was given. Failed conservative treatment is the most common indication for lumbar discectomy. Those who have not improved sufficiently and are not experiencing continued improvement might then be offered treatment by surgical excision of the disc. Such patients should be advised that this is an elective operation but that delay for longer than 3–6 months in the face of persistent and severe symptoms may ultimately compromise the best result.20,22 The latter four indications are exceptions to the 4–8 week rule. Excruciating pain may not be relieved by medical rehabilitation and interventional spine techniques and may require earlier surgical decompression. Recurrent sciatica should also receive consideration for surgery: the chance of recurrent sciatica after the second episode is 50%, and after the third episode is almost 100%.22 An example of a significant neurologic deficit may be a foot drop, or weakness that prevents normal posture, gait, or one that affects the patient’s profession or a particular skill. Any definite progression of neurologic deficit is an absolute indication for surgery. Cauda equina syndrome is relatively rare, being reported in 1–3% of patients with confirmed disc herniations.23,24 This is an orthopedic or neurosurgical emergency. Features include rapid progression of neurologic signs and symptoms, bilateral leg pain, caudal sensory deficit, bladder overflow incontinence or retention, and loss of rectal sphincter tone with or without fecal incontinence.

Indications for surgery

Contraindications for discectomy

Surgical indications, as currently recommended by the North American Spine Society (NASS) include a definite diagnosis of ruptured lumbar intervertebral disc and:20,21

The NASS and the American Academy of Orthopedic Surgeons (AAOS) have identified the following factors as absolute or relative contraindications for discectomy:20,25

Section 5: Biomechanical Disorders of the Lumbar Spine ● ● ●

Lack of clear clinical diagnosis, anatomic level of lesion, and radiographic evidence of HNP; Lack of trial of medical rehabilitation and interventional spine treatment (with the exceptions mentioned above); Disabilities with major nonorganic components (multifocal, nonanatomic, or disproportionate signs and symptoms);

● ● ●

Systemic disease processes which can negatively influence outcome of surgery (e.g. diabetic neuropathy); Medical contraindications to surgery (such as major comorbidities, or unfavorable survival); and Disc herniation at a level of instability (may need additional stabilization).

Acute low back pain + radiculopathy or HNP seen on imaging studies already done

Progressive neurological deficit or uncontrollable pain

Urgent radiographs, MRI/CT-myelogram if not already done

Mechanical (positional or activity-related) pain

Non-operative management (may combine modalities)

Cauda equina syndrome

Emergent radiographs, MRI/CT-myelogram if not already done

Surgical intervention Surgical intervention

Activity modification (maximum of 2–3 days of modified bedrest, avoid painful activity)

Physical therapy

Medications (analgesics, NSAIDs, or spinal injections)

Mechanical support (corset, bracing, walking aids)

Exercises, manipulation, traction

Passive modalities (ice, heat, ultrasound, TENS)

Re-evaluation in 4–6 weeks

If resolved, preventative education and resume normal activities

If improving, continue non-operative management

If no identifiable cause, continue non-operative management

If not improving, obtain imaging studies and additional tests as needed

Surgical intervention if Fig. 86.2 Flowchart for management of acute radiculopathy. 941

Part 3: Specific Disorders

SURGICAL PROCEDURES One only has to review the natural history of lumbar disc disease to realize that spinal surgeons play a palliative role in the management of HNP.16,26–29 Surgical procedures as treatment for lumbar HNP include the following: ●

● ● ●

Lumbar discectomy (microscopic or standard open technique): Hemilaminotomy and discectomy, Laminectomy and discectomy; Minimally invasive percutaneous techniques: Chemonucleolysis, Percutaneous discectomy (suction, shaver, laser, endoscopic tools).

The use of an operating microscope The attempt to improve visualization and illumination has led many spine surgeons to use loupes and a headlight. The authors believe the magnification and illumination built into the microscope offer many surgical advantages, the most important of which is reduced wound size and decreased tissue manipulation. The surgeon can limit the amount of tissue dissection by working through a small exposure directly over the pathology to be removed. Microsurgical techniques can also be used to preserve the ligamentum flavum and epidural fat to minimize postoperative epidural fibrosis and improve clinical results by preserving natural tissue planes.8,30 With this approach, the disc herniation can be easily removed, lateral recess stenosis can be decompressed, and nerve root manipulation is kept to a minimum. The senior author has used this technique since 1986 for most lumbar disc herniations, and has found the approach to be safe, with fewer dural tears and nerve root injuries and less postoperative epidural fibrosis than with standard discectomy.6 Table 86.1 lists the many advantages of the microscope over loupes.8,14,31 The microscope is not without its disadvantages. Peripheral vision is lost, with the field of vision limited to approximately 4–5 cm. Because of this, the surgeon needs to know detailed anatomy of the spine. This is probably the biggest disadvantage of the microscope, although it in fact forces an increased awareness by the surgeon. The line of vision is fixed through the microscope. To look over structures (to overcome tissue overhang), the patient or microscope has to be adjusted during the surgery. This can be avoided by proper retraction or dissection of tissue away from the line of vision. Focusing of the microscope has to be done manually, unlike the surgeon’s own eyes. The shortcut to maintaining focus under the microscope is to have

the anesthesiologist pump the table up or down as needed. Large instruments can block the line of vision, and the surgeon may need to look from outside the microscope periodically if this happens. Wilson et al. reported increased disc-space infection after microsurgery.32,33 This is most likely due to contamination from unsterile parts of the microscope during surgery although, as McCulloch and Young astutely point out, no one has looked at the potential for an increased infection rate when two surgeons with loupes and headlights bump heads over the wound! Recent reports by those who have long experiences with the microscope do not show any increased infection rates.6,12,14,34

Lumbar microdiscectomy Microscopic discectomy (microdiscectomy) has become the gold standard for operative treatment of lumbar disc herniations, and the latest minimally invasive percutaneous techniques have not been shown to be more effective.8,35,36 Although no statistical differences can be shown in the ultimate long-term outcomes of microscopic versus standard open discectomies,10–12,29,37–39 the microscope provides improved illumination and magnification, and patients have less morbidity and earlier hospital discharge when compared to standard discectomies.6,9–14

1. Operative setup General anesthesia is preferable because of patient comfort, airway, and sedation control. Another advantage is the option of hypotensive anesthesia. The procedure can also be done under epidural or local anesthesia with sedation, although this is not the authors’ preference. The patient’s position is always prone with the abdomen free, thus relieving pressure on the abdominal venous system and, in turn, decreasing venous backflow through Batson’s venous plexus into the spinal canal. This has the effect of decreasing bleeding from the epidural veins intraoperatively. Several frames are available for this, but the authors prefer a Wilson frame on a regular operating table because of the ease of setup. The frame is cranked up to induce flexion and opening of the interlaminar space. It is important to place the approximate spinal level of interest at the apex of the Wilson frame so the interlaminar space flexes open. When cranking the frame for increased flexion, careful attention must be paid to the position of the patient’s head and neck, as the body of the patient tends to be lifted up, thus increasing neck flexion. Additional padding may be

Table 86.1: Advantages of the Microscope Over Loupes

942

Loupes

Microscope

Magnification

Limited in amount, and fixed

Relatively unlimited and changeable during a case

Motion

Long surgery causes neck fatigue and motion of loupes

No motion of microscope

Focus

Each time surgeon looks up, refocusing is necessary to restart surgery

Microscope is in constant focus regardless of surgeon’s attention

Illumination

Not parallel to line of vision (paraxial)

Parallel to line of vision (coaxial), and stronger

Deep 3D vision

Limited when the skin incision is less than 65 mm (or surgeon’s interocular distance)

Maintained with even a 25 mm skin incision

Patient size

The larger the patient, the bigger the wound required

Neutralized (every patient is made the same size by the optics)

Teaching

Assistants excluded from vision

Assistants included

Surgeon’s neck

Fixed in flexion and requiring repositioning – fatigue during long surgeries

Spared – can be adjusted through inclinable binoculars

Section 5: Biomechanical Disorders of the Lumbar Spine

necessary to stabilize the head and neck in a neutral position. Padding underneath the shoulders may also be needed to prevent shoulder subluxation or dislocation. The microscope is prepared and draped for use. It is important to inspect the microscope and lenses, pre-set the focal length and interocular distances if possible beforehand to prevent excessive handling of the nonsterile components during surgery. Although to date there has been no statistically sound study to support the use of prophylactic antibiotics in lumbar microdiscectomies, the authors prefer to administer an intravenous antibiotic (1–2 g cefazolin) approximately half an hour before incision.

Fig. 86.4 Following skin exposure and subsequent subperiosteal elevation, the retractor in position reveals the interlaminar interval, with exposure of the upper and lower laminae. Several millimeters of the cephalad lamina and 2– 3 mm of the medial edge of the inferior facet are removed with the high-speed burr. This bone can be safely removed because the undersurface is protected by the ligamentum flavum.

2. Identification of level and side A pre-incision lateral radiograph or fluoroscopy image, with a radiopaque skin marker placed according to preoperative radiographs and anatomic landmarks will identify the appropriate incision location for the disc space to be exposed. This is best done by placing a spinal needle as straight vertically as possible approximately 2 cm from midline contralateral to the side of surgery. The side or surgery is usually the more symptomatic side, although occasionally a midline HNP can be approached from either side.

3. Skin incision and interlaminar space exposure A 2–3 cm incision is made midline or up to 1 cm lateral to the spinous process on the symptomatic side, at a level directly over the disc space based on the localizing lateral radiograph. At L5–S1 this incision tends to be directly over the interlaminar space, but as one moves up the lumbar spine, this incision will be progressively over the cephalad lamina. The dissection is carried down to the lumbodorsal fascia, which is sharply incised. The fascial incision is placed carefully just lateral to the spinous processes to avoid damage to the supraspinous–interspinous ligament complex (Fig. 86.3) and to make it easier for lateral retraction. The subperiosteal muscle dissection and elevation are confined to the interlaminar space and approximately half of the cephalad and caudad lamina. The facet capsules are carefully preserved. A Cobb elevator and bovie cautery are used. It is important to watch out for spina bifida occulta while using the Cobb for subperiosteal dissection, especially at the L5–S1 level. A framed retractor is then placed. The medial hook is usually one size smaller than the lateral muscle blade to prevent tilting of the retractor frame.

Expose the lateral border of the pars as a landmark for preserving enough of the pars during laminotomy to prevent fracture. At this time, another localizing lateral radiograph should be obtained to confirm the proper level. A forward-angled curette can be placed underneath the cephalad lamina of the interspace. With this intraoperative radiographic verification, wrong-level surgery is unlikely to occur. The radiograph will also indicate how much of the cephalad lamina needs to be removed to expose the disc space. The microscope is then brought into position (Fig. 86.4).

4. Spinal canal entry After exposure of the interlaminar space and placement of the retractor, a high-speed burr is used to remove several millimeters of the cephalad lamina and 2–3 mm of the medial aspect of the inferior facet (Fig. 86.5). Once the cephalad lamina and medial aspect of the inferior facet have been removed, the ligamentum flavum is easily seen as its bony attachments are exposed. The ligamentum attaches at the very cephalad edge of the lower lamina, but approximately halfway up the ventral surface of the upper lamina, and attaches to

s

m

s

Fig. 86.3 The curvilinear incision through lumbodorsal fascia and erector spinae fascia (s, spinous process; m, midline supraspinous ligament area) that spares the interspinous– supraspinous ligament complex.

Fig. 86.5 A small, forwardangled curette frees the ligamentum flavum from its attachment to the medial edge of the superior facet. The ligamentum flavum also can be freed from the undersurface of the upper and lower laminae. 943

Part 3: Specific Disorders

the medial aspect of the superior facet. Thus, the high-speed burr can be used relatively safely on top of the bottom half of the superior lamina as well as the medial aspect of the inferior facet. To prevent tissue overhang from impeding the microscope’s line of vision, one may burr down the bulbous side of the spinous process as well.

5. Free ligamentum flavum The ligamentum flavum is then released from the medial edge of the superior facet with a forward-angled curette. It can also be released from the undersurface of the upper and lower lamina (see Fig. 86.5). It is safest to start the curette inferolaterally toward the superior aspect of the pedicle (caudal aspect of the foramen). An unintentional plunge with the curette in this quadrant is likely to avoid damaging a nerve root because the exiting nerve root lies in the cephalad aspect of the foramen, and the traversing nerve root dives anteriorly to curve around the inferior aspect of the pedicle. A ligamentum- and epidural fat-sparing approach, by creating a flap of the ligamentum as described above, decreases postoperative epidural fibrosis and can improve results.8,30 This can, however, make it more difficult to get a good view of the nerve root, but certainly this is easier with a microscope than without one. The less-experienced surgeon may perform partial removal of these tissues. The ligamentum flap is also not recommended for large midline disc herniations (with or without cauda equina syndrome) and severely stenotic canals because the ligamentum itself occupies more room in the already severely compromised spinal canal and would also interfere with direct visualization for the delicate manipulation of the thecal sac. Figure 86.6 is a postoperative CT scan illustrating a great example of a level where bilateral laminotomies were performed to remove a broad-based disc herniation: a ligamentum- and epidural fat-sparing approach was used to minimize the greater potential scarring from bilateral laminotomies.

6. Lateral recess exposure After release of the ligamentum flavum, the medial edge of the superior facet is resected with 2–4 mm Kerrison rongeurs. This resection goes from the lower pedicle to the tip of the superior facet (Fig. 86.7). This medial facet resection decompresses any lateral recess stenosis at the level of the pedicle and up into the foramen, and allows easy access to the lateral disc space. If needed, some of the lateral ligamentum flavum, particularly into the foramen, can be removed with the Kerrison rongeurs. Fig. 86.6 A postoperative axial CT scan at a level where bilateral laminotomies were performed to remove a broad-based midline disc herniation. Note the straight and vertical facet jointsparing laminotomy margins (arrowheads). A ligamentum- and epidural fat-sparing technique was used, and the shadow of the ligamentum is visible bilaterally, extending from the base of the spinous process to the facet joints. 944

Fig. 86.7 A 3 mm or 4 mm Kerrison rongeur is used to remove the lateral recess (subarticular) stenosis (i.e. the medial edge of the superior facet) back to the pedicle of the lower vertebra and cephalad to the top of the superior facet. This bony resection removes the lateral recess (subarticular) stenosis and allows exposure of the lateral disc space.

7. Nerve root and ligamentum retraction Bipolar cautery can be used at this time to cauterize any epidural bleeding over the lateral disc space, directly cephalad to the pedicle. The authors recommend finding the pedicle, and then using it as a guide to release the epidural non-neural tissues above the disc space. At this point, a nerve root retractor can be placed on the disc space and the ligamentum flavum, epidural fat, and nerve root are retracted toward the midline, generally exposing the herniation (Fig. 86.8). Again, the bipolar can be used to cauterize any epidural veins over the disc herniation. Any free large fragments of disc can now be removed (Fig. 86.9). If needed, a forward-angled curette can be used to scrape the inferior and posterior bony margins of the foramen, using a unidirectional pulling motion. Using the bony pedicle as a starting point, it is ensured that the end of the curette does not include any neural tissue before scraping. The classic teaching is that, once inside the spinal canal, it is essential to identify the lateral border of the nerve root before using any degree of force in manipulating the nerve root and before entering the disc space. Once the nerve root is retracted medially, it is possible to become more aggressive with the Kerrison rongeur to achieve more cephalad or caudad laminar excision, as necessary. Some basic principles of Kerrison usage are:22

Fig. 86.8 A nerve root retractor is used to retract the ligamentum flavum, nerve root sleeve, and epidural fat toward midline over the herniated disc. Bipolar cautery can be used to cauterize the epidural plexus over the disc herniation.

Section 5: Biomechanical Disorders of the Lumbar Spine

Fig. 86.9 After exposure of the disc herniation, large free fragments can be removed with a pituitary rongeur, and/or the natural annulotomy from the disc herniation can be enlarged with a No. 11 blade.

● ● ●

Use the biggest rongeur that will fit; Bite at the soft tissue–bone interface if trying to remove soft tissue; If near the dura, turn the footplate as perpendicularly as possible against the dura to retract it away from the biting surfaces (remember there are three biting edges to the mouth of the Kerrison rongeur.

If the lateral edge of the nerve root cannot be found, the following are important considerations: ● ● ● ●

An axillary HNP is displacing the root laterally; Osteophytic lip of the medial edge of the superior facet may be obstructing the view and needs to be removed; Adhesions are present; or There is an anomalous root.

In such instances, it is important to remember the following basic rule: nerve roots are intimately related to pedicles. If a nerve root cannot be found, find the pedicle it is associated with and the nerve root will be beside it. Even if a nerve root is isolated, it is useful to probe the medial bony wall of the pedicle to ensure there is no other neural tissue laterally. Microsurgery is a two-handed technique: one hand holds and manipulates the root and the other hand operates. If an able assistant is present, he or she can hold the root retractor while the surgeon holds a sucker in the nondominant hand. This is a matter of surgeon preference. Some believe that root retraction by the surgeon is safer since the surgeon knows when and where to retract, while others believe that root retraction by an assistant prevents excessive forces on the root by the surgeon trying to counterbalance forceful motions with the instrument in the other hand. In either case, excessive root retraction must be avoided when: (1) the patient already has a significant neurologic deficit, (2) a very large HNP has flattened the nerve root, or (3) the spinal canal is congenitally narrowed. Retraction across midline (especially against tension) can be considered excessive.

8. Discectomy Frequently, the anular defect of the disc herniation is all that is necessary to allow cleaning out of any loose nucleus pulposus inside the disc space, although the anulotomy can be enlarged with a No. 11 blade. The herniated nuclear material is then cleaned out with straight or angled pituitary rongeurs, and small back-angled curettes.

Care should be taken not to damage or curette the endplates. The anulotomy can be performed in various shapes, which are not discussed in detail here.40,41 It has been noted, however, that upon repeat surgery the root is found more scarred down to the anulus after more aggressive anulotomies.8,22 How much disc to remove from the discal cavity is an unresolved issue. Removal of as much disc as possible implies curettage of the interspace, including possible removal of the cartilaginous endplates. Critics of this approach point out that irrespective of how long the surgeon works, it is impossible to remove all disc material in this fashion. They also argue that this method increases risk of damage to anterior visceral structures, and increases risk of chronic back pain induced by conditions such as sterile discitis and instability. Although some surgeons believe that extensive intradiscal debridement decreases the rate of recurrent HNP, there are others who refute that position.41–44 In the end, the only reasonable prospective, controlled study is Spengler’s, which suggests that limited disc excision is all that is necessary.45 The advantages of limited disc excision are less trauma to endplates and less dissection, less nerve root manipulation, a lower prevalence of infection, reduced risk of damage to structures anterior to disc space, and less disc space settling postoperatively (theoretically reducing the incidence of chronic back pain).

9. Disc space irrigation After the HNP and any remaining loose material is removed, the disc space is irrigated under some pressure with a long angiocatheter, and then the pituitary rongeur is again utilized to remove any loose fragments. The spinal canal is then palpated underneath the nerve root and across the vertebral bodies above and below for any residual fragments. In doing the limited disc excision, one must also be sure to probe under the posterior anulus both medially and laterally for loose fragments. This is an important step to ensure that no displaced or sequestered fragments are missed. Residual disc material will feel rough, whereas the native dural surface is quite smooth. In the end, the patient must be left with a freely mobile nerve root. The preoperative MRI should be carefully studied for displaced fragments, but it is important to keep in mind that fragments may have moved since the MRI was taken.

10. Closure Once the decompression is complete, the entire surgical wound is thoroughly irrigated with antibiotic-containing irrigant. Any final bleeding is controlled with bipolar cautery, thrombin-soaked gel foam, or flo-seal hemostatic gel. After complete hemostasis and removal of all gel foam, the closure is then performed in layers. Many attempts have been made to design substances to seal the laminotomy defect and prevent scar formation, including fat grafts, hydrogel, silicone, Dacron, steroids, etc.46 The authors simply prefer the ligamentum flap (Fig. 86.10).6,8,22 The dorsal lumbar fascia is closed with No. 1 or 0 sutures, the subcutaneous layer with 2-0 sutures, and the skin with 3-0 subcuticular sutures. Using this ligamentum flavum-sparing approach, blood loss should be no more than 10–20 cc. With good hemostasis, drainage of the surgical wound is not necessary. After closure, the skin can be injected with 0.5% bupivacaine with epinephrine, which provides immediate postoperative pain relief, and when injected into the paraspinal muscles also aids hemostasis. Sixty milligrams of ketorolac tromethamine (Toradol; Hoffman-La Roche, Newark, NJ) is given intravenously 20 minutes before closure of the skin, and can be continued at 30 mg every 6 hours for the first postoperative day for very effective analgesia. 945

Part 3: Specific Disorders

stabilization, and mobilization beginning at around 4 weeks after surgery. Most athletes return to their normal athletic activities within 8 weeks after surgery. However, the postoperative course is variable, and return to normal activities depends on the patient’s overall medical condition, and neurologic and overall recovery.50–52

Unusual disc herniations There are some unique situations where a microscope can be even more invaluable.

Foraminal or extraforaminal HNP

A

B

Fig. 86.10 After thorough irrigation, the nerve root retractor is released, allowing the ligamentum flavum and nerve root sleeve to return to their normal anatomic positions.

Foraminal or extraforaminal (far lateral) disc herniations occur in 3–12% of all disc herniations.53–55 They compress the exiting nerve root, not the traversing one. Attempts to remove this disc herniation through the standard interlaminar window may result in loss of a facet joint, potentially destabilizing the level.37 Most foraminal disc herniations occur at the L4–5 and the L3–4 levels, affecting the L4 and L3 roots, respectively. They tend to occur in older patients (average age 50) who have a wide disc space rather than degenerated narrow disc spaces. The usual presentation is severe anterior thigh pain of sudden onset, interfering with all functions except sitting. The very positive femoral stretch test together with the fairly negative straight leg raising will alert the examiner to the possibility of a higher lumbar disc lesion. The pain is usually so severe that the patient is not prepared to accept too long a conservative treatment program. Surgical decompression for foraminal or extraforaminal disc herniations requires a Wiltse paraspinal muscle-splitting approach.56–58 The skin incision is placed 1½ finger breadths off the midline to the affected side, and the dorsolumbar fascia opened in line with the incision (Fig. 86.11). The paraspinal muscles are bluntly split down to the intertransverse process interval. The intertransverse ligament is carefully released. Again, it is helpful to find the border of the pedicle to use as the starting point for the release, and to march to the disc space.

Axillary herniated nuclear pulposus 11. Postoperative course Many microdiscectomy procedures can be done on an outpatient basis.13,47–49 Most patients are encouraged to walk as tolerated. Sitting is also tolerated, but may be more limited. Many return to work within 5–10 days, especially those with desk-type work. All patients are required to participate in lumbar physical therapy, primary

Axillary disc herniations can occur in two ways (Fig. 86.12). First, a downward and medial migration of a disc fragment can lodge in the axilla of the dura and nerve root. This usually occurs at the L5–S1 level, and can push the S1 root into the subarticular recess anterior to the medial edge of the superior facet of S1. This root is vulnerable to damage by a Kerrison rongeur in this location. It may also be impos-

A

B A Fig. 86.11 The surgical approach for a foraminal or extraforaminal disc herniation. 946

C

Section 5: Biomechanical Disorders of the Lumbar Spine

syndrome is caused by a HNP unless proven otherwise. These ruptures can be approached microsurgically. In the case of a stenotic canal (congenital or degenerative), it is important to carefully perform interlaminar and root decompressions before attempting to mobilize the root to retrieve the disc herniation.

L4 L4

Herniated nuclear pulposus at high lumbar levels (L1–2, L2–3, L3–4)

L5

High lumbar HNPs are uncommon (5%), and when they occur they are likely to be foraminal or extraforaminal.22,57 Important skeletal S1 S1 Fig. 86.12 Axillary disc anatomy in the higher lumbar spine for the spinal surgeon to be aware A B herniations. of includes: (1) the pars are narrower, and facet integrity is easily lost with excessive laminotomy, (2) the laminae are broader, (3) the interlaminar window is narrower, (4) the inferior border of the lamina sible to mobilize the root to expose the disc space without the disc overhangs more of the disc space, (5) at L1–2, the conus cannot be fragment being extracted from the axilla first. retracted like the cauda equina at lower levels, (6) the nerve roots exit Second, upward migration of a disc fragment can cause it to lodge in more horizontally, and are less mobile, and (7) epidural veins may be the axilla of the dura and root above. This is also most common at the more prevalent. At these levels, due to limited size of the interlaminar L5–S1 disc. However, in this case, the fragment pushes the L5 root space, ligamentum excision rather than sparing is recommended. up against the L5 lamina, making it vulnerable to damage from the high-speed burr or Kerrison rongeur during the hemilaminectomy. Sometimes, the first warning of an axillary disc is the appearance of Recurrent disc rupture displaced disc material as soon as the ligamentum is retracted. In this sit- The incidence of recurrent HNP is 2–5%.6,59,60 The microscope is uation, as much of the disc material as possible must be teased out with a especially valuable in this scenario because of the scar between tissue planes, including neural elements. Adequate time must be spent blunt instrument, then the axilla and the nerve root can be identified. carefully teasing the tissues apart with a blunt instrument (e.g. bipolar, curette, Penfield, etc.) before forcefully mobilizing the nerve Double root involvement root. The incidence of complications are understandably higher in Double root lesions (i.e. changes in more than one nerve root distri- revision discectomies. bution as revealed by neurologic examination) occur in four ways.8 These are: (1) large herniated fragment migrating distally to compress two subsequent traversing nerve roots, (2) foraminal disc her- Cauda equina syndrome niation at L4–5 compressing the L4 nerve root and a furcal nerve, (3) The classic teaching in cauda equina syndrome is that: (1) this is large herniated fragment migrating proximally and compressing exit- an orthopedic emergency, and (2) a wide decompression through a ing and traversing nerve roots, and (4) conjoined nerve roots which bilateral approach is necessary. The authors agree with the first point, exit through the same foramen. All of these situations can be handled but not the second. Few disc herniations are too big to be addressed microsurgically, carefully using the techniques described above. It microsurgically. A wider hemilaminectomy may be needed. The will be necessary to perform a wider decompression by undercut- microscope is invaluable when working in the severely stenotic canal. ting the superior facet. Fortunately, most of these issues occur at the If the disc cannot be easily or totally excised unilaterally, bilateral L5–S1 level where a more aggressive removal of the facet joint is less hemilaminotomies may be done.23,24 likely to compromise stability. L5

Disc rupture at the slip level in spondylolytic spondylolisthesis In this scenario, if there is symptomatic instability (bilateral leg symptoms or significant back pain), it is necessary to fuse the unstable segment. An exception would be an older patient with a stable slip on bending films, and who has predominantly leg pain on one side. In this case a simple disc excision may be very effective.

Disc rupture at level of spondylolisthesis In a young patient (under 25–30 years), the potential for increased instability is too great not to consider concomitant stabilization. In an older patient with a spondylolytic slip that is stable on flexion–extension radiography and predominantly radicular symptoms, a simple disc excision may be indicated. An HNP at a degenerative spondylolisthesis level should not be excised without concomitant stabilization.

Disc rupture into a stenotic canal These disc herniations and their effect can be difficult to appreciate on MRI or CT-myelography. In such patients, a dominant radicular

Herniated nuclear pulposus in the adolescent patient The risk for recurrence of HNP after surgical excision is higher in adolescents than in adults. Because of the high proteoglycan content in adolescent discs, and the prevalence of disc protrusions rather than disc extrusions, some have recommended percutaneous chemonucleolysis rather than surgical intervention in this age group.22,61,62 Studies have been published with controversial results for surgical discectomy in this patient population.63–65 The authors’ opinion is that chemonucleolysis may have merit in the treatment of symptomatic disc protrusions, but discectomy is necessary in the setting of an extruded or sequestered disc causing significant or progressive neurologic deficit or pain. These extruded or sequestered fragments are frequently heavily collagenized.20,66

Midline herniated nuclear pulposus For every true midline HNP, there are probably 100 000 cases of anular bulging.22,67 This usually occurs in patients under age 40. These discs should be approached from the more symptomatic side, or if both sides are equally affected, from the side suggested by the MRI. The surgeon must be prepared to perform bilateral laminotomies if needed. 947

Part 3: Specific Disorders

Bilateral or two-level herniated nuclear pulposus Almost all clinically significant HNP present at one level. However, if a surgeon does encounter a two-level surgical HNP, addressing the higher level will avoid the problem of blood flowing into the wound from the more superficial lower level. Bilateral HNP may be treated with two separate fascial incisions.

Osteophytes Osteophytes are problems if they interfere with nerve root mobility, and need to be removed. A diffuse osteophyte is probably best left alone unless it significantly compromises the nerve root. In such a case, the annular covering is stripped off of the bone, the osteophyte is excised, and the annular flap is laid back down. This prevents the nerve root from being in contact with the raw bone, which can compromise outcome.22

Complications Complications for these discectomy procedures include dural tears, neural injury, visceral injuries, postoperative infection, recurrence of herniation, inadequate decompression, and iatrogenic instability, among others. Dural tears occur in 1–6.7% of cases, although the incidence decreases with experience.6,34,52,68–70 If possible, repair should be done by direct suture (5-0 to 7-0 silk, nylon, or polypropylene) with or without a dural patch.68 The patient should be kept flat for a few days after surgery to lower the hydrostatic pressure in the lumbar thecal sac while the repair seals. Neural injuries are rare, although the risk is greater with unusual disc herniations as described above. Visceral injuries occur when an instrument penetrates the anterior anulus. Among these, vascular injuries are the most common.68,71 If these are recognized, immediate laparotomy for surgical repair is indicated. Postoperative discitis occurs in 1% of cases or fewer in experienced hands, although clearly there is a learning curve in developing facility with the microscope. Higher infection rates (up to 7%) have been reported with the use of a microscope during surgery, although in experienced hands this has been shown not to be true.68 An MRI is the best diagnostic imaging tool. An image-guided needle biopsy may be performed to assist in appropriate antibiotic selection. Reoperation may not be necessary unless the patient develops root compression, cauda equina syndrome, or an epidural abscess. The literature reports recurrent HNP occurring anywhere from 2% to 5% after lumbar discectomy.22,72 When reoperating for a recurrent HNP, it is important to get adequate exposure of the dural sac above and below the disc space. Then using a combination of blunt (nerve hook, Penfield, bipolar) and sharp (Kerrison) dissection, the dural sac and nerve root are exposed and mobilized above the HNP. Iatrogenic mechanical instability is fortunately a rare occurrence after discectomy, even if a decompressive laminectomy was required for a stenotic canal or to excise a large disc.15 Symptomatic mechanical treatment may require surgical stabilization. Suboptimal results after discectomy surgery can be due to several other reasons that unfortunately do not have a straightforward medical or surgical treatment. While very rare, these can include epidural fibrosis, arachnoiditis, and complex regional pain syndrome.68

DISCUSSION Most modern studies utilizing microscopic techniques for treatment of herniated lumbar discs report 90–95% success rates.6,8,9–13,28,30,32– 34,38,39,60,69,72 A multicenter, prospective trial has proved what cannot be repeated often enough – if one selects patients with dominant 948

radicular pain (compared to back pain), with neurological changes and painful straight leg raises, and with a study confirming a disc rupture, one can anticipate a high level of success for discectomy, with or without a microscope.37 The rate of successful outcome drops significantly as more of these inclusion criteria are not met. Persistent back pain occurs in up to 25% of patients who undergo microdiscectomy.69,70 This has led to the opinion that it is important to save the supraspinous–intraspinous ligament complex, remove as little lamina as possible, save the ligamentum flavum as a flap, and do a limited discectomy. These steps theoretically reduce iatrogenic instability, epidural fibrosis, sterile discitis, and loss of disc height. All of these steps are facilitated by the use of a microscope, but there is no proof as of yet that these steps reduce the incidence of back pain. The most frequent cause of poor result from lumbar disc surgery is faulty patient selection due to erroneous or incomplete diagnosis. Technical errors such as wrong-level surgery, incomplete decompression, and intraoperative complications explain a small percentage of failures. A 1981 study assigned the following frequency of missed diagnoses as sources of failure: lateral spinal stenosis 59%, recurrent or persistent herniation 14%, adhesive arachnoiditis 11%, central canal stenosis 11%, and epidural fibrosis 7%. Finally, the results of repeat surgery are not as good as primary surgery, regardless of the reason or whether a microscope was used, because of scar tissue, higher incidence of complications, and larger dissections. In the past decade, there has been a substantial increase in interest in minimally invasive procedures in all areas of medicine, and particularly for spinal disorders. Several methods to remove HNP have been proposed as alternatives to standard open discectomy. Injected chymopapain can dissolve much of the central nucleus, but is not likely to act on extruded or sequestered fragments, which are often heavily collagenized.20,62,66 Likewise, percutaneous suction discectomies and removal of nucleus, either mechanically or by laser, from the center of the disc may reduce intradiscal pressure, but are unlikely to influence the effects of extruded or sequestered disc material. So although alternative, minimally invasive techniques hold considerable promise, lumbar microdiscectomy is still the gold standard for surgical treatment of lumbar HNP with radiculopathy. However, the skills and technology to remove herniated discs by such alternatives are evolving.20,73–77

References 1. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects: A prospective investigation. J Bone Joint Surg 1990; 72A:403–408. 2. Yasuma T, Koh S, Okamura T, et al. Histologic changes in aging lumbar intervertebral discs. J Bone Joint Surg 1990; 72A:220–229. 3. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 331:69–73. 4. Buirski G, Silberstein M. The symptomatic lumbar disc in patients with low-back pain: Magnetic resonance imaging appearances in both a symptomatic and control population. Spine 1993; 18:1808–1811. 5. Hardy RW. Lumbar discectomy: Surgical tactics and management of complications. In: Frymoyer JW, ed. The adult spine, principles and practice, 2nd edn. Philadelphia, PA: Lippincott-Raven; 1997:1947–1959. 6. Delamarter RB. Lumbar microdiscectomy: microsurgical technique for treatment of lumbar herniated nucleus pulposus. Instr Course Lect 2002; 51:229–232. 7. Davis H. Increasing rates of cervical and lumbar spine surgery in the United States, 1979–1990. Spine 1994; 19:1117–1124. 8. Delamarter RB, McCulloch J. Microdiscectomy and microsurgical spinal laminotomies. In: Frymoyer JW, ed. The adult spine, principles and practice, 2nd edn. Philadelphia, PA: Lippincott-Raven; 1997:1961–1988. 9. Caspar W, Campbell B, Barbier DD, et al. The Caspar microsurgical discectomy and comparison with a conventional standard lumbar disc procedure. Neurosurgery 1991; 28:78–87.

Section 5: Biomechanical Disorders of the Lumbar Spine 10. Silvers HR. Microsurgical versus standard lumbar discectomy. Neurosurgery 1988; 22:837–841.

42. Onik GM, Kambin P, Chang MK. Minimally invasive disc surgery. Nucleotomy versus fragmentectomy. Spine 1997; 22(7):827–828.

11. Tullberg T, Isacson J, Weidenhielm L. Does microscopic removal of lumbar disc herniation lead to better results than standard procedure? Spine 1993; 18:24–27.

43. Williams RW. Microdiscectomy – myth, mania, or milestone? An 18-year surgical adventure. Mt Sinai J Med 1991; 58:139–145.

12. Tureyen K. One-level one-sided lumbar disc surgery with and without microscopic assistance: 1-year outcome in 114 consecutive patients. J Neurosurg 2003; 99(3 Suppl):247–250.

44. Rogers LA. Experience with limited versus extensive disc removal in patients undergoing microsurgical operations for ruptured lumbar disc. Neurosurgery 1988; 22:82–85.

13. Singhal A, Bernstein M. Outpatient lumbar microdiscectomy: a prospective study in 122 patients. Can J Neurol Sci 2002; 29(3):249–252.

45. Spengler DM. Lumbar discectomy: results with limited disc excision and selective foraminotomy. Spine 1982; 7:604–607.

14. McCulloch JA, Snook D, Kruse CF. Advantages of the operating microscope in lumbar spine surgery. Instr Course Lect 2002; 51:243–245.

46. McCulloch JA, Young PH. Wound healing and mobilization. In: Essentials of spinal microsurgery. Philadelphia, PA: Lippincott-Raven; 1998:43–53.

15. Yasuma T, Makino E, Saito S, et al. Histological development of intervertebral disc herniation. J bone Joint Surg 1986; 68A:1066–1072.

47. Bookwalter JW, Buxch MD, Nicely D. Ambulatory surgery is safe and effective in radicular disc disease. Spine 1994; 19:526–530.

16. Weber H. Lumbar disc herniation: a controlled, prospective study with 10 years of observation. Spine 1983; 8:131–140.

48. Newman MH. Outpatient conventional laminotomy and disc excision. Spine 1995; 20:353–355.

17. Vroomen PC, de Krom MC, Wilmink JT, et al. Lack of effectiveness of bed rest for sciatica. N Engl J Med 1999; 340(6):418–423.

49. Zahrawi F. Microlumbar discectomy: is it safe as an outpatient procedure? Spine 1994; 9:1070–1074.

18. Deyo R, et al. How many days of bed rest for acute low back pain? A randomized clinical trial. N Engl J Med 1986; 315:1064.

50. Carragee EJ, Helms E, O’Sullivan GS. Are postoperative activity restrictions necessary after posterior lumbar discectomy? A prospective study of outcomes in 50 consecutive cases. Spine 1996; 21(16):1893–1897.

19. Krolner B, Toft B. Vertebral bone loss: An unheeded side effect of therapeutic bed rest. Clin Sci 1983; 64:437. 20. Errico TJ, Fardon DF, Lowell TD. Open discectomy as treatment for herniated nucleus pulposus of the lumbar spine. Spine J 2003; 3:45S–49S. 21. Carragee E. Indications for lumbar microdiscectomy. Instr Course Lect 2002; 51:223–228.

51. Wang JC, Shapiro MS, Hatch JG, et al. The outcome of lumbar discectomy in elite athletes. Spine 1999; 24(6):570–573. 52. Watkins RG 4th, Williams LA, Watkins RG 3rd. Microscopic lumbar discectomy results for 60 cases in professional and Olympic athletes. Spine 2003; 3(2):100–105.

22. McCulloch JA, Young PH. Microsurgery for lumbar disc herniation. In: Essentials of spinal microsurgery. Philadelphia, PA: Lippincott-Raven; 1998:329–382.

53. Abdullah AF, Wolber PG, Warfield JR, et al. Surgical management of extreme lateral lumbar disc herniations: a review of 138 cases. Neurosurgery 1988; 22: 648–653.

23. Kostuik J, et al. Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg 1986; 68:386.

54. Postacchini F, Montanaro A. Extreme lateral herniations of lumbar discs. Clin Orthop 1979; 138:222–227.

24. Hanley EN. The surgical treatment of lumbar degenerative disease. In: Garfin SR, Vaccaro AR, eds. Orthopaedic knowledge update: Spine. 1997.

55. Epstein NE. Foraminal and far lateral disc herniations: surgical alternatives and outcome measures. Spinal Cord 2002; 40(10):491–500.

25. Shapiro S. Cauda equina syndrome secondary to lumbar disc herniation. Neurosurgery 1993; 32:743–746.

56. Zindrick MR, Wiltse LL, Rauschning W. Disc herniations lateral to the intervertebral foramen. In: White AH, Rothman RH, Ray CD, eds. Lumbar spine surgery. St Louis: Mosby; 1987:195–207.

26. Hakelius A. Prognosis in sciatica: a clinical follow-up of surgical and non-surgical treatment. Acta Orthop Scand [Suppl] 1970; 129:1–76. 27. Gibson JN, Grant IC, Waddell G. Surgery for lumbar disc prolapse. Cochrane Database Syst Rev 2000; (3):CD001350. 28. Findlay GF, Hall BI, Musa BS, et al. A 10-year follow-up of the outcome of lumbar microdiscectomy. Spine 1998; 23(10):1168–1171. 29. McCulloch JA. Focus issue on lumbar disc herniation: macro- and microdiscectomy. Spine 1996; 21(24 Suppl):45S–56S. 30. De Divitiis E, Cappabianca P. Lumbar discectomy with preservation of the ligamentum flavum. Surg Neurol 2002; 57(1):5–13. 31. McCulloch JA, Young PH. The microscope as a surgical aid. In: Essentials of spinal microsurgery. Philadelphia, PA: Lippincott-Raven; 1998:3–17. 32. Wilson DH, Kenning J. Microsurgical lumbar discectomy: preliminary report of 83 consecutive cases. Neurosurgery 1979; 4:137–140. 33. Wilson DH, Harbaugh R. Microsurgical and standard removal of the protruded lumbar disc: a comparative study. Neurosurgery 1981; 8:422–427. 34. Salvi V, Boux E, Cicero G, et al. Microdiscectomy in the treatment of lumbar disc herniation. Chir Organi Mov 2000; 85(4)337–344. 35. Deen HG, Fenton DS, Lamer TJ. Minimally invasive procedures for disorders of the lumbar spine. Mayo Clin Proc 2003; 78:1249–1256. 36. Maroon JC. Current concepts in minimally invasive discectomy. Neurosurgery 2002; 51(5 Suppl):137–145. 37. Abramovitz JN, Neff SR. Lumbar disc surgery: results of the prospective lumbar discectomy study of the Joint Section on Disorders of the Spine and Peripheral Nerves of the American Association of Neurological Surgeons and the Congress of Neurological Surgeons. Neurosurgery 1991; 29:301–308. 38. Barrios C, Ahmed M, Arrotequi J, et al. Microsurgical versus standard removal of the herniated lumbar disc. Acta Orthop Scand 1990; 61:399–403. 39. Striffeler H, Groger U, Reulen HJ. ‘Standard’ microsurgical lumbar discectomy vs ‘conservative’ microsurgical discectomy. Acta Neurochir (Wien) 1991; 112:62–64. 40. Peacock EE Jr. Dynamic aspects of collagen biology. Part 1: Synthesis and assembly. J Surg Res 1967; 7:433–446. 41. Williams RW. Microlumbar discectomy: A conservative surgical approach to the virgin herniated lumbar disc. Spine 1978; 3:175–182.

57. McCulloch JA, Young PH. Foraminal and extraforaminal lumbar disc herniation. In: Essentials of spinal microsurgery. Philadelphia, PA: Lippincott-Raven; 1998: 383–428. 58. McCulloch JA, Weiner BK. Microsurgery in the lumbar intertransverse interval. Instr Course Lect 2002; 51:233–241. 59. Pappas CTE, Harrington T, Sonntag VKH. Outcome analysis in 654 surgically treated lumbar disc herniations. Neurosurgery 1992; 30:862–866. 60. Loupasis GA, Stamos K, Katonis PG, et al. Seven- to 20-year outcome of lumbar discectomy. Spine 1999; 24(22):2313–2317. 61. Lorenz M, McCulloch JA. Chemonucleolysis for herniated nucleus pulposus in adolescents. J Bone Joint Surg 1985; 67A:1402–1404. 62. Gogan WJ, Fraser RD. Chymopapain: a 10-year, double blind study. Spine 1992; 17:388–394. 63. Parisini P, Di Silvestre M, Greggi T, eet al. Lumbar disc excision in children and adolescents. Spine 2001; 26(18)1997–2000. 64. Silvers HR, Lewis PJ, Clabeaux DE, et al. Lumbar disc excisions in patients under the age of 21 years. Spine 1994; 19:2387–2392. 65. DeLucca PF, Mason DE, Weiland R, et al. Excision of herniated nucleus pulposus in children and adolescents. J Pediatr Orthop 1994: 14:318–322. 66. Nordby EJ, Fraser RD. Chemonucleolysis. In: Frymoyer JW (ed): The adult spine, principles and practice. 2nd edn. Philadelphia, PA: Lippincott-Raven; 1997: 1989–2008. 67. Walker JL, Schulak D, Nurtagh R. Midline disc herniations of the lumbar spine. South Med J 1993; 86:13–18. 68. McCulloch JA, Young PH. Complications (adverse effects) in lumbar microsurgery. In: Essentials of spinal microsurgery. Philadelphia, PA: Lippincott-Raven; 1998: 503–529. 69. Schutz H, Watson CPN. Microsurgical discectomy: prospective study of 200 patients. Can J Neurolog Sci 1987; 14:81–83. 70. Thomas AMC, Afshar F. The microsurgical treatment of lumbar disc protrusions. J Bone Joint Surg 1987; 69B:696–698. 71. Roberts, MP. Complications of lumbar disc surgery. In: Hardy RW, ed. Lumbar disc disease. New York: Raven Press; 1992:161–170.

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72. Weir BKA, Jacobs GA. Reoperation rate following lumbar discectomy. An analysis of 662 lumbar discectomies. Spine 1980; 5:366–370.

75. Onik GM. Percutaneous discectomy in the treatment of herniated lumbar disks. Neuroimaging Clin N Am 2000; 10(3):597–607.

73. Deen HG, Fenton DS, Lamer TJ. Minimally invasive procedures for disorders of the lumbar spine. Mayo Clin Proc 2003; 78(10):1249–1256.

76. Gill K. Percutaneous lumbar discectomy. J Am Acad Orthop Surg 1993; 1(1): 33–40.

74. Obenchain TG. Speculum lumbar extraforaminal microdiscectomy. Spine J 2001; 1(6):415–420.

77. Maroon JC. Current concepts in minimally invasive discectomy. Neurosurgery 2002; 51(5S):137–145.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ ii: Lumbar Radicular Pain

CHAPTER

87

Surgical Decompression for Spinal Stenosis Franco Postacchini, G. Cinotti and R. Postacchini

DEFINITION Lumbar spinal stenosis is an abnormal narrowing of the osteoligamentous vertebral canal and/or the intervertebral foramina, which is responsible for compression of the thecal sac and/or the caudal nerve roots; narrowing of the vertebral canal may involve one or more levels and, at a single level, may affect the entire canal or a part of it.1 Thus, abnormal narrowing of the spinal canal may be considered as stenosis if two criteria are fulfilled: the narrowing involves the osteoligamentous spinal canal, and it causes compression of the neural structures. If the concept of stenosis is not limited to the osteoligamentous canal, even disc herniation is, in the strictest sense, a stenotic condition because it causes a pathological narrowing of the spinal canal. However, the two conditions – disc herniation and stenosis – are so different in the pathogenesis and anatomoclinical characteristics, that they cannot be considered as a single pathological entity. The second criterion emphasizes the concept of compression of the thecal sac and nerve roots. The term stenosis indicates a disproportion between the caliber of the container and the volume of the content. If the content is solid or semifluid, as in the vertebral canal, the dimensional disproportion results in compression of the content by the walls of the container. However, the disproportion is not strictly related to the anteroposterior dimensions of the vertebral canal, as believed by Verbiest.2 Severe compression of the neural structures may occur even if the sagittal dimensions of the canal are within normal limits. On the other hand, a midsagittal diameter of 10 mm or less does not necessarily lead to compression of the cauda equina.3 This is probably due to the fact that the neural structures develop in harmony with the dimensions of the canal. When this does not occur, the reserve space available for the thecal sac and/or the caudal nerve roots is variably reduced and, therefore, acquired constrictive conditions of even minor degree are sufficient to cause stenosis. If the narrowing is not severe enough to cause compression of the neural structures, the spinal canal is to be considered narrow but not stenotic. Therefore, a diagnosis of stenosis cannot be made solely on the basis of measurements of the size of the vertebral canal or the area of the thecal sac in the axial sections. The radiologic diagnosis of stenosis should be predicated upon the demonstration of compression of the neural structures, whether clinically symptomatic or asymptomatic, by an abnormally narrow osteoligamentous spinal canal (Fig. 87.1).

CLASSIFICATION Site of constriction Lumbar spinal stenosis can be distinguished, based on the site of constriction, as stenosis of the spinal canal or central stenosis, isolated

stenosis of the nerve root canal or lateral stenosis, and stenosis of the intervertebral foramen (Table 87.1). In stenosis of the spinal canal, the entire area of the canal, as viewed on the axial plane, is usually constricted (Fig. 87.2). In other words, both the central portion of the canal and the lateral parts, occupied by the emerging nerve roots, are constricted. Therefore, the expression stenosis of the spinal canal is more correct than that of central stenosis, which would indicate constriction only of the central area. However, the authors will use the latter term because it has become the one commonly adopted. Central stenosis, except for the rare forms due to vertebral malformations, or sequelae of fractures or infections, is located at the level of the intervertebral space, where there are the anatomical structures, such as the intervertebral disc, the apophyseal joints, and the ligamenta flava, which can change with aging or disease.

Fig. 87.1 Central lumbar stenosis at L3–4 and L4–5 (L5 vertebra is sacralized). The thecal sac shows the posterior indentations typical of the osteoligamentous compression by the posterior vertebral arch.

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Table 87.1: Classification of Lumbar Spinal Stenosis CENTRAL STENOSIS Primary Congenital Developmental Achondroplastic Constitutional Secondary Degenerative Simple With degenerative spondylolisthesis or scoliosis Late sequelae of fractures or infections Paget’s disease Combined Association of primary and secondary forms at the same vertebral level ISOLATED LATERAL STENOSIS Primary Secondary Combined STENOSIS OF THE INTERVERTEBRAL FORAMEN Primary Secondary Combined

The nerve root canal or radicular canal corresponds to the lateral portion of the spinal canal (Fig. 87.3). This canal, which is more of an anatomical concept than a true canal, is the semitubular structure in which the nerve root, exiting from the thecal sac, travels before entering the intervertebral foramen. As for the central form, in the last decade, the term lateral stenosis has become the most widely used for this type of stenosis.

The term lateral stenosis is often used to indicate both nerve root canal stenosis and stenosis of the intervertebral foramen. The authors believe that the intervertebral foramen, which begins and ends at the level of the medial and the lateral border of the pedicle, respectively, should be considered as a distinct anatomical entity. Therefore, stenosis of the foramen should be differentiated from the other two forms of stenosis, although it can be associated, albeit rarely, with one of the two.

Type of stenosis Three forms of stenosis can be identified: primary, secondary and combined (see Table 87.1).

Fig. 87.2 MRI scan at L4–5 level showing central spinal stenosis. The spinal canal is constricted in the central portion, containing the thecal sac, as well as in the lateral portions occupied by the emerging nerve roots. 952

Fig. 87.3 Lateral stenosis at L4–5. CT scan showing constriction of the nerve root canals due to degenerative changes of the facet joints.

Section 5: Biomechanical Disorders of the Lumbar Spine

Primary forms

Secondary forms

Central stenosis

Central stenosis

This abnormality can be classified as congenital or developmental central spinal stenosis. Congenital stenosis, which is exceedingly rare, is due to congenital malformations of the spine. Developmental stenosis includes achondroplastic and constitutional forms. In the former, the midsagittal and/or interpedicular diameters of the spinal canal are abnormally short and the nerve root canals are severe narrowed due to abnormal shortness of the pedicles. In constitutional stenosis the cause of the defective vertebral development is unknown. In the authors’ experience, two types of constitutional abnormality may be identified: (1) a short midsagittal diameter of the spinal canal, and (2) an exceedingly sagittal orientation and/or shortness of the pedicles (Fig. 87.4). In the latter type, the spinal canal is abnormally narrow, mainly or only, in the interarticular diameter.

If the sagittal dimensions of the spinal canal are normal, or at the lower limits, and compression of the caudal nerve roots is the result of one or more acquired conditions, such as spondylotic changes of the facet joints, abnormal thickening of the ligamenta flava, and bulging of the intervertebral discs, then this form is defined as simple degenerative stenosis (Fig. 87.6). Very often, however, degenerative spondylolisthesis of the cranial vertebra of the motion segment is also present at one or, occasionally, two or more levels (Fig. 87.7). Degenerative spondylolisthesis is consistently responsible for narrowing of the spinal canal, but may not cause lateral or central stenosis. This is because the presence, type, and severity of stenosis is related to several factors, such as the constitutional dimensions of the spinal canal, the orientation (more or less sagittal), and the severity of degenerative changes of the facet joints, and the amount of vertebral slipping, which may in some cases play a minor role. For example, a grade I spondylolisthesis in a patient with a constitutionally large spinal canal produces no significant narrowing of the canal, would be categorized as no stenosis. In contrast, the same or even lesser grade of spondylolisthesis in a patient with a primarily narrow canal can be associated with clinically significant stenosis. The type of stenosis, that is whether stenosis is central or lateral, depends on the orientation of the articular processes and the length of the pedicles. Usually, stenosis initially presents as lateral and then central in later stages. Instability, that is hypermobility on flexion–extension radiographs, is one of the main characteristics of degenerative spondylolisthesis. However, in many cases there is no appreciable hypermobility of the slipped vertebra. The authors consider the latter condition as a potential instability, which can become unstable as a result of surgery. Such a scenario may arise following removal of a large part of one or both facet joints, unilateral or

Lateral stenosis Lateral stenosis may result from disturbances of vertebral development, particularly achondroplastic or constitutional abnormal shortness of the pedicles, even more so if associated with a trefoil configuration of the spinal canal or anomalous orientation and/or shape of the superior articular process. In this form, a primary role may be played by the intervertebral disc. A mild disc protrusion or a bulging anulus fibrosus may be enough to cause symptoms in a stenotic or only narrow radicular canal.

Stenosis of the intervertebral foramen Primary forms are found almost exclusively in the presence of abnormally short pedicles associated with a decrease in height of the intervertebral disc (Fig. 87.5).4

Fig. 87.4 CT images showing constitutional stenosis at L3–4 and L4–5. The articular processes are orientated more sagittally than normal and the pedicles are very short. The result is a constriction of the spinal canal more in the interpedicular, than in the sagittal, plane. 953

Part 3: Specific Disorders

Fig. 87.5 Effects intervertebral space narrowing on foraminal dimensions on dried vertebrae. In the presence of normal pedicle length (top and middle), even a marked decrease of the disc height does not change significantly the foraminal dimensions. However, in the presence of short pedicles (bottom), a marked decrease of the disc height causes a relevant decrease of the foraminal dimensions.

bilateral discectomy, or when destabilizing factors unable to stabilize a normal vertebra intervene, such as disc degeneration or severe degenerative changes of the facet joints. In degenerative spondylolisthesis, the intervertebral disc often bulges into the intervertebral foramen to cause stenosis. However, true stenosis of the foramen is rarely present as the foramen becomes larger in the sagittal dimensions in the presence of slipping of the cranial vertebra. A particular form of acquired stenosis is the type that is associated with degenerative scoliosis. In this instance a role may be played by the scoliotic curve in tandem with the pure degenerative changes of the facet joints and the intervertebral discs. 954

Other forms of secondary stenosis include late sequelae of fractures or infectious diseases of the spine, which, however, are rare conditions. Rarely, stenosis can occur secondary to systemic bone diseases such as Paget’s disease. Paget’s disease can lead to an increase in volume and/or deformation of one or more vertebral components.

Lateral stenosis Most often, this form of stenosis is degenerative in nature. Usually, degenerative stenosis involves only the lateral portions of the spinal canal in the initial stages and become central in more advanced stages

Section 5: Biomechanical Disorders of the Lumbar Spine

Fig. 87.8 Lateral stenosis due to a synovial cyst of the left facet joint at L4–5 level.

Combined forms

Fig. 87.6 Simple degenerative stenosis. T2-weighted sagittal MRI showing stenosis at L3–4 and L4–5. The sagittal dimension of the thecal sac is normal in size at intervertebral levels.

when spondylotic changes becomes more severe. This is particularly true for degenerative spondylolisthesis. Lateral stenosis can occur due to a cyst of the facet joint when it compress the emerging root in the nerve root canal (Fig. 87.8).

Stenosis of the neuroforamen Stenosis of the intervertebral foramen is rarely encountered, especially as an isolated condition. In most cases, foramenal stenosis is associated with a central or lateral stenosis. At times, root compression occurs when there is a lateral disc herniation or disc bulge in the presence of advanced degenerative changes of the articular processes.

Fig. 87.7 Plain radiographs of a patient with severe degenerative spondylolisthesis of L5 and mild slipping of L4.

These forms occur when primary narrowing of the spinal canal, the nerve root canal, or the intervertebral foramen is also associated, at the same vertebral level, with secondary narrowing, which is generally spondylotic in nature. Combined stenosis can be differentiated from primary stenosis by the presence of milder developmental narrowing, but more severe degenerative changes.

INDICATIONS FOR SURGERY Surgery is contraindicated for a narrow spinal canal and is generally not indicated in patients who complain only of back pain, in the absence of deformities, such as degenerative spondylolisthesis or scoliosis. In patients with an unstable motion segment who have only back pain, it is usually sufficient to perform a fusion alone if stenosis is mild, because it is unlikely that neural compression will significantly increase and become symptomatic over time after fusion of the motion segment. In patients with no hypermobility it may be useful to apply a rigid corset for 2 weeks. If the back pain improves significantly, there may be an indication for surgery. In patients with leg symptoms, surgery is indicated when comprehensive conservative management as described in other chapters of this book have been carried out for 4–6 months without resulting in significant improvement (Fig. 87.9). The exception to this recommendation is for patients with a severe motor and/or sensory deficit consistent with cauda equina syndrome, who require emergent neural decompression. When the presentation is that of weakness with associated pain, then surgery is indicated when two criteria are met. The stenosis should be advanced and the symptoms should be of less than a few months duration. If the paresis or paralysis has been present for more that 6–8 months, then it is the authors’ opinion that there can be no indication for decompression. Such an extended duration of neural compression leads to irrevocable changes and ultimately surgery offers small or no chance of improvement of muscle function. The ideal surgical candidates are less than 70 years old, without comorbidities, who have radiologic evidence of severe or very severe stenosis, long-standing leg symptoms and severe intermittent claudication, moderate or no motor deficits, and mild or no back pain. This is in contrast to patients who have mild stenosis, mild or inconsistent leg symptoms without a precise radicular distribution, a history of claudication after many hundreds of meters, no motor deficit and back pain of similar severity to, or more severe than, the leg symptoms. A less predictable outcome is associated with surgery in this latter group. 955

Part 3: Specific Disorders Asympt (narrow canal or sten)

LP

LP and chronic LBP

No treatment

Conserv treat

Conserv treat

Failure

Failure

Lat sten

Mild centr sten

Sev centr sten

Laminot (unilat or bilat)

Bilat laminot

Laminect

Decompression and fusion if wide laminect risks to create instability or sev degen adjac disc/s

Severe motor deficits

Decompression

Lat sten

Centr sten

Laminot

Laminect

Fig. 87.9 Algorithm for treatment of simple stenosis.

Usually, there is no need for spinal fusion. Arthrodesis may be indicated when there is a concern that wide surgical decompression could result in postoperative instability. Additionally, fusion may be required for the patient that is experiencing simultaneous radicular pain from spinal stenosis and axial back pain due to internal disc disruption syndrome (see Fig. 87.9).

Advanced age Surgical decompression may offer significant relief of symptoms also to patients older than 70 years.5–8 In the authors’ experience, there is no significant difference in the results of surgery between the patients in early senile age and those aged 80–90 years old, provided the stenosis is severe and the patient’s general health is satisfactory.

Comorbidity In one study,7 a high rate of comorbid illnesses was found to be inversely related to the rate of satisfactory results after surgery. Another study9 compared the long-term results of surgery in 24 diabetic and 22 nondiabetic patients. In the diabetic group there was a 41% rate of satisfactory results, compared with 90% in the nondiabetic group. Different results, however, were observed in a similar study,10 in which the outcome was satisfactory in 72% of the diabetic and 80% of the nondiabetic patients. Neither the duration of the diabetes before surgery nor its type correlated with the outcome. A mistaken preoperative diagnosis was the main cause of failure in diabetic patients. In many of the failures, diabetic neuropathy or angiopathy had elicited symptoms that had been confused with pseudoclaudication.

Previous surgery Surgery for spinal stenosis tends to give less satisfactory results in patients who had previously undergone decompressive procedures in 956

the lumbar spine.7,11–14 This is particularly true when stenosis is at the same level or levels at which the previous surgery for disc herniation or stenosis had been performed.15

Type of stenosis There is no significant difference in outcomes between the various types of central stenosis. However, patients with degenerative or combined stenosis at a single level are the best candidates for surgery because they tend to have a better outcome than those with stenosis at multiple levels. In patients with constitutional stenosis, the intervertebral disc may play a significant role in the compression of the neural structures. When the disc bulges considerably in the spinal canal, but it is not truly herniated, it may be difficult to eliminate the anterior compression of the neural structures. Consequently, less satisfactory outcomes may be obtained when compared with the cases in which the neural compression is caused exclusively by the articular processes. Patients with lateral stenosis, particularly at a single level, tend to have better results than those with central stenosis.

SURGICAL MANAGEMENT Definition of terms Decompression of the lumbar spinal canal can be carried out by total laminectomy, also defined as bilateral or complete laminectomy (Fig. 87.10). More focal decompression can be accomplished with a laminotomy, also called keyhole laminotomy, hemilaminectomy, or partial hemilaminectomy. Laminotomy consists in the removal of the caudal portion of the proximal lamina, the cranial portion of the distal lamina and a varying portion of the articular processes, together with a part of, or the entire, ligamentum flavum on the side of surgery. Laminotomy can be performed at a single level on one side or both sides (Fig. 87.11). Less frequently it is performed at multiple levels (Fig. 87.12).

Section 5: Biomechanical Disorders of the Lumbar Spine

Fig. 87.10 Total laminectomy at two contiguous levels.

The term foraminotomy indicates removal of a part of the posterior wall of the intervertebral foramen, while the term foraminectomy refers to complete excision of the wall of the foramen.

Surgical planning General concepts Surgical treatment is aimed at decompressing the neural structures by means of a total laminectomy or laminotomy at one or more vertebral levels. It is crucial to accurately plan the extent of decompression before surgery because during the operation it may be difficult to determine whether, at a certain level, the central or lateral canal is stenotic, particularly if stenosis is mild. Lack of sufficient care in planning the

A

B

Fig. 87.12 AP radiograph showing bilateral laminotomy at L2–3 to L4–5 in a patient with constitutional stenosis at those levels.

operation may give rise to inadequate decompression, which would leave areas of stenosis, or too wide a decompression, which might cause iatrogenic instability. This process entails a careful review of the history, examination, electrodiagnostic testing, and all radiologic studies. The authors invariably require flexion–extension plain radiographs to assess for instability. In addition, a high-quality MRI or multiplanar reformatted CT scan is a necessary component. Rarely does myelography need to be performed. A review of these multiple elements of the diagnostic work-up allow for thorough and accurate presurgical planning.

Fig. 87.11 Unilateral laminotomy (arrow) (A) and bilateral laminotomy (arrows) (B) at two contiguous levels. 957

Part 3: Specific Disorders

Types of stenosis Stenosis without concurrent spondylolisthesis or scoliosis Central stenosis Number of levels to decompress The stenotic levels should be distinguished accurately to levels at which the need for decompression is absolute and levels where the need is relative. In the former case, compression of the neural structures is marked or, regardless of the severity, is responsible for clinical symptoms and signs. In the latter case, compression of the neural structures is mild and asymptomatic. In most instances, one or two levels, contiguous to the area of absolute stenosis, are involved. At these levels, imaging studies (MRI, CT, myelography) usually reveal: a posterior indentation on the thecal sac; decreased sagittal and transverse diameters of the thecal sac on the axial views; lateral indentation or a mild hourglass deformation of the thecal sac; or medial deviation and/or partial filling of the nerve root emerging from the thecal sac on the coronal view. The consideration of performing a prophylactic decompression at the levels of relative stenosis stems from the evaluation of several factors, such as the patient age, the site of stenosis, the presence of disc abnormalities, and vertebral stability. In patients aged over 75 years the need for a prophylactic decompression is less than in middle-aged or early-old-age patients. Posterior compression of the thecal sac is less likely to become symptomatic than is compression of the nerve roots in the radicular canal. Marked bulging of the anulus fibrosus, which with passing time may become symptomatic, represents an indication for prophylactic decompression. In the presence of instability of the motion segment, it is usually advisable to limit the decompression in the transverse plane as much as possible. Conversely, the presence of intersomatic osteophytes producing spontaneous vertebral arthrodesis represents a guarantee against postsurgical instability. Unilateral or bilateral decompression For the intervertebral levels at which the need for decompression is absolute and stenosis is bilateral, the decompression should be performed bilaterally. This is true for patients with bilateral leg symptoms and/or signs, and for those with unilateral symptoms. When, at a given level, stenosis is severe and symptomatic on one side and mild and asymptomatic on the other, unilateral decompression may be considered, if discectomy has to be performed for associated disc disease. However, even in these cases, bilateral decompression is generally recommended. For levels at which the need for decompression is relative, the choice between unilateral and bilateral decompression should be made taking into consideration the severity of stenosis on the two sides, and the factors taken into account in determining the number of levels to decompress. In general, if total laminectomy is planned at the level of absolute stenosis, it is advisable to extend it also to the level of relative stenosis. On the other hand, when laminotomy is planned for the area of absolute stenosis, it is often sufficient to limit the decompression for the area of relative stenosis to the side of the more marked compression of the neural structures. Extent of decompression The long-term results of surgery may deteriorate with time because of regrowth of the resected portion of the posterior vertebral arch.16 This is more likely to occur when a narrow decompression is performed. The authors believe that decompression should be as wide as possible in the lateral portion of the spinal canal, while at the same time preserving vertebral stability. The optimal facetectomy is that in which the medial two-thirds of the superior and inferior articular processes are removed. An important concept is that in lumbar stenosis radicular symptoms originate from 958

compression of the nerve root after it has emerged from the thecal sac, that is in the radicular canal, rather than within the thecal sac. Compression of the thecal sac and spinal nerve roots usually occurs at the intervertebral level. To achieve adequate decompression the entire area facing the intervertebral disc needs to be addressed. That is, decompression should extend as far as half of the height of the vertebrae above and below the stenotic area. Methods of decompression Surgery for lumbar stenosis is aimed at adequately decompressing the neural structures, particularly the nerve roots in their extrathecal course, without significant compromise of vertebral stability. Preservation of vertebral stability is paramount because the disappearance of leg symptoms may not make the patient satisfied if back pain appears or worsens after surgery. This is especially true for middle-aged or early-senile-aged patients. In the past few years, the technique of multiple laminotomy, or its variants, has become widely used in the treatment of central spinal stenosis because it preserves vertebral stability better than central laminectomy does.17,18 However, a major role is still played by total laminectomy, which often allows for a more effective decompression of the neural structures. Multiple laminotomy is the treatment of choice for constitutional stenosis because the patients are usually middle-aged, the stenosis is rarely severe, and disc excision is often necessary in addition to decompression.18 Similarly, a multilevel laminotomy is preferred for degenerative or combined stenosis when narrowing of the spinal canal is mild or moderate, particularly if a disc excision has been planned. Total laminectomy is typically more effective for severe stenosis, providing that the involved segments are stable preoperatively. When this is not the case, the choice is between multiple laminotomy and total laminectomy combined with fusion of the decompressed segments. Spinal fusion In addition to degenerative spondylolisthesis and scoliosis, spinal fusion should be planned if the area to decompress is unstable or when total laminectomy and bilateral discectomy are to be performed. Spinal fusion should also be planned when there are high chances that, at surgery, the articular processes will be completely removed on both sides or when the articular processes will be excised on one side and discectomy performed bilaterally. Also, fusion will be needed for the patient complaining of chronic back pain, determined to originate from the motion segment needing decompression. Except for these situations, there is no need to carry out spinal fusion in stenotic patients undergoing decompression of the neural structures. These guidelines, previously indicated on the basis of clinical experience,15 were confirmed by a prospective, randomized study.19

Isolated lateral stenosis In this condition, only one vertebral level is usually involved. In the presence, at a single level, of a symptomatic nerve root compression on both sides, bilateral decompression should be carried out. This should be done even if on one side the leg symptoms are mild and no neurological abnormalities are detectable. When imaging studies show bilateral nerve root compression in the presence of radicular symptoms and signs on one side only, bilateral decompression should generally be planned, especially in the middleaged patient or when electrophysiological investigations show evidence of acute denervation of the clinically asymptomatic nerve root. However, in the elderly patient in which a rapid surgical procedure is desired, there can be an indication for unilateral decompression. This is particularly true when the symptomatic side is considerably more stenotic than the asymptomatic side. Discectomy should generally be planned for patients in whom preoperative investigations show evidence of a bulging intervertebral

Section 5: Biomechanical Disorders of the Lumbar Spine

disc at the stenotic level. Preoperatively, however, it is often difficult to determine the precise role played by the intervertebral disc in the etiology of nerve root compression. In these cases, the decision about whether to carry out disc excision must be made on the basis of the operative findings after exploring the canal. Spinal fusion is rarely needed in cases of isolated lateral stenosis. It is indicated when bilateral decompression is carried out at a preoperatively unstable level, particularly if a unilateral or bilateral disc excision is planned. Fusion may also be indicated in patients complaining of chronic low back pain due to disc degeneration at the stenotic level or levels.

Stenosis of the neuroforamen This type of stenosis is often better appreciated on CT or MRI. However, in the vast majority of cases, narrowing of the intervertebral foramen causes no compression of the nerve root. Osteoligamentous decompression for foraminal narrowing is rarely indicated, unless protrusion or marked bulging of the intervertebral disc coexists.

Degenerative spondylolisthesis In the authors’ experience, bilateral laminotomy, or even total laminectomy, may be carried out with no concomitant fusion in patients with mild olisthesis, no vertebral hypermobility on flexion–extension radiographs, mild central stenosis or any degree of isolated lateral stenosis, and mild or no back pain (Fig. 87.13). Similarly, in elderly patients with moderate olisthesis and marked resorption of the disc below, no vertebral hypermobility, and stenosis requiring total laminectomy, there may be no indication for fusion. This tenet is particularly applicable in the absence of significant chronic low back pain or

in the presence of comorbid diseases which require a rapid operation. The indications for monolateral laminotomy with no fusion are: moderate central stenosis in elderly patients with unilateral symptoms; lateral stenosis only on one side; and unilateral additional pathology, such as a ipsilateral synovial cyst provided there is no contralateral leg pain and no chronic back pain. In the presence of moderate or severe olisthesis, vertebral hypermobility even of mild degree, and/or severe central stenosis and chronic back pain patients should undergo decompression and fusion (see Fig. 87.13). In these instances, the association of an arthrodesis allows the surgeon to decompress the neural structures as widely as necessary. Arthrodesis should usually be limited to the involved motion segment, but this is not an absolute rule. When there is spondylolisthesis of L4, the presence of a degenerated L5–S1 disc may necessitate extension of the fusion to the sacrum. Such a procedure is performed to avoid persistent postoperative back pain, if the disc above the slipped vertebra is normal on MRI. If the disc above (L3–4) is degenerated, then fusion should be limited to the level of spondylolisthesis, particularly when surgery is mainly aimed at resolving leg symptoms. Others use discography to determine whether a concurrent fusion is necessary, feasible, and at which levels. Posterolateral (intertransverse process) fusion with no pedicle screw instrumentation is the gold standard because the fusion is less rigid and a small residual mobility of the fused vertebrae remains, which decreases the mechanical stresses on the adjacent motion segments. However, the drawbacks are the necessity of a prolonged, rigid immobilization following surgery. Posterolateral instrumented fusion, using pedicle screw fixation, has become the most common procedure (Fig. 87.14). The procedure can be done at multiple levels when olisthesis

Flexion−extension x-rays

No hypermobility

Hypermobility

Clinical features

Clinical features

No LBP

Chronic LBP

Only LP

No surg

Corset

Severe sten

Mild sten

No symp

LBP and mild asympt sten

LBP and severe sten

No surg

Fusion

Laminect and fusion

LP

40–70 y. No improvement

Improvement

Laminect and fusion

Laminot no fusion

>70 y. mild hyperm comorbidity

Laminect and bilat fusion LPB: low back pain LP: leg pain

Laminot and unilat fusion

Fig. 87.13 Algorithm for treatment of degenerative spondylolisthesis. 959

Part 3: Specific Disorders

Fig. 87.14 Postoperative radiographs taken 4 years after total laminectomy and bilateral pedicle screw instrumentation and intertransverse fusion at L4–5 in patient with degenerative spondylolisthesis and stenosis.

is present at more than one level (Fig. 87.15). In both cases it requires no, or a short period of, postoperative immobilization. Internal fixation may be bilateral or unilateral. The latter, which decreases the potential morbidity of the bilateral fixation (increased stress on the adjacent unfused segments) was found to give similar results in terms of fusion rate as the bilateral instrumentation.20 The authors have performed bilateral bone grafting and unilateral instrumentation or unilateral bone grafting and instrumentation in 36 cases with a 97% rate of solid fusion. The advantages of the unilateral instrumentation are a shorter operative time, decreased risk of neurological complications, and reduced costs. The main indications are:

A

960

B

back pain with mild segmental instability in the elderly, or concern of producing gross instability after a total laminectomy. Some surgeons prefer to perform a posterior lumbar interbody fusion (PLIF) in lieu of a posterolateral fusion. This procedure, when used in tandem with pedicle screw instrumentation, provides excellent results and a high rate of solid fusion. The devices inserted in the disc space are normally represented by cages filled with bone chips. An alternative is to use blocks of porous tantalum (hedrocel), the stiffness of which is very similar to that of subchondral bone. Animal model studies have shown bone ingrowth within the pores of the implant and maturation of the osteoid in some 3 months. The

Fig. 87.15 Degenerative spondylolisthesis at multiple levels associated with mild lumbar scoliosis. Pedicle screw instrumentation and intertransverse fusion at L2–5 with partial correction of scoliosis. The patient had complete relief of symptoms.

Section 5: Biomechanical Disorders of the Lumbar Spine

C

D

authors have used blocks of hedrocel for 3 years with excellent results of this interbody fusion (Fig. 87.16). In 16 cases followed for at least 2 years, there has been no observed migration of the implant or loosening of the pedicle screws. The authors have invariably observed a tight union between the implant and the adjacent vertebral endplates as assessed by MRI and/or plain X-rays.

Degenerative scoliosis Lumbar scoliosis, particularly of the degenerative type, is not uncommonly associated with spinal stenosis. In patients with both

A

B

Fig. 87.15—Cont’d

conditions, total laminectomy may not relieve compression of the nerve roots when their compromise is related to pedicle and facet migration and rotation. Furthermore, in scoliotic patients, decompression may lead to an aggravation of the curve and/or lateral vertebral slipping. Laminectomy alone may yield a poor outcome because of increased deformity or instability. These risks should lead one to limit the indications for decompression or, if surgery is undertaken, to concomitantly carry out a spinal fusion after correction of the curve using segmental pedicle screw instrumentation.

C

Fig. 87.16 Central stenosis in a patient with degenerative spondylolisthesis at L4–5. (A–C) Preoperative radiograph and MRI scans showing degenerative olisthesis and stenosis. (Continued) 961

Part 3: Specific Disorders

D

F

E

G

SURGICAL TECHNIQUE

Disinsertion of paraspinal muscles

Total laminectomy

The thoracolumbar fascia is incised, starting on the side of the surgeon, immediately adjacent and parallel to the tip of the spinous processes and interspinous ligaments, using an electric cautery knife. Frequently, the tip of the spinous processes can be palpated, but is not visible. In these cases, the fascia can be erroneously incised along the midline or one may inadvertently pass over to the opposite side. To avoid this, the assistant surgeon should press down the paraspinal muscles on his side using a periosteal elevator applied against the outer surface of the spinous processes. The surgeon may carry out the same maneuver on his side, while incising the fascia. Elevation of the paraspinal muscles from their insertion starts at the most cranial of the exposed vertebrae. A broad periosteal elevator is introduced deep to the muscle mass and allowed to slip along the outer surface of the spinous process and lamina to detach the paraspinal muscles from the bone surface until the lateral border of

Skin incision and superficial hemostasis The skin incision extends from the cranial edge of the spinous process above to the caudal edge of the spinous process below that of the vertebra, or the group of vertebrae, needing decompression. Dermal and subdermal vessels may be cauterized or preferably clamped together with a small portion of superficial subcutaneous tissue; clamps (usually placed at a distance of approximately 1 cm from each other) are then turned outwards of the surgical wound and held together with an elastic band anchored to the surgical drape. This method makes hemostasis of the superficial vessels very rapid. The deep portion the subcutaneous tissue may be detached from the supraspinous ligament and adjacent portions of the thoracolumbar fascia with a dry sponge. 962

Fig. 87.16—Cont’d (D,E) Functional radiographs demonstrate hypermobility of the olisthetic vertebra. (F,G) Radiographs taken after total laminectomy, bilateral pedicle screw instrumentation, and PLIF at L4–5 level.

Section 5: Biomechanical Disorders of the Lumbar Spine

the facet joints is reached. Dry sponges are then packed, using the periosteal elevator, beneath the muscle mass. This maneuver is aimed at both disengaging the paraspinal muscles from the lateral portion of the laminae and apophyseal joints, and arresting bleeding from the posterior branches of the lumbar arteries and veins. Sponges packed at the level of two contiguous vertebrae are subsequently removed and, while retracting the muscle mass, the residual musculotendinous attachments to the base of the spinous processes and interspinous ligaments are sectioned. When decompression is needed at more than one motion segment, dry sponges are again packed into the depth of the wound and the vertebrae and intervertebral spaces below are exposed. The maneuvers described above are then performed on the opposite side by the surgeon himself or the assistant surgeon. One or two self-retaining retractors, depending upon the number of exposed vertebrae, are applied. Hemostasis is completed and remnants of muscle and fat tissue still adherent to the laminae, facet joints, and yellow and interspinous ligaments are removed using gouge forceps or a large curette.

Opening of the spinal canal After exposure of the yellow and interspinous ligaments, the vertebrae included in the operative field are identified by locating the lumbosacral interspace, when exposed, or counting the spinous processes starting from the fifth lumbar. Fluoroscopic imaging should be used to confirm levels by inserting a spinal needle into one, or two contiguous, interspinous spaces. Identification, at this stage, of the individual vertebrae is extremely important, because, once the spinous processes have been removed and laminectomy started, it becomes exceedingly difficult to identify the vertebral levels. When a single intervertebral level is to be decompressed, the cranial half of the spinous process of the distal vertebra and the caudal half or two-thirds of the spinous processes of the proximal vertebra as well as the interspinous ligament are resected. Resection of the spinous process, using a sharp-angled bone biter, should be carried out as far as its base. A small curette is used to detach the ligamentum flavum from the deep surface of the proximal laminae. The curette should be introduced between the ligament and bone and maintained in close contact with the latter. Laminectomy is initiated in the central portion of the laminar arch, that is, at the level of the posterior angle of the spinal canal, not occupied by the thecal sac. The lamina can be removed using a small gouge forceps, or a punch rongeur when the spinal canal is severely stenotic. Laminectomy is then continued, alternately on one side and the other, after the ligamenta flava have been further detached with a curette from the residual ventral aspect of the laminae. The ligamenta flava are subsequently detached from the proximal border of the laminae of the distal vertebra starting from the most medial portion. The cut edge of the ligament is lifted with forceps, sectioned longitudinally using scissors or the tip of a small scalpel, and removed as extensively as possible. The lateral portion of the laminae and the inferior articular processes are removed using a rongeur. An alternative technique, which the authors prefer, is to perform laminectomy using chisels. After removal of the spinous processes and detachment of the ligamentum flavum from the lamina of the proximal vertebra, a chisel is used to remove, first, the caudal half of the lamina of the proximal vertebra and then the medial half of the inferior articular process of the same vertebra. The proximal portion of the lamina of the distal vertebra can be removed partly by the chisel (posterior portion) and partly using a rongeur (deep portion, closer to the thecal sac and nerve root). After removal of the ligamen-

tum flavum as extensively as possible and exposure of the thecal sac, the residual lateral portions of the articular processes are removed using both chisels, 1 or 2 cm in width, and punch rongeurs. When using chisels, these should be orientated at 45° in a mediolateral and posteroanterior direction to undermine the articular processes, that is to remove only the ventral portion of the bone in order to preserve vertebral stability.12 Since stenosis occurs at the intervertebral level, when performing decompression at multiple levels, care should be taken to extend laminectomy, proximally and distally, beyond the intervertebral discs located at the extremities of the stenotic area, until it is certain that the neural structures are no longer compressed.

Exploration of intervertebral discs and spinal nerve roots The spinal canal is opened laterally until the nerve root emerging from the thecal sac is visualized. The emerging root and the thecal sac are then retracted medially and the disc is exposed at each of the intervertebral levels included in the area of laminectomy. Consistency of the anulus fibrosus is tested with a blunt probe. If the anulus is hard in consistency, the disc should not be entered, even when it protrudes posteriorly. Discectomy is carried out only when the disc is herniated or, in the absence of a true herniation, it is soft in consistency and easily depressed by the probe. A right-angled blunt probe is then used to evaluate the width of the nerve root canal and the intervertebral foramen. If difficulty is encountered in introducing the probe into the nerve root canal and the foramen, removal of the articular processes should be continued and the foramen opened until complete decompression of the root is obtained. It is important to free the spinal nerve root adequately, even if this implies complete excision of the articular processes. This is rarely necessary and one should not hesitate to perform unilateral foraminectomy because it does not jeopardize vertebral stability if the disc has been preserved and the motion segment is preoperatively stable. Bilateral foraminectomy is needed very rarely and may require spinal fusion, especially when the disc has been excised.

Wound closure Where the spinous processes have been removed, the paraspinal muscles of the two sides are sutured by interrupted sutures. In these areas the thoracolumbar fascia is closed with interrupted sutures or a continuous suture, which is more rapid and better closes the fascia. Where the spinous processes have been preserved, the fascia is anchored to the supraspinous ligament. The formation of a hematoma between the subcutaneous tissue and thoracolumbar fascia can be avoided by passing a few sutures in both the deep and middle subcutaneous layer and the fascia.

Laminotomy Single level Skin incision extends from the cranial border of the spinous process of the proximal vertebra to the caudal border of the spinous process of the distal vertebra. For unilateral laminotomy, the thoracolumbar fascia is incised only on the symptomatic side, in close proximity to the spinous processes. Gradually, as the paraspinal muscles are disinserted from the bone surface, dry sponges are packed into the osteomuscular space to control bleeding and to strip the muscles as far as the lateral portion of the articular processes. A Taylor retractor is installed against the external aspect of the articular processes and held by a metal weight of some 2 kg. The 963

Part 3: Specific Disorders

ligamentum flavum is detached using a curette from the deep surface of the proximal lamina, and the distal one-third to half of it is excised using a gouge forceps or a punch rongeur. The ligamentum flavum is disinserted from the proximal border of the distal lamina. This allows a rongeur to be introduced under the lamina, about one-third of which is initially removed. Rongeurs of varying sizes are used to excise the medial half to two-thirds of the facet joint as well as the ligamentum flavum inserted on the facets. An alternative method is to use a chisel, or a high-speed microdrill, to remove a portion of the proximal lamina and the medial portion of the inferior articular process of the proximal vertebra. The remaining ligamentum flavum is excised by cutting it with a scalpel or a rongeur. Facetectomy should be extended laterally to expose the emerging nerve root: retracting the sac and the nerve root medially, the intervertebral disc is exposed and the degree of its prominence and consistency is evaluated. Disc excision is not usually necessary when the disc is hard and fibrous in consistency and does not appear to compress the nerve root. If any uncertainty exists, it is better to proceed with discectomy rather than risk leaving a disc protrusion responsible for root compression. Laminotomy of the distal vertebra is then enlarged and the medial portion of the base of the superior articular process is removed with a rongeur or a small chisel to expose the nerve root as far as the medial surface of the pedicle. A blunt probe is used to evaluate the width of the distal portion of the lateral recess and the neuroforamen, continuing the laminofacetectomy until complete decompression of the nerve root is achieved. For bilateral laminotomy at a single level, the procedure is carried out firstly on one side and then on the opposite side.

Multiple levels Bilateral laminotomy can be performed at two or more adjacent intervertebral levels. The surgical technique is similar to that described for single level laminotomy. However, when performing laminotomy at two adjacent levels on the same side, much care should be taken to leave intact, for at least 5 mm, the lamina between the two motion segments. This type of decompression is particularly indicated for patients with constitutional stenosis, in whom constriction of the spinal canal is usually moderately severe and disc excision is often required at one or more levels, and for patients with degenerative spondylolisthesis when spinal fusion is not planned.

Microsurgery Most technical difficulties encountered in performing laminotomy, particularly at a single level, are related to poor lighting of the operative field. These difficulties may be overcome with the use of the operating microscope. The microscope, by providing a vertical light beam not obstructed by the surgeon’s head or hands, ensures excellent lighting, regardless of the extent of surgical exposure, which is 2–3 or 4–6 cm long for one or two levels, respectively. Furthermore, by slanting the objective, any part of the operative field can be illuminated. Thus, surgical maneuvers may be performed with greater precision, the causes of compression of the neural structures may be more easily identified, and fewer risks are run of causing undue trauma to the emerging nerve root or thecal sac. Moreover, only occasionally is an excessively large portion of the articular processes resected or a complete facetectomy inadvertently performed when using the microscope. The microsurgical technique is very similar to the naked-eye technique in as much as the same instruments are needed, with the exception of the paraspinal muscle retractor, which should be as 964

narrow as possible. The authors use a Taylor retractor about one-third the width of the standard instrument. Excision of the laminae and articular processes can be carried out using the same instruments used for naked-eye technique, including the chisel. However, many surgeons use a high-speed microdrill for laminoarthrectomy. The microscope is particularly useful for single-level laminotomy. However, surgeons accustomed to the microscope often use this tool also for surgery at multiple levels.

RESULTS OF SURGERY Overall results Central stenosis Of the 92 patients followed by Verbiest,2 for 1–20 years, 18% had no significant symptoms. In the remaining cases, back pain was the most frequent symptom. The highest rate of excellent results was obtained in the patients with the most severe stenoses. Lassale et al.21 evaluated 128 patients 2–14 years after surgery using a grading scale of 0 to 20. Satisfactory results were observed in 83% of patients. On the grading scale, four profiles were identified: a stable result (60%), regular improvement (14%), improvement with episodic aggravation of symptoms (19%), and subsequent worsening (8%). In a prospective study22 of 140 patients, an average leg pain improvement of 82% and back pain improvement of 71% was found a mean of 3 years after surgery. Similar results were reported in other series of the 1970s and 1980s.12,23–25 In a series of 77 patients,26 average age of 65 years of age, who were followed for 2–5 years, 83% had a satisfactory result. Younger patients had a greater reduction in severity scores. However, satisfaction was similar in both older and younger patients. Postacchini et al.27 reviewed 64 patients at a mean of 8 years (range, 4–21 years) after surgery. The long-term results were excellent or good in 67% of patients and fair or poor in 33%. However, of the patients with unsatisfactory results, 15% already showed an unsatisfactory outcome in the first year after surgery. Thus, only 13% of patients had a deterioration of the result with time. The majority of the patients who underwent radiographs during the followup period and/or at the most recent follow-up showed regrowth of the resected portion of the posterior vertebral arch.16 Regrowth was marked in 13% of cases (Fig. 87.17). In two cases, the regrowth produced recurrence of stenosis, which required repeat surgery. In a study in which 37 patients were followed for a minimum of 10 years, no impairment in activity of daily living was found in 62% of the cases.28 The rate of improvement was evaluated as excellent or good in 57%, fair in 22% and poor in 22%.

Lateral stenosis Proportions of satisfactory results ranging 79–93% were obtained by several authors using laminotomy or total laminectomy.17,29–31 Venner and Crock32 reviewed 45 patients with stenosis of the S1 radicular canal and isolated resorption of the fifth lumbar disc. An excellent result was obtained by 62% and a good result by 25% of patients. Results were satisfactory in 83% of 43 cases followed for 3 years on average by Postacchini;15 good to excellent outcomes were observed in 90% of patients with preoperative motor deficit or reflex changes and in 71% of those without neurological deficits.

Degenerative spondylolisthesis Several studies, particularly in past decades, have reported satisfactory results with decompression alone.33–36 In the past two decades, fusion (with or without pedicle screw instrumentation) has been associated more and more often to decompression,37–42 with very high

Section 5: Biomechanical Disorders of the Lumbar Spine

A

B

percentages of satisfactory results. In the authors’ experience, the association of arthrodesis is mandatory in the presence of gross instability, particularly when total laminectomy is carried out. In other situations (such as mild olisthesis and potential instability or unilateral decompression, in patients with no back pain) only decompression can be performed with excellent outcomes.

References 1. Postacchini F. Lumbar spinal stenosis and pseudostenosis. Definition and classification of pathology. Ital J Orthop Traumatol 1983; 9:339–351. 2. Verbiest H. Results of surgical treatment of idiopathic developmental stenosis of the lumbar vertebral canal. A review of twenty-seven years experience. J Bone Joint Surg 1977; 59B:181–188. 3. Postacchini F, Ripani M, Carpano S. Morphometry of the lumbar vertebrae. An anatomic study in two caucasoid ethnic groups. Clin Orthop Rel Res 1983; 172: 296–303. 4. Cinotti G, De Santis P, Nofroni I, et al. Stenosis of the intervertebral foramen. Anatomic study on predisposing factors. Spine 2002; 27:223–229. 5. Herron LD, Mangelsdorf C. Lumbar spinal stenosis: results of surgical treatment. J Spinal Disord 1991; 4:26–33. 6. Johnsson KE, Udén A, Rosén I. The effect of decompression on the natural course of spinal stenosis. A comparison of surgically treated and untreated patients. Spine 1991; 16:615–619.

Fig. 87.17 Regrowth of the posterior vertebral arch after central laminectomy. (A) Early postoperative radiograph. (B) Radiograph taken 7 years after surgery showing marked regrowth of the posterior vertebral arch.

13. Herron LD, Mangelsdorf C. Lumbar spinal stenosis: results of surgical treatment. J Spinal Disord 1991; 4:26–33. 14. Nasca RJ. Rationale for spinal fusion in lumbar spinal stenosis. Spine 1989; 14: 451–454. 15. Postacchini F. Lumbar spinal stenosis. Vienna: Springer Verlag; 1989. 16. Postacchini F, Cinotti G. Bone regrowth after surgical decompression for lumbar spinal stenosis. J Bone Joint Surg 1992; 74B:862–869. 17. Aryanpur J, Ducker T. Multilevel lumbar laminotomies: an alternative to laminectomy in the treatment of lumbar stenosis. Neurosurgery 1990; 26:429–433. 18. Postacchini F, Cinotti G, Perugia D, et al. The surgical treatment of central lumbar stenosis. Multiple laminotomy compared with total laminectomy. J Bone Joint Surg 1993; 75B:386–392. 19. Grob D, Humke T, Dvorak J. Degenerative lumbar spinal stenosis. Decompression with and without arthrodesis. J Bone Joint Surg 1995; 77A:1036–1041. 20. Kabins MB, Weinstein JN, Spratt KF, et al. Isolated L4–L5 fusion using the variable screw placement system: unilateral versus bilateral. J Spinal Disord 1992; 5:39–49. 21. Lassale B, Deburge A, Benoist M. Resultatts à long terme du traitment chirurgical des stenoses lombaires operées. Rev Rheum 1985; 52:27–33. 22. Herron LD, Mangelsdorf C. Lumbar spinal stenosis: results of surgical treatment. J Spinal Disord 1991; 4:26–33. 23. Paine KWE. Results of decompression for lumbar spinal stenosis. Clin Orthop 1976; 115:96–100. 24. Hasue M, Kida H, Inoue K, et al. Lumbar spinal stenosis. A clinical study of symptoms and therapeutic results. Int Orthop (SICOT) 1977; 1:133–137.

7. Katz IN, Lipson SJ, Larson MG, et al. The outcome of decompressive laminectomy for degenerative lumbar stenosis. J Bone Joint Surg 1991; 73A:809–811.

25. Tsuji H, Tamaki T, Itoh T, et al. Redundant nerve roots in patients with degenerative lumbar spinal stenosis. Spine 1985; 10:72–82.

8. Sanderson PL, Wood PLR. Surgery for lumbar spinal stenosis in old people. J Bone Joint Surg 1993; 75B:393–397.

26. Hansray KKH, Cammisa FP, O’Leary PF, et al. Decompressive surgery for typical lumbar spinal stenosis. Clin Ortop 2001; 384:11–17.

9. Simpson JM, Silveri CP, Balderstone RA, et al. The results of operations on the lumbar spine in patients who have diabetes mellitus. J Bone Joint Surg 1993; 75A: 1823–1829.

27. Postacchini F, Cinotti G, Gumina S, et al. Long-term results of surgery in lumbar stenosis: 8-year review of 64 patients. Acta Orthop Scand 1993; Suppl 251:78–80.

10. Cinotti G, Postacchini F, Weinstein JN. Lumbar spinal stenosis and diabetes. Outcome of surgical decompression. J Bone Joint Surg 1994; 76B:215–219.

28. Iguchi T, Kurihara A, Nakayama J, et al. Minimum 10-year outcome of decompressive laminectomy for degenerative lumbar spinal stenosis. Spine 2000; 25: 1754–1759.

11. Boccanera L, Pelliccioni S, Laus M. Stenosis of the lumbar vertebral canal (a study of 25 cases operated on). Ital J Orthop Traumat 1984; 10:227–236.

29. Choudury AR, Taylor JC. Occult lumbar spinal stenosis. J Neurol Neurosurg Psychiatry 1977; 40:506–510.

12. Getty CJM. Lumbar spinal stenosis. The clinical spectrum and the results of operation. J Bone Joint Surg 1980; 62B:481–485.

30. Tile M, McNeil SR, Zarins RK, et al. Spinal stenosis. Results of treatment. Clin Orthop 1976; 115:104–108.

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Part 3: Specific Disorders 31. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al. Lumbar spinal nerve lateral entrapment. Clin Orthop 1982; 169:171–178.

37. Hanley EN. Decompression and distraction–derotation arthrodesis for degenerative spondylolisthesis. Spine 1986; 11:269–276.

32. Venner RM, Crock HV. Clinical studies of isolated disc resorption in the lumbar spine. J Bone Joint Surg 1981; 63B:491–494.

38. Knox BD, Harvell JC, Nelson PB, et al. Decompression and Luque rectangle fusion for degenerative spondylolisthesis. J Spinal Disord 1989; 2:223–228.

33. Cauchoix J, Benoist M, Chasseing V. Degenerative spondylolisthesis. Clin Orthop 1976; 115:122–129.

39. Herkowitz HN, Kurz LT. Degenerative spondylolisthesis with spinal stenosis. A prospective study comparing decompression with decompression and intertransverse process arthrodesis. J Bone Joint Surg 1991; 73A:802–808.

34. Rosenberg NJ. Degenerative spondylolisthesis. Surgical treatment. Clin Orthop 1976; 117:112–120. 35. Herron LD, Trippi AC. Degenerative spondylolisthesis. The results of treatment by decompressive laminectomy without fusion. Spine 1989; 14:534–538. 36. Epstein NE, Epstein JA, Carras R, et al. Degenerative spondylolisthesis with an intact neural arch: a review of 60 cases with an analysis of clinical findings and the development of surgical management. Neurosurgery 1983; 13:555–561.

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40. Caputy AJ, Lussenhop AJ. Long-term evaluation of decompressive surgery for degenerative lumbar stenosis. J Neurosurg 1992; 77:669–676. 41. Katz JN, Lipson SJ, Chang LC, et al. Seven-to10-year outcome of decompressive surgery for degenerative lumbar spinal stenosis. Spine 1996; 21:92–98. 42. Garfin SR, Herkowitz HN, Mirkovic S. Spinal stenosis. J Bone Joint Surg 1999; 81A:572–586.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ ii: Lumbar Radicular Pain

CHAPTER

Postoperative Rehabilitation

88

Raymond W.J.G. Ostelo and Katrien Bartholomeeusen

INTRODUCTION Patients with intractable lumbar radiculopathy, due to a lumbar disc herniation, require surgery. Lumbar discectomy is the standard of care. This invasive technique aims to release the pressure on the nerve caused by a prolapsed disc, while minimizing scar tissue formation, avoiding nerve damage and biomechanical destabilization.1 Rehabilitation following lumbar disc surgery has received far less attention than the operation itself. One could speculate that this is because after lumbar disc surgery the problems have been resolved and, therefore, rehabilitation is unnecessary. The reality is that in the long term too many patients still show considerable symptoms, reduced daily functional capacities, and disability.2,3 In other words, surgery to remove the lumbar disc protrusion does not solve all back or leg problems and a substantial number of patients continue to suffer residual complaints. That is, complaints remain or return after surgery. In general, the success rate of lumbar disc surgery varies from 60% to 90%.4–6 It has been reported that, after lumbar disc surgery, 22–45% of patients experience residual leg pain and 30–70% have residual low back pain.7–9 The range of these statistics reflects the different inclusion criteria for lumbar disc surgery and the various definitions of a successful outcome. It is often not clear from these studies what kind of post surgical care, if any, was provided to subjects in a particular study. Very specific and individualized rehabilitation is an important tool that can minimize these remaining complaints. In particular, active treatment options could be important in maximizing patients’ functional status. This chapter will focus on the active rehabilitation after lumbar discectomy. The first part of this chapter will briefly discuss the controversial diagnosis of ‘failed back surgery syndrome’ and will explain possible reasons for these less favorable outcomes. In the second part, scientific evidence regarding postoperative rehabilitation programs following lumbar disc surgery will be highlighted. For this purpose, randomized controlled trials as well as nonrandomized controlled trials were considered. This is in line with the evidence-based approach because these designs are most appropriate for establishing sound evidence. This chapter will conclude with the proposal of a treatment protocol, which when possible, is based on the evidence as described in the second part of this chapter.

A ‘FAILED’ SURGERY? For the situation where complaints remain or return, the term ‘failed back surgery syndrome’ has been used.10,11 This is a controversial term.12,13 The authors agree with Verbeek13 that this term is not particularly helpful and even authors of articles who use these diagnos-

tic terms admit that they are better avoided since they do not help to identify a cause or a treatment. After all, the only characteristics that these patients share are that they have been operated on for a lumbar disc surgery and that back-related complaints or leg pain remained or returned at some point after the operation. In contradistinction to Verbeek, the authors think that the term non-specific low back pain for this condition might also be somewhat misleading because that term is used for the general situation where the so-called ‘red flags’ have been excluded. The authors propose the term ‘residual complaints following lumbar disc surgery,’ because in the opinion of the authors that describes the situation most appropriately. First of all, it has not the negative connotation (both for surgeons and patients) that the surgery has ‘failed,’ but on the other hand it acknowledges the fact that there has been a surgery. Different underlying mechanisms before, during, and after surgery have been described that could explain the persistent symptoms, the reduced daily functional capacities, and the disability inherent in this group of patients. Knowledge of these mechanisms is important to understanding the rationale of the proposed treatment strategy.

Before surgery Before surgery, many patients have a long history of recurrent low back and leg pain. Panjabi14 assumes that, as a result of injury, degenerative disc disease and muscle weakness, the control over the neutral zone of the spinal segment is decreased, which may lead to instability. The herniated disc as part of the degenerative cascade15 affects the stability of the spine: an increase in neutral zone to range of motion ratio in the different loading directions is reported.16 The stability around the spinal segment is conserved by the sensory-motor control system.17 There is extensive evidence of changes in both of these systems in patients with low back pain. After the first episode of low back pain, the lumbar multifidus, which is an important stabilizer, is inhibited and does not spontaneously recover, even when the patient is asymptomatic.18 Furthermore, as a result of a herniated disc, abnormal changes in the characteristics and the activity of the paraspinal muscles are observed on the involved side. In addition, the contraction of the tranversus abdominus muscle, the other important stabilizer, is altered and delayed in patients with low back pain when performing upper and lower limb movements, leading to inefficient muscular stabilization of the lumbar spine.19 Lumbar proprioception, postural control, and feed forward control of the paraspinal muscles seem to be impaired in patients with sciatica.20 In general, these patients often have a long medical history of pain and functional limitation, which can lead to long-term disability, antalgic posture, muscle imbalance, and reduced cardiovascular capacities.21 Other factors that play an important role, which are superimposed upon these neuromusculoskeletal abnormalities, include psychological influences such as anxiety or problems at 967

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work. Disability and patients’ expectation regarding the surgery have also been reported.10,22,23

During surgery During surgery the functional spinal unit will be altered. The lumbodorsal fascia is incised, the paraspinal muscles are dissected and elevated off the spinous process, a portion or the entire lamina is removed, and the ligamentum flavum is incised. Depending on the size and location of the herniated fragment, a laminectomy or facet-otomy is necessary.24 The annulus fibrosis is also incised. It is obvious that injury to these tissues will necessarily interrupt the biomechanical integrity of the functional spinal unit. Another concern develops as a result of retraction of the paraspinal muscles. Even with careful dissection, damage to the medial branches of the posterior rami of the spinal nerves and denervation of the multifidus muscle can occur.25 In those instances in which the injury presumably results from ischemia, a risk factor for nerve root injury results and, moreover, the neural damage does not necessarily spontaneously recover.26 Of course, if the medial branch was surgically lysed, the probability of recovery is even lower.

After surgery In the first period after surgery, local tissue response to the surgical intervention is detected on MRI and considered as normal.27 This postoperative edema gradually decreases at 3 weeks and may last up to 6 months. There is a plethora of evidence documenting the decreased stability of the lumbar motion segment as a result of surgical intervention. In the immediate postoperative period, disc height loss may be detected27 but generally no gross instability is reported. However, in the long term, even if an increase of motion does not occur shortly after surgery, reduced stiffness of the spine is observed, resulting in some degree of increased spinal motion.28 Repetitive loading of the spine and the presence of scar tissue appear to be two of the major factors for the development of spinal instability.29 Other factors that contribute to spinal instability include a higher load on the posterior elements,30 increased development of degenerative spondylosis,31 and instability of the level above.28 Evidence shows that the sensorymotor control system that, in normal conditions, can compensate for this acquired instability may fail to provide adequate control. A loss of muscle support and disturbed innervation is observed as a result of low back pain and sciatica in conjunction with the effects of the operative procedure.32 The deep back muscles not only stabilize the local segment, but also contribute to spinal stability as a whole. The instability is reinforced, leading to increased mechanical strain and further injury. With respect to the neurological deficits, immediate recovery is observed in a number of patients, as a result of the resolution of nerve root ischemia, but in a number of patients the paresis and the sensory disturbance do not spontaneously recover.33 For a portion of patients that experience residual complaints following lumbar disc surgery there is no real diagnosis and no specialist or operation which can simply stop the pain.10,11,34,35 For those patients, and certainly for any patient with primary postoperative axial pain, the main outcome or goal of the rehabilitation program should be aimed at restoring normal function during activities of daily living and/or work. But what is the evidence for these kinds of rehabilitation programs?

EVIDENCE REGARDING POSTOPERATIVE REHABILIATION PROGRAMS In the international literature there is a surprisingly wide variation in the content of rehabilitation programs.36–38 Despite many plausible 968

theories on the effectiveness of active, as well as passive, interventions following lumbar disc surgery, sound evidence is lacking. The choice of a specific method of rehabilitation is mainly based on the personal experience of care providers or on the results of studies of generally poor methodological quality. It has been suggested that passive treatment modalities should have no place in rehabilitation following first-time lumbar disc surgery and that active treatment is of paramount importance.39 Indeed, an active rehabilitation program is considered to enhance a patient’s independence from healthcare services in the long run. Here, the focus will be on the evidence regarding active rehabilitation programs.

Methods In a systematic review that assessed the effectiveness of such programs used in the rehabilitation of patients following lumbar disc surgery,40 relevant randomized controlled trials (RCTs) and nonrandomized controlled clinical trials (CCTs) were included. This systematic review was conducted according to the method guidelines of the Cochrane Back Review Group.41 For this chapter, the literature was updated by searching PUBMED through December, 2003. RCTs or CCTs were included if they used at least one of the four primary outcome measures that were considered to be important, that is: (1) pain (e.g. VAS), (2) a global measure of improvement (overall improvement, proportion of patients recovered, subjective improvement of symptoms), (3) back pain-specific functional status (e.g. Roland Disability Questionnaire, Oswestry Scale), and (4) return to work (return to work status, days off work). Outcomes of physical examination (e.g. range of motion, spinal flexibility, degrees of straight leg raising or muscle strength), behavioral outcomes (e.g. anxiety, depression, pain behavior), and generic functional status (SF-36, Nottingham Health Profile, Sickness Impact Profile) were considered as secondary outcomes. Other outcomes such as medication use and side effects were also considered. In assessing the quality of the included studies, the criteria list recommended in the method guidelines for systematic reviews by the Cochrane Back Review Group was applied.41 Only items reflecting the internal validity were used in assessing the quality of the included studies. One point was scored for each item in which a satisfactory response was obtained, and high quality was defined as fulfilling at least five of the validity criteria. Internal validity criteria are: 1a. 1b. 2a. 2b. 3. 4. 5. 6. 7. 8. 9. 10.

Method of randomization, Concealment of randomization, Dropout rate during the intervention period, Withdrawals during follow-up, Co-interventions avoided or equal, Blinding of patients, Blinding of outcome assessment, Blinding of care providers, Intention-to-treat analysis, Compliance, Similarity of baseline characteristics, and Adequate length of follow-up

For summarizing the evidence, a rating system consisting of four levels of scientific evidence was used. 1. Strong evidence – provided by generally consistent findings in multiple high-quality RCTs. 2a. Moderate evidence – provided by generally consistent findings in multiple low-quality RCTs. 2b. Moderate evidence – provided by generally consistent findings in multiple CCTs.

Section 5: Biomechanical Disorders of the Lumbar Spine

3. Limited or conflicting evidence – only one RCT or CCT (of either high or low quality) or inconsistent findings in multiple RCTs or CCTs. 4. No evidence – no RCTs or CCTs. The treatments are clustered here according to the timing of the start of treatment. In total, 15 studies were included, eight of which were of high quality.

Results Active rehabilitation programs that start immediately postsurgery Two studies assessed neural mobilization. A high-quality RCT42 added an active and passive neural mobilization program to a standard 6-week physical therapy program that consisted of isometric and dynamic exercises. These exercises were increased in intensity from day 1 postsurgery as tolerated. The control group received the same standard physical therapy without the neural mobilization. This study revealed evidence that adding a neural mobilization program to a standard physical therapy program does not provide any additional benefits on any of the main outcome measures (level 3) on both short-term and long-term follow-up. This constitutes limited evidence (level 3) since there is only one high-quality RCT supporting this conclusion. A low-quality RCT43 compared an intensive 7-day auto-assisted straight leg raise (SLR) regime for eight times a day with a 2-hour interval with a mild straight leg raise regimen that performed this same exercise only once a day for 7 days. This study revealed no significant differences between the two neural mobilization programs on pain, disability, or SLR at the 1-week and the 6-week measurement. No data were presented with regard to re-operation rates. Hence, there is limited evidence (level 3) that an intensive straight leg raise regimen is no more effective than a mild straight leg raise regimen. A high-quality RCT44 evaluated an intensive exercise program that consisted of increasing daily activities, home training (mobilization, trunk strengthening) and later mainly intensive muscle strengthening exercises and cardiovascular exercises. The control group received no increase in daily activities, exercises only once a day, and no promotion of cardiovascular exercises. The results show that there are no statistically significant differences on any of the primary outcome measures, but some differences of the secondary outcomes. There was one re-operation (3.4%) in the intervention group and 2 reoperations (6.5%) in the control group. This is limited evidence (level 3) that there is no difference in effectiveness between an intensive exercise program and a less active program in the long term for global perceived effect, pain, and return to work.

Active rehabilitation programs that start 4–6 weeks postsurgery Two high-quality RCTs39,45 and one low-quality RCT46 compared intensive exercise programs with mild exercise programs. The two high-quality RCTs reported no statistically significant differences between groups in overall improvement at 12-month follow-up. The low quality RCT did not include a long-term follow-up. All three studies showed a statistically significant difference on functional status in favor of the intensive exercise program on short-term follow-up and in one study45 on long-term follow-up. In the two high-quality studies return to work and daily activities were statistically significantly better in the intensive exercise programs in the short-term but not over the long term. The RCTs by Danielsen45 and Yilmaz46 revealed a statistically significant improvement in short-

term pain relief in favor of the intensive program (but not longterm45). Furthermore, Danielsen45 observed 1-year re-operation rates that were negligible. The above translates to strong evidence (level 1) that intensive exercise programs are more effective in improving functional status and faster return to work in short-term follow-up and there is strong evidence that on long-term follow-up there is no difference between interventions with regard to overall improvement. There is moderate evidence (level 2) that intensive exercise programs are more effective for pain relief in the short term. For all other primary outcome measures there is conflicting evidence (level 3) with regard to long-term benefit. One high-quality RCT47 compared a behavioral graded activity program that was based on operant treatment principles and was time contingent (time dependent) with usual care as provided by physical therapists. On the post-treatment measurement, 67% of the patients treated with care as usual had recovered versus 48% of the patients treated with behavioral graded activity. This 19% difference was statistically significant. On long-term follow-up, 73% of patients receiving care as usual and 75% of patients receiving behavioral graded activity had recovered. This difference was no longer statistically significant. On all other main outcome measures there were no statistically significant or clinically relevant differences. This study provides limited evidence (level 3) that there are no long-term differences in effectiveness between a behavioral graded activity program and usual care as provide by physical therapists. One low-quality RCT48 compared a supervised exercise program to home exercises. Both interventions incorporated the same exercises and at the same intensity. Re-operation rate was negligible in both groups. There is limited evidence (level 3) that supervised exercises and home exercises are equally effective on global perceived effect, disability, pain, and mobility. One low-quality RCT49 added horseback riding (three times per week for 20 minutes per session) to an intensive 4-week rehabilitation program. There were no statistically significant differences for overall improvement in the short term. (No long-term follow-up was performed.) There was a statistically significant more rapid return to work in the intervention group. There were no statistically significant differences in pain and physical measures. This study provided limited evidence (level 3) that adding therapeutic horseback riding to a rehabilitation program is effective for return to work, but not for overall improvement. One low-quality RCT50 compared a multidisciplinary rehabilitation program that consisted of sessions with a physical therapist, psychiatrist, occupational therapist, psychologist, social worker, and an intensive back training with usual care. At 1-year follow-up, there were no statistically significant differences between groups on global perceived effect, sick leave, or re-operation rate (3.7% in both groups). This study offered limited evidence (level 3) that multidisciplinary rehabilitation and usual care are equally effective. One low-quality CCT51 added aerobic exercises to a treatment program. All outcome measures were performed only at 3 months. This is limited evidence (level 3) that adding aerobic exercises to a treatment program is not more effective on functional status, pain, and depression than exercises alone.

Rehabilitation in an occupational setting Two studies specifically included patients in a work setting. One highquality RCT52 compared a multidisciplinary rehabilitation-oriented approach in insurance medicine with usual care. This work provides limited evidence (level 3) that a rehabilitation-oriented approach in insurance medicine is more effective in affecting return to work at 969

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long-term follow-up. One low-quality CCT53 assessed a functional restoration program versus usual care. This study does not present comparisons between groups.

Comparisons among rehabilitation programs that start more than 12 months postsurgery One low-quality RCT54 compared physical agents with joint manipulations, high-tech exercise, low-tech exercise, and no treatment. The low-tech exercise consisted of a McKenzie program under supervision in addition to spine stabilization. The high-tech exercise consisted of cardiovascular exercise (bicycle), isotonic trunk muscle training (DAPRE), and isokinetic exercises in flexion–extension and left–right rotation (Cybex TEF & Torso). There was limited evidence that low-tech and high-tech exercises, initiated more than 12 months after surgery, were more effective in improving low back functional status than physical agents, joint manipulation, or no treatment, but that there are no differences between the low-tech and high-tech exercise programs. One high-quality RCT55 added hyperextension to an intensive exercise program. In the short term there was a statistically significant improvement in functional status that was equalized at long-term follow-up. There were no re-operations. There is moderate evidence (level 3) that adding hyperextension to an intensive exercise program is no more effective than intensive exercise alone on overall improvement or functional status.

Conclusion On the basis of these RCTs and CCTs it can be concluded that there is strong evidence in favor of intensive exercise programs as compared to mild exercise programs, starting 4–6 weeks after surgery. Because of the variety in the content of the programs, no firm conclusions can be drawn regarding the specific elements that are most effective. No strong evidence was found for any of the other treatments investigated. Furthermore, none of the treatments investigated seemed to carry an increased risk of re-herniation or re-operation. Therefore, it seems unnecessary for patients to restrict their activities after first-time lumbar disc surgery.

PROPOSED TREATMENT PROTOCOL As already mentioned, it is unclear what the exact content of postsurgery rehabilitation should be. The rationale for the currently described treatment protocol is based on knowledge of the consequences of the operative procedure, the phases of tissue healing, and the knowledge of the behavior of the functional spinal unit in nonspecific low back pain and sciatica. Furthermore, in addition to the evidence as described in the previous part of this chapter, the evidence of the efficacy of physical therapy modalities used in chronic low back pain and sciatica have been taken into account.56,57,58 The emphasis is on biomechanical rehabilitation, which is supported by Ostelo40 who found no differences in the effectiveness of a behaviorally graded activity program and usual care in the long term. However, this doesn’t mean that a comprehensive bio-psycho-social approach and yellow flags should be neglected. Furthermore, red flags always have to be monitored. The complete treatment program is divided in different periods predicated on the classic phases of tissue healing. The main goals are to regain the maximal functional status without symptoms, and to prevent recurrences. With this treatment program, a compliant patient, supported by a good social support system, should be able to return to work and recreational sport activities within 2 months. However, to prevent recurrence and to obtain automatic movement control, patients have to continue exercising until the autonomous stage of motor learning is 970

reached. In the autonomous stage of motor learning, according to Fitts and Posner, the patient performs the skill automatically with a low degree of attention.59 Depending on the task, the performer, and the intensity of practice, this stage can take months to reach. Finally, the described strategy forms the structure of the program which has to be adapted for each patient’s personal needs on a physical, psychological, and social level. The program should be individualized as much as possible: every patient has a different medical history, a slightly different operative procedure, a different ability to recover, and a different capacity for motor learning. Remember: ‘evidencebased practice is the integration of best research evidence with clinical expertise and patient values.’60

The protective phase of postoperative rehabilitation (hospital discharge to day 21) In this period, phase 1, the surgical area is still vulnerable to injury and has to be protected. If possible, the rehabilitation program starts immediately after discharge with a home visit to provide back-care instructions and ergonomic advice in the home environment. At this stage, judgment of the social environment can be made and family support can be emphasized or moderated. The surgical procedure is once again explained to the patient. Donceel et al.52 demonstrated that an adequate explanation to the patient, together with a rehabilitation-oriented approach, increases the rate of return to work. They also stated that when poor outcome is predicted, i.e. a high score on the VAS scale for pain, the patient needs rehabilitation and has to be guided more intensively. The surgical procedure is invasive for dorsal structures, which inherently need time to heal. In the first period, local tissue response is observed.27 This postoperative edema gradually decreases after 3 weeks and continues for up to 6 months. Consequently, for the first weeks, loaded flexion and rotation should be minimized to avoid tension on the healing tissues. To unload the disc, it is advised to avoid sitting and to load the spine as ergonomically correctly as possible in a lordotic posture. General (muscle) activation, such as brisk walking, without provoking leg symptoms, is promoted. There is no evidence that advice to stay active is harmful for either acute low back pain, sciatica, or postsurgery patients. The benefit of increasing physical activity levels as early as feasible culminates in a significant reduction of sick leave and fear–avoidance behavior.40,61

Key points phase 1 Recommendations for safe performance of daily activities: ●

●

Avoidance of re-injury but also prevention of fear–avoidance beliefs Explanation of operative procedure, Patient education and instructions; Back care Transfers, Restriction of flexion: static + dynamic, Short-term sitting; no lifting/bending/driving a car, Maintenance of a lordotic lumbar posture, Frequent posture changes, General (muscle) activation: brisk walking, three times daily, without provoking leg pain.

The general rehabilitation phase of postoperative rehabilitation (day 21 to 6 weeks) An active rehabilitation program (phase 2) is initiated from the fourth postoperative week onwards. As previously mentioned in the second

Section 5: Biomechanical Disorders of the Lumbar Spine

part of this chapter (Evidence), there is strong evidence in favor of intensive exercise programs that are initiated at the 4–6-week postoperative interval. These will enhance short-term functional recovery and a faster return to work. Equally important to consider is that none of the proposed treatment strategies seems to carry a risk of re-herniation or re-operation. There are no studies that have investigated whether active rehabilitation programs should start immediately after surgery or 4–6 weeks later. Intuitively, when considering the time interval required to affect soft tissue healing, the 3-week benchmark appears to be reasonable. In this rehabilitation program, emphasis is first made on progressive local stabilization exercises to control the increased neutral zone. Although quality changes are found in the multifidus muscles, positive alterations are observed through physical therapy treatment after surgery.62 The tranversus abdominus muscle is an important stabilizer and often loses its anticipatory function in patients with low back pain,19 but to the authors’ knowledge, no information is available regarding its functioning after discectomy. Once the multifidus muscle regains the capability to contract, local stability can be (re)trained. As a result of the previously described denervation, retraining the multifidus muscle itself can be impossible, but local stability should be achieved by compensation strategies. Extensive literature regarding local motor control and stability retraining for patients with low back is available.56 In a short-term follow-up after lumbar discectomy, lumbar proprioception and feed forward control of the paraspinal muscles seems to recover, but the postural control remains impaired.20 Therefore, if on assessment postural control is reduced, retraining is integrated in the treatment program. Additional manipulative physical therapy for the surrounding restricted joints (e.g. hip, thoracic spine) can be useful and depends on the result of the individual assessment of the lower quadrant. Currently, no high-quality studies are available proving the efficacy of mobilization of restricted joint in postdiscectomy patients. But clinical experience and evidence in chronic nonspecific low back pain63 support the use of mobilization for painful and restricted joints. When muscles are weak as the result of nerve compression, specific strengthening exercises are prescribed. The two published studies on postoperative neural mobility exercises have not shown any improvement in the time it ultimately takes to recover.42,43 On the other hand, the authors’ clinical experience and that of Butler64 suggest the implementation of neural mobilization techniques when positive neural tension signs are present. In the literature, there seems to be no clear consensus regarding the fitness level of the patient with chronic low back pain. In contrast, patients with sciatica often dramatically decrease their normal exercise behavior resulting in reduced level of cardiovascular fitness.64a In view of the absence of agreement regarding the cardiovascular and muscular conditioning status of patients with low back and their predilection to limit physical endeavors, combined with the known diminished physical status of those with radicular complaints, it is the authors’ judgment that it is exceedingly appropriate to incorporate aerobic exercises. As preparation for return to work, individualized preventive backcare techniques should be taught. Individual back training appears to be most efficient in occupational settings and should be integrated when necessary (Fig. 88.1).

Key points phase 2 ●

Increase the protection of the neutral zone: Promote the local stability system with motor control exercises, Multifidus muscle–tranversus abdominus muscle co-contraction, Unloaded positions and weight bearing, With upper and lower limb movements, Static and dynamic;

Fig. 88.1 Example exercise, phase 2. Static, unloaded, local stability with limb movement

●

Depending on the results of the assessment: Postural control exercises, Mobilization of the restricted surrounding joints, Neural mobility exercises, Aerobic exercises.

The specific rehabilitation phase of postoperative rehabilitation (6 weeks to 3 months) In this stage (phase 3) of the rehabilitation program the patient is prepared for specific loading in activities of daily living, work, more intensive axial loading, and exposure to potentially provocative situations. Spinal stabilization is progressed to more complex weightbearing positions and extended with exercises for the whole-body stability system. This functional stability depends upon integrated local and global muscle function and should provide active control over the available movement range.65 By now, the patient should reach the autonomous stage of task performance, in which a low degree of attention is required for the correct performance of motor tasks and dynamic stabilization of the spine, so it can be performed in an automatic manner during any movement pattern.66 The recovery of maximal endurance and explosive strength is incomplete 2 months after surgery.67,68 Given this fact, specific deficits in muscle strength, length, and aerobic conditioning must be identified. Focused exercises to address these inadequacies are weaved into the rehabilitation program. If the reaction of the patient to destabilizing forces is slow, specific exercises on an unstable surface are also incorporated. Although a basic notion, the need to evaluate the range of motion of the lumbar spine must be emphasized. Interestingly, there are no guidelines for mobility benchmarks due to the large variation in the population. Lumbar range does not give one the ability to discriminate between people with or without low back pain and with disability.69 Häkkinen et al.68 observed a decreased mobility of the spine 2 months postsurgery. If the mobility is judged to be restricted for that specific patient’s constitution, mobilizations of the spine are performed and self-mobilizations are taught to the patient. At this juncture, no evidence is available regarding the effect of spinal mobilization after surgery. Koes et al.63 stated that although no good randomized clinical trials are available, there certainly are indications 971

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Key points phase 3 Reintegration of functional demands of daily living, professional and sports activities: ●

● ● ●

Fig. 88.2 Example exercise, phase 3. Body stability + active control through movement range with load towards work-specific loading.

that mobilizations are effective in some subgroups of patients with low back pain. Sport-specific drills are started with an eye towards eventual return to play. Only limited data are available regarding return to sports. Watkins and Williams70 followed professional and Olympic athletes after lumbar discectomy for 2 years. The athletes returned to their competitive level at an average of 5.2 months. The indicator of readiness to return to competition was superior trunk stability, excellent aerobic condition, good performance of sportspecific skills, and sport-specific strengthening and stretching exercises. Once the patient can perform the functional demands of daily living and professional and sport activities without symptoms, treatment sessions are ended and a singular control assessment is planned 3 weeks later. Typically, the patient can be discharged at that visit (Figs 88.2, 88.3).

Promote whole body stability and active control through range of motion: Local stability, Global stability; Restore muscle function: Strength, endurance, length; Restore spinal mobility; Work and sport specific loading.

SUMMARY In this chapter the authors attempted to provide a thoughtful approach to patients who undergo lumbar spine surgery, discectomy, and the various degrees of lamina removal, but not those who have undergone fusion surgery. The vantage point used allowed the authors to address patients who do well following surgery as well as those who have a less favorable outcome. Detailed analyses of the scientific evidence regarding postoperative rehabilitation programs following lumbar disc surgery were offered. The threshold for inclusion of a peer-reviewed publication was that it was either a randomized, controlled trial or a nonrandomized, controlled trial. This leading decision was made because these are the soundest methodologic designs. The authors concluded with a treatment strategy that was based on available literature and extensive experience so that practical clinical application is immediately available to the reader. As alluded to, these programs were predicated upon a number of facts: the evidence shared in the second part of this chapter, knowledge of the consequences of the operative procedure, the phases of tissue healing, and on the knowledge of the behavior of the functional spinal unit in non-specific low back pain and sciatica. Further, the evidence of the efficacy of physical therapy modalities used in chronic low back pain and sciatica were taken into account. The treatment program emphasized an early return to normal physical functional capacities and the prevention of recurrent symptoms. In clinical settings the effectiveness of an intensive exercise program after first-time lumbar surgery leads to short-term functional recovery and rapid return to work. The proposed treatment protocol is currently under evaluation in a randomized clinical trial by the second author. This scientific inquiry is being conducted because there is need to improve the quality of evidence supporting specific methods of rehabilitation for patients after lumbar disc surgery. Ultimately, such endeavors will allow treatment to be scientifically based and facilitate future outcome research.

References 1. Delamarter RB, Coyle J, Pakozdi D. Lumbar discectomy and rehabilitation. In: Maxey L, Magnusson J, eds. Rehabilitation for the postsurgical orthopedic patient: procedures and guidelines. St.Louis: Mosby; 2001:122–150. 2. Atlas JA, Keller RB, Chang Y, et al. Surgical and nonsurgical management of sciatica secondary to a lumbar disc herniation. Spine 2001; 26(10):1179–1187.

Fig. 88.3 Example exercise, phase 3. Active control through movement range with load + restoration of muscle function and spinal mobility towards rotation. 972

3. Gibson JNA, Grant ICG, Waddell G. The Cochrane review of surgery for lumbar disc prolapse and degenerative lumbar spondylosis. Spine 1999; 24(17): 1820–1832. 4. Korres DS, Loupassis G, Stamos K. Results of lumbar discectomy: a study using 15 different evaluation methods. Eur Spine J 1992; 1:20–24. 5. Pappas CT, Harrington ET, Sonntag VKH. Outcome analysis in 654 surgically treated lumbar disc herniations. Neurosurgery 1992; 30(6):862–866. 6. Manniche C, Asmussen K, Vinterberg H, et al. Analysis of preoperative prognostic factors in first-time surgery for lumbar disc herniation, including Finneson’s and modified Spengler’s score systems. Dan Med Bull 1994; 41(1):110–115.

Section 5: Biomechanical Disorders of the Lumbar Spine 7. Weber H. Lumbar disc herniation. A controlled, prospective study with ten years of observation. Spine 1983; 8(2):131–140.

35. Slipman CW, Shin CH, Patel RK, et al. Etiologies of failed back surgery syndrome. Pain Med 2002; 3(3):200–214.

8. Dvorak J, Valach L, et al. The outcome of surgery for lumbar disc herniation. II. A 4–17 years’ follow-up with emphasis on psychosocial aspects. Spine 1988; 13(12):1423–1427.

36. Hansen JW. Postoperative management in lumbar disc protrusions. Acta Orto Scan 1964; 71(Suppl):1–47.

9. Yorimitsu E, Chiba K, Toyama Y, et al. Long-term outcomes of standard discectomy for lumbar disc herniation: a follow-up study of more than 10 years. Spine 2001; 26(6):652–657.

37. Zylbergold RS, Piper MC. Lumbar disc disease: comparative analysis of physical therapy treatments. Arch Phys Med Rehab 1981; 62(4):176–179. 38. Hurme M, Alaranta H. Factors predicting the result of surgery for lumbar intervertebral disc herniation. Spine 1987; 12(9):933–938.

10. Long DM. Failed back surgery syndrome. Neurosurg Clin N Am 1991; 2(4): 899–919.

39. Manniche C, Skall HF, Braendholt L, et al. Clinical trial of postoperative dynamic back exercises after first lumbar discectomy. Spine 1993; 18(1):92–97.

11. Fritsch EW, Heisel J, Rupp S. The failed back surgery syndrome: reasons, intraoperative findings, and long-term results: a report of 182 operative treatments. Spine 1996; 21(5):626–633.

40. Ostelo RWJG, de Vet HCW, Waddell G, et al. Rehabilitation after lumbar disc surgery. Spine 2003; 28(3):209–218.

13. Verbeek JH. Label is unhelpful. Br Med J 2003; 74(21):986–987.

41. van Tulder MW, Assendelft WJJ, Koes BW, et al. Method guidelines for systematic reviews in the Cochrane Collaboration Back Review Group for Spinal Disorders. Spine 1997; 22(20):2323–2330.

14. Panjabi M. The stabilizing system of the spine: Part I: function, dysfunction, adaptation and enhancement. J Spinal Dis 1992; (5):383–289.

42. Scrimshaw SV, Maher CG. Randomized controlled trial of neural mobilization after spinal surgery. Spine 2001; 26(24):2647–2652.

15. Kirkaldy-Willis WH. The three phases of the spectrum of degenerative cascade. In: Kirkaldy-Willis WH, Burton CV, eds. Managing low back pain. 3rd edn. New York: Churchill Livingstone; 1992:105–119.

43. Kitteringham C. The effect of straight leg raise exercises after lumbar decompression surgery – a pilot study. Physiotherapy 1996; 82(2):115–123.

12. Talbot L. Failed back surgery syndrome. Br Med J 2003; 327(7421):985–986.

16. Mimaru M, Panjabi MM, Oxland TR, et al. Disc degeneration affects the multidirectional flexibility of the lumbar spine. Spine 1994; 19(12):1371–1380. 17. Panjabi M. The stabilizing system of the spine: Part II: neutral zone and instability hypothesis. J Spinal Dis 1992; (5):390–397. 18. Hides JA, Richardson CA, Jull GA. Multifidus muscle recovery is not automatic after resolution of acute, first-episode low back pain. Spine 1996; 21(23): 2763–2769. 19. Hodges PW, Richardson CA. Altered trunk muscle recruitment in people with low back pain with upper limb movements at different speeds. Arch Phys Med Rehabil 1999; 80:1005–1012. 20. Leinonen V. Lumbar paraspinal muscle function, perception of lumbar position and postural control in disc herniation-related back pain. Spine 2003; 28(8):842–848. 21. Waddell G, Main CJ. A new clinical model of low back pain and disability. In: Waddell G, ed. The back pain revolution. London: Churchill Livingstone; 1998: 223–240. 22. Mayer T, Gatchel R, Betancur J, et al. Trunk muscle endurance measurement. Isometric contrasted to isokinetic testing in normal subjects. Spine 1995; 20(8): 920–926. 23. Lutz GK, Butzlaff ME, Atlas SJ, et al. The relation between expectations and outcomes in surgery for sciatica. J Gen Intern Med 1999; 14(12):740–744.

44. Kjellby Wendt G, Styf J. Early active training after lumbar discectomy. A prospective, randomized, and controlled study. Spine 1998; 23(21):2345–2351. 45. Danielsen JM, Johnsen R, Kibsgaard SK. Early aggressive exercise for postoperative rehabilitation after discectomy. Spine 2000; 25(8):1201–1206. 46. Yilmaz F, Yilmaz A, Medrol F, et al. Efficacy of dynamic lumbar stabilization exercise in lumbar microdiscectomy. J Rehabil Med 2003; 35(4):163–167. 47. Ostelo RWJG, de Vet HCW, Vlaeyen JWS, et al. Behavioral graded activity following first-time lumbar disc surgery: 1-year results of a randomized clinical trial. Spine 2003; 28(16):1757–1765. 48. Johannsen F, Remvig L, Kryger P, et al. Supervised endurance exercise training compared to home training after first lumbar diskectomy: a clinical trial. Clin Exp Rheumatol 1994; 12(6):609–614. 49. Rothaupt D, Laser T, Ziegelr H, et al. Die Orthopädische Hippotherapie in der postoperativen Rehabilitation von lumbalen Bandschiebenpatienten. Eine prospektive, randomisierte Therapiestudie. Sportverl. Sportschad 1997; 11:63–69. 50. Alaranta H, Hurme M, Einola S, et al. Rehabilitation after surgery for lumbar disc herniation: results of a randomized clinical trial. Inter J Rehab Res 1986; 9(3): 247–257. 51. Brennan GP, Shultz BB, Hood RS. The effects of aerobic exercise after lumbar microdiscectomy. Spine 1994; 19(7):735–739.

24. Goffin A. Microdiscectomy for lumbar disc herniation. Clincal Neurol Neurosurg 1994; 96:130–134.

52. Donceel P, Du Bois M, Laheye. D Return to work after surgery for lumbar disc herniation. A rehabilitation-oriented approach in insurance medicine. Spine 1999; 24(9):872–876.

25. Taylor H, McGregor AH, Medhis-Zadhen S, et al. The impact of self-retaining retractors on the paraspinal muscles during posterior spinal surgery. Spine 2002; 27(24):2758–2762.

53. Burke SA, Constas CK, Aden PS. Return to work/work retention outcomes of a functional restoration program. A multi-center, prospective study with a comparison group. Spine 1994; 19(17):1880–1885.

26. Matsui H, Kitagawa H, Kawaguchi Y, et al. Physiologic changes of nerve root during posterior lumbar discectomy. Spine 1995; 20(6):654–659.

54. Timm KE. A randomized-control study of active and passive treatments for chronic low back pain following L5 laminectomy. JOSPT 1994; 20(6):276–286.

27. Babar S, Saifuddin A. MRI of the post-discectomy lumbar spine: review. Clinical Radiology 2002; 7:969–981.

55. Manniche C, Asmussen K, Lauritsen B, et al. Intensive dynamic back exercises with or without hyperextension in chronic back pain after surgery for lumbar disc protrusion. A clinical trial. Spine 1993; 18(5):560–567.

28. Goel VK, Goyal S, Clark C, et al. Kinematics of the whole lumbar spine: effect of discectomy. Spine 1985; 10(6):543–554. 29. Kuroki H, Goek V, Holekamp S, et al. Contributions of flexion–extension cyclic loads to the lumbar spinal segment stability following different discectomy procedures. Spine 2004; 29(3):E39–E46. 30. Brinckmann P, Grootenboer H. Disc height, radial bulge, and intradiscal pressure from discectomy: an in vitro investigation on human lumbar discs. Spine 1991; 16(6):641–646. 31. Kambin P, Cohen LF, Brooks M, et al. Development of degenerative spondylosis of the lumbar spine after partial discectomy. Comparison of laminectomy, discectomy, and posterolateral discectomy. Spine 1995; 20(5):599–607. 32. Sihvonen T, Herno A, Paljarvi L, et al. Local denervation atrophy of paraspinal muscles in postoperative failed back syndrome. Spine 1993; 18(5):575–581. 33. Kobayashi S, Yoshizawa H, Yamada S. Pathology of lumbar nerve root compression. Part 2: Morphological and immunohistochemical changes of dorsal ganglion. J Orthop Res 2004; 22(1):180–188. 34. Schofferman J, Reynolds J, Herzog R, et al. Failed back surgery: etiology and diagnostic evaluation. Spine J 2003; 3:400–403.

56. Richardson C, Jull G, Hodges P, et al. Therapeutic exercise for spinal segmental stabilization in low back pain. Scientific basis and clinical approach. Edinburgh: Churchill Livingstone; 1999:191. 57. van Tulder MW, Ostelo RWJG, Vlaeyen JWS, et al. Behavioural treatment for chronic low back pain. Cochrane Database Syst Rev; 2000. 58. Hides JA, Jull GA, Richardson CA. Long-term effects of specific stabilizing exercises for first-episode low back pain. Spine 2001; 26(11):E243–E248. 59. Shumway-Cook A, Woollacott M, eds. Motor control: theory and practical applications. Baltimore: Williams & Wilkins; 1995. 60. Sacket DL, Rosenberg WMC, Muir Gray JM, et al. Evidence-based medicine: what it is and what it isn’t. Br Med J 1996; 312:71–72. 61. Carragee EJ, Helms E, O’Sullivan GS. Are postoperative activity restrictions necessary after posterior lumbar discectomy? A prospective study of outcomes in 50 consecutive cases. Spine 1997; 21(16):1893–1897. 62. Rantanen J, Hurme M, Fälck B, et al. The lumbar multifidus muscle five years after surgery for a lumbar intervertebral disc herniation. Spine 1993; 18(5): 568–574.

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67. Häkkinen A, Ylinene J, Tarvainne U, et al. Pain, trunk muscle strength, spine mobility and disability following lumbar disc surgery. J Rehabil Med 2003; 35(5): 236–240.

64. Butler D. Adverse neural tension disorders centered in the spinal canal. In: Butler D, ed. Mobilisation of the nervous system. Melbourne: Churchill Livingstone; 1991:231–246.

68. Häkkinen A, Kuukkanen T, Tarvainen U, et al. Trunk muscle strength in flexion, extension, and axial rotation in patients managed with lumbar disc herniation surgery and in healthy control subjects. Spine 2003; 28(10):1068–1073.

64a. Brennan GP, Ruhling Ro, Hood RS et al. Physical characteristics of patients with herniated intervertebral lumbar discs. Spine 1987; 12(7):699–702. 65. Comerford M, Mottram L. Functional stability re-training: principles and strategies for managing mechanical dysfunction. Manual Ther 2001; 6(1):3–14 66. Taylor JR, O’Sullivan P. Lumbar segmental instability: pathology, diagnosis, and conservative management. In: Twomey L, Taylor J, eds. Physical therapy of the low back, 3rd edn. New York: Churchill Livingstone; 2000:201–248.

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69. Parks KA, Crichton KS, Goldford RJ, et al. A comparison of lumbar range of motion and functional ability scores in patients with back pain: assessment for range of motion. Spine 2003; 28(4):380–384. 70. Watkins G, Williams L. Microscopic lumbar discectomy results for 60 cases in professional and Olympic athletes. Spine J 2003; 3:100–105.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain

CHAPTER

89

Lumbar Axial Pain – An Algorithmic Methodology Jason S. Lipetz

INTRODUCTION Promoting an algorithmic approach to the patient with lumbar axial pain may at first appear paradoxical. Algorithms imply a defined if not mathematical process, yet lumbar pain generators are often multifactorial and elusive. It is actually the clandestine nature of the lumbar axial pain generator and the often speculative diagnoses assigned to patients with persistent lumbar pain which warrant a more methodological diagnostic and therapeutic approach. This chapter is written in the context of an interventional spine text. The minority of patients with lumbar pain will require an interventional approach. While remarkably prevalent, most episodes of debilitating axial pain will prove short lived. The majority of patients will respond to a period of activity modification. Some will participate in a structured rehabilitation program and utilize oral analgesics or antiinflammatory agents in order to realize relief. It is the relative minority of patients whose axial pain persists in a debilitating fashion who are candidates for an interventional approach. In such cases, a more meticulous history, examination, and image review can offer guidelines for the judicious use of diagnostic and therapeutic spinal injection procedures. Spinal pain generators are typically not definitively identified by history, highlighted by imaging, or reliably provoked during physical examination. While it is always the goal to treat in a less interventional fashion, in the case of persistent lumbar axial pain, diagnostic injection techniques offer an opportunity to identify pain generators in this patient population where diagnoses might otherwise remain ill defined. Offering these challenging patients further therapeutic interventions before exhausting a more algorithmic diagnostic approach might lead the patient along a less appropriate and ineffective treatment pathway. A general algorithmic approach to the patient with axial pain can be proposed, but diagnostic and therapeutic pathways will vary depending upon the pain generator in question. Each interventional algorithm assumes that symptoms have first persisted for a reasonable period of time, i.e. 4–6 weeks. The algorithm employed should be logical and evidence based but needs to remain practical and feasible in the daily clinical setting and current medical environment. At each step in the assessment and treatment pathway, the patient should remain center stage, informed, and encouraged to play an active role in the decision-making process. Prior to diagnostic or therapeutic interventions, appropriate advanced imaging, and blood work-up if necessary, is performed to rule out a more concerning and underlying pathologic process. In this author’s practice, a positive response to a diagnostic injection requires a quantitative pain relief response of at least 80%. During the postinjection assessment, the patient’s symptom response to typically provocative postures and maneuvers is assessed. In the patient with a suspected painful intervertebral disc, lumbar discography serves as a provocative diagnostic measure but is more invasive

than the commonly employed therapeutic injection approach. In the disc algorithm, more definitive diagnostic testing is therefore uniquely deferred in favor of a more presumptive therapeutic approach in an effort to minimize the extent of spinal interventions. Once a pain generator is confirmed through completion of the diagnostic component of the algorithm, therapeutic approaches should also be considered in a logical fashion. Arguably, one’s ability to identify the origin of pain through an interventional approach, which in itself remains inexact and incomplete, remains superior and less controversial than the efficacy of the therapeutic options available to the interventionist. Less interventional treatments, defined as those which strive to reduce pain and inflammation, but maintain tissue integrity, should be offered prior to those that denervate, ablate, modulate tissue, resect or alter regional anatomy and function. When therapeutic corticosteroid injections are performed, it is the author’s practice to schedule two injections 2 weeks apart. If the first injection offers complete relief, the second is deferred. If no relief is offered after two injections, injection therapy is determined likely to be ineffective. If a component of lasting, but incomplete relief is described 2 weeks after the second injection, a third is offered. A fourth and final injection is only considered for those patients who describe an incremental and sustained response to the initial three. Injection series are ideally not repeated, but if offered in the future, this does not transpire until 6–12 months after the initial series. This number of injection procedures described finds its basis in part in a review of the literature describing the role of therapeutic epidural injections in the treatment of lumbosacral radiculopathy.1 With an increasing number of injections performed, declining therapeutic efficacy and potential local and systemic adverse corticosteroid effect should raise greater concerns.2 As more interventional and less reversible therapeutic approaches are entertained, additional and confirmatory diagnostics can be utilized to assure accurate identification of the pain generator. For those patients who ultimately fail to realize relief following an algorithmic approach or who are determined to be poor surgical candidates, a paradigm better related to chronic pain modulation is proposed. The chronic pain program can employ the use of analgesics, alternative maintenance therapies such as acupuncture and biofeedback, pyschological care, and, in select cases, a consideration of implantable pain modulating devices (Fig. 89.1). Ultimately, the patient with persistent and debilitating axial pain presents the spine specialist with unique and formidable bookend challenges. The diagnostic algorithm can prove multifaceted with initially suspected pain generators ultimately found to be inert. The therapeutic arm of the axial pain algorithm remains hindered by a general lack of more conclusively supportive and well-designed outcome studies. The common disorder of persistent axial pain continues to challenge the many disciplines of the spine care community, and the multitude of current studies examining therapeutic approaches 975

Part 3: Specific Disorders

Persistent pain which fails to improve despite relative rest, activity modification, therapeutic exercise and analgesic use

Detailed history, physical examination and imaging suggest active pain generator

Diagnostic injection procedure to confirm active pain generator

Negative response

Consider alternative pain generator

Positive response

Therapeutic injections (can be offered with targeted and diagnosis specific rehabilitation strategies)

Unsatisfactory outcome and persistent symptoms

Satisfactory outcome: algorithm concluded

Confirmatory diagnostic techniques

Negative response

Positive response

More interventional therapeutic approaches: i.e. denervation and tissue modulating techniques

Unsatisfactory outcome and persistent symptoms

Satisfactory outcome: algorithm concluded

Surgical treatments

Unsatisfactory outcome and persistent symptoms

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Satisfactory outcome: algorithm concluded

Fig. 89.1 General algorithmic approach to chronic axial lumbar pain.

Section 5: Biomechanical Disorders of the Lumbar Spine

reflects the ongoing search for more definitive treatments. This chapter will address several syndromes, which are the topic of other dedicated chapters in this text. In these dedicated chapters, meticulous descriptions of procedural techniques and a more complete review of the pertinent literature have been included. In each of the following sections, background information pertaining to the pain generator of interest will be provided first. The significance of radiographic studies, patient history, and physical examination findings will then be discussed with an inclusion of supportive literature and the author’s practice in each realm. A diagnostic and therapeutic algorithm will then be presented in a logical and sequential fashion and summarized in figure form. The chapter will conclude with a mention of axial pain of potential radicular origin, more malignant processes which can lead to axial pain, and finally, two exemplary cases in which an algorithmic approach is employed.

SACROILIAC JOINT The sacroiliac joint (SIJ) will be addressed first, as sacroiliac joint syndrome (SIJS) remains a commonly assigned diagnosis for the patient with axial pain. Prior to Mixter and Barr’s 1934 study highlighting pathology of the intervertebral disc,3 the SIJ was believed to represent the most likely pain generator in patients with low back pain. As with the other anatomic structures addressed in this chapter, the SIJ remains a viable candidate for a primary pain generator as it satisfies several criteria outlined elsewhere: first, the structure should have a nerve supply; second, it should be susceptible to diseases or injuries known to be painful; and third, it should be capable of causing pain similar to that seen clinically.4 The complex and variable innervation of the SIJ has been described in many anatomic studies.4–6 Painful SIJ conditions are known to arise from spondylarthropathies,7 infection,8 trauma,9,10 and malignancy.11 Intra-articular injections, performed both provocatively in asymptomatics12 and diagnostically in patients with chronic lumbar pain,13,14 have demonstrated the SIJ to be a potential source of pain. The prevalence of SIJS in the population with chronic low back pain has been estimated at 13–30%.13,14 SIJS, which remains a controversial diagnosis among spine practitioners, has been hypothesized to develop from degenerative change affecting the joint or altered joint mobility. The SIJ is mobile, albeit limited to 3° of rotation and only a few millimeters of glide.15,16 Radiologic or surgical pathology has not been identified in patients with SIJS, further raising pathophysiologic speculation. Bone scan has demonstrated a poor sensitivity (12.9%) in patients demonstrating a positive response to diagnostic intra-articular injections.17 Bone scan has demonstrated a sensitivity in patients with SIJS which is significantly lower than that observed when utilized to detect sacroiliitis in patients with rheumatological disease.17–20 These findings do not exclude the possibility that SIJS does not involve more mild synovial irritation which remains undetected by radionuclide imaging which relies upon an acceleration of osteoblastic activity.17 While magnetic resonance imaging (MRI) has demonstrated a high sensitivity in cases of true sacroiliitis,18,19 the role of MRI in diagnosing SIJS has also yet to be defined. At least 24.5% of asymptomatics >50 years of age demonstrate degenerative SIJ changes on plain radiographs,21,22 and similar degenerative findings in aging asymptomatics have been demonstrated utilizing computed tomography (CT) imaging.23 Similarly, no specific pathology has been described in patients undergoing surgical intervention for chronic sacroiliac joint pain.24 Sacroiliac joint pain referral patterns often localize to the sacral sulcus and buttock,12 but patients can also describe symptom referral to the medial thigh and groin,13,25–28 posterior thigh, and calf.9,13,29–31 Physical exam maneuvers utilized to detect motion irregularities have demonstrated poor intertester reliability32,33 and have been

observed to be positive in 20% of asymptomatics.34 The detection of joint motion abnormalities by physical examination,29 response to pain provocation tests such as Faber’s and Gaenslen’s maneuvers,17,29,35 and historical findings13,29 have all correlated poorly with the response to fluoroscopically guided diagnostic intra-articular injections, which have come to be recognized as the gold standard for diagnosing SIJ pain. As specific history, examination, and imaging findings have all correlated poorly with a positive response to a diagnostic intra-articular injection, it is more likely a combination of presenting factors which might lead the treating clinician to suspect the SIJ as an active pain generator and warrant introduction into the SIJ diagnostic and therapeutic algorithm. Suggestive symptoms include pain predominantly below the L5 level in the region of the sacral sulcus, with or without referral to the groin13 or more distal lower limb, and sacral sulcus tenderness to palpation.29,35,36 Additionally, patients with unilateral symptoms and a positive response to multiple provocative maneuvers may be more likely to demonstrate a positive diagnostic injection response and subsequently benefit from targeted therapeutic approaches.29,35,36 While a previous history of a fall upon the affected buttock, recent pregnancy, pelvic trauma, or an antecedent gait alteration37 also prompt this author to consider the SIJ as a pain generator, these historical points have not been demonstrated to be predictive by the available literature. For those patients who are believed to be reasonable candidates, an algorithmic approach to the SIJ (Fig. 89.2) can be initiated and a confirmatory diagnostic SIJ injection performed. Diagnostic intraarticular injections were initially described in 1938,38 and the utilization of fluoroscopic guidance was first introduced in 1979.39 It has been estimated that successful intra-articular SIJ entry is achieved in only 22% of injections performed without image guidance,40 and such blind injections performed for either diagnostic or therapeutic purposes are not included in an algorithmic approach to SIJS. Given the complexity of the anatomy and configuration of the SIJ, it would seem that this 22% figure may even be an overestimate, further amplifying the requirement of using fluoroscopic guidance. If a positive response to a guided diagnostic injection is realized, therapeutic injections should follow. Therapeutic SIJ corticosteroid injections have been advocated as an appropriate treatment for patients with persistent SIJ pain.41 A retrospective and uncontrolled study of SIJ injections in 31 patients with chronic pain of SIJ origin has suggested a lasting resultant improvement in pain, work status, and disability.42 The efficacy of these injections has been more clearly demonstrated, both prospectively and retrospectively and in a controlled fashion, in the seronegative spondyloarthropathy population.43,44 The mechanism of action of injections in patients with presumed SIJS outside of the spondyloarthropathy population remains less clear, but is presumed to arise from the well-known antiinflammatory properties of corticosteroids.28,45 The role of inflammation in SIJS remains unconfirmed. The role of injection therapy in this patient population therefore remains poorly defined. Injection therapy can be combined with a targeted physical therapy regimen which emphasizes pelvic stabilization techniques and SIJ-specific therapies. For those patients who fail to respond to therapeutic injections, a more recently described and evolving radiofrequency denervation approach to the SIJ might then be considered. The nerves which can be targeted for this approach include the L5 dorsal ramus and the lateral branches of S1–3.46 The ability to reliably target and anesthetize these nerves with fluoroscopic guidance remains less clear.47 In those patients who demonstrate a positive diagnostic response to anesthetization of these innervating branches or who demonstrate a concordant response48 with lateral branch stimulation, a denervation procedure can be trialed. The ability of such a denervation approach to successfully anesthetize the SIJ remains less clear with only 977

Part 3: Specific Disorders SIJ suspected as primary pain generator

Fluoroscopically guided diagnostic SIJ injection

Negative response

Positive response

Consider alternative pain generator

Therapeutic fluoroscopically guided SIJ injections performed in conjunction with targeted SIJ/pelvic stabilization therapies

Persistent pain

Satisfactory outcome: algorithm concluded

Consider fluoroscopically guided diagnostic L.5 dorsal ramus and sacral lateral branch block

Negative response

Positive response

Radiofrequency denervation procedure of dorsal ramus and lateral branches

Persistent pain

Satisfactory outcome: algorithm concluded

Confirmatory fluoroscopically guided diagnostic intra-articular SIJ injection

Negative response

Positive response

Consider alternative pain generator

SIJ arthrodesis

Satisfactory outcome: algorithm concluded

Persistent pain

More chronic pain management paradigm

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Fig. 89.2 General algorithmic approach to the sacroiliac joint.

Section 5: Biomechanical Disorders of the Lumbar Spine

small and uncontrolled studies suggesting a significant therapeutic response.49–52 For those patients with persistently debilitating SIJ pain who either fail to respond to denervation techniques or who demonstrate an initial negative response to L5 dorsal ramus and sacral lateral branch anesthetization, surgical arthrodesis of the SIJ can be considered as a final treatment option.50,53 In selecting candidates for SIJ fusion, those patients who demonstrated both a positive lateral branch response and an initial diagnostic intra-articular injection may be considered less likely to be false-positive SIJ patients. In these cases, it would appear that a confirmatory diagnostic injection has been employed to lessen the likelihood of an initial placebo response. As the approach to and efficacy of lateral branch anesthetization remains less well defined, any patient contemplating SIJ fusion should first demonstrate a second positive response to a confirmatory diagnostic intra-articular injection utilizing an anesthetic of different duration or a blind and placebo-controlled diagnostic injection protocol. As well, the candidacy of such individuals for surgical intervention might be further strengthened by a negative response to provocation discography.

ZYGAPOPHYSEAL JOINT The zygapophyseal joints (Z-joints) have been recognized as a potential source of lumbar pain since 1911.54 The lumbar Z-joints are paired synovial joints with an intra-articular volume capacity of 1–2 mm.55 While the more cephalad lumbar Z-joint orientation tends to be in the sagittal plane, the lower joints are more coronally situated.56 Each lumbar Z-joint is innervated by the medial branch of the dorsal ramus at the level of the joint and by the medial branch arising from the dorsal ramus of the next cephalad level.57 In 1976, Mooney and Robertson58 demonstrated that lumbar axial pain and symptoms referred to the extremity could arise from intra-articular injections of normal saline in asymptomatic volunteers. McCall et al.59 later corroborated these findings and observed a more intense pain response with injection into the capsular tissues when compared with injection into the joint’s intra-articular space. Utilizing progressive local anesthesia during surgery, Kuslich et al.60 demonstrated a pain response with stimulation of the Z-joint capsule, but the pain described by patients was often not concordant with their more debilitating axial pain. Z-joint pain, or ‘facet syndrome,’ is presumed to arise from osteoarthritic change, chondromalacia, or occult fractures.61–66 Less common conditions affecting the Z-joints including infection, ankylosing spondylitis, and villonodular synovitis have also been reported.67,68 Lumbar Z-joint fractures, capsular tears, hemorrhage, and cartilaginous injury have been observed in postmortem studies of trauma patients with normal radiographs.66 A study of 176 consecutive patients presenting with chronic lumbar pain, in which lidocaine and confirmatory bupivacaine medial branch or intra-articular diagnostic injections were employed, suggests that the Z-joint represents the primary pain generator in 15% of cases.69 Plain radiographs often reveal degenerative arthrosis of the Z-joints which strongly correlates with age, but not with symptoms of axial pain.70,71 Utilizing diagnostic intra-articular injections, degenerative Z-joint change detected by CT imaging has also demonstrated a poor correlation with pain arising from the lumbar Z-joints.72 Several studies73–75 have specifically investigated the historical and physical examination findings which might predict the Z-joint as a pain generator. In one of these studies74 a second and confirmatory diagnostic Z-joint injection was included to establish a diagnosis, and in two73,75 a positive response to only a single diagnostic injection was utilized. Patients with confirmed primary Z-joint pain were noted to describe lumbar discomfort, but pain could similarly be referred to the lower limb. Patients generally did not describe central lumbar

pain. While no particular symptoms or historical findings demonstrated a significant correlation with a positive response to diagnostic injections, patients with Z-joint pain tended to be older, without exacerbations during coughing, and without described provocation with forward flexed postures. The L5–S1 Z-joints were found to be more likely symptomatic than L4–5, with pain arising from the L3–4 and L2–3 joints much less commonly observed.69 While eliciting a concordant pain response by direct articular palpation has been described as a potential screening mechanism in patients with suspected Z-joint pain,61 the utility of this examination technique was not clearly substantiated by the aforementioned studies. Deciding which patients to introduce into the Z-joint algorithm presents a challenge to the treating clinician quite similar to that described in patients with SIJS. Radiographic evidence of degenerative change is typically not a reliable indicator, and historical and physical examination findings do not clearly correlate. As in the case of SIJS, it is neither practical or economical to subject each patient with chronic axial pain to a confirmatory diagnostic injection without a reasonable clinical suspicion. Older patients, i.e. greater than 60 years of age, presenting with uni- or bilateral axial lumbosacral pain, and with an absence of provocation during flexion and coughing, may be more likely to demonstrate pain of Z-joint origin. In the author’s practice, a Z-joint pain generator is more suspect in older patients who describe pain which is most reliably provoked by standing, ambulating, or ipsilateral extension, and relieved by sitting. These latter historical features are not supported as clearly reliable by the available literature. In the patient with suspected Z-joint pain, an algorithmic approach can be initiated (Fig. 89.3) and a confirmatory diagnostic intra-articular injection performed.69,74 There is no standard protocol for the selection of joints to anesthetize. It has been suggested that the joints with maximal tenderness during palpation can be marked and identified under fluoroscopic inspection. Alternatively, in patients with unilateral lumbosacral pain, the L4–5 and L5–S1 joints can be investigated. If more isolated posterior element arthrosis is observed radiographically, a single joint can be studied. In patients with bilateral lumbosacral pain, these joints can be bilaterally addressed in a diagnostic fashion. If the diagnostic response from the L4–5 and L5–S1 injections is negative and a midlumbar pain complaint is reported, the L2–3 and L3–4 joints can then be studied in a similar coupled and unilateral or bilateral fashion. If the patient presents with midlumbar rather than lumbosacral pain, the L2–3 and L3–4 joints might be studied first. In the author’s practice, while a radiographic correlate to Z-joint pain has yet to be defined, MRI or CT scan evidence of more advanced arthrosis is also considered in selecting joints for further study when these imaging findings correspond to the patient’s pain location. Following a positive diagnostic response, therapeutic intra-articular injections could follow. Similar to the treatment of SIJS, the therapeutic response arising from intra-articular injection with corticosteroid has not been more definitively revealed by controlled studies, and an inflammatory injury component has only been theorized. While intra-articular effusions can be observed on MRI, histologic studies have not revealed inflammatory cells in patients with spondylotic joints.61 Similarly, clinical studies have yet to identify a therapeutic effect from intra-articular injections in patients with inflammatory rheumatologic spinal conditions.61 A randomized, controlled study investigating the therapeutic benefits of intra-articular methylprednisolone, utilizing an initial single diagnostic injection screen and an intra-articular saline control, have suggested up to 46% of patients can realize significant pain relief at 6 months’ follow-up.76 Open and uncontrolled studies of fluoroscopically guided intra-articular injections suggest an 18–63% therapeutic effect for more than 6 months following injection.61,77–80 979

Part 3: Specific Disorders Zygapophyseal joint suspect as primary pain generator

Fluoroscopically guided diagnostic intra-articular z-jt injection

Negative response

Positive response

Consider alternative pain generator

Therapeutic fluoroscopically guided intra-articular Z-joint injections performed in conjunction with manual or mechanical spine rehabilitative therapies

Persistent pain

Anatomy prevents successful intra-articular injection

Satisfactory outcome: algorithm concluded

Diagnostic medial branch block followed by confirmatory diagnostic injection with second anesthetic or placebo controlled diagnostic screen

Confirmatory medial branch block

Positive response

Negative response

Radiofrequency denervation procedure to address innervating medial branches/branches

Persistent pain

Consider alternative pain generator

Satisfactory outcome: algorithm concluded

Consider more chronic pain management paradigm Fig. 89.3 General algorithmic approach to the zygapophyseal joint.

Pain relief realized following intra-articular injection might provide a window of opportunity to progress the patient in a spine rehabilitation program and graduate mechanical and manual therapies. If the patient failed to realize relief following therapeutic intra-articular injections or spondylotic anatomy prevented the performance of a diagnostic intra-articular injection, a diagnostic medial branch block81 could be utilized to confirm a diagnosis of Z-joint-mediated pain. In the setting of a positive response to medial branch block, radiofrequency neurotomy can be considered. In the patient who initially demonstrated a positive response to an intra-articular injection, the medial branch block can serve as a confirmatory diagnostic measure. For patients in whom a diagnostic intra-articular injection was not previously performed, a positive response to medial branch block should be confirmed with an additional diagnostic screen to address 980

the estimated 38% false-positive response rate with single uncontrolled blocks.74 A second and confirmatory medial branch block can be performed with a local anesthetic of different duration of action. In this scenario, the patient’s analgesic response with each test should correlate with the duration of action of the anesthetic utilized. Alternatively, the confirmatory injection can be performed with an informed patient in a blind fashion with either a saline placebo or anesthetic injected and the patient monitored for an appropriate response. The difficulty with employing local anesthetics of different duration is that the patient is required to accurately record and communicate their pain response over a period of hours which extends beyond the time spent in the office of the evaluating team. Additional response interpretation difficulties can arise in the patient who describes marked symptomatic relief after the injection of the

Section 5: Biomechanical Disorders of the Lumbar Spine

longer-acting anesthetic, but whose response does not last for as long as one would predict based upon the agent’s half-life. To avoid these confounding factors, only shorter-acting anesthetics can be utilized and the response assessed in the office setting by an independent observer. Patients who demonstrate a positive response to either variant of this double diagnostic screen can then be considered for medial branch radiofrequency denervation. While radiofrequency denervation represents a minimally invasive approach to the patient with chronic posterior element pain and localization of the innervating medial branches appears to be reliable, outcome studies are limited. Modest therapeutic responses have been described, uncontrolled small patient populations have been studied,82 and such procedures likely need to be repeated to offer sustained relief as reinervation to the painful joints can occur. A double-blind, controlled study of radiofrequency denervation versus sham lesions which employed a single diagnostic injection screen revealed only a two-point reduction in visual analog pain scores with the minority of patients realizing complete relief.83 A meticulously designed but small and uncontrolled study of medial branch neurotomy, which included electromyographic assessment of the paraspinal musculature to confirm denervation, demonstrated pronounced relief in 60% (n=9 of 460 initially screened) of patients at 12 month follow-up evaluation.82 If the denervation procedure proves helpful but the symptomatic response wanes, neurotomy can be repeated. A significant response should first be realized for at least 6–12 months.82 For those individuals with persistent axial pain of Z-joint origin which fails to improve despite the aforementioned therapies, surgical intervention in the form of posterolateral fusion should be considered only with great caution. While studies have yet to address the success of this approach in patients with Z-joint pain confirmed with a double diagnostic screen, the available literature does not suggest a correlation between posterior element pain and successful outcomes following fusion.84–86 While it may be tempting to assume that posterior element pain can be relieved by fusion, this has yet to be demonstrated. The potential remains for the fused joint to serve as an ongoing pain generator, as its painful tissue components remain after a typical posterior fusion approach. The possibility also remains that forces continue to be borne, albeit reduced, by the painful posterior elements following posterior stabilization. Finally, as mentioned in the discussion of SIJS, for any patient considered for fusion for Zjoint pain, preoperative lumbar discography, which will be further addressed in the next section of this chapter, should also be considered to rule out a contributing discogenic pain source. Discography also allows the clinician to better evaluate the anatomy and symptom response from adjacent levels. While a positive response to a double diagnostic screen would appear confirmatory for a primary Z-joint pain generator in these chronic cases, the possibility remains, potentially in a minority, that a concordant pain response will similarly be demonstrated during discography.87

INTERVERTEBRAL DISC While the sacroiliac joint and Z-joints are suspected as primary pain generators in a significant but relative minority of patients with persistent axial lumbosacral pain, the intervertebral disc has stood center stage as the most commonly suspected pain generator in patients with both debilitating chronic and more acute axial pain. Mixter and Barr’s 1934 publication described herniated lumbar discs and their relationship to nerve root compressive syndromes.3 In addition to inducing radicular complaints affecting the lower limb, the degenerative disc is also believed to be a common primary pain generator in patients with axial pain. In a study of 92 consecutive patients presenting with

chronic lumbar pain, provocative discography revealed a concordant pain response in 39%, most commonly at L4–5 and L5–S1.88 In a unique study utilizing progressive local anesthesia and selective tissue stimulation intraoperatively, Kuslich et al. demonstrated that while stimulation of the nerve root typically resulted in buttock and lower limb pain, stimulation of the disc, and in particular the anulus, most commonly resulted in a reproduction of the patient’s lumbar pain in a concordant fashion.60 The innervation of the intervertebral disc has been well defined. Abundant nerve endings with a variety of free and complex terminals have been identified in the outer third to half of the anulus fibrosus.89–91 The posterior plexus of nerves responsible for innervating the posterior anulus and posterior longitudinal ligament (PLL) is derived predominantly from the sinuvertebral nerve. The sinuvertebral nerve arises from both the somatic ventral ramus and autonomic gray ramus communicans and also supplies innervation to the ventral dura mater.92 Discitis represents a well-documented and painful condition arising from intervertebral disc infection.93,94 A noninfectious and degenerative condition labeled internal disc disruption describes a painful condition of the intervertebral disc involving a deterioration of the disc’s internal architecture with a relative maintenance of external contour. This mechanical breakdown leads to painful radial fissures which reach the outer third of the anulus fibrosus.95,96 Painful tears in the anulus are also presumed to arise, in the more acute injury setting and independent of a more gradual degenerative cascade, from flexion–rotation-type injuries.92 While abnormalities of the anulus are often not readily identified by conventional imaging techniques, discography and postdiscography CT can reveal abnormal disc architecture and painful annular tears. Advanced imaging of the lumbar spine in patients with suspected discogenic pain typically does not provide confirmatory diagnostic information. Degenerative discs can be observed in 35% of asymptomatic 20–39 year olds, and 36% of individuals older than 60 years of age will demonstrate MRI evidence of disc herniation.97 With such a high incidence of abnormal findings in patients without axial pain, the observation of degenerative discs on MRI is clearly not diagnostic in isolation. Posterior annular tears, also referred to as high intensity zone (HIZ) lesions, are more commonly observed in patients with lumbar pain but can also be observed in up to 24% of asymptomatics.98 When appreciated in symptomatic patients, those discs with HIZ lesions have been observed to be twice as likely to produce a concordant pain response during discography when compared to discs without such lesions. Lumbar MRI findings might be most telling when disc space height and hydration are observed to be well preserved. Discs with a preservation of morphology have been demonstrated to be considerably less likely to be painful.96,99,100 Patients with discogenic pain can describe unilateral or bilateral axial pain with or without symptom referral to the proximal and distal lower limb.88 In a study of patients with discogenic pain confirmed by lumbar discography, historical findings were not shown to demonstrate statistical significance in predicting a discogenic pain source.88 Patients were equally as likely to describe increased pain with sitting as with standing. Additionally, physical examination findings, including increased pain with forward flexion, did not demonstrate statistical significance to predict a discogenic pain source. In assessing patients for possible discogenic pain, the clinician might consider the findings from two previous studies examining intradiscal pressures in healthy subjects assuming various postures.101,102 If the compromised and well-innervated posterior anulus is presumed to be the primary pain generator in patients with discogenic pain those positions or activities which maximize intradiscal pressure may be most likely to lead to annular stress and activation of nociceptive fibers. In these studies, erect sitting has been demonstrated to increase intradiscal 981

Part 3: Specific Disorders

pressure only slightly more than erect standing. Standing in a forward-flexed posture significantly increases intradiscal pressure and to a greater extent than sitting in a forward-slouched fashion. Reclining while seated reduces intradiscal pressure to a considerable extent, but pressure reductions are not as great as those observed while resting supine. The greatest intradiscal pressures are observed while performing lifting maneuvers in a standing and forward-flexed posture. Valsalva maneuver has been demonstrated to increase intradiscal pressure at least as much as sitting in a forward-flexed fashion. Disc pressures are also noted to more than double during evening hours, presumably secondary to bodily fluid shifts which can lead to a morepressurized disc during morning hours. While statistical significance has not been demonstrated for particular historical findings or physical examination maneuvers, the studies of dynamic disc pressures likely offer clues in identifying patients with discogenic pain. In the author’s experience, while Z-joint pain is more likely to be observed in older patients, discogenic pain can present in patients of all ages but is particularly common in the younger patient population, i.e. 18–65 years of age. Patients might describe an initial symptomatic onset following a defined and more stressful lifting or rotational maneuver. The gardening and snow shoveling seasons are particularly common times for patients to present with acute discogenic pain following a defined stressful maneuver, but often the onset of pain is more gradual and incremental. The discomfort is described as a deepseated ache which is at times profound, forcing the patient to unload the spine and assume a supine position. Coughing and sneezing are often described as provocative and in some cases represent the initial inciting event. Patients realize increased pain with sitting, particularly during car travel or while at work or in a theater, and experience relief while resting supine with the lower extremities elevated. Standing and walking are often not as provocative, and bending and lifting maneuvers are typically avoided. Young parents and grandparents often present with axial pain of suspected discogenic origin, presumably secondary to the repetitive lifting and rotational maneuvers performed while caring for their children. Morning hours can be particularly problematic, likely secondary to increased intradiscal pressures following sleep and a prolonged period of recumbency, with a symptomatic decline after a period of ambulation and increased activity. At times, patients will describe a truncal shift, characterized by the torso being visibly and horizontally displaced relative to the pelvis, during symptomatic exacerbations. This antalgic posture is presumed to arise from asymmetric reactive paraspinal contraction and deeper-seated protective mechanisms arising from the activation of nociceptive fibers within a richly innervated and activated discogenic pain generator.103 Pain referral patterns to the lower limbs is also often reported, with such complaints described as poorly localizable, migratory, and less debilitating than the axial pain component. Some patients will even report a distal complaint of burning in the soles of the feet which coincides with worsening lumbar pain during prolonged sitting postures. For a primary mechanical and discogenic pain generator to remain suspect, the physical examination should not reveal neurologic deficits consistent with radiculopathy. While sitting, the patient is often observed to lean rearward upon the elbows in an effort to reduce the more pain-provoking axial load to the spine. With the patient supine, passive pelvic rocking, during which the examiner maneuvers the patient’s lower limbs while passively flexed at the hips and knees, may prove provocative through the introduction of a torsional load to the intervertebral discs and a painful posterior anulus. Sustained hip flexion maneuvers, during which the patient actively flexes the hips while supine with the knees extended, is also often provocative. The response to this maneuver is often most notable as the limbs are allowed to slowly descend toward the exam table surface, presum982

ably by simulating a valsalva-type maneuver with a resultant increase in intra-abdominal pressures. Sustained hip flexion or pelvic rocking may be more likely to be positive when the painful segment is at the L4–5 and/or L5–S1 levels, and may be less reliable for more cephalad segments. Pain is often reproduced with pressure applied over the lower lumbar spinous processes. In the author’s experience, standing with active forward flexion at waist with the knees extended most often reproduces axial pain in a concordant fashion. At times, transitioning from the flexed to neutral posture is the most pain-provoking maneuver. While standing extension is classically believed to be relieving, and is often observed to be so clinically, some patients will describe similar if not more intense pain during active extension maneuvers. A McKenzie approach to patient assessment has also been demonstrated to be fairly reliable in detecting pain of discogenic origin.104 Through such mechanical assessment, patients who realize symptom centralization or peripheralization following repetitive movements have been demonstrated to be more likely to demonstrate a symptomatic disc during lumbar discography. For those patients with persistent lumbosacral axial pain of suspected discogenic origin, an algorithmic approach (Fig. 89.4) can be initiated and epidural corticosteroid injections trialed. A plethora of literature, which will be more completely detailed in the appropriate chapters of this text, has described the role of transforaminal epidural injections in patients with radicular syndromes. Many uncontrolled studies,105–108 and more recently a meticulously designed randomized, prospective double-blind, controlled study1 have demonstrated the successful treatment of radiculopathy with transforaminal injection therapy. Transforaminal injections performed with fluoroscopic guidance allow for the most reliable means of administering corticosteroid to the ventral epidural space where the posterior anulus, PLL, spinal nerve, and ventral dura mater reside.109 Corticosteroids are believed to offer relief in patients with radicular syndromes by addressing the biochemical and inflammatory component of radiculopathy which has been extensively described in the literature and which will be more completely detailed in the chapters of this text addressing the pathophysiology of nerve root injury.110,111 The utilization of epidural corticosteroids in the treatment of axial lumbosacral pain, without a radicular component, is more speculative as the biochemical and inflammatory component of discogenic pain has yet to be as convincingly demonstrated.92 The pain generating processes at play in the patient with axial discogenic pain may arise from a prevailing mechanical insufficiency.112,113 Clinical studies investigating the role of epidural steroid injections have suggested but not clearly demonstrated success in the treatment of primary axial pain.114–116 The transforaminal injection approach offers the most direct means reaching the posterior anulus. Unlike the treatment of an inflamed spinal nerve where circumferential bathing of the target can be achieved, the possibility remains that the pain-generating fibers of the degenerative disc are not in direct contact with the epidural space. Alternatively, one might theorize that in the setting of a painful and incompetent anulus a component of the pain-generating process arises from the spillage of inflammatory mediators. This could lead to irritation of ventral spinal tissues such as the dura and PLL which are in intimate contact with the affected disc and are more accessible by transforaminal injection. In this author’s practice, due to concerns of iatrogenic discitis, an inability to isolate the painful disc without more interventional diagnostic measures, and a lack of supportive literature,117,118 intradiscal steroids are not offered in the treatment algorithm for discogenic pain. In the patient with a suspected discogenic pain source who presents with central or bilateral lumbosacral symptoms and an MRI which reveals multilevel, i.e. L3–4 through L5–S1, degenerative disc disease, a bilateral S1 transforaminal injection is performed. This

Section 5: Biomechanical Disorders of the Lumbar Spine Suspect persistent axial pain of discogenic origin

Fluoroscopically guided transforaminal injection therapy targeting suspected symptomatic disc(s) either bilaterally or unilaterally – can be performed in conjunction with a mechanical therapy program and spine stabilization techniques

Improved Discharge to home exercise program with appropriate postural precautions

Symptoms persist

Lumbar discography (can follow with post-discogram CT) scheduled in conjunction with pre-surgical psyche screen

Abnormal psychometric scores

Refer for appropiate consultation and psychological care

Negative

Positive one or two levels with relative preservation of disc height (i.e. 80%)

Positive one or two level with more advanced loss of disc height

IDET

Surgical stabilization with inclusion of inter-body fusion at symptomatic levels (or consider evolving technologies such as disc replacement therapy)

Symptoms persist

Consider alternative pain generator

Greater than two level positive response

Chronic, interdisciplinary pain management approach

Symptoms persist Fig. 89.4 General algorithmic approach to the intervertebral disc.

approach is offered in an effort to achieve a multilevel disc bathing effect through a cephalad push of injectate. If isolated degenerative change or a central contained protrusion with an annular tear is noted at L4–5 and disc morphology is preserved at L5–S1, a bilateral L5 transforaminal injection can be performed in an effort to maximally target the L4–5 disc. When targeting a particular disc in a unilateral or bilateral fashion, the foramen of the next caudal disc space is utilized for entry, as medication tends to spread in a cephalad fashion. No more than two injections are performed during a single procedural visit. In the patient with unilateral pain and two-level disc disease, i.e. L4–5 and L5–S1, an ipsilateral S1 and L5 injection approach is performed. Injection therapy can be offered in conjunction with a diagnosis-specific physical therapy program coordinated by a skilled therapist. In the author’s practice, success has been realized when such therapy is directed by a McKenzie certified or experienced mechanical therapist. The rehabilitation regimen should emphasize postural training, truncal strengthening, work ergonomics, and

patient education, rather than promote a more passive and modalitybased approach.119 For the patient with persistent and debilitating axial pain following an injection trial, lumbar discography and postdiscography CT imaging can be considered. The discogenic pain algorithm varies in this regard, as more-definitive diagnostic measures are deferred until initial treatments fail. We proceed in this fashion, as the majority of patients will ultimately not require discography, which is a more invasive approach than the injections previously described. A few important highlights regarding discography are warranted, as the chapters by Richard Derby and Mike Furman cover the topic in superb detail. A commonly referenced 1968 study by Holt120 raised concerns as a 37% false-positive provocative discography rate was demonstrated, and discography was labeled an unreliable diagnostic tool. This early investigation has been challenged on several fronts, and a 1990 study by Walsh et al.121 demonstrated a concordant pain response in 40% of discs studied in a small symptomatic group and a 0% false-positive 983

Part 3: Specific Disorders

rate in asymptomatic subjects. Discography remains an imperfect diagnostic tool, and subsequent studies have similarly revealed the potential for a false-positive response and in particular in patients with abnormal psychological profiles.98,122 Despite these shortcomings, discography represents an important diagnostic tool in the algorithmic approach to the patient with persistent axial pain and offers the only current means of identifying symptomatic discs. Provocative discography can be followed by CT imaging to reveal the nuclear morphology of the disc in the axial plane and further characterize the annular tears observed under fluoroscopy. Without discography, the treating clinician attempting to identify the symptomatic intervertebral disc(s) would need to rely solely upon MRI or CT imaging, which previous studies have convincingly demonstrated to be fraught with a high false-positive rate. Using an aggressive technique such as discography is essential at this point in the treatment algorithm, as the subsequent therapeutic options to be considered are among the most invasive, expensive, and controversial offered in spine care. Ideally, discography reveals a single symptomatic disc with two asymptomatic control discs also studied. In the patient with suspected single-level lower lumbar disc disease at L4–5 or L5–S1, a three-level discogram can be performed. If two-level symptomatic disc disease is suspect, i.e. at L4–5 and L5–S1, a four-level study can be performed which investigates L2–3 through L5–S1. Following such studies, if a painful disc is not identified and suspicion remains that a more cephalad disc is symptomatic, a three- or four-level discogram can be performed to investigate the upper lumbar discs. In the setting of negative discography, alternative pain generators should be pursued. In this scenario, the posterior elements or sacroiliac joints might be reconsidered as potential primary pain generators. It is the patient with discogenic pain demonstrated by discography who epitomizes the challenges before the treating spine clinician. In this more commonly encountered group of patients with chronic and persistently debilitating discogenic pain, the likelihood of successful treatment outcomes becomes quite variable. Further interventions for the patient with discogenic pain should be reserved for those with ideally one and no more than two-level disc disease.123–126 In the author’s practice, patients with greater than two-level disease are not considered appropriate candidates for further intradiscal or surgical therapies. These individuals are directed toward a chronic and interdisciplinary pain modulation approach. In conjunction with lumbar discography and prior to further interventions, and in particular in those patients for whom surgical approaches are being considered, psychological factors must be critically assessed through the use of a screening examination. Patients with abnormal psychological profiles are more likely to demonstrate false-positive findings during provocative discography, and contributing psychosocial stressors can ultimately correlate with treatment failure and ongoing disability.122,127–130 Patients with persistent pain and abnormal psychological profiles can be referred for psychological care as a component of an interdisciplinary pain management program. For those patients with one- or two-level positive discograms, intradiscal electrothermal (IDET) annuloplasty might be considered, but recent literature is now suggesting a therapeutic effect quite inferior to that initially suggested by uncontrolled trials. The potential mechanism of action of IDET remains unclear. Pain relief has been speculated to result from a coagulation of nociceptive fibers within the anulus,131,132 sealing of painful annular tears,132 collagen modulation and stiffening,131 or even a disruption of the chemical inflammatory cascade.132 A randomized, placebo-controlled trial of IDET126 has demonstrated no appreciable benefit in 50% of patients treated. Approximately 38% of patients in the treatment group realized greater that 50% pain relief, and 22% demonstrated 75% or greater reduction in pain. While the treatment group demonstrated a 984

statistically significant overall 2.4 point drop (versus 1.1 in the control group) in the visual analog scale (4.2 at 6 months post treatment versus 6.6 at baseline), the clinical significance of this pain reduction remains less clear. The IDET group demonstrated better pain relief and Oswestry Disability Scores than the control group, but improvements in the Bodily Pain and Physical Functioning scores of the SF36 were similar. These modest results were realized in a highly select patient population. Patients were screened for depression, had no prior spine surgery, had no workers compensation claim or injury litigation issues, and demonstrated no greater than 20% loss of disc space height at the treated levels. A second randomized, controlled trial,133 which studied patients with a greater baseline disability level and included workers compensation cases, demonstrated no clinically significant improvements in the treatment group. Scores from multiple outcome instruments were assessed at 6 month follow-up, and no patient was observed to realize what the authors defined as a successful clinical outcome. In those patients with single- or, at most, two-level, disc disease who fail to realize relief from IDET or who are considered poor candidates, i.e. more-advanced loss of disc space height, surgical intervention in the form of fusion can be considered. Uncontrolled outcome studies investigating lumbar fusion procedures have described varying success rates ranging of 39–93%.125,134,135 In a study of posterolateral fusion in patients with positive preoperative discography, an overall 39% good or excellent outcome was observed.125 Of the 23 patients studied, 10 were workers compensation cases, and 90% of these proved to be treatment failures. Additionally, patients out of work for more than 3 months preoperatively demonstrated poor outcomes. A study of 137 patients123 in whom discography revealed abnormal disc morphology and symptom reproduction revealed an 89% clinical success rate following either anterior or posterolateral fusion. This compared favorably to the 52% clinical success rate in patients whose radiographs revealed disc degeneration with negative preoperative discograms. A 10-year follow-up study128 of anterior fusion patients demonstrated significant or complete pain relief in 78%. A retrospective study of four fusion techniques136 suggests that anterior interbody fusion performed in conjunction with posterior fusion and instrumentation results in superior outcomes to both stand-alone anterior interbody fusion and posterolateral fusion with instrumentation. A study investigating the potential role of preoperative pressure-controlled discography in surgical planning137 demonstrated no significant difference in outcomes in patients following either anterior, posterior, or combined surgical approaches. Patients with highly sensitive discs demonstrated superior outcomes following surgical approaches which included anterior interbody fusion when compared to an isolated posterolateral fusion approach. Studies demonstrating superior outcomes following anterior interbody fusion may be consistent with either superior segmental immobilization following anterior surgery138–142 or a greater likelihood of symptom resolution only following resection of the painful intervertebral disc.143,144 At this time, the treatment algorithm ends at surgical fusion. For those patients who choose not to proceed with surgery or for whom such intervention is inappropriate, i.e. three-level disc disease or a medical history which presents too great a surgical risk, a chronic pain modulation approach can be introduced. Patients considering surgical intervention for discogenic pain should also be educated in the areas of evolving treatments and technologies for the treatment of discogenic pain. These approaches are described in greater detail in dedicated chapters within this text and include intervertebral disc replacement,145 disc nucleus replacement,146,147 disc regenerative therapies,148 and perhaps, if such technology should evolve, percutaneous fusion utilizing the introduction of bone growth factors. Ultimately, well-designed and controlled prospective studies should

Section 5: Biomechanical Disorders of the Lumbar Spine

demonstrate the superiority of these treatments to current fusion techniques in terms of clinical success, invasiveness, complications, and cost for spine clinicians to embrace such technology. As there are many exciting avenues of research in the treatment of discogenic pain, this information, along with available outcome data for current treatments, needs to be shared with patients so that they can remain educated and primary decision-makers in the algorithmic approach.

exam not further suggestive of radiculopathy, the differential needs to be expanded. The patient may be experiencing symptoms arising from a symptomatic nerve root, a primary discogenic pain source, or even pain arising from combined pain generators which include an inflamed nerve root dura and dorsal root ganglion without associated or more overt neural dysfunction. The addition of these diagnostic tools might help to further clarify such a patient’s candidacy for introduction into the axial pain generator algorithms.

EXAMPLE CASES

Case 1

Before proceeding with two cases which exemplify the algorithmic approach to the patient with persistent axial pain, a few clarifications will be highlighted. First, when the data from combined prevalence studies is considered, the three pain generators emphasized in the preceding sections may only account for approximately two-thirds of the chronic lumbar axial pain population. As the therapeutic outcomes remain inferior to one’s diagnostic abilities, an even lower percentage of this population is likely to be successfully treated through the algorithms proposed. The algorithms, though, do not only offer a logical approach through which treatment outcomes may be maximized. They also protect the patient and clinician from proceeding along even lower-yield or inappropriate treatment pathways. In this regard, an algorithm may lead the patient along an appropriate, and actually successful treatment pathway but without a more complete symptomatic resolution. Each algorithm has assumed that a detailed history, physical examination, advanced imaging, and other diagnostic studies, such as blood work-up when appropriate, have been performed prior to a more interventional approach. In this author’s practice, such screening has led to the identification of benign osteoporotic fractures, vertebral body fractures arising from metastatic disease, osteomyelitis and discitis, primary and metastatic pelvic lesions, expansile hemangiomas, renal tumors, ruptured ovarian cysts, symptomatic abdominal aortic aneurysms, cholelithiasis and pancreatic disease, and primary symptomatic osteoarthritis or avascular necrosis of the hip. Finally, before proceeding with the cases, a word about a less malignant, but commonly encountered clinical syndrome which needs to be considered when evaluating the patient with ongoing axial pain. Radicular syndromes must always remain in the differential when evaluating the patient with axial pain. Not all lumbosacral radiculopathies present with classic myotomal strength deficits or dermatomal pain distributions.149 While a consideration of radiculopathy is likely less important in the patient with isolated and central lumbar pain, the patient with lumbar pain radiating the buttock, inguinal region, or proximal limb may in fact be presenting with a less pronounced radicular syndrome. These pain distributions can be quite similar to the symptom referral patterns described for the three primary pain generators above. This possible symptom overlap emphasizes the need to perform a detailed history and physical examination. The revelation of a prior component of more distal pain radiation or weakness might provide valuable clues and elucidate a previously more overt radiculopathy. The examination should include a methodical neurologic examination in which bilateral sensation, strength, and reflexes are assessed for symmetry. If suspicion remains high, the examination and history unrevealing, and an isolated compressive lesion is appreciated on advanced imaging, additional diagnostic tools can be employed. Electrodiagnostic studies and diagnostic selective nerve root injections, which will be addressed in dedicated chapters of this text, can be included in the diagnostic algorithm in an effort to more definitively rule out a symptomatic nerve root. In the patient with radiographic evidence of an isolated compressive injury, i.e. posterolateral protrusion to the right at L4–5 with compression of the L5 root, lumbar and buttock pain on the right, and a history and

A 36-year-old woman presented with the chief complaint of lumbar and right buttock pain. Her symptoms began 8 weeks earlier after lifting a carton in her garage and then falling rearward upon her buttocks. She had initially trialed a period of activity modification, but after 2 weeks began a regular regimen of icing and over-the-counter ibuprofen. At the 1-month juncture, with only mild improvement, she visited her internist who diagnosed her with a ‘lumbar sprain’ and prescribed physical therapy and a regimen of naproxen twice daily. Four weeks later, as her symptoms persisted, an MRI of the lumbar spine was ordered, and the patient was referred to the author’s practice. Her pain diagram depicted right lower lumbar discomfort which radiated to the superior and midbuttock without involvement of the more distal limb. She described no significant past medical or surgical history. She complained of pain with prolonged sitting as well as during forward-flexed postures and lifting maneuvers. Her physical examination revealed preserved right lower extremity reflexes at the patella, Achilles, and medial hamstring tendons, intact sensation, and full strength. Active lumbar flexion while standing was pain provoking as were pelvic rocking and sustained hip flexion maneuvers. Sacral sulcus tenderness was appreciated to local palpation on the right but not on the left. Faber’s testing and Gaenslen’s maneuver were also positive on the right side. Her MRI of the lumbar spine was notable only for disc desiccation with preservation of height at L4–5 where a small right paracentral protrusion and annular tear was observed. The protrusion was not noted to compress the evolving right L5 nerve root, and no significant central or foraminal stenosis was appreciated at this or other levels. At the conclusion of her initial visit, the patient’s differential diagnosis included lumbar pain of discogenic origin and right sacroiliac joint syndrome. Her radiographs suggested an L4–5 disc pain generator, and her mechanism of injury and exacerbations with sitting, forward flexion, and provocative physical examination maneuvers were supportive of discogenic pain. Her described fall upon the buttocks, tenderness over the sacral sulcus, superior buttock pain, and response to provocative maneuvers were also potentially consistent with a sacroiliac joint process. At this point she felt that she had exhausted physical therapy and refused a further trial of therapy with a skilled therapist affiliated with the author’s practice. She wished to pursue a more interventional and definitive approach, and a diagnostic sacroiliac joint injection was planned prior to proceeding with a more empiric therapeutic injection approach. Her response to the fluoroscopically guided diagnostic intra-articular injection was negative. Minimal relief, approximately 20%, was described 30 minutes after the intra-articular injection of 2 cc of 2% xylocaine. It was then decided to proceed with a working diagnosis of discogenic pain and fluoroscopically guided right L5 transforaminal injections were planned in an effort to maximally bathe the right L4–5 intervertebral disc and protrusion to the right. Two weeks after two therapeutic injections, she described an approximate 60% reduction in her level of lower lumbar pain, and her radiating pain to the buttock was resolved. A third therapeutic injection was then performed without additional appreciable benefit. As an incremental response was not realized, no further injection therapy was planned. 985

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The patient then decided to proceed with further physical therapy with an experienced mechanical therapist and realized some additional relief after 3 weeks of treatment and the introduction of a home exercise regimen. Five months after her initial injury, describing an overall 75% improvement, but with residual lumbar discomfort which prohibited her from lifting or sitting for extended periods without pain, she requested further information regarding her treatment options. The role of lumbar discography was reviewed as a potential precursor to intradiscal annuloplasty, fusion, or, at some point in time, evolving techniques such as disc replacement therapy. The pertinent literature and range of therapeutic outcomes was referenced in our discussion. We also reviewed the option of living with her discomfort along with activity and postural modifications or trialing a more chronic pain management approach and medication trials. She decided to proceed with discography from L3–4 through L5–S1. A concordant pain response was elicited at L4–5 where an annular tear was observed without resultant pain or annular disruption at the adjacent control discs. She then wished to proceed with IDET. After her procedure and 6 weeks of graduating activity and the tapering use of an external orthosis, only mild additional relief was described, with the patient then reporting an overall 80% improvement. While her pain was as easily provoked through similar activities, her localized lumbar discomfort was not as sharp in nature. She chose to continue her home program, addressed her seating system and work station, and continued the intermittent use of nonsteroidal antiinflammatory agents. She decided that she would rather live with her current level of discomfort than pursue further interventions. The patient revealed that she was satisfied with the pain relief obtained and was pleased with her decision to undergo the IDET procedure considering the outcome realised.

Case 2 A 72-year-old male presented with the chief complaint of right lower lumbar pain. His symptoms evolved gradually over 4 months and began without a particular inciting event. He had trialed a course of COX-2-specific nonsteroidal antiinflammatory agents for 3 weeks without relief. His primary care physician suggested he was suffering from a ‘degenerative spine,’ and physical therapy was prescribed. After 6 weeks of therapy, he realized minimal relief and was graduated to a home exercise program. An MRI was ordered, and he presented with these films to his initial visit at the author’s office. He described right lower lumbar pain which radiated to the superior buttock and rarely to the inguinal region. He denied symptom radiation to the more distal lower limb. His symptoms were typically exacerbated by prolonged standing more so than during ambulation and were relieved by sitting. The past medical history was significant for benign prostatic hypertrophy and hypertension. Examination revealed intact right lower limb strength and reflexes and easily appreciated distal pulses. Passive range of motion of the right hip was not pain provoking. There was no significant sacral sulcus tenderness, but right lower lumbar paraspinal tenderness was noted to deep palpation. Sacroiliac joint provocative maneuvers were negative. Pain was reproduced with active lumbar extension and relieved with forward-flexed postures. An MRI of the lumbar spine revealed multilevel disc desiccation and a mild grade I-listhesis at L4–5. No foraminal stenosis was observed and the central canal compromise at L4–5 was graded as mild. Z-joint arthrosis was noted bilaterally at L4–5 and L5–S1 but more notably on the right where increased T2-intra-articular signal was observed. Flexion and extension radiographs revealed no translational, rotational, or angular motion abnormality at the level of the L4–5 olisthesis. At the conclusion of his initial visit, his differential diagnosis included lumbar pain of Z-joint or discogenic origin.

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As his symptoms were not exacerbated by valsalva maneuvers, exacerbated by standing and extension-biased postures, and relieved through assuming the supine, sitting or flexed positions, the posterior elements were considered more likely as his primary pain generators. His localized tenderness to palpation and asymmetric right-sided Z-joint arthroses were also considered supportive. A diagnostic right-sided fluoroscopically guided intra-articular L4–5 and L5–S1 Z-joint injection was performed utilizing 1.0 cc of 2% xylocaine into each joint. During the assessment phase, the patient described complete relief from his baseline pain during typically provocative standing and extension postures. This confirmatory diagnostic injection was followed by a right-sided therapeutic corticosteroid intra-articular injection at L4–5 and L5–S1. The first injection offered him mild relief and was followed by a second 2 weeks later. Two weeks after his second injection, he described an approximate 60% improvement when compared to his initial presentation and improved ambulation endurance. It was decided to proceed with a third. Two weeks later he described a 70% improvement in his level of right-sided axial pain. Over the subsequent 3 months, his improvements waned, but not to his baseline level. He questioned his candidacy for another injection. In the absence of a sustained incremental response, it was explained that another injection would likely also only offer transient relief. The potential outcomes following radiofrequency denervation were reviewed and a diagnostic medial branch block injection was performed on the right at L3 through L5. This confirmatory diagnostic assessment similarly resulted in complete relief from his residual pain. A radiofrequency denervation procedure to address these medial branches was then performed. The patient realized additional relief which was graded as an overall 75% improvement and increased standing and ambulation tolerance. At 10 months following this procedure, a gradual decline in response was described, and discussions were initiated regarding a possible repeat radiofrequency approach.

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125. Parker LM, Murrell SE, Boden SD, et al. The outcome of posterolateral fusion in highly selected patients with discogenic low back pain. Spine 1996; 21: 1909–1917.

98. Carragee EJ, Paragioudakis SJ, Khurana S. 2000 Volvo Award winner in clinical studies: Lumbar high-intensity zone and discography in subjects without low back problems. Spine 2001; 23:2987–2992.

126. Pauza KJ, Howell S, Dreyfuss P, et al. A randomized, placebo-controlled trial of intradiscal electrothermal therapy for the treatment of discogenic low back pain. Spine 2004; 4:27–35.

Section 5: Biomechanical Disorders of the Lumbar Spine 127. Block AR, Vanharanta H, Ohnmeiss DD, et al. Discographic pain report: Influence of psychological factors. Spine 1996; 21:334–338.

138. Lee CK, Langrana NA. Lumbosacral spinal fusion: A biomechanical study. Spine 1984; 9:574–581.

128. Penta M, Fraser RD. Anterior lumbar interbody fusion. A minimum 10-year follow up. Spine 1997; 22:2429–2434.

139. Rolander SD. Motion of the lumbar spine with special reference to stabilizing effect of posterior fusion. Acta Orthop Scand Suppl 1966; 90:1.

129. Greenough CG, Peterson MD, Hadlow S, et al. Instrumented posterolateral lumbar fusion. Results and comparison with anterior interbody fusion. Spine 1998; 23:479–486.

140. White AA, Panjabi MM. Clinical biomechanics of the spine: Biomechanical considerations in the surgical management of the spine. 2nd edn. Philadelphia: Lippincott; 1990:529–535.

130. Trief PM, Grant W, Fredrickson B. A prospective study of psychological predictors of lumbar surgery outcome. Spine 2000; 25:2616–2621.

141. Ylinen P, Kinnunen J, Laasonen EM, et al. Lumbar spine interbody fusion with reinforced hydroxyapatite implants. Arch Ortho Trauma Surg 1991; 110:250–256.

131. Saal JS, Saal JA. Management of chronic discogenic low back pain with a thermal intradiscal catheter. A preliminary report. Spine 2000; 25:382–388.

142. Zdeblick TA, Smith GR, Warden KE, et al. Two-point fixation of the lumbar spine. Differential stability in rotation. Spine 1991; 16(S):298–301.

132. Karasek M, Bogduk N. Intradiscal electrothermal annuloplasty: percutaneous treatment of chronic discogenic low back pain. Techniques Reg Anesth Pain Manage 2001; 5:130–135.

143. Saal JS, Franson RC, Saal JA, et al. Human disc PGE2 is inflammatory. Proceedings of the Sixth Annual North American Spine Society Meeting. Colorado; 1991.

133. Freeman BJC. A randomized controlled efficacy study: Intradiscal electrothermal therapy (IDET) versus placebo. Proceedings of the annual meeting of the International Society for the Study of the Lumbar Spine. Vancouver: 2003. 134. Bernard TN Jr. Lumbar discography and post discography computerized tomography: Refining the diagnosis of low back pain. Spine 1990; 15:690–707. 135. Lee CK, Vessa P, Lee JK. Chronic disabling low back pain syndrome caused by internal disc derangements: The results of disc excision and posterior lumbar interbody fusion. Spine 1995; 20:356–361.

144. Weinstein J, Claverie W, Gibson S. The pain of discography. Spine 1988; 13: 1344–1348. 145. Delamarter RB, Fribourg DM, Kanim LE, et al. ProDisc artificial total lumbar disc replacement: introduction and early results from the United States clinical trial. Spine 2003; 28:S167–S175. 146. Klara PM, Ray CD. Artificial nucleus replacement: clinical experience. Spine 2002; 27:1374–1377. 147. Sagi HC, Bao QB, Yuan HA. Nuclear replacement strategies. Ortho Clin North Am 2003; 34:263–267.

136. Vamvanij V, Fredrickson B, Thorpe JM, et al. Surgical treatment of internal disc disruption: An outcome study of four fusion techniques. J Spin Disord 1998; 11:375–382.

148. Kroeber MW, Unglaub F, Wang H, et al. New in vivo animal model to create intervertebral disc degeneration and to investigate the effects of therapeutic strategies to stimulate disc regeneration. Spine 2002; 27:2684–2690.

137. Derby R. et al. The ability of pressure-controlled discography to predict surgical and nonsurgical outcomes. Spine 1999; 24:364–371.

149. Nitta H, Tajima T, Sugiyama H, et al. Study of dermatomes by means of selective lumbar spinal nerve block. Spine 1993; 18:782–786.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain

CHAPTER

90

Medical Rehabilitation – Lumbar Axial Pain William Micheo and Carmen E. López-Acevedo

INTRODUCTION Axial low back pain is a common complaint of patients visiting physicians who practice musculoskeletal and pain medicine. The majority of these patients are diagnosed with non-specific back pain, which is presumed to be caused by muscle or ligament soft tissue damage, while many of these patients will actually have pain associated to injury to the posterior elements or the disc. These patients are thought to have a good prognosis for recovery; they improve in 4–12 weeks after the onset of pain, and the strategies of treatment used focus only on short-term management. In reality, many of these patients have future episodes of back pain associated with recurrent injury to the disc and associated structures and some will present with chronic back pain. Patients with unresolved pain may develop significant changes in the quality of their life including reduced health perception, happiness, social participation, and restriction of function.1 In addition, significant direct and indirect healthcare costs are associated with chronic low back pain.2 Low back pain should be considered a symptom of a clinical problem and not a specific diagnosis. Clinicians dealing with the rehabilitation of patients with low back pain should avoid non-specific terminology to describe the patient’s diagnosis such as lumbar strain, lumbago, or myositis. An understanding of the epidemiology of back pain, functional anatomy, and biomechanics of the spine, as well as the pathophysiology of the disease process is required to appropriately manage back pain. In addition, a complete history, physical examination, and appropriate diagnostic studies are paramount for the clinician who rehabilitates patients with this common disorder. Attempts should be made to establish a specific diagnosis for the cause of the axial back pain, which includes the site of injury with the pain generator, the clinical symptoms which require appropriate treatment, biomechanical changes associated to the tissue injury, and finally the functional abnormalities which result from the disease process. The overwhelming majority of patients with back pain will not require surgery and should be managed with conservative treatments which include rehabilitation and functional restoration.3–5 The goals of rehabilitation are to return the individual with low back pain to normal function. This requires achieving control of pain, adequate flexibility, strength, and muscle balance as well as neuromuscular coordination that would allow the return to normal activities. Evaluation, management, and rehabilitation of low back pain also require that the clinician understands the vocational and avocational demands of the patients and their goals. Unfortunately, there is limited positive scientific evidence on the results of a structured rehabilitation program in the management of back pain. In this chapter, the authors will review some of the scientific evidence available that relates to therapeutic interventions used

in rehabilitation such as physical modalities, rest and physical activity, exercise, manual therapy, and education. In addition, the authors will discuss their approach to the patient with back pain, and how they combine the available scientific information with their clinical experience in the management of this very common and often difficult patient problem.

FACTORS INFLUENCING REHABILITATION Epidemiology Understanding the patterns of injury and clinical presentation of low back pain is important for the planning of therapeutic, rehabilitative, and preventive strategies. Low back disorders are prevalent in all societies and the etiology of these disorders is multifactorial including individual/intrinsic as well as external/extrinsic factors. The annual incidence of low back pain in the general population is 5%, with many patients presenting between the ages of 30 and 50 years, and a significant number of cases resolving within 4 weeks of presentation. Of these patients, particularly the ones who present with pain at an early age, a significant number will present with recurrence of the symptoms, and some will develop chronic disability. Therefore, a functional rehabilitation program should be instituted early in the disease process.6–8 Some individual risk factors for pain are modifiable and include obesity, cigarette smoking, and low fitness level.9,10 Occupational factors associated with back pain include vibration, static work posture, flexed posture, frequent bending and twisting, lifting and material handling.11,12 Psychosocial factors associated with back pain and recurrence of symptoms include dissatisfaction with work, long duration of initial treatment, recurrent treatment, and being disabled from work.13–15 Other factors, such as heredity, may not be modifiable but also play a role in the development of low back pain. Familial predisposition to back pain and degenerative disc disease has been described and may be important in patients who present at an early age (Table 90.1).16–19 Sports and recreational activities are also associated with the development of back pain, wherein 10–15% of all sports injuries are related to the spine. Rotational, torsional, and compressive stresses to the spine are associated with the development of intrinsic disc disease.20,21 Activities in daily life that involve frequent bending and lifting may also lead to back pain. Individuals caring for elderly or disabled family members present with an increased prevalence of back pain.22

Functional anatomy and biomechanics A review of the anatomy and biomechanics of the spine is beyond the scope of this chapter; however, an understanding of the functional 991

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Table 90.1: Risk Factors for Axial Low Back Pain Epidemiologic Evidence Individual/Intrinsic

External/Extrinsic

Age

Static work postures

Gender

Prolonged sitting

Abdominal girth

Frequent lifting, pushing and pulling

Smoking

Frequent trunk rotation

Muscle weakness/loss of endurance

Vibration exposure

Reduced/excessive flexibility

Repeated lumbar flexion

Sedentary life style

Activity early in the day

anatomy as well as basic concepts of biomechanics of the lumbar spine is important for the clinician who treats and rehabilitates patients with low back pain. The basic functional unit of the lumbar spine is the three-joint complex formed by two consecutive vertebra, the intervertebral disc, and the zygapophyseal joints. The anterior elements of the lumbar spine sustain the compression loads applied to the vertebral column including body weight and loads associated with contraction of the back muscles. The posterior elements regulate the passive and active forces applied to the vertebral column and regulate motion. The zygapophyseal joints are typical synovial joints endowed with cartilage, capsule, meniscoids, and synovial membrane. The articular facets exhibit variations in both the shape of their articular surfaces and their orientation. In the lumbar spine the only movement permitted is a sliding motion in a vertical direction, executed during flexion and extension.23 Muscle function is very important for the lumbar spine since ligaments provide little static stability and in the absence of muscle activity the spine could buckle with low compressive loads. The erector spinae are composed of two major groups: the longissimus and iliocostalis. They are primarily thoracic muscles that act on the lumbar spine with a long moment arm ideal for lumbar spine extension. The small rotatores and intertransversarii muscles are basically length transducers and position sensors. The multifidi which cross 2 or 3 segmental levels are theorized to work as spinal stabilizers.24 Other muscle groups important for low back function are the quadratus lumborum, which has a direct insertion in the lumbar spine and acts as a weak lateral flexor, and the abdominal muscles which include: the transversus abdominus, internal and external oblique, and rectus abdominus. These muscles are important in flexion of the trunk, lateral bending, but most importantly help to stabilize the lumbar spine. Pelvic muscles also play a role in the kinetic chain by acting on the lumbar spine and transmitting forces from the lower extremity to the trunk and upper extremities and include: the hip flexors such as the iliopsoas, and gluteal hip extensor, as well as abductor muscles.25 The lumbar spine and related structures including ligaments and muscles receive an extensive nerve supply. The vertebral bodies, the intervertebral disc, the zygapophyseal joints, and the ligaments are all innervated and have the capacity to be pain generators, making it difficult for the clinician treating axial back pain to identify the origin of a patient’s symptoms.

Pathophysiology of injury Flexion of the lumbar spine, which involves sagittal rotation and translation, is well tolerated by the lumbar elements. Compression 992

of the lumbar spine occurs by adding body weight, muscular contraction, and the loads that are lifted by the individual. Excessive compression may injure the anterior vertebral elements, particularly the endplates. When flexion and compression are combined with rotation, shear applied to the intervertebral disc results in injury to this structure. Vertebral extension is limited primarily by bony impaction of the spinal processes or the inferior articular facet against the lamina below, and repeated extension as well as rotation activities may lead to injury of the posterior elements such as the pars intercularis.26 Lumbar disc disease associated with axial back pain is multifactorial in origin. Aging, apoptosis, abnormalities in collagen, vascular ingrowth, loads placed on the disc, and abnormal proteoglycan all contribute to disc degeneration.27 Repetitive or continuous axial overloading, associated with disc fatigue, is key in the pathogenesis of lumbosacral degenerative disease.24 Vigorous occupational activity and competitive athletic participation associated with end-range flexion and frequent turning predispose the disc to herniation and accelerated degeneration.28 These changes in the disc, which progress from herniation to subsequent internal disruption and resorption, may affect more than one functional unit and compromise spinal motion. The combined changes in the posterior joint and discs lead to arthritis, lateral recess stenosis, and central stenosis.29–31 Low back pain may result from compression of nerve tissue, inflammation of the nerve root, and the facet joint, as well as damage to the anulus fibrosus. Inflammatory mediators, such as prostaglandins and substance P, have been identified in patients with disc disease and are associated with pain in the absence of a compressive lesion.28,32 Increasing age has been associated with progressive disc degeneration which can be asymptomatic in some individuals. Changes in trabecular bone morphology and inappropriate disc matrix may be related to apoptosis, or programmed cell death, in the patient with disc disease.27,33

Clinical presentation In the individual with axial back pain, the history and physical examination are very important in the planning of a functional rehabilitation program. Pertinent information that should be obtained from the history include: the type of pain, the mechanism of injury, exacerbating and mitigating factors, and previous injuries and response to treatment strategies. The physical examination should identify limitations of motion, direction of pain exacerbation, lack of flexibility, muscle weakness and imbalance, ligamentous laxity, and neurologic as well as proprioceptive deficits. This information combined with pain diagrams, diagnostic imaging, and injection procedures allows the clinician to recognize specific characteristics of different clinical subsets.34 Clinical subsets of axial back pain include patients with acute annular tears, intrinsic disc disease, facet joint degeneration, or posterior element injury. Patients with axial back pain associated with disc disease may present with acute symptoms, chronic symptoms, or acute exacerbation of chronic symptomatology. The patient with an acute annular disc injury will present with axial pain, limited lumbar motion, intolerance to sitting, and exacerbation of symptoms with attempted flexion of the spine. The physical examination of these individuals may reveal a lateral trunk list, pain with flexion of the spine, normal neurologic examination, and typically no evidence of spinal nerve root irritation. The patient with chronic discogenic disease will present with axial back pain, intolerance to sitting as well as pain upon arising from a chair, limited capability to lift, bend, or twist.35 Physical examination will reveal soft tissue inflexibility of paravertebral muscles, fascia and ligaments as well as some muscle spasm. There may be evidence

Section 5: Biomechanical Disorders of the Lumbar Spine

of lumbar segmental hypomobility, loss of lumbar lordosis, and pain with flexion and rotation. The neurologic examination is usually normal with no evidence of root irritation.36 Individuals who present with an acute on chronic injury give the history of an excessive load or sudden trauma superimposed on previous discogenic symptoms. The physical examination is usually similar to patients that presents with an acute annular tear. Patients who present with axial back pain may also have involvement of posterior elements such as the facet joints. These individuals may present with pain in the back which may radiate to the buttocks or thighs that could worsen with extension activities such as walking downhill, prone lying, and prolonged standing. Other patients may present with a different history such as pain with flexion that is not exacerbated by sitting and still have facet joint pathology. The physical examination may reveal inflexibility of the lumbar soft tissues, hypomobility of spine segments, and pain with extension or flexion as well as rotation maneuvers. The neurologic examination and special maneuvers to identify root irritation are usually normal, and injection procedures may be required to clearly identify the facet joint as the pain generator.37 In sports, the patterns of back injury will depend on several factors which include the patient’s age and sport-specific demands. Athletes involved in sports that require trunk rotation and hyperextension usually present with axial back pain associated to posterior element injury. Repeated stresses associated to gymnastics, diving, and wrestling places the athlete at increased risk of pars interarticularis injury such as spondylolisis. These athletes may present with acute or gradual onset of pain and limited motion which restricts activity.38 Older individuals who exercise vigorously or participate in sports will generally present with injuries of the vertebral endplate and the intervertebral discs. These individuals usually present with symptoms associated to repeated flexion and trunk rotation. They may present with episodes of axial back pain and limited motion which may be accompanied by leg symptoms.39

Psychosocial factors Psychologic and social issues should be addressed in the individual with axial back pain because they may affect rehabilitation, and include coexisting anxiety, depression, family or work related stress, and lack of social support. Work dissatisfaction, fear of recurrence of pain with activity, and pending compensation are also factors that may be impediments to return to normal activity.14

BASIC CONCEPTS OF REHABILITATION Complete diagnosis of musculoskeletal injury Prior to starting rehabilitation, attempts should be made to reach a complete diagnosis of the patient with back pain including the pain generator and the biomechanical deficits. In the authors’ practice, a modification of the musculoskeletal injury model described by Kibler is used for this purpose. This model identifies the anatomic site of injury, the clinical symptoms, and the functional deficits (Table 90.2).40

Phases of rehabilitation Musculoskeletal rehabilitation combines therapeutic modalities and exercise in order to return the individual to normal function. It should start early in the disease process in order to reduce the deleterious effects of inactivity and immobilization. A medical rehabilitation program should state the goals and objectives of treatment specific for each phase of rehabilitation. The treatment should focus on optimizing the healing process, restoring the biomechanical relations between the normal and injured tissue, and finally preventing

Table 90.2: Framework for Musculoskeletal Injuries Axial Back Pain CLINICAL ATERATIONS Symptoms Back pain Sitting intolerance Pain with bending ANATOMIC ALTERATIONS Tissue injuries: vertebral end plate, intervertebral disc, facet joints Tissue overload: extensor muscles, interspinal ligaments FUNCTIONAL ALTERATIONS Biomechanical deficits: weak back extensors, tight hip flexors Adaptive behavior: avoidance of trunk flexion, rotation, prolonged sitting

recurrence of pain and chronic disability. A functional rehabilitation program emphasizes therapeutic exercise and physical activity while monitoring for exacerbation of symptoms. Rehabilitation of the patient with back pain can be divided into acute, recovery, and functional phases (Table 90.3). The acute phase addresses the clinical symptom complex and should focus on treating tissue injury. The goal at this stage should be to allow tissue healing while reducing pain and inflammation. Reestablishment of nonpainful range of motion, prevention of muscle atrophy, and maintenance of general fitness should be emphasized. Symptom control and patient education about the condition should be accomplished prior to progressing to the next rehabilitation phase. The subacute or recovery phase should focus on obtaining normal passive and active range of motion, improving muscle control, achieving normal muscle balance, and working on core strength as well as proprioception. Biomechanical and functional deficits including inflexibilities and inability to bend or lift should begin to be addressed. Functional activities should be initiated in this stage and progression without recurrence of symptoms is required prior to advancing to the next stage. The functional or maintenance phase should focus on increasing power and endurance while improving neuromuscular control. Rehabilitation at this stage should work on the entire kinematic chain, addressing specific residual functional deficits. The individual

Table 90.3: Goals in Rehabilitation of Musculoskeletal Injury Acute Phase

Recovery Phase

Functional Phase

Treat clinical symptoms

Allow tissue healing

Correct abnormal biomechanics

Protect injured tissue

Restore normal strength and flexibility

Prevent recurrent injury

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should be pain free, exhibit full range of motion, normal strength, and muscle balance prior to returning to full activity. After return to activity, disease prevention and ‘prehabilitation’ strategies to avoid recurrence of symptoms in the previously injured individual should be developed. Exercise programs which combine flexibility, stabilization, dynamic strengthening, and balance training, as well as appropriate biomechanics should be encouraged in the patient who has recovered from low back pain.

REHABILITATION OF AXIAL BACK PAIN The functional rehabilitation model of patient management should be implemented as soon as the patient presents for clinical evaluation of back pain. As previously discussed, identification of the pain generator should be attempted based on the information obtained from the history, physical examination, laboratory studies, imaging data, and diagnostic injections.41 However, in many instances, the pain generator cannot be definitely identified, and a functional approach to the rehabilitation should be undertaken after developing a working diagnosis. Patterns of pain provocation with motion, muscle weakness, inflexibility, abnormal biomechanics, and functional abnormalities can be identified, used as a starting point for treatment, and addressed in a progressive manner.

Acute phase The acute phase of treatment is the period when pain should be addressed, and the injured tissue should be protected from further damage, with the purpose of optimizing the healing process and allowing the patient to progress in the rehabilitation program. It is important to understand that a balance must be achieved between treating the pain with medications, among other passive rehabilitation therapeutic interventions, and encouraging active patient participation in their treatment early in the recovery process (Table 90.4). Medications are an important component of the acute phase of rehabilitation, and basic knowledge of their pharmacology, side effects, and interactions is required for the clinician rehabilitating the patient with back pain. Management of pain is very important at this stage because pain can inhibit muscle contraction, reduce activity tolerance, and limit progression in a rehabilitation program. Some of the therapeutic agents commonly used in the acute phase, about which the treating physicians must be knowledgeable, include nonsteroidal antiinflammatory drugs (NSAIDs), muscle relaxants, nonopioid and opioid analgesics, as well as adjuvant medications such as antidepressants and anticonvulsants. There are multiple clinical studies that show evidence that prescription of various types of NSAIDs at regular intervals provides

Table 90.4: Rehabilitation of Back Injury – Acute Phase 1. NSAIDs and other medications 2. Limited rest 3. General conditioning 4. Cryotherapy 5. Electrical stimulation 6. Protected motion 7. Isometric–static exercise 8. Basic stabilization program 9. Diagnostic and therapeutic injections

994

effective pain relief from acute low back pain.42–45 Use of over-thecounter nonselective NSAIDs can be an initial treatment option, particularly for young patients without a history of gastrointestinal problems.46 In patients with a history of gastrointestinal problems, elderly individuals, or those patients in whom less frequent dosing is important for compliance, COX-2-specific inhibitors offer a therapeutic alternative.47,48 Risk of cardiovascular disease and monitoring fluid retention, blood pressure, and renal and liver function is important for any patient being treated with NSAIDs but particularly those treated with COX-2 inhibitors. In addition, there is clinical and scientific evidence that the different types of muscle relaxants are equally effective in the management of acute low back pain.49–51 However, muscle relaxants have significant adverse effects, such as drowsiness, risk of habituation, and dependency, which require that they be used with caution. The use of low-dose regimens of muscle relaxants offer a good therapeutic alternative with reduced side effects and similar efficacy.52 In many patients, low-dose muscle relaxants are used for a short period of time, particularly at night in patients with sleep dysfunction, since they may aid in sleep. Another treatment alternative to consider in patients with acute exacerbation of chronic symptoms and sleep dysfunction associated with fatigue is antidepressant medications, particularly the tricyclic agents because of their anticholinergic sedative and analgesic effects.53 In patients that do not respond to nonopioid analgesics in combination with the previously mentioned medications, consideration can be given to a short course of opioid analgesics. Formulations which combine acetaminophen with opioid analgesics such as oxycodone or with tramadol offer a treatment alternative for patients with poor response to other treatments or those allergic to aspirin. In the authors’ clinical experience, the use of these agents does not affect participation in the rehabilitation program and, in many instances, facilitates return to activity. During the acute phase, the focus is on reducing pain and protecting injured or inflamed tissue. A common therapeutic intervention in the acute phase of rehabilitation is restricted activity and bed rest. At present, there is scientific evidence that prolonged bed rest is not effective and may be detrimental for patients with acute low back pain.54,55 Based on the best information available, bed rest should be kept to less than 2–3 days for nonradicular low back pain. Hagen et al., from the Cochrane Collaborative Group, reviewed nine clinical trials in which bed rest was used in patients with acute back pain and sciatica and concluded that there is not an important difference in the effects of bed rest when compared to exercise in this patient population and that prolonged bed rest does not appear to be indicated even in the case of sciatica.55 Hilde and colleagues, from the same Cochrane Collaborative Group, reviewed four clinical trials with a total of 491 patients in which advice to stay active was included as a treatment strategy and concluded that the best available scientific evidence suggests that physical activity has a beneficial effect for patients with acute low back pain.56 In the authors’ clinical practice, low-intensity aerobic exercise is routinely prescribed for patients with acute back pain. Walking or swimming are appropriate exercises to prescribe for patients with discogenic pain, while bicycling is adequate for those with posterior element injury. Patient education is very important and should start in the acute phase of rehabilitation. Individuals participating in the rehabilitation program should be educated in the basic concepts of the pathophysiology of their illness, patterns of back pain, and proper spine biomechanics. The patient should be oriented on how to identify changes of intensity, frequency, and duration of pain patterns, how they affect their rehabilitation, and how their medication should be taken. In

Section 5: Biomechanical Disorders of the Lumbar Spine

addition, strategies that allow the patient to cope with their pain are important and should be established early in the management process. The identification of barriers to recovery such as beliefs about the harm of physical activity, comorbid factors such as psychiatric illness, job dissatisfaction, and unemployment is important to prevent the progression to chronic pain.57–59 Physical modalities such as cryotherapy are frequently used in combination with prescribed analgesics at regular intervals. Although the physiologic effects of cold include analgesia, reduction of inflammation, and muscle spasm, making cryotherapy ideal for treatment for acute injury, there is no strong evidence in the medical literature for their benefits in the management of acute back pain.28,60,61 Standard physical therapy treatment has not been shown to be effective in changing long-term outcome of patients with back pain; however, there is a patient-perceived benefit from such treatment.62 It is the authors’ clinical experience that short-term supervised physical therapy early in the clinical course of patients with acute back pain allows a more rapid progression and transition to an activity program, and it is frequently recommended to their patients. Muscle weakness, inhibition, and imbalance particularly of trunk muscles is commonly seen in patients who present with acute or recurrent back pain. Isometric and static exercises should be initiated to retrain proper muscle firing patterns in patients with muscle inhibition and abnormal firing patterns. Identification of the neutral spine position for stabilization exercises is very important at this stage since spine stability is necessary prior to achieving mobility in exercise, work, and activities of daily living. Gradual pain-free range of motion exercises for the back, hips, and lower extremities should be instituted in the acute management. Although, these exercises are commonly used and reported to have good clinical results, there is conflicting scientific evidence that specific back exercises such as flexion, extension, or stretching produce symptomatic improvement in acute low back pain.63 Another modality often recommended in this phase of treatment is electrical stimulation for pain control. Transcutaneous electrical nerve stimulation (TENS) for analgesia has been used in the past by many clinicians treating acute back injury based on the physiologic effects of this modality, which is theorized to block pain perception at the level of the spinal cord and may also cause secretion of endogenous opioids.64 However, there is conflicting evidence for the effectiveness of these treatments in acute back pain, and recent data suggest that subthreshold TENS is not effective treatment for low back pain.65,66 There are additional data that electro-acupuncture is more effective than TENS and classic massage, particularly if indicated in combination with back exercises. This can be an effective option for the treatment of pain and disability associated with chronic low back pain.67 In that group of patients who show poor response to the initial treatment program of medications, modalities, and low-level exercise, consideration should be given to the use of interventional techniques. Injection techniques play a dual role in the acute phase of rehabilitation: that of helping in the diagnosis and identification of the pain generator, and that of an important therapeutic tool to aid in symptom control. In the authors’ treatment algorithm, the use of epidural steroid injections for discogenic pain and facet joint injections or medial branch blocks for posterior element injury is of the utmost importance, since pain control and improved tolerance to physical activity must be achieved prior to progressing to the recovery phase of treatment.

Recovery phase The recovery phase of treatment is the subacute period that focuses on restoring the biomechanical relations between the normal and

Table 90.5: Rehabilitation of Back Injury – Recovery Phase 1. Modalities: superficial heat, ultrasound, electrical stimulation 2. Range of motion exercises, static and dynamic flexibility exercises 3. Dynamic stabilization exercises 4. Closed chain exercises, proprioceptive neuromuscular facilitation 5. Dynamic strengthening exercise 6. Sport- or work-specific functional exercises 7. General conditioning 8. Gradual return to physical activity

injured tissue (Table 90.5). Patients should be advised to gradually increase their physical activity in daily living despite the existence of some pain. Physical modalities such as superficial heat, ultrasound, and electrical stimulation are commonly recommended for treatment of pain in the recovery phase. There is limited evidence in the scientific literature that selected modalities in isolation are effective in this phase of treatment; however, based on their physiologic effects of analgesia, reduction of muscle spasm, facilitation of muscle recruitment, and increased distensibility of soft tissue, they are used in the authors’ practice for a limited period of time in combination with therapeutic exercises such as flexibility training and dynamic strengthening.28,68 Massage and manipulation have been used extensively and are thought to be effective in acute pain when combined with exercises and education. However, Assendelft et al. reviewed randomized clinical trials of spinal manipulation for the treatment of low back pain and concluded that there is no scientific evidence that spinal manipulation therapy is superior to other standard or conventional modalities of treatment for pain relief in patients with acute low back pain.69 The medical literature is not clear and gives conflicting evidence for the use of spinal manipulation for exacerbations of pain or chronic pain, with some studies reporting good short-term results in acute exacerbations.70–72 In the authors’ practice, patients with acute pain or exacerbation of baseline chronic symptoms are referred for manual therapy with good subjective results of pain reduction and increased mobility. In the recovery phase, flexion- or extension-biased exercise should be prescribed based on the identification of the direction that exacerbates the symptoms. The McKenzie approach uses a mechanical assessment of the patient to identify direction of pain exacerbation and has been advocated by many clinicians. The centralization phenomenon or the reduction of pain with preferential direction of motion has been associated with good prognosis for recovery.73 Patients with axial pain secondary to discogenic disease may benefit from extension exercises while patients with posterior element or facet syndrome may benefit from flexion exercises.74 Care should be taken when exercising patients to extreme ranges of motion, since these positions may increase the compressive load to the intervertebral discs.24 There is some evidence that exercises may be effective for patients in the subacute or chronic stage of treatment and may slightly reduce the risk of additional back problems or work disability.75 The intensity of the exercises should be monitored, increased gradually depending on the clinical response, with a specific prescription, and in some instances even in the presence of some pain.76,77 995

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Strengthening of the core musculature has become important in the rehabilitation of patients with back pain. The muscles that are targeted for exercise training include the multifidi, quadratus lumborum, abdominals, and hip girdle muscles. Back stabilization exercises in the neutral spine position are used to initiate strengthening of the back and pelvic core musculature. McGill and others have looked at exercises that could be safely used for strengthening in patients with back pain and these include the curl-up, side bridge, and bird dog or quadruped exercise. Endurance training with a high number of exercise repetitions rather than high-resistance strength training should be emphasized in the patient with back pain at this stage.25,78,79 In the recovery phase, the stabilization program should progress in difficulty, moving from stable to unstable surfaces.80 As the patient’s symptoms improve, inflexibilities and muscle imbalances of specific muscles such as the hip rotators, iliopsoas, and hamstrings should be addressed. Dynamic flexibility training in sagittal, frontal, and transverse planes of motion should be started gradually (Fig. 90.1). Progression of the aerobic and conditioning program is continued during this phase.25 Analgesic and antiinflammatory medications can be prescribed at this point of the treatment program only to facilitate a gradual increase in activities, but should be prescribed for a fixed period of time. Opioid analgesics remain an alternative for patients with no relief from other medications and have been reported to increase back exercise performance in those with intolerance to exercise secondary to pain.81 Local injections and interventional techniques such as epidural, facet, and medial branch blocks or radiofrequency denervation could also be considered at this point in the rehabilitation of patients. When attempting higher levels of activity, symptomatic individuals may benefit from these procedures to control pain and allow participation in the exercise program.82,83 Special patient populations addressed with interventional procedures in this stage include athletes and individuals who need to return to heavy labor. It is the authors’ clinical goal to reduce the fear of activity in these patients.

Complementary medicine approaches to pain management which include acupuncture and relaxation techniques have also been used in this stage of rehabilitation; however, the effectiveness of these treatments in long-term management is not clear.84 The authors recommend using acupuncture to their chronic patients with acute exacerbations who show slow response to treatment, including integrating muscle relaxation and visualization techniques, who present with activity-related anxiety. The functional phase of treatment emphasizes restoration of function for work and activities of daily living (Table 90.6). Another important objective of this phase of treatment is the prevention or reduction of physical or mental disability as well as improving the patient’s quality of life. The final goal is to prevent dependence on medical treatment and allow the patient the transition to exercising on his or her own. At this stage, patients with disabling low back problems who fail to progress in treatment should be referred to a multidisciplinary or behavioral pain management program.85,86 Factors that may predict the failure of an interdisciplinary program in returning the individuals to work include those patients involved in compensation claims and those with a subjective feeling of being disabled.87,88

Functional phase In the functional phase, progression of trunk strengthening is emphasized. Exercises with gym balls, rotational patterns, and eccentric loading of the spine are emphasized (Fig. 90.2). Rainville et al.77 and Cohen and Rainville89 have reported the use of aggressive quota-based exercise programs with the intent of reducing disability and altering fears about functional activities. Their results demonstrate that this is an effective treatment strategy in patients with chronic pain. Improvement in pain intensity and frequency, posture, self-efficacy with activity, and well-being, in addition to increased return to work status, have been documented 6 months to 1 year following rehabilitation.90–92 Finally, normal spine mechanics for sports and work activities and progression of functional training is required prior to allowing the athlete to return to competition or the individual to return to full activity.

Fig. 90.1 Transverse plane rotational exercises. 996

Section 5: Biomechanical Disorders of the Lumbar Spine

Table 90.6: Rehabilitation of Back Injury – Functional Phase 1. Analgesic medications 2. Power and endurance exercises 3. Increase multiple-plane neuromuscular control exercises 4. General flexibility program

low back pain. More studies are required prior to recommending their widespread use.99–101 Another factor to be considered during the rehabilitation process is modification of activity and the work environment. Simple strategies such as establishing a standing rest period after sitting for 50 minutes to 1 hour has been shown to reduce the compressive load on the lumbar spine.102 In addition, avoidance of prolonged flexion and rotation activities during the rehabilitation process should be encouraged.

5. Trunk and extremity strengthening program

SUMMARY

6. Injection techniques

Rehabilitation of axial back pain requires comprehensive knowledge in the areas of epidemiology, anatomy, biomechanics, and pathophysiology of the disease process. This knowledge combined with a thorough history, physical examination, and diagnostic evaluation will allow the clinician to reach a complete diagnosis that includes the suspected pain generator and the functional deficits. This information is necessary to establish a rehabilitation plan that treats the patient’s symptoms, corrects the biomechanical deficits, allows return to normal function, and improves the quality of life. The rehabilitation program is divided in three separate phases with each one having specific goals. The acute phase has the goals of reducing the patient’s symptoms and protecting injured tissues; the recovery phase has the goals of allowing tissue healing as well as achieving normal strength and flexibility; and the functional phase has the goals of correcting abnormal biomechanics as well as returning the patient to normal function and preventing long-term disability. Components of the rehabilitation program that have been shown to be effective in the acute treatment of back pain include a short period of bed rest, low-level physical activity, patient education, and medications. In the recovery phase, flexion and extension exercises, stabilization training, and core strengthening programs have been shown to be clinically successful. Treatment strategies that have been effective in the functional phase include quota-based strengthening exercises and interdisciplinary rehabilitation in patients that fail other treatment options. Therapeutic modalities, manual techniques, and complementary medicine treatments are used based on their clinical effect with reported good results in the short-term management of back pain. However, in well-controlled, randomized clinical trials, there is a lack of scientific validation of their effects in the long-term care of patients with back pain.

7. Work modification 8. Improvement in sports specific techniques

Lumbar supports and braces have been used with the goal of preventing either the onset or recurrence of low back pain. However, the medical literature has not shown effectiveness for this intervention.93–95 In a rehabilitation program, lumbar supports may be used to provide short-term patient comfort, allow participation in an exercise program, and enhance trunk proprioceptive training.96 Special consideration should be given to the use of bracing in patients with axial back pain suspected of having spondylolisis.38 Interventional and injection techniques should also be considered in this stage of patient management. Butterman has used spinal steroid injections for degenerative disc disease in patients with chronic symptoms and acute exacerbations for temporary improvement in pain and function that allows return to activity.97 Zygapophyseal joint injections and radiofrequency denervation for the treatment of patients with zygapophyseal joint-mediated pain can also be considered in the functional phase. Sparse scientific evidence for the long-term effectiveness of these treatments has been evaluated by Slipman et al. in a critical review of the medical literature. However, these treatments remain viable options in the individual with posterior element symptoms and activity intolerance.98 Other techniques that are used for chronic low back pain and have gained recent acceptance include botulinum toxin injections and prolotherapy. Although these treatment are safe, with good anecdotal results when used for addressing the soft tissues as pain generators, there is no scientific evidence documenting their effectiveness in the treatment of chronic

Fig. 90.2 Advanced stabilization exercises. 997

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Interventional techniques should be considered part of the rehabilitation armamentarium and integrated into the different stages of treatment. They should be used to reduce pain in the acute phase, to allow an increase in activity tolerance in the recovery phase, and finally to manage symptoms exacerbation in the functional phase of rehabilitation.

27. Martin MD, Boxell CM, Malone DG. Pathophysiology of lumbar disc degeneration: a review of the literature. Neurosurg Focus 2002; 13(2). Online Available: http://www.medscape.com/viewarticle/442440

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain

CHAPTER

Manipulation and Manual Methods

91

John J. Triano

INTRODUCTION Central axis pain is, perhaps, the core enigma of spine disorders. The diagnosis is one often made by exception and involving many forms of trial therapy before conclusion. Like all other sources of spine pain, the diagnosis may be confounded by the presence of other potential pain generators that have overlapping clinical and physical symptoms. Discogenic pain has variable presentation from primary, centralized aching spinal and paraspinal pain to bizarre sclerotomal pain of the lower extremities. Severity may wax and wane as patients undergo differing levels of weight-bearing load to their spine with episodes of overstrain to the disc material. Various forms of treatment from medication to spinal manipulation give relief that is temporary. Exercise may be relieving or aggravating. In a retrospective study, Smith and colleagues1 noted that 68% of patients with positive discography improved without surgery over a 4-year interval while 24% deteriorated. Some patients require more treatment to relieve their suffering than others. However, weight-bearing and activity intolerance is a consistent pattern among the various presentations of central axis pain. This section will discuss the foundation and application of spinal manipulation from a chiropractic perspective in the management of central axis spine pain. It is, perhaps, an axiom of today's healthcare environment that the approaches in spine care between chiropractors and allopathic physicians are perceived to somehow be diametrically opposed to each other. Such perceptions are the legacy of the sociopolitical conflicts of the twentieth century and its remnants that persist even today. This discussion contends that the facts of patient care make the approaches complementary and demands a greater need for integration of efforts by all providers to achieve the broadest benefit for patients. No more obvious a point of distinction is available than that of the treatment of discogenic, central axis pain syndromes. The key purposes for providing treatments (Fig. 91.1) are to relieve suffering, improve function, and maximize healing capacity. The nonoperative allopathic methods most often employ biochemical mediators to manage symptoms, followed by biomechanical interventions to modify loading of the spinal tissues to reduce local stress concentrations and strengthen core muscles while maximizing pain-free flexibility. The chiropractic methods seek to minimize or alter local physical tissue stress through the use of applied forces and moments, followed by interventions to modify behaviors that load the tissues, strengthen muscle and increase trunk stiffness, and improve painfree flexibility. Should either approach be insufficient, a surgical consultation can be considered. The practical difference, ignoring the debates over disciplinary jargon, is the relative emphasis on the best means to reduce tissue stress, inflammation, and pain. The allopathic view relies heavily on chemical intervention to block pain and suppress inflammation followed by efforts to reduce tissue stress. The

Allopathic methods

Chiropractic methods

Analgesics, anti-inflammatory, fomentation, injections

Manipulation, continuous passive motion, mobilization, neuromuscular therapy, herbal preparations, fomentation

Symptom control:

Patient activation: Assurance, resume activity to tolerance, patient education Rehabilitation: Flexibility exercise, muscular endurance & strengthening Maximum benefit Discharge to episodic management

Surgical consult, lifestyle modifications, chronic pain management

Fig. 91.1 Convergence of approach in the management of discogenic, central axis pain syndromes for chiropractic spinal manipulation versus allopathic disciplines.

chiropractic view prefers to alter the mechanical environment, allowing inflammation and pain to subside. Patients often consult both types of care simultaneously without disclosing to either. Increasing professional interactions between the groups suggest that a meaningful number of cases may benefit from both approaches. Only in recent years has there been quantitative evidence to understand the mechanical lesion treated by manipulation as well as the effects of the treatment itself. Moreover, the evidence suggests how the ‘subluxation lesion’ may contribute to symptom episodes in patients with discogenic pain. Spinal manipulation is a mechanically applied therapy used to relieve nociceptive pain and improve function. A number of clinical and physiological effects are known2–4 and their attributes require appropriate and skillful application to achieve safe and successful outcomes.5–9 The clinical benefit from use of these procedures has been studied10,11 in subacute and chronic back pain cases, a heterogeneous 1001

Part 3: Specific Disorders

population of patients including many with central axis pain. This chapter will discuss the theoretical underpinnings of spinal manipulation and its use in the management of central axis pain.

THE BASIS OF SPINAL MANIPULATION The lesion

Load step

Spinal manipulation is the use of controlled forces and moments applied to the spine or pelvis. Application of the loads may be manual or mechanically assisted. The intention of load application is to reduce local stress concentration within the intervertebral articulations and disc, improve function, and to reduce the associated local and, when present, remote symptoms. The mechanism of the manipulable spinal lesion is characterized biomechanically as a buckling event. These phenomena have been observed in orthopedics for some time among some patients with an unstable wrist carpus12,13 and are associated with multiarticular kinetic chain systems like the spine that rely on biarticular muscles for establishing local mechanical equilibrium and control. Detailed review of the biomechanics of these lesions can be found elsewhere.14–16 Briefly, buckling may involve single functional spinal units or an entire spinal region. They are caused by a mismatch in timing or amplitude of response between the local and regional muscular control systems (Fig. 91.2). A local shift of intersegmental joint configuration occurs within the bounds of normal range

that is disproportionate to the task at hand. Symptoms arise from the increase in local tissue strain. The clinical presentation of the patient and the exact symptoms depend on the identity of the tissues strained to injury threshold and the presence of comorbid conditions. The mismatch between the demand of spinal load and appropriate local intersegmental stiffness results in a sudden shift in relative joint configuration (Fig. 91.3). That is, there is a disproportionate repositioning of the joint within the bounds of its normal functional range. Instead of supporting the patient's posture and activity with minimum local tissue strain, the new configuration may result in a local stress concentration leading to symptoms of the involved tissue. Effectively, while the buckled equilibrium may be functional, it is with increased cost in terms of comfort. These types of buckling phenomena have now been observed under biomechanical testing conditions in vitro for isolated segments17–19 as well as the lumbar region20 and, by happenstance, during experimental studies of weight lifters when an unexpected injury occurred.16,21 The factors associated with development of local buckling are found in Table 91.1. Prior injury or degenerative disease potentiates buckling, allowing it to occur more easily, effectively lowering the critical load requirements and reducing the ultimate load capacity. Figure 91.4 describes the chain of events leading to symptoms.

0

0.5

1

1.5

2

2.5

3

Angular displacement (deg) Fig. 91.3 The mismatch between the demand of spinal load and appropriate local intersegmental stiffness results in a sudden shift in relative joint configuration.

Regional control muscles

Local control muscles

Table 91.1: Etiologic factors for local joint buckling events based on available biomechanical experiments in vitro and in vivo15,16

Fig. 91.2 Dual spinal stabilizing muscle systems. (Left) Regional stabilizers drive overall postural configurations to perform tasks. (Right) Local stabilizers coordinate intersegmental stiffnesses and movement to minimize joint structural stresses. Bergmark (1987) and McGill (2002). 1002

Causative

Facilitating

Sudden incremental load after prolonged static posture

Vibrating environments

Unexpected load

Disc damage

Rapid load events (500 lb/sec) Uncoordinated/fatigued effort

Section 5: Biomechanical Disorders of the Lumbar Spine

governing diagnostic interpretation is the partitioning of patient response to applied loads into categories of those that relieve or those that aggravate symptoms. Results that reduce symptoms and any referred or radicular pain components are the desired motions for directing the choice of procedure and the application of manipulative methods. Joint or nerve blocks may be helpful in identifying the pain generator (facet, sacroiliac, or nerve root) and quelling local inflammatory responses that may be interfering with patient recovery. Therapeutic trials provide an inexpensive and timely means to evaluate manipulation as a treatment option. Patients who are good candidates tend to show rather quick symptomatic response, resulting in noticeable improvement generally within a 2-week interval from onset of care.

Manipulable lesion (buckling)

Stress concentration

Neurogenic pain

Non-neurogenic pain

Inflammation

Neural sensitization

Local segmental/ central axis pain

Radicular/ pseudoradicular symptoms

Manipulation skill and control factors

Reduce response threshold

Sensitization to normal motions

Fig. 91.4 The chain of events leading to symptoms.

Diagnostic findings The determination of a manipulable lesion in isolation is relatively straightforward but is made more complicated by the presence of other pathology. Table 91.2 provides a review of findings warranting a trial of spinal manipulation. Unraveling symptoms that may respond to manipulative methods, however, is easily achieved through a trial therapy interval. Provocative testing can be used to identify the specific directions of loading that give comfort and relieve symptoms. Such maneuvers guide the selection of treatment procedures that match patient needs. These maneuvers apply controlled forces and moments, often involving postural positioning or tasks, to the suspected dysfunctional joint. Based on knowledge of any comorbid pathoanatomical diagnosis and associated findings (palpation sensitivity, flexibility, orthopedic/neurologic testing and imaging/laboratory test results), initial trials of provocation are performed in an effort to reduce local tissues stress. The principal

Table 91.2: Signs and symptoms of the isolated manipulable lesion Local back pain with or without limb pain absent progressive neural signs Focal sensitivity to manual pressure Local muscular hypertonicity with or without tender points Limited joint compliance in mid-range position and/or end-range limitations with pain on overpressure testing Reproduction of symptoms with joint compliance or end-range motion testing Local soft tissue edema Altered local skin turgor, temperature or color

Manipulation, like all other therapy, must be performed using sufficient skill and knowledge. Applications include the ability to use thrusting and nonthrusting techniques where appropriate, which requires an in-depth clinical assessment and differential diagnosis.22 Used in trained hands, these methods are remarkably safe.23–25 Evidence shows that minimally skilled individuals are ineffective in producing good outcomes6 with recovery from a symptomatic episode. Efforts to extend one's practice into the field of manipulation based on superficial weekend training programs may be pedagogically wrong and potentially dangerous.26,27 Effective treatment needs to be administered with sufficient threshold, dosage, and duration using appropriate procedures that account for patient stature and coincident pathology. Threshold is defined as the application of necessary and sufficient joint load to effect a change in its behavior and symptoms. Threshold levels are a function of patient joint stiffness, soft tissue viscoelastic properties, and muscular tension that may vary themselves, based on age, severity or acuteness of symptoms, and patient anxiety levels. Assessment of tissue condition to guide application of the procedures is a skill developed through supervised practice and experience. In cases where there are multiple tissue elements involved (e.g. reactive muscle tension, capsular swelling, adhesions, hemorrhage), sequential procedures may be necessary. Staged procedures can speed the removal of local fluid or breakdown interstitial adhesions without exceeding patient tolerance for more severely injured or sensitive tissues. Choice of treatment modality is dependent on the presence or absence of pain during the examination (provocation testing). Empirically, patients with localized pain seem to respond better to impulse loads as long as the preliminary joint positioning can be engaged without difficulty.22 Patients who are unable to be effectively positioned or have chronic or referred pain may initially benefit more rapidly using procedures without impulse. Effective dosage and duration of therapy varies with patient cooperation on reducing aggravating factors, performing recommended exercises to gain stability, the presence of other pathology or degenerative change, and condition severity. In general practice, initial treatment dosage is 2–3 sessions per week. Haas et al.28 have shown a direct relationship between treatment frequency and outcome scores for pain and disability for patients with chronic low back pain. A statistically significant linear relationship noted greater improvement for patients treated 3–4 times per week over a 3-week period. Across the literature, the average number of treatment sessions to maximum improvement for uncomplicated cases ranges from 8 to 18 with a range of approximately 1–40 treatments, depending on complexity and complications.29,30 1003

Part 3: Specific Disorders

TREATMENT METHODS Manual therapy concerns itself with the treatment of functional disturbances of muscle and joints including their local or remote symptoms. There are a number of ways in which manual therapy has been divided for discussion. Manipulation is a specific form of manual method that uses rapid impulse loads to the body structures. Manipulation can be quantitatively differentiated from other methods on the basis of speed of application14 and the differing response of the body tissues to rapid loading. While many systems of manual treatment methods exist, including manipulation, the common factor is the controlled application of loads (forces and moments) to the spine. The various approaches may be most easily understood when broken down into their biomechanical control parameters. Such classifications also help to align treatment objectives to therapeutic goals. That is, the body's biomechanical response to load application will depend on tissue properties and their reserve viscoelastic and stiffness characteristics. The various procedures span a spectrum of force and moment amplitude, speed, and direction of application that are designed to influence joint and disc strain and normalize mobility. The therapeutic loads can arise from two primary sources. They are generated either by action of the treating physician or from patient muscle action (stretching, relaxing, or contracting) under the guidance of the provider. Depending on the clinical discipline base (chiropractic, osteopathy, or manipulative medicine) of the provider administering these procedures, the specific name will vary (Table 91.3). Guided patient muscle action may be termed neuromuscular therapy, muscle energy, or counterstrain maneuvers. Provider-induced motions are typically characterized by repetition rate, speed, and amplitude and fall under the terms manipulation or adjustment and mobilization. Finally, various assistive devices that may be used to control the patient motion direction, rate, and amplitude are termed mechanically assisted procedures. These latter may be coupled with manipulation methods to provide motion assisted manipulation procedures.

Guided patient muscle activation Neuromuscular therapy (NMT) utilizes direct muscle action as well as associated neuromuscular reflex mechanisms to improve mobility and normalize muscle tone. Its action is based on the principle that inhibited or weakened agonists or competition of hypertonic antagonists may limit joint function. For example, spinal motion of rotation may be limited by inhibited contralateral transversospinal groups or by shortened ipsilateral transversospinal muscles. The pattern is determined by provoking local joint motion and determining its relative compliance in a direction and contrasting that with the presence of muscle tenderness and relative hypertonicity.22 There are three types of NMT, their use being dependent on whether the desired effect is to relax hypertonic agonists or strengthen them or to relax hypertonic antagonists as noted below. NMT1: Agonist muscle considered weakened or hypotonic. 1. Engage the functional motion barrier; 2. Select appropriate agonists; 3. Teach agonistic tension in the direction of movement to direction to increase the joint flexibility; a. Use passive motion to help position the patient; b. Use cutaneous stroking/tapping to facilitate muscle recruitment; 4. Homecare: 2–5-second repetitions.

1004

NMT2: Postisometric relaxation of shortened, tonic antagonists muscles 1. Passively stretch the shortened muscle limiting the motion; 2. Hold and have the patient isometrically contract the agonist muscle in a direction to increase the joint flexibility; 3. Gently stretch further during postisometric relaxation phase for 3–10 seconds; 4. Repeat steps 1–3 from the new position up to 4 cycles; 5. Homecare: muscle stretching for phasic and tonic muscles. NMT3: Mobilization using reciprocal inhibition of the antagonists 1. Identify the shortened muscles restricting motion; 2. Use NMT3 if contraction of the shortened muscle is painful (often when radicular pain is present); 3. Passively position at the functional barrier; 4. Contract in direction of motion restriction for 5–10 seconds; 5. Use manual mobilization (see below) in the same direction. Muscle energy techniques are essentially the same as NMT1. Counterstrain, on the other hand, is a different approach, based on the effort to shorten muscles that are tense in association with defined, painful trigger points that are palpated as tense nodular areas of soft tissue of reduced compliance. The painful point may reside in the muscle or be at a referred site typical for each muscle. The operator positions the joint to shorten the affected muscle and produce mild strain in its antagonist. The position continues to be refined until the local area of tenderness is reduced or disappears. The position is held for about a minute and a half to give time for proprioceptive adaptation within the muscle. When the tenderness has been resolved and position held for sufficient time, the limb is slowly returned to a neutral joint position so as not to introduce a rapid stretch to the previously sensitive stretch reflex receptors. These methods are often used for patients with acute strain injury and locally tissues to direct loading. They are also considered useful in older or frail patients. Whereas the action of NMT procedures is directed in altering joint mobility through muscle action (stretching, relaxation, and isometric tensing), the mechanism of muscle energy and counterstrain is believed to be more associated with the effects of direct alteration of muscle tone. As noted by Murphy31 the restoration of joint functional range and normal muscle tone arises from several hypothesized benefits. They include relaxing hypertonic muscle to decrease oxygen demand and local pain, increasing circulation to the area to wash out metabolic waste products, and promoting greater venous and lymphatic drainage to reduce edema.

Provider-induced loading Loads applied by the treating doctor to the patient's spine are controlled in terms of their speed, amplitude, displacement, frequency, duration, and direction. They may be induced manually, through use of instrumented treatment tables and devices, or a combination of both. The procedures fall into categories of continuous passive spinal motion (CPM); mobilization; high-velocity, low-amplitude (HVLA) thrusting techniques, and mechanically assisted procedures (see Table 91.3). Slow, externally applied procedures such as continuous passive motion (CPM), mobilization methods, and flexion distraction techniques result in decreasing internal disc pressures,32 as shown in Figure 91.5. Other benefits include the dispersion of local edema,15,33 prevention or disruption of joint adhesions and stimulation of connective tissue healing34–36 within functional limits. The slow, cycled motions influence time-dependent viscoelastic characteristics within the affected tissues, shifting fluid between various body compartments.

*

Manual + mechanical Manual + mechanical

CPM + HVLA Impulse hammers

Mechanically assisted HVLA

Manual

Manual

HVLA

Manual

Grades I–IV Manual

Manual

Flexion-distraction (F/D)

Flexion–distraction + auxiliary pressures

Mechanical

Continuous passive motion (CPM)

Agonist & Antagonist

Mobilization

Unloaded spinal motion

Counterstrain

Agonist muscle

Agonist muscle

NMT 3 (Analogous to NMT 1)

Antagonist muscle

Agonist muscle

NMT 1 NMT 2

Application

Subcategory

BW, patient body weight; ** BMI, patient body mass index.

Provider-induced loads

Neuromuscular therapy

Guided patient muscle action

Muscle energy

Category

Therapeutic loading source

Impulse

Periodic+high speed / impulse

High speed / impulse

Periodic / cyclic

Periodic / cyclic

Single, short duration impulse (<20 msec); focused small relative displacements, very low–low load, simple load vectors, uniaxial load vectors

Superimposed, CPM augmented HVLA

Single impulse (32–140 msec), focused small relative displacements, low to high load, complex load vectors

Very low speed (0.0–0.5 Hz), large multisegmental displacements, intermediate load, complex load vectors

Low speed (0.50–2.00 Hz), large multisegmental displacements, intermediate (?) load, complex load vectors

Very low speed (0.0–0.5 Hz), large multisegmental displacements, low load, complex load vectors

Very low speed (0.0–0.5 Hz), low load (<20% BW*, <5% BMI*), large multisegmental displacements (angular), complex load vectors (sagittal, frontal, axial) possible

Periodic / cyclic

Periodic / cyclic

Joint positioning for maximum comfort and relaxation of affected muscles

Isometric contraction of agonist muscle for direction of increased flexibility

Reciprocal inhibition of antagonistic muscles to direction of intended increased flexibility

Postisometric relaxation of muscle antagonistic to direction of intended increased flexibility

Isometric contraction of agonist muscle for direction of increased flexibility

Characteristics

Muscle relaxation

Tensile muscle loading

Tensile muscle loading with joint at functional barrier

Stretch > contract > stretch

Tensile muscle loading

Type of Load

Table 91.3: Loading source, category, and characteristics of types of manual treatment procedures

Section 5: Biomechanical Disorders of the Lumbar Spine

1005

Part 3: Specific Disorders

A

mmHg

600 400

Intradiscal pressure

200 0

Degrees

−4

Table motion

−6 −12 20 seconds B

Fig. 91.5 Flexion–distraction and CPM methods both passively move the spine while in an unloaded, recumbent posture. Intradiscal pressures are reduced with the downstroke of the table. (Intradiscal pressure recording courtesy of M.R. Gudavalli.)

Pulsed procedures include high-velocity, low-amplitude (HVLA) methods that impart a rapid thrust to the body segments bounding the joint of interest and transmitting forces and moments through the vertebral disc and surrounding structures. These methods tend to more quickly influence relative functional restrictions in vertebral motion and local tissue strains. In general, where a patient can be comfortably positioned for these procedures, they are considered by some to be more effective in achieving a more quick clinical change in the patient's condition.22 Formal training in HVLA methods requires intense rehearsal of a series of procedures for each region of the spine. The names of the procedures, once again, may vary based on the discipline in which the doctor has been trained. Once familiar with the basic procedures, skilled providers can frequently modify procedures to meet individual clinical needs under unusual and novel circumstances to provide safe and effective treatment. With the exception of the contraindications noted in Table 91.7 (below), the presence of local pathology or prior surgical intervention is not a contraindication to use of manipulative methods. The skilled provider can modify procedures to accommodate the pathology or can elect nonpulsing methods as may be appropriate. Procedure modifications include the selection from the various procedural options, adaptation of applied forces, moments and motions, as well as variation of patient postures. Triano and Schultz7 demonstrated effectively that the specific load components acting on the spine can be increased or decreased accordingly through strategies that combine these factors. For the most common system of manipulation used by chiropractors, the diversified method, there are as many as 45 different approaches to the lumbar spine, 17 to the thoracic, and 25 to the cervical region. Patients with disc protrusion that is aggravated by extension maneuvers may receive manipulative 1006

treatment by minimizing extension moments. In like manner, desired directions that relieve may be accentuated as necessary. Adaptation of forces and moments applied by provider-induced loading requires the adjustment of control factors (Table 91.4) enhancing or diminishing specific load components in order to accommodate stature, comorbid pathology, or postoperative changes.37 Control strategies fall into two categories. Patient factors include postural positioning to open or close the articulations of the target segments. Once positioned, the loads may be applied using static prepositioning or with dynamic oscillation manually or through therapeutic tables that mechanically assist. The acceleration of the patient's body segments induces inertial loads within the target joints that will either add to or subtract from the provider-induced loads. The operator may elect to further modify the application point, force and moment amplitudes, directions, rate, and duration. Figures 91.6A–D demonstrate examples of differing control strategies based on patient positioning. The resulting changes in loads transmitted through the targeted lumbar spine were reported by Triano and Schultz7 and are shown in Table 91.5. In Figure 91.6A, treatment to the lumbosacral spine is delivered with a combination of muscular effort through the arm and use of upper body mass to generate the applied loads. The patient has been positioned without any lateral bend or twisting of the torso. This strategy will create, within the targeted level, a relatively low flexion moment while boosting the tendency for lateral shear and lateral bending. Figure 91.6B modifies the initial position by inducing a prepositioning of lumbar flexion and left axial rotation. Under these conditions, the patient’s left intervertebral foramen and zygapophyseal joint will be maximally opened during the impulse delivery. Figure 91.6C uses the same patient positioning as in Figure 91.6B but a different loading application point. This procedure, originally conceived as treatment of the sacroiliac joint, accentuates flexion moments at the lumbosacral region while providing relatively little anterior shear and a moderate level of additional lateral bending or rotation component. Finally, Figure 91.6D demonstrates the use of a long-lever maneuver that alters how the provider uses his/her body mass to affect loading of the spine. Here, the application of load to the lumbosacral segments is derived through arm action as before but with pressure from the hip acting through the patient's flexed femur. This strategy will accentuate spinal axial rotation, depending on the degree of patient prepositioning, while moderating or minimizing all other components. While knowledge of the control strategies is helpful, their application comes from understanding of manipulation dynamics and how the loads are developed. The total load acting on the target joint is

Table 91.4: Control strategies for provider-induced loading manual methods Patient-based factors

Provider-based factors

Patient posture

Preload amplitude

Initial conditions

Load direction

Static posture

Load peak amplitude

Dynamic motion

Load impulse rate

Mobilization

Load duration

Mechanically assisted

Transient pulse Sustained

Section 5: Biomechanical Disorders of the Lumbar Spine

A

B

C

D

Fig. 91.6 (A) Treatment applied to the lumbosacral segments using a patient positioning strategy to provide low flexion moment and higher lateral shear and lateral bending. See the text for details. (B) Positioning to maximally open the left intervertebral foramen and zygapophyseal joint by adding torso flexion and left axial rotation to the procedure shown in Fig. 91.6A. (C) A pelvic procedure applied through the ischial tuberosity may be used to treat the sacroiliac joint or to modify loads acting on the lumbosacral spine by enhancing flexion moment, limiting anterior shear. (D) Long-lever procedures apply operator body mass differently than those in Figs 91.6A–C. Body mass is applied here through the contact between the provider's hip and the patient's flexed thigh.

the sum of the applied forces and moments with the inertial forces and moments derived from the motions induced by the patient's body segment masses. A third factor is the relative muscular activity surrounding the joint which can attenuate the loads transmitted, acting either as dampers if tight during the delivery of the procedure or as an after-load if contracting in response. Table 91.6 relates the characteristics of the loads themselves as dependent factors to the parameters that influence them as independent factors. For the purposes here, intrinsic muscle action is assumed as an insignificant value, an ideal sought by each provider through various relaxation techniques.

Motion-assisted methods are also available that couple CPM and HVLA methods (Fig. 91.7), taking advantage of momentum to either amplify or diminish the amplitude of loads passing through the targeted joint system while preserving the speed effects. Therapeutic joint loading may also be accomplished through the directed application of patient positioning and internal muscular action. Termed neuromuscular therapy (NMT) in European medical circles,22 or divided into categories of muscle energy and counterstrain techniques in North American osteopathic practice, these methods focus patient effort to assist in resolving local tissues strains. 1007

Part 3: Specific Disorders

Table 91.5: Manipulation load components organized by hierarchy in producing individual load components7 Loading action at the lumbosacral segments

Hierarchy of effectiveness (procedure + initial patient position yields load amplitude)

Flexion

MPar = HIar >LLar >LLur = MPur > HIur

Rotation

LLar = MPar > HIar

Lateral bending

HIur > MPur >LLur = HIar > MPar > LLar

Lateral shear

HIur > MPur = HIar >LLur > MPar > LLar

Axial compression

HIar > MPar > LLar

Anterior shear

MPar > MPur >LLur = LLar > HIar > HIur

Procedures: MP, mammillary push procedure; HI, hypothenar ischium; LL, long lever. Patient positioning: ar, axially rotated; ur, unrotated.

DIAGNOSTIC INDEPENDENCE OF MANIPULATION Significant cross-discipline confusion exists regarding the issue of pathoanatomical diagnosis. The disarray of thought revolves around two factors. First is the failure of the medical model to adequately predict treatment outcomes as a function of pathoanatomical diagnosis.38 The second is the continuing inability to quantitatively measure the manipulable lesion (buckling event) in a clinical setting. Spine dysfunction and disease is a continuum of interrelated severity and stages that may arrest with local healing or progress based on many

extrinsic and intrinsic variables. Despite the occasional clarion calls for a ‘specific diagnosis’ to drive selection of treatment for a predictable outcome, widespread evidence shows that only the extremes of some pathology reach that level of predictability. For the remainder, significant proportions of the population have abnormal structure on X-ray or advanced imaging that is clinically silent. Others with no identifiable abnormality suffer serious activity limitation because of pain. Likewise, patients with asymptomatic pathoanatomy may become symptomatic under given circumstances. These factors were discussed under the section on the evidence of buckling as the mechanism of the spinal lesion. Both those with pathoanatomy and those without are included among those patients who may benefit from use of manipulation methods in their care. Providers skilled in performing manipulation deal with biomechanical relationships among different tissue components. Pathoanatomical diagnosis, while unable to drive specific treatment successfully, remains an important part of treatment planning. Knowledge of existing pathology, along with information from the patient's examination, form a significant part of the treatment plan. The intent is to alter local tissue strains, particularly at the suspect pain generator, reducing pain and fostering normal healing as necessary. Thus, the tissue involved, local geometry, and pathomechanics form the starting point for procedure selection. The final procedure results from the feedback of provocation testing. The objective of altering local tissue strains, then, forces the doctor to view diagnosis differently. It is less from a classical perspective and more as a means of anticipating necessary modifications. For example, presence of degenerative spondylosis or a disc bulge narrowing the lateral recess will cause the provider to identify patient positioning for delivery of the treatment that will facilitate a maximum volume of the canal and recess. Similarly, patients with radicular syndrome must be positioned and treated using methods that decompress the offended

Table 91.6: Factors governing the development of load parameters during HVLA spinal manipulation Independent factors Postural configuration Phase

Dependent factors

Patient

Operator

Gravity

Muscular effort

Inertial load

Amplitudes**

−

+

+

+

−

Directions

+

+

−

+

−

−

−

+

+

−

−

−

−

+

−

Preload procedure setup ***

Magnitudes

*

Stability* Dynamic impulse Amplitudes**

−

−

+

+

+

Cycles

−

−

+

+

+

Directions

***

Durations Magnitudes Slopes

**

*

*

+

+

+

+

+

−

−

−

+

+

−

−

+

+

+

−

−

+

+

+

There are four magnitude quantities: 2 for loads (force & moment) & 2 for slopes, which are equivalent to the speed of force and moment development. ** Each factor has six components (3 forces & 3 moments). Only two of the three components are mathematically independent as they are mechanically coupled to the magnitudes by the equation M = (C12 + C22 + C32). *** There are six direction components (3 force & 3 moments) which may be defined as positive or negative with respect to a reference frame. From: Triano JJ, Rogers CM, Combs S, et al. Developing skilled performance of lumbar spine manipulation. J Manip Physiol Ther 2003; 26:539–548.

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Section 5: Biomechanical Disorders of the Lumbar Spine

A 500

400

Newtons

300

200

Review and best evidence synthesis of the English and Northern European literature on randomized trials by Bronfort and colleagues11 summarizes the information on utility of manipulation methods in contrast to sham and alternate treatments. For acute episodes, there is moderate evidence that HVLA provides more short-term pain relief than mobilization methods and detuned diathermy, and limited evidence of faster recovery than a commonly used physical therapy treatment strategy. For patients with more chronic pain, HVLA has an effect similar to11 or better than10 use of nonsteroidal antiinflammatory medication. It is effective in the short term when compared with placebo and general practitioner care, and in the long term compared to physical therapy. There is limited evidence that HVLA is superior to chemonucleolysis for disc herniation in the short term. Triano et al.,43 in a small sample of patients, showed evidence that painful internal disc derangement on CT discography will respond with symptom reduction using HVLA procedures. In a trial contrasting the effects of medication management versus manipulation, Giles and Muller10 showed that the highest proportion of early suppression of symptoms was found for manipulation at 27.3% with medication achieving 5%. In those not reaching asymptomatic status, manipulation achieved the best overall results as reported by pain scales, Oswestry scores, and range of motion. However, the data do not strongly support the use of only manipulation or only nonsteroidal antiinflammatory medication for the treatment of chronic spinal pain.10 As evidenced by patients who often elect to consult medical providers and chiropractors simultaneously without informing either, there appears to be a synergistic effect from both.

CASE EXAMPLES 100

0 −100 B Fig. 91.7 Measures of the summation effect of superimposing the momentum of CPM (lower trace) with the HVLA procedure (upper trace sums HVLA + CPM) at the lumbosacral junction.

nerve and are generally identified by those postures that are relieving rather than provoking of discomfort. Only those patients with distinct contraindications cannot undergo a trial of manipulation.

TREATMENT EFFECTIVENESS As in all other forms of treatment, the Hawthorne or placebo effect plays a role in treatment outcome. In numerous studies, chiropractic patients record greater satisfaction with their treatment experience than when they are attended by other providers,39,40 an observation often triggering the assumption of placebo as the sole operational mechanism. At least two controlled clinical trials have addressed the question of placebo effect directly.41,42 In both studies, all treatment groups showed improvement over time. However, the patients receiving thrusting procedures demonstrated significantly greater and more rapid rates of improvement from their symptoms and in their ability to function than in the control group. While physician attention, in any form, appears to benefit patients with back pain, the data also shows that, at least for thrusting techniques of manipulation, there is a treatment-specific advantage beyond the non-specific effects.

Figure 91.8 shows the discogram of a 36-year-old female patient with chronic low back pain onset following a heavy lifting incident 6 months earlier. Medical management and physical therapy procedures had failed. An intradiscal electrothermal therapy procedure was attempted following discography, yielding 2 months of pain relief. With renewed symptoms, she became increasingly weightbearing and activity intolerant with low back and pseudoradicular leg pain. Her range of motion, particularly in flexion, was limited to 30 degrees. The spinous processes of L4 and L5 were tender and there was significant muscle tone asymmetry in the paraspinal group and quadratus lumborum. Efforts to test midrange joint compliance reproduced pain when extension, right bending, or axial rotation provocation was attempted. The patient was initially treated with in-office prone CPM in flexion with left lateral bending (Fig. 91.9) followed by left lateral decubitus position using left lateral bending CPM coupled with flexion (Fig. 91.10). As CPM methods helped reduce immediate discomfort, motion-assisted HVLA was applied with the patient in left lateral decubitus posture with CPM in right lateral bending. Home exercise focused on flexibility in range of motion and spine stabilizing exercises. She experienced good relief of symptoms and a gradual return to normal activities of daily living over a period of 7 weeks. The patient remained sensitive to heavy lifting, push–pull tasks, and sudden or awkward trunk postures. Over a 3-year period, she has experienced decreasing frequency of episodes at 1–2 per year requiring 1–2 weeks of treatment.

SAFETY AND CONTRAINDICATIONS No discussion of the use of spinal manipulation would be complete without addressing the issue of safety. Rare reports of adverse effects from spinal manipulation to the lumbar spine have been recorded.24 Based on the rate of utilization for these procedures in 1009

Part 3: Specific Disorders

A

B

Fig. 91.8 Internal disc derangement at L4–5 by discogram showing a fissured disc from annular tears anteriorly and at the 3 o'clock position with extravasation.

Fig. 91.10 Left lateral bending with left lateral decubitus CPM. (From Bougie and Morganthal, with permission Triano J. 2001.) Fig. 91.9 Prone CPM in flexion with left lateral flexion coupling. (From Bougie and Morganthal, with permission Triano J. 2001).

CONCLUSIONS the reported literature, the incidence of serious complication is negligible (<1:107). Cauda equina syndrome is the most serious adverse event suspected to follow spinal manipulation, with less than 30 cases reported since the early twentieth century. The proposed mechanism of injury is hypothesized to be the spinal manipulative loads applied to an already significantly compromised disc. Presence of undiagnosed neurologic deficit or the appearance of progressive deficit should result in immediate cessation of treatment and further diagnostic work-up. The contraindications to manipulation are based on the pathomechanics of specific conditions rather than an extensive epidemiological database. Table 91.7 lists the relative and absolute contraindications. 1010

Spinal manipulation consists of a series of procedures of varying intensity and method of application. Its application is designed to reduce tissue strain and local affects. The manipulable lesion is a buckling event arising from the happenstance of critical loading under susceptible conditions. Superimposition on existing pathology may explain why so many members of the population have asymptomatic pathoanatomical lesions and others whose similar pathology may be symptomatic. In the case of central axis pain from discogenic sources, mechanical reduction of local stress through manipulation appears to provide relief. Coupled with use of medication as necessary, manipulation control of symptoms may facilitate reconditioning and strengthening of the trunk. Patients may be made more functional as they undergo the long process of recovery that natural history suggests for most.

Section 5: Biomechanical Disorders of the Lumbar Spine

Table 91.7: Relative and absolute contraindications to spinal manipulation with examples of exceptions Contraindications

Exceptions

Undiagnosed progressive neurologic deficit

None

Undiagnosed loss of bowel or bladder control

None

Cauda equina syndrome

None

Procedures incompatible with the direction of unstable motion

None

Bone weakening disorders

Sites distant to the pathologic site may undergo manipulation if appropriate

Primary or metastatic tumor

Sites distant to the pathologic site may undergo manipulation if appropriate

Acute fracture

Stable compression fracture of the anterior column

Bleeding disorder

Unloaded motion procedures may be used avoiding extremes of motion

Acute inflammatory rheumatoid disease or septic joints.

None

References 1. Smith SE, Darden BV, Rhyne AL, et al. Outcome of unoperated discogram-positive low back pain. Spine 1996; 21:1394–1395. 2. Herzog W. The mechanical, neuromuscular and physiologic effects produced by the spinal manipulation. In: Herzog W, ed. Clinical biomechanics of spinal manipulation. New York: Churchill Livingstone; 2000:191–207. 3. Pickar JG. Neurophysiological effects of spinal manipulation [review] [127 refs]. Spine Journal: Official Journal of the North American Spine Society. 2002; 2:357–371. 4. Pickar JG, Sung PS, Kang Y. The effect of a spinal manipulation's impulse speed on l0w-threshold mechanoreceptors in lumbar paraspinal muscles. J Chiro Educat 2004; 18:25–26. 5. Cohen E, Triano JJ, Mcgregor M., et al. Biomechanical performance of spinal manipulation therapy by newly trained vs. practicing providers: does experience transfer to unfamiliar procedures? J Manip Physiol Ther 1995;18:347–352. 6. Curtis P, Carey T, Evans P, et al. Training primary care physicians to give limited manual therapy for low back pain: patient outcomes. Spine 2000; 22:2954–2959. 7. Triano J, Schultz AB. Loads transmitted during lumbosacral spinal manipulative therapy. Spine 1997; 22:1955–1964. 8. Triano JJ, Bougie JD, Rogers CM, et al. Procedural skills in spinal manipulation: does preparation matter? Spine 2003; In submission. 9. Triano JJ, Rogers CM, Combs SB, et al. Quantitative feedback vs. standard training for cervical and thoracic manipulation. J Manip Physiol Ther 2003; 26:131–138. 10. Giles LG, Muller R. Chronic spinal pain syndromes: a clinical pilot trial comparing acupuncture, a nonsteroidal anti-inflammatory drug, and spinal manipulation [see comment]. J Manip Physiol Ther 1999; 22:376–381. 11. Bronfort G, Haas M, Evans RL, et al. Efficacy of spinal manipulation and mobilization for low back pain and neck pain: a systematic review and best evidence synthesis. Spine J 2004; 4:335–336. 12. Landsmeer JMF. Studies in the anatomy of articulation. I: the equilibrium of the ‘intercalated’ bone. Acta Morphol Neerl Scand 1961; 3:287–321. 13. Landsmeer JMF. Atlas of the anatomy of the hand. New York: Churchill Livingstone; 1976. 14. Triano J. The mechanics of spinal manipulation. In: Herzog W, ed. Clinical biomechanics of spinal manipulation. New York: Churchill Livingstone; 2000:92–190. 15. Triano J. Biomechanics of spinal manipulation. Spine 2001; 1:121–130. 16. McGill SM. Low back disorders. Human Kinetics 2002; 17. Wilder DG, Pope MH, Seroussi RE, et al. The balance point of the intervertebral motion segment: an experimental study. Bull Hosp Jt Dis Orthop Inst 1989; 49:155–169.

20. Crisco JJ III, Panjabi MM, Yamamoto I., et al. Euler stability of the human ligamentous lumbar spine. Part II: experiment. Clin Biomech 1992; 7:27–32. 21. Cholewicki J, Mcgill SM, Norman RW. Lumbar spine load during the lifting of extremely heavy weights. Med Sci Sports Exer 1991; 23:1179–1181. 22. Schneider W, Dvorak J, Dvorak V, et al. Manual medicine therapy. New York: Theime Medical Publishers; 1988. 23. Haldeman S, Rubinstein SM. Compression fractures in patients undergoing spinal manipulative therapy. J Manip Physiol Ther 1992; 15:44–48. 24. Haldeman S, Rubinstein SM. Cauda equina syndrome in patients undergoing manipulation of the lumbar spine. Spine 1992; 17:1469–1473. 25. Haldeman S, Rubinstein SM. The precipitation or aggravation of musculoskeletal pain in patients receiving spinal manipulative therapy. J Manip Physiol Ther 1993; 16:47–50. 26. Triano JJ, Bougie J, Rogers C, et al. Procedural skills in spinal manipulation: do prerequisites matter? Spine J 2004; 4:557–566. 27. Schneider G. Manual therapy techniques for the cervical spine require special skills. (Comment on Refshauge et al., Austr J Physiother 48:171–179) [comment]. Austr J Physiother 2002; 48:314. 28. Haas M., Groupp E, Kraemer DF. Dose–response for chiropractic care of chronic low back pain. Spine 2004; 4:574–583. 29. Triano JJ, Hondras M, McGregor M. Differences in treatment history with manipulation for acute, subacute, chronic and recurrent spine pain. J Manip Physiol Ther 1992; 15:24–30. 30. Haldeman S, Chapman-Smith D, Peterson DH. Guidelines for chiropractic quality assurance and practice parameters. Gaithersburg, MD: Aspen Publishers; 1993: 1–216. 31. Murphey T. Myofascial Techniques, in: DiGiovanna EL, Schiowitz S (Eds). An osteopathic approach to diagnosis and treatment. Philadelphia: JB Lippincott; 1991. 32. Gudavalli MR, Cox JM, Baker JA, et al. Intervertebral disc pressure changes during the flexion-distraction procedure for low back pain. ISSLS 1997; 165–166. 33. Triano J. Manipulative therapy in the management of pain. In: Tollison CD, Satterthwaite JR., Tollison JW, eds. Clinical pain management: a practical approach 3rd edn. Philadelphia: Lippincott, Williams & Wilkins; 2002:109–119. 34. O'Driscoll SW, Kumar A, Salter RB. The effect of the volume of effusion, joint position and continuous passive motion on intraarticular pressure in the rabbit knee. J Rheumatol 1983; 10:360–363. 35. Salter RB. The biologic concept of continuous passive motion of synovial joints. The first 18 years of basic research and its clinical application. Clin Orthop 1989; 242:12–25.

18. Wilder DG, Pope MH, Magnusson M. Mechanical stress reduction during seated jolt/vibration exposure. Semin Perinatol 1996; 20:54–60.

36. Kim HK, Kerr RG, Cruz TF, et al. Effects of continuous passive motion and immobilization on synovitis and cartilage degradation in anigen induced arthritis. J Rheumatol 1995; 22:1714–1721.

19. Ogon M, Bender BR, Hooper DM, et al. A dynamic approach to spinal instability. Part II: hesitation and giving-way during interspinal motion. Spine 1997; 22:2859–2866.

37. Triano J. Managing geriatric spine patients. In: Bougie J, Morganthal P, eds. The aging body. New York: McGraw Hill; 2001.

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Part 3: Specific Disorders 38. Haldeman S. Presidential address, North American Spine Society: Failure of the pathology model to predict back pain. Spine 1990; 15:718–724.

42. Triano JJ, McGregor M, Hondras MA, et al. Manipulative therapy versus education programs in chronic low back pain. Spine 1995; 20:948–955.

39. Cherkin D, Hart LG, Rosenblatt RA. Patient satisfaction with family physicians and general internists: is there a difference? J Fam Pract 1988; 26:543–551.

43. Triano J, Vanharanta H, McGregor M. Manipulation for painful disc syndrome. Washington, DC: NASS; 1995.

40. Carey TS, Garrett J, Jackman A. The outcomes and costs of care for acute low back pain among patients seen by primary care practitioners chiropractors, and orthopedic surgeons. N Engl J Med 1995; 333:913–917.

44. Triano JJ, Rogers CM, Combs S, et al. Developing skilled performance of lumbar spine manipulation. J Manip Physiol Ther 2003; 26:539–548.

41. Hadler NM, Curtis P, Gillings A. Benefit of spinal manipulation as adjunctive therapy for acute low back pain: a stratified controlled trial. Spine 1987; 12:703–706.

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45. Bergmark A. Mechanical stability of the human lumbar spine. 1–85. 1987. Lund University, Department of Sold Mechanics. Ref Type: Thesis/Dissertation.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain

CHAPTER

Injection Procedures

92

Rajeev K. Patel and Clifford R. Everett

BACKGROUND The natural history of low back pain has been reported to be quite favorable in some studies and is often quoted to patients as such. It has been reported that 40–50% of patients are symptom free within 1 week and up to 90% have resolution of symptoms without medical attention in 6–12 weeks.1–4 However, recent studies suggest that lumbar axial pain is a more significant condition characterized by acute exacerbations and variable periods of remission. Deyo and Tsui-Wu5 reported 33.2% of patients with low back pain reported symptoms with a duration of less than 1 month, with 33% reporting pain for 1–5 months and 32.7% reporting pain for longer than 6 months. Recurrence rates from 60–85% have been reported in the first 2 years following an acute episode of low back pain.6,7 More recently, Von Korff et al.8 observed that over a 2-year follow-up period, 44% report chronic symptoms (defined as more than 90 days of back pain in the previous 6 months). In this study, most patients were experiencing low levels of back pain with 20% rating their pain as 4 or greater on a 0–10 scale; 13% rated their current pain as 5 or greater and only 8% reported pain of 6 or greater. Furthermore, Von Korff et al.8 reported that 15–20% of primary care patients with low back pain show moderate to severe activity limitations during a 1-year follow-up period after the initial episode has resolved.

PATHOPHYSIOLOGY Descriptions of the treatment for low back pain dates to Hippocrates (460–370 BC), with the reporting of joint manipulation and the use of traction.9 It often is theorized that the onset of low back pain is associated with bipedal ambulation and that this transformation in the mechanics of locomotion is the inciting evolutionary event that has made the lumbar spine susceptible to a relatively accelerated rate of degenerative disease. Degeneration is universal to the structures that comprise the basic functional spinal unit, which is composed of two adjacent vertebral bodies, the intervertebral disc, and the two zygapophyseal (Z-) joints at the same segment functioning as a tri-joint complex. As humans age, endure various micro- and macrotraumas, and undergo changes in body habitus that alter and unevenly distribute biomechanical forces on the lumbar spine, there is a natural progression of degeneration of the lumbar motion segment with corresponding anatomic, biomechanical, radiologic, and clinical findings.10 It is this evolution that provides the insight into the root cause of lumbar spinal pain syndromes. The posterior elements of the lumbar spinal functional unit bear less weight than the anterior elements in all positions. During sitting, the anterior elements bear over 90% of the forces transmitted through the lumbar spine, whereas during standing, this fraction decreases to approximately 80%.10 As the degenerative process progresses, the

relative anterior to posterior force transmission approaches 50%.10 The spine functions best within a realm of static and dynamic stability. The bony architecture and associated specialized soft tissue structures, especially the intervertebral disc, provide static stability. Dynamic stability, however, is accomplished via a system of muscular and ligamentous supports which act in concert during various functional, occupational, and avocational activities. The overall mechanical effect of these structures maintains the histologic integrity of the tri-joint complex. The net shear and compressive forces must be maintained below respective critical minimums in order to maintain the integrity of the tri-joint articulation. Persistent, recurrent, nonmechanical and/or excessive forces to the motion segment beyond minimal thresholds leads to microtrauma to the disc and Z-joints, which triggers and continues the degenerative process.10 This degenerative cascade, as described by Kirkaldy-Willis,10 is the widely accepted pathophysiologic model describing the degenerative process and ensuing spinal segment dysfunction as it affects the lumbar spine and its individual motion segments. This process is described as occurring in three phases in a progressive longitudinal manner over time. These phases are a continuum with a gradual transition rather than three distinct, clearly definable stages. Although the etiology of spinally mediated lumbar axial pain is variable and not always clearly definable, there are a finite number of potentially painful structural components of the lumbar spine, and the aforementioned degenerative cascade provides insight on the process by which these components develop pathology and can become symptomatic.

BASIC SCIENCE EVIDENCE OF INFLAMMATORY MECHANISMS IN DISCOGENIC-MEDIATED PAIN SYNDROMES The anterior elements of the lumbar spine, most notably the intervertebral disc, are currently thought to be the primary source of the vast majority of spinally mediated lumbar axial pain syndromes. Several theories cite a traumatically induced acute annular tear as the inciting pathologic event. Others theorize the natural result of aging is the sole etiology of pathology of the lumbar disc. However, these models do not explain spontaneously occurring annular tears and disc degeneration in the young. Therefore, the cause of lumbar disc disease is most likely multifactorial. Various genetic, environmental, autoimmune, inflammatory, traumatic, infectious, toxin-induced, and other factors may alone, or in various combinations, result in the initiation and progression of degeneration of the intervertebral disc in a way that has not yet been elucidated. However, to some degree, the basic science literature has been able to elucidate the inflammatory mechanisms of discogenic mediated lumbar axial pain syndromes. In 1987, McCarron 1013

Part 3: Specific Disorders

et al.11 published a study in which they reported on the incitation of an inflammatory response upon injection of autologous nucleus pulposus into the epidural space of dogs. In addition, they reported that a delay in the treatment of this inflammatory process could result in tissue fibrosis and cellular damage. In 1990, Saal et al.12 demonstrated significantly increased level of PLA2, the rate-limiting enzyme in the arachidonic acid cascade, activity in lumbar HNP further demonstrating the inflammagenic properties of nuclear material. In 1996, further study helped elucidate the biochemical factors by which the nucleus pulposus elicits an inflammatory process. Takahashi et al.13 demonstrated the presence of inflammatory cytokines, including IL-1a+b, IL-6, TNF, GMCSF, and L-B4, in herniated nucleus pulposus (HNP). Kang et al.14 reported increased levels of MMPs, nitric oxide, IL-6, and PGF2 in the culture media of HNP. These properties may in part be explained by the fact that the nucleus pulposus, a remnant of the embryonic notochord, is sheltered from the bloodstream during embryologic development and may therefore be construed as an antigen upon presentation to the immune system when entering the ventral aspect of the epidural space.15 Subsequently, epidural steroid injections (ESI) have become commonly employed interventions in treating spinally mediated lumbar axial pain syndromes thought to be potentially due to an inflammatory mechanism based on the aforementioned basic science literature as it pertains to specific discogenic induced spinal syndromes.

EVOLUTION OF INTERVENTIONAL SPINE PROCEDURES The initial reports of epidural injections almost a century ago reported the instillation of cocaine into the epidural space to treat lumbago and sciatica. In the early 1900s, epidural injection of local anesthetic was used to treat intractable sciatica.16 In 1952, Robecchi and Capra17 reported success with the first ESI in treating lumbar and associated sciatic pain. Presently, ESIs are a commonly utilized intervention in the management of spinally mediated lumbar axial syndromes both with and without associated radicular symptomatology. Several studies have shown that up to 40% of blind (nonfluoroscopically guided) ESIs may erroneously deliver the injectate superficially into the soft tissues or inadvertently deep into the subarachnoid space, which may result in serious complications.18–21 Therefore, we strongly advise that any type of ESI be performed under real-time fluoroscopic guidance with contrast-enhanced visualization of flow within the epidural space to the target site prior to the injection of medication unless otherwise contraindicated. In 1972, Winnie et al. emphasized the importance of placing the medication as close to the site of pathology as possible for the clinician to optimize outcome. They demonstrated improvement in 80% of patients in whom corticosteroids were infused at the site of pathology.22 This logical concept must be considered when determining which of the three commonly utilized epidural access routes, transforaminal, interlaminar, or caudal, is utilized when performing an ESI.

EFFICACY OF TRANSFORAMINAL ESI FOR LUMBAR AXIAL PAIN SYNDROMES WITH RADICULAR INVOLVEMENT The optimal route for injection of corticosteroids into the epidural space at the site of pathology in patients with discogenic-mediated lumbar axial pain syndromes with corroborative radicular involvement is via the transforaminal route. This approach allows the clinician to deliver the injectate, composed of a combination of 6–12 mg of betamethasone and 0.5–1 cc of 1% lidocaine, precisely to eradicate the known inflammatory response emanating from the potentially inflammagenic HNP focally on the specific inflamed nerve root sleeve (Fig. 92.1). The efficacy of this approach has been demonstrated in 1014

Fig. 92.1 An AP view of a right L5 selective nerve sleeve injection (note the contrast dye hugging the inferior and medial aspect of the right L5 pedicle consistent with the anatomical location of the right L5 nerve root).

four different randomized, prospective, double-blind, controlled clinical trials. Riew et al.23 reported results of a prospective, randomized, controlled, double-blinded study using fluoroscopically guided lumbar transforaminal injections in 55 patients with imaging evidence of nerve root compression and corroborative radicular symptoms. Twenty-eight patients received bupivacaine and betamethasone, and 27 received only bupivacaine. At follow-up (13–26 months) 33.3% of the bupivacaine group decided not to have surgery, versus 71.4% of the bupivacaine and betamethasone group. This difference in surgical rates was statistically significant ( p<0.004). This controlled study demonstrates the beneficial effect of precisely delivered corticosteroids in obviating the need for operative treatment in patients with HNP and/or spinal stenosis. Kraemer et al.24 published a study in which they reported long-term pain relief with transforaminal ESI in a study in which 49 patients with lumbar radicular pain were randomized into a corticosteroid group and control group. Karppinen et al.25,26 reported on 160 consecutive patients with symptomatic herniated discs with no prior history of lumbar spine surgery randomized into either a corticosteroid group or normal saline group. Outcome measures obtained at 2 weeks, 3 months, and 6 months included pain relief, sick leave, medical costs, the Nottingham Health Profile, and the future requirement for surgical intervention. They reported that transforaminal ESI provided significant short- and long-term improvement in all of the aforementioned outcome measures. Thomas et al.27 reported results of a prospective, randomized, controlled, doubleblinded study comparing the relative effectiveness of fluoroscopically guided lumbar transforaminal ESIs versus blind interlaminar ESIs in patients with radicular pain. They demonstrated the superiority of transforaminal ESIs in all of a variety of outcome measures including finger-to-floor lumbar flexion, daily activity including work and avocational function, and Dallas pain scores. This direct comparison study underscores the importance of fluoroscopic guidance as well as delivering medication accurately and precisely to the site of a potential ongoing inflammatory response. In a non-blinded, randomized, prospective study by Butterman,28 transforaminal ESIs provided efficacy measured by reducing symptomatology and disability and obviating surgery at a follow-up of up to 3 years in patients with large (>25% of the cross-sectional area of the spinal canal) symptomatic lumbar herniated discs. Butterman28 also reported that in those patients who

Section 5: Biomechanical Disorders of the Lumbar Spine

had short-term improvement or ineffectiveness of transforaminal ESIs and required surgical discectomy, there was no adverse affect in the outcome of that surgery from the temporal delay caused by the trial of transforaminal ESIs. In addition to the aforementioned randomized clinical outcome studies, several prospective nonrandomized clinical trials on the efficacy of transforaminal ESI also strongly suggest the beneficial effects of transforaminal ESIs for HNP causing lumbar axial pain with corroborative radicular pain. For example, Weiner and Fraser29 showed 21 out of 28 patients with a computed tomography (CT) documented HNP and corroborative lower extremity pain receiving a single transforaminal infusion of betamethasone and 1% Xylocaine injectate had moderate or complete pain relief not requiring surgery at an average of 3.4 years follow-up. Lutz et al.30 reported on 69 patients, with an average of 22 weeks of symptoms, with magnetic resonance imaging (MRI) evidence of an HNP and radicular pain. Patients underwent an average of 1.8 transforaminal injections of betamethasone and 1% Xylocaine followed by a 6–12-week course of lumbar spine stabilization therapy. They reported a successful outcome, as defined by a 50% or greater reduction in pain and return to near-previous level of functioning, in 75% of patients at an average of 80 weeks follow-up. In a retrospective evaluation, Wang et al.31 demonstrated significant symptom improvement in both the short and long term and the avoidance of discectomy in 77% of patients with lumbar disc herniations treated with one to six transforaminal ESIs. With respect to the interventional treatment of lumbar axial pain syndromes with corroborative radicular pain due to spinal stenosis, the previously stated Riew et al.23 study reported on the effectiveness of transforaminal ESI as it incorporated spinal stenosis in addition to HNP as the underlying etiology to their subjects symptomatology. In addition, Delport et al.32 conducted a retrospective review of treating symptomatic spinal stenosis a subgroup of which underwent transforaminal ESI. They reported that of 140 subjects, over 70% had symptom improvement and were at least somewhat satisfied with their response, over 50% reported sustained improvement in their function, and only 29% of the 140 subjects ultimately underwent surgical decompression. Botwin et al.33 conducted a prospective cohort outcome study assessing the efficacy of transforaminal ESIs in the treatment of symptomatic degenerative spinal stenosis. Thirty-four subjects were followed for 1 year. They reported that 75% of the patients had a successful long-term outcome as defined as >50% symptom reduction. They also reported more than 50% of the subjects improved standing and/or walking tolerance. The aforementioned literature strongly suggests that transforaminal ESI should be the standard of care index interventional spine procedure for patients with spinally mediated lumbar axial pain syndromes associated with radicular involvement due to HNP and/or spinal stenosis when more conservative measures have failed. Furthermore, in the case of the majority of HNPs, the known phagocytic immunologic response and consequent benign anatomic natural history assists in the relatively high rate and long-term success of transforaminal ESIs.34,35

CONCEPTUAL PATHOPHYSIOLOGIC MECHANISMS OF LUMBAR AXIAL PAIN SYNDROMES WITHOUT RADICULAR INVOLVEMENT DUE TO A DISCOGENICMEDIATED INFLAMMATORY RESPONSE Some important inferences from the aforementioned literature on the successful long-term treatment of HNP-associated lumbar axial pain syndromes with corroborative radicular involvement may be extracted that, when combined with known previously stated

basic science literature and lumbar spinal anatomy, suggest a possible utilization for transforaminal ESIs in the interventional treatment of discogenic-mediated lumbar axial pain without radicular involvement. The similarities in the basic ideologies by which the initial incorrect thought processes of compression as the sole mechanism of radicular pain due to HNP requiring discectomy as stated nearly a century ago by Mixter and Barr36 mirror recent theory that motion segment instability and/or structural disc pathology is the sole mechanism of discogenic-mediated lumbar axial pain without radicular involvement. In the decades subsequent to Mixter and Barr’s36 landmark article identifying HNP pathology as a key source of lumbar axial and radicular pain, there have been many attempts to identify the precise pathophysiologic mechanism of discogenicmediated lumbar axial pain without radicular involvement. As stated earlier in this chapter, over the years, there have been key pieces of literature to suggest that a tear in the outer one-third of the anulus of the intervertebral disc may be the most common etiology of acute spinally mediated lumbar axial pain.10,37 As with the painful sequelae of most degenerative spinal conditions, improvement and eventual remission within 6 weeks is the natural history. However, subacute symptoms can persist and the mechanism for this may be inflammatory in nature.38 The basic science literature discussed earlier in this chapter has repeatedly and clearly demonstrated the inflammagenic properties of the intervertebral disc, particularly the nucleus pulposus when it is exposed to the ventral epidural space.13–17,38 This literature lends credence to the mechanisms by which transforaminal ESI effectuate symptom relief on a molecular basis. Therefore, the possibility of a focally contained inflammatory response to a centrally or paracentrally contained herniated disc is entirely possible and may be instrumental in pain generation as well as inhibition of the natural healing processes known to exist. In fact, a contained HNP may chemically sensitize the posterior longitudinal ligament, resulting in axial pain in a fashion similar to that of inflammatory radicular pain due to an HNP sensitizing a nerve root. Furthermore, patients with internal disc disruption syndrome in which an annular fissure extends from the nucleus pulposus to the outer one-third of the anulus (which may or may not be associated with a HNP) and may pierce through the outer anulus and intermittently or consistently communicate microscopic amounts of nuclear material to the ventral epidural space ensuing in an intermittent and/or ongoing focal discogenicinduced inflammatory response (Fig. 92.2). This pathophysiologic model may explain why a randomized, prospective, double-blind clinical trial performed by Simmons et al.39 failed to demonstrate a statistically significant benefit to intradiscal corticosteroid infusions when compared to placebo. The aforementioned hypothesis suggests the inflammatory response occurs in the ventral portion of epidural space on the floor of the spinal canal juxtapositioned to the afflicted intervertebral disc(s) rather than within nuclear material encased by the anulus fibrosus.

EFFICACY OF TRANSFORAMINAL ESI FOR LUMBAR AXIAL PAIN SYNDROMES WITHOUT RADICULAR INVOLVEMENT To date, there have been only two nonrandomized, retrospective studies reporting on the outcome of transforaminal ESI on spinally mediated lumbar axial pain due to discogenic pathology without imaging evidence of nerve root involvement. One is a subgroup reported by Rosenberg et al.40 stating greater than 50% pain reduction after one year in 59% of patients. The other study reported by Manchikanti et al.41 on patients with spinally mediated lumbar axial pain treated by one of three interventions: (1) blind interlaminar 1015

Part 3: Specific Disorders Anterior (ventral)

Posterior (dorsal)

Route of infusion of transforaminal ESI Posterior longitudinal ligament

Location of discogenic-induced focal inflammatory response on spinal canal

Vertebral body

Inferior articular process Superior articular process

Spinal process

Nucleus pulposus Articular intervertebral disc

Neural foramen

Annulus fibrosis

Spinal process

Vertebral body Outer 1/3 of annulus containing a complex network of pain transmitting nerve fibers

Spinal canal

ESI, (2) fluoroscopically guided caudal ESI, and (3) fluoroscopically guided transforaminal ESI, states that superior short- and long-term pain relief is achieved via the transforaminal route. This conclusion makes anatomical sense as transforaminal ESIs likely distribute injectate more focally to the ventral epidural space when compared to interlaminar and caudal route and therefore are more target specific when attempting the deliver medication to a possible focal posterior discogenic-induced inflammatory response. We are in no way suggesting that transforaminal ESI should be utilized for low back pain in general. However, based on the previously described history of spinal disorders, spinal anatomy, basic science literature, inferences from the current class I evidence in the interventional treatment of HNP and ensuing inflammatory radicular pain, and some preliminary retrospective data, as well as our own anecdotal experience, transforaminal ESIs may be a possible spinal intervention in the treatment of discogenic-mediated lumbar axial pain. Certainly, further study is required in the form of randomized, double-blinded, placebo-controlled clinical trials to elucidate the role, if any, of transforaminal ESIs in the treatment of discogenic-mediated lumbar axial pain without radicular involvement. As previously implied, the best route for infusion of corticosteroids into the ventral epidural space in patients with a potential component of focal posterior discogenic inflammatory response is the transforaminal route. In many cases, the specific level of discogenic pathology has not yet been elucidated at the algorithmic point of consideration of ESIs for the treatment of lumbar axial pain thought to be potentially due to a discogenic inflammatory etiology. In fact, more than one segmental level may be contributing to inflammation in the ventral aspect of the lumbar epidural space. Therefore, unless imaging strongly suggests one segment, the S1 transforaminal ESI is recommended (Figs 92.3, 92.4). This route allows the clinician to mechanically drive the corticosteroid injectate, typically 12–18 mg of betamethasone, diffusely along the floor of the lumbar spinal canal via a pressure effect utilizing 3–5 cc of 1% lidocaine in an attempt to quell potential inflammation along the ventral epidural space incited by leakage of nuclear material. In those patients where one-level 1016

Fig. 92.2 Authors’ rendition of the pathophysiologic model by which an intermittent or continual posterior discogenic inflammatory response may occur in the ventral portion of the epidural space due to leakage of nuclear inflammogens.

Fig. 92.3 An AP view of a left S1 transforaminal ESI (note the outline of the left S1 root sleeve inferior and medial to the left S1 pedicle as well as the degree of dispersion of contrast dye upon cephalad flow into the inferior portion of the lumbar spinal canal with maintenance of ipsilateral flow cephalad to the L4 level).

disease is strongly suspected, a smaller volume of local anesthetic may be infused after the corticosteroid dose at the foraminal level below the suspected level to deliver the corticosteroids in the cephalad direction more focally on the ventral aspect of the spinal canal at the posterior aspect of the suspicious intervertebral segment. In cases where a nonhealing annular tear(s) exists communicating nuclear material to the ventral epidural space, mediation of the inflammatory response may create a more optimal environment for spontaneous healing of the annular tear.

Section 5: Biomechanical Disorders of the Lumbar Spine

Fig. 92.4 A lateral view of the S1 transforaminal ESI demonstrating relative ventral flow of contrast dye on the floor of the spinal canal flowing cephalad to the L4 level.

Technique of performing transforaminal ESI Transforaminal ESI absolutely requires fluoroscopic guidance in order for the site of pathology to be precisely targeted. The transforaminal route is the optimal access for delivering an injectate on the lumbar nerve sleeve and/or the ventral portion of the epidural space. Transforaminal ESIs are performed with the patient prone on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. Realtime fluoroscopy is utilized to identify the pedicle corresponding to the foramina through which injectate is to be delivered. In patients with a transitional segment, either a lumbarized S1 vertebral body or sacralized L5 vertebral body, the interventional spine specialist will need to count the vertebral bodies beginning with L1 after the most caudal rib (T12) to establish that the appropriate pedicle is identified. Once the targeted pedicle is correctly identified, the c-arm should be rotated ipsilaterally until the superior articular process of the juxtapositioned caudal vertebral body comes into view and advances to the medial portion of the targeted pedicle on the created oblique view. The targeted pedicle should now take on an ovoid shape once the correct degree of rotation is achieved as opposed to the circular shape on a true anteroposterior (AP) image with the lumbar spinous processes in the midline. Then, a skin wheal utilizing a combination of 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate42 is raised just inferior to the midline portion of the targeted pedicle on the oblique image. A long-handled sponge clamp is utilized to guide a 20-gauge, 3.5 inch spinal needle through the raised skin wheal in a bull’s-eye manner (the needle hub concentrically outlines the needle tip (Fig. 92.5) just inferior to the midline portion of the targeted pedicle until a change in tissue resistance is appreciated or until the spinal needle hub abuts the skin. If the needle abuts skin prior to a change in tissue resistance, the 3.5 inch spinal needle is then utilized as an introducer and is positioned to align its tip to the midline portion of the targeted pedicle and a 25-gauge, 6 inch needle is guided through the index needle until a change in tissue resistance is appreciated. In either instance, the needle tip should then feel stable or locked into position if it has entered the targeted foramen. Verification of needle tip placement is achieved by rotating the

Fig. 92.5 An oblique view of a right L5 transforaminal ESI demonstrating the bull’s-eye approach to needle advancement visualized as a black dot with a thin concentric ring circumscribing the needle tip just inferior to the mid portion of the right L5 pedicle.

c-arm in a manner that provides a true midline AP image. The needle tip is then slowly advanced to the six-o’clock position, proximated just inferior to the targeted pedicle. The lumbar spinal nerves exit the spinal canal just inferior and medial to the midposition of the corroborative pedicle on the AP image. Needle placement just superior to the spinal nerve and just inferior to the pedicle is confirmed by visualization of contrast medium centrally hugging the pedicle both inferiorly and medially as well as spreading cephalad along the ipsilateral ventral portion of the spinal canal, bathing the posterior aspect of the intervertebral discs as well as peripherally along the lumbar spinal nerve sleeve. Care must be taken and technique must be precise throughout needle advancement to maintain the bull’s-eye approach at all times via real-time fluoroscopy to prevent straying of the needle away from the targeted foramen. Inadvertent curvature of the needle outside the confines of the bull’s-eye approach may result in the needle tip hitting periosteum, such as the targeted pedicle if the needle tip strays superiorly, punctured viscus if the needle tip strays anteriorly towards the retroperitoneal and/or abdominal cavity, or punctured spinal nerve extraforaminally if the needle tip strays inferiorly. In some instances when performing a transforaminal ESI through the L5–S1 foramen, the targeted inferior aspect of the midline of the L5 pedicle may be accessible only by ipsilateral rotation due to one or a combination of a high-riding pelvis, significant loss of disc space height, large L5 transverse process, L5–S1 fusion, or a L5 on S1 spondylolisthesis. These obstacles can be overcome with a variable degree, depending on the severity of the aforementioned anatomical variations, of cranial to caudal tilt which will in effect move the pelvis inferiorly, creating direct access to the inferior portion of the targeted L5 pedicle. In cases of performing transforaminal ESI through the L5–S1 foramen in patients with a partially or completely sacralized L5 vertebral body, the approach is similar to that utilized when performing sacral transforaminal ESIs. When performing S1 transforaminal ESI, the skin wheal is raised superior and lateral to the targeted S1 pedicle. The needle is advanced through the skin wheal via a long-handled sponge clamp in the direction of the X-ray beam at a 45° angle to gently abut sacral periosteum just lateral to the S1 pedicle. Then, the needle is slightly withdrawn, reoriented inferiorly and medially, and slowly advanced, sliding to just inferior to the midline of 1017

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the S1 pedicle into the targeted foramen. A slight suction or vacuum phenomena may be felt as the needle tip enters the targeted sacral foramen. A similar approach is utilized for L5–S1 transforaminal ESI in patients with partial or complete sacralization of the L5 vertebral body; however, the skin wheal is raised lateral and inferior to the targeted L5 pedicle and the needle too is advanced superiorly and medially after depth is achieved by contacting periosteum.

Indications and efficacy of interlaminar ESI The interlaminar route most likely continues to be the most widely utilized approach to accessing the lumbar epidural space for ESI in the treatment of spinally mediated lumbar axial pain syndromes; however, there is little in the published randomized literature to suggest longterm efficacy.43–49 Carette et al.43 demonstrated short-term improvement in radicular complaints in patients with HNP but no difference between control and treated groups at 3 months in a prospective, randomized, double-blind, controlled trial. In a prior prospective, randomized, double-blind, controlled trial, Cuckler et al.44 demonstrated no significant improvement in both the short and long terms in patients with lumbar axial pain due to HNP and/or spinal stenosis. Ridley et al.48 reported statistically significant long-term benefit (6-month follow-up) to interlaminar ESIs in patients with lumbar axial and radicular pain in a randomized, placebo-controlled outcomes trial. Lending credence to the variables influencing such outcomes studies are the previously mentioned studies that report up to 40% of blind interlaminar ESI do not enter the epidural space even in experienced hands.18–21 Furthermore, an intrinsic problem with interlaminar ESI is that even when the physician is able to correctly place the needle tip into the epidural space, the dorsal aspect of the spinal canal is infused. Therefore, interlaminar ESIs are likely delivering injectate dorsal to the thecal sac and at a site relatively distal to the ventrally located pain-generating structures.

Technique of performing interlaminar ESI Interlaminar ESIs are performed under X-ray guidance with the patient prone or in the lateral decubitus position on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidoneiodine and the region is draped in a sterile fashion. The correct level, taking into account the possibility of a transitional segment, is verified by the process previously stated in the technique portion of the transforaminal ESI section. Then, with fluoroscopic imaging, the inferior ipsilateral aspect of the lamina corresponding to the site of pathology is visually confirmed. A skin wheal utilizing a combination of 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate is raised.42 A 20- or 22-gauge, 3.5 inch spinal needle is carefully guided to abut the ligamentum flavum as resistance is felt. One of two techniques can be utilized for advancement into the dorsal epidural space. Firstly, the spinal needle can be slowly advanced using a loss of resistance technique. A ‘pop’ may be felt and/or heard when the ligamentum flavum is pierced and the needle tip has entered the epidural space. Otherwise, the stylet can be removed and a glass syringe filled with 5 cc of normal saline is attached to the needle hub. The spinal needle is slowly advanced with modest pressure being simultaneously applied to the plunger. Once a drop in resistance is encountered, the ligamentum flavum has been pierced and the dorsal epidural space has been infiltrated. The needle tip position is assessed on AP and lateral images and verified by the injection of contrast medium. Once needle confirmation is achieved, an injectate combination of 12–18 mg of betamethasone and 5–10 cc of lidocaine and/or normal saline is slowly infused. 1018

Indications and efficacy of caudal ESI The caudal ESI may be safer than other routes of ESI due to a substantially lower risk of inadvertent dural puncture and subsequent subarachnoid injection, as the dural sac rarely extends beyond the S1–2 level. The published randomized clinical outcomes literature as a whole provides a contradictory picture on both short- and longterm efficacy of caudal ESI in the treatment of lumbar axial pain with or without radicular involvement in patients both prior to and post surgical decompression.41,50–54

Technique of performing caudal ESI Caudal ESIs are performed with the patient prone on the fluoroscopy table. The skin overlying the sacrococcygeal area is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. The clinician should then identify the right and left sacral cornu via palpation or fluoroscopic guidance, as the sacral hiatus is located between these two landmarks. A skin wheal utilizing a combination of 2–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate is raised.42 A 22-gauge, 3.5 inch spinal needle is carefully guided at a 45° angle through the sacrococcygeal ligament and into the sacral canal hiatus near the superior portion of the gluteal cleft and then advanced slightly into the sacral canal no further than the inferior edge of S2. The needle tip position is assessed on AP and lateral images and verified by the injection of contrast medium and observance of cephalad flow. Once needle confirmation is achieved, 12–18 mg of betamethasone is injected followed by an infusion of 5–15 cc of lidocaine and/or normal saline to assist in the cephalad spread of the corticosteroid to the lumbar epidural space via a direct mechanical pressure effect in the cephalad direction.

Timing of ESI The optimal timing for administration of ESIs has not yet been elucidated. It is standard practice for patients to undergo more conservative palliative measures (i.e. nonsteroidal antiinflammatory drugs (NSAIDs), lumbar spine stabilization physical therapy) prior to being considered for ESIs; however, the clinician must be wary not to delay ESIs when more conservative treatments do not seem to be helping. Delaying aggressive treatment may allow an ongoing inflammatory process to result in fibrosis and possibly cellular damage.13 It is unknown how often ESIs can be administered. Practitioners will often wait as long as 2 weeks prior to reassessing a patient for a response to an injection for possible re-injection. This practice became popular after Swerdlow and Sayle-Creer suggested that corticosteroids infused into the epidural space may remain in situ for up to 2 weeks.55

INTRADISCAL INJECTIONS OF BIOLOGICS FOR DISCOGENIC MEDIATED LUMBAR AXIAL PAIN SYNDROMES Patients with discogenic mediated lumbar axial pain have, at least a component of, a structural anatomic lesion within the outer annulus of the intervertebral disc. This lesion may or may not communicate with the nucleus pulposus and is conceptually regarded as the inciting pathologic event that progresses over time and results in degeneration of the disc and, potentially, discogenic mediated pain. Intradiscal infusions of active biologics may represent the future in the prevention of this progression and repair of structural lesions within the intervertebral disc. In vitro studies have demonstrated a cellular response of intervertebral disc cells to exogenous bone morphogenetic protein (BMP).

Section 5: Biomechanical Disorders of the Lumbar Spine

These studies have demonstrated improved disc height and signal changes on MRI suggestive of repair of the intervertebral disc following intradiscal administration of BMP to discs damaged via chemical and mechanical methods. In a rabbit model, Miyamoto et al.56 demonstrated that intradiscal infusion of osteogenic protein -1 (OP-1, BMP-7) restored the biomechanical properties of the degenerated intervertebral disc. Furthermore, An et al.57 demonstrated that infusion of OP-1 intradiscally resulted in increased disc height and proteoglycan content. In addition, Takegami et al.58 reported that intervertbral disc cells exposed to interleukin-1 alpha lost no intrinsic ability to upregulate proteoglycan synthesis in response to OP-1 stimulation. In fact, he went on to describe that the reformed matrix was actually richer in proteoglycans than that prior to interleukin-1 alpha exposure. Interestingly, Yoon et al.59 demonstrated that infusion of adenovirus carrying Lim Mineralization Protein – 1 increases disc production of proteoglycans as well as bone morphogenic proteins. In a rat model, Kawakami et al.60 demonstrated both enhancement of the extracellular matrix as well as inhibition of pain-related behavior with intradiscal OP-1 injection into painful degenerated discs. Based on these initial in vitro studies, it has been proposed that intradiscal infusion of BMP to a degenerated dessicated disc may initiate repair of the disc, manifested clinically as reduction in lumbar pain and concomitant improvement of physical function and potentially manifested structurally as a radiographic increase in disc height and/or an increase in MRI disc signal intensity. This author is a principal investigator in a multicenter phase 1 study evaluating infusion of a BMP into single level symptomatic degenerative disc disease in humans. Although transforaminal ESIs targeted on the floor of the spinal canal at a focal discogenic mediated inflammatory response holds promise for some patients episodic chemically induced discogenic pain as previously described (Fig. 92.2), randomized prospective double-blinded studies done by both Simmons et al.61 as well as Khot et al.62 have demonstrated no statistically significant benefit of intradiscal infusion of corticosteroids for discogenic pain diagnosed by provocative lumbar discography. Other biologics that have been reported upon but whose role has not yet been elucidated include infusions of hematopoietic precursor stem cells, methylene blue and ozone (O3). For example, Haufe et al.63 reported no reduction in discogenic pain at one year follow-up in patients who underwent intradiscal infusion of hematopoietic precursor stem cells harvested from the pelvic bone marrow. Peng et al.64 demonstrated that 87% of patient with chronic discogenic pain who met inclusion criteria for lumbar interbody fusion surgery but were instead treated with intradiscal injection of methylene blue were able to report marked improvement in pain and physical function. In 2004, Muto et al65 reported on 2200 patients treated with intradiscal oxygen-ozone injection reporting no side effects and a 75–80% success rate at 6 and 18 months. Buric et al66 conducted a prospective case series reporting on chemonucleolysis via ozone injections in 30 patients with non-contained disc herniations. They stated 90% of patients had a statistically significant improvement in pain and function as measured by VAS and Roland Morris Disability Questionnaires. Of course, further study is required before any of the aforementioned intradiscal infusions of various biologics can be regarded as a generally acceptable or standard of care intervention for discogenic lumbar axial pain syndromes.

PATHOPHYSIOLOGY OF Z-JOINTMEDIATED LUMBAR AXIAL PAIN SYNDROMES The lumbar Z-joint is the primary posterior element structure thought to be a potential etiology of spinally mediated lumbar axial

pain. The rationale is derived from conclusions drawn from the conceptual model of the lumbar spine degenerative cascade as initially described by Kirkaldy-Willis,10 as previously reported within this chapter, as well as properties intrinsic to the Z-joint. As outlined earlier in this chapter, the posterior elements take on more axial load in certain positions (standing) as well as with increasing age. Anatomically, the Z-joint is a true diarthrodial joint with articular and subchondral cartilage, a small meniscus, a capsule, and a fluidfilled synovium encased in synovial lining. The initiating event that is thought to implicate the Z-joint as an etiology of lumbar axial pain is synovitis and the resultant synovial reaction which occurs as a result of the shift in axial loading from the anterior elements to the posteriorly situated Z-joints due to the temporally related incompetence of the intervertebral disc. On the other hand, it is theorized that the aforementioned initiating pathology to the synovial capsule can result in a younger population when induced by sudden, unexpected flexion–extension moments as occurs commonly in motor vehicle trauma. The Z-joints are able to accommodate the increased load up to a critical maximum at which point synovial pathology ensues leading to eventual progressive destruction of the cartilaginous articular surface when facet joint weight bearing exceeds the critical maximum. Acute, recurrent, and/or chronic inflammation can result in these synovial joints filling with fluid and distending. This distention may result in pain perception because of mechanical and/or chemical stimulation of the richly innervated synovial capsule. Evidence suggests that the Z-joint’s synovial capsule has a complex innervation provided by small, C-type pain fibers.67 Furthermore, the majority of mechanosensitive somatosensory units found within the Z-joint were discovered to be group III high-threshold, slow-conduction units, which are thought to mediate nociception.68–70 Therefore, the Z-joint can result in nociception by osteochondral and/or capsular mechanisms similar to those found in other extensively studied degenerated joints, such as the hip or knee. Capsular laxity can result and the accompanying subluxation can stretch and/or tear the richly innervated capsule leading to one or a combination of inflammatory or structural lumbar axial pain syndromes emanating from the lumbar Z-joint. Another potential mechanism for nociception arising from lumbar Z-joint has not been recognized until recently. In most diarthrodial joints, prolonged immobilization can lead to a cascade of joint changes. These may include, among other things, capsular stiffness leading to contracture, decrease in synovial fluid production, and tightening of para-articular muscles, all leading to joint rigidity. In some cases, complete ankylosis may accompany extreme inactivity, immobilization, and inhibition of function. In such cases, mechanical loads applied to the rigid joints typically can produce pain, which may be related to capsular stretching/tearing, synovial irritation from cartilage fragmentation due to poor nutrition, and/or muscle spasm from sudden stretching of immobilized, debilitated muscle. In chronic lumbar axial pain conditions, patients often splint segments of the lumbar spine, and the chronic immobilization may lead to nociception. Stretching the involved joint–muscle complex is the obvious physiologic therapeutic modality. Unfortunately, pain and fear-avoidance may prevent some pain-sensitive patients from complying with such logical medical advice. Nevertheless, the Z-joint can be the source of pain associated with these mechanisms, particularly after chronic persistent or chronic episodic lumbar axial pain conditions have produced disability for longer than 6 months.71

Diagnosis of Z-joint-mediated lumbar axial pain syndromes Revel et al. suggested certain clinical features including age greater than 65 years, pain not exacerbated by coughing, hyperextension, 1019

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forward flexion, rising from forward flexion, or extension–rotation, or mitigated by recumbence, may be suggestive for a Z-joint etiology to lumbar axial pain.72,73 However, more recent studies demonstrate that no physical examination finding(s), including segmental rigidity, are specific for Z-joint-mediated lumbar axial pain.74,75 Although the aforementioned features on clinical presentation reported by Revel et al.72,73 may suggest the Z-joint as a possible etiology of lumbar axial pain and enter the Z-joint into the differential diagnosis, anesthetic blockade is currently the gold standard by which the diagnosis is ultimately made.76 Two methods are currently accepted: (1) a dual-block paradigm eliciting a positive response for the halflife duration of both a short- and long-acting local anesthetic performed on separate occasions, or (2) a single-block paradigm eliciting a positive response from a local anesthetic blockade with a negative response from a placebo control performed on separate occasions.

Efficacy of lumbar Z-joint injections in Z-jointmediated lumbar axial pain syndromes There has yet to be a study to determine the efficacy of intra-articular steroid injections of the lumbar Z-joints in patients diagnosed with Z-joint-mediated pain via a dual-block paradigm or placebo-controlled single-block paradigm. Carette et al.77 designed and implemented the best study to date assessing the efficacy of intra-articular corticosteroid injections of the lumbar Z-joints for Z-joint-mediated lumbar axial pain. They reported on 101 patients with lumbar axial pain diagnosed with Z-joint-mediated pain via a single intra-articular anesthetic blockade providing 50% pain reduction randomized into either a normal saline group and corticosteroid group. At 1 month, 42% of the corticosteroid group and 33% of the normal saline group reported significant pain relief (thus a one-third placebo response rate and requirement of a dual-block paradigm for diagnosis). There was a statistically significant difference in marked pain relief at 6-month follow-up between the corticosteroid group (46%) and normal saline group (15%). Carette et al.77 argued that intra-articular steroid Z-joint injections were not effective since the percentage of patients with long-term pain relief was low; however, one could retort that the inclusion criteria was detrimental to the study outcome because of the failure to exclude a placebo response. A more recent randomized, single-blind clinical trial by Mayer et al.75 found that fluoroscopically guided Z-joint injections with supervised stretching exercises when compared to exercise alone (control group) in patients with chronic disabling work-related lumbar spinal disorders demonstrated that incorporating Z-joint injections significantly increased lumbar range of motion (ROM) in all planes as well as lumbar mobility relative to the control group. However, Mayer et al.64 also observed that there was no increase in the improvement of pain and disability of the Z-joint injection group relative to the control group. The key point in this paradigm of segmental rigidity is that the purpose for the injection/exercise approach is to increase motion in spinal segments noted specifically to be rigid. The added goal of facilitating functional rehabilitation involving para-articular muscle strength, endurance, and coordination becomes possible only after joint mobility has been restored. This study demonstrated significant ROM gains were also present in the exercise-only control group, but that significantly greater improvements were noted when Z-joint injections were added to the standardized exercise program. It was also noted that only 17% of the patients meeting criteria for segmental rigidity also met criteria for Z-joint syndrome, as determined by the response to the Z-joint injections. As such, it appears that the entity of lumbar axial pain of Z-joint origin is noncongruent with the entity of segmental rigidity. More study of the relationships between these two phenomena is required, as comprehension will 1020

ultimately determine the prescription and efficacy of comprehensive treatment programs. The nonrandomized outcome studies offer varying short- and longterm results in the utilization of intra-articular Z-joint corticosteroid injections in the treatment of lumbar axial pain. For example, Lynch and Taylor78 reported total pain relief in nine of 27 patients receiving intra-articular Z-joint injections and partial relief in another 16 of those 27 patients. However, none of the 15 patients receiving extraarticular corticosteroid injections reported complete pain relief and only eight of the 15 reported partial pain relief. Destouet et al.79 reported significant pain relief for 1–3 months in 62% of their patient sample and 38% reported 3–6 months of pain relief. Murtagh80 reported that 54% of his patient sample claimed up to 6 months significant pain relief. Mironer and Somerville81 only reported 28% of patients in their study reporting significant long-term pain relief. Two separate retrospective outcome studies demonstrated approximately 50% of patients reporting short-term pain relief with much lower percentages of patients (approaching 8%) reporting long-term relief at 12 months.82,83

Technique of performing lumbar intra-articular Z-joint interventions Lumbar intra-articular Z-joint injections are performed with the patient prone on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. The correct level, taking into account the possibility of a transitional segment, is verified by the process previously stated in the technique portion of the transforaminal ESI section. Real-time fluoroscopy is utilized to rotate the c-arm ipsilaterally until the medial and lateral edges of the targeted Z-joint are clearly visualized. Local anesthesia is achieved by infiltrating the skin, creating a skin wheal raised just medial to the midline or inferior aspect of the joint with a combination of approximately 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate.42 Real-time fluoroscopy is utilized to advance a 22-gauge, 3.5 inch spinal needle in a bull’s-eye fashion so that the needle tip abuts the lateral edge of the middle to inferior portion of the Z-joint. The spinal needle is then slightly withdrawn and directed just medially into the capsule of the targeted Z-joint. Approximately 0.1–0.3 cc of contrast can be utilized to verify needle placement, visualized by the presence of an hourglass-shaped arthrogram or portion thereof (Figs 92.6–92.8). Once needle tip confirmation is achieved, a combination of 0.5–0.8 cc of betamethasone and 0.2–0.5 cc of 1% lidocaine can be injected, dependent on the degree of compromise of the synovial capsule and the ensuing capacity to accommodate an infusion of volume.

Efficacy of medial branch injections in Z-joint-mediated lumbar axial pain syndromes Medial branch neural blockade is also performed in the treatment of lumbar axial pain of Z-joint etiology. Manchikanti et al.84 prospectively randomized 73 patients diagnosed with Z-joint mediated lumbar axial pain via a dual anesthetic block paradigm into one of two groups treated with therapeutic medial branch injections. One group received local anesthetic and sarapin whereas the other received a mixture local anesthetic, sarapin, and corticosteroid. Significant pain relief was achieved in both groups with a mean duration of relief greater than 6 months. In addition, physical, functional, psychological status, and return to work status were all improved. Of note, the efficacy of radiofrequency neurotomy of the medial branch of the corroborative spinal nerves has been

Section 5: Biomechanical Disorders of the Lumbar Spine

Fig. 92.6 An oblique view demonstrating a medial to lateral approach to the right L4–5 Z-joint. The needle tip is directed toward the inferior portion of the joint space. (Note that rotation must be adequate in order to clearly visualize the edges of the inferior articular process of L4 and superior articular process of L5.)

Fig. 92.8 An oblique view of a left L4–5 intra-articular Z-joint injection with visualization of a classic hourglass arthrogram pattern filling the superior and inferior capsules.

trial, North et al.86 demonstrated the short-term efficacy of medial branch blocks with a local anesthetic, but long-term improvement was infrequent.

Technique of performing medial branch injections

Fig. 92.7 An infusion of 0.2 cc of contrast dye demonstrates filling of the joint space and visualization of the right L4–5 Z-joint partial arthrogram.

demonstrated for patients diagnosed by a dual-block paradigm by Dreyfuss et al.76 In a nonrandomized study by Manchikanti et al,85 a retrospective analysis of 180 patients all diagnosed with Z-joint-mediated lumbar axial pain via a dual-anesthetic paradigm, three groups of 60 patients were evaluated, the groups receiving medial branch blocks with local anesthetic, local anesthetic and sarapin, or local anesthetic, sarapin, and corticosteroid. To summarize, the results of this retrospective study reported that diagnostic medial branch blocks alone had shortterm therapeutic effects which were enhanced by the addition or sarapin and/or corticosteroid. In another nonrandomized clinical

Medial branch neural blockade is performed with the patient in the prone position on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. The correct level, taking into account the possibility of a transitional segment, is verified by the process previously stated in the technique portion of the transforaminal ESI section. The c-arm is rotated until the eye of the ‘Scottie dog’ is clearly visualized on an oblique image. Local anesthesia is achieved by infiltrating the skin, creating a skin wheal raised over the eye of the ‘Scottie dog’ with a combination of approximately 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate.42 A 22-gauge 3.5 inch spinal needle is advanced in a bull’s-eye manner to the eye of the ‘Scottie dog,’ representing the junction of the base of the corroborative transverse process and the superior articular process under fluoroscopic guidance. Injections must be performed at the level of the involved joint and the adjacent superior segmental level as both of these medial branches will contribute innervation to the targeted Z-joint. For example, the L4–5 Z-joint is innervated by the medial branches of the dorsal rami of both the L3 and L4 spinal nerves. Injectate consists of 0.5 cc of 1% or 2% lidocaine.

CONTRAINDICATIONS AND COMPLICATIONS OF INTERVENTIONAL SPINE PROCEDURES Contraindications to interventional spine procedures include possible pregnancy (secondary to the potential adverse effects of fluoroscopic radiation on the fetus), hypersensitivity to any component of the injectate, bacteremia, full anticoagulation, and bleeding diathesis. Other concerns are elevations of serum glucose levels in diabetics, elevations of blood pressure in hypertensive patients, and fluid 1021

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retention in congestive heart failure patients. The use of aspirin and other NSAIDs have not been demonstrated to predispose patients to any significant bleeding while receiving ESIs.87 Potential complications of fluoroscopically guided interventional spine procedures include increased pain, hypersensitivity reactions, dural puncture, subarachnoid injection, anaphylaxis, infection, unmasking of preexisting systemic infection, epidural abscess, increased pain, fever, epidural bleeding and/or hematoma, bladder dysfunction with urinary retention, weakness, permanent neural element damage via penetrating trauma, intravascular injection resulting in local anesthetic toxicity such as seizure, cardiac arrhythmia or arrest, and death. However, these events are quite rare. Botwin et al.88 reported no major complications and less than a 10% rate of minor complications, all of which resolved without hospitalization, in 207 patients undergoing 322 fluoroscopically guided lumbar transforaminal ESIs.

PHYSICAL REHABILITATION Physical rehabilitation is a key modality on the treatment of patients with spinally mediated lumbar axial pain. Physical therapy programs prescribed specifically to address the primary site of injury and secondary sites of dysfunction can provide a means of treatment with or without adjuvant medications and interventional spine procedures. Back schools and other training programs that are not job specific have not been shown to be statistically effective; however, programs that integrate the job requirements into the training program show statistical significant results.89 Relative rest, which restricts all occupational and avocational activities, for up to the first 2 days following an acute episode may be indicated to help calm down initial pain symptoms and relieve fatigue. Rest for longer periods of time has not been shown to be beneficial, and may be harmful, potentially causing deconditioning, loss of bone density, decreased intradiscal nutrition, loss of muscle strength and flexibility, and increased segmental stiffness.90 Passive modalities are valuable during the initial 48 hours of relative rest to aid in pain relief, but protracted courses of passive treatments become counter-productive as they place the patient in a dependent role instead of participating in an active, function maximizing rehabilitation program. One of the most important components of any back care program is education. Education should include an explanation of the natural history of an acute, subacute, and chronic disc injury. In addition, education should include training in proper body mechanics and lumber ergonomics during various functional, occupational, and avocational activities. The greatest successes in health education can be seen in two great medical problems, heart disease91 and cancer.92 Education has had a direct effect on decreasing the prevalence of smoking, from 40% of the population in 1965 to 29% in 1987.93 An education-based low back paradigm is inexpensive and begins with providing reassuring information to the patient. The seeds of the educational approach exist in back schools, functional restorative programs, and innovative prevention and rehabilitation strategies. LaCroix found that 94% of patients with a good understanding of their condition returned to work, whereas only 33% of patients with a poor understanding of their condition returned to employment.94 Reassurance that activity is helpful promotes return to function. Back school provides information on spine anatomy and function and was found to be one of only three interventions identified by the Quebec Task Force on Spinal Disorders as effective for patients in randomized, controlled trials.95 Myofascial manual techniques may be employed to increase soft tissue pliability when secondary myofascial tightness is present. If the aforementioned measures are appropriate and completed, then an active, dynamic, outpatient lumbar spine stabilization rehabilitation program should be prescribed. In addition, rehabilitation of other associated components of the functional kinetic chain may be appropriate, as these 1022

structures may also be affected. A dynamic lumbar spine stabilization rehabilitation program is aimed at maintaining a neutral spine position throughout various daily activities. An extension bias is commonly employed to help reduce intradiscal pressure. This position allows for a balanced segmental force distribution between the intervertebral disc and Z-joints, provides functional stability with axial loading to help minimize the chance for acute dynamic overload upon the discs, minimizes tension on ligaments and fascia planes, and alleviates symptoms. Repetition is key in increasing flexibility, building endurance, and developing the required muscle motor programs that activate a series of key multimuscular contractions subconsciously that maintain the lumbar spine in a neutral position throughout static and dynamic activities. For athletes, the aforementioned program can be combined progressively with sport-specific polymetrics to help the lumbar spine maintain a neutral position during high-intensity, unpredictable, reaction-intensive sports. Another method for rehabilitation of athletes is to train them in maintaining a neutral spine position in the individual motions of their sport, then subsequently grouping these component motions into a new, safe, stable spine movement. Cardiovascular fitness training is an important component to a comprehensive rehabilitation program as it assists in providing the endurance necessary to prevent fatigue of the spine-stabilizing musculature.

CASE STUDIES Case study 1 S.G. is a 36-year-old male with a history of occasional spontaneously resolving short-term (less than 1 week duration) low back pain episodes who presents to a spine specialist complaining of 12 weeks of worsening low lumbar axial pain initiated while lifting a heavy television set helping a friend move into a house. The patient states his symptoms are located across the width of the low back without lower extremity radiation. He qualifies his pain as a constant, deep, dull ache worsened with prolonged sitting, especially riding in his car, as well as with twisting motions when bent forward. The patient reports lumbar extension and staying active seem to provide some symptom mitigation. Physical examination reveals some tenderness and spasm to palpation over the bilateral low lumbar paraspinal musculature. Lumbar flexion is significantly limited due to worsening of the patient’s lumbar pain; however, lumbar extension alleviates the patient’s lumbar pain. In addition, the patient reported increasing lumbar pain with decreasing angle acuity during sustained hip flexion. Sacroiliac joint stress maneuvers and provocative maneuvers were not pain provoking. The lumbosacral spinal neurologic examination was normal. Plain films of the lumbar spine ordered by the patient’s primary care physician revealed moderate loss of disc height posteriorly at the L5–S1 segment. Physical therapy had been initiated 10 weeks previously with minimal improvement. The patient reports that mostly passive modalities had been employed in therapy for pain and spasm control, as several attempts at advancement to an active extension-biased McKenzie stabilization program proved too difficult due to pain provocation. An MRI of the lumbar spine was ordered, revealing focal degenerative disc desiccation at the L5–S1 segment with reactive endplate edema and a highintensity zone lesion posteriorly (Figs 92.9, 92.10). A diagnosis of discogenic lumbar axial pain was made and the patient underwent two therapeutic bilateral S1 transforaminal ESIs. After the second procedure, the patient reported greater than 90% alleviation of his lumbar pain. Physical therapy was reinitiated, resulting in nearcomplete symptom resolution. The patient understood the key to obtaining long-term success with management of his disc disease included compliance with his home exercise program and proper

Section 5: Biomechanical Disorders of the Lumbar Spine

lumbar spine mechanics during all activities. Although the patient continues to have occasional lumbar pain episodes, he reports that these episodes resolve within a few days with rest, activity modification and/or mild analgesics.

Case study 2

Fig. 92.9 T-weighted sagittal and axial images of a high-intensity zone lesion located within the posterior rim of the L4–5 intervertebral disc. Note the high signal intensity of the lesion easily visualized due to the backdrop of a dark, desiccated intervertebral disc.

A.D. is a 61-year-old female who presents to an interventional spine specialist with a 1-year history of slowly worsening left-sided lumbar axial pain of spontaneous onset. The patient reports focal lumbar pain just to the left of midline of the low lumbar spine without lower extremity radiation and qualifies the symptoms as a dull ache which worsens with prolonged standing and becomes sharp with left-sided lumbar extension. Physical examination reveals tenderness upon deep palpation over the left side of the low lumbar spine and limitation of lumbar extension by 50%, eliciting sharp left-sided lumbar pain. The patient had a normal lumbosacral spine neurologic examination. Imaging of the lumbar spine revealed varying degrees of degenerative changes throughout the lumbar spine. Z-joint arthropathy was found at all segmental levels with the left side affected worse than the right. In addition, asymmetric levels of fluid were noted in the left L4–5 and L5–S1 Z-joints. A presumptive diagnosis of left lumbar Z-joint syndrome was made and the patient underwent successive diagnostic intra-articular injections of the left lumbar Z-joints. The diagnostic left L5–S1 was negative but the left L4–5 level proved positive. Subsequent therapeutic left intra-articular L4–5 Z-joint injections resulted only in short-term pain improvement. The presumptive diagnosis of left L4–5 Z-joint syndrome was verified via medial branch blocks of the L3 and L4 spinal nerves via a dual-block paradigm. This test proved positive and subsequent radiofrequency ablation of the medial branches of the dorsal rami of the left L3 and L4 spinal nerves provided 75% relief of the patient’s left-sided lumbar pain. Physical rehabilitation focusing on lumbar spine stabilization exercises and core strengthening was stressed to the patient as an important adjunct in optimizing spinal health in the future.

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Fig. 92.10 T-weighted sagittal and axial images of a high-intensity zone lesion located within the posterior rim of the L4–5 intervertebral disc. Note the high signal intensity of the lesion easily visualized due to the backdrop of a dark, desiccated intervertebral disc.

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Section 5: Biomechanical Disorders of the Lumbar Spine 68. Ashtar IK, Aston BA, Gibson SJ, et al. Morphological basis for back pain: The demonstration of nerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum. J Orthop Res 1992; 10:72–78. 69. Yamashita T, Cavanaugh JM, El-Boly AA, et al. Mechanosensitive afferent units in the lumbar facet joint. J Bone Joint Surg [Am] 1990; 72:865–870. 70. Yamashita T, Cavanaugh JM, Ozaktay AC, et al. Effect of substance P on mechanosensitive units of tissues around the facet joint. J Orthop Res 1993; 11:205–214. 71. Mayer T, Robinson R, Pegues P, et al. Lumbar segmental rigidity: can its identification with facet injections and stretching exercises be useful? Arch Phys Med Rehabil 2000; 81:1143–1150. 72. Revel ME, Listrat VM, Chevalier XJ, et al. Facet joint block for low back pain: identifying predictors of a good response. Arch Phys Med Rehabil 1992; 73(9):824–828. 73. Revel M, Poiraudeau S, et al. Capacity of the clinical picture to characterize low back pain relieved by facet joint anesthesia. Proposed criteria to identify patients with painful facet joints. Spine 1998; 23(18):1972–1976.

82. Lau LS, Littlejohn GO, Miller MH. Clinical evaluation of intra-articular injections for lumbar facet joint pain. Med J Aust 1985; 143:563–565. 83. Lippitt AB. The facet joint and its role in spine pain. Management with facet joint injections. Spine 1984; 9:746–750. 84. Manchikanti L, Pampati V, Bakhit CE, et al. Effectiveness of lumbar facet nerve blocks in chronic low back pain: a randomized clinical trial. Pain Physician 2001; 4:101–117. 85. Manchikanti L, Pampati V, Fellows B, et al. Prevalence of lumbar facet joint pain in chronic low back pain. Pain Physician 1999; 2:59–64. 86. North RB, Han M, Zahurak M, et al. Radiofrequency lumbar facet denervation: analysis of prognostic factors. Pain 1994; 57:77–83. 87. Horlocker TT, Wedel DJ, Offord KP. Does preoperative antiplatelet therapy increase the risk of hemorrhagic complications associated with regional anesthesia? Anesth Analg 1990, 70:631–634. 88. Botwin KP, Gruber RD, et al. Complications of fluoroscopically guided transforaminal lumbar epidural injections. Arch Phys Med Rehabil 2000; 81(8):1045–1050.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain

CHAPTER

Radiofrequency Denervation

93

Atul L. Bhat

INTRODUCTION Low back pain is ubiquitous to mankind by virtue of our upright posture. Traditionally, it has been believed that most episodes of spinal pain are short lived and that at least 90% of patients with low back pain recover in about 6 weeks with or without treatment.1–3 Contrary to this prior assumption of only 10–20% patients experiencing recurrent or chronic symptoms after an initial episode of low back pain, recent literature puts that number as high as 35–79%.4–7 The challenge lies, in this subgroup of subjects, to identify the specific pain generator so that appropriate interventional therapy may be initiated as and when indicated. The study by Kuslich et al.8 identified along with intervertebral disc, dura, ligaments, fascia, and muscles, zygapophyseal or facet joints as capable of transmitting pain in the low back region. Even prior to this anatomical study, Goldthwait9 in 1911 first recognized lumbar zygapophyseal joints as potential source of low back pain. He believed that joint asymmetry could result in pain secondary from nerve root pressure. Subsequently, in 1933, Ghormley10 first coined the term ‘facet syndrome’ as lumbosacral pain with or without sciatic pain, occurring after a twisting or rotary strain of the lumbosacral region. Badgley11 in 1941 suggested that facet joints by themselves could be a primary source of low back pain separate from the nerve compression component. However, it was not until 1963 when Hirsch et al.12 demonstrated that the low back pain distributed along the sacroiliac and gluteal areas with referral to the greater trochanter could be induced by injecting hypertonic saline in the region of the lumbar facet joints. In 1976, Mooney and Robertson,13 and three years later McCall et al.14 used fluoroscopy to confirm the location of intra-articular lumbar facet joint injections in asymptomatic individuals, demonstrating reproduction of back and leg pain after injection of hypertonic saline. Eventually, Marks15 in 1989, followed by Fukui et al.16 in 1997, described the distribution of pain patterns after stimulating the lumbar facet joints. Recent literature17 indicates that the prevalence of chronic lumbar zygapophyseal joint-mediated pain has a wide range that varies from 15% in the relatively younger patients, with confidence limits of 10–20%. This prevalence can be as high as 40% among the elderly population with confidence limits of 27–53%.18

ANATOMY The lumbar facet or zygapophyseal joints are paired, true synovial, diarthrodial joints that form the posterior aspect of the respective intervertebral foramina. The joint consists of hyaline cartilage, a synovial membrane, a fibrous capsule, and nociceptive fibers transmitted via the medial branches of the dorsal rami.19,20 These facet joints are innervated by the medial branches of the dorsal rami (posterior

primary rami) that exit the intervertebral foramina. The posterior primary rami travel posteriorly over the base of the transverse process. The dorsal ramus divides into a medial, an intermediate, and a lateral branch. The lateral branch ascends from the dorsal ramus just before it reaches the transverse process. The medial branch passes under the mammilloaccessory ligament and sends branches to the adjacent facet joint, the facet joint below, and the more medial erector spinae muscles. Thus, the joint is typically innervated from a branch at the same level and a branch originating from the foramen above. In contrast, the dorsal ramus at the fifth lumbar vertebral level (L5) travels between the ala of the sacrum and its superior articular process, which divides into the medial and lateral branches at the caudal edge of the process, the medial branch continuing medially, where it innervates the lumbosacral joint.21–23 Neuroanatomical studies12,24–26 indicate that the facet joint capsule is richly innervated, containing both free and encapsulated endings, and can undergo extensive stretch under physiological loading.27 It has been reported that protein gene product (PGP) 9.5, substance P (SP), calcitonin gene-related peptide (CGRP), dopamine β-hydroxylase (DBH), vasoactive intestinal polypeptide (VIP), neural peptide Y (NPY), and choline acetyl transferase (chAT) immunoreactive (IR) fibers are present within the human facet joint capsule.21,26,28–30 Ashton et al.31 confirmed immunoreactivity for SP, CGRP, and VIP in surgically removed human facet joint capsule. A subsequent anatomical study confirmed higher concentration of inflammatory cytokines in facet joint tissue from patients with lumbar spinal stenosis than in lumbar disc herniations, suggesting that these cytokines may have some contribution to the etiology of symptoms in degenerative spinal stenosis.32

PATHOPHYSIOLOGY With aging, the changes that occur in the zygapophyseal joints are the same as those seen in any diarthrodial joint. The earliest change is synovitis, which may persist with the formation of a synovial fold which projects into the joint space itself. Later, degenerative changes set in gradually, and eventually become more marked. Eventually, the capsular laxity allows for subluxation of the joint surfaces. Continued degeneration mainly due to repeated torsional strains results in the formation of subperiosteal osteophytes, and possibly subchondral synovial cysts. The end result is that of gross articular degeneration, with almost complete loss of articular cartilage, and formation of bulbous zygapophyseal joints and marked periarticular fibrosis. The pathogenesis of a degenerative cascade in the context of a threejoint complex involving the intervertebral disc and the adjacent zygapophyseal joint also leads to the assumption that the degenerative changes within the disc are also believed to lead to associated facet degeneration.33–35 1027

Part 3: Specific Disorders

PAIN PATTERNS The clinical presentation of lumbar zygapophyseal joint-mediated low back pain appears to overlap considerably with the presentation of low back pain due to various other etiologies. Lumbar facet joints have been shown to be capable of producing pain in the low back and referred pain in the lower extremity in normal volunteers.13–16 McCall et al.14 concluded that pain referral patterns overlap between the upper and lower lumbar spine. Marks15 also studied patterns of pain induced from lumbar facet joints, from the posterior primary rami of L5, and from the medial articular branches of the posterior primary rami from T11 to L4. He observed no consistent segmental or somatic referral pattern. Marks also concluded that pain referred to the buttocks or trochanteric region occurred mostly from the L4 and L5 levels, while inguinal or groin pain was produced from L2 to L5. This latter finding led to the conclusion that the nerves innervating the joints gave rise to distal referral of pain more commonly than the facet joint itself. Fukui et al.16 concluded that the major site of referral pain from the L1–2 to L4–5 joints was the lumbar region itself. However, stimulation of the L5–S1 joint caused referred spinal pain as well as gluteal pain. Referred pain into the lower extremities was not observed by Fukui et al.16 as was reported by Mooney and Robertson.13 However, it must not be overlooked that in the study by Mooney and Robertson, the relatively large volume of the injectate (3 cc) used may very well have inadvertently anesthetized structures other than the facet joint intended. In essence, these studies indicate that there is no clear dermatomal or somatic pattern that is diagnostic of lumbar facet joint-mediated pain and an overlap with a varied pattern is the norm.

DIAGNOSIS All this being said, there is no identified correlation between a clinical picture or any imaging study used, such as the magnetic resonance imaging (MRI), computed tomography (CT) scan, single photon emission computed tomography (SPECT), or radionuclide bone scan in diagnosing pain mediated via the lumbar zygapophyseal joint.36–40 Simple static radiographs of the lumbar spine, and also dynamic images including standing flexion–extension films, may reveal evidence of arthritis involving the lumbar zygapophyseal joint as commonly in asymptomatic individuals as in patients with axial low back pain. What remains contentious is how lumbar zygapophyseal joint-mediated pain should be diagnosed. Another point not to be overlooked is the fact that psychological factors can be involved in cases of chronic low back pain. Long before the monumental work of Freud, it was recognized that emotional states could be associated with physical symptoms in the absence of an organic pathology. Consequently, it behooves the primary spine care provider to learn how to identify these patients, how to diagnose their conditions, how to treat them, and how, when, and from whom to seek consultation. Unless chronic spinal pain is simultaneously understood and treated from a musculoskeletal and psychological perspective, treatment failure will be the norm. Treatment modalities directed only at a physical or mechanical problem will not be sufficient or helpful if there is an associated unrecognized or ignored psychological problem. Diagnosis is the cornerstone of a rational treatment approach to any kind of illness. Spine physicians confronted with a patient describing chronic or ongoing back pain are pressed to establish a diagnosis. Appropriately, any clues derived from the history and from the physical examination are pursued toward that end. Schemata describing the great classifications of disease illustrate the breadth and scope of physical pathologic conditions that can be associated with low back pain. Thus, the differential diagnosis in a patient presenting with chronic low back encompasses 1028

numerous entities. Clinical problems tend to become complex when there is difficulty in establishing a diagnosis or when then the treatment options are unclear or difficult to implement. In approximately a quarter of the patient population there is a coexisting lesion responsible for the patient’s symptoms. Up-to-date laboratory and imaging techniques notwithstanding, nothing supplants and nothing exceeds the diagnostic accuracy of a thorough history and a careful physical examination. Because the causes of back pain are legion and involve virtually every organ system as well as the psyche, a truncated history, focused only on the spine should be avoided. A tunnel vision, essentially blinding oneself, will only lead to diagnostic followed by therapeutic pitfalls.

Diagnostic injections The only available means of establishing a diagnosis of lumbosacral zygapophyseal joint-mediated pain is to utilize diagnostic injections. Diagnostic blockade of a structure with a nerve supply with ability to generate pain can be performed to test the hypothesis that the target structure is the source of symptoms. If pain is relieved by blocking the medial branch or the zygapophyseal joint itself, the joint may be considered prima facie to be the source of pain.41 Pain relief is considered as the essential criterion, rather than provocation of pain from stimulating the target area. The choice lies with the spine interventionist whether to pursue an intra-articular zygapophyseal joint injection or anesthetize the medial branches of the dorsal rami that innervate the target joint. Debate continues regarding the appropriateness of intra-articular injections or medial branch blocks. For diagnostic intra-articular injection only a small volume (0.5–0.8 cc) of the local anesthetic agent is to be injected. Using small aliquots of local anesthetic will minimize extravasation of the anesthetic agent and necessarily diminish the frequency of a false-positive response. In essence the specificity of the diagnostic injection is enhanced. A small amount (0.2 cc) of contrast medium should be instilled to ensure an intra-articular spread. A partial arthrogram ensures appropriate needle placement and protects against false appreciation of joint entry and venous infiltration.42 Similarly, when a medial branch block is performed, contrast should be instilled prior to the actual injection of the anesthetic agent to ensure against venous uptake. Theoretically, medial branch injections may be more specific because there is a less likelihood of anesthetizing the epidural space or the neural foramina as long as the anesthetic volume is limited to 0.5 cc. The author prefers to peruse an intraarticular injection in the younger patient population where the joint is not affected by significant arthritis. A medial branch block is preferred in the elderly where it may be technically difficult to access the severely arthritic zygapophyseal joint or when lack of adequate joint space is suspected. Kaplan et al.43 did find that medial branch blocks can fail to anesthetize the target joint in a minority of cases, ostensibly in 11% but possibly in as many as 31%, based on 95% confidence interval intervals. These authors have postulated that an aberrant or additional innervation of the targeted joint may provide for a pathway for persistent nociception. While not refuting the ability of the medial branch blocks to positively diagnose zygapophyseal joint pain, they warn that facet joint pain may be underdiagnosed by such diagnostic blocks. Based on the response to a single diagnostic injection, the prevalence of the lumbar zygapophyseal joint pain in patients with chronic low back pain demonstrates a wide range of 7.7–75%.42,44–50 This wide range in numbers may represent a selection bias, variable population subsets, or even placebo responders. Similarly, a diagnosis cannot be made reliably on the basis of a single diagnostic injection, and falsepositive rates as high as 38% have been demonstrated.51 To increase the sensitivity of these diagnostic injections it has been suggested

Section 5: Biomechanical Disorders of the Lumbar Spine

that controlled diagnostic injection should include placebo injections utilizing normal saline.41 This may be accurate theoretically but is not practically viable, logistical, or ethical to use placebo injections in all patients presenting with low back pain presumably of lumbar facet origin. An attractive, reasonable alternative is the use of comparative local anesthetic blocks using two local agents with different duration of actions on two separate occasions.52–55 A double-block diagnostic injection involves the use of two different anesthetic injections, each with a different duration of action. A true-positive response to comparative local anesthetic injections is one in which the patient experiences pain relief for a shorter duration when a short-acting agent is used and for a longer duration when a long-acting agent is utilized. A triple-block paradigm requires three injections. The first uses a short-acting anesthetic agent. If a positive response is obtained, the patient is subjected to a series of two blinded injections. One injection uses intraparticular anesthetic agent, whereas the second is an extraparticular injection with saline. However, again it may not be logistically possible or ethically sound to use such regimens in a conventional practice on every patient. Once a diagnosis of lumbar zygapophyseal joint-mediated pain is established, therapeutic intra-articular zygapophyseal joint injection utilizing a steroid preparation or medial branch block can be utilized. These procedures have been described elsewhere in this textbook. The efficacy of such interventions may not be long lived and repeat injections may need to be performed on an individual basis. Most interventionist spine physicians limit the frequency of intra-articular steroid injections to 2–4 per year. However, there are no data to support or refute this number. From anatomical studies of the innervation of the facet joint it is clear that the medial branch of the dorsal ramus supplies sensory innervation to the joint. Radiofrequency neurotomy of medial branch of the dorsal ramus eliminates this sensory input for a considerably longer duration of time as compared with simple medial branch block and may be used in patients with the goal of achieving long-lasting pain relief.56 In the classic conception of pain, afferent nerves that are exposed to noxious stimuli transmit ascending pain signals through the dorsal horn to the brain where sensory perception is processed. This simplistic conception of pain has now been superseded and augmented by new evidence of pain signaling through many additional pathways. In addition to the psychological component of the perception of pain mediated by cultural, behavioral, and experimental influences, pain signaling can be modified within both the periphery and central nervous system to produce a self-sustaining, vicious cycle of pain syndromes. In the periphery, the imbalance of small and large fibers transmitting pain signals at the dorsal horn have been implicated in sustaining pain impulses even after the stimulation of the afferent nerve has been eliminated. Centrally, chronic pain may be mediated by changes in neuronal function in the dorsal horn or in biochemical mediators involved in descending signals of pain perception. This being said, it is rather naïve or too simplistic to assume almost complete resolution of lumbar pain will occur after attacking the medial branches of the presumably affected zygapophyseal joints.

REVIEW OF LITERATURE SUPPORTING CLINICAL EFFECTIVENESS OF LUMBAR RADIOFREQUENCY Historically, interventional management of lumbar zygapophyseal joint pain started with the use of a knife-cut in the region of the lumbar facet joint for denervation. Rees57 reported immediate relief of pain in 998 of 1000 patients suffering from ‘intervertebral disc syndrome’ using this technique. Shealy58,59 introduced the procedure

in North America but, after a large number of operations, changed to a radiofrequency coagulation lesion through a probe placed in the region of the nerve supply of the facet joint. Many investigators have studied the effectiveness of radiofrequency denervation of medial branches of the lumbar zygapophyseal joint, of which only four are prospective studies. These include two randomized, controlled trials by van Kleef et al.60 and Leclaire et al.,61 one double-blind, controlled study by Gallagher et al.,62 and a case series by Dreyfuss et al.55 In each of these studies, patients were included when they had failed to respond to traditional conservative treatment, such as a trial of bed rest, medications, and physical therapy. However, the inclusion or exclusion criteria were inconsistent across the studies. Gallagher et al.62 included patients with low back pain for at least 3 months and used diagnostic injections of 0.5 cc of 0.5% bupivacaine in and around the lumbar zygapophyseal joint. Patients with good or equivocal response to this injection within 12 hours were randomized to undergo either a lumbar facet joint denervation or placebo treatment. Radiofrequency lesions were performed for 90 seconds at a temperature of 80°C. McGill pain questionnaire63 and the visual analog scale (VAS)64 were used at 1 month but only the VAS at 6 months. Statistical comparison of pain scores was conducted using the Kruskal-Wallis and Mann Whitney U tests. Reduction in pain scores was approximately 50% at 1 month and was sustained at 6 months. The only difference in pain scores were seen when comparing people, all of whom met the inclusion criteria of a good response to an initial injection using 0.5 cc of 0.5% bupivacaine. The only statistical differences in pain scores in the post-treatment group occurred during comparing patients with a good initial response to local anesthetic injection but proceeding to a sham procedure. The randomized, controlled trial of van Kleef et al.60 included 31 patients with low back pain of at least 12 months. These were injected with 0.75 cc of 1% lidocaine about the two medial branches innervating a particular zygapophyseal joint. Patients were evaluated 30 minutes after this injection. Those with at least a 50% relief on a four-point Likert scale (0–30% pain relief was considered as no relief; 30–50% was defined as moderate; 50–80% pain relief was good, and 80% or more was considered as pain free) were randomized. Radiofrequency probes were placed in both groups but only one group underwent the actual radiofrequency lesioning for 60 seconds. Patients were followed for at least 12 months and the outcome measures included the VAS instrument, Oswestry disability index, and global perceived effect. At 8 weeks, a higher rate of success in the treatment group compared to the control group was noted. Subsequent log rank test showed a statistically significant difference ( p=0.02) at 3, 6, and 12 months. Leclaire et al.61 performed a diagnostic intra-articular facet joint block with 0.5 cc of lidocaine 2% and 0.5 cc of 40 mg of triamcinolone acetonide. Significant relief of low back pain for at least 24 hours in the week after this injection was considered as positive. For each nerve, radiofrequency neurotomy was performed at two locations, one at the proximal portion and another at the distal portion of the dorsal ramus with the temperature controlled at 80°C for 90 seconds. For patients in the control group the temperature of the probe was maintained at 37°C. Follow-up assessments were undertaken at 4 and 12 weeks when the disability questionnaire, the visual analog scale, the triaxial dynamometry, and the return to work assessment was repeated. The primary analysis was based on the intention to treat principle. At the end of 4 weeks, there was an improvement in the Roland-Morris score65 by 8.4% and 2.2% in the radiofrequency and control groups, respectively. However, at 12 weeks there was no significant difference in the Roland-Morris,65 Oswestry disability,66 VAS,64 strength/mobility, and return-to-work status in both groups. 1029

Part 3: Specific Disorders

Dreyfuss et al.55 used 0.5 cc of lidocaine 2% for the initial zygapophyseal joint injection. A positive response was defined as at least 80% relief of pain lasting longer than 1 hour. At the end of 1 week, this group of patients underwent another diagnostic injection using bupivacaine 0.5%. Subjects experiencing greater than 80% relief, lasting longer than 2 hours, were included in the study. The technique used by Dreyfuss et al.55 was different in that the radiofrequency ablation was performed for 8–10 mm along the length of the target nerve with the temperature being maintained at 85°C. The outcome measures included VAS,64 Roland-Morris questionnaire,65 prescription analgesic medication, McGill pain questionnaire,63 ShortForm (SF)-36 general health questionnaire,67,68 North American Spine Society (NASS)69 treatment expectations, isometric push and pull, dynamic floor-to-waist lift, and isometric above-shoulder lifting tasks. In addition, a needle electromyography of the L2–L5 bands of the multifidus muscle was performed before and at 8 weeks after the radiofrequency denervation. Patients were evaluated with at least a 12 month follow-up. Statistical analysis was performed using median scores and interquartile ranges of all outcome measures, Friedman two-way analysis of variance, Wilcoxon paired test, and Spearman correlation coefficients. Sixty percent of patients experienced at least a 90% pain reduction, whereas 87% of patients experienced at least a 60% reduction in pain. This effect lasted for 12 months. Fortyseven percent of patients obtained absolute reduction of at least 5 in the VAS,64 and 60% obtained relative reduction of at least 3. They noted that, even for patients who experienced pain for more than 5 years, radiofrequency denervation of the medial branch was helpful, cost effective, and less time consuming than other interventions such as exercise-based physical therapy or manipulative care. The results of needle electromyography warrants a special mention, with 11 of 15 patients sustaining 100% denervation, whereas 4 achieved partial denervation. A critical review of each of these studies is of prime importance if one is to derive a deep understanding of this therapeutic intervention for the treatment of lumbar zygapophyseal joint mediated pain. Each study used a small sample size, with van Kleef et al.60 and Dreyfuss et al.55 using only 15 subjects each in the treatment group. Gallagher et al.62 and Leclaire et al.61 did not specify how a successful outcome to the diagnostic injections was objectively rated. Dreyfuss et al.55 and Leclaire et al.61 were the only two sets of authors who followed their patients for at least 12 months. There were also discrepancies noted in reporting the diagnostic injection. Gallagher et al.,62 in their abstract, mention that the solution used was a combination of local anesthetic agent with steroid, whereas the main text of the paper states that the solution used was only local anesthetic. Van Kleef et al.60 used a double-blind, placebo-controlled injection paradigm. Unfortunately, patients were selected on the basis of a single positive diagnostic injection which, as discussed previously, is known to have a false-positive rate of approximately 38%.51 The technique used by van Kleef et al.61 was different, such that the electrodes were placed at an angle to the target nerve. Laboratory studies have shown that the electrode must lie parallel to the nerve if the nerve is to be optimally and maximally coagulated.56 This may explain why van Kleef et al.60 obtained only modest results. Similarly, van Kleef et al.60 and Dreyfuss et al.55 included subjects with low initial VAS scores. Although Dreyfuss et al.55 used the strictest inclusion criteria in their prospective audit, they unfortunately treated only a small sample size. By performing two different diagnostic injections with two anesthetic agents, each with a different duration of action, they tried to eliminate the false-positive responders. Also, during the radiofrequency denervation, the electrodes were placed meticulously to optimize coagulation of the nerve. As previously stated, these authors conducted a needle electromyography of L2–L5 bands of multifidus 1030

before and at 8 weeks after the denervation. Although electromyographic evidence of denervation indicates that the radiofrequency ablation successfully coagulated the assessed medial branch, such an outcome did not correlate with symptom improvement. However, this study did not include a control group. In the Leclaire et al.61 study, the inclusion criteria was significant relief of low back pain for more than 24 hours after the facet injection. Roland-Morris score65 was used as an important outcome measure, which is a measurement of functional limitation and not of pain relief. A more in-depth questionnaire on pain, such as the McGill Pain Questionnaire,63 possibly could better identify the therapeutic response in these patients. These conflicting trials, discussing the use of radiofrequency denervation in the management of lumbar zygapophyseal joint-mediated pain, highlight the use of varied inclusion criteria, varied treatment, lack of uniform outcome measures, use of concurrent interventions, and lack of a sufficient follow-up. A detailed review of these deficiencies and critical analysis of the relevant peer-reviewed publications can be found elsewhere.70,71 A more recent anatomical study undertaken by Lau et al.72 validates the prime importance of placement of electrodes parallel to the target nerve. This underscores the fact that a meticulous technique will lead to superior results. Because of the insufficient quantity of high-quality studies, it is evident that prospective, randomized, controlled trials with uniform inclusion and exclusion criteria and assessing an appropriate number of subjects in each are necessary, as dictated by a power analysis. Additionally, such studies should use a standardized treatment, uniform outcome measures, and have an adequate follow-up duration of at least 12 months. The Agency for Health Care and Policy Research describes evidence rating for management of low back pain in adults.73 For the development of these guidelines, a rating schema was used to assess the strength or efficacy of a treatment or procedure. They offered five levels of strength: level I (conclusive): research-based evidence with multiple relevant and high-quality scientific studies; level II (strong): research-based evidence from at least one properly designed randomized, controlled trial of appropriate size (with at least 60 patients in each arm) and high-quality or multiple adequate scientific studies; level III (moderate): evidence from well-designed trials without randomization, single group pre-post cohort, time series, or matched case-controlled studies; level IV (limited): evidence from well-designed nonexperimental studies from more than one center or research group; and level V (intermediate): opinions of respected authorities, based on clinical evidence, descriptive studies, or reports of expert committees. Critical review of the literature reveals that the type and strength of efficacy evidence for radiofrequency neurotomy in managing lumbar zygapophyseal joint-mediated pain is level III evidence.

CONCLUSION In summary, the process of establishing a diagnosis of lumbar zygapophyseal joint-mediated pain, the techniques used to make this diagnosis and implementing an effective treatment algorithm has evolved extensively over the past three decades since Mooney and Robertson proposed the posterior joints of the lumbar spine as a potential source of low back pain (Fig. 93.1). The question is not whether the syndrome of lumbar zygapophyseal joint pain exists but how to come to an accurate diagnosis and how to treat it effectively. The challenge lies in the accurate diagnosis of this entity so that appropriate interventional therapy may be instituted. Regardless of the approach used, the diagnosis can only be affirmed using, at a minimum, a double-block paradigm due to the low positive predictive value of a single diagnostic injection. If attractive, compelling results

Section 5: Biomechanical Disorders of the Lumbar Spine Axial pain on extension/rotation single stance extension facet arthrosis on imaging studies

5. Cassidy D, Carroll L, Cote P. The Saskatchewan health and back pain survey. Spine 1998; 6. Carey TS, Garrett JM, Jackman A, et al. Recurrence and care seeking after acute low back pain. Results of a long-term follow-up study. Med Care 1999; 37:157–164. 7. Van Den Hoogen HJM, Koes BW, Deville W, et al. The prognosis of low back pain in general practice. Spine 1997; 22:1515–1521.

Conservative care (therapy/medications)

8. Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back pain and sciatica: A report of pain response to tissue stimulation during operation on the lumbar spine using local anesthesia. Orthop Clin North Am 1991; 22:181–187.

No relief

Consider interventional therapy

9. Goldthwait JE. The lumbosacral articulation: An explanation of many cases of lumbago, sciatica, and paraplegia. Boston Med and Surg J 1911; 164:365–372. 10. Ghormley RK. Low back pain. With special reference to the articular facets, with presentation of an operative procedure. JAMA 1933; 101:1773–1777. 11. Badgley CE. The articular facets in relation to low back pain and sciatic radiation. J Bone Joint Surg 1941; 23:481.

Diagnostic intra-articular block with 2% lidocaine or medial branch block

12. Hirsch D, Inglemark B, Miller M. The anatomical basis for low back pain. Acta Orthop Scand 1963; 33:1. 13. Mooney V, Robertson J, The facet syndrome. Clin Orthop 1976; 115:149–156. 14. McCall IW, Park WM, O’Brien JP. Induced pain referral from posterior elements in normal subjects. Spine 1979; 4:441–446.

Negative: think of lumbar myofascial pain, enthesopathy

Positive

15. Marks R. Distribution of pain provoked from lumbar facet joints and related structures during diagnostic spinal infiltration. Pain 1989; 39:37–40. 16. Fukui S, Ohseto K, Shiotani M, et al. Distribution of referral pain from the lumbar zygapophyseal joints and dorsal rami. Clin J Pain 1997; 12:303–307.

Two sets of diagnostic blocks with lidocaine and bupivacaine at different times

17. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints: Is the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–1137. 18. Schwarzer AC, Wang S, Bogduk N, et al. Prevalence and clinical features of lumbar zygapophyseal joint pain. Ann Rhem Dis 1995; 54:100–106.

Positive

Negative: exclude facet pain

19. Bogduk N, Engel R. The menisci of the lumbar zygapophyseal joints. A review of their anatomy and clinical significance. Spine 1984; 9:454–460. 20. Bogduk N, Twomey LT. Clinical anatomy of the lumbar spine, 2nd edn. London: Churchill Livingstone; 1991. 21. Pedersen HE, Blunck CFJ, Gardner E. The anatomy of lumbosacral posterior rami and meningeal branches of spinal nerves (sinu-vertebral nerves). J Bone Joint Surg [Am] 1956; 38A;377–391.

Therapeutic block with steroid and lidocaine

22. Bogduk N, Wilson AS, Tynan W. The human lumbar dorsal rami. J Anat 1982; 134:383–397. 23. Bogduk N. The innervation of the lumbar spine. Spine 1983; 8(3):286–293.

Recurrence

24. Jackson HC, Winkelmann RK, Bickel WH. Nerve endings in the human spinal column and related structures. J Bone Joint Surg [Am] 1966; 48A:1272

Medial branch blocks

Repeat therapeutic block

25. Bogduk N. Nerves of the lumbar spine. In: Clinical anatomy of the lumbar spine and sacrum, 3rd edn. New York: Churchill Livingstone; 1997:127–143. 26. Suseki K, Takahashi Y, Takahashi K, et al. Innervation of the lumbar facet joints. Spine 1997; 22:477–485.

Radiofrequency denervation Fig. 93.1 Effective treatment algorithm.

are to be achieved following a lumbar radiofrequency denervation, the clinician needs to follow two basic but often overlooked steps: establish an accurate diagnosis of lumbar facet syndrome and then, during treatment, adhere to a meticulous placement of electrodes.

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Part 3: Specific Disorders 36. Wiesel SW, Tsourmas N, Feffer HL. A study of computer assisted tomography I: The incidence of positive CAT scans in an asymptomatic group of patients. Spine 1981; 9:549–551. 37. Jensen M, Brant-Zwawadzki M, Obuchowski N. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 2:69–73. 38. Schwarzer AC, Wang S, O’Driscoll D, et al. The ability of computed tomography to identify a painful zygapophyseal joint in patients with chronic low back pain. Spine 1995; 20:907–912. 39. Ryan PJ, Di Vadi L, Gibson T, et al. Facet joint injection with low back pain and increased facetal activity on bone scintigraphy with SPECT: A pilot study. Nucl Med Commun 1992; 13:401. 40. Schwarzer AC, Scott AM, Wang S, et al. The role of bone scintigraphy in chronic low back pain: Comparison of SPECT and planar images and zygapophyseal joint injection. Aust NZ J Med 1992; 22:185. 41. Bogduk N. International Spinal Injection Society guidelines for the performance of spinal injection procedures: Part 1: Zygapophyseal joint blocks. Clin J Pain 1997; 13:292–297. 42. Dreyfuss PH, Dryer SJ, Herring SA. Contemporary concepts in spine care: Lumbar zygapophyseal (facet) joint injections. Spine 1995; 20(18):2040–2047. 43. Kaplan M, Dreyfuss P, Halbrook B, et al. The ability of lumbar medial branch blocks to anesthetize the zygapophyseal joint: A physiologic challenge. Spine 1998; 23(17):1847–1852. 44. Carette S, Marcoux S, Truchon R, et al. A controlled trial of corticosteroid injections in the facet joints for chronic low back pain. N Engl J Med 1991; 325:1002–1007. 45. Carrera GF. Lumbar facet joint injection in low back pain and sciatica: Preliminary results. Radiology 1980; 137:665–667. 46. Carrera GF, Williams AL. Current concepts in evaluation of the lumbar facet joints. Crit Rev Diagn Imaging 1984; 21:85–104. 47. Destouet JM, Gilula LA, Murphy WA, et al. Lumbar facet joint injection: Indication, technique, clinical correlation, and preliminary results. Radiology 1982; 145:321–325. 48. Destouet JM, Murphy WA. Lumbar facet block: indication and technique. Orthop Rev 1985; 14:57–65. 49. Helbig T, Lee CK. The lumbar facet syndrome. Spine 1988; 13:61–64. 50. Raymond J, Dumas JM. Intra-articular facet block: diagnostic test or therapeutic procedure? Radiology 1989; 151:333–336. 51. Schwarzer AC, Aprill CN, Derby, et al. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophyseal joints. Pain 1994; 58:195–200. 52. Bonica JJ. Local anesthesia and regional blcoks. In: Wall PD, Melzack R, eds. Textbook of pain, 2nd edn. Edinburgh: Churchill Livingstone; 1989:724–743. 53. Bonica JJ, Buckley FP. Regional analgesia with local anesthetics. In: Bonica JJ, ed. The management of pain. Philadelphia: Lea & Fibeger; 1990:1883–1966. 54. Boas RA. Nerve blocks in the diagnosis of low back pain. Neurosurg Clin North Am 1991; 2:806–816. 55. Dreyfuss P, Halbrrok B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophyseal joint pain. Spine 2000; 25(10):1270–1277.

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56. Bogduk N, Macintosh J, Marshland A. Technical limitations to the efficacy of radiofrequency neurotomy for spinal pain. Neurosurgery 1987; 20:529–535. 57. Rees WES. Multiple bilateral subcutaneous rhizolysis of segmental nerves in the treatment of the intervertebral disc syndrome. Ann Gen Pract 1971; 16:126–127. 58. Shealy CN. The role of spinal facets in back and sciatic pain. Headache 1974; 14:101. 59. Shealy CN. Facet denervation in the management of back and sciatic pain. Clin Orthop 1976; 115:157–164. 60. Van Kleef M, Barendse GAM, Kessels A, et al. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine 1999; 24(18):1937–1942. 61. Leclaire R, Fortin L, Lambert T, et al. Radiofrequency facet joint denervation in the treatment of low back pain: a placebo-controlled clinical trial to assess efficacy. Spine 2001; 26(13):1411–1417. 62. Gallagher J, Petriccione di Vadi PL, Wedley JR, et al. Radiofrequency facet joint denervation in the treatment of low back pain: a prospective controlled double-blind study to assess its efficacy. Pain Clin 1994; 7(3):193–198. 63. Melzack R. The McGill pain questionnaire: Major properties and scoring methods. Pain 1975; 1:277–299. 64. Huskisson EC. Visual analog scales. In: Melzack R, ed. Pain measurement and assessment. New York: Raven Press; 1983:33–37. 65. Roland M, Morris R. A study of the natural history of back pain. Part I: Development of a reliable and sensitive measure of disability in low-back pain. Spine 1983; 8:141–144. 66. Fairbank JC, Couper J, Davies JB, et al. The Oswestry low back pain disability questionnaire. Physiotherapy 1980; 66(8):271–273. 67. McHorney CA, Ware JE, Raczek AE. The MOS 36-item short-form health survey (SF-36): II. Psychometric and clinical tests of validity in measuring physical and mental health constructs. Med Care 1993; 31:247–263. 68. Ware JE, Sherbourne CD. The MOS 36-item short-form health survey (SF-36): I. Conceptual framework and item selection. Med Care 1992; 30:473–483. 69. Daltroy LH, Cats-Beril WL, Katz JN, et al. The North American Spine Society lumbar spine outcome assessment instrument: reliability and validity tests. Spine 1996; 21:741–749. 70. Niemisto L, Kalso E, Malmivaara A, et al. Radiofrequency denervation for neck and back pain: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2003; 28:1877–1888. 71. Slipman CW, Bhat AL, Gilchrist RV, et al. A critical review of the evidence for the use of zygapophyseal injections and radiofrequency denervation in the treatment of low back pain. Spine J 2003; 3:310–316. 72. Lau P, Mercer S, Govind J, et al. The surgical anatomy of lumbar medial branch neurotomy (facet denervation). Pain Med 2004; 5:289–298. 73. Bigos SJ, Boyer OR, Braen GR, et al. Clinical practice guideline number 4: Acute low back problems in adults. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services, December 1994. AHCPR Publication 95-0642.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disk Disorders ■ iii: Lumbar Axial Pain

CHAPTER

94

Lumbar Provocation Discography: Clinical Relevance, Sensitivity, Specificity, and Controversies Michael B. Furman, William A. Ante, and Ryan S. Reeves

INTRODUCTION Lumbar provocation discography is a commonly used diagnostic procedure utilized to determine the presence or absence of discogenic pain at a specific spinal segment. Although discography has been proposed as the criterion standard for identifying discogenic pain [NASS statement], the test is controversial. Skeptics argue that newer diagnostic tests such as MRI scans make discography obsolete and the test should be discontinued unless its utility can be validated.1 This chapter will discuss the clinical relevance of lumbar provocation discography by correlating discography findings with the standard clinical work-up, and by its ability to help guide treatment. Additionally, we will describe controversies in technique and interpretation.

CORRELATION OF LUMBAR PROVOCATION DISCOGRAPHY WITH HISTORY AND PHYSICAL EXAMINATION FINDINGS Various studies have attempted to correlate history and physical examination findings with the diagnosis of discogenic pain by discography and to compare these findings with respect to treatment outcome (Fig. 94.1). Simmons and Segil2 reported a diagnostic accuracy of 44% for clinical examination and 82% for discography based on ability to predict symptomatic level as confirmed by successful clinical result after surgery. They did not specify any particular tests used preoperatively, but used the following in follow-up examinations: straight leg raise, neurologic examination including reflexes, sensory or motor, range of motion, and tenderness. Although they correlated discogram results with these physical examination techniques, no other outcome instruments were correlated. Schwarzer et al.3 found that no historical or clinical examination finding that they studied in 92 patients could accurately identify patients with internal disc disruption as diagnosed by provocation discography. Historical findings sought were pain increased or was relieved by sitting, standing, or walking. Pain referral patterns studied were pain into the buttock, groin, thigh, calf, or foot and whether the pain was unilateral, bilateral, or midline. Physical examination findings performed included provocation of pain with forward flexion, extension, rotation, combined rotation with extension, or straight leg raising making either back or leg pain worse.3 There was a trend (lowest p values obtained) with historical finding of pain increased with sitting ( p=0.13), pain increased with standing ( p=0.13), but also pain relieved with sitting ( p=0.16) and physical examination finding of pain increased with forward flexion ( p = 0.16). There was a negative trend (highest p values obtained) with a historical finding of pain increased with walking ( p=0.89) or physical examination finding of pain increased with extension.

Young et al.4 prospectively examined 81 patients with clinical examination and various diagnostic injections and found a weak but statistically significant correlation of discogenic pain as diagnosed by discography with centralization of pain with repeated end-range movements ( p=0.025, Phi=0.5). Although localization of a specific symptomatic level was not studied, 47% of those with positive discograms had ‘retreat of referred symptoms from the periphery toward the midline of the spine’ (centralization) during the standard McKenzie evaluation. Centralization was not seen with zygapophyseal joint pain as diagnosed by single intra-articular injection. Furthermore, all patients with a positive discogram (15 of 24 total discograms) reported pain when rising from sitting. A positive correlation ( p=0.02) was, however, also noted in patients with sacroiliac joint pain. Donelson et al.5 also prospectively studied 63 patients with chronic low back pain to evaluate the ability of the McKenzie mechanical lumbar assessment to diagnose discogenic pain and assess annular competence as determined by provocation discography. Seventyfour percent of centralizers and 69% of peripheralizers had a positive discogram as defined as exact pain reproduction accompanied by an abnormal image (nucleogram/CT), provided no pain was reproduced at an adjacent control level. The disc was interpreted as having a complete annular disruption or noncontained pathology if there was poor resistance to injection and contrast spread through the anulus to the epidural/perineural or peridiscal space. The disc was interpreted as having an intact outer anulus or contained pathology if there was firm resistance to injection even if contrast leaked from the disc at peak injection pressure. Of the centralizers, 91% had a competent anulus. Of the peripheralizers, 54% had a competent anulus. Of the patients whose symptoms did not change with repeated end-range movement, only 12.5% had a positive discogram. These differences were significant. The localization of a specific symptomatic level was not addressed and, therefore, these maneuvers could only be used for screening but not for identifying specific symptomatic disc levels for targeted interventional treatment. A ‘bony vibration stimulation test’ or ‘vibration pain provocation’ was described by Yrjama and Vanharanta and the results of bony vibration were compared to the results of provocation discography.6 The studies assumed provocation discography as the reference standard and compared the bony vibration stimulation test by itself or in combination with either ultrasound or MRI. The bony vibration stimulation test described utilized a Braun 3-D electric toothbrush as a modified vibrator device with a frequency of vibration of 42–50 Hz. The patient was laid on the more symptomatic side. The lumbar spinous processes were sequentially compressed with the vibrator's head in either the on or off position. If there was more pain with vibration than without vibration and this pain was described as concordant, the test was classified as ‘painful.’ 1033

Part 3: Specific Disorders

Left

Left

Right

Right

Right

B

A

Fig. 94.1 Pain drawings can be an important clinical tool in the prescreening evaluation. By having a patient diagram the location of their pain, a more streamlined approach to the patient can be pursued. (A) is an ideal discography candidate with axial back pain. (B and C) could potentially be screened out since patients with major components of radicular and whole body pain are suboptimal discography candidates.

Left

Right

Right

C

Thirty-eight patients were studied with the bony vibration stimulation test, ultrasound, and provocation discography.7 Discs were graded by ultrasonographic findings. Grade 0 was a normal disc. Grade 1 discs showed a hyperechoic lesion in the inner anulus. Grade 2 discs demonstrated a hyperechoic lesion in the outer anulus. Grade 3 discs showed a hyperechoic area extending outside the disc. When used alone, the bony vibration stimulation test yielded a sensitivity of 65% and a specificity of 58%. In the patients with a grade 1 or grade 2 disc, the sensitivity was 90% and specificity 75%. In the patients who had a grade 3 disc and pain on bony vibration the sensitivity and specificity were 50%. The authors also studied 33 patients with low back pain, correlating the results of bony vibration stimulation test and MRI with

1034

the results of provocation discography.8 When used alone, the bony vibration stimulation test yielded a sensitivity of 63% and specificity of 44%. If patients with history of previous lumbar surgery were excluded, the sensitivity was 61% and specificity 67%. In patients with or without previous history of surgery who had MRI findings of ‘partial annular rupture’ (as defined as irregular or absent intranuclear cleft images or bright-signal nuclear material into the outer anulus on T2-weighting), the sensitivity was 88% and specificity 50%. If the patients with previous surgery were excluded from this group, the sensitivity was 88% and the specificity 75%. The only false-positive finding in this group was a patient who was ‘hypersensitive’ and felt pain at all levels tested. If a ‘total annular rupture’ (defined as

Section 5: Biomechanical Disorders of the Lumbar Spine

T2-weighted or proton density images showing discontinuity of the low-signal band representing the outer rim of the anulus) was seen, the sensitivity decreased to 47% and specificity to 50%. These studies were, however, limited by their small sample sizes. Provocation discography was regarded as the reference standard for determining a symptomatic level without comparison to postprocedural outcome. Additionally, the findings of both bony vibration stimulation test and provocation discography were not recorded according to a specific spinal level. Finally, the protocol for discographic examination and interpretation was not fully elaborated.

UTILITY OF POSTDISCOGRAM COMPUTED TOMOGRAPHY Discography was originally used as an adjunctive to myleography to visualize lateral herniations (Fig. 94.2). There are, however, fundamental limitations to using discograms exclusively as an imaging tool. The classic nucleogram patterns viewed with anteroposterior (AP) and lateral

Fig. 94.2 Discography showing a far lateral herniation.

A The above normal nucleogram is described as a cottonball pattern where the contrast is a centralized mass within the nucleus

B The above normal nucleogram is described as a lobular pattern where the contrast is also centralized with two distinct arcs juxtaposed to the superior and inferior end plates

radiographs have been described as both normal and degenerative. Quinnell is credited with the original description of interpreting radiographic images of discography although he never proposed a classification scheme.9 He discussed the importance of monitoring contrast flow and volume to help improve the interpretation of the nucleograms. In 1986, Adams et al. initially classified nucleogram patterns into five categories; cottonball, lobular, irregular, fissured, and ruptured (Fig. 94.3).10 Cottonball and lobular patterns are thought to be normal variations, while fissured and ruptured are pathological. An irregular pattern is considered intermediate between these normal and pathological presentations. Adams et al. hypothesized the pathological patterns were due to disc degeneration. Cottonball nuclear patterns show the contrast central to the disc with an ovoid appearance (Fig. 94.3A). Lobular nuclear patterns also show the contrast centralized within the disc; however, there are two distinct arcs that may or may not be contiguous (Fig. 94.3B). An irregular pattern shows some tracking of the contrast outside the central nucleus without extension to the outer anulus (Fig. 94.3C). Although the contrast is intranuclear with irregular nucleograms, the small crevices and clefts exhibit early evidence of degeneration. Fissured nucleograms extend to the posterior annular margin, while ruptured nucleograms demonstrate complete radial tears and show contrast spread into the epidural space (Figs 94.3D, 94.3E).10 Adams speculated that by viewing the first four types of nucleograms, a natural progression of disc degeneration can be seen. Postdiscogram CT scans provided a more comprehensive view of the disrupted anulus (Figs 94.4–94.6). Axial views allowed a more detailed view of pathological contrast patterns than the AP and lateral radiographs (see Figs. 94.3C, 94.3D, 94.3E). The disorganized patterns seen on radiographs now coalesced into structured images, demonstrating organized annular tears with circumferential spreading. In 1989, Thomas Bernard published a case series of 250 patients who underwent both discography and postdiscography CT.11 He showed that computed tomography scanning after discography was not only able to define the type of herniation and disc architecture (protrusion, extrusion, sequestration, or internal disc disruption), but it could also be used to rationalize false-positive levels in the setting of non-nuclear injections (annular injections) (Fig. 94.4). In 1987, Sachs et al. organized the previously inexactly described axial contrast patterns into the Dallas discogram scale (Fig. 94.5).12

C The above nucleogram is described as irregular. This pattern is considered an intermediate between normal and pathological. The pattern contains tracking outside the central nucleus without annular extension

D The fissured nucleogram is pathological. Characteristically, it displays extension of contrast into the outer margins of the anulus

E The above pathological nucleogram is ruptured. There is a complete tear in the anulus with contrast extension into the epidural space

Fig. 94.3 Illustrated examples of Adams's nucleogram classifications. 1035

Part 3: Specific Disorders

A

Fig. 94.4 Postdiscography CT with left-sided inner annular injection: (A) axial and (B) coronal views.

B

A Grade 1 spread into the inner 1/3 of the annulus

B Grade 2 spread into the outer 1/3 of the annulus

C Grade 3 extension of contrast beyond the outer annulus

D

E

F

Category 1: Spread of contrast in < 10% of the annulus

Category 2: Spread of contrast through < 50% of the annulus

Category 3: Contrast extending into > 50% of the annulus

Fig. 94.5 Illustrated is the annular description for the radial tear findings and circumferential degenerative findings for the original Dallas discogram scale described by BL Sachs et al. In (A), the radial extension of contrast moving away from the inner nucleus is shown. Grading of 1–3 is based upon the radial spread of the contrast towards the anulus (A–C). (D–F) The percentage quadrant distribution of circumferential spread displays the amount of degeneration within each disc. In addition to radial extension, grade 1–3 is also used to describe circumferential extension (D–F). Addition modifiers are meant to be employed to specify the areas of annular leakage as anterior, posterior, lateral, posterolateral, anterior, and posterior.

Sachs's original description was based on the appearance of the anulus. This allowed objective categorization of the anulus, classifying both degeneration and annular disruption separately. Sachs's grading 1036

of the Dallas discogram scale is based on a four-point scale of 0 to 3, with zero defined as normal. Annular disruption defined as ‘leaking/protrusion/annular fissuring’ is based on the radial spread of the contrast away from the center of the nucleus to the periphery (Fig. 94.5A–C). Grade 1 is defined as spread within the inner third of the anulus; grade 2 is into the outer third of the anulus, while a grade 3 is defined as moving beyond the outer anulus.12 Degeneration findings were based on the circumferential distribution of contrast contained in quadrants of the anulus (Fig. 94.5D–94.5F). Grade 1 was defined as local spread in less than 10% of the anulus. Grade 2 was defined as partial spread or less than 50%, while grade 3 was defined as greater than 50% spread of contrast across the anulus. The development of the Dallas discogram scale not only allowed a new perspective to classify annular degeneration and disruption, but it also increased the inter-rater reliability when interpreting these findings. Sachs et al. were able to show 91% reproducibility and 88% repeatability when using the Pearson correlation test.12 Furthermore, they showed how standard AP and lateral discogram radiographs may appear normal until viewed axially. This reproducibility helped validate the Dallas discogram scale. Aprill and Bogduk soon added a grade 4 to the disruption scale.13 Approximately 10 years after its original description, Schellhas et al. expanded upon the three-grade disruption classification system to propose the modified Dallas discogram scale. The modified Dallas discogram scale incorporates both aspects of degeneration described as circumferential involvement as well as annular disruption depicted as radial contrast extension. The definitions of grades 0–2 remained the same. Grade 3 was expanded slightly to include either focal or radial extension of contrast into the outer third of the anulus, with a limitation of circumferential spread less than 30 degrees. Grade 4 was defined the same as grade 3, but with greater than 30 degrees of circumferential spread into the outer anulus. Grade 5 is a full-thickness tear, either focal or circumferential, with extension of contrast outside the anulus (Fig. 94.6).14

CORRELATION OF LUMBAR PROVOCATION DISCOGRAPHY WITH LUMBAR MRI Lumbar MRI is a sensitive means to investigate anatomic abnormalities of the low back. However, even asymptomatic subjects have been noted to have significant spinal pathology on imaging, including disc protrusion or

Section 5: Biomechanical Disorders of the Lumbar Spine

extrusion with or without neural compromise.15–17 Therefore, although MRI demonstrates pathology, it does not necessarily reveal whether the abnormality is causing a patient's symptoms. The correlation between MRI findings and provocative discography results has been investigated. The common goal of these studies was to determine whether imaging findings could predict the presence of concordant discogenic pain. If imaging studies could reliably predict discography findings, discography was unnecessary. The accuracy of MRI findings such as the high-intensity zone (HIZ) and endplate changes in determining symptomatic levels have been compared to the results of discography.18

High-intensity zone A

B

C

The high-intensity zone in the lumbar spine was first described by Aprill and Bogduk (Fig. 94.7)13 as a high-intensity zone (HIZ) seen on T2-weighted, sagittal images and defined by the authors as a highintensity signal (bright white) located in the substance of the posterior anulus fibrosus. The HIZ must be clearly dissociated from the signal of the nucleus pulposus because it is surrounded superiorly, inferiorly, posteriorly, and anteriorly by the low-intensity (black) signal of the anulus fibrosus and because the HIZ has an appreciably brighter signal than the nucleus pulposus. Aprill and Bogduk investigated a subset of 41 patients who had both MRI and discography with postdiscography CT scan. The HIZ was identified in 28% of patients with low back pain sent for lumbar MRI. All discs with HIZ had abnormal imaging on postdiscography CT with either a modified Dallas discogram scale grade 3 or grade 4 annular tear, specifically a radial tear extending into the outer third of the anulus without (grade 3) or with (grade 4) circumferential contrast encompassing an arc of greater than 30 degrees. When compared to reproduction of pain by disc stimulation, the HIZ had a high correlation with exact or similar pain with a sensitivity of 63%, specificity of 97%, and positive predictive value of 95%. For exact pain reproduction, the sensitivity was 82% and specificity 89%. Schellhas et al.14 sought to reproduce Aprill and Bogduk's findings with a similar study. In their retrospective analysis of 100 HIZs in 63 symptomatic patients, all discs with HIZ were internally deranged with annular disruption, 87 of 100 HIZ discs were concordantly

HIZ

D

E

Fig. 94.6 Illustrated is the annular description for combination of radial tears and degenerative findings in the Modified Dallas discogram scale ultimately proposed by K.P. Schellhas et al. (A) Grade 1 of 5, unchanged from the original description, demonstrates extension within the inner third of the annulus. (B) Grade 2 of 5, also unchanged from the original description, illustrates extension into the outer third of the annulus. (C) Grade 3 of 5 reveals radial extension of contrast into the outer third of the annulus, with a limitation of circumferential spread less than 30 degrees. (D) Grade 4 of 5 demonstrates extension of contrast into the outer annulus with greater than 30 degrees of circumferential spread into the outer annulus. (E) Grade 5 of 5 illustrates a full thickness tear (focal in this example, although it may be circumferential) with extension of contrast freely into the epidural space.

Fig. 94.7 T2-weighted image shows a highintensity zone (HIZ) at L4–5. As originally described by Aprill and Bogduk in the British Journal of Radiology in 1992, an HIZ is an area of brightness or high signal intensity located in the posterior anulus fibrosus, distinctly separate from the nucleus pulposus and brighter than the nucleus on T2weighted images. 1037

Part 3: Specific Disorders

painful at discography, and all 87 of these concordantly painful HIZcontaining discs had grade 3 to grade 5 annular tears on their modified Dallas discogram scale. Their schema is identical to Aprill and Bogduk's; however, they further stratified the Dallas discogram and added grade 5 to identify those discs which had a ‘full-thickness tear, either focal or circumferential, with extra-anular leakage of contrast.’ Individual discs could be classified into two categories, such as grade3/grade 5 or grade 4/grade 5.14 After the symptomatic group was analyzed, 17 asymptomatic volunteers underwent MRI without discography in an attempt to determine the prevalence of HIZ in patients not exhibiting low back pain (LBP). Only 1 of 17 (5.9%) of lifelong asymptomatic volunteers had a lumbar MRI with an HIZ. Those volunteers who never had prior LBP had a younger average age as compared to the symptomatic group (29.6 years old versus 37.5 years old). Other similar studies correlating HIZ with positive provocation discography have shown poor sensitivity of 26%, high specificity of 90–95.2%, positive predictive values of 40–88.9%, and negative predictive value of 47–83%.19 The interobserver reliability of HIZ also varies. Aprill and Bogduk found that out of 67 images, the two observers agreed on the presence of HIZ in all but one (1.5%). Though both observers noted the abnormality, the two disagreed on its meeting the criterion of brightness due to poor-quality film. However, Smith et al.19 only found fair to good interobserver reliability with a kappa value of 0.57 with 95% confidence interval 0.44–0.70. The original description by Aprill and Bogduk13 only included HIZ located in the posterior anulus and had a prevalence of 28%. The clinical significance of the HIZ was further studied by Rankine et al.20 in a patient population without neural compression. When including HIZs in any aspect of the anulus, the prevalence in a specialty spine surgery clinic was 45.5%. Most of these were posterior (77%) followed by posterolateral (22%). The HIZ was associated with moderate disc degeneration as assessed by signal reduction on T2-weighted sagittal images. There was no correlation of presence of HIZ with clinical features such as age, duration of symptoms, Oswestry score, or Schober's extension–flexion range of motion testing. There was also no correlation with patient history of employment, pain above or below the knee, or the positions or activities worsening pain. No physical examination findings studied predicted the presence of HIZ. The examination findings tested were paraspinal muscle spasm, spinal tenderness, straight leg raise, neurologic testing with reflexes, myotomal and dermatomal testing, and Waddell's testing. Correlation of HIZ presence with positive provocative maneuvers producing concordant axial pain with forward bending or extension/quadrant loading was not measured.

Endplate degeneration on MRI Magnetic resonance signal intensity changes adjacent to vertebral endplates have been described and are associated with degenerative disc disease.21 Modic classified these endplate changes into two types, while others have expanded their classification to three.22 Type 1 endplate changes have decreased signal on T1-weighted images and increased signal intensity on T2-weighted images. Type 2 endplate changes have increased signal on T1-weighted images and isointense or slightly increased T2-weighted image signal intensity. Type 3 endplate changes have a decreased signal intensity on both T1-weighted and T2weighted images. Kokkonen et al.18 compared endplate degeneration to pain provocation on discography and to the original Dallas discogram description which included three grades of annular disruption. Modictype endplate degeneration was found to have a strong correlation with disc (anular) degeneration. There was no correlation between endplate degeneration and ‘disc rupture’(annular rupture) and no correlation between endplate degeneration and pain provocation by discography. 1038

Based on these data, provocation discography would not necessarily be positive for those who have pain associated with endplate changes.

LUMBAR PROVOCATION DISCOGRAPHY AND ITS PREDICTIVE VALUE FOR TREATMENT AND PROGNOSIS Discography is a presurgical technique used to identify concordantly painful disc(s) and to verify that adjacent discs are negative for concordant pain prior to a therapeutic interventional procedure. Together with imaging studies, the provocation of concordant back pain during disc pressurization is used to confirm one's clinical impression that a specific disc is a source of pain. The procedure is usually performed in patients with predominately axial pain who have failed conservative management and are considering more invasive treatments such as percutaneous intradiscal or open discal procedures based on the results of discography. Because the results of discography are used to justify interventional treatments, the results should have predictive value for treatment success or prognosis. Although several studies compare the results of discography to decision formulation and outcome, most of the studies have methodological shortcomings such as the use of nonvalidated and/or subjective outcome scales. Additionally, many early studies were done before the routine use of MRI and CT and used discography to identify a disc herniation while today discography is used to ‘prove’ a disrupted disc is the source of the patient's axial pain. The studies which correlate discography with clinical outcome after procedures assume that (1) the treatment chosen is appropriate for the given lesion, and (2) the procedure accomplished its intended goal (i.e. successful fusion, adequate decompression, etc.). This may have valid grounds and gives valuable information if there is a strong correlation of a discographically proven lesion with successful clinical outcome. If poor results are obtained from the surgical procedure, either the test (discography) or the treatment (specific procedure) is suspect. In 1975, Simmons and Segil retrospectively reported the value of discography for the cervical, thoracic, and lumbar spine by accurately localizing a symptomatic spinal level based on postoperative results.2 Lumbar discograms were performed at 995 levels in 393 patients. Discogram results were assessed by patient pain response, amount and resistance to injection, and discographic appearance by Collis criteria, which describes discs as normal, degenerate, or protruded. Various clinical examinations were compared to the results of surgery on a scale with poor, fair, good, or excellent categories based on patient rating, complaints, occupation, activities, examination findings, and radiographic findings. It was assumed that if the patient was relieved of preoperative symptoms or was significantly improved after surgery, that the level of surgery selected by a certain test was accurate. Specific diagnoses and numbers for each were not reported but lumbar surgeries performed were ‘discotomy,’ ‘discotomy and fusion’ (usually posterolateral and intertransverse), and fusion alone without laminectomy. Overall, 94% of these lumbar surgery patients had satisfactory (fair to excellent) results. Diagnostic accuracy for these surgical outcomes was 44% for clinical examination, 71.5% for routine radiography, 45.6% for myelography, and 82% for discography. Specificity, sensitivity, falsepositive, and false-negative rates were not addressed. In 1979, Brodsky and Binder23 performed a retrospective study of patients who underwent discography. The authors performed discography only if the myelogram was negative but the patient was clinically thought to have discogenic pain. Specific indications included complaints which were atypical or without localizing neurologic signs, a myelogram which was equivocal or indeterminate, and a myelogram which was positive at one level while symptoms were suggestive of another. Discography was also performed to evaluate discs adjacent

Section 5: Biomechanical Disorders of the Lumbar Spine

to a herniated disc. Decision-making was ‘significantly influenced’ by the discogram in 77.9% of cases. Decision-making would have been the same without discogram in 22.1%. Positive discography was confirmed with surgery in 55.8% of the cases. In 1988, Calhoun et al. prospectively studied the predictive value of symptom reproduction during provocation discography as a guide to planning spine surgery for symptomatic intervertebral discs in the absence of nerve root compression.24 All 195 patients had lumbar provocation discography at L4–5 and L5–S1, most at L3–4, and some at L2–3 and all underwent lumbar surgery including anterior or posterior fusion and/or laminectomy. With at least 2-year followup, surgical success was based on whether the surgical objective was achieved radiographically (successful fusion, etc.) and clinical result was based on complete or significant relief of symptoms, resumption of work and/or normal activities, and no intake of analgesics. Failure to achieve these results was ‘clinical failure.’ There were 137 patients who had a painful injection of a morphologically diseased disc in which 89% had significant clinical relief. There were 25 patients who had technically successful surgery for a morphologically abnormal disc but without symptom production on disc injection, and in these patients only 52% had significant symptomatic relief while most of the remaining 48% had no clinical benefit. Additionally, morphologically abnormal discs that did not cause symptoms during disc injection that were adjacent to symptomatic discs were found in 43 patients. These levels were not included in levels of surgical intervention and significant clinical benefit was 95% (41 of 43) in these patients. Of six patients who were surgically treated despite normal discography, only 50% had clinical benefit. Overall, comparing lumbar provocation discography to clinical outcome after technically successful surgery yielded an 82% accuracy rate, 90% sensitivity, and 9.7% false-negative rate. ‘Accuracy’ was defined by combining the 137 patients who had a positive discogram and did well with surgery (true positive) and the 25 patients who had morphologic abnormal discs but no symptoms on discogram. Also in 1988, Blumenthal et al.25 used provocation discography to diagnose internal disc disruption (IDD) with the main purpose of the study being to evaluate the efficacy of anterior lumbar fusion as a treatment for IDD. All 34 patients underwent provocation discography and anterior fusion with average follow-up of 29 months. The diagnosis of IDD required radiographic signs of degeneration and discography with concordant pain reproduction with ‘instillation of small amounts of contrast.’ Successful treatment was defined as return to work or normal activities and either no medications or use of NSAIDs only. Fusion success was judged by radiographs only. The successful fusion rate was 73 %, but successful clinical treatment rate was 74%. Four cases were indeterminate for fusion. Of those with healed grafts, 73% had clinical success while only 62.5% of those with nonunion had clinical success. Of those patients with a successful clinical result, 81% had evidence of fusion while only 56% of the clinical failures had evidence of fusion. The authors cite higher previous fusion rates of 91–96%.Wetzel et al. performed a retrospective review of 48 patients, with a minimum follow-up of 2 years, who had lumbar arthrodesis based on provocation discography results.26 All were symptomatic for a mean time of 34.4 months prior to discography. Pain reproduction was graded as concordant or nonconcordant. The discography protocol did not, however, include a negative control disc. Fifty-four percent were single-level discographies, presumably without a control level. Two- and three-level discographies accounted for 31% and 14.5%, respectively. Sixty three-levels were graded as positive based on a concordant pain response. Seventy-five percent of patients had a single-level positive discogram, but 72% of these ‘single-level positive’ patients only had a single level studied. Two-level and three-level positive results were obtained in 18.9% and 6.2%, respectively. However, of the two-level positive discs, 77.8% only had a two-level discogram. None of the previously operated levels was included in discography. Fusion was

performed to include all symptomatic levels determined by discography. Previously operated discs were included in fusion if they were adjacent to symptomatic discs. Anterior and posterior fusion techniques with and without varying instrumentation were performed. The clinical outcome was evaluated on the criteria of Zucherman which includes subjective symptom improvement, functional limitations, and amount of analgesic use. Categories were poor, fair, good, and excellent. Success of fusion was also assessed radiographically. At mean 35-month (range 24–65 months) final follow-up, there was a 46% (n=22) satisfactory clinical outcome with solid arthrodesis in 47.9% (n=23). All patients who had satisfactory clinical outcome had a solid fusion. Conversely, 95.7% of patients who had a solid fusion had a satisfactory clinical outcome. None of the patients who had nonfusion had a satisfactory outcome. Therefore, if the surgical goal of fusion of the symptomatic levels as determined by provocation discography was obtained, the clinical success rate was 95.7%. This study was limited by its retrospective nature, small sample size, discography technique as judged by today's standards, and varying operative techniques. Derby et al. retrospectively evaluated pressure-controlled discography for its ability to predict surgical outcomes for interbody fusion, intertransverse fusion, combination fusion, or nonsurgical treatment.27 The study's premise is that pressure-controlled manometric discography may allow improved and more specific diagnosis and categorization of discogenic pain and may have the potential to predict outcome of surgery (Fig. 94.8). The positive discs found on provocation discography of 90 patients were classified as ‘chemically sensitive,’ ‘mechanically sensitive,’ or ‘indeterminate’ based on pain provocation at specific values above ‘static opening pressure.’ ‘Opening pressure’ is the manometric reading taken when injected contrast is first visualized entering the disc on fluoroscopy. Derby et al. classified a chemically sensitive disc as one which has positive concordant pain provocation of (1) immediate onset when less than 1 mL of contrast is visualized reaching the outer anulus, or (2) at less than 15 psi above opening pressure. These discs were considered the ‘most positive’ since the lowest pressures resulted in significant concordant pain. A disc was classified as ‘mechanically sensitive’ when concordant pain was noted between 15 psi and 50 psi above opening pressure. A disc was categorized as ‘indeterminate’ when concordant pain occurred between 51 and 90 psi above opening pressure. A disc was classified as normal if no pain occurred at pressures up to 90 psi above opening pressure. Thirty-six patients with chemically sensitive discs were identified. Clinical out-

Fig. 94.8 Manometry has become an invaluable tool in the interrogation of painful discs. Several brands are currently available, with slight differences in the manometry meter and the ways to dispense the contrast while pressurizing the disc. 1039

Part 3: Specific Disorders

comes were based on the Patient Satisfaction Index adapted from the NASS low back pain outcome instrument, numerical rating scale for pain, and a modified ADL scale. ‘Favorable outcome’ was defined as at least two favorable outcomes of the three scales. There was no significant difference in patient outcome between those who underwent interbody/combined fusion versus those who had intertransverse fusion if pressure-controlled discographic classification was not considered. However, those patients who had chemically sensitive discs were found to have an 89% rate of favorable outcome with interbody/combined fusion, 20% favorable outcome with intertransverse fusion, and only 12% favorable outcome with nonoperative treatment. Although this study was limited by its small sample size and retrospective, nonrandomized nature, it demonstrates that lowpressure-sensitive discs may have a different pathobiology and respond differently to treatment than discs that are concordantly painful at higher pressures.28 Derby et al. went on to perform a pilot study in which 32 patients were prospectively followed before and after undergoing IDET.29 Percutaneous treatment was based on chronic low back pain for more than 6 months, axial pain comprising at least 60% of pain symptoms, negative neurologic and neural tension testing, and failure of conservative management. All had at least one positive disc (mean 2.04 symptomatic discs) on provocation discography as defined as provocation of at least 6/10 concordant pain accompanied by an abnormal nucleogram. The discs were classified as low-pressure discs if there was pain produced at minimal pressure less than 15 psi above opening pressure or high-pressure discs if pain was produced at more than 15 psi above opening pressure. Low-pressure discs comprised 37.5% of the discs and high-pressure discs were more common and comprised 62.5% of the discs. If there were more than two positive discs, a ‘clinical decision was made as to which discs were likely to be most symptomatic, and … included’ in the treatment levels. Outcome was assessed using Roland-Morris Disability Questionnaire and Visual Analogue Scale, NASS Low Back Pain Outcome Assessment Instrument Patient Satisfaction Index, and a general activity questionnaire. Favorable outcome was defined as improvement of three or four of the tools while nonfavorable outcome was defined as worsening of three or four of the tools. No change was recorded for all other results. Overall, 62.5% had a favorable outcome, 25% had no change, and 12.5% had a nonfavorable outcome. Among the low-pressure-sensitive discs, 75% had a favorable outcome while 55% of the high-pressuresensitive discs had a favorable outcome. Thus, patients who had lowpressure-sensitive discs tended to do better that those patients whose discographic pain was reproduced at higher pressures. This study was only a pilot study and was limited by small numbers of patients as well as the fact that the study population included patients with multilevel disc disease. There were also no data reported that compared pretreatment pain and disability scores between the low- and high-pressure disc groups. The heating protocol had been changed during the course of the study. Rhyne et al.30 retrospectively reviewed 25 cases in which patients who had single-level positive provocation discography did not undergo surgical treatment. The patients had been offered posterolateral fusion but refused due to fear of complications, insurance denial, knowledge of acquaintances who worsened after surgery, or desire to change lifestyle and live with the pain. The patients had a mean follow-up of 4.9 years and completed clinical evaluation including Roland-Morris disability scale and pain scale of Million et al. These scales were filled out twice, one representing their current status and the second to represent the recall of their status at the time of discography. Based on this assessment, 68% of patients improved, 8% had no perceived change in status, and 24% worsened. No patient was pain-free or free of disability. Of those who improved, pain improved an average of 39% and 1040

disability decreased an average of 42%. Patients who reported improvement had a shorter history of low back pain (3.5 years versus 11 years) and were older (45 years old versus 33 years old). Psychiatric disease was present in 66.7% of those who worsened. This study is certainly flawed in that not only is it a retrospective study, but the subjects were asked to retrospectively enter data to reflect their status an average of 5 years prior to the time of the study. However, it does demonstrate that 68% perceived an improvement. In summary, these studies suggest that provocation discography is useful in the preoperative planning and prognostication for certain procedures. Discs that have been found to cause concordant pain on disc stimulation may also improve spontaneously. However, due to methodological insufficiencies and differences in these studies, more research is needed in the form of prospective, randomized trials with adequate sample size and validated outcome measures. The use of manometry may decrease the false-positive rate of provocation discography.

VALIDITY AND FALSE-POSITIVE RATES OF PROVOCATION DISCOGRAPHY AS A DIAGNOSTIC TOOL Holt's classic study questioned discography's value, concluding that the false-positive rate of discography in asymptomatic volunteers was 36% based on the ratio of abnormal discographic images to the number of satisfactory disc injections.31 Holt's work has been widely criticized. Simmons et al. ‘acknowledge[d] that Holt's study was appropriate for its time,’ but noted subsequent advances in nonirritating contrast dye and radiologic equipment.32–34 In their reassessment they noted Holt's high failure rate for proper needle placement, which was 30% for the lower two disc levels (site of most disc pathology), 37% for L5–S1, and 23% for L4–5. The selection process for asymptomatic volunteers (who were prison inmates) was not clearly defined and there were discrepancies within the text. Additionally, only disc morphology, and not pain provocation, was considered in calculation of false positives. If pain response and disc morphology were considered, then reanalysis demonstrates that the true negative rate would be 74%. If only patients with successful injections were considered, then the accuracy rate of discography would be 81.9% despite the use of highly irritating contrast material (Hypaque). ‘Major advances in the techniques of discography’ occurring after Holt's 1968 study prompted Walsh et al.33 to perform a similar study in 1990, reevaluating discography's value and specificity using ‘current techniques’ and more precise methodology. They used the much less irritating contrast, iopamidol, instead of diatrizole. More importantly, they included pain provocation evaluation. They rated the pain reproduction according to intensity, presence of pain-related behavior, and pain similarity (concordancy) for symptomatic patients. A ‘positive pain-related response’ to disc injection was recorded if the subject exhibited two or more types of pain behavior and rated the pain intensity a 3 or more (‘bad’ on a scale 0 to 5). Pain behaviors considered were guarding/bracing/withdrawing, rubbing, grimacing, sighing, or verbalizing. (Inter-rater reliability for these was 92.6%.) Because asymptomatic subjects could not report ‘concordant’ pain, they were termed ‘positive’ if there was an abnormal disc morphology with positive ratings for pain intensity and pain behavior. Symptomatic control patients required a typical rating for pain similarity to be called ‘positive.’ They included two groups: an asymptomatic group of young men and a symptomatic control group determining interobserver reliability for pain response evaluation and semiblinding the raters as to which participants were asymptomatic. The asymptomatic test subjects demonstrated an abnormal discographic disc morphology in 17% but a false-positive rate of 0% based on pain response. Even if more liberal criteria were used such as only minimal pain (at least

Section 5: Biomechanical Disorders of the Lumbar Spine

1 on a scale of 5) or presence of only one pain behavior, the falsepositive rate would have been 3% and 7%, respectively. Because the false-positive rate was lower than that of the Holt study (0% as compared to 36%), Walsh et al. concluded that the ‘single most important way to improve the specificity of discography is to incorporate assessment of pain into the definition of a positive discogram.’ Carragee and colleagues have extensively studied the possibility of false-positive results obtained from provocation discography in clinical practice (Table 94.1). Tanner and Carragee35 suggest that ‘the reproduction of concordant pain has less diagnostic utility that [sic] often assumed, particularly if there is pathology in a similar sclerotomal region.’ Initially, Carragee et al. presented case studies in which patients with positive lumbar discography were later found to have other painful processes such as sacroiliac joint abnormalities and posterior element neoplasm.36 With these in mind, they appropriately sought to test the validity of provocation discography and determine its false-positive rates among various subjects by replicating and extending Walsh et al.'s study. They reasoned that in order to check the validity of any clinical test, it is essential to know how many subjects

without a given disease will test positive with a particular test for that disease. Also, the relative risk of certain subsets of subjects will affect the meaning of the test. Therefore, they took as their starting point the use of asymptomatic control subjects.35 Their first study applied ‘experimental disc injections’ to subjects with no previous history of low back pain to evaluate the pain responses and pain-related behaviors in the experimental setting. Its aim was to test the ‘first assumption in discography’ that ‘stimulation of a disc in an asymptomatic individual will not cause a significant sensation of pain.’37 Twenty-six volunteers with an mean age of 43 years were selected from three sources: patients being followed after cervical surgery with best results and pain free (n=10), patients from the same cervical surgery cohort but with the worst results and with cervical-related chronic pain(n=10), and finally patients meeting the DSM-IV criteria for somatization disorder (initial n=10). All were asymptomatic for low back pain. Provocation discography was performed according to the protocol of Walsh et al.33 with a ‘positive’ result scored if the pain response was greater than or equal to 3 out of 5, but only if accompanied by two or more pain behaviors (inter-rater agreement was 97.4%).37

Table 94.1: Summary of studies from Eugene J. Carragee, M.D., et al. Publication

Objective

Conclusion

Positive provocation discography as misleading finding in the evaluation of low back pain. Chicago, IL: North American Spine Society; 1997.

To compare results and outcomes with Walsh's 1990 discography results.

Patients with positive lumbar discography were later found to have other painful processes such as sacroiliac joint abnormalities and posterior element neoplasm. The reproduction of concordant pain has less diagnostic utility than assumed, particularly if there is pathology in a similar sclerotomal region.

False-positive findings on lumbar discography: Reliability of subjective concordance assessment during provocative disc injection. Spine 1999; 24(23):2542–2547.

To determine if patients subjective interpretation of pain concordancy during provocative discal injections is reliable.

In patients without a history of low back pain, lumbar discography is able to concordantly produce pain from a posterior iliac crest bone graft harvest site, questioning the reliability of concordant pain production originating from discal pathology.

The rates of false-positive lumbar discography in select patients without low back pain symptoms. Spine 2000; 25:1373–1381.

To test the null hypothesis of discography; ‘the first assumption in discography’ that ‘stimulation of a disc in an asymptomatic individual will not cause a significant sensation of pain.’

When performing discography according to Walsh's criteria (IASP criteria was NOT used) the rate of false-positive findings may be low in patients without chronic pain conditions and normal psychometric profiles. However, when performing discography in patients with annular disruption, chronic pain, or abnormal psychometric testing, concordant injections are very common.

Lumbar high-intensity zone and discography in subjects without low back problems. Spine 2000; 25(23):2987–2992.

To investigate the prevalence and significance of HIZ in symptomatic and asymptomatic patients and compare discography results between the two groups.

The presence of a HIZ does not represent a diagnosis of internal disc disruption, while the same percentages of discs with HIZs were found to be painful during discography in both symptomatic and asymptomatic populations.

Provocative discography in patients after limited lumbar discectomy: a controlled, randomized study of pain response in symptomatic and asymptomatic subjects. Spine 2000; 25(23):3065–3071.

To investigate the intensity of pain after lumbar discectomy in both symptomatic and asymptomatic patients.

When performing discography according to Walsh's criteria (IASP criteria was NOT used) the rate of false-positive findings were reported to be 40% in the asymptomatic group. In the symptomatic postsurgical group, 70% of patients experienced provoked pain during discography.

Prospective controlled study of the development of lower back pain in previously asymptomatic subjects undergoing experimental discography. Spine 2004; 29:1112–1117.

To determine if asymptomatic patients who underwent discography with positive findings would proceed to develop back pain after discography and up to 4 years later.

Independently, a positive discogram can be a poor indicator of developing low back pain.

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They found that disc stimulation was ‘false positive’ in at least one disc in 10% of subjects in the pain-free group and 40% of those with chronic pain (cervical-related chronic pain). Of the somatization group, 40% (n=4) dropped out before discographic injection and two others stopped the procedure after only one or two disc levels were injected. Of those remaining in the somatization group who completed all disc injections, 75% (3 of 4 subjects) had a least one-level positive discogram. If the somatization subjects who had at least one disc injected were considered, then there was an 83% rate of subjects with false-positive pain provocation. When correlating radiologic (MRI and discogram) findings with pain provocation in subjects who completed at least 3 disc injections, there were no positive injections in the 31 radiologically normal discs, 11% (2 of 18) positive disc injections in the intermediate disruption discs (abnormal MRI and discographic nucleogram but no extension of dye to the outer anulus), and 37% (10 of 26) positive disc injections in the annular disruption discs (discogram with dye extension to or through the anulus). Patients on disability who completed three disc injections (4 of 5) had an 80% false-positive rate. Subjects with active worker's compensation or personal injury claims had an 89% rate (8 of 9) of false-positive injections. All subjects in the somatization group had some type of ongoing compensation claim which confounded separation of those two variables. A positive discogram correlated with an elevated modified Zung Depression Test and Modified Somatic Pain Questionnaire. This study has been criticized on the basis that ‘concordant pain,’ paramount in provocation discography, cannot, by definition, be tested in asymptomatic individuals.34 In response, Tanner and Carragee point out that all clinical tests must be evaluated in part by the results obtained in asymptomatic or disease-free persons.35 Bogduk re-analyzed Carragee's data in this study using IASP criteria (Table 94.2): that is, concordant pain with an intensity of 6/10, abnormal morphology, and at least one painless control level.38 Specifically, he imposed the criteria that the suspect disc(s) be surrounded by at least one painless adjacent disc. He also applied the manometric criteria for pressure of injection. When at least one adjacent disc was required to be painless in order to call a given level positive, the false positives in the chronic pain group fell from 40% to 20%. But the rate remained stable for the no-pain group (10%) and somatization group (75%). Bogduk then used two different manometric parameters to analyze Carragee's data. Under the criterion that the pressure of disc injection be less than 50 psi, the false-positive rates of both the chronic pain and somatization groups fell. The false-positive rates for the chronic pain group decreased to 10% (original 40%) while the somatization group had a resultant 50% false-positive rate (original 75%). If the stricter criterion of disc injection pressure less than 15 psi (called the ‘chemically sensitive disc’ by some) is used, then the false-positive rates fall to 0% in the pain-free group, 0% in the chronic pain group, and 25% in the somatization group. Additionally, Bogduk stated that because of the small sample size, confidence intervals should be used, and with these adjustments found that the false-positive rates either became zero or the confidence intervals overlapped zero even in the somatiza-

Table 94.2: IASP criteria for positive discography P0 control level Concordant locational pain Pain intensity ≥ 6/10 Morphological disc changes

1042

tion group. Based on this reanalysis of Carragee et al.'s data, Bogduk suggested using the criterion of 50 psi in general clinical practice to restore sensitivity but 15 psi in patients with suspected or known somatization. In order to evaluate false-positive rates of ‘concordant’ back and buttock pain, Carragee et al. devised a study in which patients who had never had low back pain prior to posterior iliac crest bone grafting for nonlumbar spinal reasons were evaluated with provocation discography for concordant bone graft donor site pain.39 Eighty-five percent of subjects (7 of 8) experienced similar or exact pain. Sixty-four percent of discs caused similar or exact pain. Of the discs with annular tears, 70% (7 of 10) caused similar or exact pain reproduction of the patient's usual iliac crest bone graft harvest site. In this small sample of 8 patients and 24 discs, 50% of subjects had false-positive concordant donor site pain on disc stimulation if pain magnitude, concordancy, and demonstration of pain behavior are all considered. Carragee et al., again, did not use the IASP criteria. If these data are reanalyzed with IASP criteria, 25% of subjects would have false-positive findings if disc injection pressure was less than 50 psi, or a 12.5% false-positive rate for less than 15 psi. Still, these results call into question whether a patient can reliably distinguish pain from discogenic versus nondiscogenic sources. After the rates of false positives in subjects without previous history of low back and/or buttock pain due to spinal pathology were evaluated, Carragee et al. next sought to determine the rate of positive disc injection in patients who had a previous history of lumbar-related complaints.40 They no longer called these ‘false positive,’ presumably to eliminate the association with concordancy of pain response. They performed provocative discography on 20 patients from a cohort who had a previous history of symptomatic single-level lumbar pathology, underwent subsequent limited posterior discectomy 2–10 years prior to the study, but were now asymptomatic. They compared the rates of positive injection in this group to a control group of 27 subjects who were symptomatic with persistent or recurrent lumbar or lower limb symptoms after similar surgery 14 months to 6 years prior to the study. Twenty-six percent of these symptomatic patients had normal psychometric scores. In the asymptomatic group, 40% of subjects had positive provocation disc injection at the level of previous surgery while only 10% (2 of 20) of asymptomatic subjects had a positive provocation if only the nonsurgically treated discs were considered. In total, 45% of the asymptomatic group had at least one positive provocation injection. All previously surgically treated discs that had significant pain on injection had discographic grade 2 to 3 tears with dye penetrating to or through the outer anulus. Sixty-three percent of symptomatic subjects had a positive pain response at the level of previous surgery. If the symptomatic group was subdivided according to psychometric scores, those with normal psychometrics had a 43% rate of positive provocation (all concordant) while those with abnormal psychometrics had a 70% rate of positive provocation (86% of which were concordant). The intensity of pain was significantly rated as higher in the symptomatic group with abnormal psychometrics (3.4 of 5) versus those in both the asymptomatic group and the symptomatic group with normal psychometrics (both 2.1 of 5). In reanalyzing this asymptomatic group data with IASP criteria for manometric injection, the positive provocation rate in previously surgically treated discs would decrease to 35% if pressure on injection was less than 50 psi or to 25% if pressure on injection was less than 15 psi. Of unoperated discs, the positive rate would fall to 5% if either the less than 50 psi or less than 15 psi criteria was used. If the requirement for a pain-free adjacent control disc is also required, then the positive rate falls to 25% if less than 50 psi is used, or 15% if less than 15 psi is used. Still, previously operated discs may be more likely to be painful on injection than discs which have never been operated on.

Section 5: Biomechanical Disorders of the Lumbar Spine

In summary, the Carragee et al.40 studies point out the fact that false-positive results can occur in discography as with any clinical test. These false positives are more likely in those with abnormal psychometric scores, specifically somatization disorder, and in previously operated discs. Bogduk has pointed out that adherence to the IASP criteria can decrease the false-positive results to an acceptable level. O'Neill and Kurgansky published a retrospective study of 253 patients in an attempt to further delineate false-positive rates and offer suggestions to increase specificity.41 Particularly, they wanted to determine if the distribution of disc pain thresholds would organize into subgroups to help identify false positives. To accomplish this, they incorporated pressure-controlled discography through manometry. By correlating the manometry information with false-positive findings from Carragee's asymptomatic populations,36,37,39,40,42 they were able to select out for false positives. They concluded that there was a 100% chance of false positives above 50 psi. Pressures ranging 10–25 psi had a 50% chance of being a false positive. However, discs with pain responses at 0–10 psi were most likely true positives. Based on these data, there appears to be a bimodal distribution of true positives. One population of true positive were those who had positive pain responses with cut-off values above 25 psi and below 50 psi ; the other population of patients were those who had pain responses at less than 10 psi. However, it was difficult to confirm that the latter are true positive due to testing limitations..

DISCOGRAPHY COMPLICATIONS Passing a needle into the disc has risks that should be recognized and anticipated before they occur. Perhaps the most common reaction or complication to any procedure is a vasovagal episode. This involuntary reaction of the parasympathetic nervous system causes reflex bradycardia and vasodilatation. Patients should be monitored with pulse oximetry, pulse rate, and blood pressure. A vagal episode is recognized by an audible slowing of the pulse rate and is usually accompanied by perfuse sweating and nausea. Increasing the intravenous fluids and raising the legs will usually restore cerebral perfusion, but 0.5–1 mg of intravenous atropine can be administered and incremental intravenous doses of 5–10 mg of ephedrine may be required in more severe reactions Other common reactions include paravertebral muscle pain and potential contusions from local punctures. Less common complications include nerve injury, dural puncture, bowel perforation, epidural abscess, local cellulitis, and allergic reactions to contrast agents, topical iodine and prophylactic antibiotics. These risks can usually be avoided by using proper techniques and due diligence. The ventral ramus crosses the posterolateral quadrant of the target disc and is vulnerable to direct trauma, but the risk is minimized by slowly advancing the needle medial and under the root in the safe triangle and redirecting the needle when the patient complains of buttock or leg pain. Dural puncture and bowel perforation is possible but should not occur if one uses proper technique and carefully monitors the advancing needle with both AP and lateral imaging. An individual with a pendulous abdomen may have an increased risk of bowl perforation and subsequent disc space infection because the retroperoteneum is pushed posteriorly. Placing these patients in a lateral decubitus position may help avoid this potential complication. Local cellulitis can be avoided with strict adherence to sterile techniques, but if it occurs it is treated with cold compresses and empiric coverage for group A streptococci and Staphylococcus aureus. Allergic reactions to drugs utilized can potentially be avoided with through histories. Patients with a serous allergic reaction to iodine and shell-

fish can be pretreated with prednisone 50 mg p.o. 24 hours before the procedure, prednisone 50 mg p.o. 12 hours before the procedure, and benadryl 50 mg p.o. 1 hour before the procedure or i.v. at the time of the procedure. The most serious potential complication is disc space infection. Before antibiotic prophylaxis became routine, the reported rate of discitis ranged from 2.3% per patient and 1.3% per disc to 0.1% per patient and 0.05% per disc.43 The most common causative organisms are S. aureus and S. epidermidis. The reported incidence of discitis may be reduced by using a double-needle techniques and preprocedural antibiotics.44 In 1990, Osti et al.45 designed an experimental discography model using sheep. They added cefalozin to the intradiscal suspension or administered it intravenously 30 minutes prior to intradiscal inoculation of bacteria. The prophylactic treatment prevented any radiographic, macroscopic, or histological signs of discitis. In a follow-up study of 127 patients this protocol also prevented disc space infection following discography and became the basis of the routine use of intravenous antibiotics (e.g. 1 g of cefalozin) prior to discography, adding antibiotics to the injected contrast, or the use of both intravenous and intradiscal antibiotics.

CONTROVERSIES Although the issue of discography itself remains controversial, there are subjects within the procedure itself which should be addressed in order to further increase its diagnostic utility.

False-negative results False-negative results could occur because there is a rupture through the outer anulus or endplate and one is not able to pressurize the disc. Rapid injection of contrast will raise the dynamic pressure to over 50 psi, but whether this technique reduces false-negative results or increases false-positive results is unknown. Other potential causes of false-negative results include oversedation or injected local anesthetics.

Sources for false-positive results Potential anatomic sources of false-positive findings are adjacent structures which are mechanically or chemically irritated. Possibilities include distension of the zygapophyseal joints or the posterior longitudinal ligament. Some have even advocated performing medial branch blocks prior to lumbar discography. Commonly, initial pressurization will provoke significant concordant pain, but repressurization will be significantly less painful and not meet the criteria for a positive response. Although one could argue that this is not a positive response, interpretation is not standardized. Pressurizing an adjacent symptomatic disc is also a potential cause of false-positive results. There is an assumption that when injecting an intervertebral disc (IVD) and checking its pain response, adjacent intervertebral discs are not pressurized. Therefore, any pain response is believed to be solely attributed to the IVD level injected. Some practitioners have anecdotally observed that pressurizing IVDs with normal anatomy occasionally results in significant pain when there is an immediately adjacent nonruptured pathologic IVD. These practitioners believe that if this adjacent pathologic IVD is later anesthetized, the original normal-appearing IVD will no longer be painful with IVD injection. If validated, such a response supports the theory that a positive pain response may be caused by pressurizing an adjacent pathologic IVD and not from the injected IVD. On the other hand, preliminary data suggest that pressurizing an intact lumbar disc to pressures exceeding 100 psi will not result in any measurable pressure changes in the adjacent discs.45a 1043

Part 3: Specific Disorders

Is analgesic response validated? Instead of, or in addition to, the provocative response, some discographers use pain relief following intra-discal injection of local anesthetic to help determine whether the disc is symptomatic. An invalidated emerging technology call functional analgesic discography by Kyphon Inc, evaluates a dynamic analgesic response post procedurally. Intra-discal analgesic is injected via a catheter into the suspected pain generator. The patient is then asked to perform various functional activities that typically cause their pain. Although this may help validate single level positive discs, multilevel functional pathology is more challenging unless near 100% relief of symptoms can be obtained after single level disc anesthesia is performed. Certain interpretative challenges remain given multilevel interpretations. Currently there are no published studies correlating clinical outcome to results of analgesic lumbar discography.

Does needle insertion site affect discography results? Discogenic pain often lateralizes to one side. Some discographers, therefore, advocate approaching the target disc contralateral to the patient's more painful side to theoretically differentiate index pain from needle insertion pain on nondiscal structures.46 For example, a patient with predominantly right-sided back pain (index pain) would be investigated with needle entry left of midline. Needle insertion ipsilateral to the patient's index pain has been speculated to increase the false-positive rate. False-positive pain reproduction could occur by stimulation of the adjacent spinal nerve, soft tissue, or osseous structures. Stimulation of a nerve root usually causes a characteristic lancinating pain that is different than the dull, aching pain provoked by contrast injection. However, residual pain after needle repositioning may still cause interpretive challenge to the patient and physician. Cohen et al.47 attempted to determine if needle insertion affected discography results. Retrospective analysis of 127 discography patients who all had a right-sided approach due to limitations of their fluoroscopic unit revealed no significant difference in the rate of positive results among patients with midline, left-sided, or right-sided pain. Unfortunately, one limitation of the study was the lack of any correlation to radiological findings. There was no analysis of left- or right-sided MRI findings and how those results may have factored in on the outcome of discography. The authors concluded that the side from which discography is performed had no effect on results of provocation discography. No ‘gold standard’ or postdiscography treatment outcomes were correlated. Instead, they based their conclusion on the assumption that their population should theoretically have an anticipated equal incidence of rightand left-sided pain source. Slipman et al.48 investigated the commonly held notion that the site of pain reproduced during discography should correspond to the side of their annular tear in one-level positive discography. In their retrospective study, they found a random correlation between the side of a concordantly painful, CT visualized annular tear and the lateralization of one's perceived pain. Slipman et al. postulated that there are two possible theories to describe this finding. There may be a misperception of the origin of the somatic referred signal to the brain occurring via a convergent sensory pathway or possibly a remote pain source independent from the stimulated disc. Until more conclusive studies are completed, we recommend consideration of performing discography with needle entry contralateral to the patient's more painful side unless the physician faces tactical problems imposed by c-arm or procedure suite limitations. 1044

Does needle insertion into a normal or abnormal morphological disc result in damage? One of the more elusive topics concerns the potential for transitory or permanent iatrogenic disc injury secondary to disc puncture or disc pressurization. Carragee et al.42 published a prospective, controlled study to determine whether asymptomatic subjects develop low back pain after discography. They performed discography on 50 asymptomatic patients. The attempt of the study was to determine if asymptomatic patients with positive LBP on discography were not actually false positives but possible true positives predicting ‘near-term future chronic LBP.’ All 50 patients were followed for up to 4 years. There was no conclusive evidence that a painful injection was an independent predictor of developing low back pain in patients without any abnormal psychometric scores. They also determined whether the presence of high-intensity zones (HIZs) or annular fissures seen on MRI and discographic nucleograms were predictive factors for developing LBP. They compared their findings to the previous studies that demonstrated that an area of HIZ in the outer anulus is an independent finding and not necessarily directly related to LBP.14 Caragee et al. found a weak association with late-onset LBP episodes with HIZ and annular fissured nucleograms subsequent to discography. These two studies suggest that the late onset of permanent disc injury in previously asymptomatic patients is purely coincidental or, at best, a subclinical finding. Studies performed in the 1940s evaluated the potential of disc punctures to cause a disc herniation.49 Hirsch could not alter a normal disc to any structural pathology from needle penetration. In 1984, Kahanovitz et al. looked at the histological effect of discography in dogs.50 They injected the L1 through L6 discs. The first intervertebral disc was used as a control without any needle perforation or intradiscal substance introduction. The next level was punctured without any infusion of an injectate. The third level underwent injection of saline, while the fourth and fifth discs underwent injection of Hypaque and metrizamide contrast agents. All 10 dogs were eventually sacrificed at 2, 4, 6, 8, and 10 weeks postdiscography. The discs underwent gross examination as well as saffranin-O mucopolysaccharide staining during histological examination. There was no discernable histological difference in any dog at any level, nor was there evidence of any inflammatory response or annular necrosis. In 1989, Robert Johnson published results from 34 patients who underwent a second discogram.51 The purpose of the study was to determine whether previously normal nucleograms became abnormal within a 2–28-month period of time. He hypothesized that discography does not cause disc herniation or other types of disc damage. Unfortunately, the methodology was flawed. Discography was not performed according to prescribed IASP and ISIS standards (Tables 94.2, 94.3). Furthermore, limited information could be gathered from the outcome because of inadequate statistical analysis of data, the limited number of discs reported, and the constrained means of data collection. Despite these shortcomings, this study demonstrates that within the 42 discs that were initially normal, eight of the discs were fissured on follow-up discograms. The pain was reported as similar or concordant within seven discs, while one disc did not provoke pain. Within all 42 discs with normal nucleograms, there was no evidence of herniation of nuclear material. Three of eight patients with abnormal discs underwent fusions subsequent to the primary discogram. The initially normal discs, now adjacent to the level of fusion, developed abnormal nucleograms. However, the mechanism for these segment changes are not necessarily from the initial discogram, but could be caused by altered biomechanics, surgical trauma, or another unknown cause.

Does antibiotic use mitigate complication rates? Before antibiotic prophylaxis became a routine component of disc stimulation, reported rates of discitis varied. Preprocedural antibiotics are

Section 5: Biomechanical Disorders of the Lumbar Spine

Table 94.3: ISIS scoring sheet for provocative pain responses Variable

Segments studied

Concordant levels

Points

Concordant pain Pain > 5/10 Pain > 7/10 Pressure < 50 psi Pressure < 15 psi

30 5 5 10 10

Sum of rows

L2–3

L3–4

L4–5

L5–S1

L2–3

L3–4

L4–5

L5–S1

Subtotal Divide subtotal by number of concordant discs. Enter result in this row. Control levels

Points

No pain Pain at < 50 psi Pain at < 15 psi Total of sums of rows below the double line Interpretation: > 70 points = POSITIVE 40–60 points = INDETERMINATE < 40 points = NEGATIVE

30 −10 −10

1. For each disc studied (see columns), enter the appropriate score for each of the variables indicated (rows). For discs with CONCORDANT PAIN, Enter 30 if the concordant pain is produced Enter 5 if the pain produced is greater than 5/10 Enter another 5 if the pain produced is also greater than 7/10 Enter 10 if the pressure at which pain occurred is anything less than 50 psi Enter another 10 if the pressure is also less than 15 psi For discs at CONTROL LEVELS, i.e. not concordant pain, Enter +30 if the disc was painless Enter −10 if pain occurred at a pressure less than 50 psi Enter another −10 if pain occurred at a pressure also less than 15 psi 2. For the CONCORDANT DISCS, add up the scores in each row, and record the sum of each row in the column labeled Sum of rows. 3. Add up the sums of the rows for all concordant discs, i.e. all scores above the double line. Divide this total by the number of concordant discs, and record the quotient in the cell indicated, immediately below the double line, in the column labeled Sum of rows. 4. For the NON-COCORDANT DISCS, add up the scores in the rows, taking heed of any negative numbers, and record the sum of each row in the column labeled Sum of rows. 5. Add up the total of the Sums column below the double line, taking care to heed negative numbers. 6. Interpret the result.

now the standard of care. Osti et al.'s landmark 1990 publication presented the most compelling evidence to date supporting the use of prophylactic antibiotics.45 We are unaware of any recent studies that have compared infection rates with and without prophylactic antibiotics.

Should psychometrics be routinely performed prior to discography? Caragee demonstated that individuals with primary somatization disorders are likely to have positive discograms regardless of disc architecture.37 In addition, Block et al. previously showed that patients with elevation of select scales in the Minnesota Mutiphasic Personality Inventory were more likely to over-report pain during discography.52 Both studies suggest that psychometrics should be performed prior to discography. If psychometrics demonstrate concomitant anxiety or depression, the results of discography should be more strictly evaluated.

Can discographic data guide treatment? Elaborate descriptions are available for fluoroscopic AP and lateral and postdiscography CT axial contrast patterns that try to classify stages of radial and concentric spread of contrast. In addition, some discographers record manometry data to help determine whether the discogram meets the criteria of a positive response, and most require

the provocation of 6/10 or greater concordant pain provocation at less than 50 psi above opening pressure. Treatments for internal disc disruption are still evolving and range from the most conservative (rest, therapy, bracing) to the maximally invasive 360 fusions, or disc replacements. Newer, evolving treatments include biological treatments and gene therapy. Currently, however, an ideal treatment for internal disc disruption. There is currently work in progress retrospectively comparing outcome data with the information obtained during discography. Perhaps we can eventually establish specific criteria based on imaging and pressure data to direct treatment.

Are the current standards reliable? When is a disc ‘positive?’ Determining whether a disc is a source of pain is more an art than a science. For example, performing a ‘sham injection’ may help one uncover over-reactive or deceitful responses. One may fake an injection by going through all the motions such as holding the syringe, clicking the fluoroscopy pedal, and asking the patient if they are experiencing any of their typical pain. If the patient responds inappropriately to this sham injection, the quality of information obtained from the rest of the procedure is dubious. 1045

Part 3: Specific Disorders

Likewise, any unexpected behavioral responses should be recorded. Examples include concordant pain response during local skin anesthetic injection and hysterical reactions during the procedure. Although difficult to interpret accurately, many discographers perform a repeat ‘confirmatory’ pressurization following initial concordant pain provocation and most will require equal or similar pain provocation on the repeat pressurization before calling the disc ‘positive.’ There are, however, no generally accepted standards, and whether the initial or succeeding response is the most accurate assessment could be argued either way. Current IASP and ISIS discography criteria are outlined in Tables 94.2 and 94.3. IASP standards are concrete. ISIS standards further objectify the results by including manometry and attempt to interpret a questionably positive disc through an elaborate scoring system. To their credit, they attempt to objectify factors which are measurable. However, neither criterion takes into account factors which would compromise data interpretation, such as awareness of a pain response to sham injections or reproducibility of pain with repeat pressurization of a specific disc. Unlike bimodal test outcomes which fall into groups of positive or negative, such as stool guaiac or pregnancy testing, discography requires interpretation. One's judgment must be based on a combination of many sources of information, including clinical, radiological, psychological, and pain provocation data. Discogram findings should be reproducible and there should be a negative response to a ‘sham’ injection. An inaccurate interpretation may lead to a failed surgery. Judging the reliability of the data will always remain an art.

CONCLUSIONS Lumbar discography is a diagnostic test that helps one determine whether a particular intervertebral disc is a source of pain. Properly performed and interpreted, discography is an invaluable tool. Together with the history, physical examination, and radiological studies, discography will identify asymptomatic discs and provide confirmatory evidence that a particular disc is the source of the patient's pain. Because this information is often used to determine at which levels to perform a percutaneous or open surgical procedure, accurate and precise interpretation of the results is vital.

10. Adams MA, Dolan P, Hutton WC. The stages of disc degeneration as revealed by discograms. J Bone Joint Surg [Br] 1986; 68:36–41. 11. Bernard TN. Lumbar discography followed by computed tomography: refining the diagnosis of low-back pain. Spine 1990; 15:690–707. 12. Sachs BL, Vanharanta H, Spivey MA, et al. Dallas discogram description: a new classification of CT/discography in low-back disorders. Spine 1987; 12:287–298. 13. Aprill C, Bogduk N. High-intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. Br J Radiol 1992; 65(773):361–369. 14. Schellhas KP, Pollei SR, Gundry CR, et al. Lumbar disc high-intensity zone: correlation of magnetic resonance imaging and discography. Spine 1996; 21:79–86. 15. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg [Am] 1990; 72: 403–408. 16. Boos N, et al. Volvo Award in Clinical Science: the diagnostic accuracy of MRI. Spine 1995; 20(24):2613–2625. 17. Weishaupt D, et al. MR imaging of the lumbar spine: prevalence of intervertebral disk extrusion and sequestration, nerve root compression, end plate abnormalities, and osteoarthritis of the facet joints in asymptomatic volunteers. Radiology 1998; 209:661–666. 18. Kokkonen S, et al. Endplate degeneration observed on magnetic resonance imaging of the lumbar spine: correlation with pain provocation and disc changes observed on computed tomography discography. Spine 2002; 27:2274–2278. 19. Smith BM, Hurwitz EL, Solsberg D, et al. Interobserver reliability of detecting lumbar intervertebral disc high-intensity zone on magnetic resonance imaging and association of high-intensity zone with pain and annular disruption. Spine 1998; 23:2074–2080. 20. Rankine JJ, et al. The clinical importance of the high-intensity zone on lumbar magnetic resonance imaging. Spine 1999; 24(18):1913–1920. 21. Modic MT, et al. Degenerative disc disease: assessment of changes in vertebral body marrow with MR imaging. Radiology; 1988; 166:193–199. 22. Miller G. The spine. In: Berquist T. MRI of the musculoskeletal system, 2nd edn. New York: Raven Press; 1990. 23. Brodsky AE, Binder WF. Lumbar discography: its value in diagnosis and treatment of lumbar disc lesions. Spine 1979; 4(2):110–120. 24. Calhoun E, et al. Provocation discography as a guide to planning operations on the spine. J Bone Joint Surg [Br] 1988; 70(2):267–271. 25. Blumenthal SL, et al. The role of anterior lumbar fusion for internal disc disruption. Spine 1988; 13(5):566–569. 26. Wetzel FT, et al. The treatment of lumbar spinal pain syndromes diagnosed by discography: lumbar arthrodesis. Spine 1994; 19(7):792–800. 27. Derby R, et al. The ability of pressure-controlled discography to predict surgical and non-surgical outcomes. Spine 1999; 24(4):364–372. 28. Carragee EJ. Point of view. Spine 1999; 24(4):371–372.

References 1. Nachemson A. Lumbar discography – Where are we today? [Editorial comment]. Spine 1989; 14(6):555–557. 2. Simmons EH, Segil CM. An evaluation of discography in the localization of symptomatic levels in discogenic disease of the spine. Clin Orthopaed Rel Res 1975; 108:57–69.

30. Rhyne AL III, et al. Outcome of unoperated discogram-positive low back pain. Spine 1995; 20(18):1997–2001. 31. Holt EP. The question of lumbar discography. J Bone Joint Surgery [Am] 1968; 50:720.

3. Schwarzer AC, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995; 20(17):1878–1883.

32. Simmons JW, et al. A reassessment of Holt's data on ‘The question of lumbar discography.’ Clin Orthopaed Rel Res 1988; 237:120–123.

4. Young S, Aprill C, Laslett M. Correlation of clinical examination characteristics with three sources of chronic low back pain. Spine J 2003; 3:460–465.

33. Walsh TR, Weinstein JN, Spratt KF, et al. Lumbar discography in normal subjects: a controlled, prospective study. J Bone Joint Surg [Am] 1990; 72(7):1081–1088.

5. Donelson R, et al. A prospective study of centralization of lumbar and referred pain: a predictor of symptomatic discs and annular competence. Spine 1997; 22(10):1115–1122.

34. Wetzel FT. Point of view. Spine 2000; 1381. 35. Tanner C, Carragee EJ. Letter to editor in response. Spine 2001; 26(8):995–996.

6. Yrjama M, Vanharanta H. Bony vibration stimulation: a new, non-invasive method for examining intradiscal pain. Eur Spine J 1994; 3:233–234.

36. Carragee E, Tanner C, Vittum D, et al. Positive provocation discography as a misleading finding in the evaluation of low back pain. Chicago, IL: North American Spine Society; 1997.

7. Yrjama M, Tervonen O, Vanharanta H. Ultrasonic imaging of lumbar discs combined with vibration pain provocation compared with discography in the diagnosis of internal annular fissures of the lumbar spine. Spine 1996; 21(5):571–574.

37. Carragee EJ, Tanner CM, Khurana S, et al. The rates of false-positive lumbar discography in select patients without low back pain symptoms. Spine 2000; 25:1373–1381.

8. Yrjama M, Tervonen O, Kurunlahti M, et al. Bony vibration stimulation test combined with magnetic resonance imaging: Can discography be replaced ? Spine 1997; 22(7):808–813.

38. Bogduk N. An analysis of the Carragee data on false-positive discography. International Spinal Injection Society Scientific Newsletter Summer 2001; 4 (2):3–10.

9. Quinnell RC. Pressure standardized lumbar discography. Br J Radiol 1980; 53(635):1031–1036.

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29. Derby R, Eek B, Chen Y, et al. Intradiscal electrothermal annuloplasty (IDET): a novel approach for treating chronic discogenic back pain. Neuromodulation 2000; 3(2):82–88.

39. Carragee EJ, Tanner CM, Yang B, et al. False-positive findings on lumbar discography: reliability of subjective concordance assessment during provocative disc injection. Spine 1999; 24(23):2542–2547.

Section 5: Biomechanical Disorders of the Lumbar Spine 40. Carragee EJ, Chen Y, Tanner CM, et al. Provocative discography in patients after limited lumbar discectomy: a controlled, randomized study of pain response in symptomatic and asymptomatic subjects. Spine 2000; 25(23):3065–3071. 41. O'Neill C, Kurgansky M. Subgroups of positive discs on discography. Spine 2004; 29(19):2134–2139. 42. Carragee EJ, et al. Prospective controlled study of the development of lower back pain in previously asymptomatic subjects undergoing experimental discography. Spine 2004; 29:1112–1117.

46. Endres S, Bogduk N. Practice guidelines and protocols: lumbar disc stimulation. ISIS 9th Annual Scientific Meeting Syllabus. Sep 2001; 1456–1475. 47. Cohen SP, Larkin T, Fant GV, et al. Does needle insertion site affect discography results? A retrospective analysis. Spine 2002; 27(20):2279–2283. 48. Slipman CW, Patel RK, Zhang L, et al. Side of symptomatic annular tear and site of low back pain: is there a correlation ? Spine 2001; 26(8):E165–E169. 49. Hirsch C. An attempt to diagnose the level of disc lesion clinically by disc puncture. Acta Orthop Scand 1948; 18:131–140.

43. Bogduk N, Aprill C, Derby R. Discography. In: White AH, ed. Spine care, vol. 1. St Louis: Mosby; 1995:219–238.

50. Kahanovitz N, et al. The effect of discography on the canine intervertebral disc. Spine 1986; 11:26–27.

44. Fraser RD, Osti OL, Vernon-Roberts B. Discitis after discography. J Bone Joint Surg [Br] 1987; 69:26–35.

51. Johnson RG. Does discography injure normal discs? An analysis of repeat discograms. Spine 1989; 14:424–426.

45. Osti OL, Fraser Rd, Vernon-Robers B. Discitis after discography: the role of prophylactic agents. J Bone Joint Surg [Br] 1990; 72:271–274.

52. Block AR, Vanharanta H, Ohnmeiss DD, et al. Discographic pain report: influence of psychological factors. Spine 1996; 21:334–338.

45a. Furman MB, Lee TS, Puttlitz KM et al. Lumbar provocative discography: evaluation of possible disc pressurization. Proceedings of the North American Spine Society Mid Year Meeting – Meeting of the Americas II, 2002 [abstract].

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain

CHAPTER

95

Intradiscal Steroids and Prolotherapy: Clinical Relevance, Outcomes and Efficacy Michael B. Furman, Ryan S. Reeves and William A. Ante

Internal disc disruption treatments are evolving. This chapter focuses on alternative intradiscal treatments distinct from the well-recognized ones (i.e. electrothermal annuloplasty, nucleoplasty, chemonucleolysis) discussed elsewhere in this book. In particular, this chapter focuses on intradiscal steroid injections and intradiscal prolotherapy. We discuss the rationale, efficacy, and potential therapeutic effects of these interventions based on a comprehensive literature review.

RATIONALE FOR INTRADISCAL STEROID INJECTIONS Inflammatory processes theoretically contribute to discogenic pain. Nucleus pulposus material leaks along radial tears into or through the annular fibers causing a local inflammatory response with associated pain. Studies have shown the presence of both inflammatory mediators1 and inflammatory cells2–4 within herniated nuclear material. The high-intensity zone, often seen in symptomatic individuals, may represent inflamed grade 3 to 5 annular fissures with neovascularization.5–7 Corticosteroid administration has been used since the 1950s to treat symptomatic degenerative intervertebral discs. However, its efficacy and mechanism of action remained controversial. Feffer8 first described using intradiscal hydrocortisone injections for its antiinflammatory properties, attempting to reverse the degenerative process. He also suggested that it had a polymerizing effect and could thus heal annular tears and restore the disc's biomechanical load-bearing properties. He proposed this hypothesis after observing that rheumatoid arthritis patients' synovial fluid viscosity increased after intra-articular hydrocortisone injections. This was attributed to polymerization of the hyaluronic acid's polysaccharide component. The synovial fluid's depolymerized hyaluronic acid is replaced by fluid with normal viscosity within 4 days.9 Leao stated that in degenerative processes, the interfibrillar substance's mucopolysaccharide can have an abnormal sulfuric chondroitin cleavage. The polymerization caused by hydrocortisone could repair the connection.10 Based on findings of accelerated disc degeneration following intradiscal Depo-Medrol administration, some11 have proposed that this agent may exert its therapeutic effect by reduction of disc bulging or protrusion.

INTRADISCAL STEROID INJECTION TECHNIQUE The intradiscal steroid injection's disc access and technique is essentially the same as that used for provocation discography.12–15 When indicated, the steroids are administered into the symptomatic level immediately after positive diagnostic disc stimulation using the same spinal needles. However, the discography's contrast volume and the

disc's capacity may limit this technique. Intranuclear injection should distribute medication into contiguous radial fissures and annular tears.

INTRADISCAL STEROID INJECTION EFFICACY Table 95.1 summarizes this section’s studies. In 1956, Feffer described using intradiscal steroids for low back and sciatic pain.16 He injected a hydrocortisone and iodopyracet solution during a single-level discography procedure using a modified Erlacher technique. The injected solution included 3 cc of 35% iodopyracet and 1 cc of 50 mg hydrocortisone. The total injectate volume varied with the patient’s intradiscal capacity The two lowest lumbar discs were routinely injected with a few days between injections. Occasionally, he injected more cephalad levels, depending on the patient's clinical scenario. If the first injection provided adequate relief, another level was not injected. Sixty patients were studied. None of the five patients with normal nucleograms had any symptom improvement. At a maximum 8-month follow-up, 37 patients (67%) of those with abnormal nucleograms had symptom improvement, with ‘permanent’ remission in 33 patients. Symptoms improved but then recurred in four patients at 2 weeks (one of four patients), 2 months (one of four), and 3 months (two of four). There was no improvement in 18 patients (33%) of those patients with abnormal nucleograms. This study did not detail its patient inclusion criteria, patient demographics, or outcome measurement method. In 1969, Feffer published a retrospective review in which he evaluated 244 patients who had undergone therapeutic intradiscal hydrocortisone injection.8 Discography was performed using a posterolateral approach with an injectate composed of 25 mg hydrocortisone per 1.5 cc contrast dye. Initially, the contrast agent Diodrast was used but was subsequently replaced with Hypaque due to the ‘better contrast’ obtained on radiographic imaging. Feffer stated that, ‘In most cases, two interspaces were injected, although a conscientious effort was made to correlate the levels treated with the clinical picture.’ At an average follow-up of 7.3 years (range 4–10 years), 46.7% had ‘permanent remission’ while 53.3 % had response failure defined as either no initial response to injection or relapse of symptoms. They reported complications on both their study population as well as all other discograms performed in their center over the previous 4 years. These included postprocedural spinal headaches, one case of disc infection requiring interbody fusion and a missed intrathecal meningioma which was previously misdiagnosed for lack of a prediscography myelogram. Radiographs obtained routinely 2 years after discography did not reveal accelerated disc degeneration.

1049

1050 Steroid Hydrocortisone (50 mg)

Hydrocortisone (25 mg)

Depo-Medrol (40–80 mg)

Triamcinolone hexacetonide (2 ml with no dose given) Depo-Medrol (80 mg)

Depomedrone or lederspan Depo-Medrone (40 mg)

Sample size

60

244

42

30

25

105

98

Author

Feffer 1956

Feffer 1969

Wilkinson and Schuman

Bertin

Simmons

Bull

Khot

Table 95.1: Intradiscal injection efficacy studies

No significant change vs. saline control

24% better

43% improvement on VAS; 36% functional improvement (Per Oswestry)

36.6% good results, 36.6% moderate results, 26.7% poor results

Lumbar: 31% good results for > 3 months. Cervical: 25% good results

46.7% permanent remission

55% (33) patients with complete resolution; 62% (37) with improvement

Improvement

1 year VAS and Oswestry

8 weeks

10–14 days VAS and Oswestry

1–3 months

2.4 year (average)

4–10 years

8 months

Follow-up

Validated Outcome measures, double blinded RCT, large sample size. No intermittent shortterm outcomes prior to 1 year.

Comparison of Modic changes and response rates. Retrospective abstract publication, no dose given.

Small sample sized, short follow up.

Limited methodology, nonvalidated outcome scale.

Prospective-non randomized trial; Nonvalidated outcome scale, no blinding, variable steroid dose. See Table 95.2.

Retrospective review; multiple discs injected at once, no true statistical analysis, no validated outcome measures.

No outcome measures or inclusion/ exclusion criteria or patient demographics.

Comments

Part 3: Specific Disorders

Section 5: Biomechanical Disorders of the Lumbar Spine

Older patients or those with primarily back symptoms responded better to intradiscal steroids while gender and neurologic deficit did not affect results. Disc characteristics in patients with positive results were analyzed. Patients with ‘posterior degeneration only’ also had more favorable responses. This was defined by discographic results demonstrating an intact anulus anteriorly and laterally, without hypertrophic or bony changes. The degree or direction of the disc protrusion did not affect prognosis. This study was limited by its retrospective nature, lack of validated outcome measures, nonstandard discography technique and reporting as compared to today's methods. The discography protocol did not include a control level or emphasize obtaining concordant pain responses. Also, the data tables presented were not easily decipherable, nor was the data statistically analyzed. In 1980, Wilkinson and Schuman15 performed a prospective, nonrandomized intradiscal Depo-Medrol study investigating degeneratively mediated lumbar and cervical axial pain. Inclusion criteria required greater than 6 months' symptom duration despite aggressive noninvasive therapy which was not defined. No patient was considered an ideal surgical candidate since they lacked any neurologic deficits. The study included 29 lumbar and 13 cervical patients. Myelography was reportedly normal in almost all patients except for degenerative changes. ‘Contrast and/or anesthesia discography’ was performed prior to the initial therapeutic intradiscal injection. Nearly all patients had pathology, most having a single-level abnormal disc. The study protocol changed after the first eight lumbar injections: Depo-Medrol increased from 30–40 mg to a dose of 60–80 mg into one or two discs. Each subject in the cervical group received 40–80 mg of Depo-Medrol. Average follow-up was 2.4 years with a 1-year minimum. This assessment was either a clinical examination or simply a referring orthopedist report. Outcomes were documented using a three-point Likert scale. ‘Good’ was defined as significant pain improvement for at least 3 months, ‘limited’ results denoted significant pain relief from 10 days to 3 months, and ‘none’ referred to no improvement or improvement lasting less than 10 days (Tables 95.2 and 95.3) For the 45 intradiscal injections in the 29 patients with lumbar disc disease, including those with previous lumbar surgery, and mainly axial low back pain with little or no lower limb radicular pain, 31% had good results lasting more than 3 months, 15% had limited relief, and 54% responded poorly (see Table 95.2). In patients with predominantly radicular pain, 37% had good results, 31% had limited relief, while 42% responded poorly. If patients with previously surgically treated lumbar discs were considered alone (8 patients), 23% had good results, 15% had limited relief, and 62% did poorly. In the patients who only received 40 mg or less of Depo-Medrol, 12% had good results, 26% had only limited relief, and 62% did poorly. If only the injections in patients with axial low back pain who had never had surgery and received ‘full dose steroid therapy’ of 80 mg are considered (n=13 injections), then 54% responded with good results, 15% had limited relief, and 31% had poor results. If only the injections in patients with lumbar radicular pain who never had surgery and received full-dose steroid therapy were considered (n=10 injections), then 40% gave good results, 30% limited results, and 30% poor results. Eighteen patients subsequently underwent lumbar surgery. Twelve of these were from the group that did not receive any clinical benefit from intradiscal injection and similarly only 2 (17%) of these received good results, 4 (33%) limited results, and 6 (50%) poor results from surgery. Eighteen injections in 13 patients with cervical disc disease were also studied (see Table 95.3). None had previous cervical surgery and all received 60–80 mg of Depo-Medrol (80 mg/mL). For those with mainly axial neck pain, 25% had good results, 50% had limited relief, and 25% did poorly. For those with predominantly cervical radicular

symptoms, 20% had good results, 30% had limited relief, and 50% did poorly. Nine cervical patients subsequently underwent anterior interbody surgery with 5 (56%) having good results from surgery. None of the patients who had good results from cervical intradiscal injection underwent surgery. The only complications reported were occasional spinal headaches and minor menstrual irregularity. No disc infections or increased disc degeneration were encountered. Based on these data, the authors conclude that intradiscal steroid injections may be beneficial for those with discogenic pain but may have more efficacy for axial pain than radicular pain. The study included only patients who had symptoms for longer than 6 months without improvement despite conservative care. Theoretically, this reduces the possibility that improvement in patients' symptoms after intradiscal steroid treatment was due merely to the natural course of the disease process. Unfortunately, this study was limited by small sample size, lack of validated outcome measures, the nonrandomized and nonblinded nature, and heterogeneity of dosages of steroid used. The data were not subjected to formal statistical analysis and the discography technique was not fully elaborated In 1990, Bertin et al.17 studied the effect of triamcinolone hexacetonide for acute, subacute, and chronic sciatica with a prospective, nonrandomized study. Each patient had sciatica with evidence of ‘disc protrusion,’ ‘discal hernia,’ or ‘epidural fibrosis’ by CT scan or ‘saccoradiculography’ (myelography). Operational definitions for disc protrusion, discal hernia, and sciatica were not given. The presenting sciatica symptoms were resistant to conservative care including rest, nonsteroidal antiinflammatory drugs, and, occasionally, epidural steroid injections. Each patient underwent discography followed by intradiscal injection of local anesthetic combined with 2 mL of triamcinolone hexacetonide. The exact dosage was not given. Followup occurred at 1 and 3 months following injection. There were 30 patients who had a mean age of 46 years (range 25–63 years) and mean duration of symptoms of 36 months (range 1 month to 10 years). Outcomes were categorized according to the authors' idiosyncratic criteria. Good results were defined as return to work or normal activity, discontinuation of analgesics and/or antiinflammatory drugs, and absence of clinical signs of radiculopathy. Moderate results were defined as commencement of restricted occupational or recreational activity, ‘improvement but insufficient’ reduction of axial or appendicular pain, and continued use of antiinflammatories or analgesics. Poor results yielded no change in pain and no return to work. The only two complications reported were one case of transient urinary retention and one case of foot dorsiflexion weakness that persisted at 1 year. Due to the small number of patients (n=30), Woolf's G test was utilized. There was no significant difference between the results at 1 versus 3 months although there was a trend for diminished number of good results and an increase in poor results with the number of moderate results remaining relatively unchanged. After 3 months, 36.6% had good results, 36.6% had moderate results, and 26.7% had poor results. Essentially, one-third of patients had a good, moderate, or poor result. Duration of symptoms of less than 6 months and CT-scan appearance of disc herniation ( p<0.001, g=11.65) or fibrosis ( p<0.001, g=11.65) predicted a good prognosis whereas a poor prognosis was more likely when there was an antecedent occupational accident (0.025< p <0.05, g=4.76), symptom duration of greater than 6 months (0.01< p < 0.025, g=8.644), and a CT-scan appearance of disc protrusion ( p<0.001, g=11.65). The authors' distinction between disc protrusion and discal hernia was not defined. Factors that did not affect results were gender (g=6.9×10−4), age (g=0.149), spinal stiffness (g=0.8), presence of Lasegue's sign (g=2.197), disc level (g=1.92), history of disc surgery (g=0.346), and zygapophyseal joint arthropathy (g=2.7). The authors suggested limiting the indication for intradiscal steroid injection to sciatica due 1051

1052

54%

15%

31%

Predominantly axial LBP ± previous surgery. (n = 26 injections)

42%

31%

37%

Predominantly radicular pain (n = 19 injections)

25%

50%

25%

Predominantly axial cervical pain (n = 8 injections)

50%

30%

20%

31%

15%

54%

30%

30%

40%

No history of previous surgery. Predominantly radicular pain. Full dose Depo- Medrol = 80 mg (n = 10 injections)

**

**

56%

Patients progressing to anterior interbody surgery after not responding to intradiscal injections (n = 9)*

No history of previous surgery. Predominantly axial LBP. Full dose Depo-Medrol = 80 mg (n = 13 injections)

‘Good’ was defined as significant improvement in pain for at least 3 months, ‘limited’ results denoted significant pain relief from 10 days to 3 months, and ‘none referred to no improvement or improvement lasting less than 10 days. * None of the patients who had good results from cervical intradiscal injection underwent surgery. ** Not broken down in the article.

No improvement or improvement lasting less than 10 days

None

Significant improvement in pain from 10 days to 3 months

Limited

Significant improvement in pain for at least 3 months

Good

RESULTS

Cervical intradiscal steroid injections (18 injections, 13 pts)

62%

26%

12%

Depo-Medrol ≤ 40 mg (n = 8 pts)

Predominantly cervical radicular pain (n = 10 injections)

62%

15%

23%

History of previous surgery (n = 8 pts)

Table 95.3: Wilkinson and Schuman: cervical intradiscal steroid injection

No improvement or improvement lasting less than 10 days

None

Significant improvement in pain for at least 3 months

Limited

Significant improvement in pain for at least 3 months

Good

RESULTS

Lumbar intradiscal steroid injection (45 injections, 29 pts)

Table 95.2: Wilkinson and Schuman: lumbar intradiscal steroid injection

Part 3: Specific Disorders

Section 5: Biomechanical Disorders of the Lumbar Spine

to a disc protrusion when the symptoms were of less than 6 months duration. They also suggested symptomatic epidural fibrosis could constitute an indication, but were less demonstrative about this. The authors did not specify any criteria for diagnosing symptomatic epidural fibrosis. The methodology was limited, since it was nonrandomized and nonblinded, analyzed a small sample size, and used an outcome measure that had not been validated. Likewise, neither the discography technique nor the interpretation method was described. Finally, the operational definitions distinguishing ‘discal hernia’ and ‘disc protrusion’ were not described. Simmons et al.14 evaluated the efficacy of intradiscal steroids (Depo-Medrol) in 25 patients, aged 18–50 years, who experienced low back pain due to single-level lumbar disc disease diagnosed using provocation discography. Other inclusion criteria included no prior surgery, 6 weeks of axial back pain that failed to improve with conservative care, and an MRI that did not reveal a sequestered fragment. Patients were then randomized to one of two study arms and prospectively assessed. The therapeutic group received an unreported volume of 80 mg/mL of Depo-Medrol and the control group was given 1.5 mL of 0.5% Marcaine. The Oswestry Pain Questionnaire, visual analogue scale (VAS) and pain diagram were evaluated. These were completed before and at 10–14 days following discography and intradiscal injection. The timing of intradiscal injection relative to discography was not specified but is implied to immediately follow the provocation discography. If no improvement was reported after 10–14 days, surgery was offered, when appropriate. There was no statistically significant difference in outcomes reported using chi-square analysis between the two groups. A trend was reported for improvement in the Depo-Medrol group (21%, 3 of 14) versus the Marcaine group (9%, 1 of 11). Forty-three percent of the Depo-Medrol group and 36% of the Marcaine group showed some degree of improvement in VAS scales although no specific improvement threshold was required to be categorized as receiving benefit. The Oswestry Pain Questionnaire data revealed functional improvement in 36% of the Depo-Medrol group and 27% of the Marcaine group. There were no complications observed in either group. Unfortunately, the small sample size (14 patients in the DepoMedrol group and 11 in the Marcaine group), and a short follow-up interval (10–14 days) precludes the ability to identify which treatment cohort's aspects predict a better or worse outcome. Additionally, although the concentration of Depo-Medrol administered was specified (80 mg/mL), the volume and dosage was not given. Most discs can only accept a limited volume and, therefore, it is unknown if all discs in the study received the same dosage. Bull retrospectively studied the efficacy of intradiscal depomedrone or lederspan administration during a discography procedure on degenerative lumbar discs in relation to Modic changes.18 Of 105 patients, 61 had no Modic changes, 20 had type I Modic changes, and 24 had type II Modic changes. At 8 weeks postinjection, patients were classified as better (complete resolution or significant improvement allowing return to normal activities), same, or worse. Worsening occurred temporarily in seven patients, four in the non-Modic group and three in the type I Modic group. No worsening occurred in the type II Modic group. In the non-Modic group, 8 (13%) were better and 49 (87%) were the same. In the Type I Modic group, 4 (20%) were better and 13 (80%) were the same. In the type II Modic group, 13 (54%) were better and 11 (46%) were the same. For statistical analysis with chi-square analysis with Yates correction, the seven patients with worsening were placed in the ‘same’ group. There was a significant difference between the type II Modic group and the nonModic group (p<0.02). There was no significant difference between the type I Modic group and the non-Modic group (p>0.5). Based on these findings, the authors concluded that patients with MRI findings

of type II Modic changes may have an inflammatory response and may, therefore, respond to intradiscal steroid injection. This study was limited in that it was published in abstract form only, did not include dosages of medications, and was retrospective. Khot et al.19 also produced a randomized, controlled trial comparing intradiscal injection of 1 cc of 40 mg Depo-Medrol to 1 cc of normal saline in a total of 98 patients (120 enrolled, 98 completed) with chronic axial low back pain without radicular pain who had failed at least 6 weeks of conservative care. All patients had concordant pain generation of a degenerate disc on provocation discography and were given the intradiscal injection postdiscography. Sixty patients were randomized into each group. Of these, 46 in the Depo-Medrol group and 52 in the saline group completed the trial. The patients were prospectively followed in clinic and by postal questionnaire at 1 year with a visual analogue score for pain and an Oswestry Disability Index. At 1 year, there was no significant change in pain or disability for both groups. The saline group had a mean change in disability of 3.4 while the Depo-Medrol group had a mean change in disability of 2.3. The saline group had a median change in pain score of 0 (interquartile range −1 to +1) while the Depo-Medrol group had a median change in pain score of 0 (interquartile range −0.25 to +1). Ten patients did not complete the study due to undergoing surgery and were not included in the final analysis. Of these, 6 were in the Depo-Medrol group and 4 were in the saline group. Complications were not reported. This study's strengths were its use of validated outcome measures, larger sample size than previous studies and the fact that it was a double-blinded, randomized, controlled trial. Unfortunately, outcomes were only assessed at 1 year without regard to the intervening time periods such as 1–2 weeks, 4–6 weeks, 3 months, and 6 months. It is possible that the therapeutic time period was missed. Additionally, in 1980, the study by Wilkinson and Schuman15 suggested that 80 mg of Depo-Medrol provided better results than 40 mg of Depo-Medrol. Thus, Khot et al. may not have used an adequate dose of methylprednisolone acetate or Depo-Medrol. Additionally, the study conclusions may not be applicable to other corticosteroids. There has been one coccygeal intradiscal steroid injection investigation evaluating coccydynia symptom relief.20 Radiographs were obtained in two positions: (1) the lateral standing position after standing 5–10 minutes, thus allowing the coccyx to regain a neutral position, and (2) a dynamic film taken laterally after 1 minute of sitting on a hard stool with the back slightly extended in a position where the patients experienced the most pain. Measurement changes in sagittal angulation and displacement in 91 patients with chronic coccydynia and 25 volunteers without low back or coccygeal pain were compared. Based on these comparisons, patients with coccydynia were classified into three categories based on the dynamic coccygeal motion or angulation amount: (1) normal, (2) hypermobile if there was more than 25° flexion, and (3) luxation if there was more than 25% slippage. In the control group, the mean mobility ranged from 0 to 70 degrees with a mean of 9.3±5.7 degrees. Only two control patients had less than 20% luxation. In the symptomatic group, 28.6% had luxation, 19.8 % were hypermobile, and 51.6% had normal coccygeal mobility. In 86 patients, coccygeal discography was performed to inject prednisolone acetate into the involved articulation, which could exist as disc, synovial joint, or as intermediate structure. The researchers used Maigne's previously described technique for coccygeal discography.21 The sacrococcygeal or intercoccygeal disc was entered from a midline posterior approach with the patient in a lateral decubitus position using an image intensifier. The dosage of steroid was not detailed. At a follow-up of approximately 2 months postprocedure, 1053

Part 3: Specific Disorders

improvement was reported in 50% of the patients with luxation or hypermobility whereas only 27.5% of the symptomatic patients with normal coccygeal motion improved with a statistical difference between groups (p=0.033). Unfortunately, the outcome measurement method was not described. In summary, intradiscal corticosteroid injection efficacy studies have methodologic flaws but demonstrate the technique is relatively safe and provides modest clinical discogenic pain improvement for selected patients. Older patients with predominantly axial pain have better outcomes8,15 and the response appears dose-dependent. All investigations used only one agent and therefore the results may not be applicable to other corticosteroids. Each injectate may have unique characteristics such as solubility, duration of action, and extent of accelerated disc degeneration. The supposed inactive ingredients contained in the corticosteroid preparation may also need to be considered.11

INTRADISCAL CORTICOSTEROIDS: ADVERSE SIDE EFFECTS Accelerated disc degeneration Accelerated disc degeneration has been reported with intradiscal Depo-Medrol and also its component preservative, polyethylene glycol (PEG). Using a rabbit model, Aoki et al.11 found that injections of either PEG alone or Depo-Medrol (methylprednisolone acetate) caused nucleus pulposus cell disappearance in 2 of 2 rabbits and intradiscal calcification deposition in 2 of 3 rabbits examined by electron microscopy 24 weeks after injection. There were no abnormal findings when rabbits were sacrificed and evaluated at 12 weeks or before. There was also no such degeneration with intradiscal saline or Solu-Medrol (methylprednisolone sodium succinate) injection. The authors suggested that postintradiscal steroid injection disc degeneration may actually be the mechanism for the clinical improvement. Kato et al.13 also pointed out that progressive disc degeneration and subsequent contraction may reduce a herniated disc.

Spinal calcification and ossification Intraspinal ligament and intraepidural space calcification or ossification has been reported after intradiscal triamcinolone and betamethasone injections.22–25 In Japan, there is a relatively higher prevalence of posterior longitudinal ligament ossification. Ito et al.26 retrospectively reviewed lower lumbar radiographs in 183 Japanese patients before and 1 year after lumbar intradiscal betamethasone injection and found no statistically significant increase in spinal canal ossification and calcification risk. Ossification and calcification either developed or increased in the anulus fibrosus outer layer or posterior longitudinal ligament in 3.8% of patients. Of the 193 discs injected with contrast but without betamethasone, 2 disc levels (1.0 %) developed calcification or ossification. Of the 304 discs that received both contrast and betamethasone, 5 (1.9%) disc levels developed calcification or ossification. Of the discs in the lower three lumbar levels that did not receive either contrast or betamethasone, 1 (1.9%) disc level developed calcification or ossification. None of the cases was severe enough to cause dural compression on CT or MRI. The preparation's nonsteroidal additives may affect or cause the phenomenon but this was not tested. Additionally the conclusions of this study are based on the use of betamethasone and may not be applicable to other corticosteroid preparations.

INTRADISCAL PROLOTHERAPY Prolotherapy has been a controversial topic since Louis Schultz's 1937 description.27 Prolotherapy substances theoretically stimulate the growth or initiate sclerosis of ligaments, tendons, cartilage, and 1054

bone. It has been used to treat recalcitrant musculoskeletal conditions and has gained escalating popularity over the past decade. Although it is currently utilized for many conditions, from headaches to lateral epicondylitis, the following discussion will focus on the current published outcome studies for low back pain and its application for intradiscal treatment. Intradiscal prolotherapy or ‘restorative injections’ has been reported in two publications to date.28,29 Klein et al.29 published a prospective pilot study on 30 patients in which a mixture of glucosamine and chondroitin sulfate combined with hypertonic dextrose and dimethylsulfoxide (DMSO) was injected. The authors theorized that the injectate could cause chondrocyte stimulation and secondary repair of degraded cartilage within the lumbar discs. The mixture utilized in this study was divided into thirds; {1/3} consisted of contrast, {1/3} was 50% dextrose, while the remaining {1/3} consisted of a concentration of 0.5% chondroitin sulfate, 20% glucosamine hydrochloride, 12% dimethylsulfoxide (DMSO) and 2% bupivicaine. According to the authors, the glucosamine and chondroitin sulfate was theorized to enhance proteoglycan synthesis, whereas the hypertonic saline was theorized to induce growth factor release, as well as to suppress factors that may potentially impair restoration.30–32 The contrast was used to determine if the entire 1–2 cc of injectate was deposited into the disc. If there was any fluoroscopic evidence of epidural spread, the injection was terminated. Klein et al. chose 30 consecutive patients who had all failed to respond or responded poorly to multiple treatment including medications, therapy, percutaneous procedures (including IDET), and surgery. All patients were considering further surgical procedures. It was the authors' intent to enroll patients with refractory low back pain that had failed multiple interventions. The patients were presumed to all have discogenic pain based upon discography results. Eighty percent of the cohort had discogenic pain at two or more levels. Seven of the patients had previously failed IDET at one level. Of those patients, six underwent subsequent treatment with prolotherapy to the same level that had previously been treated with IDET while one patient had a different level treated. Six patients (20%) had failed previous surgery with the surgical cohort split 50% between either a previous laminectomy (three patients) or fusion (three patients). The patients who had a previous lumbar fusion surgery had a single-level fusion and were symptomatic via discography at adjacent unfused levels. Additionally, the authors also simultaneously performed intraarticular zygapophyseal joint injections with 20% glucosamine hydrochloride, 12% dimethylsulfoxide (DMSO) and 2% bupivicaine. The 0.5% chondroitin sulfate was omitted from the zygapophyseal joint injectate because of previous experience resulting in irritation with select patients. By evaluating pre- and posttreatment Roland-Morris disability scores and the visual analogue scale, the authors found that 57% of the patients had good or excellent response based upon a 50% minimum improvement in the Rolland-Morris questionnaire and VAS. Forty-three percent of patients failed to receive 50% relief of pain or disability. The entire surgical cohort (46% of the failure group) did not demonstrate any benefit. The lack of a control group and the inclusion of simultaneous zygapophyseal joint injections are significant flaws affecting the study's results. Derby, who co-authored the above study with Klein, published an additional pilot study comparing IDET and intradiscal prolotherapy outcomes.28 They retrospectively compared the two treatment groups' visual analogue scale, satisfaction rate and pain flares preand postprocedure. Except for the addition of five patients, Derby's intradiscal prolotherapy cohort are the same as those in the Klein publication. A total of 35 patients had restorative therapy. Sixty-eight percent had discogenic pain at two or more levels (80% without the

Section 5: Biomechanical Disorders of the Lumbar Spine

additional five patients). Seven of the patients had previously failed IDET at one level. Six of these seven patients underwent subsequent intradiscal prolotherapy directed at the previous IDET treatment level. One patient had intradiscal prolotherapy into a disc without previous IDET. Seventeen percent had previously failed surgery, or 20% if one excludes the additional five patients. Injection of a solution containing glucosamine and chondroitin sulfate combined with hypertonic dextrose and DMSO was undertaken. There are no comments about co-treatment with zygapophyseal joint injections after intradiscal prolotherapy as in the Klein publication. The IDET group included 74 patients with single-level pathology diagnosed with positive discography documenting an annular tear. The demographic stratification was similar to the prolotherapy group, with an average age of 41.6 years, compared to 42.0 years for the intradiscal injection group. Pre- and postprocedural visual analogue scales, subjective satisfaction and improvement questions, activity level, and patient's pain distribution were collected. When comparing pain relief and disability, the authors found statistically significant relief for both groups, although restorative therapy fared slightly better than IDET. Based on the study results, Derby postulates that prolotherapy could be an early alternative to IDET in discogenic low back pain treatment.

CONCLUSIONS Intradiscal injections may provide clinical discogenic pain improvement, but their overall effects seem modest. The corticosteroid studies have design flaws that limit their ability to confirm or refute the therapeutic benefits. Intradiscal prolotherapy is a novel approach that has yet to be fully elucidated. The trials have shown modest improvement in a small patient cohort whose pain was previously refractory to other treatments. Unfortunately, these restorative disc injection studies are by no means comprehensive and also contain methodological flaws. More comprehensive intradiscal corticosteroid and restorative disc injection studies are needed to fully establish their therapeutic benefit

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11. Aoki M, Kato F, Mimatsu K, et al. Histologic changes in the intervertebral disc after intradiscal injections of methylprednisolone acetate in rabbits. Spine 1997; 22(2):127–132. 12. Barnsley L. Steroid injections: effect on pain of spinal origin. Best Pract Res Clin Anaesthesiol 2002; 16(4):579–596. 13. Kato F, Mimatsu K, Kawakami N, et al. Changes in the intervertebral disc after discography with intradiscal injection of corticosteroids observed by magnetic resonance imaging (MRI). J Neurol Orthop Med Surg 1993; 14:210–216. 14. Simmons JW, McMillin JN, Emery SF, et al. Intradiscal steroids: a prospective double-blind clinical trial. Spine Supplement 1992; 17(6):S172–S175. 15. Wikinson HA, Schuman N. Intradiscal corticosteroids in the treatment of lumbar and cervical disc problems. Spine 1980; 5(4):385–389. 16. Feffer HL. Treatment of low-back and sciatic pain by the injection of hydrocortisone into degenerated intervertebral discs. J Bone Joint Surg [Am] 1956; 38(3): 585–592. 17. Bertin P, Rochet N, Arnaud M, et al. Intradiscal injection of triamcinolone hexacetonide for acute, subacute, and chronic sciatica. Results at 3 months an openprospectus study of 30 cases and review of the literature. Clin Rheumatol 1990; 9:361–366. 18. Bull TM, Sharp JM. The efficacy of intra-discal steroid injection compared to Modic changes in degenerative lumbar discs. J Bone Joint Surg [Br] 1998; 80 Supp I:47. 19. Khot A, Bowditch M, Powell J, et al. The use of intradiscal steroid therapy for lumbar spinal discogenic pain: a randomized controlled trial. Spine 2004; 29(8): 833–837. 20. Maigne J-Y Tamalet B. Standardized radiologic protocol for the study of common coccygodynia and characteristics of the lesions observed in the sitting position: clinical elements differentiating luxation, hypermobility, and normal mobility. Spine 1996; 21(22):2588–2593. 21. Maigne J-Y, Guedj S, Straus C. Idiopathic coccygodynia: Lateral roentgenograms in the sitting position and coccygeal discography. Spine 1994; 19(8):930–934. 22. Debiais F, Bontoux D, Alcalay M, et al. Calcification after intra-disk injection of triamcinolone hexacetonide in lumbar disk hernia: evaluation of therapeutic results. Rev Rhum Mal Osteoartic 1991; 58:565–570. 23. Duquesnoy B, Debiais F, Heuline A, et al. Poor results of intradiscal triamcinolone hexacetonide in the treatment of sciatica due to intervertebral disc herniation. Presse Med 1992; 21:1801–1804. 24. Menei P, Fournier D, Alhayek G, et al. Necrotic inflammatory granuloma and calcification after intradiscal injection of triamcinolone hexacetonide. Rev Rhum Mal Osteoartic 1991; 58:605–609. 25. Menkes CJ, Vallee C, Giraudet-Le-Quintrec JS. Calcification of the epidural space following an intradiscal injection of triamcinolone hexacetonide. Scand J Clin Lab Invest 1954; 6(4):295–302. 26. Ito S, Usui H, Maruyama K, et al. Roentgenographic evaluation of ossification and calcification of the lumbar spinal canal after intradiscal betamethasone injection. J Spinal Disord 2001; 14(5):434–438. 27. Schultz L. A treatment for subluxation of the temporomandibular joint. JAMA 1937; 190:1032–1035.

3. Virri J, et al. Comparison of the prevalence of inflammatory cells in subtypes of disc herniations and associations with straight leg raising. Spine 2001; 26(21): 2311–2315.

28. Derby R, et al. Comparison of intradiscal restorative injections and intradiscal electrothermal treatment in the treatment of low back pain. Pain Physician 2004; 7:63–66.

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6. Aprill C, Bogduk N. High-intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. Br J Radiol 1992; 65(773): 361–369. 7. Ross JS, Modic MT, Masaryk TJ. Tear of the anulus fibrosus: Assessment with CdDPTA-enhanced MR imaging. Am J Roentgenol 1990; 154:159–162. 8. Feffer HL. Therapeutic intradiscal hydrocortisone: a long-term study. Clin Orthopaed Rel Res 1969; 67:100–104. 9. Sundblad L, Egelius N, Jonsson E. Action of hydrocortisone on the hyaluronic acid of joint fluids in rheumatoid arthritis [French]. Presse Med 1989; 18(34):1707.

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10. Leao L. Intradiscal injection of hydrocortisone and prednisolone in the treatment of low back pain. Rheumatism 1960; 16:72–77.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain

CHAPTER

96

Intradiscal Electrothermal Annuloplasty Peter C. Gerszten and William C. Welch

INTRODUCTION Spine specialists have been frustrated by the lack of effective treatments for chronic low back pain. The intervertebral disc is believed to be the source of low back pain in as many as 40% of patients with chronic low back pain.1–4 The results from conservative therapies are frequently poor in this patient population. Over the years, a number of intradiscal techniques to either shrink or remove disc material believed to be causing lumbar pain and/or radiculopathy have been described.5 These techniques include interbody fusion, posterolateral fusion, microdiscectomy, arthroscopic discectomy, automated percutaneous lumbar discectomy, chymopapain, as well as other procedures.6–10 Recently, a new technique has been developed that involves the percutaneous insertion of a thermal resistance probe with controlled heating of the disc material.11–14 This technique is known as intradiscal electrothermal annuloplasty (or IDET). Intradiscal electrothermal annuloplasty was developed as a minimally invasive procedure for the treatment of pain due to degenerative disc disease.15 The procedure has been used in the lumbar spine of patients who have failed conservative treatment regimens and who might otherwise be candidates for a spinal fusion procedure. The IDET procedure was developed by two brothers, Drs. Jeffrey and Joel Saal, specialists in physical medicine and rehabilitation. The procedure was developed to offer patients with chronic discogenic low back pain an option other than chronic pain management for spinal fusion.16 The IDET procedure is specifically devised to treat degenerative disc disease resulting in chronic low back pain. Thermal energy had been shown to induce tissue shrinkage in cadaveric and animal models.17–20 Saal and Saal hypothesized that thermal energy might have a role in the treatment of so-called ‘internal disc disruption,’ and, thus, in chronic low back pain.13 This proposition led to the development of a catheter to deliver intradiscal electrothermal annuloplasty therapy.17

Nociceptors may accompany this vascular growth and account for the presence of sensory nerve supply in the inner anulus (Fig. 96.1). In the normal intervertebral disc, sensory nerves do not penetrate beyond the outer one-third of the anulus fibrosus.1 In degenerative disc disease, however, an association has been demonstrated between the ingrowth of nerves expressing substance P and disc degeneration. Disc degeneration and disc injury are associated with centripetal growth of nerve fibers in the disc, which would provide a morphologic basis for true discogenic pain. It is this ingrowth of nerve fibers that is believed to be the source of back pain of discogenic origin.

INTRADISCAL ELECTROTHERMAL THERAPY The theoretic basis for IDET is that targeted thermal energy within the pathologic disc is designed to shrink collagen fibrils, cauterize granulation tissue, and coagulate nerve tissue in the posterior anulus fibrosus.13,16 When temperatures above 65°C were applied to cadaveric shoulder capsules, studies have shown shrinkage of the specimen and, histologically, hyalinization of the collagen (Fig. 96.2).18 The procedure is supported by basic science research performed by investigators who assess in vitro temperature mapping and demonstrated that

PATHOPHYSIOLOGY OF DISC DEGENERATION AS IT RELATES TO IDET The pathophysiology and origins of low back pain of discogenic origin are incompletely understood.21 One theory hypothesizes that small, post-traumatic peripheral tears of the anulus fibrosus lead to an acceleration in the dehydration of the intervertebral disc, with resultant fraying of the nucleus pulposus.17,22 Studies using annular trauma in a sheep model support this theory.23 The intervertebral disc is surrounded by an external continuous plexus of interlacing nerve fibers. Contributions to this network occur ventrally from a plexus surrounding the anterior longitudinal ligament and dorsally from a plexus surrounding the posterior longitudinal ligament.21 Vascular ingrowth also has been observed in peripheral tears of the anulus.

Fig. 96.1 Schematic drawing of an annular fissure with ingrowth of nociceptor fibers. 1057

Part 3: Specific Disorders • Heat-sensitive bonds break at 60⬚C • Crystalline extended structure begins to uncoil • As molecule contracts, its diameter increases Heat Collagen triple helix module

Table 96.1: Selection criteria for IDET Fig. 96.2 Demonstration of the thermal modulation and shrinkage of collagen in response to IDET.

thermal resistance catheter heating conducted temperatures sufficient to coagulate nerve endings and to contract collagen.24 Bono et al.25 documented in a cadaver model the temperature sufficient for collagen denaturation and nociceptive ablation were detected at distances greater than previously documented. These data suggest that the proposed heat-dependent mechanism of action in intradiscal electrothermal therapies are achieved in most discs. Among other factors, intraspecimen variability of maximum temperatures may help explain the somewhat inconsistent clinical results following intradiscal electrothermal therapy. One in vitro study, however, suggested that the temperatures developed during intradiscal electrothermal therapy were insufficient to alter collagen architecture or stiffen the treated motion segment acutely.26 Kleinstueck et al.26 also investigated the biomechanical effects of IDET on vertebral motion. It is plausible that the heated catheter denatures and shrinks the collagen fibrils, thus stabilizing the motion segment. In this cadaveric study, there was an increase in motion at the IDET-treated levels. This investigation, however, did not take into account the effects of subsequent scarring that would occur over time in vivo. Subsequent scarring may result in stiffening and stabilization of the motion segment over a period of time consistent with the clinical relief of pain at 1–3 months. Other studies27 have shown a similar triad of biologic repair in the therapeutic effect (maintenance of shrinkage, secondary scarring and thickening, and destruction of sensory fibers). Gross pathology before and after treatment demonstrates shrinkage of the nuclear matrix.17 Although the in vivo response has not yet been proven, IDET is likely successful in denervation of the anulus fibrosus through temperature modulation.28

Intrusive low back pain for more than 3 months Failure to achieve adequate improvement with comprehensive nonoperative treatment No medical or other systemic causes for the low back pain Physical examination No neurologic deficits Normal straight leg raise test MRI scan and X-ray films Not definitive for a specific pathologic condition known to cause low back pain such as disc herniation, spinal stenosis, spondylolisthesis, etc. Disc desiccation is not a specific pathologic condition No greater than 25% loss of disc height Psychological No irreversible psychological barriers to recovery Motivated patient with realistic expectations Criteria for internal disc disruption satisfied

Table 96.2: Contraindications for APLD INCLUSION CRITERIA Duration of symptoms of at least 3–6 months Failed 6 weeks conservative care Abnormal disc morphology Predominance of low back pain symptoms Concordant pain reproduced on discography EXCLUSION CRITERIA

INDICATIONS FOR INTRADISCAL ELECTROTHERMAL The indications for IDET are generally felt to be similar to those for interbody fusion, and apply the same diagnostic and treatment criteria. As with most treatments, patient selection may be the single most important criterion for a successful outcome. Discogenic low back pain is the most common condition treated with IDET, and its presence is the primary selection criterion. Patients should have chronic low back pain in the absence of other readily identifiable structural abnormalities. Discogenic pain is most often defined as unremitting, persistent low back pain that is worse with axial loading and improved with recumbency. The low back pain is greater than leg pain. This is a nociceptive pain and not a neuropathic pain syndrome.29 Patient selection criteria for the IDET procedure are similar to those used for spinal fusion for degenerative disc disease of the lumbar spine (Table 96.1).15 Several authors have published strict inclusion criteria as well as exclusion criteria (Table 96.2).13,30,31 The primary indication is unremitting, persistent low back pain. An additional criterion is a failure of satisfactory improvement with a nonoperative care program that includes back education, activity modification, a progressive and intensive exercise program, a trial of physical therapy, and use of oral nonsteroidal antiinflammatory drugs. These authors have described the failure of the conservative (nonoperative) treatment as a minimum 6-month period of comprehensively applied nonoperative treatment with the patient reporting persistent pain and disability, 1058

Abnormal neurological findings/ compressive lesion Severe disc degeneration Segmental instability Other medical conditions Consideration of previous surgery

dissatisfaction with quality of life, and a desire to pursue alternative treatment options. Physical examination should include a normal neurological examination with a negative straight leg raising sign. Imaging studies are necessary in the diagnostic evaluation process. Magnetic resonance imaging (MRI) confirms the presence of disc degeneration, desiccation, high-intensity zones (Modic endplate changes), and loss of disc height (Fig. 96.3). Contained disc fragment herniations may also be present. Extruded and free fragments of disc cannot be effectively treated using this procedure, but patients with these lesions may be treated for discogenic low back pain with the proviso that the fragments will be unchanged after treatment. We do not feel that a focal protrusion of a disc is a contraindication to performing the IDET procedure. The authors have not seen a single clinical case in which a disc herniation occurred after the IDET procedure. There does not appear to be any increased risk if undertaken in such discs. Karasek and Bogduk11,30 state that the major indication for IDET is internal disc disruption, not merely discogenic pain. This internal disc

Section 5: Biomechanical Disorders of the Lumbar Spine

Fig. 96.3 Sagittal T2-weighted MRI demonstrating disc desiccation with a posterior ‘highintensity zone’ consistent with an annular tear.

disruption may be diagnosed by a combination of disc stimulation (‘provocative discography’) that produces concordant pain with no pain replication at adjacent levels, and a computed tomography (CT) scan after discography that reveals an annular tear. Both criteria must be met in order for the discogram to be considered ‘positive.’ The author often employs provocative discography, conducted by an unbiased interventional spine physician.13 This diagnostic study is used to confirm the clinical suspicions, and its results may be used as exclusionary criteria for patients with multilevel disease. Postdiscography CT also provides technical information regarding placement of the intradiscal catheter by evaluating the location and degree of annular disruption (Fig. 96.4). In addition, if a skilled interventional spine physician has difficulty placing a 20-gauge needle into the L5–S1 disc space, one can reasonably expect to have similar difficulties placing an even large needle into the same intervertebral space for the IDET procedure.

Another group of patients considered for IDET are those with multilevel degenerative disc disease in whom multilevel interbody fusion is being considered. These patients may benefit from combined-modality treatment including a fusion at the most affected level and IDET at the less symptomatic level. Kapural et al. reported that the pain relief and Pain Disability Index were significantly better in patients with a single- or two-level degenerative disc disease than in the multiple degenerative disc disease group.32 The exclusion criteria for IDET initially presented by Saal and Saal12 included patients with inflammatory arthritides, nonspinal conditions that could mimic lumbar pain, and prior surgery at the symptomatic levels. The authors’ exclusion criteria include lumbar spinal instability that would require fusion and the presence of infection or malignancy at the level requiring treatment. Multilevel disease (three or more levels of disc disease documented on MRI or discography) is a relative but not necessarily absolute contraindication to IDET. Finally, a greater than 75% loss of normal disc height is also a relative contraindication to the procedure.

IDET TECHNIQUE The authors perform the IDET procedure in a standard operating room in an outpatient setting. The technique consisted of placing the patient on a Jackson Table (Orthopaedic Systems, Inc., Union City, CA) in a prone position. Intravenous sedation is given and C-arm fluoroscopy is utilized to obtain anteroposterior, oblique (‘needle eye view’), and lateral images. The treatment level is localized and local anesthesia is applied to the skin 6–9 cm lateral to the midline (Fig. 96.5). In this approach, the anatomical triangular working zone described by O’Neill et al., Kambin, and Parke is used (Fig. 96.6).5,9,33 This ‘working triangle’ avoids the exiting nerve root. The IDET set includes a 17-gauge needle and stylet. The needle is directed toward the center of the disc under fluoroscopic guidance, and the anulus is punctured. The thermal-resistance catheter is inserted through the needle into the disc (Fig. 96.7). The catheter is coiled within the disc as it is deflected by the annular fibers (Fig. 96.8). The tip of the catheter is directed to the posterior aspect of the disc in such a manner that the heating elements of the catheter remained on the symptomatic side. Therefore, the needle is inserted on the side contralateral to the patient’s pain (or annular tear seen on postdiscography axial CT images) (Fig. 96.9). The catheter temperature is increased along an electronically programmed protocol

Use discography approach for needle placement 8–10cm

35˚–45˚

Fig. 96.4 Postdiscography axial CT image demonstrating a posterior annular tear with extravasation of contrast material.

Fig. 96.5 Cross-section through lumbar region demonstrating entry point of the catheter. 1059

Part 3: Specific Disorders Angles of approach to lumbar discs

Kambin's triangle

Axial view Triangular working zone

Fig. 96.6 Diagrams demonstrating the working triangles and safety zone for catheter placement.

Intradiscal portion (shown flexed)

Radiopaque distal tip

Tip pre-curve direction indicator Needle/connector

Thermocouple

Proximal shaft markings

Radiopaque proximal marker Thermal resistive heater Pre-curved guiding tip Fig. 96.7 Schematic drawing of the IDET catheter.

over 13 minutes to 90°C and is allowed to remain at that temperature for 4 minutes. The temperature of the catheter is initially 65°C and is increased by 1°C every 30 seconds until the target temperature is reached. A single heating treatment is administered. The authors do not inject antibiotics into the disc space. The catheter and needle are then removed as a single unit.

A

Other authors have also described their technique for the IDET procedure. Derby et al.34 stated that when there has been significant posterior annular disruption, it is sometimes difficult to navigate the catheter anywhere but the outermost annular fibers. In these cases, one can easily reach temperatures that denervate the outer anulus at temperatures and times at or below 60°C tissue temperature which would correspond to 85°C measured temperature in the original IDET catheter. Karasek and Bogduk30 emphasize that the catheter position at all times should be buried between the lamellas of the anulus fibrosis some 5 mm deep to its outer surface. Of note is that Freeman et al.35 stated that the IDET did not produce denervation of the experimentally induced posterior annular lesion in a sheep model. After assessing the temperatures in thermal dose distribution during IDET, Kleinstueck et al.36 reported temperatures were not reliably produced in clinically relevant regions, such as the posterior anulus. A more recent study by Bono et al.25 have refuted this finding. Patients with multilevel disease undergo treatment at other involved level(s) using the same protocol. New catheters and needles are used at each level. Patients with only back pain and no leg pain undergo treatment on the opposite disc side (i.e. bilateral) as well. Patients are discharged after 2 hours of observation. Following the

B

Fig. 96.8 (A) Anteroposterior fluoroscopic image demonstrating the IDET catheter coiled in the disc space. (B) Lateral fluoroscopic image demonstrating the IDET catheter coiled in the disc space. Note how the distal catheter lies adjacent to the posterior annular fissure. 1060

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Fig. 96.9 Schematic drawing of the ideal position of the catheter during the IDET procedure. The flexible tip is in position with the flexed catheter resting along the inner portion of the posterior wall of the anulus fibrosus. The markings demonstrate the area exposed to thermal energy during the procedure. (Image Courtesy of Smith & Nephew, Inc.)

procedure, patients are instructed to resume their usual activities as tolerated after 24 hours. The authors do not routinely prescribe a lumbar orthoses after the procedure. This is the authors’ own protocol. Many practitioners place different restrictions upon their patients as well as prescribe a lumbar orthoses after the procedure.

REVIEW OF PUBLISHED CLINICAL DATA Since 1998, there have been over 40 peer-reviewed articles and abstracts that have presented clinical outcomes associated with the IDET procedure.2,13,30,37 The initial publication regarding IDET was from the Saal brothers in 2000.12 These investigators reported a series of 91 patients who were chosen from a population pool of 1116 consecutive patients presenting with chronic low back pain of >3 months duration. Of the 91 patients who did not respond to nonoperative care, 62 underwent IDET as an alternative to spinal fusion and 29 remained in a control group to assess the impact of natural history on symptom resolution.38 At 12 and 24 months, the mean decrease in Visual Analog Scale (VAS) score was 3.52±2.30 and 3.41±1.96, respectively. Based upon these initial data, the authors concluded that a statistically significant improvement in pain was obtained in patients with chronic discogenic low back pain treated with IDET. The wide variations in definitions of success that have been used to evaluate the outcomes of IDET therapy make comparisons among studies difficult.39 A meta-analysis published in 2001 reviewed 11 studies involving 704 patients.2,30,37,40,41 This meta-analyses showed a clinically significant improvement in pain and physical functioning post-IDET. The reported outcomes from the published and presented clinical studies seem to attest to the efficacy and safety of IDET. In eight studies that utilized the VAS to assess pain outcome, all reported decreases in the VAS. The results of the meta-analysis of changes in VAS scores derived from a total of 448 patients demonstrated a p-value of p<0.0001 for a significant decrease in pain of at least two points at a minimum of 6 months post-treatment. Combining a total of 448 patients in the literature, McGraw et al.38 found a mean decrease in pain following the IDET of 2.7 points on the VAS scale.

A meta-analysis of five studies was performed that evaluated the Physical Function Scale of the SF-36 for a total of 404 patients.38 The results of a meta-analysis addressing SF-36 Bodily Pain scores found an overall mean significantly greater than 7 points ( p<0.0001), supporting a clinically significant improvement in bodily pain post-treatment. Freedman et al.39 reported an overall success rate of 65% in the management of chronic discogenic low back pain in active-duty soldiers. Wetzel et al.28 published their review of several studies and concluded that the pain resulting from lumbar disc disease may be diminished by IDET. All the studies projected a positive therapeutic effect. They stated that all the studies, however, suffered from the same methodological flaws. All studies utilized a prospective cohort design or a nonrandomized, prospective design with a biased control. A review by Biyani et al.21 concluded that IDET is a potentially beneficial treatment for internal disc disruption in carefully selected patients as an alternative to spinal fusion. In the authors’ own study, IDET was found to be effective in 75% of patients in improving their chronic low back pain at 1 year.31 Karasek et al.11,30 summarize the literature by stating that strict adherence to their proposed selection criteria results in a 60% chance of obtaining at least 50% relief of pain and a 20% chance of obtaining complete pain relief. Bogduk and Karasek42 similarly found 54% of patients had a 50% reduction in pain, and 20% achieved complete relief of their pain. With a 2-year follow-up, these investigators found the long-term results of IDET to be stable and enduring. Derby et al.2 and Lee et al.43 also found this long-term duration of pain relief. Finally, a randomized, double-blind, placebo-controlled trial evaluating the efficacy of IDET for the treatment of chronic discogenic low back pain with 6-month outcomes data has recently been published.44 In this study of 64 patients, a statistically significant improvement in pain levels was documented when compared with the control group as determined by the outcome instruments of SF-36, Visual Analog Scale, Oswestry Disability Index, Beck Depression Inventory (BDI), and Work Status Questionnaire. Primary eligibility criteria for this study were as follows: age 18–65 years; low back greater than leg pain present for greater than 6 months duration; failure to improve after at least 6 weeks of nonoperative care, including antiinflammatory and analgesic medications and a physical therapy and/or home directed lumbar exercise program; low back pain exacerbated by sitting or standing and relieved by lying down; a score less than 20 on the Beck Depression Scale; no surgical interventions within the previous 3 months and less than 20% disc height narrowing on lateral plane film radiographs. Of 1360 individuals who were prepared to submit to randomization, 260 were found potentially eligible after clinical examination and 64 became eligible after discography. The primary objective of the study was to compare the improvement in pain and physical function between groups. Post hoc analyses were conducted that summarized the proportions of patients who at 6 months obtained 25%, 50%, and 75% relief of pain relative to pretreatment levels. Percentage relief of pain at follow-up was calculated for each patient as the difference between the postoperative pain score from baseline, divided by the baseline score, and converted to a percentage. Both groups exhibited significant improvements in pain scores, but the improvement in the IDET group was significantly greater than in the sham group ( p=0.045). A similar pattern of improvement occurred in the Bodily Pain Scores of the SF-36 but was not significantly different between the two groups ( p=0.086). Both groups improved with respect to Physical Functioning on the SF-36 ( p=0.050), although with no significant differences between groups; but on the Oswestry Disability Scale, the IDET group achieved significantly better outcomes ( p=0.05). With respect to categorical outcomes, statistically significant differences in favor of the IDET group occurred both for absolute 1061

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change and for relative changes in pain scores as measured by the VAS. Furthermore, more substantial differences were found when the main outcomes were stratified according to baseline scores. It emerged that IDET was significantly more effective for patients with pain scores less than 70 at inception and for patients with poor function or greater disability at inception. Reciprocally, IDET had no significantly greater effect than sham treatment for patients with low disability or who had already had good physical function. Few interventions that the authors perform for spinal disorders have undergone such a rigorous, randomized, placebo-controlled trial as this one. The authors concluded that the efficacy of IDET could not be attributed wholly to a placebo effect. In summary, many studies by independent researchers have been published that suggest a positive therapeutic benefit of the IDET procedure.

COMPLICATIONS Intradiscal electrothermal annuloplasty appears to be a safe procedure. Few complications have been reported, and the authors’ own experience has reflected this. The most common difficulty has been inserting the needle into the L5–S1 disc space, particularly in men. In only rare cases can this level not be treated and the procedure aborted. In the authors’ extensive clinical experience, there have been no postoperative infections or nerve root injuries. Another treatment-related problem that may occur is difficulty in threading the catheter into the disc space once the needle is adequately positioned. Threading the catheter may be difficult if the needle tip is positioned against the endplate or if the disc is extremely degenerated (i.e. collapsed). A 75% or greater loss of disc height makes it extremely difficult to properly position the catheter within the disc space. Should this difficulty arise, it is extremely important not to force the catheter into the disc space because the catheter can be sheared off by the needle tip. Additionally, the catheter and needle must be removed as a single unit once the catheter is extended past the needle tip.29 McGraw et al. reported a single minor complication of temporary radicular pain in a series of 30 patient.38 Saal and Saal13 reported no complications in their study of 62 patients followed to 24 months. Wetzel et al.28 reported a minimal complication rate in a series of 75 patients. A study specifically addressing the risk factors for failure and complications of IDET found a 10% complication rate in a series of 79 patients.45 However, all of these complications were minor and self-limited. A single case of cauda equina syndrome caused by device malpositioning has been reported.46 Finally, Djurasovic et al.47 reported a single case of osteonecrosis of the adjacent vertebral bodies after an IDET procedure. Other major series report no additional complications for the IDET procedure.15,16,30,31,38,42,43,48 With over 50 000 IDET procedures performed in the United States to date, there have been no reports of discitis.1 However, this remains a potential complication. One explanation for the absence of discitis cases is the coaxial nature of the catheter system, such that the catheter that is applying the heat to the posterior anulus does not contact the skin, which would be the source of infection.34 In summary, IDET is a safe procedure, and there is no evidence to suggest that IDET is harmful to patients, either clinically or biomechanically.

SUMMARY The IDET procedure was developed as a minimally invasive procedure for the treatment of pain due to degenerative disc disease. This chapter presents a summary of the currently available clinical data regarding the indications and clinical outcomes of the IDET procedure. In light of good and excellent reported outcomes, excellent 1062

patient satisfaction, and few reported complications, IDET has been advocated as a viable treatment option for chronic discogenic low back pain refractory to nonoperative therapy.35 The IDET technique is performed by a variety of physician specialties involved in the care and management of patients with chronic low back pain of discogenic origin. IDET is currently widely being used for the treatment of this condition. The IDET procedure has gained widespread popularity and is being performed in numerous centers throughout the United States. IDET is a safe procedure that appears to be moderately effective in relieving pain of discogenic origin. It may be an alternative to lumbar interbody fusion in patients who cannot or wish not to undergo a major fusion procedure. The complication rate is very low and recovery time is minimal, especially compared with an interbody fusion operation. Finally, there is no evidence to suggest that IDET is harmful to patients, either clinically or biomechanically.

References 1. Coppes M, Marani E, Thomeer R, et al. Innervation of ‘painful’ lumbar discs. Spine 1997; 22:2342–2350. 2. Derby R, Eek B, Chen Y, et al. Intradiscal electrothermal annuloplasty (IDET): a novel approach for treating chronic discogenic back pain. Neuromodulation 2000; 3:82–88. 3. Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back pain and sciatica: a report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia. Orthop Clin North Am 1991; 22:181–187. 4. Schwarzer A, April C, Derby R, et al. The relative contributions of the disc and zygapophyseal joint in chronic low back pain. Spine 1994; 19:801–806. 5. O’Neill C, Derby R, Kenderes L. Precision injection techniques for diagnosis and treatment of lumbar disc disease. Sem Spine Surg 1999; 11:104–118. 6. Turner JA, Ersek M, Herron L, et al. Patient outcomes after lumbar spinal fusions. JAMA 1992; 268:907–911. 7. Fritzell P, Hagg O, Wessberg P, et al. Lumbar fusion versus nonsurgical treatment for chronic low back pain: a multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine 2001; 26:2521–2532. 8. Welch WC. Intradiscal electrothermy (IDET) – patient selection criteria. Cleveland Clinic/University of Cincinnatti Winter Neuroscience Symposium (Snowmass, Colorado); 2001. 9. Kambin P. Alternative to open lumbar discectomy: Arthroscopic microdiscectomy. In: Lange A, ed. Operative spinal surgery. Stanford, CT: Appleton & Lange; 1999. 10. Onik G, Maroon J, Davis GW. Automated percutaneous discectomy at the L5–S1 level. Use of a curved cannula. Clin Orthop 1989; 238:71–76. 11. Karasek M, Bogduk N. Intradiscal electrothermal annuloplasty: percutaneous treatment of chronic discogenic low back pain. Techn Reg Anesthes Pain Manage 2001; 5:130–135. 12. Saal J. Intradiscal electrothermal therapy for the treatment of chronic discogenic low back pain. Operat Tech Orthopaed 2000; 10:271–281. 13. Saal JA, Saal JS. Intradiscal electrothermal treatment for chronic discogenic low back pain: a prospective outcome study with minimum 1-year follow-up. Spine 2000; 25:2622–2627. 14. Saal JS, Saal JA. Management of chronic discogenic low back pain with a thermal intradiscal catheter: a preliminary study. Spine 2000; 25:382–388. 15. Heary RF. Intradiscal electrothermal annuloplasty: The IDET Procedure. In: Resnick DK, Haid Jr RW, eds. Surgical management of low back pain. Rolling Meadows: Kristine Rynne Mednansky; 2001:143–150. 16. Saal JA, Saal JS. Intradiscal electrothermal treatment for chronic discogenic low back pain. Spine 2002; 27:966–974. 17. Wetzel TF, McNally TA. Treatment of chronic discogenic low back pain with intradiskal electrothermal therapy. J Am Acad Orthop Surg 2003; 11:6–11. 18. Hayashi K, Thabit GI., et al. The effect of thermal heating on the length and histologic properties of the glenohumeral joint capsule. Am J Sports Med 1997; 25:107–112. 19. Obrzut S, Hecht P, Hayashi K, et al. The effect of radiofrequency energy on the length and temperature properties of the glenohumeral joint capsule. Arthroscopy 1998; 14:395–400. 20. Naseef GI, Foster T, Trauner K, et al. The thermal properties of bovine joint capsule: The basic science of laser-and radiofrequency-induced capsular shrinkage. Am J Sports Med 1997; 25:670–674.

Section 5: Biomechanical Disorders of the Lumbar Spine 21. Biyani A, Andersson GBJ, Chaudhary H, et al. Intradiscal electrothermal therapy a treatment option in patients with internal disc disruption. Spine 2003; 28:S8–S14. 22. Otsi O, Vernon-Roberts B, Moore R, et al. Annular tears and disc degeneration in the lumbar spine: A post-mortem study of 135 discs. J Bone Joint Surg [Br] 1992; 74:678–682. 23. Otsi O, Vernon-Roberts B, Fraser R. Annulus tears and intervertebral disc degeneration: An experimental study using an animal model. Spine 1990; 15:762–767. 24. Ashley J, CGharpuray V, Saal J, et al. Temperature distribution in the intervertebral disc: a comparison of intranuclear radiofrequency needle to a novel heating catheter. Proceedings of the 1999 Bioengineering Conference, 1999;77.

35. Freeman BJ, Walters RM, Moore RJ, et al. Does intradiscal electrothermal therapy denervate and repair experimentally induced posterolateral annular tears in an animal model? Spine 2003; 28(23):2602–2608. 36. Kleinstueck FS, Diederich CJ, Nau WH, et al. Temperature and thermal dose distributions during intradiscal electrothermal therapy in the cadaveric lumbar spine. Spine 2003; 28(15):1700–1708; discussion 1709. 37. Singh V. Intradiscal electrothermal therapy: a preliminary report. Pain Phys 2000; 3:367–373. 38. McGraw JK, Silber JS. Intradiscal electrothermal therapy for the treatment of discogenic back pain. Appl Radiol 2001; 30:1–6.

25. Bono CM, Iki J, Jolata A, et al. Temperatures within the lumbar disc and endplates during intradiscal electrothermal therapy: formulation of a predictive temperature map in relation to distance from the catheter. Spine 2004; 29(10):1124–1131.

39. Freedman BA, Cohen SP, Kuklo TR, et al. Intradiscal electrothermal therapy (IDET) for chronic low back pain in active-duty soldiers: 2-year follow-up, Spine J 2003; 3:502–509.

26. Kleinstueck F, Diederich C, Nau W, et al. Acute biomechanical and histological effects of intradiscal electrothermal therapy on human lumbar discs. Spine 2001; 26:2198–2207.

40. Wetzel T, et al. IDET to treat discogenic low back pain: preliminary results of a multi-center prospective trial, presented at the annual meeting of the International Society for the Study of Lumbar Spine, Adelaide, Australia. Not yet published.

27. Arnoczky S, Aksan A. Thermal modification of connective tissues: Basic science considerations and clinical implications. J Am Acad Orthop Surg 2000; 8:305–313.

41. Liu B, Manos R, Criscitiello A, et al. Clinical factors associated with favorable outcomes using intradiscal electrothermal modulation (IDET). 15th Annual Meeting North American Spine Society. New Orleans; 2000.

28. Wetzel FT, McNally TA, Phillips FM. Intradiscal electrothermal therapy used to manage chronic discogenic low back pain: new directions and interventions. Spine 2002; 27:2621–2626. 29. Welch WC, Gerszten PC. Alternative strategies for lumbar discectomy: intradiscal electrothermy and nucleoplasty. Neurosurg Focus 2002; 13:1–6. 30. Karasek M, Bogduk N. Twelve-month follow-up of a controlled trial on intradiscal thermal annuloplasty for back pain due to internal disc disruption. Spine 2000; 25:2601–2607. 31. Gerszten PC, Welch WC. Intradiscal electrothermy techniques. Congress of Neurological Surgeons Annual Meeting, Pain Section. San Antonio, Texas, Congress of Neurological Surgeons; 2000. 32. Kapural L, Mekhail N, Korunda Z, et al. Intradiscal thermal annuloplasty for the treatment of lumbar discogenic pain in patients with multilevel degenerative disc disease. Anesth Analg 2004; 99(2):472–476.

42. Bogduk N, Karasek M. Two-year follow-up of a controlled trial of intradiscal electrothermal annuloplasty for chronic low back pain resulting from internal disc disruption. Spine J 2002; 2:343–350. 43. Lee MS, Cooper G, Lutz GE, et al. Intradiscal electrothermal therapy (IDET) for treatment of chronic lumbar discogenic pain: a minimum 2-year clinical outcome study. Pain Phys 2003; 6:443–448. 44. Pauza K, Howell S, Dreyfuss P, et al. A randomized, placebo controlled trial of intradiscal electrothermal therapy for the treatment of discogenic low back pain. Spine J 2004; 4(1)27–35. 45. Cohen SP, Larkin T, Abdi S, et al. Risk factors for failure and complications of intradiscal electrothermal therapy: a pilot study. Spine 2003; 28:1142–1147. 46. Hsia A, Isaac K, Katz J. Cauda equina syndrome from intradiscal electrothermal theapy [Letter]. Neurology 2000; 55:320.

33. Parke W. Anatomy of the spinal nerve and its surrounding structures. Semin Orthop 1991; 6:65–71.

47. Djurasovic M, Glassman SD, Dimar II JR, et al. Vertebral osteonecrosis associated with the use of intradiscal electrothermal therapy. Spine 2002; 27:E325–E328.

34. Derby R, Kleinstueck FS, Diederich CJ, et al. Temperature and thermal dose distributions during intradiscal electrothermal therapy in the cadaveric lumbar spine. WMJ 2004; 101(8):4–5.

48. Lutz C, Lutz GE, Cooke PM. Treatment of chronic lumbar diskogenic pain with intradiskal electrothermal therapy: a prospective outcome study. Arch Phys Med Rehabil 2003; 84:23–28.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain

CHAPTER

Surgical Treatment of Axial Back Pain

97

James Zucherman, Vikram Parmar, Ken Hsu and Matthew Hannibal

INTRODUCTION Severe axial back pain represents one of the most challenging problems in spine surgery. Seventy to 85% of people have low back pain at some time. It is considered the second most common cause of appointments to physicians in the United States.1 The social and economic burden incurred by treatment of axial back pain is high and accounts for 2% of the gross domestic product.2,3 Surgical options remain controversial in spite of the fact that back pain producing lumbar degenerative disc disease is the most common cause of operative intervention on the spine. Though many treatments are in use, results have been somewhat unsatisfactory, even with aggressive fusion procedures. The causes of axial back pain are multifaceted and still not well understood although the technologies for diagnosis and treatment have grown significantly in the past 30 years. Among the problems in treating low back pain are a lack of an adequate nomenclature for the differential diagnosis, lack of complete understanding of specific pathophysiologic-based pain generators, the presence of anatomic segmental overlap of sources of pain, its frequency as a source of somatization of psychogenic stressors, and the likely adaptive changes of the pain perception system which alter response to chronic nociceptive stimuli over time. This chapter focuses on the surgical treatment of axial back pain.

PATHOPHYSIOLOGY Degenerative disc disease (DDD) has been defined as a clinical syndrome characterized by manifestations of disc degeneration and symptoms related to those changes. Disorders of the spinal motion segment are generally accepted to be a source of low back pain. Degenerative changes in components of the motion segment seem to be associated with release of nociceptor stimulating chemical mediators; cytokines, nitric oxide, phospholipase A2 and others have been implicated.4 Anatomically, there are several sources of nociceptors which include the facet joint capsules, perivascular tissue, periosteum, outer anulus, and major traversing roots and rootlets.5 In the authors' experience, and that of others in the literature, the damaged posterior anulus is the most common source of axial back pain syndromes.6 The dorsal root ganglia, which house the sensory cell bodies, have been identified as a likely modulator of low back pain.5,7 Chronic injury has been shown experimentally to increase sensitivity to mechanical stimulation.8 Upregulation and downregulation of various neuropeptides has been associated with peripheral injury and it seems likely that similar changes occur with chronic peripheral nociceptive stimulation.9 The better understood in this group of axial back pain causes are disc herniation, radiographic

segmental instability, and spinal stenosis. For these causes, there is a general agreement on basic approaches for diagnosis and treatment, though this is better defined when radicular symptoms are present. Less understood anomalies of the intervertebral disc as a source of low back pain include internal disc disruption syndrome, isolated disc resorption, and painful degenerative disc disease. In clinical practice ‘internal disc disruption syndrome’ as originally described by Harry Crock seems to run on a continuum with painful degenerative disc disease,10 the former being the most extreme manifestation and the latter, when asymptomatic, representing its antithesis. Why a similarappearing lesion is well tolerated in many and severely disabling in some is not clear and thus the approach to diagnosis and treatment is often controversial.11 The number of fusions in the United States continues to rise yearly with over 50% being performed for symptomatic degenerative disc disease, or internal disc disruption syndrome (IDD) without herniation. IDD was first described as a pathological condition of the disc causing low back pain with or with out lower extremity radiation with minimal deformation of the disc anatomy.11 Historically, it was accepted that the intervertebral disc had no nociceptive ability and no innervations. Anatomic research has revealed that the outer layers of the anulus fibrosus and endplates are innervated from the sinuvertebral nerve branches and their rich innervations in the periannular connective tissue.4,9 As the disc undergoes degeneration, it loses its ability to convert nucleus compressive loads to tensile anulus loads, resulting in further stresses and degeneration of the endplates, facets, and anulus. In addition, disc degeneration may cause pain at other locations. Collapse of a degenerated disc may increase pressures on the facet joints, thereby leading to facet overload and painful facet arthropathy. A degenerated disc may also extrude nuclear material and irritative chemicals into nociceptive-rich locations such as the posterior lateral spinal canal, resulting in radicular-like pain.11

PRESENTATION DIAGNOSIS AND CLINICAL COURSE Most cases of axial back pain resolve over time with conservative care. There is 70% spontaneous improvement after 5 years in a study of a group suffering from chronic low back pain. Eighty percent of the group that did not improve had other mitigating factors present, such as psychosomatic issues.12 Although the low back pain from degenerative disc disease usually improves spontaneously, a significant number of patients do not improve, and may even have worsening symptoms and disability. There are currently no reliable diagnostic methods differentiating disabling painful internal disc disruption syndrome from asymptomatic degenerated discs and there is disagreement on indications for fusion when compared to nonsurgical 1065

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treatments. Clinical examination is usually characterized by low back pain with or without extremity radiation. The diagnosis of isolated, mechanical (activity and posture related) low back pain should only be made after first excluding less common conditions such as tumors, deformity, infection, ongoing neurologic injury, visceral disease, etc. Flexion postures such as sitting, forward leaning, and bending are typically aggravating due to increases in disc pressure in these positions. For most patients, lying recumbent usually relieves the symptoms. Some patients are intolerant of lumbar flexion to the extent that supine reclining increases pain that is only relieved when lying prone. The group that responds with diminished pain in lumbar hyperextension positions, in the authors' experience, can frequently overcome symptoms by nonsurgical means. Maintenance of static postures is intolerable in many of the more severely afflicted patients. This is presumably related to viscoelastic creep of segmental soft tissues. Degenerative discs may be associated with referred, sclerotomal pain to the buttocks and lower extremity. On physical examination, confirmatory findings are localized near midline tenderness to one or more segments by anterior and posterior palpation, reproduction of symptoms by vibration, and increased pain reproduction with sustained positions of increased disc load such as lumbar flexion. Neurologic examination should be normal. Range of motion is limited in all directions and there may be a Gowers' sign on return from forward lumbar flexion. For surgical consideration, clinical history should include marked disability in sitting, static positioning, lifting, bending, and driving intolerance. Relative and absolute contraindications to surgery include secondary social or economic gain, psychological risk factors such as a history of sexual or psychological abuse, addiction, and dysfunctional family support systems currently or historically. All patients should have demonstrated failure of aggressive nonoperative care for at least 6 months. Plain films may be interpreted as negative or only show typical age-related disc degenerative changes such as endplate sclerosis, uncinate spurring, loss of disc height, and facet degeneration. Flexion– extension lateral views may reveal segmental instability not apparent on static films. When changes are primarily localized to one segment, there is a high likelihood that the segment is the source of symptoms. Spondylolisthesis or spondylolysis may be an incidental finding. It is also not uncommon that the segment above is involved and may be the cause of the back pain. In larger spondylolytic slips the discs are under tension instead of compression, and typically do not cause back pain without marked translational instability evident on bending films. Unfortunately, frequently there are multiple degenerative segments or none, which makes identifying the source of back pain more difficult. In evaluating pain due to disc degeneration, magnetic resonance imaging (MRI) is the most commonly employed modality since it can directly infer the degree of hydration in the nucleus pulposus. A degenerated disc will show the area of the nucleus pulposus to have decreased signal on T2-weighted images.13,14 First described by Zucherman et al.15 and more recently by Aprill and Bogduk,16 the presence of a high-intensity zone on T2-weighted MRI images correlates with a positive provocative discogram.15,16 However, recent studies have shown that in an asymptomatic group of volunteers who had a high-intensity zone on MRI, there was a 69% rate of false positives on discography.17 Small annular tears and tears that are not connected to the central nucleus may also evade MRI and discogram detection.16 Modic changes are another commonly used criterion to evaluate disc degeneration. Modic changes can be divided into three types. Type one reflects an acute disruption and fissuring of endplates, which leads to ingrowth of vascularized fibrous tissue into the marrow of the adjacent vertebral body. This tissue exhibits diminished signal on T1 images and increased signal on T2 images.18 In chronic 1066

degeneration (type two), the bone marrow undergoes fatty degeneration, thereby showing an increased T1 and an isointense T2 signal. Type three changes reflect extrinsic bone sclerosis, which is manifested as a decreased signal on both T1- and T2-weighted images. The most widely used diagnostic tool for identifying the painful degenerative disc disease is lumbar provocative discography. However, even these findings have been shown to not correlate well with the presence or absence of low back pain. Discography provides information regarding pain response and pressure response, and gives details on the degree of annular disruption. However, the value of discography still remains controversial. There is a large variation in the patient's pain response, patient's mental state, and even the physician's skill in performing the study. Historically, discography was first reported on by Lindblom in 194819 as a method to identify herniated discs in the lumbar spine. It was also noted that a reproduction of the patient's usual sciatica sometimes occurred during injection of the contrast material. With subsequent use, it was noted that familiar back pain was sometimes reproduced during the test. The finding caused some to begin using the test to evaluate lumbar discs as the origin of patients' chronic low back pain. From early use of discography, the meaning of a painful injection has been unclear. It is unknown if a disc that is painful when injected can be reliably designated as the cause of clinically significant low back pain. In an effort to improve the specificity of discography in diagnosing discogenic pain, some investigators have used additional criteria beyond pain reproduction on injection. The primary criteria for a positive disc injection are pain of significant intensity on disc injections and a reported similarity of that pain to the patient's usual, clinical discomfort. Other clinical investigators have held more complex, stringent, and sometimes idiosyncratic criteria for positive injections including: negative control disc, concordant pain, dye penetration on injection, demonstration of pain behavior, maximum pressure on injection, and only one or two positive discs. Most clinicians require that at least one additional ‘control’ disc be examined. The control injection should ideally be ‘negative’ to confirm a positive study. It is not clear whether this means an adjacent ‘control’ disc injection must be ‘painless,’ or just not significantly painful in intensity. It is also not clear whether a painful but discordant disc satisfies the ‘negative control’ requirement. Most discographers have required that painful injection be considered negative if the sensation is clearly unfamiliar. On the other hand, it is not clear how exact a reproduction is required for a ‘positive test.’ Some investigators advocate that only an exact reproduction be accepted while others do not. Some investigators have maintained that dye penetration must extend to or through the outer anulus, scoring a ‘true’ positive injection in addition to the presence of pain with the injection. Others have indicated that ‘behavioral’ signs of pain such as guarding, withdrawal, or grimacing must accompany the presence of pain for the test to be considered positive. Finally, some have argued that pain elicited during low-pressure injections be considered positive because of the concern that high-pressure injections may cause deflection of the vertebral endplates or cause rupture of membranes over sealed and presumably asymptomatic fissures. Recent work has revealed a 10% false-positive rate among asymptomatic volunteers, with rates going up to 83% in volunteers with a diagnosis of an unrelated somatization disorder. Another study revealed up to a 40% positive pain reproduction following discography performed in asymptomatic patients who had prior discectomies. In another study, a group of patients without low back pain who had recent posterior iliac crest graft for nonspine-related procedures underwent discography. Fifty percent of patients experienced pain that was similar to or an exact reproduction of pain at the iliac crest bone graft harvest sites.1,17,20–27 These results question the ability of patient to separate spinal from

Section 5: Biomechanical Disorders of the Lumbar Spine

nonspinal sources of pain on discography. Provocative discography purports to identify a subgroup of low back pain syndromes in which the primary cause of the patient's symptoms is the disc itself, apart from any other structural or psychological processes. By this theory, the successful alteration of the offending disc and solid arthrodesis or arthroplasty should result in outcomes equal to those achieved for spinal fusion with known primary structural pain generators such as unstable spondylolisthesis. However, discography studies have shown that discographic pain response can be of significant intensity in discs not actually causing the patient's primary pain. Also, certain ‘asymptomatic discs’ are more likely to be painful on injection, such as discs with annular fissures or discs after prior surgery. Studies also revealed that individuals with certain psychosocial characteristics are more likely to report higher pain intensity levels with disc injections than others, such as those with psychological stressors, chronic pain states, litigation involvements, and so forth. The failure to achieve consistent clinical success after spinal fusion for presumed discogenic pain is usually attributed to the morbidity of surgery or poor patient selection. Therefore, in the patient with a single arthritic or annular disrupted lumbar segment, without emotional troubles, with a stable family and occupational support, no history of chronic or unexplained pain syndromes and any compensation issues, discography may be helpful in confirming that the disrupted segment does hurt while the adjacent segments do not.1,17,20–28 We recommend, that discography be performed by those experienced in the technique and surgical ramifications, using strict criteria for interpretation. Furthermore, discography results need to be correlated carefully with the clinical history and physical examination to avoid surgical failures.

TREATMENT The vast majority of patients with painful degenerative disc disease can be managed nonoperatively. The first task is to optimize the patient's physiologic status. This involves increasing cardiovascular fitness and placing the patient in a smoking cessation program. Most patients with painful disc disease have exacerbation of symptoms with flexion, so extension exercises as well as low-impact aerobic exercise such as swimming and cycling are helpful if tolerated in a conditioning program. In the authors' experience, isometric neutral stabilization and hyperextension exercises are commonly effective. Robin McKenzie has pioneered and refined extension-based stabilization. It is the authors' belief that instruction in minute-by-minute comprehensive daily body mechanic control and posture management can diminish the repetitive stimulation of the damaged section of the disc anulus and facilitate recovery in some patients. Back pain and work loss is less in people who maintain a regular exercise regimen. Hip and hamstring stretching, buttock and abdominal strengthening, and hyperextension exercises to strengthen the gluteus and paravertebral muscles are frequently successful in controlling symptoms.29,30 Nonsteroidal antiinflammatory medication and acetaminophen can provide improved symptoms in some patients. Muscle relaxants may have an effect in treatment of acute flares of low back pain symptoms but are not recommended for chronic use.29,30 In general, operative intervention is only offered to patients where surgery is expected to improve the results of the natural course of the disease (Fig. 97.1). In these patients, disability is great and no indication of nonsurgical recovery is suggested by history. Discectomy has been performed in the past for treatment of patients with incapacitating low back pain from painful degenerative disc disease. Currently, there is no accepted indication to treat degenerative disc disease with isolated discectomy. Discectomy is indicated for a patient with incapacitating radicular symptoms resulting in compressive neuropathy from a herniated nucleus pulposus which is progressive or which

Axial back pain

Chronic back pain (>6 months)

Acute axial pain (<6 weeks)

Sub-acute axial back pain (>6 weeks)

Bed rest/ reversal of injury mechanism/P.T./ NSAIDs/ analgesics

Facet blocks/epidural blocks/pain films/MRIs/ lifestyle change/ vocational change/ weight control

If instability shown, consider fusion

If facet block (+), consider rhizotomy

Consider MRI

If MRI (–),consider CT/discogram

If MRI abnormal >2 segments, consider CT/discogram

If MRI shows focal abnormalities (1–2 segments), may consider fusion, arthroplasty, unconventional procedures*

Discogram negative, chronic pain management program

Discogram positive,(1–2 levels), consider fusion, arthroplasty, unconventional procedures*

Fig. 97.1 Flowchart for low back pain, which includes unconventional procedures: IDET, APLD, nucleoplasty, abdominoplasty.

has failed a 6-week trial of nonoperative treatment. Symptoms may include incapacitating sciatica (extremity pain) with or without a neurologic deficit. The patient may have low back pain in concert with these symptoms but axial back pain as a primary complaint is a relative contraindication to discectomy, which may or may not relieve back pain. We suspect the larger the protrusion is more likely to have a favorable response for isolated back pain. There have been a variety of disc debulking procedures described over the years as a less-invasive means to eliminate symptoms resulting from compressive neuropathy without the morbidity known to occur with conventional discectomy procedures. They have not to date been shown to be effective for axial back pain without neural compression. Chemonucleolysis as a treatment for patients with low back pain (primarily from herniated discs) was originated by Thomas, who noted that a proteolytic enzyme called papain had affinity for the ground substance (i.e. proteoglycans) of all cartilage in the body. Many studies in humans during the 1970s led to chymopapain being implanted in over 16 000 patients before FDA approval was granted.31,32 However, chemonucleolysis fell out of favor.33 First, multiple studies demonstrated the superiority of surgery over chymopapain injection.34 Ziegler reported in 126 patient a 98% success rate for patients undergoing surgical excision versus a 60% success rate for patients receiving chymopapain. Furthermore, chemonucleolysis actually caused recurrent low back pain in 54% of the patients, compared to only 5% receiving surgery.35 Watters et al. also demonstrated a superior patient satisfaction with surgery. This group reported a 1067

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disturbing rate of sequestered disc herniation in the chemonucleolysis group requiring reoperation.36 The second factor leading to the decline of chemonucleolysis related to the fact that there is no significant alteration of the natural history of a lumbar disc herniation treated conservatively when compared to one following chymopapain injection. In part, this is related to the fact that patients with a large disc herniation have much poorer results than do patients with lumbar disc bulges or protrusions (i.e. disc contained in the anulus). Finally, there were unique complications with chymopapain use,37–39 such as anaphylactic responses and unpredictable neurologic deficits. Anaphylactic shock was reported to be as high as 1 in 5000. Agre reviewed the neurologic complications following chymopapain injection and found cerebral hemorrhage, seizures, paraparesis, paraplegia, subarachnoid hemorrhage, and death.39 Automated percutaneous lumbar discectomy (APLD) has been used for some time as a minimally invasive variation of open discectomy. The working principle is that removing a portion of the nucleus pulposus relieves the intradiscal pressure, thereby alleviating irritation in the nerve root and the nociceptive fibers in the anulus fibrosus. Even proponents of this procedure recommend that APLD be limited to contained disc protrusions. Relative to the natural history of a herniated disc, APLD in several studies has not provided superior results though morbidity is quite low. Furthermore, there is a lack of well-constructed scientific studies evaluating its effectiveness.33,40 Other minimally invasive procedures include percutaneous laser nucleolysis of the intervertebral lumbar disc and percutaneous disc decompression with electrothermal nucleoplasty. In the hope of avoiding intraoperative trauma to dura and nerve roots, and preventing intraneural and perineural scar formation when approaching lumbar discs, Nerubay et al. used a carbon dioxide laser to vaporize a protruding nucleus pulposus.41 After performing an initial trial in dogs to determine the amount of laser energy necessary to vaporize the nucleus pulposus, a prospective study of 50 patients was performed. Good and excellent results were achieved in 74% of the patients, with four patients requiring subsequent operative intervention. Patients with sequestered fragments or bony lateral stenosis did not benefit from the procedure. Four complications of nerve root irritation (three which resolved) were attributed to thermal damage cause by warming of the cannula.42 The authors, however, were careful to point out that strict patient selection is crucial to the outcome. Proponents of percutaneous nucleoplasty claim that the use of radiofrequency (RF) energy removes nucleus material and creates small channels within the disc. Using this coblation technology, coagulation and ablation are combined to form channels in the nucleus and theoretically decompress the herniated disc. A recent study on three fresh human cadavers measured intradiscal pressure at three points: before treatment, after each channel was created, and after treatment. The results revealed that intradiscal pressures were markedly reduced in young cadavers, while it changed very little in older specimens.43 Further studies with animal and prospective human trials are needed before any conclusions can be reached about the clinical efficacy of the technique. The wide abdominal rectus plication (WARP) is another procedure for axial back pain.44 The WARP abdominoplasty is based on the theory that contraction of the abdominal muscles via the attachments to the lumbodorsal fascia results in abdominal wall stiffening, increased intra-abdominal pressure, and resultant diminished intradiscal pressure. When a ‘stretched out’ or an adynamic segment exists in the anterior abdominal wall (such as with some women following pregnancy), the internal oblique and transverses abdominus are not at physiologic length. This laxity prevents maximum force generation with contraction and thereby weakens abdominal support that is usually present via the attachments to the lumbodorsal fascia. 1068

The surgical procedure involves plicating the right side to the left side of the rectus fascia, thus converting the flat rectus muscle into a tube. This diminishes trunk girth and reduces abdominal cavity size and therefore tightens the anterior abdominal–lumbodorsal fascia muscle complex. In the largest series reported to date, the author reported increased height in the intervertebral space on both the MRI and on lateral spine radiographs postoperatively in all 25 patients. The back pain was reduced postoperatively in all except one patient. The author limited the inclusion criteria to patients with a positive abdominal compression (TAC) test, weak internal oblique-transversus abdominus Cybex muscle test, and to those patients with back pain undergoing elective abdominoplasty. The TAC test involves applying manual pressure to the abdomen, which gives relief in some patients. The procedure may be a consideration in patients with abdominal wall insufficiency, relief with abdominal corset or binde, and or a positive TAC. The authors have had some success in a consecutive series of 23 selective patients. The literature provides success rates varying from 17% to 92% with surgical fusion.45–53 Many techniques have been utilized and range from the simple posterior fusion without bone graft to most extensive anterior–posterior fusion with pedicle instrumentation. The goal of the operation is to limit sensory stimuli and tissue inflammation across the segment by stopping mechanical motion.11 Since the patient population likely have facilitated segmental and/or central nervous system (CNS) nociception, complete obliteration of motion is the goal. Traditionally, posterolateral fusion has been the standard surgical technique. Success rates have been variable and reported as high as 90% using rate of apparent solid fusion and removal of pain and return to work as criteria. Poor results are associated with pseudoarthrosis, workman's compensation and being out of work longer than 3 months.54–59 Pedicle screw instrumentation has been added to the procedures to decrease nonunion rates (Figs 97.2, 97.3). Recent studies have shown that adding instrumentation increases fusion rates by 20%.59–65 Also, proponents of instrumentation feel that these constructs offer immediate stability and allow an expedited postoperative recovery (Fig. 97.4). Current practice for painful degenerated discs among many surgeons is posterolateral fusions augmented with pedicle screw instrumentation. Anterior lumbar interbody fusion (ALIF) is growing in popularity as a primary procedure for low back pain due to degenerative disc disease or as a salvage procedure for individuals who have failed posterior procedures. Concerns about paraspinal muscle damage, the desire for more complete removal of the disc, restoration of disc height have primarily retained interest in this procedure.66–69 Crock46 considered ALIF the procedure of choice for IDD. Studies suggest that any motion across the disc space (as may persist after posterolateral fusion) may be a source of continued back pain.70–72 The advantages of ALIF include: proximity of fixation close to the center of spinal motion, complete excision of the central disc material, placement of fusion graft under compression, availability of a large surface area for fusion, availability of a virgin operative site in patients with prior posterior procedures, and the ability to provide a stable anterior column support to diminish torsional and bending force on supplemental posterior instrumentation. Proponents of ALIF advocate that even after solid posterior fusion, motion may still occur anteriorly thorough the disc, causing continued pain. This is due to the plasticity of bone, the variation in degree of posterolateral fusion confluence and rigidity, and the greater distance to the center of vertebral motion. Increased stability of the ALIF would therefore increase the fusion rate while more completely eliminating motion at the operative disc space since the fusion mass is at the center of motion of the spine. Originally, tricortical iliac crest bone graft was

Section 5: Biomechanical Disorders of the Lumbar Spine

Fig. 97.4 Posterior lumbar interbody fusion with instrumentation. Fig. 97.2 Posterolateral fusion with instrumentation, AP view.

Fig. 97.3 Posterolateral fusion with instrumentation, sagittal view.

placed in the disc spaces. This has been replaced over time by femoral ring allografts and threaded cages of various materials in order to remove the morbidity of autogenous bone grafting. Interbody fusion, while providing structural support for the anterior column, indirectly decompresses the foramina and nerve roots via restoration of disc height through distraction. Threaded interbody cages, when used in place of femoral ring allograft, increase surface contact and initial fixation between the bone and bone graft. They can also be implanted through mini-invasive approaches. As an alternative to traditional open retroperitoneal and transperitoneal approaches, laparoscopic transperitoneal and endoscopic-assisted retroperitoneal approaches allow for minimally invasive placement of ALIF devices. Using this technique, Loguidice et al. reported 80% clinical success71 while Newman and Grinstead reported 86% success based on rate of fusion, pain relief, and return to work.68 Anterior/posterior combined (360 degree) fusions have historically been used for multilevel fusions and deformity (Fig. 97.5). Recent advances in mini-invasive approaches (resulting in less patient morbidity) and the surgeon's desire to completely obliterate motion across the disc have made this technique more common for axial back pain. Lower nonunion rates and greater ease in the ability to control lordosis are among the reasons cited by authors to put the patient through this more invasive procedure. Authors have reported up to 88% fusion rates using this technique but only a 63% clinical success, showing those two factors are not mutually inclusive.72–75 Cloward, in 1945, introduced the posterior lumbar interbody fusion (PLIF) as a method of achieving an anterior arthrodesis with a posterior surgical approach.45 A wide posterior decompression is performed, allowing retraction of the dural sleeve and nerve roots for complete disc excision and anterior column fusion. This approach allows for a more complete disc excision, restoration of disc height and reproduction of lumbar lordosis, root decompression, solid mechanical arthrodesis, immediate load sharing and structural support, large surface area for fusion between the endplates 1069

Part 3: Specific Disorders

Fig. 97.5 Posterior lumbar interbody fusion/posterolateral (not drawn) fusion with instrumentation.

and avoidance of a second anterior approach.55,76 One report with average 18-month follow-up revealed a greater than 90% fusion rate with an 89% success rate based on pain relief, return to work, and outcome scoring scales.70 Disadvantages include possible graft displacement, pseudoarthrosis, increased bleeding, dural tears, nerve root injury, and risk of epidural fibrosis due to nerve retraction. PLIF is contraindicated in patients with preexisting, significant epidural fibrosis and those with osteopenic bone. Damage to the nerve roots is a principal concern with PLIF procedures.77 Steffee et al. reported that a failed PLIF ‘has a worse outcome than failure of any other fusion procedure.’78 The upper (exiting) nerve root, when performing a PLIF, traverses the interspace just out of direct view in the lateral recess and can be damaged when grafts are inserted into the disc space. Exploration of patients with a post-PLIF radiculopathy reveals epidural fibrosis for which there is no good solution. Revision options are limited following a PLIF. A noninstrumented PLIF may be converted to an instrumented PLIF and an instrumented PLIF may be revised to an anterior fusion but this is difficult and fraught with complications. Concerns about nerve root damage and epidural fibrosis66,77 led Harms et al.79 to popularize a variant of the PLIF called a transforaminal lumbar interbody fusion (TLIF). Using a more lateral posterolateral approach than with a PLIF, unilateral excision of the facets allows increased exposure of the disc space without putting undue tension to the dura and the nerve roots. Unlike with PLIF where transpedicular instrumentation is optional, with the TLIF it is mandatory. Also, a TLIF is well suited for a muscle-splitting Wiltse approach, thereby preserving the posterior ligamentous complex and decreasing problems associated with retraction and muscle damage.79 Pedicle fixation adds stability and the capacity for early mobility following surgery and is advantageous to return to optimal function. Lumbar fusion has been offered as a solution to treat low back pain when nonsurgical treatment fails. It has been reported that the rate of lumbar fusions in the United States rose 100% between 1980 and 1070

1990.3 However, fusion for low back pain continues to be controversial. Some researchers feel that low back pain is a multifactorial entity and fusion is hastily undertaken without accurately determining whether the patient's symptoms would actually be improved without fusion. Reported success rates of fusion range from 52% to 92%. Reports can be criticized for being mostly retrospective and uncontrolled without uniform criteria on how to measure a successful outcome. Three recent trials merit discussion. Lee et al. reported 89% success for fusion on a 62-patient group suffering from chronic low back pain. The study had stringent criteria for inclusion and the author claimed a 92% return to work rate in patients who had been out of work for longer than 4 months. However, the results did not include the success of nonsurgical treatment in the group of patients and the report was retrospective in nature.70 The study by Fritzell et al.,80 as part of the Swedish Lumbar Spine Study Group, was a randomized controlled multicenter study followed with a 2-year follow-up by an independent observer. The goal was to determine whether fusion was superior to nonsurgical treatments in treatment of patients with resistant low back pain. The authors reported a significant difference in reduction of low back pain, decrease in the Oswestry scores, and reduction of depressive symptoms using the Zung scale.81 Seventy-five percent of the surgical group, at the conclusion of the trial, would go through the treatment again without knowing the result. But not many of the patients would consider themselves ‘cured’ using the above-mentioned criteria.12,55,76,81 Butterman et al. compared the results of lumbar fusion surgery in groups of patients with multiple diagnoses. Success rates varied from 69% to 100% depending on the group. Along with the retrospective nature of the study, once again, the outcome scale suffered from a lack of stringency.82 Future developments to improve the rate of successful fusions will likely involve stimulation of fusion at the genetic level. The use of biotechnology solutions to stimulate bone growth has led to important discoveries. Recombinant human bone morphogenetic protein-2 (rhBMP-2) is now available for use with a tapered, threaded intervertebral fusion cage (LT cage, Medtronic Sofamor Danek, Minneapolis, MN) for the clinical treatment of degenerative disc disease. The success of an initial pilot trial in 14 patients83 gave the impetus to pursue a pivotal prospective, randomized trial involving 143 patients implanted with the LT cage filled with rhBMP-2 versus 136 patients implanted with LT cage filled with iliac crest autograft. One hundred percent fusion was achieved in the BMP group and 95.6% fusion in the autograft group. There were no significant differences in the Oswestry scores between the groups, while 32 of the 136 patients receiving the iliac crest bone graft experienced some degree of donor site pain after 2 years following surgery.84 A prospective, randomized trial of posterior lumbar interbody fusion comparing 36 rhBMP-2 versus 35 cases with autograft showed equal success using Oswestry, leg pain, and back pain scores as criteria.85 Finally, a recent pilot study investigating the difference between rhBMP-2 and autograft in posterolateral fusions has revealed increased fusion rates and higher scores in back and leg pain scales in the rhBMP-2 group.86 Early work in Sweden investigating the ability of rhBMP-7 versus autograft to achieve posterolateral fusions has also been promising.87 The current consensus is that recent trials have demonstrated the ability of rhBMP-2 to achieve a high fusion rates and can substitute for autogenous bone graft in both interbody and intertransverse applications. In addition, serology testing has not demonstrated a significant antibody response to rhBMP-2 following implantation.88 Intradiscal electrothermal therapy (IDET) has been developed by Drs. Jeff Saal and Joel Saal as an alternate treatment to spinal fusion for patients incapacitated secondary to discogenic pain. IDET is performed in the operating room where a flexible intradiscal catheter

Section 5: Biomechanical Disorders of the Lumbar Spine

with a temperature-controlled thermal resistive coil is inserted into the nucleus until it penetrates the inner layers of the anulus fibrosus. As the electrode is advance, the outer layers of the anulus deflects it in a circumferential course toward the affected side. At its resting position, the electrode traverses the posterior midline of the anulus fibrosus. At this point, the thermal coil is heated to 90°C per protocol. After appropriate heating, the catheter is removed and the patient is discharged home with immediate ambulation.7 The theory of why IDET alleviates symptoms is based on two principles. The first is that previous studies have shown that temperatures above 45°C destroy nociceptors in the anulus.89 Also, a second hypothesis states that raising the temperature to 60°C induces denaturation and shrinkage of collagen.90 This shrinkage could potentially stabilize the motion segment at the disc and theoretically remove the pain generator. Lee et al. showed a decrease in motion of the operated spinal segment in all planes of testing after IDET with no significant difference in stability in a study of five cadaver specimens with the posterior elements intact.91 Studies testing both hypotheses have been conflicting, and it is clear that there is no consensus on the biologic effect of IDET on the intervertebral disc. The success rates in clinical trials have also been variable, ranging from 23% to 71%.92,93 To establish IDET as a worthwhile treatment, more research needs to be performed at a basic science level to elucidate the biomechanical and physiological effects on the intervertebral discs. Despite its unproven efficacy, IDET continues to be used to treat LBP, partly because it is a technically easy procedure to perform and has few complications. Until long-term data show the benefit of IDET in altering the course of painful degenerative disc disease, the procedure remains an unproven option. Clinical studies supporting the effectiveness of chondroitin and glucosamine for the treatment of osteoarthritis were the impetus to a group of clinicians to explore their effectiveness in treating low back pain when injecting these substances into the intervertebral disc. The hypothesis is that injection of these substances would promote a reparative response in the disc. Thirty patients who had lumbar discography used to reproduce low back pain took part in the study. Lumbar intervertebral discs were injected with a solution of glucosamine and chondroitin combined with dimethyl sulfoxide (to enhance diffusion of the substrates throughout the disc), and pretreatment Roland-Morris disability scores and visual analog scores (VAS) were compared with 1-year follow-up post-test values of these scores. Seventeen of 30 patients (57%) were found to have improved markedly with 72% and 76% improvements in the Roland-Morris and VAS scores, respectively. There were no complications or serious side effects. The authors were the first to admit that the study had a weakness because it was nonprospective in nature and had no control or comparison group. The authors could not give a sound scientific explanation for the biochemical effects of the injections. However, the absence of any severe adverse effects and the fact that there was a large subgroup of patients who were very pleased allowed the authors to justify further studies to look for the effects of these injections.94 The current hypothesis is that the reduction in pain and disability is due to favorable alterations in the intervertebral disc to promote repair. Further clinical and basic science trials will be needed to prove or disprove this hypothesis. Because of the concerns with lumbar fusion procedures, there is a significant amount of interest in total disc replacement (TDR). Proponents of TDR state that it would potentially relieve symptoms, prevent long-term issues associated with fusion, and also remove the diseased disc mechanism, the ‘pain generator.’ The other major goal of disc replacement surgery is to maintain and restore normal segmental spinal motion by restoring the disc space height and segmental lordosis. Achieving this goal also allows indirect decompression of foraminal stenosis and protects adjacent levels from iatrogenically

accelerated degeneration.95 From a clinical standpoint according to current pivotal FDA trials, general indications for disc replacement surgery include: patients with back pain greater than leg pain not responsive to appropriate nonsurgical treatment, symptomatic oneor two-level disc changes associated with collapse, symptomatic early stage disc changes identified by MRI and/or discogram in the absence of marked facet arthritis, and patients without prior history of back surgery at the affected level. Contraindications include severe facet joint arthrosis, spinal instability, altered posterior elements secondary to prior surgery, infection, spondylolytic spondylolisthesis, and metabolic bone diseases. There is a paucity of data in the literature today concerning total disc replacement. The Charite disc replacement has the most associated data. The Charite has gone through three generations of modifications since its development in 1984. There have been device failures with earlier designs, but few device failures with the most recent model (Fig. 97.6). Buttner-Janz et al., in 1989, reviewed the initial clinical experience of 62 patients, and submitted that there were 83% very satisfactory results or results that was ‘better-than-before’ the operation.96 David, in 1993, reviewed his results with the Charite in 22 patients. He had a minimum of a 1-year follow-up and 65% excellent or good results.97 He concluded

A

B

Fig. 97.6 Total disc arththoplasty (Adapted from a drawing by S.B. Charite III, Link, Branford, CT). 1071

Part 3: Specific Disorders

that the disc replacement procedure had a very narrow application, and artificial disc replacement, in his opinion, was not a routine procedure. Griffith, in 1994, had the first multicenter, multisurgeon, retrospective review of the Charite.98 There were 93 patients in which the Charite 3 device was inserted. The most common diagnosis was degenerative disc disease, in 52%, and the most common level implanted was the L4–5 level. The follow-up was 11.5±8.4 months. He reported a significant functional and pain improvement, although there was no work status change in the patients evaluated. There was a 6.5% incidence of migration, subsidence, and dislocation. He concluded that prospective, randomized studies were needed to compare artificial disc replacement versus fusion procedures. Cinotti et al., in 1996, also performed a one-surgeon retrospective review of 46 Charite 3 devices. He had a minimum of a 2-year follow-up. The diagnoses were approximately 50% degenerative disc disease and 50% failed disc excision. They had a 69% satisfactory result for one-level procedures, and a 40% satisfactory result with two-level procedures.10 They hypothesized that the poorer results in two-level procedures were because the device was difficult to implant at two levels because of excessive distraction that had to be performed at the second level; additionally, at the second level, a smaller device needed to be inserted, and this device needed to be inserted more anteriorly, very likely contributing to decreased range of motion at that second level. They concluded that, in their hands, success was less than that seen in fusion cases. The Charite, in their opinion, was not suitable for two levels, and they also determined that prospective, randomized studies were needed to evaluate disc replacement versus fusion procedures. The ProDisc total disc prosthesis completed its FDA pivotal trial in 2003. The ProDisc has a modular design with a superior and inferior cobalt–chrome endplate (Fig. 97.7). Additionally, the inferior endplate allows for a polyethylene insert to be snapped into place, utilizing a locking mechanism. The earlier ProDisc results have been evaluated by their inventor, Dr. Marnay. He had an outside organization perform a prospective review of 61 of his cases. Ninety-five percent were available for follow-up at 7–11 years. Thirty-three percent of these procedures were performed at two levels. At follow-up, all of the prostheses were intact and functioning, and there was no evidence of subsidence or migration. Additionally, there were no revisions or removals, and 92.7% of the patients were satisfied or entirely satisfied. They concluded that there was no difference in results in one- or two-level implantations, and there were no device-related safety issues.99 Weichert et al. reported a 6-month follow-up of 16 ProDisc patients where the mean VAS score improved from 7.0 to 1.9 and the Oswestry Pain Score improved from 23.3 to 10.2.100 Bertagnoli and Kumar published results of a 108-patient series with a follow-up period of 3–24 months. They reported that 91% of patients had an excellent outcome, 8% a good outcome, and 1% a fair outcome.101 The obvious drawback was that the specific criteria used to make the classification

Fig. 97.7 Total disc arthroplasty (Adapted from a drawing by ProDisc, Synthes, Paoli, PA). 1072

system were not clearly defined. Postoperative complications commonly associated with lumbar disc replacement procedures include: (1) abdominal wall hematomas, (2) vascular injury, (3) dural tears, (4) nerve injury, (5) retrograde ejaculation in males, and (6) migration of the prosthesis. Total disc replacement is in its infancy. The early studies of Marnay and the ProDisc as well as the Charite trials are encouraging. Two additional prostheses are in pivotal trials at this time (Maverick (Medtronic, Minneapolis, MN and FlexiCore (SpineCore, Summit, NJ) (Figs 97.8, 97.9). The FlexiCore is prearticulated and inserted as one piece. The FlexiCore and Maverick are both all-metallic disc replacements. These FDA supervised studies are prospective, controlled and randomized, and outcomes are being measured using standard patient-based assessments such as the Oswestry low back pain questionnaire, SF-36 and VAS. As spine surgeons learn more about total disc replacement, proper indications are being developed. It is unclear at this time which of these prostheses, if any, is most efficacious. Our experience with 85 ProDisc and FlexiCore implantations suggests they are associated with less morbidity, less surgery, and shorter healing time than fusions. FDA trial results, soon to be available, will hopefully shed light on these potential advantages. Investigational prosthetic nucleus replacements purport the same advantages as those provided by total disc replacements. In addition, they may have utility as a postdiscectomy alternative maintaining disc height and possibly preventing recurrence. By replacing the disc nucleus following discectomy, pain related to chemical irritation of neural tissue from extruded products from the native nucleus would be reduced. Two emerging prosthetic nucleus devices use hydrogels. These substances mimic the nucleus by absorbing water to increase in size and fill the disc space. The largest amount of data is available on the PDN (prosthetic disc nucleus; Raymedica, Minneapolis, MN) (Fig. 97.10). The hydrogel core of the device absorbs water and expands to fill the nuclear cavity. The hydrogel is prevented from escaping by the outer jacket. Ray has reported 4-year follow-up results with 90% decrease in Oswestry scores in patients.102 The indications for implantation of the device was back pain with or without

Fig. 97.8 Total disc arthroplasty (Adapted from a drawing by FlexiCore, SpineCore, Summit, NJ).

Fig. 97.9 Total disc arthroplasty (Adapted from a drawing by Maverick, Sofamor Danek, Memphis, TN).

Section 5: Biomechanical Disorders of the Lumbar Spine

Fig. 97.10 Prosthetic disc nucleus (Adapted from a drawing by Raymedica PDN, Raymedica, Minneapolis, MN).

leg pain, related to painful degenerated discs which were refractory to nonsurgical treatment. Although early reports are hopeful, trials involving PNDs are complicated by device displacement occurring at a relatively high rate (6%). Ray has explanted 10% of the devices from his patients. It is important to avoid any of the many pitfalls present with surgical treatment of painful degenerative disc disease. Improper patient selection is a common error. Patients with psychosomatic issues, who smoke, have pending litigation claims, are receiving workman's compensation, and those who have been out of work for an extended period of time often have poorer outcomes with fusions for degenerated discs. Correct identification of the proper level of pain generator is also vital to the success of the surgery and is most challenging in some cases. Novel and new surgical approaches which do not have prospective, controlled long-term studies reported in peer-reviewed journals should be looked at with some skepticism as a treatment for this challenging problem. Thanks to demands of the FDA, we are getting a fair amount of scientific data in regard to total disc replacement procedures. In the authors' opinion there is no one best approach or procedure for axial back pain and we perform most of the available procedures in different situations. For example, in a case of collapsed (<2 mm disc height) radiographically stable L5–S1 disc with no need for posterior decompression, an anterior interbody fusion with femoral ring cages with or without BMP has a high fusion success rate greater than 85%.103 Since the segment is collapsed, not contributing much to motion, and frequently has marked facet joint arthropathy; a simple fusion is usually successful and does not create much additional load transfer to other segments. Arthroplasty is also of low morbidity in our experience, but in this case example the need for restoration of disc height, which can stretch the neural elements if fibrosis is present, and the presence of chronic facet disease, can cause residual symptoms in some patients. Adjacent segment stress transfer of a fused lumbosacral segment is a significant concern but is less than at lower segments, especially if the fusion is at L4–5, which leaves the L5–S1 level between two rigid segments, the sacrum and the L4–5 fusion. All degenerative discs with disc heights approaching 2 cm are best treated with total disc arthroplasty if available, or circumferential fusion with instrumentation.103 The increased mobility of these segments makes a technically successful fusion more difficult. We have been well satisfied with total disc arthroplasty in this subgroup in 1–2-year follow-up in single and double levels to date. Much less surgical intervention is required than in the circumferential fusion. When fusion is employed in tall discs in lumbar levels above L5–S1, we prefer either a TLIF with pedicle instrumentation or an anterior– posterior combined procedure with pedicle instrumentation placed

posteriorly through a percutaneous or paraspinal muscle-splitting approach. The open or percutaneous paraspinal approaches seem to spare early and possibly late morbidity by avoiding extensive muscle retraction required for traditional midline approach. If spinal canal decompression is needed, a midline approach is utilized and usually a TLIF is placed since the exposure for the TLIF becomes part of the decompression for the nerve roots. We rarely consider surgery and even more rarely fuse patients who appear to have significant pain generation from more than two segments without neural compression. Emerging technology such as dynamic posterior stabilization offered by Dynesis (Zimmer, Warsaw, IN) and multilevel total disc replacement, when released by the FDA, may possibly help some in this unfortunate group. The unproven thermal energy and disc debulking techniques discussed earlier have the rationale of not frequently making patients permanently worse. Their success is expectantly low in this patient population but other approaches are still available if, in the future, they fail. One must keep in mind that the desperation of some individuals due to failure of all modes of nonsurgical management and severity of their disability drives them to seek surgical solutions, whether appropriate or not, by surgeons willing to perform these procedures. In many cases, risk factors for failure may make good surgical outcomes so remote that surgery is inappropriate.

CONCLUSION The lower back is a common focus of pain for patients with other structural and supratentorial disorders. The spinal surgeon must develop expertise in selecting good surgical candidates. Reliance on scientific, methodic analysis when available is required for the highest success rate. Recent trends in improved surgical clinical research study design, such as patient-based statistically validated outcomes tools, prospective, randomized trials which are now usually a new technology requirement of the FDA, and insurance payer requirements of peer-reviewed research demonstrating outcome efficacy of surgical treatments are moving us in the right direction as never before. Though objective analysis is currently deficient, there is little doubt from many good clinical outcomes that a portion of the population with severe refractory axial back pain can be helped by surgery. The art and science of doing the most good and the least harm lies in both thorough and rigorous selection criteria, and meticulous diagnostic and surgical execution.

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Section 5: Biomechanical Disorders of the Lumbar Spine 68. Newman M, Grinstead G. Anterior lumbar interbody fusion for internal disc disruption. Spine 1992; 17:831–833. 69. Stauffer R, Coventry M. Anterior interbody lumbar spinal fusion: analysis of Mayo Clinic series. J Bone Joint Surg [Am] 1972; 54:456–468. 70. Lee C, Vessa P, Lee J. Chronic disabling low back pain syndrome caused by internal disc derangements: the results of disc excision and posterior lumbar interbody fusion. Spine 1995; 20:356–361. 71. Loguidie V, Johnson R, Guyer R, et al. Anterior lumbar interbody fusion. Spine 1988; 13:366–369. 72. Vamanij, Fredrickson V, Thorpe B, et al. Surgical treatment of internal disc disruption. J Spinal Disord 1998; 11:375–382. 73. Selby D, Frymoyer J. Circumferential (360 degree) spinal fusion. The adult spine: principles and practice. In: Frymoyer J. ed. The adult spine. New York: Raven Press; 1991:1989. 74. Kozak J, O'Brien J. Simultaneous combined anterior and posterior fusion: an independent analysis of a treatment for the disabled low back pain patient. Spine 1990; 15:4322–4328. 75. Leufven C, Nordwall A. Management of chronic disabling low back pain with 360 degrees fusion: results from pain provocation tests and concurrent posterior lumbar interbody fusion, posterolateral fusion, and pedicle screw instrumentation in patients with chronic disabling low back pain. Spine 1999; 24:2042–2045. 76. Stromqvist B, Jonsson B, Fritzell P, et al. The Swedish National Register for Lumbar Spinal Surgery: Swedish Society for Spinal Surgery. Acta Orthop Scan 2001; 72:99–106. 77. Zucherman J, Delong B. Posterior lumbar interbody fusion, clinical series and technical aspects. In: White A, ed. Lumbar spine surgery 1st edn. St. Louis, Missouri: CV Mosby; 1987. 78. Steffee A, Biscup R, Sitkowski D. Posterior lumbar interbody fusion and plates. Clin Orthop 1988; 227:99–102. 79. Harms J, Leszensky D, Stoltz D, et al. True spondylolisthesis reduction and monosegmental fusion in spondylolisthesis. In: Bridwell K, DeWald R, eds. Textbook of spinal surgery, 2nd edn. Philadelphia: Lippincott-Raven; 1997:1337. 80. Fritzell P, Hagg O, Wessberg P, et al. 2001 Volvo Award winner in clinical studies: lumbar fusion versus non-surgical treatment for chronic low back pain: a multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine 2001; 26:2521–2532. 81. Zung W, Richards C, Short M. Self-rating depression scale in an outpatient clinic: further validation of the SDS. Arch Gen Psychiatry 1965; 14:6508–6515. 82. Butterman G, Garvey T, Hunt A, et al. Lumbar fusion results related to diagnosis. Spine 1998; 23:116–127. 83. Boden S, Zdeblick T, Sandhu H, et al. The use of rhBMP-2 in interbody fusion cages. Definitive evidence of osteoconduction in humans: A preliminary report. Spine 2000; 25(3):376–381. 84. Burkus J, Gornet M, Dickman C, et al. Anterior lumbar interbody fusion using rhBMP-2 with tapered interbody cages. J Spinal Disord Tech 2002; 15:337–349. 85. Alexander J, Branch CJ, Haid RJ, et al. An analysis of the use of rhBMP-2 in PLIF constructs: clinical and radiographic outcomes. Annual Meeting of the American Association of Neurological Surgeons and Congress of Neurological Surgeons Section on Disorders of the Spine and Peripheral Nerves. Orlando, Florida, USA, 2002.

86. Boden S, Kang J, Sandhu H, et al. Use of recombinant human bone morphogenetic protein-2 to achieve posterolateral lumbar spine fusion in humans: a prospective, randomized clinical pilot trial: 2002 Volvo Award in clinical studies. Spine 2002; 27:2662–2673. 87. Johnsson R, Stromqvist B, Aspenberg P. Randomized radiostereometric study comparing osteogenic protein-1 (BMP-7) and autograft bone in human noninstrumented posterolateral fusion: 2002 Volvo Award in clinical studies. Spine 2002; 27:2654–2661. 88. Sandhu H. Bone morphogenetic proteins and spinal surgery. Spine 2003; 15S: S64–S73. 89. Houpt J, Conner E, McFarland E. Experimental study of temperature distributions and thermal transport during radiofrequency current therapy of the intervertebral disc. Spine 1996; 21:1808–1821. 90. Hecht P, Hayashi K, Cooley A, et al. The thermal effect of monopolar radiofrequency energy on the properties of joint capsule. An in vivo histologic study using a sheep model. Am J Sports Med 1998; 26:808–814. 91. Lee J, Lutz G, Campbell D, et al. Stability of the lumbar spine after intradiscal electrothermal therapy. Arch Phys Med Rehab 2001; 82:120–122. 92. Saal J, Saal J. Intradiscal treatment for chronic low back pain: Prospective outcome study with a minimum 2-yr follow-up. Spine 2002; 27:966–974. 93. Karasek M, Boduk N. Twelve month follow-up of a controlled trial of intradiscal thermal annuloplasty for back pain due to internal disc disruption. Spine 2000; 25:2601. 94. Klein R, Eek B, O'Neill C, et al. Biochemical injection treatment for discogenic low back pain: a pilot study. Spine J 2003; 3:220–226. 95. Hsu K, Zucherman J, White A. The long-term effect of lumbar spine fusion: deterioration of adjacent motion segments. In: Yonenobu K, Ono K, eds. Lumbar fusion and stabilization. Tokyo: Springer-Verlag; 1993:54–64. 96. Buttner-Janz K, Scheilnack K, et al. Biomechanics of the S.B. Charite lumbar intervertebral disc endoprosthesis. Int Orthop 1989; 13:173–176. 97. David T. Lumbar disc prosthesis. Spine 1993; Eur Spine J 254–259. 98. Griffith S. A multicenter retrospective study of the clinical results of Link SB Charite intervertebral prosthesis. The initial European experience. Spine 1994; 19:1842–1849. 99. Marnay T. Lumbar disc arthroplasty, 8–10 year results using titanium plates with a polyethylene inlay component. American Academy of Orthopedic Surgeons. San Francisco, California. USA, 2001. 100. Weichert K, Mayer H, Marnay T, et al. ProDisc. Results of a multicenter prospective clinical trial. Spine arthroplasty conference. Munich, Germany, 2001. 101. Bertagnoli R, Kumar S. Indications for full prosthetic disc arthroplasty: a correlation of clinical outcome against a variety of indications. Eur Spine J 2002; 11(Suppl 2):S124–S130. 102. Ray C. Prosthetic disc nucleus. Spine Arthroplasty Conference. Munich, Germany, 2001. 103. Implicito D, Hsu K. Disc space geometry as a predictor of fusion solidity. Abstracts of the International Society of the Study of the Lumbar Spine. Burlington, Vermont, 1996.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ ii: Spondylolisthesis

CHAPTER

Spondylolisthesis: Epidemiology and Assessment

98

Santhosh A. Thomas

INTRODUCTION Etymologically, the term spondylolisthesis derives from Greek roots spondylos (vertebra) and olisthesis (to slip or slide down). It is now well established that spondylolisthesis is a broad group of disorders with the common basis of slippage of a vertebra over another vertebra. Spondylolisthesis was described as early as 1782 by a Belgian obstetrician who noted narrowing of the birth canal due to gross displacement of the fifth lumbar vertebra over the sacrum.1 Killian first used the term spondylolisthesis in 1854 to describe the displacement of fifth lumbar vertebra over the sacrum.2 Far-reaching anatomic studies by Naugebauer in 1888 showed that the forward displacement could occur by a defect in the pars interarticularis and less commonly with an intact but elongated pars.3 The direction of the spondylolisthesis or slippage is defined according to the displacement of the upper (olisthetic) vertebra as in anterolisthesis or retrolisthesis. The intervertebral discs, superior and inferior articular process (also referred to as zygapophyseal joints or facet joints), ligaments and paravertebral muscles work together to provide segmental stability.4–9 Dysfunction of the disc and horizontalization of the lamina and the articular process have been implicated as factors responsible for the development of spondylolisthesis.10–13 This may also occur if there is weakening of the supporting ligaments, muscular weakness or degenerative changes of the articular processes. The upper lumbar vertebrae are subjected to posteriorly oriented sheer forces and the lower lumbar vertebrae to anteriorly directed forces. During the aging process, the intervertebral discs undergo degenerative changes resulting in the loss of water and elasticity.5 Disc height is reduced, leading to loss of the intervertebral disc space height that leads to spinal instability. The vertebrae may begin to slip relative to another vertebra.14–18 The L4 and L5 vertebrae are particularly prone to this stress.

CLASSIFICATION Spondylolisthesis is classified based on the etiology of the slippage of the vertebra. Individual attempts were made to create classification but Wiltse, Macnab, and Newman merged their concepts, leading to the most commonly accepted classification (Fig. 98.1).19 1. Congenital or dysplastic: caused by congenital defects of L5 and/ or the upper sacrum; 2. Isthmic: caused by pars interarticularis defects; 3. Degenerative: due to articular process degeneration or abnormal orientation; 4. Traumatic: caused by fracture or dislocation of the lumbar spine, not involving the pars; 5. Pathologic: due to infection, malignancy either primary or metastatic, or other types of abnormal bone (e.g. osteogenesis imperfecta); 6. Iatrogenic/postsurgical.

Congenital or dysplastic spondylolisthesis is due to agenesis or insufficiency of the superior articular process (Fig. 98.2). This abnormality can lead to forward slippage due to inability to resist the stress and force placed on these joints under normal conditions. It is more commonly noted in childhood when a patient presents with an episode of severe back pain, hamstring tightness, and rarely a neurological compromise that leads to the work-up. Dysplastic spondylolisthesis typically occurs at the L5–S1 level, and particularly in young patients. It is always accompanied by a congenital anomaly of S1 (usually spina bifida) and often a vertebral arch anomaly of L5. Females are more often affected than males. The fundamental defect is in the L5–S1 facet joint that is dysplastic. A large degree of slip can occur including spondyloptosis in which the L5 has completely slipped off S1. Isthmic spondylolisthesis is the most common subtype and is caused by pars interarticularis defects (Fig. 98.3A, B). Subtype A is hypothesized to occur in individuals who have a congenitally weakened pars, but many do not and the lesion arises de novo. Subtype B includes individuals who have an elongated but intact pars. This is believed to be secondary to repeated fracture and subsequent healing of the stress fracture in the pars. Subtype C is due to acute fracture of the pars interarticularis.

INCIDENCE The pars interarticularis is the pivotal point where the maximum stress concentration is located. It is the connecting link between the pedicle, lamina, transverse process, and the two articular processes. The defect in the pars interarticularis is due to stress or fatigue fracture, which can allow forward slippage of one vertebra over the adjacent vertebra. The normal lumbar lordosis can lead to forward slippage. In the lumbar spine, isthmic spondylolisthesis occurs with the following frequencies: at the L5–S1 level (82.1%), L4–5 level (11.3%), L3–4 level (0.5%), L2–3 level (0.3%), and other levels (5.8%).20 White men appear to have the highest prevalence (6.4%) and black women the lowest (1.1%). This may indicate a gender and racial difference.21 Degenerative spondylolisthesis is second in frequency only to isthmic spondylolisthesis and is believed to be due to intersegmental instability. It is primarily a condition that affects older adults. Two leading theories on etiology are dysfunction of the intervertebral disc, and the horizontalization of the lamina.11,13,22 Degenerative spondylolisthesis occurs more often in women than men, ranging from a ratio of 2:1 to as high as 6:1.23–25 Women who have borne children have a significantly higher incidence of degenerative spondylolisthesis compared to nulliparous women (28% versus 16.7%). In contrast, men have a 7.5% incidence. Sanderson and Fraser suggest that females are more prone to developing degenerative spondylolisthesis, and the incidence 1077

Part 3: Specific Disorders

I Dysplastic

Normal

II-A Break in pars interarticularis

III Degenerative

II-B Elongated but intact pars

IV Fracture other than pars

of slippage increases with pregnancy.26 A familial component has also been implicated. Ryan reported on 73-year-old twin brothers with symptomatic spinal canal stenosis and lumbar degenerative listhesis involving the L4–5 level.27 In degenerative spondylolisthesis, Vogt et al. noted in radiographs of 788 white women with a mean age of 71.5 1078

II-C Acute fracture

Pathological

Fig. 98.1 Classification of spondylolisthesis.

years that 73% of the spondylolisthesis was located at L4–5, 28% at the L5–S1 level, followed by 12% at L3–4 level (10% of patients had multilevel listhesis).28 In stark contrast, a study by Merbs on New Mexico Pueblo skeletons revealed 79% of listhesis occurring at the L5–S1 level.23 Prevalence of spondylolisthesis increased with

Section 5: Biomechanical Disorders of the Lumbar Spine Lateral view

Posterior view

L3 L4

L5 Hypoplastic superior sacral facet joint S1

S1

Fig. 98.2 Dysplastic (congenital) spondylolisthesis with hypoplastic superior articular process with an intact pars interarticularis.

Intact but elongated pars

L5

S1

A

B

Fig. 98.3 (A) Isthmic spondylolisthesis with pars interarticularis defect. (B) Isthmic spondylolisthesis with intact but elongated pars interarticularis.

increasing age. Progression of slippage occurs in 30% of patients.29 Due to the inherent increased mobility created by a degenerative spondylolisthesis, it is not surprising that synovial cysts are frequently identified. These mass occupying structures arise from the facet joints and can reside in the lateral foramen or in the central spinal canal.30,31 Degenerative spondylolisthesis was more likely to develop in patients who underwent fusion than in the general population.32 Traumatic spondylolisthesis is caused by a fracture or dislocation of the spine not involving the pars interarticularis. Pathologic spondylolisthesis is due to localized or generalized infection, malignancy, or other types of bone disease (e.g. osteogenesis imperfecta, Paget's disease). Iatrogenic or postsurgical spondylolisthesis is due to partial or complete loss of posterior supporting structures due to a surgical procedure. Patients with spondylolisthesis may present with a very broad spectrum of complaints. Symptoms and complaints may also vary over time. Presentation may range from asymptomatic in some patients to having mild through severe back pain which may be intermittent or persistent. In addition, patients may present with or

without radicular complaints. There may not be any complaints of back pain despite signs and symptoms of nerve root compression or cauda equina syndrome. The most common pain pattern associated with spondylolisthesis is a dull, aching pain in the back, buttocks, and posterior thigh. The source of pain is likely multifactorial. The pars nonunion may be a source33 and ligamentous stretch may lead to local muscle spasm at the unstable vertebral segment. Disc degeneration is noted in 67% at the level of the slip.34 Saraste's study of spondylolysis and spondylolisthesis suggests that disc degeneration may contribute to symptoms, as a strong correlation was noted between disc degeneration and low back pain in patients with spondylolysis.35 Often, the central canal is not as compromised, as the neural foramina at the level of the slip and, in some instances degenerative changes may further compromise the neural foramina leading to nerve root compression.36 With an emphasis on healthier lifestyles, many are getting involved in athletic activities. This has led to an increase in participation in various sports at recreational and at more competitive levels. Numerous skeletally immature athletes are also participating in these activities. Many of these growing children are at a higher risk for various musculoskeletal injuries including spinal trauma. Factors that contribute to these injuries includes poor techniques, rapid increase in training frequency, use of improper equipment, inappropriate footwear, and variable playing fields, along with musculoskeletal weakness and inflexibility.37–40 In athletes with persistent back pain, isthmic spondylolisthesis is noted in up 50%. It has a prevalence rate of 4–5% in children at 6 years of age. The prevalence slightly increases by age 18 to 6%.41 The etiology of an isthmic spondylolisthesis is a defective or weakened pars interarticularis that is further injured with repetitive motion or stress. Certain clinical features help distinguish stress fractures from isthmic spondylolisthesis. These include genetic predisposition, rare callous formation, young age of onset, relatively minor inciting trauma, and a low incidence of spontaneous bony union.42 The greatest forces occur at the L5–S1 articulation.38,43 Anatomically, the position of the sacrum creates compressive forces and anterior shear on the neural arch.43–45 Bipedal stance further exacerbates these forces.37 Erector spinae musculature plays an important role in supporting the posterior elements in an erect posture. Extension of lumbar spine leads to closure of facet joints. When additional extension forces are applied, these forces are transmitted to the neural arch.43 It is believed that repetitive motion leads to the higher prevalence of spondylolisthesis seen in athletes. The most commonly implicated movement in injury to the pars interarticularis is hyperextension. Up to 20% of pars defects may be unilateral.46–49 Repetitive rotation motion is implicated in unilateral defects. Football and gymnastics are believed to be the sports with the highest risk, but other sports including hockey, diving, wresting, volleyball, pole vaulting, racquet sports, and weight lifting have also been implicated. A fourfold increase in spondylolisthesis was noted in helicopter pilots in comparison to transport pilots and cadets, suggesting that repetitive minor stress and vibrational force, without acute fracture, can cause lumbar spondylolisthesis.50

DIAGNOSIS Physical examination may reveal some tenderness to palpation over the involved region. In the late or advanced stages, the patient may present with distortion of the pelvis and trunk. There may be some restriction noted with side-to-side motion along with some guarding, especially in a presentation with acute onset. Forward flexion may be limited due to hamstring tightness. Hamstring tightness is common but it may not be observed in a flexible athlete. Hamstring tightness 1079

Part 3: Specific Disorders

was believed to be due to traction on the cauda equina; however, all grades of spondylolisthesis can present with hamstring tightness and it is seldom accompanied by neurologic signs.51–53 Several nerve roots (L4 to S3) innervate the hamstring muscles and a very severe single lesion would be necessary to produce such a massive involvement. The development and perpetuation of hamstring tightness may be an attempt by the body to reestablish the patient's center of gravity by attempting either to control the unstable segment or to rotate the pelvis into a more vertical position. Significant slip can lead to lumbosacral kyphosis and trunk shortening.54–58 Forward slip of the lumbar spine leads to a compensatory thoracolumbar hyperlordosis, which can present with an anteriorly protruding inferior rib cage. In highgrade slips, a clinician may be able to observe a palpable step-off sign or depression at the involved level. Other findings may include tight hip flexors, relative thoracic kyphosis, and positive one-leg hyperextension test. Athletes with lumbar spondylolisthesis may also present with a dull backache that is amplified with hyperextension and rotation motion.54 Gait abnormalities may observed in some patients with spondylolisthesis. Compensation for the hamstring tightness, lumbosacral kyphosis (vertical tilting), compensatory lumbar hyperlordosis, and the flexion deformity at the hips and knees leads to a spondylolisthetic gait. It is characterized by a waddle with limited hip flexion, a wide base of support, and a shortened stride length.52,54,57,59 Neurologic deficits are uncommon and the straight leg raising test is usually negative. Indeed, this is a difficult maneuver to perform because of the previously described hamstring tightness. In nearly half of the patients who require surgical intervention, radicular pain and varying degrees of nerve root dysfunction are present.60–62 The fifth lumbar root is more often involved as it approaches the L5 neural foramina. Osteophytes or hypertrophic facet joints can further affect the compression. Any involvement of bladder dysfunction may be due to involvement of the sacral roots, which can be further evaluated with urologic studies including a cystometrogram.

ASSOCIATED CONDITIONS Other conditions have been noted to occur with spondylolisthesis. Spina bifida occulta has been reported to be present along with isthmic defects, with a reported incidence of 24–70%. In dysplastic spondylolisthesis, spina bifida occulta occurs in about 40% of the cases. In contrast, the incidence of spina bifida occulta in adults without spondylolisthesis is about 6%. This defect, in which there is incomplete fusion of the posterior arch, likely permits added stresses on the pars interarticularis allowing it to fracture.57,59,63,64 Congenital defects such as sacral spina bifida and hypoplasia of posterior sacral development was found in 94% of dysplastic and 32% of isthmic spondylolisthesis patients.65 Scoliosis is another entity noted in patients with spondylolisthesis. The incidence ranges between 15% and 43%.66–69 Those requiring surgery are noted to have an approximately 30% incidence (range 23–48%). The scoliosis may be due to, or worsened by, muscle spasms. Distortion of the pelvis and trunk may become apparent in the late stages of grade II spondylolisthesis, but are frequently present by the time the slip reaches grade III. Surgery may correct this secondary deformity.53,64,66,70–72 Posterior disc protrusion at the level of the slip is rare, with an incidence approaching 5%.55,56 There have been no reported cases of spondylolysis or spondylolisthesis at birth. The earliest documented case was in a 4-month-old infant whose parents had noted some deformity in the lower back. In that case the spondylolisthesis was confirmed radiographically. The child developed a wide-based shuffling gait with lower extremity in lateral rotation at the age of 15 months.73,74 Rosenberg et al. evaluated 143 lifelong nonambulatory adult patients and found no cases 1080

of a pars defect.75 An overall incidence of spondylolisthesis was 4.4% in a group of 500 6-year-olds and it progressed to 6% by adulthood in the same population.63 An overall incidence of spondylolisthesis 8.02% was noted in a group of 3152 athletes evaluated by Soler and Calderon. A higher incidence of 26.7% was noted in throwing sports such as discus and shot put. Gymnastics, a sport that often involves hyperextension, was noted to have an incidence of 16.9%, rowing 16.9%, and swimming 10.2%.76 Elite athletes are not exempt from these findings. Jones et al. compared division 1 college football players' pre-participation radiographs to controls. It was noted that the rate of spondylolysis was 4.8% in these athletes and 6% in the control group. The rate of spondylolisthesis was slightly less with 3.8% in the group of athletes and 3.6% in the control group.77 Shaffer et al. reviewed questionnaires completed by NFL and 25 NCAA team physicians. The known prevalence of spondylolisthesis was 1%.78 Other studies have reported 10.1–50% spondylolysis rates for down-lineman. Degenerative spondylolisthesis in the cervical spine was noted to have a prevalence of 5.2%.79 Studies by Vogt et al.80,81 did not support a relationship between anterolisthesis and diabetes. Prevalence of isthmic lumbar spondylolisthesis was 5.7% and there was no significant sex difference in a group of diabetics.82 AfricanAmerican women are 2–3 times more likely to develop anterolisthesis than Caucasian women.81 Oophorectomized Japanese women83 were noted to have an increased prevalence of anterolisthesis, but among older Caucasian women, neither oophorectomy nor use of estrogen was related to the prevalence of listhesis.80 There is support in the literature for a familial component associated with spondylolisthesis. Among first-degree relatives, spondylolisthesis was noted to be 27–69% with the dysplastic type being more prevalent (33%). The familial incidence in first-degree relatives over the age of 10 years was noted to be 40%.84

PROGRESSION A number of factors contribute to the risk of progression: decreased skeletal maturity as seen in the younger age group, slip greater than 50%, slip angle greater than 40–50 degrees (0–10 is normal), domeshaped sacrum, female gender, and dysplastic versus isthmic spondylolisthesis. Slippage that progresses occurs predominantly during puberty and has an association with spina bifida occulta.85 A study of 255 patients who were followed for a minimum of 20 years revealed a mean slip progression of 4 mm with 11% of adolescents and 5% of adults progressing to greater than 10 mm.35 Mean initial slip was 10.1% in a group of 86 young athletes between the ages of 6 and 20 years with spondylolysis or spondylolisthesis over a period of 4.8 years. In this study, 47% of the patients had no progression of their slip, 9% improved, and 44% had slip progression. A slip progression of 10% or more was noted in 12%. One of the 86 athletes had a progression of greater than 20%. No increased risk was associated with spina bifida occulta or continued activity. An increased risk of progression was associated with puberty, increased slip angle, and sacral inclination.86 Several authors have described the assessment of spondylolisthesis by utilizing various calculations on plain radiographs.87–91 Meyerding's classic description92 in 1931 grades the spondylolisthesis as the percentage of anterior displacement of the superior vertebral body on the lower body. The vertebra is divided into four quarters. Grade I slips are displaced from 0% to 25%, grade II from 26% to 50%, grade III from 51% to 75%, and grade IV from 76% to 100% (Fig. 98.4). Spondyloptosis, or grade V, is more than 100% (Fig. 98.5). The most often used method today, first described by Talliard and later used by Laurent and Osterman, describes the degree of slip of L5 as an exact percentage of the anteroposterior diameter of the top of the first

Section 5: Biomechanical Disorders of the Lumbar Spine

A

L5 I

II

III

L4 B

L5

IV S1 A – ⫻100 = % Slip B

Slip angle (Lumbosacral joint angle) Fig. 98.6 Measurement of percentage of slip (% slip = (A / B) × 100; SI, sacral inclination; slip angle between arrows).

S1 Grade 1 – 1–25% Grade II – up to 50% Grade III – up to 75% Grade IV – 76 –100%

Fig. 98.4 Meyerding's classification of spondylolisthesis. L3

L4 L5 S1

Fig. 98.5 Spondyloptosis.

views, and bilateral obliques should be obtained. The lateral film will best identify the spondylolisthesis or slippage. Vertebral instability is generally multidirectional94 but the displacement is measured in one plane. Progression and instability in spondylolisthesis are evaluated with lateral radiographs. The pars can be seen on the lateral film. Spondylolysis refers to the radiolucent defect in the pars interarticularis. If the defect is large, it can be viewed on nearly all plain films of the lumbar spine. Oblique views will demonstrate most but not all of the pars defects. The commonly referred to description of the ‘collar’ on the neck of the Scotty dog of LaChapelle is noted on the oblique film (Fig. 98.7). In severe slips, the AP radiograph will show the L5 vertebra ‘end-on’ through the sacrum, the so-called reverse Napoleon hat sign (le chapeau). The hat in reality is upside down and not reversed. Obvious pathology is often absent in plain films. Lateral slipping, or laterolisthesis, is almost always associated with vertebral rotation and scoliosis. A standing AP view is needed to evaluated scoliosis. Supine flexion–extension views should be utilized in

sacral vertebra.93 Sacral inclination is the relationship of the plane of the sacrum to the vertical plane. The sacrum tends to a more vertical position with increasing slips. The slip angle, also known as sagittal rotation angle or lumbosacral kyphosis, is the relationship determined by a line along the posterior border of S1 and the inferior endplate of L5. The slip angle and percentage of slip may predict the risk of future slip progression (Fig. 98.6).

A B

C

D

DIAGNOSTIC WORK-UP Treatment Most commonly, patients with spondylolisthesis, unless accompanied by neurological deficits or evidence of instability, should have a trial of conservative care. This includes modification of activities, physical therapy, bracing, and a trial of analgesics as the first line of treatment of symptomatic spondylolisthesis.

F A = Superior articular process B = Pedicle C = Transverse process D = Inferior articular process E = Pars defect or spondylolysis F = Lamina

Diagnostic imaging If no significant improvement is noted with conservative measures, further evaluation is indicated. Spine X-rays with multiple views, standing anteroposterior (AP), lateral film, flexion and extension

E

Spondylolysis

Fig. 98.7 Scotty dog. 1081

Part 3: Specific Disorders

evaluating both sagittal and translational mobility or instability. There are limitations with the functional radiographs. The reproducibility of functional radiographs is difficult. A slight variation in patient positioning or in gantry tilting may result in 10–15% variation in the range of vertebral displacement. In order to obtain accurate and reproducible measurements, the patient positioning and direction of the X-ray beam must be consistent.95 The method to measure the displacement is still not standardized when it comes to functional radiographs.96 Radiographic landmarks used for the measurement vary among many reported studies. The gonadal dose of radiation for the lumbar spine should be considered. Caution is warranted: there is little evidence linking instability with symptoms or progression. Given the indolent nature of most cases of spondylolisthesis, care should be taken to avoid attributing symptoms solely to the slippage, but consideration must be given to other findings, including neurologic involvement. These finding should be investigated beyond the diagnostic plain radiographs. As well, low back pain could emanate from a lumbar disc that is not at the listhetic segment. In cases of degenerative slippage, the facet joint(s) may be the source of discomfort. Computed tomography (CT) and magnetic resonance imaging (MRI) allow evaluation of the axial plain, and plain radiographs allow evaluation of sagittal and coronal planes. CT is ideal for defining bony detail. It has added much to the plain radiographs and myelographic evaluation of spondylolisthesis. Teplick et al.97 found CT to be more sensitive in the diagnosis of pars defects, especially thin sclerotic lesions. Thus, CT may occasionally afford more information in highrisk athletes with negative bone scans and suspected stress fracture. It is crucial that the CT sections be angled to cut as nearly as possible at right angles across the pars lesion. It is often the only method to differentiate a congenital or isthmic spondylolisthesis. The presence of a grade I spondylolisthesis may be missed if only the axial images are evaluated. Sagittal and coronal reformatting of high-resolution axial images adds a new perspective to foraminal stenosis and gives a three-dimensional relationship between anatomic anomalies, slips, fractures, or osteophytes. The presence of a pseudobulging disc at the level of the slip can also be evaluated by using a midline sagittally reformatted image. A deformity of the involved neural foramina in spondylolisthesis, described as a ‘flattening’ on axial CT scan with multiplanar reconstruction, has been reported. The foramen assumes a bilobed appearance, and instead of vertical-oblique it becomes more horizontal.98,99 Magnetic resonance imaging can provide information regarding interruption of the cortical margins of the pars defect seen on sagittal images, with short TR/TE and long TR/short TE images showing the lysis better than the long TR/TE images.100 It can also provide detailed information on neural elements, including the exiting nerve root in the foramen. It should be obtained in cases with neurologic deficits. MRI has demonstrated great sensitivity to bone marrow abnormalities. An interruption in the continuity of marrow signal cannot be completely attributed to a break in the pars interarticularis. Any process that replaces marrow (i.e., lytic or blastic metastasis or bony sclerosis) can alter the marrow signal. Partial volume averaging of a superior facet spur and adjacent pedicle as seen in degenerative facet disease can similarly affect the marrow signal. Sclerosis of the pars interarticularis is seen most often with spondylolysis when there is minimal spondylolisthesis.101 Radionuclide scintigraphy (technetium-99) is most sensitive for diagnosing suspected early unilateral or bilateral stress fractures in the child and young athlete with relatively acute symptoms. It is only positive in 17% of patients with chronic pain who present with large and sclerotic pars defects.102–105 Thus, its usefulness is limited in patients with more chronic symptoms. 1082

Bone scan may be beneficial in patients with negative plain radiographs, but persistent pain and symptoms that are suggestive of a pars injury. A negative plain radiograph and a positive bone scan suggest a recent injury. These studies are very sensitive in showing an inflammatory response, but unfortunately are non-specific and poorly localize lesions. A bone scan is incapable of distinguishing between increased metabolic activity in the vertebral body and the posterior neural arch. Acute and healing fractures will exhibit metabolic activity of a fracture, but chronic or healed non-unions will not demonstrate increased radiotracer uptake. Identifying a pars defect that is positive or negative on a bone scan is not associated with any specific prognostic information. Single-photon emission computed tomography (SPECT) scanning is more sensitive than conventional bone scans, plain radiography (including oblique views), and CT scanning in showing early lesions. SPECT can identify sites of increased metabolic activity that were thought to be normal on bone scans.105

CONCLUSION Spondylolisthesis is a common cause for back pain. Symptoms may include back pain and less commonly neurologic deficit or radicular pain. Symptoms usually respond to such nonoperative measures as rest, activity modification, physical therapy, bracing, and oral medications. Radiographic work-up may provide additional information including the degree of slippage or instability, but there are no conclusive studies to evaluate spondylolysis. Conservative care should be the mainstay of treatment but if there is no significant improvement in pain control, quality of life, or instability is noted in patients with spondylolisthesis, surgical options should be entertained.

Acknowledgment The author would like to thank his wife Sapna and daughters Alyss and Nicole for their endless patience and support.

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45. Sward L, Hellstrom M, Jacobsson B, et al. Spondylolysis and the sacro-horizontal angle in athletes. Acta Radiol 1989; 30:359–364. 46. Roche MB. Healing of bilateral fracture of the pars interarticularis of a lumbar neural arch. J Bone Joint Surg [Am] 1950; 32:428–429. 47. Roche MB, Rowe GG. Incidence of separate neural arch and coincident bone variations: a survey of 4200 skeletons. Anat Rel 1951; 109:233–252.

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55. Boxall D, Bradford DS, Winter RB, et al. Management of severe spondylolisthesis in children and adolescents. J Bone Joint Surg [Am] 1979; 61:479–495.

25. Herron LD, Trippi AC. L4–5 degenerative spondylolisthesis: the result of treatment by decompressive laminectomy without fusion. Spine 1989; 14:534–538. 26. Sanderson PL, Fraser RD. The influence of pregnancy on the development of degenerative spondylolisthesis. J Bone Joint Surg [Br] 1996; 78:951–954. 27. Ryan MD. L4–5 degenerative spondylolisthesis in monozygous twins. Spine 1994; 19:985–986. 28. Vogt MT, Rubin D, San Valentin R, et al. Lumbar olisthesis and lower back symptoms. Spine 1998; 23:2640–2647. 29. Matsunaga S, Sakou T, Morizono Y, et al. Natural history of degenerative spondylolisthesis: pathogenesis and natural course of the slippage. Spine 1990; 15:1204–1210. 30. Parlier-Cuau C, Wybier M, Nizard R, et al. Symptomatic lumbar facet joint synovial cysts: clinical assessment of facet joint steroid injection after 1 and 6 months and long-term follow-up in 30 patients. Radiology 1999; 210:509–513.

56. Dandy DJ, Shannon MJ. Lumbo-sacral subluxation (group I spondylolisthesis). J Bone Joint Surg [Br] 1971; 53:578–595. 57. Bunnell WP. Back pain in children. Orthop Clin North Am 1982; 13:587–604. 58. Wiltse LL. Spondylolisthesis in children. Clin Orthop 1961; 21:156–163. 59. Turner RH, Bianco AJ. Spondylolysis and spondylolisthesis in children and teen agers. J Bone Joint Surg [Am] 1971; 53:1298–1306. 60. Davis IS, Bailey RW. Spondylolisthesis: indications for lumbar nerve root decompression and operative technique. Clin Orthop 1976; 117:129–134. 61. Gill GG, Manning JG, White HL. Surgical treatment of spondylolisthesis without spine fusion. J Bone Joint Surg [Am] 1955; 37:493–520. 62. O'Brien JP, Mehdian H, Jaffray D. Reduction of severe lumbosacral spondylolisthesis. Orthop Trans 1988; 12:620. 63. Fredrickson BE, Baker D, McHolick WJ, et al. The natural history of spondylolysis and spondylolisthesis. J Bone Joint Surg [Am] 1984; 66:699–707.

31. Reust P, Wendling D, Lagier R, et al. Degenerative spondylolisthesis, synovial cyst or the zygapophyseal joints, and sciatic syndrome: Report of two cases and review of the literature. Arthritis Rheum 1988; 31:288–294.

64. Laurent LE, Osterman K. Operative treatment of spondylolisthesis in young patients. Clin Orthop 1976; 117:85–91.

32. Hambly MF, Wiltse LL, Raghavan N, et al. The transition zone above a lumbosacral fusion. Spine 1998; 23:1785–1792.

65. Wiltse LL, Widell EH Jr, Jackson DW. Fatigue fracture: the basic lesion in isthmic spondylolisthesis. J Bone Joint Surg [Am] 1975; 57:17–22.

33. Zindrick MR, Lorenz MA. The nonreductive treatment of spondylolisthesis. Semin Spine Surg 1989; 1:116–124.

66. Fisk JR, Moe JH, Winter RB. Scoliosis, spondylolysis, and spondylolisthesis: their relationship as reviewed in 539 patients. Spine 1978; 3:234–245.

34. Bosworth DM, Fielding JW, Demarest L, et al. Spondylolisthesis: a critical review of a consecutive series of cases treated by arthrodesis. J Bone Joint Surg [Am] 1955; 37:767–786.

67. Libson E, Bloom RA, Shapiro Y. Scoliosis in young men with spondylolysis or spondylolisthesis. A comparative study in symptomatic and asymptomatic subjects. Spine 1984; 9:445–447.

35. Saraste H. Long-term clinical and radiographic follow up of spondylolysis and spondylolisthesis. J Pediatr Orthop 1987; 7:631–638.

68. McPhee IB, O'Brien JP. Scoliosis in symptomatic spondylolisthesis. J Bone Joint Surg [Br] 1980; 62:155–157.

36. Edelson JG, Nathan H. Nerve root compression in spondylolysis and spondylolisthesis. J Bone Joint Surg [Br] 1986; 68:596–599.

69. Rick JR, Winter RB, Moe JH. The lumbosacral articulation and its relationship to scoliosis. J Bone Joint Surg [Am] 1974; 56:445.

37. Cook PC, Leit ME. Issues in the pediatric athlete. Orthop Clin North Am 1995; 26:453–464.

70. Bosworth DM, Fielding JW, Demarest L, et al. Spondylolisthesis: a critical review of a consecutive series of cases treated by arthrodesis. J Bone Joint Surg [Br] 1955; 37:767–786.

38. Harvey J, Tanner S. Low back pain in young athletes: a practical approach. Sports Med 1991; 12:394–406. 39. Hutchinson MR. Low back pain in elite rhythmic gymnasts. Med Sci Sports Exerc 1999; 31:1686–1689.

71. Hodgson AR, Wong SK. A description of a technique and evaluation of results in anterior spinal fusion for deranged intervertebral disk and spondylolisthesis. Clin Orthop 1968; 56:133–162.

40. Stinson JT. Spine problems in the athlete. Md Med J 1996; 45:655–658.

72. McPhee IB, O'Brien JP. Reduction of severe spondylolisthesis. Spine 1979; 4:430-434.

41. Fredrickson BE, Baker D, McHolick WJ, et al. The natural history of spondylolysis and spondylolisthesis. J Bone Joint Surg [Am] 1984; 66:699–707.

73. Oakley RH, Carty H. Review of spondylolisthesis and spondylolysis in paediartic practice. Br J Radiol 1983; 57:877–885.

42. Wiltse LL, Hutchinson RH. Surgical treatment of spondylolisthesis. Clin Orthop 1964; 35:116–135.

74. Borkow SE, Kleiger B. Spondylolisthesis in the newborn; a case report. Clin Orthop 1971; 81:73–76.

43. Alexander MJL. Biomechanical aspects of lumbar spine injuries in athletes: A review. Can J Appl Sport Sci 1985; 10:1–20.

75. Rosenberg NJ, Bargar WL, Friedman B. The incidence of spondylolysis and spondylolisthesis in nonambulatory patients. Spine 1981; 6:35–38.

44. Sward L. The thoracolumbar spine in young athletes: current concepts on the effects of physical training. Sports Med 1992; 13:357–364.

76. Soler T, Calderon C. The prevalence of spondylolysis in Spanish elite athletes. Am J Sports Med 2000; 28:57–62.

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Part 3: Specific Disorders 77. Jones DM, Tearse DS, El-Khoury GY, et al. Radiographic abnormalities of the lumbar spine in college football players. A comparative analysis. Am J Sports Med 1999; 27:335–338.

93. Laurent LE, Osterman K. Operative treatment of spondylolisthesis in young patients. Clin Orthop 1976; 117:85–91.

78. Shaffer B, Wiesel S, Lauerman W. Spondylolisthesis in the elite football player: an epidemiologic study in the NCAA and NFL. J Spinal Disord 1997; 10:365–370.

94. Pope MH, Panjabi M. Biomechanical definitions of spinal instability. Spine 1985; 10:255–256.

79. Kopacz KJ, Connolly PJ. The prevalence of cervical spondylolisthesis. Orthopedics 1999; 22:677–679.

95. Danielson B, Frennered K, Irstam L. Roentgenologic assessment of spondylolisthesis: a study of measurement variations. Acta Radiol 1988; 29:345–351.

80. Vogt MT, Rubin D, Valentin RS, et al. Lumbar olisthesis and lower back symptoms in elderly white women: the study of osteoporotic fractures. Spine 1998; 23:2640–2647.

96. Putto E, Tallroth K. Extension–flexion radiographs for motion studies of the lumbar spine: a comparison of two methods. Spine 1990; 15:107–110.

81. Vogt MT, Rubin DA, Palermo L, et al. Lumbar spine listhesis in older AfricanAmerican women. Spine J 2003; 3 255–261. 82. Virta L, Ronnemaa T, Laakso M. Prevalence of isthmic lumbar spondylolisthesis in nondiabetic subjects and NIDDM patients. Diabetes Care 1994; 17:592–594. 83. Imada K, Matsui H, Tsuji H. Oophorectomy predisposes to degenerative spondylolisthesis. J Bone Joint Surg [Br] 1995; 77:126–130. 84. Wynne-Davies R, Scott JHS. Inheritance and spondylolisthesis. A radiographic family survey. J Bone Joint Surg [Br] 1979; 61:301–305. 85. Blackburne JS, Velikas EP. Spondylolisthesis in children and adolescents. J Bone Joint Surg [Br] 1976; 59:490–494. 86. Muschik M, Hahnel H, Robinson PN, et al. Competitive sports and progression of spondylolisthesis. J Pediatr Orthop 1996; 16:364–369. 87. Burkhardt E. Spondylolisthesis. Schweizerische Med Wochensch 1940; 70:1093-1101. 88. Marique P. Le spondylolisthesis. Acta Chir Belg Suppl 1951; 3:3–89. 89. Meschan I. Spondylolisthesis. A commentary on etiology, and an improved method of roentgenographic mensuration and detection of instability. Am J Roentgenol 1945; 53:230–243. 90. Newman PH. A clinical syndrome associated with severe lumbo-sacral subluxation. J Bone Joint Surg [Br] 1965; 47:472–481. 91. Taillard W. Le spondylolisthesis chez l'enfant et l'adolescent. Acta Orthop Scand 1955; 24:115–144.

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92. Meyerding HW. Spondylolisthesis. Surg Gynecol Obstet 1931; 54:371–377.

97. Teplick JG, Laffey PA, Berman A, et al. Diagnosis and evaluation of spondylolisthesis and/or spondylolysis on axial CT. Am J Neuroradiol 1986; 7:479–491. 98. Rothman SLG, Glenn WV. CT multiplanar reconstruction in 253 cases of lumbar spondylolysis. Am J Neuroradiol 1984; 5:81–90. 99. Rothman SLG, Glenn WV, Kerber CW. Multiplanar CT in the evaluation of degenerative spondylolisthesis. A review of 150 cases. Comput Radiol 1985; 9:223–232 100. Grenier N, Kressel HY, Schiebler ML, et al. Isthmic spondylolysis of the lumbar spine: MR imaging at 1.5 T. Radiology 1989; 170:489–493. 101. Johnson DW, Farnum GN, Latchaw RE, et al. MR imaging of the pars interarticularis. Am J Roentgenol 1989; 152:327–332. 102. Lusins JO, Elting JJ, Cicoria AD, et al. SPECT evaluation of unilateral spondylolysis. Clin Nucl Med 1994; 19:1–5. 103. Papanicolaou N, Wilkinson RH, Emans JB, et al. Bone scintigraphy and radiology in young athletes with low back pain. Am J Roentgenol 1985; 145:1039–1044. 104. Pennell RG, Maurer AH, Bonakdarpour A. Stress injuries of pars interarticularis: radiologic classification and indications for scintigraphy. Am J Roentgenol 1985; 145:763–766. 105. Collier BD, Johnson RP, Carrera GF, et al. Painful spondylolysis or spondylolisthesis studied by radiography and single-photon emission computed tomography. Radiology 1985; 154:207–211.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ ii: Spondylolisthesis

CHAPTER

Spondylolisthesis: Medical Rehabilitation and Interventional Spine Techniques

99

Alexander C. Simotas and Peter J. Moley

INTRODUCTION Patients presenting with lumbar spine complaints who have radiographs showing spondylolisthesis may experience painful or neurologic symptoms from a variety of clinical entities. The evaluation and treatment prescription should evolve from a biopsychosocial model that has been suggested for low back pain.1–8 Radiographic features, neuromuscular function, psychological, social factors and medical comorbities must be considered as a part of the overall disease when formulating the treatment plan. The most commonly used classification system for spondylolisthesis is based on Wiltse, Newman, and Macnab (Table 99.1).9 This chapter will focus primarily on treatment of problems associated with isthmic and degenerative types. Dysplastic spondylolisthesis is characterized by dysplasia of the sacrum and facet joints. The condition is usually seen in the first decade of life and can be associated with a high-grade slip. Traumatic spondylolisthesis is extremely rare and associated with additional spinal trauma and fractures. Iatrogenic spondylolisthesis can occur with the weakening of posterior column supportive structure that is removed during surgical decompression. Isthmic spondylolisthesis is caused by a spondylolytic defect in the pars; Nonoperative treatment for acute isthmic spondylolysis – a common presentation of adolescent low back pain – is discussed in a separate chapter. A complete radiographic evaluation is important. The degree of vertebral subluxation or slip is characterized as 0–25% for grade 1, 26–50% grade 2 , 51–75% grade 3, 76–100% grade 4, and complete for grade 5 (spondyloptosis). The severity of central or foraminal stenosis should be noted. Although it is unclear whether low-grade adult spondylolisthesis is an independent risk factor for low back

pain, the classification of spondylolisthesis into subsets may be useful in directing care. One such broad scheme classifies spondylolisthesis into the three following subsets: degenerative spondylolisthesis (DS); degenerative spondylolisthesis with spinal stenosis (DSSS); and lytic or isthmic spondylolisthesis (IS). Other radiographic findings that also should be considered include sagittal and coronal plane alignment deformities, the presence of lateral listhesis, degenerative facet disease, and the relative degree of spondylosis.

PATHOANATOMIC CONSIDERATIONS Degenerative spondylolisthesis (DS) is a segmental degenerative process characterized by facet joint arthrosis and segmental subluxation (Fig. 99.1). Multiple causes may initiate the process of subluxation but facets with a sagittal alignment are probably an important contributing factor.10–12 As the posterior elements move forward with the vertebral body,13,14 the inferior articulating processes eventually can move forward enough to abut the superior endplate of the caudal vertebral body. This may explain why the degree of degenerative spondylolisthesis is usually only grade 1 or 2. Intervertebral disc space narrowing may occur simultaneously or later in the overall process.11,15

Table 99.1: The most commonly used classification system for spondylolisthesis Type 1 Dysplastic Type 2 Isthmic (includes 3 subclasses) 1. lytic fracture of the pars 2. elongated but intact pars 3 acute pars fracture Type 3 Degenerative Type 4 Traumatic Type 5 Iatrogenic Based on Wiltse, Newman, and Macnab.9

Fig. 99.1 Axial MRI of L4–L5 degenerative spondylolisthesis complicated by a ligamentum flavum cyst. Facet joint proliferation and deterioration result in subarticular, lateral recess and central canal stenosis most significantly affecting L5 roots. 1085

Part 3: Specific Disorders

It remains unclear if the degree of subluxation has any correlation to the severity and presence of back pain or diability. Matsunaga et al. followed 145 patients with degenerative spondylolisthesis for a minimum of 10 years and observed no correlation between changes in clinical symptoms and progression of spondylolisthesis.16,17 The occurrence of increased translation or angular motion on flexion radiographs can be noted, although the relevance to different treatment outcomes is unclear Those with DS may initially present with the insidious onset of low back pain with or without thigh pain that could be attributed to facet joint disease.16–19 Leg pain, which may occur in early stages, in the absence of significant spinal stenosis, is often quickly responsive to treatment. In the later stages both lateral and central spinal stenosis may develop secondary to zygapophyseal joint hypertrophy, ligamentum flavum buckling, and/or disc protrusion. Neurogenic claudication secondary to spinal stenosis causes referred pain into the buttocks and lower limbs while walking, and is relieved when the patient sits or bends forward. Degenerative spondylolisthesis with spinal stenosis represents a more severe anatomic disease.20–24 There is evidence that patients presenting with severe back and leg pain who have radiographic findings of severe central stenosis will respond poorly to medical rehabilitation and interventional spine treatment.25,26 In addition to symptoms caused by central stenosis, entrapment of nerve roots within the lateral recess and intervetebral foramen may cause radicular symptoms. For example, a superimposed foraminal disc protrusion may cause symptomatic L4 radiculopathy. A posterolateral disc protrusion at the L4–5 or asymmetric facet joint arthrosis may cause unilateral radiculopathies affecting the L5 nerve root. Isthmic spondylolisthesis (IS) is caused by a defect in the pars interarticularis which allows anterior translation to occur in the absence of facet joint arthrosis. The distortion of the foramina by the proximal pars stump may cause dynamic or static compression of the exiting nerve roots (Figs 99.2, 99.3).27–31 Although foraminal stenosis is common, central canal stenosis usually is absent in low-grade IS. In large measure, this is due to the fact that the most common level afflicted with IS is L5–S1; the most capacious portion of the spinal canal in the lumbar spine (Figs 99.4, 99.5). Clinical studies suggest that the amount of slip will not significantly progress in adult IS.32–38 It is also unclear whether isolated IS is a primary cause of chronic low back pain. A thorough evaluation of other causes of low back pain should be conducted in all patients who present with low back pain and IS.39,40 Recalcitrant episodes of unilateral leg pain, or back pain associated with leg or thigh radiation, may be attributable to foraminal radiculopathy. Symptoms unrespon-

Fig. 99.2 Sagittal CT-myelogram reconstruction of a grade 2 L5–S1 lytic spondylolisthesis showing foraminal entrapment of the L5 nerve root. This patient was subsequently successfully treated with an L5–S1 transforaminal epidural injection. 1086

Fig. 99.3 Sagittal MRI showing lytic L4–5 spondylolisthesis with entrapment of the exiting L4 root.

A

B Fig. 99.4 (A, B) MRI images of a patient with L5–S1 degenerative spondylolisthesis suffering with longstanding low back and thigh pain who was treated successfully with 1.5 years of complete pain relief with bilateral L5–S1 facet intra-articular corticosteroid injections.

Section 5: Biomechanical Disorders of the Lumbar Spine

A

Fig. 99.5 (A, B) AP and oblique fluoroscopic views of L5–S1 transforaminal epidural injection performed on a patient with a chronic low-grade L5–S1 lytic spondylolisthesis.

B

sive to oral medications and physical therapy will often respond to transforaminal epidural steroid injections. In addition to spinal pathology, degenerative disease in the hip and lower extremities needs to be considered. Clinical evaluation should assess lower extremity flexibility. Short hamstring and iliopsoas muscles may increase the stress on lumbar lordosis and the lumbopelvic motion relationship. Patients with significant restrictions may greatly benefit from physical therapeutic stretching. A kyphotic posture, adopted to reduce pincer effect of lordosis in spinal stenosis, will secondarily lead to shortening of the hip flexors. Chronically shortened hip flexors will aggravate the condition by forcing the patient to effectively increase lordosis when attempting to stand erect.

Table 99.2: Symptom-directed therapeutic interventions in lumbar spondylolisthesis Leg pain

Back/thigh pain

Myofascial pain

NSAID

+

+

+

TCA/ anticonvulsant

+/−

0

+

ESI before PT

Mild stenosis

Moderate/ severe

−

−

−

+

+

+

+

+

MEDICAL REHABILITATION AND INTERVENTIONAL SPINE PROGRAM

ESI if PT fails PT

+

+

++

+

A step-wise approach to treatment can be divided conceptually into three independent but overlapping phases: pain control, stabilization, and a conditioning phase. Treatment interventions can include oral medications, behavioral modifications, physical therapeutics and therapeutic exercise, bracing, and a variety of injection procedures. Therapeutic decisions should be made on the basis of the clinical and radiographic evaluation. Categorizing patient complaints into back pain, leg pain, and myofascial pain can help organize treatment options (Table 99.2). Leg pain not directly attributable to radiculopathy may be caused by somatic referral, hip bursitis, osteoarthritis of the hip or knee, or myofascial pain.41 During the first phase, pain is reduced through oral or injected medication and behavior modification. Bed rest for up to 1 week is reserved for patients presenting with the acute onset of lumbar radiculopathy accompanied by a significant neurologic motor deficit (e.g. foot drop). Otherwise, bed rest should be limited to no more than 2 days. Patients should also be advised to avoid of repetitive extension loading activities. Patients with radiculopathy unresponsive to oral medications, particularly in DSSS, often do not tolerate or benefit from physical therapy. Typically, these individuals require the administration of a transforaminal or interlaminar epidural steroid injection prior to continuation of further physical therapy. Patients with back pain alone should undergo a reasonable trial of oral medication, physical therapy, and/or bracing prior to considering injection interventions.

Facet injections

−

−

++

+

Cardiovascular conditioning

+/−

+/−

+

++

Oral medications Medications for the treatment of various forms of lumbar spondylolisthesis have not been studied. In a large meta-analysis of low back pain,42 there is good evidence supporting the use of nonsteroidal antiinflammatory medications and acetaminophen in the treatment of acute pain, and fair evidence for the use of muscle relaxants. Using these medications may help allow the patient to continue in a physical therapy program. The efficacy of drug therapy for chronic low back pain is less clear. Current controversy surrounds the use of narcotic medication for chronic low back pain.43–46 Patients with significant radiculopathy can be treated with a course of oral corticosteroids and nonsteroidal antiinflammatory medication for 1 week. Although unproven, NSAIDs may be more effective in the treatment of DS because of the presence of facet arthrosis. Anticonvulsant and antidepressant medications should be also be considered for all patients with myofascial pain and for patients presenting with dysesthetic leg pain, especially if the leg pain is nocturnal. Gabapentin has become one of the off-label anticonvulsant drugs most commonly prescribed in the treatment of spinal pain, and 1087

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although the mechanism is unknown, a recent study suggests that gabapentin may be useful in the treatment of patients with neuropathic or myofascial pain.25 A newer variation of gabapentin, pregabelin, may prove to be an even more effective agent. Currently, it is approved in the US for the treatment of neuropathic pain developing from postherpetic neuralgia or diabetic peripheral neuropathy. The mechanism of pain relief for tricyclic medications may be independent from their effect on depression. The positive effects seem to depend on two mechanisms: the blockade of norepinephrine uptake, and its antagonist action on the N-methyl D-aspartate receptor.8,22,27

Physical therapy The initial step in prescribing a physical therapy program depends upon a detailed musculoskeletal assessment. Evaluation of biomechanical relationships is an integral part of this process. Patients who present with concomitant osteoarthritis of the lower extremities (hip, knee, ankle), causing restricted and painful joint range of motion (ROM), will require special consideration. Lower extremity flexibility should be assessed in all patients. Short hamstring and iliopsoas muscles may increase the stress on lumbar lordosis and the lumbopelvic motion relationship. Patients with significant restrictions may greatly benefit from physical therapeutic stretching. A kyphotic posture, adopted to reduce pincer effect of lordosis in spinal stenosis, will secondarily lead to shortening of the hip flexors (Fig. 99.6). Chronically shortened hip flexors will aggravate the condition by forcing the patient to effectively increase lordosis when attempting to stand erect. Early in the treatment program a strategy of pain reduction is implemented to provide sufficient symptom relief to allow the patient to participate in an active therapy program. Progressive exercise may help to increase lumbopelvic muscular stabilization and maintain a better posterior pelvic tilt. It also may improve cardiovascular conditioning and other factors that enhance soft tissue function. The intent of the early therapy is, when possible, to restore and elongate soft tissue changes (hamstrings, hip flexors, paraspinals) that have occurred secondary to stenosis and radiculopathy. Patients may tolerate exer-

Iliotibial band

Quadriceps

Gluteus maximus Tendon Hamstrings

Fig. 99.6 Shorter hip flexors will lead to anterior pelvic rotation and an increase in the effective lumbar lordosis required to resume erect posture. 1088

cise, such as stationary bicycle, performed with the lumbar spine in a flexed posture. Particularly at the outset, patients may require the assistance of a trained therapist when exercising. However, the goal of such therapy should be to establish a more permanent independent exercise program. Studies on low back pain suggest that strong secondary psychologic benefits are derived from positive self-efficacy concepts, and confrontational rather than avoidance behavioral strategies.9,19,32 These strategies are reinforced by the reasonable return to activity program and independent daily exercise program. The benefits of this positive health belief system may be more important than the physiologic counterpart of exercise. Despite this fact, many patients who do not tolerate the transition to exercise may receive benefit from limited passive treatments such as therapeutic modalities of heat, ultrasound, and soft tissue mobilization. When a significant amelioration of painful symptoms occurs, a vigorous cardiovascular conditioning exercise program is typically introduced. While maintaining flexibility and some degree of trunk strength through a program of daily exercise seems to make sense, only fitness has been implied as preventive for lower back pain.1 Patients may be advised to partake in regular and slowly progressive amounts of safe aerobic exercise (exercise bicycle, swimming pool exercise). For cardiovascular conditioning, the authors have found that the upright stationary bicycle is well tolerated. Other patients with a more extensive history of back pain may perform better on recumbent bicycle. Patients are encouraged to increase their tolerance to treadmill in order to develop upright endurance. More functionally advanced patients may be able to use stair climbers or a stairmaster, but these activities present more obvious difficulties to many elderly patients whose balance and coordination may be affected or whom may have hip or knee osteoarthritis. Most patients will be able to exercise on the elliptical machines that build lower extremity endurance and balance without the same degree of axial impact loading.47 Many patients with lytic or degenerative spondylolisthesis of varying severity may be able to successfully return to most sport activities. High-grade spondylolisthesis should be a contraindication to participation in contact sports. Patients can be encouraged to perform exercise and noncontact sports to tolerance. Many can engage in running and tennis even after having experienced significant episodes of radiculopathy (Fig. 99.7). The hypothetical rationale for assessment-based physical therapy requires an understanding of the pathoanatomic process associated with each type of spondylolisthesis. For example, in DSSS, a flexion-biased movement and exercise program is preferable. There are relatively few specific studies confirming the outcome effects of specific therapy.15,47 Sinaki et al.15 reported on the outcomes of 48 patients with symptomatic back pain secondary to spondylolisthesis treated conservatively for 3 years. They compared the outcomes of flexion-biased and extension back strengthening exercise programs. The patients were divided into two groups: those performing flexion, and those performing extension back strengthening exercises. Flexion exercise consisted of partial sit-ups, pelvic tilts, and chest-to-thigh exercises. Extension exercises consisted of upper back extension from the prone position and hip extension from the prone position. At 3 years, overall recovery rate was 62% for the flexion group and 0% for the extension group. O’Sullivan et al.47 prospectively compared the effect of a spine stabilization exercise program with non-specific exercise therapy in 44 patients with spondylolisthesis or spondylolysis. Subjects were randomly assigned to one of the two treatments. At 30 months, the stabilization exercise group experienced significant benefits while those in the non-specific exercise therapy group did not. While the majority of the patients, whose average age was 30 years, appeared to experience chronic low back pain it is unclear how the authors established that symptoms were specifically related to chronic IS.

Section 5: Biomechanical Disorders of the Lumbar Spine

A

B

Bracing Bracing may play a role in early protection of a painful segment while the patient begins a comprehensive stabilization program. In addition to support of the area, both the warmth and proprioception48 gained by the brace may lead to patient comfort. Bracing may be the best option, particularly for debilitated patients when physical therapy would be either difficult or simply pose a health risk. The role of bracing has been studied most extensively in acute IS presenting in young or adolescent patients and is discussed in detail by Frank Lagatutta (see Ch. 129). There is little or no literature investigating the clinical effect of bracing in the conservative management of degenerative spondylolisthesis or spinal stenosis.49 Some authors have advocated a 4–6 week trial of brace management. We have found that soft or semirigid lumbar supportive braces are sufficient for patient comfort and ease of use. Braces will generally be tolerated better by thin than obese patients. Many patients with uncomplicated spondylolisthesis may find that a properly fit spinal orthotic provides comfort and pain relief. Bracing may be indispensable in patients suffering with spondylolisthesis complicated by additional spinal alignment and mechanical problems such as scoliosis, uncompensated scoliosis, lateral listhesis, or hyperlordosisis. The most important aspect of bracing is whether the patient will actually use the device. The authors’ experience is that patients rarely tolerate rigid bracing, whether custom made or the soft spinal variety. Since these orthotics are costly, a realistic appraisal of probable usage should be undertaken prior to providing a prescription for their purchase.

INTERVENTIONAL SPINE TECHNIQUES FOR SPONDYLOLISTHESIS Rationale for use: hypothetical mechanisms Incorporating spinal injection procedures into the rehabilitation program of patients with spondylolisthesis can be an effective tool. When other medical rehabilitation fails (e.g. physical therapy, oral medications) interventional treatment is well recognized as a potent therapeutic aide. As with the development of the medical rehabilitation component of treatment the anticipated success of an injection procedure will depend upon a careful clinical and radiographic assessment of the patient. Ultimately, this allows the spine clinician to determine which spinal structures are pertinent to symptomatic complaints, choosing a logical sequence of treatment interventions, and proper execution of what often are technically demanding procedures (Table 99.3). A detailed evaluation of this nature will maximize the potential benefit of this

Fig. 99.7 (A) An anecdotal but nonetheless noteworthy case of a gentleman who maintained a high-level exercise lifestyle since his youth in spite of a long known history of high-grade lumbosacral spondylolisthesis. Sagittal MRI scan reveals grade 4 or 5 listhesis resulting in canal stenosis across the dome of the sacrum and severe L5 foraminal stenosis (not captured here). (B) Axial MRI show significant L5–S1 stenosis with S1 roots in lateral recesses. At the age of 50, he continues to run upwards of 30 miles per week, in addition to biking and swimming extensively, and has run several marathons. A few episodes of radiculopathy were treated with physical therapy and were self-limited.

therapeutic modality. The extent to which it is used in specific clinical scenarios is a matter of greater controversy and the subject of ongoing investigations. Their effectiveness in maintaining reasonable outcomes in patients with more severe presentations of disease who are otherwise healthy candidates for surgery is one area of debate, whereas treatment is more widely supported for mild to moderate disease.24,50 There is a hypothetical rationale for the use of a spinal injection using glucocorticoids. The pathophysiology explanation for this hormonal therapy stems from evidence that biochemical and neurochemical inflammatory mediators play a role in the occurrence of lumbar radiculopathy.51–57 Inflammatory mediators may also play a role in the pathophysiology of some low back pain when factors including facet joint degenerative arthritis and lumbar radiculopathy are at play.58,59 As previously stated, one should remember that the severity of symptoms is unrelated to the pathologic abnormalities observed with imaging studies. As well, radiographic studies of degenerative spondylolisthesis and spinal stenosis have revealed that radiographic severity imperfectly correlates with symptoms.60–62

Scientific data supporting the use of injections in spondylolisthesis Several reports are available reporting on outcomes of lumbar spinal stenosis treated with epidural steroids.26,63–68 None of these has contained sufficient data to analyze an effect on subgroups with spondylolisthesis. No data are available on the effect of lumbar facet injections and DS. Facet joint injections have questionable efficacy when used on facet joint low back pain in general when defined by response to anesthetic facet block.69–74 Despite this fact, the case for use of facet injections in degenerative spondylolisthesis is intuitively apparent because of the specific aberrant pathomechanics of the disease.13,19 The beneficial effect of epidural steroid injections on patients with DSSS is suggested by several studies assessing those patients with symptoms of lumbar spinal stenosis. Botwin et al. prospectively evaluated 34 stenosis patients for 1 year treated with transforaminal epidural steroid injections.63 Seventy-five percent of patients had successful long-term outcome, reporting at least a >50% reduction between preinjection and postinjection pain scores. Numerous other medical rehabilitation and interventional spine outcome studies for lumbar spinal stenosis have been published.2,16,18,21,31 In 1992, Johnsson et al.75 reported on 32 patients followed up for an average of 49 months (range10–103 months). Fifteen percent of the patients were improved, 70% were the same, and 15% were worse. In that study, the authors did not specify if patients received epidural steroid injection. 1089

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Table 99.3: Injection strategies in lumbar spondylolisthesis Symptoms

Targeted structure

Procedure

DSSS (i.e. L4–5 level)

Leg pain > back pain

L5 root – central

1. IL* ESI 2. L5-S1 TF ESI

DSSS with severe stenosis

Back pain

L5 or S1 roots Facet joint OA Mild radicular pain

L5 –S1 or S1 TF ESI Facet injection IL* ESI or L5-S1 TF ESI

DS L4-5

Back and thigh pain > leg pain

Facet joint OA

1. L4–5 facet joint IA† inj 2. IL* ESI

DS L4–5 complicated by foraminal stenosis (foraminal HNP, scoliosis, facet DJD)

Thigh and leg pain > back pain

L4 root

L4-L5 TF ESI

Chronic L5-S1 IS

Unilateral leg pain Back pain

L5 root – foraminal ? Specific structure-segmental sensitivity/ ‘instability’

L5-S1 TF# ESI Caudal, bilateral S1TF or L5-S1 IL*

*

IL = interlaminar = Intra-articular # - Transforaminal †

In 1996, Atlas and colleagues,64 at 12 months, assessed the outcomes of 81 patients who were treated surgically and 67 patients who were conservatively treated. Although the conditions of those who underwent surgery were clinically and radiographically more severe than in the conservative care group, their outcomes were superior. Only 28% of patients who were treated conservatively reported that their pretreatment symptoms of pain were better or totally abated and for 15% the pain was much worse. An important point to make is that only 18% of patients in the conservative care group were treated with epidural steroid injections. Perhaps a careful strategy of oral medications, specific physical therapy, and injection techniques that are predicated on the pathology, history and exam would provide better outcomes. Certainly, that is the authors’ experience, but it remains an unproven perspective until further scientific inquiry is undertaken. In 1996, Swezey68 reported on the outcomes of 47 patients who had been evaluated 5 years earlier for lumbar spinal stenosis. Patients had symptoms of neurogenic claudication, and CT or MRI findings of moderate to severe stenosis (43 patients) or severe spondylosis by plain radiographs (4 patients). Treatments included education regarding ergonomics and flexion exercise, analgesic medications, intermittent pelvic traction (11 patients), and epidural steroids (13 patients). Eleven patients required laminectomy. Of the patients who were treated conservatively, 43% were improved, while the symptoms of neurogenic claudication were unchanged in 30%. The current authors studied outcomes of 49 patients with stenosis with an average 33 month follow-up (range 16–55) treated with aggressive medical rehabilitation and interventional spine care.26 Eighty-eight percent received an epidural steroid injection. At a mean follow-up time of 33 months, 9 required surgery, 5 were worse, 12 unchanged, 11 mild, and 12 sustained improvement. Thirty percent of patients felt none or mild overall pain. Twenty-two of the 49 studied patients with stenosis also had DSSS. These 22 patients tended to have worse outcomes, but without reaching statistical significance (e.g. 6 of the 22 with DSSS required surgery).

Radiographic and clinical factors to consider The radiographic factors to consider when determining which injection technique or approach to use in patients with spondylolisthesis include assessing the severity and levels of central and or foraminal spinal ste1090

nosis, rating the degree of anterior and/or lateral spondylolisthesis, and assessing the severity of facet joint arthrosis. It is also critically important to analyze concurrent sagittal or coronal plane deformities and their mechanical relationship to generation of pain. Patients may experience symptoms of pain that can be localized to one or more of the following regions: low back, buttock, thigh, and leg. It is helpful to conceptually organize the patient complaints into these categories.

Sequence and timing considerations Epidural steroid injection is generally indicated when other conservative therapies have failed to satisfactorily control pain, or if the intensity is such that engaging in a therapy program is not feasible. While some clinicians have advocated an administration of three epidural injections, usually spaced 1–2 weeks apart, there are no current data to support that this strategy is more effective than a wait and see approach after one initial injection. Additionally, most clinicians perform spinal injections with radiographic control.76,77 The use of fluoroscopy confirms the delivery of medication to the targeted spinal level. Such precision is a special concern for patients with spondylolisthesis. Foraminal stenosis and facet joint arthopathy, common features of the disease, are probably best treated by transforaminal and intra-articular injections which can only be performed correctly with the assistance of radiographic guidance. Most patients with severe symptoms will require more than one injection intervention. A second injection can be repeated within 1–4 weeks. A sufficient interval should transpire to allow the clinician to judge the patient response. In the event that there is no benefit realized following the first injection, a different injection should be considered. For partial responses, a second injection performed within a month of the first may help to solidify gains. Most patients are unlikely to benefit from three or more fluoroscopically confirmed epidural injections during the course of 6–12 months.

Integrating injections with overall management Integrating different levels and stages of treatment into an overall plan is critical to the success of medial rehabilitation and interventional spine treatment for symptomatic spondylolisthesis. Usually, patients present with a mixture of back, thigh, and leg complaints. As stated throughout this chapter, a thorough study of the history, examination, and radiologic findings is essential to achieving success.

Section 5: Biomechanical Disorders of the Lumbar Spine

Unfortunately, even though that process is undertaken, the determination of which injection to perform, where in the spine, and when to do it represents an art form. Although one conceptualizes the process in a methodical way, there are no studies that provide the necessary guidance. As a typical example, a patient suffering with degenerative spondylolisthesis may have excellent relief of leg pain by the administration of a well-placed epidural steroid injection or selective nerve root block. Residual back pain, presumably related to facet joint arthropathy and subluxation may require augmenting therapy later on with fluoroscopically guided facet injections or flexion-biased trunk stabilizing exercise programs and hip flexor range of motion. Some patients with residual back and thigh pain and additional scoliosis deformity may require a period of spinal bracing. In others, the pain may be a consequence of disc pathology, and an interlaminar injection or transforaminal epidural may be needed.

INTERVENTIONAL PROCEDURES

Transforaminal injections Transforaminal epidural steroid injection has become a frequently used epidural route of delivery for many physicians treating their patients with lumbar spondylolisthesis. Some clinicians may prefer to try an interlaminar or caudal epidural steroid injection as an initial treatment before proceeding to the transforaminal route of administration. The transforaminal injection ensures delivery of medication to the targeted nerve root. In the case of degenerative L4–5 spondylolisthesis, spinal stenosis is often present more dramatically at the level of listhesis than other spinal levels. As a result, the central canal tapers at this level. Interlaminar injection at L4–5 may be difficult to perform if there is severe segmental stenosis. Injections placed above and below this tend to diffuse away from the level of stenosis. The transforaminal epidural offers the most direct method of injection. The traversing L5 root is best approached by performing an L5–S1 transforaminal epidural (on the most severely affected side). Needle place-

Trigger point injections Trigger point injections have been widely used by clinicians over the years for problems of lower back pain and sciatica alike. Their widespread use suggests there is some basis for their efficacy but there are no scientific data to support this belief.42 Patients with spondylolisthesis may present with clinical examination findings or exaggerated tenderness in paraspinal, gluteal, or piriformis muscles. Injections to these tender areas may reach the muscles or to some underlying structures such as facet joint arthropathy, trochanteric or gluteal bursitis, and sciatic nerve. Relief may come from resolution of muscle tenderness and spasm, or (when corticosteroid is included in the injection) treatment of the underlying structure, or both. These typical areas of tenderness may be seen in some patients with spondylolisthesis and may be considered as part of the clinical presentation. It is unclear whether these symptoms will resolve with specific spinal injections or whether they require additional therapy. In the authors’ view, it is reasonable to use trigger point therapy (usually with corticosteroid and local anesthetic) on one or two occasions in such patients before proceeding to the more invasive spinal injection procedures. A

Epidural steroid injections Rationale Epidural steroids in spondylolisthesis are indicated for recalcitrant leg pain that can be attributed to radiculopathy. They may also be used in patients with recalcitrant back and/or thigh pain. Many such patients will respond favorably to epidural injection, presumably because these symptoms are caused by a mild form of radiculopathy. Many, but not all, patients with degenerative spondylolisthesis will develop central spinal stenosis, especially in later stages of the disease.16,18,19 Usually, the most severe stenosis will occur at the listhesis level. Normally such patients will respond more favorably to injection targeting the most severely compressed nerve roots, and the rationale for the therapy is the same as has been noted for lumbar stenosis. Central stenosis seems to carry a worse outcome than isolated foraminal stenosis.78 The transiting root will usually be more diseased than the exiting (foraminal root) (Fig. 99.8). The initial injection should target this level. Conversely, patients with lytic spondylolisthesis, with the exception of high-grade severity cases, are unlikely to develop central stenosis at the listhetic level. They often suffer with leg pain symptoms related to foraminal root entrapment and will more likely benefit from injection at the level of entrapment. Lytic spondylolisthesis at the L5–S1 level, particularly those of grade 2 or 3 severity, may develop severe foraminal entrapment (of L5 nerve roots) in adult life. These cases can present a technical challenge for the interventionist.

B Fig. 99.8 (A) Axial MRI of patient with L4–5 spondylolisthesis showing severe subarticular stenosis of the L5 nerve roots (arrows) who presented with left leg pain. (B) Oblique fluoroscopic radiograph of the L5–S1 transforaminal epidural performed on the same patient. The spinal needle (red arrow) is placed just posterior to the L5–S1 facet joint. 1091

Part 3: Specific Disorders

ment just under the L5 pedicle will allow medication flow first to the L5–S1 foramen and L4–5 lateral recess before proceeding into the remainder of the L4–5 epidural space (Fig. 99.9). Patients with bilateral leg pain may be treated with bilateral transforaminal injections. Alternatively, the physician may treat the more severely affected side and hope that some contralateral spread will occur, as it often does. L4 radiculopathies can occur in L4–5 spondylolisthesis. Although less common, foraminal radiculopathies in spondylolisthesis often occur when there is superimposed scoliosis, severe facet arthropathy, or foraminal disc herniation (Figs 99.10, 99.11).

A

B

Some physicians shy away from performing an epidural injection at the most severely affected level and shift the injection down one level hoping to ‘float’ the medication upwards in a more gentle fashion. This may be a reasonable approach. In such a circumstance, an S1 transforaminal epidural would be used to treat an L4–5 DSSS (Fig. 99.12). Concerns with performing the L5–S1 transforaminal epidural include creating too much procedural pain, further sensitizing a severely compressed and inflamed nerve root, and the risk of causing further compression injury incurred by injecting a severely compressed level. These concerns are reasonable, but there are no available reports to support their validity. The degree of L4–5 stenosis and radiculopathy

C

Fig. 99.9 (A–C) Sagittal and axial MRI scans of patient with L4–5 spondylolisthesis with leg pain complaints. She was successfully treated by L5–S1 transforaminal ESI. Note the sharp obstruction of contrast flow at the stenotic L4–5 level.

A

1092

B

Fig. 99.10 A 52-year-old woman with a known history of scoliosis and episodic low back pain presented with symptoms of severe L4 radiculopathy. Routine radiographs showed both anterior and lateral listhesis of L4 on L5. Superimposed was a scoliosis mildly decompensated to the left and with its concavity across the affected segments. MRI demonstrated mild L4/5 segmental central but significant foraminal stenosis noted in (A). In (B), facet arthropathy is more prominent on the left side. An L4–5 transforaminal epidural steroid injection

Section 5: Biomechanical Disorders of the Lumbar Spine

C

D

Fig. 99.11 An axial MRI of a 64-year-old woman who developed an L3–4 lateral disc herniation where she is also noted to have a grade 1 degenerative spondylolisthesis. She responded favorably after receiving an L3–4 foraminal epidural steroid injection.

A

B

Fig. 99.10 Cont’d (C) provided excellent initial relief. She subsequently received L3–4 and L4–5 facet and L5–S1 transforaminal injections and went on to complete recovery.

can be severe enough to effect both L5 and S1 roots, such that injections from the S1 transforaminal approach may be equally or more effective than the L5–S1 transforaminal (Fig. 99.13). Foraminal stenosis such as that noted with lytic spondylolisthesis (IS) is also best treated by transforaminal epidural steroid injection. As in the case of L5–S1 IS, the exiting (L5) nerve root becomes entrapped in the intervertebral foramen by the pars lysis, and the onslaught of vertical (up–down) narrowing in the foramen. Performing a L5–S1 transforaminal epidural, particularly in cases of grade 2 and above spondylolisthesis, can be technically demanding. The sacral lordosis is usually significant and the sacrum has a high horizontal inclination. The L5 vertebra pitches forward and horizontal, deeper within the pelvis. The oblique needle approach is often blocked by the narrow walls of the iliac crest and posterior spine elements which are bunched up by the lordosis (Fig. 99.14). One possible solution is to use a coaxial double-needle technique with double bending. In this case the first spinal needle (usually 20-gauge, 3.5 in) is bent at its tip. The second needle (25-gauge, 6 in) is curved more dramatically

Fig. 99.12 (A) MRI of a patient with L4–5 degenerative spondylolisthesis. (B) Axial MRI of same patient shows severe central and right lateral recess stenosis. Additionally, there is severe facet joint arthropathy. (Continued) 1093

Part 3: Specific Disorders

C

Fig. 99.12 Cont’d (C, D) Right L5–S1 transforaminal epidural was performed followed by a L4–5 facet injection to address both thigh and distal leg complaints. Note the obstruction of epidural contrast at the L4–5 disc space level.

D

Fig. 99.13 Axial MRI demonstrating stenosis associated with degenerative spondylolisthesis. The patient presented with severe leg pain and dense L5 and S1 radiculopathy as assessed by MRI. An L5–S1 and an S1 transforaminal ESI was administered with good results. A

Fig. 99.14 AP X-ray of high-grade L5–S1 spondylolisthesis. The L5 vertebra is rotated nearly horizontal and anterior to the sacrum (white arrows). The sacral ala (black arrows) is actually rostral to the L5 transverse process. The L5–S1 foramen lies in a plane between the two, making needle access with standard techniques impossible.

than the first, such as to afford the most acute 90° turn of the needle upon passing deep to the obstructing posterior elements. This allows a passage to the deeper-seated L5–S1 foramen (Fig. 99.15). Radiculopathies that occur after laminectomy surgery without fusion for DSSS often result from residual foraminal stenosis at the level of listhesis. Decompression surgery may have the effect of worsening the degree of vertebral subluxation and can potentially aggravate or initiate radicular symptoms of foraminal stenosis. The presence of even a small degree of scoliosis or asymmetric disc space collapse can amplify the problem. In such cases, a transforaminal 1094

B

Fig. 99.15 (A) Fluoroscopic image of L5–S1 transforaminal ESI using a doubleneedle/double-bend technique. (B) Lateral fluoroscopic view of a L4–5 transforaminal ESI. Degenerative spondylolisthesis is present at both L3–L4 and L4–L5.

epidural is the procedure of choice. In the case of a decompressed L4–5 spondylolisthesis, a patient can experience residual L4 radicular pain. The target for needle placement, normally the undersurface of the L4 pedicle at its root from the vertebral body, can be deceiving in such cases because of distortion of the spatial relationships caused by the spondylolisthesis. The L4 vertebral body sits more anterior (or deeper) than the L5 body; the L4 nerve root and its passage in the L4–5 intervertebral foramen have moved further anterior alongside the elongated L4–5 facet joint than might be expected.

Section 5: Biomechanical Disorders of the Lumbar Spine

Interlaminar and caudal epidural injections

Choosing levels

Some clinicians will routinely use caudal or interlaminar injection as the initial procedure. The caudal approach is safe, usually easy to perform, and small needle manipulations will insure a bilateral spread of injection. Observation of contrast penetration suggests most of the injection will spread onto the L5 and sacral roots, but doubtfully above this level. In spite of this limitation, many clinicians will employ the caudal technique for stenosis problems up to the L3–4 level. The interlaminar technique can be an effective means of delivering epidural steroid injections for lumbar radiculopathies. Technical shortcomings make this a less commonly used procedure for fluoroscopically guided injections in spondylolisthesis. Injectant flow is difficult to control and less liable to spread in the stenotic lateral recess and foramen. In cases of severe stenosis, there is a greater risk of dural puncture and, in some cases, it is technically impossible to perform due to degenerative diminution of the interlaminar space Furthermore, even with careful midline placement, interlaminar injectant spread is frequently unilateral only. Nonetheless, the interlaminar epidural may be a good way to spread epidural steroid medication in cases where multilevel stenosis accompanies the spondylolisthesis. If possible, an injection placed in between two levels of stenosis will be contained and spread amongst the roots affected (i.e. for L2–3, L3–4, L4–5 stenosis, a placement at the L3–4 level).

Typically, in degenerative spondylolisthesis, the facet joint has been remodeled to assume a more sagittal axis. An injection targeting the aperture of the joint is often best approached from a more AP fluoroscopic projection than the oblique projections usually used. For many patients, chronic back pain and DS will have more than one level of facet joint degenerative arthropathy with or without other levels of spondylolisthesis. These patients may also have hyperlordosis of the lumbar spine. Often, multilevel facet injections are needed, although an initial trial of facet injections at the level of DS is a reasonable way to initiate therapy. Scientific data supporting the use of facet injections for spondylolisthesis are surmised from clinical outcome studies regarding the efficacy of facet injections for non-specific low back pain.69,71,74 There is also speculation as to whether radiographic findings such as facet joint arthropathy can be used to identify ‘facet joint pain.’73,81,82 The authors are not aware of any study with sufficient numbers of patients to specifically identify efficacy of this intervention for spondylolisthesis. At best they can postulate that the pathomechanics of DS and the increased stress to posterior elements of the spine suggest that facet injections may be effective. The efficacy of facet injections in patients with IS is somewhat more dubious. In such cases, transmission of load forces across the neural arch is interrupted by the pars lysis. Usually, the facet joint below the lysis will appear on radiographs not to have undergone any degenerative change. Some clinicians have suggested injection of the pars defect as a diagnostic or therapeutic tool for patients with chronic low back pain. The rationale is unclear since chronic low-grade lytic spondylolisthesis does not always result in chronic low back pain and in those cases where it is imputed as the cause, it is less than clear that the pars region is a focal pain generator. It has been substantiated that the fibrous union of a pars interarticlaris fracture contains neural elements.83 Some spine interventionists attempted to perform diagnostic pars interarticualris fracture injections. In one unreported series of 50 cases, not a single diagnostic injection, using 0.5 cc of 2% xylocaine, was reported as positive (Slipman C. Unpublished). There may be a role for therapeutic corticosteroid facet injections in athletes with healed or chronic spondylolysis and persistent chronic low back pain. The supernormal stresses in their sport activity (i.e. gymnasts, football lineman, cricket bowlers) sustained to the posterior elements of their spine which presumably caused their stress reaction or fracture, may persist in causing facet joint arthropathy. For these reasons, some clinicians have noted anecdotally success in cases of recalcitrant back pain in high-level athletes.

Outcome studies There are limited scientific data available regarding the efficacy of medical rehabilitation and interventional spine treatment for lumbar spinal stenosis.26,63,64,66,79,80 The extent to which such information can be applied to patients with spondylolisthesis is unclear. Patients with spondylolisthesis and stenosis may have better or worse outcomes than patients with stenosis alone. None of the available studies regarding spinal stenosis explicitly identify the occurrence of spondylolisthesis, nor do they contain significant numbers of cases to study outcome efficacy.

Facet joint injection Rational The rationale for using facet injections in the treatment of patients with spondylolisthesis emerges from several observations. The degenerative deterioration of the facet joint that occurs with the progression of degenerative spondylolisthesis suggests it has a central role in pain and inflammation, prima facie. Facet joints are a primary restraint for anterior listhesis so they are presumable receiving accentuated stress and shear forces. Patients with degenerative spondylolisthesis often present in the earlier phases of disease with symptoms of back and thigh pain, which is a proven pain referral pattern of the lumbar facet joints.16,18,19 Radiographically guided intra-articular facet injection may be the injection treatment of choice in patients with lumbar degenerative spondylolisthesis presenting with back, buttock, and thigh pain or combinations thereof. Facet injections for these patients, especially those presenting without significant concomitant stenosis, may be more effective than epidural steroid injection. Nonetheless, may clinicians may opt to use the epidural steroid as the initial procedure. A reason underpinning this decision is the overall greater scientific evidence for their efficacy than for facet injection in patients with back pain and sciatica.69,71,74 A second reason is that the facet joint injection into a degenerated structure is more tedious and technically demanding to perform.

Radiofrequency denervation Radiofrequency denervation (RFD) of lumbar facet joints by medial branch nerve ablation may be effective in limiting chronic low back pain in patients with DS who have already experienced relief from facet joint block procedures. There is scant medical evidence to support the long-term efficacy of RFD. A limited number of studies suggest about a 60% carryover rate of success from facet block to RFD and the authors suspect the success may be even less in cases of spondylolisthesis. RFD may be considered in patients with proven facet joint arthropathy and DS, for whom corticosteroid injections poses greater medical risk (diabetes, congestive heart failure).

SUMMARY Patients presenting with back pain with or without leg pain and radiographic evidence of spondylolisthesis represent a spectrum of different clinical entities with potentially different associated out-

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comes. The radiographic assessment of spondylolisthesis does not automatically determine outcome or treatment. Radiographic assessment is more involved than simply identifying the presence or severity of spondylolisthesis. Specifically, DS, DSSS, and IS appear to have a different pathoanatomy and clinical course. Other radiographic variables that must be considered include sagittal and coronal plane deformity, and the extent of spondylotic changes. Most importantly, the proper diagnosis and characterization of the patient’s condition involves a synthesis of clinical and radiographic information. A clinical evaluation of the patient history of pain and disability, history of medical comorbities, and psychologic and social factors are extremely important. Additionally, physical examination findings of neuromuscular status, flexibility, soft tissue sensitivity, and general fitness also should be conducted. The implementation of medical rehabilitation and interventional spine therapeutic strategies requires the symptoms to be conceptually organized into categories of back, buttock, thigh, leg, or pain. The combination of symptom location and provocative influences aid in determining the relative contribution of facet, disc, root or myofascial pain. Using this paradigm enables the spine clinician to devise an individualized conservative care program. Similarly, such a process prevents the repeated institution of failed conservative measures when surgical treatment is required.

References 1. Karjalainen K, Malmivaara A, van Tulder M, et al. Multidisciplinary biopsychosocial rehabilitation for subacute low back pain among working age adults. Cochrane Database Syst Rev 2000; CD002193. 2. Schultz IZ, Crook JM, Berkowitz J, et al. Biopsychosocial multivariate predictive model of occupational low back disability. Spine 2002; 27(23):2720–2725. 3. Wand BM, Bird C, McAuley JH, et al. Early intervention for the management of acute low back pain: a single-blind randomized controlled trial of biopsychosocial education, manual therapy, and exercise. Spine 2004; 29(21):2350–2356. 4. Seers K. Review: intensive multidisciplinary biopsychosocial rehabilitation reduces pain and improves function in chronic low back pain. Evid Based Nurs 2002; 5(4):116.

18. Frymoyer JW. Degenerative spondylolisthesis: diagnosis and treatment. J Am Acad Orthop Surg 1994; 2(1):9–15. 19. Newman PH. Degenerative spondylolisthesis. J Bone Joint Surg 1976; 58(2): 184–192. 20. Bassewitz H, Herkowitz H. Lumbar stenosis with spondylolisthesis: current concepts of surgical treatment. Clin Orthop 2001; 384:54–60. 21. Grobler LJ, Robertson PA, Novotny JE, et al. Decompression for degenerative spondylolisthesis and spinal stenosis at L4–5. The effects on facet joint morphology. Spine 1993; 18(11):1475–1482. 22. Herkowitz HN, Kurz LT. Degenerative lumbar spondylolisthesis with spinal stenosis. A prospective study comparing decompression with decompression and intertransverse process arthrodesis. J Bone Joint Surg [Am] 1991; 73(6):802–808. 23. Rosenberg NJ. Degenerative spondylolisthesis: surgical treatment. Clin Orthop 1976; 117:112–120. 24. Wiltse LL, Kirkaldy-Willis WH, McIvor GW. The treatment of spinal stenosis. Clin Orthop 1976; 115:83–91. 25. Du Priest CM. Nonoperative management of lumbar spinal stenosis. J Manip Phys Ther 1993; 411–414. 26. Simotas AC, Dorey FJ, Hansraj KK, et al. Nonoperative treatment for lumbar spinal stenosis. Clinical and outcome results and a 3-year survivorship analysis. Spine 2000; 25(2):197–203. 27. Johnson AC, Power TC. Combined neurosurgical–orthopedic approach to the correction of radiculopathy and instability in spondylolysis and spondylolisthesis. Int Surg 1984; 69(4):345–350. 28. Rosomoff HL. Lumbar spondylolisthesis: etiology of radiculopathy and role of the neurosurgeon. Clin Neurosurg 1980; 27:577–590. 29. Stears JC. Radiculopathy in spondylosis/spondylolisthesis. The laminar/ligamentum flavum process. Acta Radiol Suppl 1986; 369:723–726. 30. Saifuddin A, Burnett SJ. The value of lumbar spine MRI in the assessment of the pars interarticularis. Clin Radiol 1997; 52(9):666–671. 31. Virta L, Osterman K. Radiographic correlations in adult symptomatic spondylolisthesis: a long-term follow-up study. J Spinal Disord 1994; 7(1):41–48. 32. Lonstein JE. Spondylolisthesis in children. Cause, natural history, and management. Spine 1999; 24(24):2640–2648.

5. Nielson WR, Weir R. Biopsychosocial approaches to the treatment of chronic pain. Clin J Pain 2001; 17(4 Suppl):S114–S127.

33. Danielson BI, Frennered AK, Irstam LK. Radiologic progression of isthmic lumbar spondylolisthesis in young patients. Spine 1991; 16(4):422–425.

6. Truchon M. Determinants of chronic disability related to low back pain: towards an integrative biopsychosocial model. Disabil Rehabil 2001; 23(17):758–767.

34. Saraste H, Brostrom LA, Aparisi T. Prognostic radiographic aspects of spondylolisthesis. Acta Radiol Diagn (Stockh) 1984; 25(5):427–432.

7. Karjalainen K, Malmivaara A, van Tulder M, et al. Multidisciplinary biopsychosocial rehabilitation for subacute low back pain in working-age adults: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2001; 26(3):262–269.

35. Saraste H. Spondylolysis and spondylolisthesis. Acta Orthop Scand Suppl 1993; 84–86.

8. Waddell G. Biopsychosocial analysis of low back pain. Baillières Clin Rheumatol 1992; 6(3):523–557. 9. Wiltse LL, Newman PH, Macnab I. Classification of spondylolysis and spondylolisthesis. Clin Orthop Relat Res 1976; 117:23–29. 10. Berlemann U, Jeszenszky DJ, Buhler DW, et al. Facet joint remodeling in degenerative spondylolisthesis: an investigation of joint orientation and tropism. Eur Spine J 1998; 7(5):376–380. 11. Berlemann U, Jeszenszky DJ, Buhler et al. The role of lumbar lordosis, vertebral end-plate inclination, disc height, and facet orientation in degenerative spondylolisthesis. J Spinal Disord 1999; 12(1):68–73.

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17. Matsunaga S, Ijiri K, Hayashi K. Nonsurgically managed patients with degenerative spondylolisthesis: a 10- to 18-year follow-up study. J Neurosurg 2000; 93(2 Suppl):194–198.

36. Seitsalo S, Osterman K, Poussa M, et al. Spondylolisthesis in children under 12 years of age: long-term results of 56 patients treated conservatively or operatively. J Pediatr Orthop 1988; 8(5):516–521. 37. Seitsalo S. Operative and conservative treatment of moderate spondylolisthesis in young patients. J Bone Joint Surg [Br] 1990; 908–913. 38. Seitsalo S, Osterman K, Hyvarinen H, et al. Progression of spondylolisthesis in children and adolescents. A long-term follow-up of 272 patients. Spine 1991; 16(4):417–421. 39. Andersson GB. What are the age-related changes in the spine? Baillières Clin Rheumatol 1998; 12(1):161–173. 40. Ventura JM, Justice BD. Need for multiple diagnosis in the presence of spondylolisthesis. J Manipulative Physiol Ther 1988; 11(1):41–42.

12. Cinotti G, Postacchini F, Fassari F, et al. Predisposing factors in degenerative spondylolisthesis. A radiographic and CT study. In Orthop 1997; 21(5):337–342.

41. Spivak JM. Current concepts review: degenerative lumbar spinal stenosis. J Bone Joint Surg [Am] 1998; 80(7):1053–1066.

13. Farfan HF. The pathological anatomy of degenerative spondylolisthesis. A cadaver study. Spine 1980; 5(5):412–418.

42. Deyo RA. Drug therapy for back pain. Which drugs help which patients? Spine 1996; 21(24):2840–2849.

14. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al. Pathology and pathogenesis of lumbar spondylosis and stenosis. Spine 1978; 3(4):319–328.

43. Bartleson JD. Evidence for and against the use of opioid analgesics for chronic nonmalignant low back pain: a review. Pain Med 2002; 3(3):260–271.

15. Sinaki M, Lutness MP, Ilstrup DM, et al. Lumbar spondylolisthesis: retrospective comparison and three-year follow-up of two conservative treatment programs. Arch Phys Med Rehabil 1989; 70(8):594–598.

44. Breckenridge J, Clark JD. Patient characteristics associated with opioid versus nonsteroidal antiinflammatory drug management of chronic low back pain. J Pain 2003; 4(6):344–350.

16. Matsunaga S, Sakou T, Morizono Y, et al. Natural history of degenerative spondylolisthesis. Pathogenesis and natural course of the slippage. Spine 1990; 15(11):1204–1210.

45. Mullican WS, Lacy JR. Tramadol/acetaminophen combination tablets and codeine/ acetaminophen combination capsules for the management of chronic pain: a comparative trial. Clin Ther 2001; 23(9):1429–1445.

Section 5: Biomechanical Disorders of the Lumbar Spine 46. van Tulder MW, Koes BW, Bouter LM, et al. Management of chronic nonspecific low back pain in primary care: a descriptive study. Spine 1997; 22(1):76–82.

65. Hoogmartens M, Morelle P. Epidural injection in the treatment of spinal stenosis. Acta Orthop Belg 1987; 53(2):409–411.

47. O’Sullivan PB, Phyty GD, Twomey LT, et al. Evaluation of specific stabilizing exercise in the treatment of chronic low back pain with radiologic diagnosis of spondylolysis or spondylolisthesis. Spine 1997; 2959–2967.

66. Onel D, Sari H, Donmez C. Lumbar spinal stenosis: clinical/radiologic therapeutic evaluation in 145 patients. Conservative treatment or surgical intervention? Spine 1993; 18(2):291–298.

48. McNair PJ, Heine PJ. Trunk proprioception: enhancement through lumbar bracing. Arch Phys Med Rehabil 1999; 80(1):96–99.

67. Rydevik BL, Cohen DB, Kostuik JP. Spine epidural steroids for patients with lumbar spinal stenosis. Spine 1997; 22(19):2313–2317.

49. Prateepavanich P, Thanapipatsiri S, Santisatisakul P, et al. The effectiveness of lumbosacral corset in symptomatic degenerative lumbar spinal stenosis. J Med Assoc Thai 2001; 84(4):572–576.

68. Swezey RL. Outcomes for lumbar stenosis: A five-year follow-up study. J Clin Rheumatol 1996; 129–134.

50. Kirkaldy-Willis WH, Burton CV. Managing low back pain. New York: Churchill Livingstone; 1992:254–256. 51. Burke JG, Conhyea D, McCormack D, et al. Human nucleus pulposus can respond to a pro-inflammatory stimulus. Spine 2003; 28(24):2685–2693. 52. Habtemariam A, Virri J, Gronblad M, et al. The role of mast cells in disc herniation inflammation. Spine 1999; 24(15):1516–1520. 53. Kang JD, Georgescu HI, McIntyre-Larkin L, et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 1996; 21(3):271–277. 54. Miyamoto H, Saura R, Harada T, et al. The role of cyclooxygenase-2 and inflammatory cytokines in pain induction of herniated lumbar intervertebral disc. Kobe J Med Sci 2000; 46(1–2):13–28.

69. Carrera GF. Lumbar facet joint injection in low back pain and sciatica: preliminary results. Radiology 1980; 137(3):665–667. 70. Carrera GF, Williams AL. Current concepts in evaluation of the lumbar facet joints. Crit Rev Diagn Imaging 1984; 21(2):85–104. 71. Dreyfuss PH, Dreyer SJ, Herring SA. Lumbar zygapophyseal (facet) joint injections. Spine 1995; 20(18):2040–2047. 72. Jackson RP, Jacobs RR, Montesano PX. 1988 Volvo Award in Clinical Sciences. Facet joint injection in low back pain. A prospective statistical study. Spine 1988; 13(9):966–971. 73. Lau LS, Littlejohn GO, Miller MH. Clinical evaluation of intra-articular injections for lumbar facet joint pain. Med J Aust 1985; 143(12–13):563–565. 74. Lilius G, Laasonen EM, Myllynen P, et al. Lumbar facet joint syndrome. A randomised clinical trial. J Bone Joint Surg [Br] 1989; 71(4):681–684.

55. Claman HN. Corticosteroids and lymphoid cells. N Engl J Med 1972; 287(8): 388–397.

75. Johnsson KE, Rosen I, Uden A. The natural course of lumbar spinal stenosis. Clin Orthop 1992; 279:82–86.

56. Rinehart JJ, Sagone AL, Balcerzak SP, et al. Effects of corticosteroid therapy on human monocyte function. N Engl J Med 1975; 292(5):236–241.

76. Mehta M, Salmon N. Extradural block. Confirmation of the injection site by X-ray monitoring. Anaesthesia 1985; 40(10):1009–1012.

57. Weinstein SM, Herring SA, Derby R. Contemporary concepts in spine care. Epidural steroid injections. Spine 1995; 20(16):1842–1846.

77. White AH. Injection techniques for the diagnosis and treatment of low back pain. Orthop Clin North Am 1983; 14(3):553–567.

58. Igarashi A, Kikuchi S, Konno S, et al. Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders. Spine 2004; 29(19): 2091–2095.

78. Porter RW, Hibbert C, Evans C. The natural history of root entrapment syndrome. Spine 1984; 9(4):418–421.

59. Willburger RE, Wittenberg RH. Prostaglandin release from lumbar disc and facet joint tissue. Spine 1994; 19(18):2068–2070. 60. Boden S, Davis D, Dina T, et al. Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg 1990; 72(3):403–408. 61. Herno A, Airaksinen O, Saari T. Computed tomography after laminectomy for lumbar spinal stenosis. Patients’ pain patterns, walking capacity, and subjective disability had no correlation with computed tomography findings. Spine 1994; 19(17):1975–1978. 62. Herno A, Airaksinen O, Saari T, et al. The predictive value of preoperative myelography in lumbar spinal stenosis. Spine 1994; 19(12):1335–1338. 63. Botwin KP, Gruber RD, Bouchlas CG, et al. Fluoroscopically guided lumbar transformational epidural steroid injections in degenerative lumbar stenosis: an outcome study. Am J Phys Med Rehabil 2002; 81(12):898–905.

79. Amundsen T, Weber H, Nordal H, et al. Lumbar spinal stenosis: conservative or surgical management?: a prospective 10-year study. Spine 2000; 25(11):1424–1436. 80. Dilke TF, Burry HC, Grahame R. Extradural corticosteroid injection in management of lumbar nerve root compression. Br Med J 1973; 2(5867):635–637. 81. Revel ME, Listrat VM, Chevalier XJ, et al. Facet joint block for low back pain: identifying predictors of a good response. Arch Phys Med Rehabil 1992; 73(9): 824–828. 82. Schwarzer AC, Wang SC, O’Driscoll D, et al. The ability of computed tomography to identify a painful zygapophyseal joint in patients with chronic low back pain. Spine 1995; 907–912. 83. Eisenstein SM, Ashton IK, Roberts S, et al. Innervation of the spondylolysis ‘ligament.’ Spine 1994; 19(8):912–916.

64. Atlas SJ, Deyo RA, Keller RB, et al. The Maine Lumbar Spine Study, part iii. 1-year outcomes of surgical and nonsurgical management of lumbar spinal stenosis. Spine 1996; 21(15):1787–1794.

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Section 5

Biomechanical Disorders of the Lumbar Spine ■ ii: Spondylolisthesis

CHAPTER

Surgical Management of Isthmic, Dysplastic and Degenerative Spondylolisthesis

100

Yizhar Floman INTRODUCTION

INDICATIONS FOR SURGERY

Spondylolisthesis is a common radiological and clinical condition that may arise as a result of different developmental and pathological processes. Although the classification system proposed by Wiltse, Newman, and McNab is the most widely accepted1 there is no consensus which classification system is the most appropriate for clinical decision-making.1–3 Most authorities agree that the presence or absence of an isthmic defect or elongated pars in conjunction with the presence or absences of dysplastic changes are the most important features of any classification system.2,3 Some types of spondylolisthesis occur only in adults (i.e. degenerative), while others are encountered mostly in children and adolescents (dysplastic). Although isthmic spondylolisthesis is present in both children and adolescents as well as in adults, the clinical presentation and natural history of this type of spondylolisthesis differ in the two age groups. It is obvious, therefore, that the recommended management of isthmic spondylolisthesis in adolescents may differ from the desirable management in adults. Some types of spondylolisthesis require simple and standard surgical management, others require the most complex and challenging surgery. Many reports on the surgical management of spondylolisthesis lump together different types of spondylolisthesis, different age groups, and are at best anecdotal and retrospective. Only a few well-conducted outcome studies4–6 on the surgical management of spondylolisthesis have been published on well-defined populations with similar types of vertebral slip (isthmic or degenerative). It is not surprising, therefore, that the surgical management of the various types of spondylolisthesis is not yet standardized and depends among other factors on the severity of the slip. Therefore, the type and extent of the surgical management is often controversial. This controversy is well reflected in the literature.7 The goal of surgery in spondylolisthesis is to reconstruct the normal anatomy whenever possible (pars repair), to restore the normal sagittal profile of the spine (reduction), to sacrifice as few motion segments as possible and, by doing the above, alleviate back and leg pain to promote daily and recreational activities. Since there is no standard type of operation, the most suitable surgical solution should be tailored to the individual case, taking into consideration not only gender, chronological age, and the amount of the slip but also the presence of dysplastic and/or degenerative changes, as well as the global sagittal balance. The most common types of spondylolisthesis encountered clinically are isthmic, dysplastic, and degenerative, and these types will be discussed in detail in this chapter. The rare types of spondylolisthesis such as traumatic, pathologic, or iatrogenic will not be discussed in this chapter, although these should be managed according to the same guidelines outlined throughout the chapter.

The indications for surgical intervention in spondylolisthesis are the same as in any other spinal pathology: pain that does not respond to medical rehabilitation and interventional spine management, functional impairment, neurological deficit, and progressive deformity (vertebral slip).

Adolescents Wiltse and Jackson8 outlined the guidelines for the management of spondylolysis and spondylolisthesis in children. Failure of adequate conservative management (discussed in the previous chapter), may dictate the need for surgical intervention, including surgical stabilization.9 In general, most low-grade isthmic slips are managed successfully with nonoperative treatment and only one-third of patients will require surgery.10 Adolescents and young adults with spondylolysis may be managed with pars interarticularis repair. Surgical stabilization should be strongly considered, in symptomatic adolescents with slips between 25% and 50%, and in asymptomatic individuals in whom slip progression is documented radiologically. Surgical stabilization is mandatory in slips greater than 50%, or when the slip angle exceeds 45 degrees, even in the absence of symptoms, as further slip progression will certainly occur.8,11,12

Adults In adults with low back pain and/or sciatica, the mere presence of spondylolysis or minimal olisthesis is not by itself an indication for surgery. Symptoms may not be directly related to these abnormalities, which probably developed many years prior to the current complaint. The cause of pain may be the result of a lesion elsewhere in the spine. Nevertheless, after the fourth decade of life some adults with a mild slip present with back and leg pain, due to superimposed degenerative changes either at the slip level or at the level above the spondylolisthesis. In addition, adult slip progression secondary to the degeneration of the disc at the slip level may occur in up to 20% of adults with low-grade isthmic slip.13 If conservative measures fail to control low back and or leg pain, operative treatment may be indicated.4,14

OPTIONS FOR SURGICAL MANAGEMENT In general, the surgical options in the management of spondylolysis and spondylolisthesis are as follows: pars repair, neural decompression without or with stabilization, and fusion (without or with decompression). Spinal fusion can be approached with various techniques: (1) posterolateral in situ fusion with or without instrumentation, (2) circumferential in situ fusion (anterior interbody or posterior

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interbody fusion), (3) slip reduction and posterolateral fusion or circumferential procedures with or without sacral dome resection, and (4) in spondyloptosis slip reduction or L5 excision and fusion of L4 to the sacrum.

Spondylolysis: pars repair A direct repair of a pars defect, which is in essence a stress fracture, is a logical operative solution in patients with symptomatic spondylolysis. Repair of the pars restores normal anatomy, without loss of segmental motion, and does not require an extensive surgery since fusion is avoided.15 It may also reduce mechanical stress on the adjacent spinal levels. A prerequisite for the procedure is the presence of a type IIA pars defect1 and a nondysplastic posterior arch, together with a normal disc and facet joints at the involved level. To better delineate which patients are suitable candidates for pars repair, lidocaine infiltration of the pars under fluoroscopy may be helpful. Postinjection pain relief and the presence of a pars defect smaller than 7 mm, are the best predictors for clinical success of this surgical procedure.15,16 Pars repair can also be considered in individuals with a minimal slip without disc degeneration. There are several operative methods available to achieve this goal. The most commonly used techniques are Buck’s screw fixation,17 Scott’s transverse process wiring,18 or Morscher’s hook screw device.19 Biomechanical testing has demonstrated that pars screws or devices that rely on pedicle screw fixation provide better mechanical stability and minimize stress across the pars defect.20 In all pars repair techniques the need to excise the pars pseudoarthrosis, freshen the bone edges, and to apply locally cancellous bone graft is of utmost importance. A brace is worn after surgery for at least 8–12 weeks. Bradford and Iza18 reported on their experience with the Scott’s wiring technique in 22 patients. They found that the clinical outcome of the Scott’s wiring was favorable in 80% of the patients, and 90% obtained a pars defect fusion. Johnson and Thompson21 found that the clinical outcome of the Scott’s wiring was favorable in individuals with spondylolysis younger than 25 years of age. Buck reported on his experience with the Buck screw in 75 patients. The surgical outcome was good in 88%.17 Hefti et al.19 reported on their experience with the Morscher hook screw technique for direct repair of the pars in 33 patients. Pain relief was attained in 79% of patients and a healed pars was observed in 73%. The largest series of patients with pars repair published to date included 113 individuals who underwent pars repair with the Morscher device and were followed for an average of 11 years.16 Union of the pars defect was achieved in 87%. Pseudoarthrosis rates were found to be four times higher in patients older than 20.16

Decompression in isthmic and dysplastic spondylolisthesis When radicular pain, as opposed to back pain, is the main complain of the patient, even in the absence of neurological deficit, neural decompression may be in indicated. Gill22 suggested removing the loose posterior elements and the fibrocartilagenous pars defect in order to decompress the neural elements without performing arthrodesis, and argued that this was the management of choice for symptomatic spondylolisthesis. He indeed published a report of a series of patients in whom pain alleviation was achieved with laminectomy alone, without arthrodesis. However, when one considers that spondylolisthesis is by definition an unstable condition, surgical damage to the posterior ligamentous structures by performing a laminectomy will render the spine even more unstable. Indeed, Gill himself noted some increase in the amount of vertebral slip in about 40% of his patients. Others have documented a more pronounced postoperative slip progression following laminectomy without fusion, not only in children and 1100

adolescents but also in young adults under the age of 40.8,11,23,24 Gill’s laminectomy, when performed alone, is mentioned only to be condemned, especially in children and adolescents. Carragee considers it futile performing decompressive laminectomy in adults with mild isthmic slip without neurological signs as it does not improve the clinical outcome and may increase the rate of pseudoarthrosis following noninstrumented spondylodesis.5 Combining decompressive laminectomy with pedicular screw fixation will provide better clinical results.5 Carragee’s experience echoes earlier reports that decompression is not always mandatory in patients with radicular pain. Posterolateral fusion alone will often eliminate radicular symptoms.25,26 The absolute indications for decompression in spondylolisthesis are: symptomatic radiculopathy with motor deficit, or sphincteric involvement. While isthmic spondylolisthesis is a pathological condition in which ‘canal expansion’ is the rule (as the loose lamina remains behind the slipped body), dysplastic spondylolisthesis is a pathological condition that leads to significant spinal canal stenosis (the lamina remains intact and by slipping forward constricts the cauda equina). Therefore, in cases of symptomatic, dysplastic spondylolisthesis with a forward slip greater than 25%, a laminectomy should always be performed.

Posterolateral in situ fusion In low-grade olisthesis For more than five decades in situ posterolateral fusion with iliac crest bone graft was the most commonly applied surgical procedure for low-grade isthmic spondylolisthesis and is considered even today as the gold standard, especially in children and adolescents.24 Although anatomical reduction of the slip may be desirable, restoration of function with minimal risk to the patient is the ultimate goal of surgery in spondylolisthesis. In low-grade slips in situ arthrodesis carries a minimal risk, and leads to good or excellent clinical results in most patients. Reports on the successes of in situ posterolateral monosegmental fusion with or without Gill’s decompression date back to the late 1950s and early 1960s.27,28 Two retrospective studies reviewed almost 300 patients, and reported greater than 80% fusion rates and a clinically asymptomatic postoperative result.27,28 Wiltse and Jackson8 popularized the paraspinal approach for in situ arthrodesis. The procedure is carried out through a midline skin incision, followed by bilateral incision of the thoracolumbar fascia and bilateral muscle splitting through the sacrospinalis with exposure of the lateral gutters and the transverse processes. Arthrodesis extends from the transverse processes of L5 to the sacral alae. Autologous iliac crest bone graft is laid down. The results of in situ fusion are good to excellent in most cases with fusion rates of 68–100%.8,29–31 Postoperative management may include cast or brace immobilization, although many surgeons do not apply postoperative immobilization at all.8,31 Postoperative immobilization may be recommended if decompression was performed in addition to the spondylodesis or in patients with slips greater than Meyerding 2. Decompression should be performed in conjunction with arthrodesis whenever a focal neural deficit correlating with the spinal imaging is present.11 It was already noted that some surgeons8,25,26 do not perform decompression in conjunction with arthrodesis in both adolescents and adults, as in situ fusion alone was found to eliminate neurologic symptoms. In general, the results obtained in adults with in situ fusion are not as good as in children and adolescents,32–34 not only because of the associated degenerative changes which may be present above and at the slip level, but also due to smoking status and workmen’s compensation claims.33 Haraldsson and Wilner34 conducted a comparative study of posterolateral fusion in adolescents and adults and noted that only 57% of adults with a lumbosacral slip who underwent fusion had a good clinical result as opposed to the 95% successes rate obtained in

Section 5: Biomechanical Disorders of the Lumbar Spine

children and adolescents. In contrast to the different clinical outcome observed in the two groups, fusion rates approached 100% in both adolescents and adults.34 More recently, and in considerable contrast to the last three cited reports,32–34 Moller and Hedlund4 reported a high success rate of in situ fusion in adults with low-grade slips. One hundred and eleven patients were randomly allocated to either an exercise program or posterolateral fusion. At a minimum 2-year follow-up, patients subjected to surgical fusion had statistically superior results on both the Disability Rating Index and the visual analog scale.4 Moller and Hedlund4 concluded that posterolateral fusion is a method supported by evidence-based medicine standards to reduce back pain and functional disability in adult isthmic spondylolisthesis. They also reported that the results of noninstrumented fusion were as good as those attained with instrumentation14 The clinical results obtained by Moller and Hedlund are even more striking since Gill’s decompression was carried out in two-thirds of the patients (all with sciatic pain) in both the noninstrumented and instrumented groups (personal communication). This author’s own personal experience with decompression and fusion in adult isthmic spondylolisthesis is similar.35 Between January 1999 and July 2003, 25 consecutive adults with symptomatic lumbosacral isthmic slip (average age 50 years) underwent surgery for slips ranging from grade 1 to 4. All cases had a Gill procedure, instrumentation, and posterolateral fusion (Fig. 100.1).35 Back and leg pain relief was achieved in all with radiological evidence of solid fusion. The results of fusion surgery in adults with isthmic spondylolisthesis are certainly better than those observed in adults undergoing fusion for purely degenerative disc disease.36 The combination of mechanical instability associated with spondylolisthesis, compounded by the development of degenerative changes with or without neural compression, will respond more favorably to spondylodesis.13

A

In high-grade olisthesis In situ fusion is not only efficient in low-grade olisthesis but also in patients with high-grade slips. Because the transverse process of L5 may be dysplastic and small and lies too deep to be accessed, in situ fusion of high-grade slips may extend from the ala to the transverse process of L4. Postoperative immobilization in high-grade slips is mandatory. Casting or bracing with thigh extension (in one leg) should be instituted for a least 2–3 months. Johnson and Kirwan37 collected 17 patients with slips greater than 50% managed by in situ fusion. Sixteen of the 17 patients had a good clinical result. Reynolds and Wiltse published a similar-sized series and similar success rate.38 No change was observed in the degree of slip or sagittal rotation at the final follow-up X-ray.38 These authors noticed that with the attainment of a solid fusion (approximately 7 months postoperatively), pain, hamstring tightness, overall cosmetic appearance, and posture were improved. Peek et al.25 reviewed eight adults with grade 3 and 4 slips, who were managed by in situ fusion without decompression. Again, good results were recorded in all patients, including resolution of neural deficits, even though no neural decompression was performed. Boxall et al. also reported that pain, gait abnormalities, hamstring tightness, and neural deficit all resolve with in situ fusion without concomitant decompression.12 Seitsalo et al.39 collected 93 adolescents (mean age 14.8 years) who underwent surgery for high-grade spondylolisthesis with long-term follow-up. Ninety-four percent of the patients obtained satisfactory clinical results with in situ fusion only. Another study from the same institution found that in situ fusion results in adolescents compared favorably with the results of surgical slip reduction accompanied by both anterior and posterior fusion; however, in the latter group postoperative complications were more common.40

B

Fig. 100.1 (A) Lateral X-ray of the lumbosacral junction of a 58-year-old female, taken 8 years after in situ instrumentation and fusion of a grade 2+ isthmic spondylolisthesis. (B) Anteroposterior X-ray of the same patient. Note the solid posterolateral L5–S1 fusion. 1101

Part 3: Specific Disorders

Drawbacks of in situ fusion in high-grade slips Despite the impressive excellent functional results obtained with bilateral lateral in situ fusion, there are several drawbacks with this technique when managing high-grade slips. In high-grade slips, the fusion mass is subjected to tension, flexion, and shearing forces. Attaining a solid fusion can be endangered by repetitive stress fractures in the fusion mass leading to gradual slip progression. Indeed, some authors report a high incidence of pseudoarthrosis (up to 45%) in patients with high-grade slips undergoing in situ arthrodesis.11,12,39,41–43 In addition, an increase in the slip angle (15–20 degrees) and the degree of slip (up to 33% increase) were noted as well despite an apparently solid fusion mass.12,41,42 Slip progression was found to occur in the first 6 months after surgery. Although in situ fusion is considered a simple and safe surgical technique, neural injury is possible. Schoenecker et al.44 collected 189 patients who underwent in situ fusion for high-grade slip at several major US spine centers. Twelve of them (6%) developed cauda equina symptoms following in situ fusion. In less than 50% of these patients did the cauda equina injury recover. Patients at risk for developing postoperative cauda equina dysfunction were those with slip angles greater than 45 degrees. Schoenecker44 postulated that the cauda equina injury was probably the result of intraoperative slip progression that occurred due to loss of muscle protection during anesthesia as well as the surgical destabilizing effect. Radiculopathy of the first two sacral roots is common before surgery in many patients with high-grade slips. This is explained by the fact that the S1 and S2 roots tent over the vertical sacrum. In addition, in many of the patients there is also evidence for L5 radiculopathy. The likelihood for intraoperative neural injury in high-grade slips is thus compounded. Other drawbacks of in situ arthrodesis in high-grade slips are the inability to address poor posture, cosmetic appearance, and altered gait. Patients with high-grade slips have hip and knee flexion contractures and a vertical pelvis that are compensatory mechanisms to maintain sagittal balance in the presence of a severe lumbosacral kyphosis. They also have protruding ribs due to compensatory thoracolumbar hyperlordosis. The shortcomings of in situ stabilization create a role for slip reduction in the management of high-grade spondylolisthesis.

Slip reduction The advantages of slip reduction in conjunction with arthrodesis are numerous and include: improved spine biomechanics, better nerve root decompression (usually by an indirect effect of the reduction), better opportunity to obtain fusion as the fusion is no longer under the influence of tension and anterior shear forces, improved posture, and better cosmetic appearance.45 As well, reduction is associated with less postoperative slip progression. Reduction of the angular deformity is probably more important than reduction of the translational deformity since the angular roll is the main factor leading to lumbosacral kyphosis. Slip reduction may be achieved by either closed or open methods. Numerous techniques of slip reduction are described.

Closed reduction Although the initial attempts at closed reduction of spondylolisthesis date back to the 1920s 1930s, Scaglietti et al.46 should be credited for popularizing the practice of closed reduction of spondylolisthesis. Other strong proponents of closed reduction are Marchetti and Bartolozzi.2 Closed reduction is reserved mainly for children and adolescents. A closed reduction may be accomplished by longitudinal traction on a Risser or Cotrel table, combined with pelvic and hip extension. Reduction is done while the patient is awake, achieved 1102

gradually, and is followed by immobilization in a bilateral hip spica. Bilateral lateral fusion is then performed in the reduced position through a window in the cast. The patient is kept recumbent for 3 months following reduction and spondylodesis. Scaglietti et al.46 reported a 50% reduction of the slip grade as well as a decrease in the slip angle. Several series of cast reduction and fusion were published.41,47–51 Bradford reported that posterolateral fusion and cast reduction decreased the average preoperative slip angle of 33 degrees by two-thirds.49 Two of the 22 patients developed a transient L5 weakness (both were also managed by skeletal traction).49 Bradford and Boachie-Adjei later reported on a modification where posterior decompression, sacral dome osteotomy, and L4–S1 fusion were followed by closed reduction with halo skeletal traction and anterior strut grafting.50 Burkus et al.51 advocated the performance of bilateral lateral fusion and decompression, if necessary, followed by gradual cast reduction. Burkus et al. reported the long-term results of in situ arthrodesis combined with closed reduction and compared them to the results obtained with in situ fusion without reduction.51 Out of 42 adolescents reported, 24 were fused in situ and then reduced in a cast, while the other 18 underwent posterolateral fusion without reduction. Although in most cases where closed reduction was attempted some correction of translation and slip angle was achieved, clinical results were similar in both groups of patients. However, patients who underwent reduction had less late progression of the deformity, less sagittal translation, a smaller lumbosacral kyphosis, and a lower incidence of pseudoarthrosis. Today, closed reduction should be reserved to children and adolescents with the most complex deformities, while in the majority of adolescents and adults with high-grade slips instrumented reduction and fusion are preferable.

Pedicle screw fixation and reduction of spondylolisthesis Modern internal fixation of the spine is based on pedicle screw fixation. Pedicle screws impart excellent control and fixation of all 3 columns of the spine and allow efficient slip reduction together with restoration of sagittal alignment and stabilization of the spine in the corrected position. In addition, pedicle screw fixation may also enhance the rate of fusion.52 Pedicle screws alone may provide for instrumented reduction in a ‘supple’ slip by way of rod or plate contouring into the desired lordosis. In more stiff deformities, screw–bolt reduction devices such as the SOCON spondylolisthesis reduction apparatus provide for further slip reduction (Fig. 100.2). This assembly enables posterior translation of the slipped vertebra and the levered forces are applied to both L5 and S1 vertebrae. Matthiass and Heine were the first to popularize a slip reduction device although Schollner was the originator of the technique.53 Matthiass and Heine performed L5– S1 discectomy with sacral dome resection when necessary, manual levered reduction of L5 combined with posterior translation by means of the screw-bolt–sacral plate and posterolateral arthrodesis. Almost 46% of the patients without preoperative neurologic deficit developed postoperative motor deficits, mostly transitory.53 Steffee and Sitkowski employed a similar technique and combined both screwbolt reduction with the VSP plate as well as levered reduction by means of a ‘persuader.’54 Ten percent of patients developed transient L5 radiculopathy.55 Other series reported an even higher rate of L5 root lesions.56 Why is L5 nerve root injury common during slip reduction of high-grade olisthesis? Petraco et al. studied the relationship of the L5 root and the degree of vertebral slip in an in vitro model.57 They found that the risk of stretch injury to the L5 nerve during reduction of a high-grade slip was not linear, with 71% of the total strain in the nerve occurring during the second half of the reduction.

Section 5: Biomechanical Disorders of the Lumbar Spine

A

B

C

Fig. 100.2 (A) Lateral X-ray of the lumbosacral junction of a 29-year-old female with a grade 4 isthmic spondylolisthesis. The slip has progressed from a grade 2 olisthesis during a span of 6 years (X-ray taken at age 23 not shown). (B) Sagittal MRI of the same patient showing the marked degenerative and dysplastic changes. (C) Same patient as in A and B, after instrumented reduction with the SOCON device and TLIF with the B-Twin interbody expandable cage. Complete slip reduction was realized.

They concluded that partial reduction was safer than complete reduction and that correction of the lumbosacral kyphosis had a protective effect on the L5 nerve.57 In his ‘point of view’ relating to the Petraco study, Hensinger wrote: ‘Spine surgeons should temper their enthusiasm for obtaining complete reduction, which is esthetically more pleasing but may significantly increase the neurological risk to the patient.’58 During the process of reduction, the L5 nerve root may also be entrapped outside the spinal canal when it passes underneath the lumbosacral/iliolumbar ligamentous complex.59 In high-grade slips it is also possible to injure proximal lumbar roots, as considerable acute lengthening of the spine occurs during slip reduction.60 A few important points must be emphasized whenever reduction of highgrade slips is considered: (1) the patient should be positioned on the operating table with flexed knees to relax the sciatic nerve; (2) it is sometimes necessary to keep the knees flexed for about a week after surgery; (3) it is important, when feasible, to monitor the L5 and S1 roots during surgery; (4) sacral screws should have a bicortical purchase; (5) consider screw purchase at S2 or, alternatively, iliac screws;43 and (6) consider Jackson’s intrasacral fixation to enhance the biomechanical strength of the construct.61 Despite the numerous advantages of pedicle screw fixation, pedicle screw-based slip reduction remains controversial because it is associated with a considerable rate of surgical complications.7 Thus, there are legitimate arguments for both slip reduction and in situ fusion. The high percentage of neural complications reported with instrumented slip reduction led Bradford to the conclusion that: ‘instrumented reduction cannot be regarded as a routine method for treating spondylolisthesis … since there are alternative less risky procedures with satisfying clinical results.’7 Poussa et al.40 compared two groups of adolescents with severe slips managed operatively. One group underwent instrumented reduction and fusion while the other group underwent in situ fusion. Although both groups achieved the same functional and clinical results, the reduction group had more complications and reoperations.

Anterior-posterior resection reduction (staged or combined) Early attempts at slip reduction, especially those of high-grade slips, led to the conclusion that anterior surgery was necessary for both release and to ensure a solid fusion. Staged or combined procedures are reserved almost exclusively for high-grade slips. In the anterior procedure, anterior discectomy and release, partial sacrectomy if needed, and anterior arthrodesis are performed. Two weeks later, Gill’s laminectomy and levered reduction with internal fixation and fusion are performed.62 Postoperative immobilization should be considered in order to achieve fusion and a good clinical result. The sequence of anterior and posterior surgical interventions is variable among surgeons.62 Many authors have utilized traction either preoperative, between the staged procedures, or after surgery, in the form of 90–90 traction, halo-femoral traction or halo-pelvic traction to facilitate slip reduction.41,48,50,63 Balderston and Bradford,48 for example, combined both spinous process traction wires that were connected to an outrigger and halo pelvic traction. More recently, Bradford and Boachie-Adjei50 reported on the long-term follow-up of spondylolisthesis managed by anteroposterior resection reduction. Although the slip angle was reduced from 71 degrees to 31degrees, the percentage of slip was not changed appreciably following surgery. Three of the 22 patients in the report developed new neural deficits, although nine of the 10 patients with preoperative neural sequelae improved following surgery. O’Brien et al.63 reported similar results following the latter type of procedure. Most of the series reporting on staged procedures found a high incidence of neural complications in up to 25% of patients.41,55,56,64

Gradual instrumented reduction To overcome the alarming incidence of neural complications associated with pedicle screw slip reduction, Edwards developed and refined the concept and the technique of gradual instrumented reduction of 1103

Part 3: Specific Disorders

spondylolisthesis.45 Edwards claims that gradual reduction is possible by simultaneous application of three corrective forces: distraction, posterior translation, and lumbosacral extension. It is important to have a two-point sacral fixation (at S1 and S2) during the reduction maneuver to withstand the considerable forces needed for reduction and restoration of sagittal alignment. The viscoelastic stress relaxation of the soft tissues during gradual reduction enables stretching of the anterior contracted nonosseous structures. In addition, Edwards claims that the restoration of full anatomical alignment obviates the need for interbody grafting. Others disagree with the latter statement and would recommend a TLIF or PLIF whenever possible (Fig. 100.3).56,65,66 According to Edwards,45 the main indications for gradual slip reduction are: (1) sacral root irritation leading to symptoms of impaired bowel and bladder control; (2) a progressive slip greater than 50%; (3) major trunk deformity with sagittal decompensation; and (4) pain or neural deficit combined with two or more risk factors such as a large

A

C

1104

slip angle, a trapezoid L5, a rounded sacrum, female adolescent and symptoms of sacral nerve root stretching. It must be stressed that gradual slip reduction should be reserved for a small, selected group of patients because even in the best hands reduction of high-grade slips is associated with a substantial complication rate.7 With this technique, Edwards was able to achieve the following results in a group of 18 patients with high-grade slips: 91% correction of the slip was realized, the final lumbosacral kyphosis was reduced to 4 degrees, and a solid fusion was obtained in 94% of the patients. Slip reduction resulted in an average of 32 mm of trunk height gain. There was a 5% incidence of transient unilateral L5 nerve root weakness.45 Hu and associates reported their experience with the Edwards gradual slip reduction in 16 patients with a high-grade slip.64 The average preoperative slip was reduced from 89% to 29% and the slip angle was reduced from 50 degrees to 24 degrees. Three patients had neurologic impairment postoperatively (19%); one did not resolve. Four patients

B

Fig. 100.3 (A) Lateral X-ray of the lumbosacral junction of a 32-yearold male with a grade 2 isthmic spondylolisthesis. (B) Sagittal MRI of the same patient showing the marked degenerative changes and the pseudoherniation. (C) Same patient as in A and B, after instrumented reduction with the SOCON device and a Brantigan carbon cage as a TLIF (see the metallic makers in the cage).

Section 5: Biomechanical Disorders of the Lumbar Spine

had hardware failure (25%). Ten patients had an excellent result, five patients had a good result, and one patient had a fair result.64

Spondyloptosis In spondyloptosis, the lumbar spine slips completely off the sacrum and the inferior endplate of L5 rests facing the anterior part of the sacrum. The loss of sacral support appears to be the most significant difference between high-grade spondylolisthesis and spondyloptosis.45 Attempts at spine fusion without reduction in spondyloptosis usually result in loss of fixation and nonunion.47 Therefore, there is a need for reduction in spondyloptosis.45 (Reduction of spondyloptosis is associated with considerable lengthening of the spine, which will result in significant stretching of the lumbar roots.) According to Edwards,45 reduction of spondyloptosis is feasible if only up to 3–5 cm of lengthening of the course of the lumbar roots is anticipated. More lengthening is not tolerated without loss of neural function. Additional contraindications for reduction are: a slip angle of 50 degrees or more, rigid lumbar lordosis, long duration of the ptosis, age 20 or older, or previous attempts at fusion. In such cases, resection of the sacral dome and the lower part of L5 may provide an additional 3 cm of possible lengthening during reduction.45 Nerve root monitoring and a wake-up test are important adjuncts to the technique. Initially, temporary rods from the ala to L1 are placed. Wires are attached to the lumbar pedicle screws and connected to a traction bridge hanging over the operation table. The wires are attached to weights to initiate posterior translation. A laminectomy, L5–S1discectomy, and sacral dome osteotomy are performed. Gradual reduction is then started, approximately 1 hour per slip grade. Following reduction, L4–S1 fixation is performed with posterolateral fusion. Edwards’s results of ptosis reduction were as follows: 88% slip reduction, preoperative kyphosis reduced from 36 degrees kyphosis to 23 degrees lordosis (a 59 degree correction) and a 25% neural complication rate, mostly unilateral L5 nerve root lesions.45

Vertebrectomy of L5 (Gaines procedure) Another way the tackle the problem of spondyloptosis is by a ‘shortening’ procedure that is accomplished by resection of the L5 body. Huizenga67 and Gaines and Nichols68 were the first in the English literature to describe L5 resection and L4–S1 fusion in spondyloptosis. The Gaines procedure consists of two stages. First, the lumbosacral junction is approached retroperitoneally or transperotoneally. The L5 body is resected to the base of the pedicles together with the two adjacent discs (L5–S1, L4–5). In the second stage (performed either under the same anesthesia or after 2 weeks), a midline posterior approach is undertaken through which the lamina and pedicles of L5 are removed, L4 is reduced onto the sacrum, and pedicle instrumentaion of L4–S1 is performed with bone-on-bone fusion or with an intervening interbody cage. Postoperative brace immobilization is recommended.69 Even this ‘shortening’ procedure is associated with an enormous incidence of iatrogenic neural deficit – 75%!69

Jackson’s sacral fixation technique The sacrum serves as the foundation of every lumbosacral fixation. Jackson61 pointed out four reasons why sacral fixation may by troublesome: (1) difficult local anatomy; (2) poor bone quality frequently encountered in the sacrum, even in nonosteopenic individuals; (3) the posterior position of the implants with respect to the center of gravity and the axes of spinal angulation in the sagittal plane; and (4) large lumbosacral loads exerting flexural bending moments and cantilever pull-out forces. Jackson61 developed a new concept of sacral instrumentation. He uses sacral screws with closed oblique canals and strong ductile rods. The rod, which is introduced through the oblique canal sacral screw, is driven into the sacrum

itself more distally. This creates the so-called ‘sacroiliac buttress’ and allows the instrumentation to be fixed to the anterior sacrum, resisting the posterior pull-out forces. In situ contouring allows for effective reduction of the slip. Jackson’s two main indications for the technique are spondylolytic spondylolisthesis and long instrumented fusions to the sacrum performed for deformity, malalignment, and imbalance. TLIF or PLIF are important adjuncts to this technique.

Alternative methods Bohlman’s fibular dowel technique Smith and Bohlman70 reported yet another variation of lumbosacral fixation. They performed posterior decompression, posterolateral arthrodesis from L4 to S1, as well as inserting a fibular graft that was passed from the back of S1 through the L5–S1 disc and into the L5 body. They performed this procedure on 11 patients, most of them adults with high-grade slips accompanied by neurologic deficit including cauda equina syndrome. Utilizing this technique through a single posterior approach, they achieved a 100% fusion rate and resolution of neural deficit. Esses et al.71 and also Roca et al.72 utilized the same technique with equally successful fusion rates and clinical improvement.

Trans-sacral transvertebral interbody fixation The spondylolisthetic deformity is fixed in situ by advancing the S1 pedicle screw through superior sacral endplate through the L5–S1 disc and into the L5 body.73 This fixation provides immediate threecolumn fixation of the lumbosacral junction. It is a good method for salvage of failed spondylolisthesis fusion or in cases with advanced disc degeneration at the slip level where reduction is not feasible or contraindicated (Fig. 100.4). This technique may allow partial reduction to be combined with trans-sacral interbody fixation.74,75

In conclusion In situ fusion without instrumentation is the treatment of choice in children and adolescents with grade 1–2 spondylolisthesis although pedicle screw fixation may obviate the need for postoperative bracing. In adults with mild to moderate olisthesis with disc degeneration at the slip level, the adjacent cephalad disc should be investigated, including the performance of provocative discography. If it is found to be a pain generator it should be incorporated in the spondylodesis. The role of anterior column support in adults with low-grade slips has not been established. Patients with mild to moderate slips with marked disc space narrowing should be managed with posterior decompression, pedicle screw instrumentation, and posterolateral fusion (Fig. 100.5). Patients with spondylolisthesis with a relatively preserved disc space height or patients undergoing slip reduction should probably be subjected to posterior lumbar interbody fusion (PLIF or TLIF) in addition to posterolateral fusion and pedicle screw fixation. Patients with advanced slip accompanied by advanced degenerative changes should undergo decompression with transacral interbody screw fixation ending in the L5 body. Posterior instrumentation should be attempted in all grade 3–4 supple slips. If a good correction of the lumbosacral kyphosis is obtained, fixation from L5 to the sacrum is sufficient, provided that TLIF or PLIF are performed. Posterior grafting with extension cast reduction is feasible in young patients with a flexible deformity that exceeds grade 4 slippage. Anteroposterior resection reduction should be reserved for stiff deformities, such as autofusion in high-grade slips. The procedure usually entails anterior resection, release and interbody fusion followed 2 weeks later by laminectomy, posterior dome osteotomy, and reduction by instrumentation. The procedure entails considerable 1105

Part 3: Specific Disorders Adult low-grade isthmic slip, disc at slip level: Normal

Normal

Degenerated disc

Worn out

Reduction with ped. screw fixation

No reduction, ped. screw fixation

No reduction, ped. screw fixation

No reduction

PLIF & post. lateral fusion

PLIF & post. lateral fusion

Post. lateral fusion

Transacraltransdiscal fixation

A

Adult high-grade isthmic slip “Supple” slip

Relatively “stiff”

Relatively “stiff”

“Stiff”

Reduction with ped. screws

“Sacrectomy” & discectomy

Part. slip reduction

Combined resection procedure

PLIF

PLIF

Transacraltransdiscal fixation

Pedicular fixation to L4

Fig. 100.5 Flowchart of treatment options for adult isthmic slip.

B Fig. 100.4 (A) Lateral X-ray of the lumbosacral junction of a 53-year-old female with a grade 3 isthmic spondylolisthesis. Note the marked disc space narrowing with anterior osteophytes. (B) Same patient as in A after trans-sacral interbody fixation of L5–S1.

incidence of complications: up to 30% root deficit and up to 25% nonunion. It must be stressed that treatment of severe slippage continuous to pose a therapeutic challenge and that instrumented reduction is at best controversial.

Degenerative spondylolisthesis Patients with degenerative spondylolisthesis usually present with symptoms after the fourth or fifth decade of life. There is a female preponderance, the condition is more common in patients with diabetes mellitus, and the prevalence of the condition increases with age.76 The condition arises secondary to disc and facet joint degeneration. Degenerative spondylolisthesis is not a pure translatory deformity but rather a rotatory subluxation.77 As such, the slip does not exceed 30% of the width of the vertebra below. Only after decompressive surgery without spondylodesis may the slip exceed 50% and 1106

rarely even more. The most common symptoms leading to operative intervention are severe spinal claudication or sciatica accompanied by mild low back and buttock pain unresponsive to medical rehabilitation and interventional spine care. Occasionally, a foot-drop or signs of cauda equina compression are the presenting symptoms leading to surgical intervention. The main goal of surgery is to decompress the stenotic canal associated with degenerative spondylolisthesis. By performing decompression of the neural elements, relief of sciatica and/or neurogenic claudication is expected. Pedicle-to-pedicle decompression has been advocated. The extent of facet resection has been debated from preservation of the facets to partial facet resection or to complete excision of the posterior joints.76 Frequently, during decompression 50% of the facets are sacrificed or the pars interarticularis is breached. The disc should be left intact unless a frank extrusion is noted. The main problem with decompressive surgery in degenerative spondylolisthesis is the occurrence of postoperatvie slip progression. Slip progression following surgery for degenerative spondylolisthesis is a common occurrence and may be associated with a bad clinical result.78 Progression can occur even when concomitant arthrodesis without instrumentation has been performed.79 Preoperative radiographic and anatomical risk factors associated with the postoperative development of slip progression include a well-maintained disc height, the absence of degenerative osteophytes, and sagittally oriented facet joints.80 Because postoperative slip progression is associated with a mediocre clinical outcome, arthrodesis should be considered. The role of arthrodesis in the operative treatment of lumbar spinal stenosis with associated degenerative spondylolisthesis has been the subject of much discussion. Laus et al. reported clinical success after decompression alone in a group of patients who had degenerative spondylolisthesis with spontaneous ‘stabilization’ of the pathological segment by spondylotic osteophytes.81 Others also advocated decompressive surgery

Section 5: Biomechanical Disorders of the Lumbar Spine

alone.82 Herkowitz and Kurz,6 in 1991, published a prospective, randomized study comparing the clinical results obtained with decompression alone and with decompression and intertransverse fusion. Fifty consecutive patients with degenerative spondylolisthesis were randomly assigned to one of the treatment groups. Follow-up averaged 3 years. Herkowitz and Kurz found a significantly better clinical outcome in patients who underwent arthrodesis in addition to decompression. Although 36% of the patients did not achieve a solid fusion, good clinical outcome was possible in the presence of pseudoarthrosis. Fishgrund et al.83 in a prospective, randomized study in patients with degenerative spondylolisthesis compared the results of decompression and noninstrumented fusion to those with instrumented arthrodesis. Although the rate of pseudoarthrosis was 55% in the noninstrumented group, compared to only 17% in the instrumented group, the clinical results were the similar. Fishgrund et al. concluded that the fusion status did not affect the clinical outcome.83 More recently, however, Kornblum et al.84 in a long-term follow-up study (5–14 years, 92 months on average) found that by obtaining a solid fusion a statistically significant better clinical outcome was achieved in patients operated on for degenerative spondylolisthesis. Eighty-six percent of those with a solid fusion had a good to excellent outcome as compared to only 56% of patients with a pseudoarthrosis. There is enough evidence in the literature to advocate the use of instrumentation to ascertain a higher fusion rate.52,79 Indeed, Booth et al. reported on a 100% fusion rate in patients with degenerative spondylolisthesis managed by decompression and instrumented fusion. After 5 years, 85% of the patients who had a solid fusion maintained a satisfactory clinical outcome.85

Conclusion In conclusion, in most cases of degenerative spondylolisthesis decompression and fusion are recommended. While noninstrumented fusion may be considered in patients in whom the facet joints have been preserved, instrumentation in addition to posterolateral fusion is strongly recommended in patients in whom the zygapophyseal joints were sacrificed, as pedicle screw instrumentation is associated with better fusion rates. Although instrumentation is associated with more surgical complications and reoperations, care after surgery is easier with instrumentation and there is no need for postoperative immobilization. Decompression alone is seldom indicated. Occasionally, it may be considered in patients with advanced disc degeneration with anterior osteophytes with no detectable motion on dynamic X-rays.

References

8. Wiltse LL, Jackson W. Treatment of spondylolisthesis and spondylolysis in children. Clin Orthop 1976; 117:92–100. 9. Stanton RP, Meehan P, Lovell WW. Surgical fusion in childhood spondylolisthesis. J Pediatric Orthop 1981; 5:411–415. 10. Pizzutilo P, Hummer RA. Nonoperative treatment for painful adolescents with spondylolisthesis J. Pediatric Orthop 1989; 9:538–540. 11. Laurent LE, Osterman K. Operative treatment of spondylolisthesis in young patients. Clin Orthop 1976; 117:85–91. 12. Boxall D, Bradford DS, Winter RB, et al. Management of severe spondylolisthesis of children an adolescents. J Bone Joint Surg [Am] 1979; 61:479–495. 13. Floman Y. Progression of lumbosacral isthmic spondylolisthesis in adults. Spine 2000; 25:342–347. 14. Moller H, Hedlund R. Instrumented and non-instrumented posterolateral fusion in adult spondylolisthesis. A prospective randomized study, part 2. Spine 2000; 25:1716–1721. 15. Sue PB, Esses SI, Kostuik JP. Repair of pars interarticularis defect. The prognostic value of pars infiltration. Spine 1991; 16:S445–S448. 16. Ivanic GM, Pink TP, Achatz W, et al. Direct stabilization of lumbar spondylolysis with a hook screw: mean 11-year follow-up period for 113 patients. Spine 2003; 28:255–259. 17. Buck JE. Further thoughts on direct repair of the defect in spondylolysis. J Bone Joint Surg [Br] 1979; 61:123. 18. Bradford DS, Iza J. Repair of the defect in spondylolysis and minimal degree of spondylolisthesis by segmental wire fixation and bone grafting. Spine 1985; 10: 673–679. 19. Hefti F, Seelig W, Morscher E. Repair of lumbar spondylolysis by hook screw. Internat Orthpaed 1992; 16:81–85. 20. Deguchi M, Rapoff AJ, Zdeblick TA. Biomechanical comparison of spondylolysis fixation techniques. Spine 1999; 24:328–333. 21. Johnson GV, Thompson AG. The Scott wiring technique for direct repair of lumbar spondylolysis. J Bone Joint Surg [Br] 1992; 74:426–430. 22. Gill GG. Long-term follow-up of patients with spondylolisthesis treated by excision of the loose lamina with decompression of the nerve roots without spinal fusion. Clin Orthop 1984; 182:215–219. 23. Osterman K, LindholmTS, Laurent LE. Late results of removal of the loose posterior element (Gill’s operation) in the treatment of lytic lumbar spondylolisthesis. Clin Orthop 1976; 117:121–128. 24. Lonstein JE. Spondylolisthesis in children: cause, natural history and management. Spine 1999; 24:2640–2647. 25. Peek RD, Wiltse LL, Reynolds JB, et al. In situ arthrodesis without decompression for grade III and IV isthmic spondylolisthesis in adults who have severe sciatica. J Bone Joint Surg [Am] 1989; 71:62–68. 26. de Loubresse CG, Bon T, Deburge A, et al. Posterolateral fusion for radicular pain in isthmic spondylolisthesis. Clin Orthop 1996; 323:194–201. 27. Bosworth D, Fielding JW, Demarest L, et al. Spondylolisthesis: a critical review of consecutive series of cases treated by arthrodesis. J Bone Joint Surg [Am] 1955; 37:767. 28. Henderson ED. Results of the surgical treatment of spondylolisthesis. J Bone Joint Surg [Am] 1966; 48:61–64.

1. Wiltse LL, Newman PH, McNab I. Classification of spondylolysis and spondylolisthesis. Clin Orthop 1976; 117:23–29.

29. Lenke LG, Bridwell KW, Bullis D, et al. Results of in situ fusion for spondylolisthesis. J Spinal Disord 1992; 5:433–442.

2. Marchetti PG, Bartolozzi P. Classification of spondylolisthesis as a guideline for treatment. In: Bridwell KH, DeWald RL, eds. Textbook of spinal surgery, 2nd edn. Philadelphia, New York: Lippincott-Raven; 1997:1211–1254.

30. Frennered AK, Danielson BI, Nachemson AL, et al. Midterm follow-up of young patients fused in situ for spondylolisthesis. Spine 1991; 16:409–416.

3. Hammemberg KW. Spondylolysis and spondylolisthesis. In: DeWald RL, ed. Spinal deformities. A comprehensive text. New York, Stuttgart: Thieme; 2003:787. 4. Moller H, Hedlund R. Surgery versus conservative management in adult isthmic spondylolisthesis. A prospective randomized study: Part 1. Spine 2000; 25: 1711–1715. 5. Carragee EJ. Single-level posterolateral fusion, with or without posterior decompression, for the treatment of isthmic spondylolisthesis in adults. A prospective, randomized study. J Bone Joint Surg [Am] 1997; 79:1175–1180.

31. Hensinger RN, Lang JR, MacEwin D. Surgical management of spondylolisthesis in childhood and adolescence. Spine 1976; 1:207–215. 32. Hanley EN, Levy JA. Surgical treatment of isthmic spondylolisthesis. Analysis of variables influencing results. Spine 1989; 14:48–50. 33. Schnee CL, Freese A, Ansell W. Outcome analysis for adults with spondylolisthesis treated with posterolateral fusion and transpedicular screw fixation. J Neurosurg 1997; 86:56–63. 34. Haraldsson S, Wilner S. A comparative study of spondylolisthesis in operations on adolescents and adults. Arch Orthop Traum Surg 1983; 101:101–105.

6. Herkowitz HN, Kurz LT. Degenerative lumbar spondylolisthesis with spinal stenosis: a prospective study comparing decompression with decompression and intertransverse process arthrodesis. J Bone Joint Surg [Am] 1991; 73:802–808.

35. Floman Y, Millgram MA, Ashkenazi E, Rand N. Outcome of fusion procedures in isthmic spondylolisthesis presenting in the adult. 23rd annual meeting of the Israeli Orthopedic Association, Tel Aviv; December, 2003.

7. Edwards CC, Bradford DS. Controversies. Instrumented reduction of spondylolisthesis. Spine1994; 19:1535–1537.

36. Buttermann GR, Garvey TA, Hunt AF, et al. Lumbar fusion results related to diagnosis. Spine 1998; 23:116–127.

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Part 3: Specific Disorders 37. Johnson JR, Kirwan EO. The long term results of fusion in situ for severe spondylolisthesis. J Bone Joint Surg [Br] 1983; 65:43–46.

62. DeWald RL, Faut MM, Tadonio RF, et al. Severe lumbosacral spondylolisthesis in adolescents and children. J Bone Joint Surg [Am] 1981; 65:619–626.

38. Reynolds JB, Wiltse LL. The treatment of severe spondylolisthesis in the young. Orthop Transactions 1989; 13:27.

63. O’Brien JP, Mehdian H, Jaffray D. Reduction of severe lumbosacral spondylolisthesis. Clin Orthop Relat Res 1994; 300:64–69.

39. Seitsalo S, Osterman K, Hyvarinen H, et al. Severe spondylolisthesis in children and adolescents. A long-term review of fusion in situ. J Bone Joint Surg [Br] 1990; 72:259–265.

64. Hu SS, Bradford DS, Transfeldt EE, et al. Reduction of high-grade spondylolisthesis using Edwards instrumentation. Spine 1996; 21:367–371.

40. Poussa M, Schlenzka D, Seitsalo S, et al. Surgical treatment of severe isthmic spondylolisthesis in adolescents. Reduction or fusion in situ? Spine 1993; 18:894–901. 41. Bradford DS, Godfreid Y. Staged salvage reconstruction of grade IV and V spondylolisthesis. J Bone Joint Surg [Am] 1987; 69:191–202. 42. Seitsalo S, Osterman K, Hyvarinen H, et al. Progression of spondylolisthesis in children and adolescents: a long term follow up of 272 patients. Spine 1991; 16:417–421. 43. Molinari RW, Bridwell KH, Lenke LG, et al. Complications in the surgical treatment of pediatric high-grade isthmic dysplastic spondylolisthesis. Spine 1999; 24: 1701–1711. 44. Schoenecker PL, Cole HO, Herring JA, et al. Cauda equina syndrome after in situ arthrodesis for severe spondylolisthesis at the lumbosacral junction. J Bone Joint Surg [Am] 1990; 72:369–377.

66. Fabris DA, Costantini S, Nena U. Surgical treatment of severe L5–S1 spondylolisthesis in children and adolescents. Results of intraoperative reduction, posterior interbody fusion and segmental pedicle fixation. Spine 1996; 21:728–733. 67. Huizenga BA. Reduction of spondylolisthesis with staged vertebrectomy. Orthop Transac 1983; 7:21. 68. Gaines RW, Nichols WK. Treatment of spondylolisthesis by two-stage L5 vertebrectomy and reduction of L4 onto S1. Spine 1985; 10:680–686. 69. Lehmer SM, Stefffee AD, Gaines RW. Treatment of L5–S1 spondyloptosis: Staged L5 resection with reduction and fusion of L4 onto S1. Spine 1994; 19:1916–1925. 70. Smith MD, Bohlman HH. Spondylolisthesis treated by a single-stage operation combining decompression with in situ posterolateral fusion and anterior fusion. J Bone Joint Surg [Am] 1990; 72:415–420.

45. Edwards CC. Reduction of spondylolisthesis. In: Bridwell KH, DeWald RL, eds. Textbook of spinal surgery, 2nd edn. Philadelphia, New York: Lippincott-Raven; 1997:1317–1335.

71. Esses SI, Natout N, Kip P. Posterior interbody arthrodesis with fibular strut graft in spondylolisthesis. J Bone Joint Surg [Am] 1995; 77:172–176.

46. Scaglietti O, Frontino G, Bartolozzi P. Technique of anatomical reduction of lumbar spondylolisthesis and its surgical stabilization. Clin Orthop 1976; 117:164–175.

72. Roca J, Ubierna MT, Caceres E, et al. One-stage decompression and posterolateral and interbody fusion for severe spondylolisthesis. Spine 1999; 24:709–714.

47. Bradford DS. Treatment of severe spondylolisthesis: a combined approach, reduction and stabilization. Spine 1979; 4:423–429.

73. Grob D, Humke T, Dvorak J. Direct pediculo-body fixation in cases of spondylolisthesis with advanced intervertebral disc degeneration. Eur Spine J 1996; 5: 281–285.

48. Balderston RA, Bradford DS. Technique for achievement and maintenance of reduction for severe spondylolisthesis using spinous process traction wiring and external fixation of the pelvis. Spine 1985; 10:376–382. 49. Bradford DS. Closed reduction of spondylolisthesis: an experience in 22 patients. Spine 1988; 13:580–587. 50. Bradford DS, Boachie-Adjei O. Treatment of severe spondylolisthesis by anterior and posterior reduction and stabilization. J Bone Joint Surg [Am] 1990; 72: 1060–1066. 51. Burkus JK, Lonstein JE, Winter RB, et al. Long term evaluation of adolescents treated operatively for spondylolisthesis: a comparison of in situ arthrodesis only with in situ arthrodesis and reduction followed by immobilization in a cast. J Bone Joint Surg [Am] 1992; 74: 693–704. 52. Zdeblick TA. A prospective randomized study of lumbar fusion. Preliminary results. Spine 1993; 18:983–991.

74. Smith JA, Deviren V, Berven S et al. Clinical outcome of trans-sacral interbody fusion after partial reduction for high-grade L5–S1 spondylolisthesis. Spine 2001; 20:2227–2234. 75. Bartolozzi P, Sandri A, Ricci M. One-stage posterior decompression-stabilization and trans-sacral interbody fusion after partial reduction for severe L5–S1 spondylolisthesis. Spine 2003; 28:1135–1141. 76. Frymoyer W. Degenerative spondylolisthesis: diagnosis and treatment. J Am Acad Orthoped Surgeons 1994; 2:9–15. 77. Farafan HF. The pathological anatomy of degenerative spondylolisthesis: a cadaver study. Spine 1980; 5:412–418. 78. Mardjetko SM, Connolly PJ, Shott S. Degenerative lumbar spondylolisthesis. A meta-analysis of literature 1970–1993. Spine 1994; 19:S2256–S2265.

53. Matthiass HH, Heine J. The surgical reduction of spondylolisthesis. Clin Orthop 1986; 203:34–44.

79. Bridwell KH, Sedgewick TA, O’Brien MF, et al. The role of fusion and instrumentation in the treatment of degenerative spondylolisthesis with spinal stenosis. J Spinal Disord 1993; 6:461–472.

54. Steffee AD, Sitkowski D. Reduction and stabilization of grade IV spondylolisthesis. Clin Orthop 1988; 227:82–89.

80. Robertson PA, Grobler LJ, Novotny JE, et al. Postoperative spondylolisthesis at L4–5. The role of facet joint morphology. Spine 1993; 18:1483–1490.

55. Ani DM, Kepller L, Biscup RS, et al. Reduction of high-grade slips with VSP instrumentation. Report of a series of 41 cases. Spine 1991; 16:S302–S310.

81. Laus M, Tigani D, Alfonso C, et al. Degenerative spondylolisthesis: lumbar stenosis and instability. Chir Org Mov 1992; 77:39–49.

56. Boos N, Marchesi D, Zuber K, et al. Treatment of severe spondylolisthesis by reduction and pedicular fixation. Spine 1993; 18:1655–1661.

82. Herron LD, Trippi AC. The result of treatment by decompressive laminectomy without fusion. Spine 1989; 14:534–538.

57. Petraco DM, Spivak JM, Cappadona JG, et al. An anatomic evaluation of L5 nerve stretch in spondylolisthesis reduction. Spine 1996; 21:1133–1138.

83. Fischgrund JS, Mackay M, Herkowitz HN, et al. Degenerative lumbar spondylolisthesis with spinal stenosis: a prospective, randomized study comparing decompressive laminectomy and arthrodesis with and without spinal instrumentation. Spine 1997; 22:2807–2812.

58. Hensinger RN. Point of view. Spine 1996; 21:1139. 59. Kleihaus H, Albrecht S, Noack W. Topographic relations between the neural and ligamentous structures of the lumbosacral junction: In-vitro investigation. Eur Spine J 2001; 10:124–132. 60. Transfeldt EE, Dendrinos GK, Bradford DS. Paresis of proximal lumbar roots after reduction of L5–S1 spondylolisthesis. Spine 1989; 14:884–887. 61. Jackson RP. Jackson’s intrasacral fixation and segmental correction with adjustable contoured translating axes. Spine: State of the Art Review 1994; 8:307–341.

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65. Harms J, Rolinger H. A one-stager procedure in operative treatment of spondylolistheses: dorsal traction–reposition and anterior fusion. Z Orthop Ihre Grenzgeb 1982; 120:343–347.

84. Kornblum MB, Fischgrund JS, Herkowitz HN, et al. Degenerative lumbar spondylolisthesis with spinal stenosis: a prospective long-term study comparing fusion and pseudoarthrosis. Spine 2004; 29:726–733. 85. Booth KC, Bridwell KH, Eisenberg BA, et al. Minimum 5-year results of degenerative spondylolisthesis treated with decompression and instrumented posterior fusion. Spine 1999; 24:1721–1727.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ iii: Instability

CHAPTER

Instability: Clinical Manifestations and Assessment

101

Ashley Lewis Park

INTRODUCTION Lumbar segmental instability is an important but often unrecognized cause of chronic low back pain (LBP). It has been a controversial and poorly understood topic, primarily because of the varying definitions and usage among the several disciplines involved in the treatment of spinal disorders.1 Traditionally, one of the most obvious manifestations of lumbar instability has been the radiographic diagnosis of spondylolisthesis,2,3 with increased segmental motion reported in patients with chronic LBP.4–7 However, lumbar segmental instability (‘microinstability’) also has been cited as a cause of chronic LBP in patients without an injury to the osseous spine,8 with a number of studies reporting increased and abnormal intersegmental motion in these patients.9–11

DEFINITION OF SPINAL INSTABILITY Numerous biomechanical and clinical definitions have been developed to describe spinal instability; however, most, including the one adopted by the American Academy of Orthopaedic Surgeons, imply excessive motion beyond normal constraints.12–16 Despite a multitude of biomechanical, radiographic, and clinical studies, ‘normal’ motion of the lumbar vertebral segments continues to be a topic of debate because of the lack of standardized measurements in normal subjects.17 Correlating clinical instability and radiographic instability also has been difficult because of the overlap of symptomatic and asymptomatic motion patterns. Additionally, conventional radiography often is insensitive and unreliable in detecting abnormal or excessive intersegmental motion.18,19 Conceptually, therefore, as with other spinal conditions, radiographic abnormalities (more specifically, abnormal motion of a single motion segment) are considered significant only if they confirm the clinical finding (of lumbar segmental instability) at the corresponding symptomatic level.14 As the pathomechanics of the lumbar spine have become better understood, definitions of spinal instability have been developed that incorporate both the mechanical aspect and the clinical consequence. In 1992, Panjabi defined spinal instability as a region of laxity around the neutral position of a spinal segment, called the neutral zone, and more precisely as a decrease in the capacity of the stabilizing systems of the spine to maintain intervertebral neutral zones within physiological limits within which there is no major deformity, no neurological deficit, and no incapacitating pain.20 This definition is useful because it describes the quality of motion throughout the range of motion rather than relying solely on the total range of motion values for diagnosis.21

THE NEUTRAL ZONE CONCEPT AND THE SPINAL STABILIZING SYSTEM The neutral zone concept of segmental instability is based on the observation that the load-displacement curve of the spine is nonlinear (i.e. the ratio of the load applied to the displacement produced is not consistent), with minimal resistance to intervertebral motion occurring within the neutral zone and increased resistance to intervertebral motion occurring at the end-ranges of spinal motion.22 This concept has been described as a ‘ball in a bowl’ (Fig. 101.1). The ball rests in a bowl created by flipping the extension part of the load-displacement curve around the displacement axis. The ball moves easily within the base of the bowl (the neutral zone), but requires greater effort to move in the steeper part of the bowl (the end-ranges of motion). The shape of the bowl is analogous to spinal stability: a deeper bowl, such as a wine glass, represents a more stable spine, while a shallower bowl, such as a soup plate, represents a less stable spine (Fig. 101.2).22 The total range of motion of a spinal motion segment, therefore, can be divided into a neutral zone and an elastic zone. The neutral zone is the initial spinal motion which is produced against minimal internal resistance, whereas the elastic zone is motion nearer to the end-range of movement that is produced against significant internal resistance.23 In order for the stabilizing system of the spine to be effective, it must limit the excursion of spinal motion within a segment and maintain the proper ratio of neutral to elastic motion.23 Biomechanical studies of the stabilizing system of the spine have provided insight into the roles of the various components providing

Load

ROM

ROM

Flexion

NZ

NZ Dispacement

Extension A

B

Fig. 101.1 Load-displacement curve. (A) Spinal segment subjected to flexion and extension loads exhibits a nonlinear load displacement curve, indicating a changing relationship between the applied load the displacements produced. (B) A ‘ball in a bowl’ is a graphic analogy of the load-displacement curve. (Adapted from Panjabi MM. Clinical spinal instability and low back pain. J Electromyogr Kinesiol 2003; 13:371–379.)

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Part 3: Specific Disorders ROM

NZ

ROM NZ

Fig. 101.2 Representation of different spinal stabilities. Using the analogy of a ball in a bowl to represent the load-displacement curve of the spine (Fig. 101.1), a deep champagne glass and a shallow soup plate represent a more and a less stable spine, respectively. (Adapted from Panjabi MM. Clinical spinal stability and low back pain. J Electromyogr Kinesiol 2003; 13:371–379.)

spinal stability. The stabilizing system of the spine is composed of three subsystems: (1) the spinal column or passive subsystem, (2) the spinal muscles or active subsystem, and (3) the neural control unit.20,22 Because, under normal conditions, the three subsystems work in harmony to provide mechanical stability, their functions are interrelated, and decreased function of one subsystem may result in increased demands on the others to maintain stability.24,25 The various components of the spinal column generate transducer information about the mechanical status of the spine, such as position, load, and motion of each vertebra, and the neural control unit computes the needed stability and generates the appropriate muscle pattern (Fig. 101.3).23 A comprehensive knowledge of the three subsystems of the lumbar spine is essential in understanding spinal stabilization and clinically evaluating patients with LBP.

The passive subsystem The passive subsystem consists primarily of the vertebral bodies, zygapophyseal joints and joint capsules, spinal ligaments, and passive

Neural control units

Spinal colum (Transducers) Vertebral position SPINAL LOADS Spinal motions

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Spinal muscles (Actuators) Muscle ACTIVATION pattern

Fig. 101.3 Spinal stabilization system has three subsystems: spinal column, muscles surrounding the spine, and motor control unit. (Adapted from Panjabi MM. Clinical spinal instability and low back pain. J Electromyogr Kinesiol 2003; 13:371– 379.)

tension from the musculotendinous units.20 The passive subsystem plays its most important stabilizing role in the elastic zone of the spinal motion (i.e. near the end-ranges of motion).25 Serial sectioning26,27 and mathematical modeling25,28 have been used to investigate the relative contributions of structures to segmental stability. Spinal flexion is stabilized primarily by the posterior ligaments of the spine (interspinous and supraspinous ligaments), the zygapophyseal joints and joint capsules, and the intervertebral discs,28,29 while end-range extension is stabilized primarily by the anterior longitudinal ligament, the anterior aspect of the anulus fibrosus, and the zygapophyseal joints.25,27 Rotational movements of the lumbar spine are stabilized mostly by the intervertebral discs and the zygapophyseal joints.30 Although not studied extensively, the intertransverse ligaments appear to play an important role in segmental stability during side-bending movement.26 Because afferent nerve fibers capable of conveying proprioceptive information are present in most of the structures of the passive subsystem, including the intervertebral discs, the zygapophyseal joint capsules, and the interspinous and supraspinous ligaments,24,31 these structures may function as force transducers in the neutral zone, sensing changes in position and providing feedback to the neural control subsystem.20,26,31 Injury to the passive subsystem, such as intervertebral disc degeneration or disruption of the posterior ligaments of the spine, may increase the size of the neutral zone, increasing the demands on the active and neural control subsystems to avoid the development of segmental instability.20,22,32

The active subsystem The active subsystem of the spinal stabilizing system consists of the spinal muscles and tendons. The active and neural control subsystems are primarily responsible for spinal stability in the neutral zone, where passive resistance to movement is minimal.20,27 Without musculotendinous support, the lumbar spine is highly unstable at very low applied loads.33 The relative contributions of different muscle groups to lumbar spine stability have not been clearly delineated, despite much research.34–38 The contributions of the deeper, unisegmental muscles differ from those of the more superficial multisegmental muscles, such as the abdominal and erector spinae muscles.34 Because of their small size, their close proximity to the center of rotation for spinal movements, and their high concentration of muscle spindles,39,40 the unisegmental muscles of the lumbar spine, such as the intertransversarii and the interspinalis muscles, are believed to function primarily as force transducers, providing feedback on spinal position and movements to the neural control subsystem.20 The larger multisegmental muscles are responsible for producing and controlling movements of the lumbar spine, primarily lifting and rotational movements. The lumbar erector spinae muscle group provides most of the extensor force required for most lifting tasks,41 while rotation is produced primarily by the oblique abdominal muscles.35 Both of these muscles have few or no direct attachments to the lumbar spinal motion segments and, therefore, do not exert forces directly on individual motion segments. The multifidus muscle, which originates from the spinous process of the lumbar vertebrae and forms a series of repeating fascicles attaching to the inferior lumbar transverse process, the ilium, and the sacrum, provides segmental control. The multifidus muscle functions as a stabilizer during lifting and rotational movements of the lumbar spine.42 Although not studied extensively, the quadratus lumborum muscle is believed to be the primary active stabilizer during movements in the frontal plane.43

Section 5: Biomechanical Disorders of the Lumbar Spine

The role of the abdominal muscles in spinal stability has been suggested to be the generation of extensor force during lifting tasks, either by increasing intra-abdominal pressure or by creating tension in the lumbodorsal fascia.36,44 Research indicates, however, that the abdominal muscles are not capable of generating substantial extensor force through these mechanisms.37,42 The abdominal muscles are primarily flexors and rotators of the lumbar spine.45 The oblique abdominal and transverses abdominis muscles, with their more horizontal orientation, are thought to contribute to spinal stability by creating a rigid cylinder around the spine and by increasing the stiffness of the lumbar spine.38,46 Continuous activity of the transverses abdominis muscle has been demonstrated throughout flexion and extension movements of the lumbar spine.47

Pain free NZ A

B

The neural control subsystem The neural control subsystem receives input from structures in the passive and active subsystems that allows it to determine the specific requirements for maintaining spinal stability and to act through the spinal musculature to stabilize the spine.20,38,48 Dysfunction of the neural control system may place other spinal structures at risk for injury,20 and the risk of reinjury may be increased if proper functioning of the neural control system is not restored after injury.48 No evidence has linked poor neuromuscular control to an increased risk of initial injury to the lumbar spine, but several studies38,49–52 have shown that patients with LBP often have persistent deficits in neuromuscular control, indicating that recovery of proper function of the neural control subsystem is not automatic following an initial injury. Increased postural sway and slower reaction times have been identified in patients with LBP compared to subjects without LBP.49–51 Luoto et al.50 found in patients undergoing rehabilitation that improvements in reaction time correlated with reduced disability, indicating that neuromuscular control deficits often persist after lumbar spine injury and that reduction in these deficits correlates with improvement in functional status. The neural control system also may help stabilize the spine in anticipation of an applied load. Hodges and Richardson38,52 reported that transverses abdominis and multifidus muscle activity consistently preceded active extremity movement in subjects without LBP, but in patients with LBP the contraction of the transverses abdominis muscles was delayed, possibly indicating deficient neural control. Further research is needed to clarify the role of neural control in patients with LBP, but these preliminary findings indicate that enhancing neural control may be an important consideration in the prevention and rehabilitation of LBP.

A HYPOTHESIS THAT RELATES MOTION TO PAIN The relationship between abnormal intervertebral motion and low back pain is inherent in the definition of clinical spinal instability. In theory, therefore, if intervertebral motion is decreased in a patient with LBP, pain also should be decreased. This assumption is the basis for low back treatments involving surgical fusion, muscle strengthening, and muscle control training.23 Based on the hypothesis that severe LBP is caused by instability between lumbar segments, Olerud et al.53 used external fixation to produce ‘instantaneous fusion’ of selected lumbar spinal segments in 18 patients with chronic severe LBP; 17 patients experienced ‘remarkable relief ’ of pain. The authors suggested that this test could be used to identify unstable segments before surgery. Panjabi et al.,54 in a biomechanical cadaver study of the cervical spine, found that after sta-

C

Fig. 101.4 Hypothesis to relate motion to pain. A ball-in-a-bowl analog representing the motion-pain hypothesis. (A) Control spine with neutral zone (NZ) within pain-free zone. (B) Painful spine has greater NZ bringing the pain-free zone within it. (C) Stabilized spine has decreased NZ and, therefore, is pain-free. (Adapted from Panjabi MM. Clinical spinal instability and low back pain. J Electromyogr Kinesiol 2003; 13:371–379.)

bilization with external fixation the average range of motion decreased by 39.3%, while the neutral zone decreased by an average of 68.8%. Using the ‘ball in a bowl’ analogy, Panjabi23 formulated a hypothesis to relate motion to pain (Fig. 101.4). He postulated that in people without spinal pain the neutral zone and range of motion are normal and the ball moves freely within the pain-free zone (Fig. 101.4A). Injury to or degenerative changes in a spinal column component result in an increase in the neutral zone and the ball moves freely over a larger distance, beyond the pain-free zone (Fig. 101.4B). The spinal stabilizing system reacts to decrease the neutral zone by activating the muscles or by adaptive stiffening of the spinal column over time (e.g. formation of osteophytes) (Fig. 101.4C). The spine also may be stabilized by surgical fusion, muscle strengthening, and retraining of the neuromuscular control system. In the analogy, the ball is now anchored and the spine is again pain free. This hypothesis is unproven and must be validated by future clinical studies.23

CLINICAL ASSESSMENT OF LUMBAR INSTABILITY General classification and evaluation Lumbar segmental instability can be viewed as a purely movement syndrome (Table 101.1): microinstability (without osseous injury) in which directional patterns of motion produce an observed lack of movement control and related symptoms within the neutral zone or may be associated with other conditions (Table 101.2),55

Table 101.I: Directional patterns in syndromes causing microinstability Flexion pattern Extension pattern Lateral shift pattern Multidirectional pattern

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Part 3: Specific Disorders

Table 101.2: Conditions associated with lumbar segmental instability I. Fractures and dislocations II. Infections involving anterior columns A. With progressive loss of vertebral body height and deformity despite treatment with antibiotics B. With progressive neurologic symptoms despite treatment with antibiotics (if accompanied by progressive loss of vertebral body height and deformity) III. Primary and metastatic neoplasms A. With progressive loss of vertebral body height and deformity B. With progressing neurologic symptoms not resulting from direct tumor involvement of the spinal cord, cauda equina, or nerve roots (e.g. caused by progressive loss of vertebral body height and deformity) C. Postsurgical (after resection of neoplasm) IV. Spondylolisthesis A. Isthmic spondylolisthesis 1. L5–S1 progressive deformity in a child, particularly when accompanied by radiographic risk signs (this lesion is rarely unstable in adults) 2. L4–5 deformity (probably unstable in adults) V. Degenerative instabilities A. Primary instabilities 1. Axial rotational instability 2. Translational instability 3. Retrolisthetic instability 4. Progressing degenerative scoliosis 5. Disc disruption syndrome B. Secondary instabilities 1. Post-disc excision – subclassified according to the pattern of instability as described under primary instabilities 2. Postdecompressive laminectomy a. Accentuation of preexisting deformity b. New deformity (i.e. no deformity existed at the time of original decompression; further subclasssified as for primary instabilities) 3. Postspinal fusion a. Above or below a spinal fusion, subclassified as for primary instabilities b. Pseudoarthrosis 4. Postchemonucleolysis VI. Scoliosis (any progressive deformity in a child – subclassified by the criteria of the Scoliosis Research Society From: Hazlett JW, Kinnard P. Lumbar apophyseal process excisions and spinal instability. Spine 1982; 7:171–176.

which are discussed in other chapters. In general, the principles derived from traumatic conditions also are applicable to infections and tumors, which produce instability by mechanical weakening of the anterior and middle columns of the spine. For the evaluation of acute spinal injuries caused by trauma, tumor, or infection, White and Panjabi developed a checklist (Table 101.3) based on anatomy, biomechanics, and clinical observations with the goal of establishing reproducible guidelines.56 In chronic degenerative clinical instability, however, the link between objective findings, which usually are radiographic, and clinical symptoms is not clear and can be confused by coexisting degenerative conditions such as stenosis or spondylolisthesis. An ongoing challenge is to develop diagnostic tests that are both sensitive and specific enough to clearly identify segmental instability. Traditionally, the diagnosis of instability has been based on radiographic observations and measurements. Although disc space narrowing, air within the disc, and calcification of the disc have been observed with spinal instability,57–60 as have hypertrophic changes of the facet joints and claw osteophytes, these are signs of degeneration, not specifically of instability, and are

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not consistently correlated with symptoms. Macnab61 described the traction spur, which is a horizontal osteophyte arising at the attachment of the outer fibers of the anulus on the anterior and lateral aspects of the vertebral body, 2 mm away from its disc surface. This spur is thought to result from excessive tensile stresses applied to the outer vertebral body through the annular fibers as a consequence of segmental instability. No direct, statistically valid, clinical significance of the traction spur, however, has been established. Knutsson62 described a method for diagnosing segmental instability based on lateral radiographs of the lumbar spine taken with the patient in maximal active extension while standing and in maximal active flexion while sitting. He defined instability as 3 mm or more of anterior translation measured between flexion and extension radiographs. Flexion–extension radiographs have now become the standard by which segmental instability is diagnosed. A variety of methods have been developed to more precisely quantify these displacements63–66 either on neutral views or by comparison of flexion and extension views. The amount of anterolithesis considered indicative of instability varies from

Section 5: Biomechanical Disorders of the Lumbar Spine

Table 101.3: Checklist for the diagnosis of clinical instability in the lumbar spine Element

Point value

Anterior elements destroyed or unable to function

2

Posterior elements destroyed or unable to function

2

−8 B1

Radiographic criteria Flexion–extension radiographs Sagittal plane translation >4.5 mm or 15% Sagittal plane rotation >15° at L1–2 and L3–4 >20° at L4–5 >25° at L5–S1 OR Resting radiographs Sagittal plane displacement >4.5 mm or 15% Relative sagittal plane angulation >22°

4 26

−10 B3

Relative sagittal plane angulation

Cauda equina damage

3

Dangerous loading anticipated

1

TOTAL OF 5 OR MORE = UNSTABLE From: White AA, Panjabi MM. Clinical biomechanics of the spine. Philadelphia: JB Lippiincott; 1990.

3 mm to 6 mm or 6–15% of the width of the adjacent vertebra (Fig. 101.5).19,55 Suggested criteria for instability include a relative sagittal angulation of more than 22 degrees on resting radiographs (Fig. 101.6) or more than 15 degrees at L1–2, L2–3, and L3–4 levels, more than 20 degrees at the L4–5 level, and more than 25 degrees at the L5–S1 level on flexion–extension films (Fig. 101.7).67 Limitations in these techniques are that the ranges

B

A

B2

Fig. 101.5 Measurement of sagittal plane translation or Abnormal if: displacement. If translation or A > 4.5mm displacement is 4.5 mm or 15% of the or sagittal diameter of the A –  100 > 15% adjacent vertebra, it is B considered abnormal. (Adapted from White AA III, Panjabi MM. Clinical biomechanics of the spine, 2nd edn. Philadelphia: JB Lippincott; 1990.)

B2 − B1 = 34 B2 − B3 = 36 Abnormal > 22

Fig. 101.6 Measurement of relative sagittal plane angulation of L3–4 functional spine unit (FSU) on a sagittal plane angulation or more than 22 degrees is abnormal and potentially unstable in the lumbar spine. (Adapted from White AA III, Panjabi MM. Clinical biomechanics of the spine, 2nd edn. Philadelphia: JB Lippincott; 1990.)

of normality have not been well established and the accuracy in measurement is low.68,69 Additionally, variations in the exact technique used, large variability in the motion characteristics of individuals without LBP, and high false-positive rates using the established criteria have resulted in questions about the usefulness of flexion–extension radiographs.53,69 Because of the intraand interobserver errors in assessing instability radiographically, Spratt et al.70 recommended that a minimum of 4 mm of forward displacement at L3–4 and L4–5 and displacement of more than 5 mm at L5–S1 are necessary to accurately measure instability. Many other techniques using lateral bending films, bipolar radiography, multidirectional reconstruction, computer digitization, and stereophotogrammetry have been investigated in measuring spinal motion and determining instability.59,71 These methods, however, have not achieved practical clinical use and have not established specific criteria for spinal instability. Perhaps most indicative of chronic instability is the radiographic progression of malalignment or deformity over time, the best two examples of which are degenerative spondylolisthesis and degenerative scoliosis. Newman and Stone72 determined that in degenerative spondylolisthesis progression averaged 2 mm every 4 years. Similar observations have been made about adult degenerative scoliosis 73 and, to a lesser degree, retrolithitic deformities. Of all the radiographic observations and measurements mentioned, however, none has statistically proved to be specifically associated with significant clinical symptoms.57–59,69,71,74 In order to establish a diagnosis of spinal instability, therefore, the clinician must correlate the biomechanical environment and radiographic observations with the patient's clinical history and physical examination. 1113

Part 3: Specific Disorders

Sagittal plane rotation A − B = 8 − (−18) = 26

−18 B 8

A

Abnormal if: L1–2, L2–3, or L3–4 > 15 or L4–5 > 20 or L5–S1 > 25

1114

Fig. 101.7 Measurement of sagittal plane rotation of L4–5 functional spinal unit on dynamic (flexion–extension) lateral radiographs. (Adapted from White AA III, Panjabi MM. Clinical biomechanics of the spine, 2nd edn. Philadelphia: JB Lippincott; 1990.)

To date, no diagnostic gold standard for segmental instability has been identified. Historically, patients complain of chronic and recurrent pain localized to the low back or radiating into the lower extremities and associated with high levels of functional disability.58 Because the condition is mechanically based, the pain typically worsens with greater loads on the spine such as general activity, lifting, standing, sitting, and motions such as bending or twisting. Kirkaldy-Willis and Farfan suggested that segmental instability is a condition in which ‘minor perturbations produce acute pain.’14 Conversely, the pain is relieved by lying supine, the position that places the least mechanical load on the lumbar spine.75 Patients most commonly describe their back pain as recurrent, constant, catching, locking, giving way, or associated with a feeling of instability.76 Several researchers have reported similar physical examination findings that are consistent with a movement–control problem within the neutral zone:14,56,77 (1) active spinal movement with good ranges of spinal mobility but with ‘through-range’ pain or a painful arc rather than end-of-range limitation of motion, and (2) the inability to return to erect standing from forward bending without the use of the hands to assist in this motion. Segmental shifts or hinging were frequently associated with the painful movement. Deep abdominal muscle activation during the provocative movement often reduced or eliminated pain. Neurological examination and neural tissue provocation tests were generally normal.78

by which patients can be evaluated and movement dysfunction analyzed in a segment-specific and individual manner. Common to all the microinstability syndromes are the patient's subjective feeling of instability and an objectively observed lack of movement control and related symptoms within the neutral zone, all of which are associated with an inability to initiate co-contraction of the local muscle system within this zone. The local muscle system consists of muscles that attach directly to the lumbar vertebrae and are responsible for providing segmental stability and directly controlling the lumbar segments. The lumbar multifidus, psoas major, quadratus lumborum, the lumbar parts of the lumbar iliocostalis and longissimus, transverses abdominis, the diaphragm, and posterior fibers of the oblique abdominis internus form part of this local muscle system. Patients may develop compensatory movement strategies that ‘stabilize’ the motion segment out of the neutral zone and towards an end-range position (such as flexion, lateral shift, or extension). This is achieved by the recruitment of global system muscles and by generating high levels of intra-abdominal pressure during low-load tasks. The global muscle system consists of large torque-producing muscles that act on the trunk and spine without directly attaching to it. These muscles include the rectus abdominus, obliquus abdominus externus, and the thoracic part of the lumbar iliocostals; they provide general trunk stabilization but are not capable of exerting a direct segmental influence on the spine.76,78

Clinical syndromes of microinstability

Flexion pattern of microinstability

The directional nature of instability based upon the mechanism of injury, resultant site of tissue damage, and clinical presentation is well understood in the knee and shoulder but poorly understood in the lumbar spine. Based on experimental and radiological data, Dupuis et al.64 concluded that the location of the dominant lesion in the motion segment determines the pattern of instability manifested. Because the motion within the lumbar spine is three-dimensional and involves coupled movements, tissue damage is likely to cause movement dysfunction in more than one direction.76 The descriptions of microinstability syndromes have been developed from clinical observation and are based on the mechanism of spinal injury, the resultant tissue damage, the reported and observed aggravating activities, and movement problems relating to a specific movement quadrant or quadrants. These descriptions provide a basis

Patients with flexion pattern microinstability, the most common type, complain of central back pain and relate their injury to either a single flexion–rotation injury or to repetitive strains relating to flexion–rotation activities. Symptoms and ‘vulnerability’ are aggravated by flexion–rotation movements and patients are unable to sustain semiflexed postures (Fig. 101.8). A loss of segmental lumbar lordosis at the level of the ‘unstable motion segment’ often is noticeable when the patient is standing and is accentuated in sitting postures because patients tend to hold the pelvis in a degree of posterior pelvic tilt. Lower lumbar segmental lordosis is further decreased in flexed postures and usually is associated with increased tone in the upper lumbar and lower thoracic erector spinae muscles, with an associated increase in lordosis in this region. During forward bending, patients have a tendency to flex more at the symptomatic level

Section 5: Biomechanical Disorders of the Lumbar Spine ‘Unstable’ movement zone Flexion

Left side bending

Neutral zone

‘Unstable’ movement zone Flexion

‘Stable’ movement zone

Right side bending

Extension

Left side bending

Neutral zone

‘Stable’ movement zone

Right side bending

Extension

Fig. 101.8 Unstable movement zone: flexion pattern. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)

Fig. 101.9 Unstable movement zone: extension pattern. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)

than at the adjacent levels, usually producing an arc of pain and an inability to return from flexion to neutral without use of the hands to assist the movement. During backward bending, extension often is less in the affected segment than in the more proximal segments. Specific movement testing reveals an inability to differentiate anterior pelvic tilt and low lumbar spine extension independent of upper lumbar and thoracic spine extension. Movement tests such as squatting, sitting with knee extension or hip flexion, ‘sit to stand,’ and forward-loaded postures reveal an inability to control a neutral segmental lordosis, with a tendency to segmentally flex at the unstable motion segment, posteriorly tilt the pelvis, and extend the upper lumbar and thoracic spine. Specific muscle tests reveal an inability to activate the lumbar multifidus in co-contraction with the deep abdominal muscles at the ‘unstable’ muscle segment within a neutral lordosis. Many patients are unable to assume a neutral lordotic lumbar spine posture, particularly in four-point kneeling and sitting. Attempts to activate these muscles commonly are associated with bracing of the abdominal muscles with a loss of breathing control and excessive coactivation of the thoracolumbar erector spinae muscles and external oblique. This is associated with a further flattening of the segmental lordosis at the unstable motion segment, often resulting in pain. Palpation reveals a segmental increase in flexion and rotation mobility at the symptomatic motion segment.

During forward bending, these patients tend to hold the lumbar spine in lordosis (particularly at the level of the unstable motion segment), with a sudden loss of lordosis at the midrange of flexion that usually is associated with an arc of pain. During return-to-neutral, they tend to hyperlordose the spine segmentally before the upright position is achieved, with pain on returning to the erect posture and the necessity to assist the movement with the use of the hands. Specific movement tests reveal an inability to initiate posterior pelvic tilt independent of hip flexion and activation of the gluteals, rectus abdominis, and external obliques. Specific muscles tests also reveal an inability to co-contract the segmental lumbar multifidus with the deep abdominal muscles in a neutral lumbar posture, with a tendency to ‘lock’ the lumbar spine into extension and brace the abdominal muscles. Attempts to isolate deep abdominal muscle activation commonly are associated with excessive activation of the lumbar erector spinae, external oblique, and rectus abdominis and an inability to control diaphragmatic breathing. Palpation reveals a segmental increase in extension and rotation mobility at the symptomatic motion segment.

Extension pattern of microinstability Patients with extension pattern microinstability relate their injury to an extension–rotation incident or repetitive trauma usually associated with sporting activities involving extension–rotation. Their symptoms are aggravated by extension and extension–rotation movements and activities such as standing, fast walking, running, swimming, and overhead activities such as throwing (Fig. 101.9). When the patient is standing, segmental lordosis at the unstable motion segment usually is increased, sometimes with an increased level of segmental muscle activity at this level and anterior pelvic tilt. Extension activities reveal segmental hinging at the affected segment with a loss of segmental lordosis above this level and associated postural ‘sway.’ With the patient prone, hip extension and knee flexion movement tests reveal a loss of co-contraction of the deep abdominal muscles and dominant patterns of activation of the lumbar erector spinae that cause excessive segmental extension–rotation at the unstable level.

Lateral shift pattern of microinstability The recurrent lateral shift pattern of microinstability usually is unidirectional and is associated with unilateral low back pain, usually reported to occur during reaching or rotating in one direction with the spine flexed (Fig. 101.10). This is the same movement direction that patients report as ‘injuring’ their back. Their standing posture is similar to that of patients with flexion pattern microinstability, with a loss of lumbar segmental lordosis at the affected level, but with an associated lateral shift at the same level. Palpation of the lumbar multifidus muscles with the patient standing commonly reveals resting muscle tone on the side of the shift, and atrophy and low tone on the contralateral side. The lateral shift is accentuated when the patient stands on the foot ipsilateral to the shift. When walking, the patient has a tendency to transfer weight through the trunk and upper body rather than through the pelvis. Sagittal spinal movements cause a further lateral shift at the midrange of flexion, usually associated with an arc of pain. With the patient supine, rotary and lateral trunk control is lost in the direction of the shift, with asymmetrical leg loading and unilateral bridging, and during four-point kneeling trunk control is lost when one arm is flexed. Sitting-to-standing and squatting movements usually 1115

Part 3: Specific Disorders ‘Unstable’ movement zone Flexion

Left side bending

Neutral zone

‘Stable’ movement zone

Right side bending

REHABILITATION OF INSTABILITY

Extension Fig. 101.10 Unstable movement zone: lateral shift pattern. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)

reveal a tendency towards lateral trunk shift with increased weightbearing on the side of the shift. Specific muscle testing reveals an inability to bilaterally activate segmental lumbar multifidus in co-contraction with the deep abdominal muscles, with dominance of activation of the quadratus lumborum, lumbar erector spinae, and superficial lumbar multifidus on the side ipsilateral to the shift and an inability to activate the segmental lumbar multifidus on the contralateral side.

Multidirectional pattern of microinstability The most serious and debilitating of the clinical presentations, multidirectional microinstability frequently is associated with a traumatic injury and high levels of pain and functional disability. Provocative movements are described as multidirectional (Fig. 101.11), all weight-bearing postures are painful, and pain-relieving positions during weight-bearing are difficult to obtain. Locking of the spine commonly is reported after sustained flexion, rotation, and extension postures, and patients may assume a flexed, extended, or laterally shifted spinal posture. Excessive segmental shifting and hinging patterns may be present in all movement directions, with ‘jabbing’ pain and associated back muscle spasm. Assuming neutral lordotic spinal positions is very difficult, and attempts to facilitate lumbar

‘Unstable’ movement zone

Flexion

Left side bending

Neutral zone

Right side bending

Extension Fig. 101.11 Unstable movement zone: multidirectional pattern. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.) 1116

multifidus and transverses abdominis co-contraction (especially during weight bearing) usually are associated with a tendency to flex, extend, or laterally shift the spine segmentally, with associated global muscle substitution, bracing of the abdominal wall, and pain. Palpation reveals multidirectional increased intersegmental motion at the symptomatic level. High levels of irritability and an inability to tolerate compression loading in any position indicate a poor prognosis for conservative exercise management.

A recent focus in the rehabilitation of patients with chronic low back pain has been the training of specific muscles, such as the transverses abdominis, diaphragm, and lumbar multifidus, involved in the dynamic stability and segmental control of the spine based on the identification of specific motor control deficits in these muscles.79–81 Once the faulty movement pattern or patterns are identified, the individual components of the movement are isolated and the muscles are retrained for functional tasks specific to the patient's needs. O'Sullivan et al. have reported reductions in pain and functional disability with this exercise training approach in patients with chronic low back pain and a diagnosis of lumbar segmental instability.76,80,82 In its simplest form, this exercise program represents the process of motor learning; three stages have been described in the learning of a new motor skill (Fig. 101.12).76,83

First stage of rehabilitation The first stage of rehabilitation is cognitive and requires a high level of patient awareness so that they can isolate the co-contraction of the local muscle system without global muscle substitution. The goal of the first stage is to train the specific isometric co-contraction of the transversus abdominis with the lumbar multifidus at low levels of maximal voluntary contraction and with controlled respiration during weight-bearing with neutral lordosis. This is accomplished by training independence of the pelvis and lower lumbar spine from the thoracic spine and hips to achieve a neutral lordosis without global muscle substitution and by training central and lateral costal diaphragm breathing control. The patient learns to maintain neutral lordosis and facilitate the ‘drawing up and in’ contraction of the pelvic floor and lower and middle fibers of the transverses abdominis with gentle controlled lateral costal diaphragm breathing and without global muscle substitution. If accurate co-contraction cannot be obtained in weight-bearing postures such as sitting or standing, non-weight-bearing postures, such as four-point kneeling, prone, or supine, can be used. The goal is to teach the patient to achieve bilateral activation of segmental lumbar multifidus (at the unstable level) in co-contraction with the transverses abdominis and controlled lateral costal diaphragm breathing while maintaining a neutral lordosis. This should be done with the patient sitting and standing, with correction to posture as needed. If global muscle substitution occurs (i.e. breathing control is lost, muscle fatigue occurs, or resting pain is increased), the patient is instructed to stop the co-contraction. The inhibition of global muscle substitution is mandatory if appropriate co-contraction is to be obtained. The actions of the obliquus externus abdominis and rectus abdominis muscles can be inhibited by having the patient focus on the pelvic floor contraction and on optimal postural alignment during weight-bearing; ensuring upper lumbar lordosis and lateral costal diaphragm breathing also are beneficial to open the sternal angle. The thoracolumbar erector spinae muscles can be inhibited by having the patient avoid thoracic spine extension and excessive lumbar spine lordosis, focus on independence of pelvic

Section 5: Biomechanical Disorders of the Lumbar Spine

Isolate LMS

Train LMS control

Train LMS functionally

and low lumbar spine movement from thoracic spine and hip movement, and continue lateral costal diaphragm breathing. Palpatory and electromyogram (EMG) biofeedback and muscle release techniques also are helpful. Training is done for 10–15 minutes at least once a day in a quiet environment. Once a pattern of muscle activation has been isolated, the contractions must be done with postural correction while sitting and standing and with the ‘holding’ time of the contraction increased from 10 to 60 seconds before it can be integrated into functional tasks and aerobic activities such as walking. At this stage, a degree of pain control is expected in these postures, which provides a powerful biofeedback for the patient. Three to 6 weeks may be required to achieve this stage.

Second stage of rehabilitation The second stage of rehabilitation is associative, where the focus in on refining a particular movement pattern. The aim of this stage is to identify two or three faulty and pain-producing movement patterns based on the examination and break them down into component movements with high repetitions (50–60). The patient is taken through these steps while isolating the co-contraction of the local muscle system. This is done first with the spine in a neutral lordotic position, then with normal spinal movement, always maintaining segmental control and pain control. This can be done for such movements as sit-to-stand, walking, lifting, bending, twisting, and extending. Patients practice the movement components every day and gradually increase the speed and complexity of the movement pattern until

Fig. 101.12 Stages of rehabilitation based on a motor learning model (LMS, local muscle system). (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)

they can move smoothly and freely. They are encouraged to carry out regular aerobic exercise such as walking while maintaining correct postural alignment, low-level local muscle system co-contraction, and controlled respiration. This helps increase the muscle tone and aids in making the pattern automatic. Patients also are encouraged to perform the co-contractions in situations where they experience or anticipate pain or feel ‘unstable.’ This is essential to having the patterns of co-contraction become automatic. This stage can last from 8 weeks to 4 months, depending on the patient, the degree and nature of the pathology, and the intensity of practice. Once the motor pattern is learned and becomes automatic, patients often report the ability to carry out previously aggravating activities without pain. Although they now no longer require the formal specific exercise program, they are instructed to maintain local muscle system control functionally with postural awareness, while maintaining regular levels of general exercise.

Third stage of rehabilitation The third stage of rehabilitation is the autonomous stage, in which correct performance of motor tasks requires only a low degree of attention.83 At this stage, patients can automatically stabilize their spine during functional demands of daily living. The success of specific exercise intervention in achieving automatic patterns of muscle recruitment has been validated by surface EMG data and reports of long-term good outcomes in patients who completed the protocol.80,82,84 1117

Part 3: Specific Disorders Identify the symptomatic motion segment and correlate this with radiological findings if present

2. Nachemson A. Instability of the lumbar spine. Neurosurg Clin North Am 1991; 2:785–790. 3. Pope M, Frymoyer J, Krag M. Diagnosing instability. Clin Orthop 1992; 296:606–667. 4. Friberg D. Functional radiography of the lumbar spine. Ann Med 1939; 21:341–346.

Identify direction specificity of the instability problem

Determine the neuromuscular strategy of dynamic stabilization

5. Mimura M. Rotational instability of the lumbar spine; a three-dimensional motion study using biplane X-ray analysis system. Nippon Seikeigeka Gakkai Zasshi 1990; 64:546–559. 6. Montgomery D, Fischgrund J. Passive reduction of spondylolisthesis on the operating room table: a retrospective study. J Spinal Disord 1994; 7:167–172. 7. Wood K, Popp C, Transfeldt E, et al. Radiographic evaluation of instability in spondylolisthesis. Spine 1994; 19:1697–1703. 8. Long D, BenDebba M, Torgenson W. Persistent back pain and sciatica in the United States: patient characteristics. J Spinal Disord 1996; 9:40–58. 9. Sihvonen T, Partanen J. Segmental hypermobility in lumbar spine and entrapment of dorsal rami. Electromyogr Clin Neurophysiol 1990; 30:175–180.

Observe for loss of dynamic trunk stabilization during functional movement and limb loading

Identify local muscle dysfunction and faulty patterns of global muscle substitution

Determine the relationship between symptoms and local muscle system control Fig. 101.13 Recommended flow diagram for physical examination assessment to determine spinal instability. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)

10. Gertzbein S. Segmental instability of the lumbar spine. Semin Spinal Surg 1991; 3:130–135. 11. Lindgren K, Sihvonen T, Leino E, et al. Exercise therapy effects on functional radiographic findings and segmental electromyographic activity in lumbar spine instability. Arch Physical Med Rehab 1993; 74:933–939. 12. Gertzbein SD, Seligman J, Holtby R, et al. Centrode patterns and segmental instability in degenerative disc disease. Spine 1985; 10:257–261. 13. Kirkaldy-Willis WH. Presidential symposium on instability of the lumbar spine. Introduction. Spine 1985; 10:254. 14. Kirkaldy-Willis WH, Farfan HF. Instability of the lumbar spine. Clin Orthop 1982; 165:110–123. 15. Panjabi MM, Thibodeau LL, Crisco JJ, et al. What constitutes spinal instability? Clin Neurosurg 1988; 34:313–339. 16. Pope MH, Panjabi M. Biomechanical definition of spinal instability. Spine 1985; 10:255–256. 17. Boden SD, Wiesel SA. Lumbosacral segmental motion in normal individuals. Have we been measuring instability properly? Spine 1989; 15:571–576.

SUMMARY Lumbar segmental instability continues to be a diagnostic challenge. Correlating clinical instability and radiographic instability has been difficult because of the overlap of symptomatic and asymptomatic motion patterns. Additionally, conventional radiography often is insensitive and unreliable in detecting abnormal or excessive intersegmental motion. As the pathomechanics of the lumbar spine have become better understood, however, defining instability in terms of quality of motion throughout the range of motion rather than relying solely on the traditional total range of motion values for diagnosis has been useful in providing a basis by which patients can be evaluated in a segment-specific and individual manner (Fig. 101.13). Lumbar segmental instability can be viewed as a purely movement syndrome: microinstability (without osseous injury) in which directional patterns of motion produce an observed lack of movement control and relative symptoms within the neutral zone or may be associated with other conditions. With increasing understanding of the relative involvement of different muscle groups contributing to lumbar stability, diagnosis-specific rehabilitation protocols are being developed to assist in the assessment and treatment of patients with lumbar instability. Good results have been reported with such an approach using a motor learning model in which the faulty movement pattern or patterns are identified and the components of the movement are isolated and retrained into functional tasks specific to the patient's individual needs. Scientific trials comparing this approach to other treatment methods are required to validate its efficacy.

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69. Hayes MA, Howard TC, Gruel CR, et al. Roentgenographic evaluation of lumbar spine flexion–extension in asymptomatic individuals. Spine 1989; 14:327–381.

45. McGill SM, Norman RW. Potential of lumbodorsal fascia forces to generate back extension moments during squat lifts. J Biomed Eng 1988; 10:312–318.

70. Spratt KF, Weinstein JN, Lehmann TR, et al. Efficacy of flexion and extension treatments incorporating braces for low back pain patients with retrodisplacement, spondylolisthesis, or normal sagittal translation. Spine 1993; 18:1839–1849.

46. Gardner-Morse MG, Stokes IAF. The effects of abdominal muscle coactivation on lumbar spine stability. Spine 1998; 23:86–91. 47. Cresswell AG, Gundstrom H, Thorstensson A. Observations on intra-abdominal pressure and patterns of abdominal intramuscular activity in man. Acta Physiol Scand 1992; 144:409–481.

71. Shaffer WD, Weinstein J. Segmental spinal instability. A survey of measurement techniques. Semin Spine Surg 1991; 3:124–149. 72. Newman PH, Stone KM. The etiology of spondylolisthesis. J Bone Joint Surg [Br] 1963; 45:39–59.

48. Gardner-Morse MG, Stokes IAF, Laible JP. Role of muscles in lumbar spine stability in maximum extensor efforts. J Orthop Res 1995; 13:802–808.

73. Grubb SA, Lipscomb MJ, Conrad RW. Degenerative adult-onset scoliosis. Spine 1988; 13:241–245.

49. Luoto S, Taimela S, Hurri H, et al. Psychomotor speed and postural control in chronic low back pain patients: a controlled follow-up study. Spine 1996; 21:2621–2627.

74. Hayes MA, Tompkins SF, Herndon WA, et al. Clinical and radiological evaluation of lumbosacral motion below fusion levels in idiopathic scoliosis. Spine 1988; 13:1161–1167.

50. Luoto S, Hurri H, Alaranta H. Reaction times in patients with chronic low-back pain. Eur J Phys Med Rehabil 1995; 5:47–50.

75. Nachemson AL. The lumbar spine: an orthopaedic challenge. Spine 1976; 1:59–71.

51. Nies N, Sinnott PL. Variations in balance and body sway in middle-aged adults: subjects with healthy backs compared with subjects with low-back dysfunction. Spine 1991; 16:325–330.

76. O'Sullivan PB. The efficacy of specific stabilizing exercise in the management of chronic low back pain with radiological diagnosis of lumbar segmental instability. PhD thesis, Curtin University of Technology, Western Australia, 1997.

52. Hodges PW, Richardson CA. Contraction of the abdominal muscles associated with movement of the lower limb. Phys Ther 1997; 77:132–142.

77. Paris S. Physical signs of instability. Spine 1985; 10:277–278.

53. Olerud S, Sjostrom L, Karlstrom G, et al. Spontaneous effect of increased stability of the lower lumbar spine in cases of severe chronic back pain. The answer of an external transpeduncular fixation text. Clin Orthop 1986; 203:67–74. 54. Panjabi MM, Lydon C, Vasavada A, et al. On the understanding of clinical instability. Spine 1994; 19:2643–2650. 55. Hazlett JW, Kinnard P. Lumbar apophyseal process excisions and spinal instability. Spine 1982; 7:171–176. 56. White AA, Panjabi MM. Clinical biomechanics of the spine, 2nd edn. Philadelphia: JB Lippincott; 1990. 57. Boden SD, Weisel SW, Laws E Jr, et al. The aging spine. Philadelphia: WB Saunders; 1991. 58. Boden SD, Frymoyer JW. Segmental instability: overview and classification. In: Frymoyer JW, ed. The adult spine: principles and practices, 2nd edn. New York: Raven Press; 1997. 59. Mirkovic S, Garfin SR. ‘Segmental’ instability as related to the degenerative disc. Semin Spine Surg 1991; 3:119–123. 60. Vo P, MacMillan M. The aging spine: clinical instability. South Med J 1994; 1987: S26–S35.

78. O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12. 79. O'Sullivan P, Twomey L, Allison G. Dynamic stabilization of the lumbar spine. Crit Rev Phys Rehab Med 1997; 9:315–330. 80. O'Sullivan P, Twomey L, Allison G. Evaluation of specific stabilizing exercise in the treatment of chronic low back pain with radiological diagnosis of spondylolysis and spondylolisthesis. Spine 1997; 15:2959–2967. 81. Richardson C, Jull G. Muscle control – pain control. What exercise would you prescribe? Manual Therapy 1995; 1:2–10. 82. O'Sullivan P, Twomey L, Allison G, et al. Specific stabilizing exercise in the treatment of chronic low back pain with clinical and radiological diagnosis of lumbar segmental instability. Third Interdisciplinary World Congress on Low Back Pain and Pelvic Pain, Vienna, Austria, 1998. 83. Shumway-Cook A, Woollacott M. Motor control – theory and practical applications. Baltimore: Williams & Wilkins; 1995. 84. O'Sullivan P, Twomey L, Allison G. Altered abdominal muscle recruitment in back patients following specific exercise intervention. J Orthop Sports Phys Ther 1998; 27:1–11.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ iii: Instability

CHAPTER

102

Fusion Surgery Andrew Perry, Choll W. Kim and Steven R. Garfin

INTRODUCTION Fusion has been used for decades to manage a variety of spinal disorders. However, the incidence of spinal fusion surgery varies among countries and among regions within a country. During its infancy, spinal fusion surgery typically involved extensive muscle dissection, copious amounts of autogenous bone graft, bracing, and prolonged bed rest. The introduction of spinal instrumentation provided an opportunity to increase the rate of successful fusion, decrease the recovery period, minimize the cardiopulmonary and musculoskeletal deconditioning resulting from immobility, and allow surgeons to perform more complex spinal reconstructive surgeries. Initial fusion techniques were primarily posterior, but anterior column support was subsequently developed to minimize the failure rates associated with the use of posterior instrumentation. Anterior column fusion can be achieved with bone graft material secured within the disc space from either an anterior or posterior approach. Anterior column fusion has inherent advantages as it occurs along the weight bearing portion of the lumbar spine (80% anterior versus 20% posterior), has superior blood supply, and a superior ability to maintain sagittal alignment. At present, controversy still exists concerning the indications for spinal fusion, the type of procedure to perform, the choice of graft material, and the use of instrumentation. The most widely accepted indication for spinal fusion is instability, which may arise from trauma, tumor, infection, and degenerative disease. Instability may also arise iatrogenically from the surgical treatment of these aforementioned conditions. With the improvement of surgical techniques, along with the development and marketing of spinal instrumentation, there has been a noticeable trend toward the increasing use of spinal instrumentation.1 In general, the goal of surgical fusion is to produce a solid arthrodesis through the segments considered unstable. This is true regardless of the surgical technique used or the approach taken. The end result should be a well-aligned and stable spine that is capable of protecting the neural elements and alleviating pain.

INDICATIONS The indications for surgical fusion of the lumbar spine for instability are not clearly defined. Much of the rationale for fusion has been based on expert opinion and retrospective studies. Over the last decade, there has been increased interest in designing objective studies that use validated outcome measures of success. This is evidenced by the development of a plethora of outcome assessments tools. This differing opinion of surgeons concerning the precise indications for fusion has led to a wide discrepancy in the rate of fusion surgery in various parts of the world. Although there is agreement regarding instability as an indication for fusion, there is a lack of consensus on the precise definition of

instability. The clinical manifestations and assessment of instability of the spinal column are discussed in detail in the previous chapter. In general, the various methods for determining spinal instability are either for trauma, degenerative conditions, or tumor. The White and Panjabi ‘checklist approach’ and the Denis classification system remain the most recognized methods of determining instability in the setting of trauma.2 Recently, Gertzbein and coworkers have developed a detailed description of thoracolumbar fracture patterns that can also be helpful in determining instability.3,4 Gaines and coworkers utilize a ‘load-sharing’ system to determine the stability of the anterior column in the setting of burst fractures.5,6 This system is useful for determining when anterior reconstruction is necessary or when short-segment posterior instrumented fusion may be helpful to treat burst fractures. Whichever system is used, instability due to trauma must take into consideration the mechanism of injury, the degree of deformity, and the location of injured ligamentous and bony structures. Instability due to degenerative conditions is typically described as relative instability. Relative instability due to these conditions is thought to lead to abnormal intervertebral motion which in turn causes pain. It is uncertain whether excessive sagittal translation on flexion–extension radiographs along with high-intensity zones seen on T2-weighted magnetic resonance imaging (MRI) images, endplate irregularities, and Modic changes on MRI, result from relative instability. This type of instability can insidiously develop into spondylolisthesis, degenerative scoliosis, and/or painful disc degeneration. As well, the surgical treatment of these disorders can lead to iatrogenic instability. For destructive lesions, particularly tumors, the degree of vertebral body and/or pedicle involvement and the degree of deformity enter into in the determination of instability.5–7 At present, no method of systematically assessing impending instability exists for infectious processes. Other forms of instability, such as inflammatory, congenital, degenerative, and postoperative instability, are not well assessed with grading systems such as those described by Gaines and coworkers. Once instability is determined, surgical treatment generally requires adequate correction of deformity, reconstruction of bony defects, and fusion of the affected segments. The choice of method by which surgical correction is performed remains a challenging task.

TECHNIQUE The method by which surgery is performed depends on the cause and character of the instability. The available methods of treatment include anterior, posterior, or combined anterior–posterior surgical approaches. General guidelines have some degree of support either in the literature or by consensus (Fig. 102.1). 1121

Part 3: Specific Disorders Trauma

Tumor

Infection

Iatrogenic

Instability

Anterior-only lesion

Anterior column intact

Posterior-only lesion

Anterior column deficient

No canal compromise Normal bone

Osteoporotic bone

Posterior instrumented fusion

Anterior and posterior lesion

Anterior column intact

Posterior fusion

Pseudoarthrosis risk

Anterior column deficient

Posterior fusion

Posterior fusion + anterior interbody fusion

Significant deformity

Canal compromise

Anterior strut + posterior fusion

Anterior strut + posterior fusion Anterior strut + anterior instrumentation

Anterior strut + anterior instrumentation

Fig. 102.1 Algorithm for the surgical treatment of instability via fusion. Instability due to trauma, tumor, infection, as well as iatrogenic induced instability are discussed. Instability due to degenerative conditions such as spondylolisthesis, scoliosis, and disc disease are discussed in previous chapters.

Anterior lesions When instability is due to a lesion that is primarily anterior, surgical stabilization can be performed from an anterior approach. This anterior approach generally involves discectomy, perhaps corpectomy, structural grafting and anterior instrumentation. Anterior surgery is indicated if there is canal compromise due to the anterior lesion, if anterior column stability is deficient, or a previous posterior procedure has failed to stabilize the segment(s). The load-sharing classification system of Gaines and coworkers is one method of determining the integrity of the anterior column.5,6 The load-sharing classification system describes the integrity of the anterior column in the setting of trauma. However, this concept can be applied to other lesions of the anterior column. If there is no significant osteoporosis or deformity that requires correction, then anterior strut grafting with anterior instrumentation will provide sufficient stabilization (Fig. 102.2). However, certain conditions warrant posterior surgery, either together with the anterior surgery or posterior surgery alone. Posterior surgery alone can be used to treat lesions that are otherwise anterior if the anterior column has sufficient stability and there is no need for decompression. In some cases, such as when there is no neurologic deficit, posterior-only surgery can be used to indi1122

rectly reduce retropulsed fragments of bone. Posterior surgery may be further entertained if there are anteriorly exposure risks, such as previous abdominal surgery or severe obesity. Posterior fusion may also be necessary if there is significant osteoporosis. In the setting of osteoporosis, anterior surgery alone may be inadequate in achieving spinal stability (Fig. 102.3).

Posterior lesions When instability stems from a posterior lesion, posterior surgery via instrumented fusion is usually the best option (Fig. 102.4). Unfortunately, instability due to a purely posterior lesion is relatively uncommon. The most common such lesion is the Chance fracture involving a flexion–distraction injury. If there is severe osteoporosis, additional levels may be added to the construct. The length of posterior instrumentation can be extended as necessary to achieve stability without much added difficulty. If necessary, pedicle screws can also be reinforced with bone cement to achieve better fixation in osteoporotic bone. Interbody fusion can be performed posteriorly via transforaminal lumbar interbody fusion (TLIF) or posterior lumbar interbody fusion (PLIF) to improve fusion rates, especially in long fusions or in fusions to the sacrum.

Section 5: Biomechanical Disorders of the Lumbar Spine

C

A A

B

C

Fig. 102.2 L2 pathologic fracture due to metastatic adenocarcinoma. (A) T2-weighted sagittal MRI showing pathologic fracture of L2. (B) T1 axial image with contrast showing canal stenosis. (C) Postoperative radiographs after L2 corpectomy, anterior cage strut, and anterior instrumentation.

Combined anterior–posterior lesions In combined lesions of both the anterior and posterior columns, the surgical approach is dictated by several factors. The first issue is whether anterior surgery is necessary. Anterior surgery is nec-

B

D

Fig. 102.4 Metastatic erosion of posterior elements. (A) Lateral radiograph showing posterior element bony destruction. (B) Sagittal MRI showing canal compromise. (C) Axial CT image showing bone erosion of facets, right pedicles, lamina, and spinous process. (D) Lateral radiograph after resection, decompression, and posterior instrumented fusion.

essary if there is isolated or predominantly anterior canal compromise requiring decompression or if anterior column stability is compromised. Anterior surgery is usually in the form of strut or structural grafting. If there is good bone stock and no significant deformity, then anterior instrumentation may be all that is needed. If there is no canal compromise and the anterior column is stable, posterior instrumented fusion alone is sufficient to obtain stability. If there is osteoporosis, the levels of posterior fusion can be increased for improved fixation. When the anterior column is deficient and it is combined with severe deformity, osteoporosis, or infection, then anterior strut graft fusion combined with posterior instrumentation is necessary (Fig. 102.5).

FACTORS AFFECTING THE OUTCOME OF FUSION SURGERY A

B

Fig. 102.3 Construct failure after anterior-only treatment of a osteoporotic burst fracture. (A) Lateral radiograph immediately after vertebral corpectomy, allograft strut fusion, and anterior instrumentation. Black dotted lines highlight endplates above and below the fusion site. (B) Lateral radiograph 4 weeks after surgery. Black dotted lines highlighting the endplates show interim kyphosis above the construct. The vertebral body above has collapsed into the superior screws.

Achieving arthrodesis and determining when this occurs are still problems that confront the spine surgeon. In general, spinal fusion is a nonphysiological operation that attempts to achieve bone formation in a site where this does not normally occur. In addition to the local and systemic factors that influence typical fracture healing, mechanical factors also influence the healing process during spinal fusion. These mechanical factors include the distance to be bridged by the fusion mass, the magnitude and planes of motion, and the structural properties of the graft. For convenience, the factors that affect successful spinal arthrodesis can be grouped into local, biologic, and surgical factors. 1123

Part 3: Specific Disorders

the graft material is to be placed also plays an important role in determining the outcome of fusion. Decortication allows vascularization of the fusion bed. In addition, it is important to remove avascular tissue such as scar tissue during surgery since a fusion bed with excessive scar tissue is less likely to achieve successful fusion.

Biologic factors Nutrition C

A

Malnutrition is associated with reduced cognitive function, poor wound healing, impaired muscle function, decreased bone mass, immune dysfunction, anemia, delayed recovery from surgery, and ultimately increased morbidity and mortality.7 Nutritional deficiencies can be confirmed using various studies such as total white blood cell count, serum albumin and total protein, transferrin levels, nitrogen balance, and anthropometric measurements.

Hormones

B

D

Fig. 102.5 Spinal osteomyelitis and epidural abscess. (A) Contrastenhanced sagittal MRI showing osteomyelitis of L5 and S1 along with anterior and posterior epidural abscesses. (B) Contrast-enhanced axial MRI showing circumferential infection. There are also abscesses in the right paraspinal muscles. (C) Lateral radiograph after surgical treatment. Treatment involved L5 and partial S1 laminectomies and right L5–S1 facetectomy. (D) Second stage partial L5–S1 corpectomies with cage strut graft were followed by third stage posterior instrumented fusion.

Smoking

The physiologic and biomechanical forces acting on the healing of anterior interbody and posterolateral fusions are quite different. Anterior interbody fusions are revascularized through the vertebral bodies themselves and the graft material used in the interspace is under compressive loading. Bone healing is favored under conditions of axial loading and stability. As such, interbody fusion tends to occur more readily than posterolateral spinal fusion. In a posterolateral fusion, revascularization is primarily derived from the bony surface of the transverse process and surrounding muscle tissue. In this region, there are few or no compressive forces acting on the graft material. Consequently, the posterolateral spinal fusion environment generally does not tolerate the use of purely osteoconductive materials as stand-alone substitutes. At this site, osteoinductive substitutes are more likely to be successful as extenders or enhancers for spinal fusion. In the anterior spine, purely osteoconductive substitutes may be suitable when they are rigidly immobilized.

The pathophysiological effects of smoking are multidimensional and include arteriolar vasoconstriction, cellular hypoxia, demineralization of bone, and delayed revascularization. Cigarette smoking also inhibits osteoblastic activity resulting in decreased rate of successful unions, with slowed bone healing and prolonged treatment.12,13 It appears that cigarette smoke has a greater impact upon cancellous bone than cortical bone, and causes decreased bone healing around implants. The constituents of cigarette smoke, and not only nicotine, seem to be more important.14,15 Complication rates after surgery and the rate of nonunion in smokers has been shown to be consistently higher than in nonsmokers.16,17 In a recent prospective clinical study designed to determine the effects of smoking on the healing of tibial deformities, half of the smokers and only one-fifth of nonsmokers developed complications.18 Smokers required an average of 16 days more treatment. Delayed healing and pseudoarthroses were more common in smokers than nonsmokers. The risk ratio for smokers to develop complications as compared to nonsmokers was 2.5.18 For spinal fusion, an increased rate of pseudoarthrosis has been observed following posterolateral lumbar spine grafting or anterior cervical interbody fusion in smokers.19 Smoking had a significant negative impact on healing and clinical recovery after these procedures.

Fusion site

Drugs

Arthrodesis depends on ingress of osteoprogenitor and inflammatory cells from the fusion bed and from the surviving bone cells located in the bone graft. Bone healing is greatly affected by the local blood supply along with the availability of osteoprogenitor cells. The fusion bed vascular supply is a source of supportive nutrients, a vehicle for endocrine signals, and a pathway for the recruitment of osteoprogenitor and inflammatory cells. The preparation of the bony surfaces where

Many drugs such as methotrexate and Adriamycin can inhibit bone formation if administered in the early postoperative period. Nonsteroidal antiinflammatory drugs (NSAIDs) act by inhibiting action of cyclooxygenase (COX) enzymes and decreasing production of prostaglandins (PGs). This can result in diminished bone formation, healing, and remodeling. These effects seem to be greater with nonselective COX inhibitors, such as ketorolac, than with selective COX-2 inhibitors

Local factors Location

1124

Thyroid hormones have a direct stimulatory effect on cartilage growth and maturation, and promote bone healing.8 These hormones are required for the synthesis of somatomedins by the liver.9 Growth hormone promotes bone healing by increasing calcium absorption from the intestine, and promoting bone formation and mineralization.8 Androgens and estrogens are considered important for skeletal development and preventing age-related bone loss. Estrogens may increase bone mineralization through their effect on increasing serum parathyroid hormone (PTH).10 Excess corticosteroids can negatively affect bone healing by decreasing synthesis of the major components of the bone matrix. These steroids have also been shown to inhibit the differentiation of osteoblasts from mesenchymal cells.11

Section 5: Biomechanical Disorders of the Lumbar Spine

at therapeutic levels.20 Ketorolac also decreases bone mineralization and endochondral ossification in a dose-dependent manner.21 Other NSAIDs, such as diclofenac, can also significantly delay fracture healing.22 The timing of administration of NSAIDs also appears important. In animal studies, the earlier indometacin was resumed postoperatively, the greater was its negative effect on intertransverse process arthrodesis.23 Recombinant bone morphogenetic protein-2 (BMP-2), however, seems to show promise for combating the inhibitory effect of ketorolac on bone formation during spinal arthrodesis.24 It has been observed that longer duration of administration of selective COX inhibitors decreases the rate of successful fusion.25 In a recent study, however, it was found that the perioperative (shortterm) administration of celecoxib had no apparent effect on the rate of nonunuion at 1 year following surgery. In this study, patients had elective decompressive lumbar laminectomy and instrumented spinal fusion. In addition, the use of the selective COX-2-specific NSAID resulted in a significant reduction in postoperative pain and opioid use following surgery.26 As such, short-term administration of selective COX inhibitors for perioperative pain, unlike long-term use, appears to be a reasonable therapeutic option. AGE The effects of aging on spinal fusion are multifactorial. With the elderly there is often a decrease in food intake secondary to reduction in appetite. If prolonged, this can lead to a decline in nutritional status. Bone healing, including spinal fusion is affected by the nutritional status of the individual.7 Common medical conditions, such as renal and cardiac insufficiency, may exist in the elderly and can affect bone healing. The clinical observation that incisional wounds also heal less well in the aged may be secondary to these coexisting pathologies.27 The number of osteogenic stem cells may be more deficient in the elderly than in younger individuals. In animal studies, the numbers of osteoprogenitor cells present in the bone marrow from aged rats were 65% lower than the amount found in young adults. These cells were also 10 times less likely to differentiate in vitro and to form bone in vivo.28 However, bone-stimulating growth factors may have a role in increasing the bone-forming capacity of aged bone in the future.29,30 During aging, bone mass loss, structural continuity, and strength gradually diminish. Osteoporotic bone is weak and difficult to stabilize with spinal instrumentation. Although gradual bone loss starts at 30 years of age, an accelerated rate of loss occurs after menopause in women. Men also experience bone loss, but in a more insidious fashion. The rate of successful fusion in elderly individuals of both sexes with osteoporotic bone tends to be lower.31

Surgical factors Approaches The surgical approach can affect the outcome of lumbar fusion. Fritzell et al. studied the outcomes of fusion surgery using three different, well-accepted techniques of lumbar fusion.32 In their randomized prospective study, they show that posterolateral fusion without instrumentation achieves arthrodesis in 72% of patients. With the addition of posterior instrumentation, the fusion rate increased to 87%. For patients treated with combined posterior instrumented fusion and interbody fusion (i.e. circumferential fusion) the fusion rate was 91%. Overall, the fusion rates for grafts used in circumferential, posterior interbody, anterior interbody, and posterolateral fusions methods are about 91% , 89%, 86%, and 85%, respectively.1

Instrumentation It is well established that spinal instrumentation increases the likelihood of successful fusion. Fischgrund et al. demonstrated that the fusion rate with instrumentation was twice that obtained without

instrumentation for patients with degenerative spondylolisthesis.33 Zdeblick observed statistically greater fusion rates in patients with rigid instrumentation than those without. In his study, the fusion success with semirigid instrumentation (plate/screw system) was not different from that obtained without instrumentation.34 In contrast, Thomsen et al. found that the fusion rates were not significantly different between instrumented (supplementary pedicle screw fixation) and noninstrumented groups for patients undergoing posterolateral lumbar spinal fusion.35 Perhaps the best perspective regarding the impact of instrumentation on the fusion rate was revealed in a meta-analysis of the outcomes of lumbar fusion surgeries that were reported in the literature from 1970 to 2000.1 In this study, the average instrumented fusion rate (89%) was significantly higher than the noninstrumented fusion rate (84%). The fusion rates with semirigid instrumentation and rigid instrumentation were not significantly different (91% and 88%, respectively). In addition, both semi-rigid and rigid stabilization resulted in significantly higher fusion rates than no instrumentation (p=0.019, p=0.022, respectively).

Number of levels fused The number of levels fused is an important factor that can dramatically affect the outcome of spinal fusion. In a retrospective study, the length of hospital stay, operative time, amount of intraoperative blood loss, and transfusion requirements were closely related to the number of levels fused for patients having revision posterior lumbar spine decompression, fusion, and segmental instrumentation. The arthrodesis rate also decreased with number of levels fused.36 Exact figures of fusion rates with number of levels fused vary according to the disease or condition in question, the approach, and whether the fusion was augmented with bone growth enhancers. In a meta-analysis study which assessed data obtained from fusions done over the past 20 years, the mean fusion rates were 89% in one-level operations, 69% in two-level operations, and 71% when three or more levels were fused.1

Graft source The choice of graft material can influence the outcome of a spinal fusion. During spinal arthrodesis, graft material may not only provide structural support but may also possess osteogenic, osteoconductive, and/or osteoinductive properties. The osteogenic potential of a graft is determined by the number of viable cells that can form bone or differentiate into bone-forming cells. Osteogenic grafts are usually obtained from fresh autologous bone and bone marrow cells. Osteoconduction is the physical property of a graft that allows vascular ingrowth and infiltration of osteogenic precursor cells. Osteoconductive grafts act as nonviable scaffolds that support the healing response. Examples are autologous and allograft bone, bone matrix, collagen, and calcium phosphate ceramics. Osteoinduction is the ability of a substance or factor to stimulate an undetermined osteoprogenitor cell to differentiate into an osteogenic precursor. The most common source of graft material is autogenous bone from the iliac crest. This is still considered the gold standard. However, due to the morbidity of autograft harvesting along with its limited supply, allograft bone and synthetic bone substitutes are being used with increasing frequency. Autograft cancellous bone has all three ideal transplant properties: osteogenicity, osteoconductivity, and osteoinductivity. It possesses a large trabecular surface area for new bone formation and contains viable bone cells. Cortical autologous bone grafts have less capacity for new bone formation but are ideal when structural support is needed. Allograft bone can be procured in greater quantities than autografts. Allografts are incorporated more slowly and to a lesser 1125

Part 3: Specific Disorders

degree than autografts. Fresh-frozen grafts are stronger, more immunogenic, and more completely incorporated than freezedried grafts. In most studies, fusion using autograft bone leads to higher fusion rates than fusion, using allograft or synthetic bone substitutes alone. In a selected comparison, uninstrumented interbody fusion using autograft was compared with uninstrumented interbody fusion using autograft/allograft mixtures. The fusion rates were 88% and 82%, respectively, and were not statistically different.37 If used anteriorly, allografts are well suited for reconstructive procedures and have good fusion rates, especially if combined with posterior fusions. When used with BMP-2, the effectiveness of an allograft can be increased. In one study, patients undergoing anterior lumbar fusion surgery with structural threaded cortical allograft bone dowels showed higher rates of fusion, improved neurologic status, and lower back and leg pain when compared with the autologous control group.38 Considering the possible complications associated with harvesting iliac crest bone, the use of allogenic bone appears justified.39,40 Xenografts have been used in orthopedic surgery and have included cow horn and bovine bone. Due to the immune response evoked by the host to these materials, xenografts are not commonly used in spine surgery.

Graft morphology The size of a structural bone graft, its positioning, and elasticity should be considered when used for lumbar fusions. A larger graft with low stiffness should be favored from a mechanical point of view. Stiff bone grafts increase stresses on adjacent endplates.41 Placement of a bone graft in a more anterior location can better resist flexion moments and decreases the tensile forces acting on the posterior ligaments. Bone grafts placed at a posterior site are better in resisting torsional moments and decreasing contact force of the facet joint in the fused segment.42 The degree to which these aforementioned observations may influence the long-term clinical outcome of spinal fusion is unclear.

Bone morphogenic proteins The osteoinductive potentials of bone morphogenic proteins have been well described. Recombinant human BMP-2 has been approved by the FDA for single-level interbody fusions of the lumbar spine. In the first prospective, multicenter study involving 279 patients with degenerative lumbar disc, the fusion rate at 24 months was higher for the BMP-treated group compared with those who received autogenous iliac-crest bone graft (94.5% versus 88.7%).43 Clinical trials have shown that rhBMP-2-filled fusion cages can eliminate the need for harvesting iliac crest graft.44,45 The benefits of BMPs in other applications of spinal fusion are currently under study.

Interbody cages Intervertebral cages or spacers were developed to prevent the collapse and pseudoarthrosis seen with bone-only interbody fusions. Initially, the early types consisted of vertically placed titanium mesh cylinders and rectangular carbon fiber cages. Later, this was followed by the development of stand-alone threaded Bagby and Kuslich (BAK) intervertebral cages. Threaded intervertebral cages usually stabilize a segment through distraction and tensioning of the annular and ligamentous structures. By partially reaming the endplates, one may expose cancellous bone for arthrodesis, increasing the likelihood for successful fusion.46 Anteriorly placed threaded cages significantly stabilize the motion segment in all directions except extension. With posteriorly placed cages, there is less stability as a result of the facetectomy required for placement of the device. Interbody cages may 1126

be implanted via a variety of surgical approaches to the disc space, with or without supplemental posterior fixation. For single-level degenerative disc disease, anteriorly placed intervertebral threaded cages have shown a high degree of clinical success.47 Both patient selection and technical expertise seem equally important in determining patient outcome.47 Patients with multilevel disease, normal (tall) looking disc on radiographs, or with osteoporotic bone, have a higher incidence of complication and failure. Posteriorly or transforaminally placed cages which are supplemented by pedicle screws seem successful for the treatment of spondylolisthesis.47 For the management of pure discogenic pain without collapse, multilevel disc disease, or disc degeneration in elderly patients, the use of cages is less certain.47

Electrical stimulation During the last 20 years, electrical stimulation has shown promise for improving the success rate of spinal fusion. The maximum benefit, in terms of an increased successful fusion rate, is estimated to be approximately 10%. At present, the types of electrical stimulation used as adjuncts to spinal fusion includes direct current electrical stimulation (DCES), pulsed electromagnetic fields (PEMF), combined magnetic fields (CMF), and capacitive coupling. These devises are usually implanted close to the fusion mass intraoperatively or worn externally. Internal devices utilize DCES. Their mechanism of action is thought to involve the attraction of charged proteins, growth factors, and bone-forming cells to the fusion site. They may also alter the function of voltage-gated channels with activation of cyclic AMP and triggering of a second messenger cascade. Other proposed mechanisms include Faradic reactions at the cathode–bone graft interface with formation of OH and H2O2. This reduces the local oxygen tension (PO2) and slightly increases the pH. The end result of both the electric field effects and the Faradic products is a stimulation of calcium uptake.48–50 Increased pH stimulates osteoblastic bone formation and mineralization but inhibits osteoclastic bone resorption. The end result is an increased rate of new bone formation.51 In contrast to DCES, PEMF devices generate an electromagnetic field across the spinal fusion area and are worn externally, usually 3–8 hours per day for 3–6 months. As these braces can be removed by patients, noncompliance can potentially hinder treatment.52 Successful arthrodesis can also be obtained with shorter application times. In a prospective study by Linovitz and coworkers, successful outcomes for one-level or two-level fusions (between L3 and S1) without instrumentation, either with autograft alone or in combination with allograft, were obtained when the combined magnetic field device was worn for 30 minutes per day for 9 months.53 Such devices with shorter wearing times may have better patient acceptance. The mechanism of action of PEMF is not well understood, but is thought to involve alterations in cell membrane potentials and parahormone receptors of bone cells. An increase in calcium influx into bone cells, promotion of calcification, and vascularization also occurs with PEMF. PEMF may also be capable of altering the production of cytokines, and increasing the expression of bone morphogenic protein (BMP)-2 and BMP-4 mRNA by cells. In ovariectomized rats, PEMF stimulation can decrease local production of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6) and inhibit osteoclastogenesis.54 A possible effect on prostaglandin E2 (PGE2) levels is also suggested.55 PEMF seems to enhance cellular differentiation and does increase the number of bone-forming cells. This stimulatory effect is greatest during the early stages of bone healing.56 However, there may be some place for PEMF stimulation in the later stages of treatment in cases of nonunion. For example, in

Section 5: Biomechanical Disorders of the Lumbar Spine

patients with symptomatic pseudoarthrosis after lumbar spinal fusion, pulsed electromagnetic field stimulation has been shown to be an effective nonoperative salvage approach to achieving fusion.57 In one study, 67% of patients who were treated with a pulsed electromagnetic field device worn consistently 2 hours a day for at least 90 days achieved fusion. Treatment was equally effective for posterolateral fusions (66%) as with interbody fusions (69%).57 Since 1985 when the first report of the clinical efficacy of PEMF on spinal fusion was published, numerous studies have demonstrated the benefits of electrical stimulation for improving the success rate of spinal fusion surgery.58,59 Not all modes of electrical stimulation are equally effective in promoting successful spinal arthrodesis. Clinical data reveal superiority of DCES to PEMF, particularly when used to enhance posterior spinal fusions. Capacitive coupling seems superior to PEMF, and perhaps DCES as an adjunct to posterior spinal fusion.60

Demineralized bone matrix Demineralized bone matrix (DBM) is prepared by decalcification of cortical bone. It is less immunogenic than allograft bone graft. The active components consists of several glycoproteins including BMPs. Preclinical investigations on the use of DBM in the spine have shown promising results. However, clinical studies on the effects on DBM on spinal fusion are lacking. In one study, titanium mesh cages and coralline hydroxyapatite combined with DBM were effective for anterior interbody fusion of the lumbar spine when used as part of a rigidly instrumented circumferential fusion.61 DBM was also effective in reducing the amount of autologous bone graft required for successful lumbar spinal fusion.62 Further clinical studies are needed to clearly establish the usefulness of DBM in spinal fusion.

SUMMARY Spinal fusion for the treatment of lumbar instability remains a complex topic. Accurate determination of lumbar instability requires evaluation of multiple factors, including patient disease, cause/mechanism of injury, location of injury, and anticipated demands of the patient. The decision for surgery requires a careful appraisal of all of these factors if high success rates are to be achieved. Determining the method by which the surgery is performed, whether to use instrumentation, along with choosing the proper graft type and deciding upon the appropriateness of including adjunctive materials is equally complex. When these key decisions are correctly instituted, the ultimate goal of fusion – achieving spinal function by protecting the neural elements, restoring spinal alignment, and alleviating pain and disability associated with instability – will be achieved.

References 1. Bono CM, Lee CK. Critical analysis of trends in fusion for degenerative disc disease over the past 20 years: influence of technique on fusion rate and clinical outcome. Spine 2004; 29(4):455–463; discussion Z5.

7. Einhorn TA, Bonnarens F, Burstein AH. The contributions of dietary protein and minerals to the healing of experimental fractures. A biomechanical study. J Bone Joint Surg [Am] 1986; 68(9):1389–1395. 8. Udupa KN, Gupta LP. The effect of growth hormone and thyroxine in healing of fractures. Indian J Med Res 1965; 53(7):623–628. 9. Schalch DS, Heinrich UE, Draznin B, et al. Role of the liver in regulating somatomedin activity: hormonal effects on the synthesis and release of insulin-like growth factor and its carrier protein by the isolated perfused rat liver. Endocrinology 1979; 104(4):1143–1151. 10. Gallagher JC, Riggs BL, DeLuca HF. Effect of estrogen on calcium absorption and serum vitamin D metabolites in postmenopausal osteoporosis. J Clin Endocrinol Metab 1980; 51(6):1359–1364. 11. Pereira RM, Delany AM, Canalis E. Cortisol inhibits the differentiation and apoptosis of osteoblasts in culture. Bone 2001; 28(5):484–490. 12. Hoogendoorn JM, Simmermacher RK, Schellekens PP, et al. [Adverse effects of smoking on healing of bones and soft tissues]. Unfallchirurg 2002; 105(1):76–81. 13. Harvey EJ, Agel J, Selznick HS, et al. Deleterious effect of smoking on healing of open tibia-shaft fractures. Am J Orthop 2002; 31(9):518–521. 14. Cesar-Neto JB, Duarte PM, Sallum EA, et al. A comparative study on the effect of nicotine administration and cigarette smoke inhalation on bone healing around titanium implants. J Periodontol 2003; 74(10):1454–1459. 15. Nociti FH Jr, Cesar NJ, Carvalho MD, et al. Bone density around titanium implants may be influenced by intermittent cigarette smoke inhalation: a histometric study in rats. Int J Oral Maxillofac Implants 2002; 17(3):347–352. 16. Ishikawa SN, Murphy GA, Richardson EG. The effect of cigarette smoking on hindfoot fusions. Foot Ankle Int 2002; 23(11):996–998. 17. Adams CI, Keating JF, Court-Brown CM. Cigarette smoking and open tibial fractures. Injury 2001; 32(1):61–65. 18. Toksvig-Larsen S. Cigarette smoking delays bone healing: a prospective study of 200 patients operated on by the hemicallotasis technique. Acta Orthop Scand 2004; 75(3):347–351. 19. Hilibrand AS, Fye MA, Emery SE, et al. Impact of smoking on the outcome of anterior cervical arthrodesis with interbody or strut-grafting. J Bone Joint Surg [Am] 2001; 83A(5):668–673. 20. Gerstenfeld LC, Thiede M, Seibert K, et al. Differential inhibition of fracture healing by non-selective and cyclooxygenase-2 selective non-steroidal anti-inflammatory drugs. J Orthop Res 2003; 21(4):670–675. 21. Ho ML, Chang JK, Wang GJ. Effects of ketorolac on bone repair: A radiographic study in modeled demineralized bone matrix grafted rabbits. Pharmacology 1998; 57(3):148–159. 22. Beck A, Krischak G, Sorg T, et al. Influence of diclofenac (group of nonsteroidal anti-inflammatory drugs) on fracture healing. Arch Orthop Trauma Surg 2003; 123(7):327–332. 23. Riew KD, Long J, Rhee J, et al. Time-dependent inhibitory effects of indomethacin on spinal fusion. J Bone Joint Surg [Am] 2003; 85A(4):632–634. 24. Martin GJ Jr, Boden SD, Titus L. Recombinant human bone morphogenetic protein2 overcomes the inhibitory effect of ketorolac, a nonsteroidal anti-inflammatory drug (NSAID), on posterolateral lumbar intertransverse process spinal fusion. Spine 1999; 24(21):2188–2193; discussion 2193–2194. 25. Gerstenfeld LC, Einhorn TA. COX inhibitors and their effects on bone healing. Expert Opin Drug Saf 2004; 3(2):131–136. 26. Reuben SS, Ekman EF. The effect of cyclooxygenase-2 inhibition on analgesia and spinal fusion. J Bone Joint Surg [Am] 2005; 87A(3):536–542. 27. Viidik A, Mosekilde L, Quirinia A. [Research on aging: biological perspectives]. Ugeskr Laeger 1992; 154(42):2884–2889. 28. Quarto R, Thomas D, Liang CT. Bone progenitor cell deficits and the age-associated decline in bone repair capacity. Calcif Tissue Int 1995; 56(2):123–129.

2. White AA, Panjabi M. Clinical biomechanics of the spine. Philadelphia: Lippincott; 1990.

29. Blumenfeld I, Srouji S, Lanir Y, et al. Enhancement of bone defect healing in old rats by TGF-beta and IGF-1. Exp Gerontol 2002; 37(4):553–565.

3. Gertzbein SD, Seligman J, Holtby R, et al. Centrode patterns and segmental instability in degenerative disc disease. Spine 1985; 10(3):257–261.

30. Sumner DR, Turner TM, Cohen M, et al. Aging does not lessen the effectiveness of TGFbeta2-enhanced bone regeneration. J Bone Miner Res 2003; 18(4):730–736.

4. Gertzbein SD, Seligman J, Holtby R, et al. Centrode characteristics of the lumbar spine as a function of segmental instability. Clin Orthop 1986; 208:48–51.

31. Tunturi T, Kataja M, Keski-Nisula L, et al. Posterior fusion of the lumbosacral spine. Evaluation of the operative results and the factors influencing them. Acta Orthop Scand 1979; 50(4):415–425.

5. McCormack T, Karaikovic E, Gaines RW. The load sharing classification of spine fractures. Spine 1994; 19(15):1741–1744. 6. Parker JW, Lane JR, Karaikovic EE, Gaines RW. Successful short-segment instrumentation and fusion for thoracolumbar spine fractures: a consecutive 4½-year series. Spine 2000; 25(9):1157–1170.

32. Fritzell P, Hagg O, Wessberg P, et al. 2001 Volvo Award Winner in clinical studies: Lumbar fusion versus nonsurgical treatment for chronic low back pain: a multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine 2001; 26(23):2521–2532; discussion 2532–2534.

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Part 3: Specific Disorders 33. Fischgrund JS, Mackay M, Herkowitz HN, et al. 1997 Volvo Award winner in clinical studies. Degenerative lumbar spondylolisthesis with spinal stenosis: a prospective, randomized study comparing decompressive laminectomy and arthrodesis with and without spinal instrumentation. Spine 1997; 22(24):2807–2812.

47. Zdeblick TA, Phillips FM. Interbody cage devices. Spine 2003; 28(15 Suppl): S2–S7.

34. Zdeblick TA. A prospective, randomized study of lumbar fusion. Preliminary results. Spine 1993; 18(8):983–991.

49. Brighton CT, Friedenberg ZB, Black J, et al. Electrically induced osteogenesis: relationship between charge, current density, and the amount of bone formed: introduction of a new cathode concept. Clin Orthop 1981; 161:122–132.

35. Thomsen K, Christensen FB, Eiskjaer SP, et al. 1997 Volvo Award winner in clinical studies. The effect of pedicle screw instrumentation on functional outcome and fusion rates in posterolateral lumbar spinal fusion: a prospective, randomized clinical study. Spine 1997; 22(24):2813–2822. 36. Zheng F, Cammisa FP Jr, Sandhu HS, et al. Factors predicting hospital stay, operative time, blood loss, and transfusion in patients undergoing revision posterior lumbar spine decompression, fusion, and segmental instrumentation. Spine 2002; 27(8):818–824. 37. Urist MR, Dawson E. Intertransverse process fusion with the aid of chemosterilized autolyzed antigen-extracted allogeneic (AAA) bone. Clin Orthop 1981; 154: 97–113. 38. Burkus JK, Transfeldt EE, Kitchel SH, et al. Clinical and radiographic outcomes of anterior lumbar interbody fusion using recombinant human bone morphogenetic protein-2. Spine 2002; 27(21):2396–2408. 39. Ehrler DM, Vaccaro AR. The use of allograft bone in lumbar spine surgery. Clin Orthop 2000; 371:38–45. 40. Wimmer C, Krismer M, Gluch H, et al. Autogenic versus allogenic bone grafts in anterior lumbar interbody fusion. Clin Orthop 1999; 360:122–126. 41. Cheng CK, Chen CS, Liu CL. Biomechanical analysis of the lumbar spine with anterior interbody fusion on the different locations of the bone grafts. Biomed Mater Eng 2002; 12(4):367–674.

50. Brighton CT, Friedenberg ZB. Electrical stimulation and oxygen tension. Ann NY Acad Sci 1974; 238:314–320. 51. Oishi M, Onesti ST. Electrical bone graft stimulation for spinal fusion: a review. Neurosurgery 2000; 47(5):1041–1055; discussion 1055–1056. 52. Mooney ML, Carlson P, Szentpetery S, et al. A prospective study of the clinical utility of lymphocyte monitoring in the cardiac transplant recipient. Transplantation 1990; 50(6):951–954. 53. Linovitz RJ, Pathria M, Bernhardt M, et al. Combined magnetic fields accelerate and increase spinal fusion: a double-blind, randomized, placebo controlled study. Spine 2002; 27(13):1383–1389; discussion 1389. 54. Chang K, Hong-Shong Chang W, Yu YH, et al. Pulsed electromagnetic field stimulation of bone marrow cells derived from ovariectomized rats affects osteoclast formation and local factor production. Bioelectromagnetics 2004; 25(2):134–141. 55. Chang K, Chang WH. Pulsed electromagnetic fields prevent osteoporosis in an ovariectomized female rat model: a prostaglandin E2-associated process. Bioelectromagnetics 2003; 24(3):189–198. 56. Diniz P, Shomura K, Soejima K, et al. Effects of pulsed electromagnetic field (PEMF) stimulation on bone tissue-like formation are dependent on the maturation stages of the osteoblasts. Bioelectromagnetics 2002; 23(5):398–405.

42. Zander T, Rohlmann A, Klockner C, et al. Effect of bone graft characteristics on the mechanical behavior of the lumbar spine. J Biomech 2002; 35(4):491–497.

57. Simmons JW Jr, Mooney V, Thacker I. Pseudoarthrosis after lumbar spine fusion: nonoperative salvage with pulsed electromagnetic fields. Am J Orthop 2004; 33(1):27–30.

43. Burkus JK, Gornet MF, Dickman CA, et al. Anterior lumbar interbody fusion using rhBMP-2 with tapered interbody cages. J Spinal Disord Tech 2002; 15(5): 337–349.

58. Mooney V. A randomized double-blind prospective study of the efficacy of pulsed electromagnetic fields for interbody lumbar fusions. Spine 1990; 15(7):708–712.

44. Haid RW Jr, Branch CL Jr, Alexander JT, et al. Posterior lumbar interbody fusion using recombinant human bone morphogenetic protein type 2 with cylindrical interbody cages. Spine J 2004; 4(5):527–538; discussion 538–539. 45. Mummaneni PV, Pan J, Haid RW, et al. Contribution of recombinant human bone morphogenetic protein-2 to the rapid creation of interbody fusion when used in transforaminal lumbar interbody fusion: a preliminary report. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine 2004; 1(1):19–23. 46. Sasso RC, Kitchel SH, Dawson EG. A prospective, randomized controlled clinical trial of anterior lumbar interbody fusion using a titanium cylindrical threaded fusion device. Spine 2004; 29(2):113–122; discussion 121–122.

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48. Baranowski TJ Jr, Black J, Brighton CT, Friedenberg ZB. Electrical osteogenesis by low direct current. J Orthop Res 1983; 1(2):120–128.

59. Mooney V, McDermott KL, Song J. Effects of smoking and maturation on longterm maintenance of lumbar spinal fusion success. J Spinal Disord 1999; 12(5): 380–385. 60. Kahanovitz N. Electrical stimulation of spinal fusion: a scientific and clinical update. Spine J 2002; 2(2):145–150. 61. Thalgott JS, Giuffre JM, Klezl Z, et al. Anterior lumbar interbody fusion with titanium mesh cages, coralline hydroxyapatite, and demineralized bone matrix as part of a circumferential fusion. Spine J 2002; 2(1):63–69. 62. Girardi FP, Cammisa FP Jr. The effect of bone graft extenders to enhance the performance of iliac crest bone grafts in instrumented lumbar spine fusion. Orthopedics 2003; 26(5 Suppl):s545–s548.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar

CHAPTER

103

Failed Back Surgery Jerome Schofferman

Failed back surgery syndrome (FBSS) is a non-specific term that implies the final outcome of surgery did not meet the expectations of both the patient and the surgeon that were established before surgery.1 It should not and does not suggest that the patient failed to get total pain relief or did not return to full function. The surgeon’s expectations for the results in a specific surgical patient should be based on published medical evidence, the type of structural problem, the number and types of prior surgeries the patient has had, the psychological health of the patient, and the skills and experience of the surgeon. For example, expectations after discectomy in a patient with radiculopathy due to a single disc herniation, no prior back surgeries, good psychological health, ability to work, and with private health insurance should be high. Conversely, expectations for a multilevel salvage surgery for pseudoarthrosis and spinal stenosis despite two prior surgeries in an injured worker who also has two painful discs will be far lower. It is the responsibility of the surgeon to convey realistic expectations to the patient. The patient must also have realistic expectations, and must rely to some degree on the surgeon’s input. In patients with chronic pain, an improvement in 0–10 numerical rating scale (NRS) or visual analog score (VAS) of 1.8 units is equivalent to a change in pain of about 30%, which will be considered by most patients as a ‘somewhat satisfactory result.’2 An improvement in NRS or VAS of 3 units or more is equivalent to a change in pain of about 50%, which most patients will consider an ‘extremely satisfactory result.’ Interventional spine specialists have many options to treat patients with FBSS. It appears that the best outcomes occur when the treatment is matched to the patient’s particular pathology. The pain specialist must understand the nature of FBSS to accurately diagnose the structural disorder and thereby render the most specific treatment.

In 1981, Burton et al. reported an analysis of several hundred patients with FBSS.3 They found that about 58% had lateral canal stenosis (foraminal stenosis), 7–14% had central canal stenosis, 12–16% had recurrent (or residual) disc herniations, 6–16% had arachnoiditis, and 6–8% had epidural fibrosis. Other less common causes in their series included neuropathic pain, chronic mechanical pain, painful segment (disc) above a fusion, pseudoarthrosis, foreign body, and surgery performed at the wrong level. They were unable to establish a definitive diagnosis in less than 5% of their patients despite the fact that their study was done early in the computed tomography (CT) scan era and well before magnetic resonance imaging (MRI) scans. They did use discography. There have been major advances in diagnostic testing since the Burton paper. In 2002, Waguespack et al.4 and Slipman et al.5 each independently reported their results of evaluations of patients with FBSS (Table 103.1). Waguespack et al. performed a retrospective review of 187 patients who presented to a tertiary care spine center. They established a predominant diagnosis in 95% of their patients. Slipman et al. performed a similar study in which they reached a diagnosis in more than 90% of patients as well. In these two recent studies the most common structural causes of FBSS were foraminal stenosis (25–29%), painful disc (20–22%), pseudoarthrosis (14%), neuropathic pain (10%), recurrent disc herniation (7–12%), instability, facet pain (3%), and sacroiliac joint pain (2%), among some others (Table 103.2). Several authors have presented their unquantified impressions and experiences regarding the causes of FBSS. Fritsch et al.6 reviewed 136 patients who had revision surgeries after clinical failure of an initial laminectomy and discectomy, and found a high prevalence of recurrent disc herniations and instability. Kostuik7 reviewed the potential causes of failure of decompression, but provided no quantitative data.

STRUCTURAL ETIOLOGIES OF FAILED BACK SURGERY In this section, the author will briefly review the most common structural causes of FBSS based on published data.3–5 These are lateral canal stenosis (foraminal stenosis), recurrent or residual disc herniation, one or more painful discs, neuropathic pain, facet joint pain, and sacroiliac joint pain. It is interesting to note that the causes of FBSS and the causes of chronic low back pain (LBP) are quite similar. By combining a careful history, physical examination, and specialized testing, the structural cause of FBSS can be delineated in more than 90% of patients.4,5 In some patients, the structural cause of the FBSS was present prior to surgery and was not adequately addressed (e.g. painful disc, lateral canal stenosis, facet or sacroiliac joint [SIJ] pain). In others the problem occurred after surgery, either as a direct consequence of the surgery (e.g. SIJ pain after fusion, pseudoarthrosis, etc.) or as new and unrelated pathology.

Table 103.1: Most Common Causes of Failed Back Surgery in Three Reported Studies Diagnosis

Burton (1981) (3)

Waguespack (2002) (4)

Slipman (2002) (5)

Lateral stenosis

58%

29%

25%

HNP

12–16

7

12

Painful discs

N/A

20

22

Neuropathic pain

6–16

10

10

Total %

76–90%

66

69

All numbers are % HNP = herniated disc

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Part 3: Specific Disorders

Table 103.2: Differential Diagnosis of Common Causes of FBS by Symptoms, Signs, Radiology, and Injections Diagnosis

Symptoms

Signs

Radiology

Injections

Lateral canal stenosis

Leg pain > LBP Relief with sitting

Loss of lumbar lordosis

MRI: foraminal stenosis

Relief with transforaminal epidural

Painful disc

LBP; ? worse with sitting

Restricted flexion in standing MRI: degenerated disc(s)

No sustained relief

Neuropathic pain

Leg pain Burning Dysesthesia

Hypoalgesia Allodynia

No alternative diagnosis

No sustained relief

Facet joint pain

Left or right LBP

?Facet tenderness

Not specific

Medial branch block relieves pain

Recurrent HNP

Vary with location. Leg pain > LBP

Variable

HNP on MRI

Epidural may provide temporary relief

SI joint pain

Gluteal pain with referral to leg and groin

May have + provocative testing

Not helpful

SI joint injection relieves pain

LBP = Low Back Pain HNP = disc herniation +/– May be helpful DDD = degenerative disc disease SIJ = sacroiliac joint CT = computed axial tomography MRI = magnetic resonance imaging

In this chapter, the author has used functional definitions which are a composite of those proposed by the North American Spine Society8 and the International Association for the Study of Pain,9 modified by personal clinical experiences.

Lateral canal stenosis Lateral canal stenosis was found in 25–29% of FBSS patients in the more recent studies, but was twice that 25 years ago.3–5 The lower prevalence in later studies may be due to better preoperative recognition of the condition and more meticulous decompression. Lateral canal stenosis usually presents with pain that is predominantly in one leg or buttock region (see Table 103.2). The leg and gluteal pains are usually worsened by standing and walking and improved by sitting. MRI or CT scan must show narrowing of the nerve root lateral canal at the index level or an adjacent segment. Lateral canal stenosis may be characterized as ‘up-down stenosis’ due to loss of disc space height or ‘front-back stenosis’ due to facet hypertrophy and osteophyte formation. There is usually at least temporary relief of leg pain after transforaminal epidural blockade of the suspected nerve root.10,11 It is important to differentiate lateral canal stenosis from neuropathic pain and from mixed pain syndrome because the treatments are different. Stenosis is treated with flexion-biased body mechanics, transforaminal corticosteroid injections, and/or surgical decompression. Neuropathic pain is better treated with medications (anticonvulsants, tricyclic antidepressants, opioids) or spinal cord stimulation. Mixed pain syndromes may require both types of treatment.

Painful discs One or more painful discs were the cause of FBSS in about 21% of patients.3–5 Painful discs may occur at the index level, adjacent level, and occasionally at the level of a prior posterolateral fusion.11 In the Waguespack study,4 painful discs were responsible for FBSS in 31 (17%) patients who did not have prior fusion and 5 (3%) additional 1130

patients had a painful disc at a level contained within a prior solid fusion. It is clear that discs have the substrate to become painful. They are richly innervated with nerve endings that have the potential to be nociceptive.12,13 In the normal disc, nerve endings are limited to the outer third of the anulus. In the degenerated disc, there is proliferation of nerve endings, and in 40% of severely degenerated discs, the nociceptors have grown inward to reach the nucleus.12 Discogenic pain presents with LBP with or without referred buttock or leg pain (see Table 103.2). Painful discs usually appear desiccated and may be narrowed on MRI scan. Schwarzer et al. found no symptoms or signs that are specific for discogenic pain,14 but there may be a few clues.15 Discogenic pain is usually worsened by sitting and by transition from sitting to standing.15 Pain may be improved somewhat by standing or walking. During examination, pain is usually worsened by flexion during standing, which is also decreased due to pain. There may be tenderness over the spinous processes, but not over the facet joints. Discography is often used to confirm the clinical impression of discogenic pain. It is controversial in chronic LBP and even more so in patients with FBSS.16–18 In every instance, discography must be interpreted very carefully and only in conjunction with the history, examination, imaging studies, and psychological status of the patient.19 The value of discography at a disc that has had prior surgery is not totally clear, but may be useful when carefully interpreted.13 When the diagnosis of discogenic pain is suggested by history and examination, MRI shows only the one bad disc, and other potential causes of LBP are excluded, there is probably no need to perform discography. If discography is used in the setting of FBSS and probable discogenic pain, it is probably most useful to prove other discs are not involved. Discogenic pain is difficult to treat. Intensive 4–6 week interdisciplinary functional rehabilitation programs may be helpful. Medications, particularly opioids and tricyclic antidepressants, can reduce pain. Surgery can be useful for patients with severe pain. There are no published reports to justify minimally invasive intradiscal procedures in the setting of FBSS.

Section 5: Biomechanical Disorders of the Lumbar Spine

Disc herniation Recurrent or residual disc herniation occurred 7–12% of patients with FBSS.3–5 In the presence of epidural or perineural fibrosis and a nerve root that is surrounded by scar, a disc herniation may cause more leg pain than expected if there were no fibrosis. The symptoms of recurrent or residual disc herniation (HNP) depend on its location (see Table 103.2). A midline HNP presents as discogenic LBP. Posterolateral HNP will usually present with a predominance of leg pain in the distribution of a single dermatome, but if the disc is sufficiently damaged internally, there can be a significant amount of low back pain as well. There will be MRI evidence of the disc herniation. Treatment depends upon the pain. Leg pain can be treated by physical therapy, epidural corticosteroids, and other medications. If these fail, discectomy may help. However, LBP rarely responds to discectomy alone, and requires fusion surgery.

Neuropathic pain Neuropathic pain was the predominant problem in 9% of the author’s patients.4 Burton et al. observed neuropathic pain in less than 5% of their patients.3 It is not clear if there has been an increase in nerve root injury or an increased recognition of neuropathic pain. Nerve roots can be damaged during surgery, but damage is more likely due to prolonged unrelieved compression by spinal stenosis or disc herniation. The incidence of arachnoiditis may be decreasing, perhaps because oil-based myelography is no longer performed. Neuropathic pain implies that pain arises from nerve injury or dysfunction. There is a predominance of leg pain, which is usually present in one or two adjacent dermatomes. In classic presentations, the pain is described as burning or dysesthetic, but in neuropathic disorders and FBSS this may not be the case (see Table 103.2). Pain is usually constant but it may be worsened by activity because the damaged nerve is sensitized and minor biomechanical changes may worsen pain. In pure neuropathic pain, there is no evidence of nerve root compression on MRI or CT scan. Neuropathic pain must be distinguished from neurogenic pain, a phrase the author uses to imply that a nerve is being compressed or irritated by structural pathology such as residual foraminal stenosis or HNP described above. Again there are also patients with mixed pain syndromes who have compressive lesions on scan (stenosis, HNP) but who also have irreversible nerve damage from the longstanding compression.

Facet syndrome Pain that arises from the facet joint is responsible for the pain in about 3% of patients with FBSS and 15–30% of patients with chronic LBP.5,20 The facet joint is susceptible to inflammation, damage during surgery, or the mechanical stresses of fusion at a segment below. There are no data that specifically address the symptoms or signs of facet syndrome in patients with FBSS, but several papers have addressed the problem in chronic LBP.15,20–24 Schwartzer et al. felt there were no symptoms typical for facet joint pain, although the presence of midline LBP was not likely in facet syndrome.21 Others feel there are symptoms that are suggestive (see Table 103.2).22,24 Pain is more likely to be experienced just lateral to the midline and is frequently referred to one or both gluteal regions. Pain is better when the patient is lying supine.22 It is less severe sitting than standing or walking, and pain is not worsened during transition from sitting to standing.25 Examination findings are not specific, but there may be tenderness with palpation directly over the joints but not over the spinous processes, and more pain with extension than flexion while standing. As discussed elsewhere in this text, the diagnosis of facet joint pain is made by intra-articular infusion of local anesthetic or block-

ade of the medial branches of the primary dorsal rami that serve the putative painful joint. The preferred treatment is radiofrequency neurotomy (RFN), which is successful in a high percentage of wellselected patients.26–29 RFN generally relieves pain for 9–12 months and then it can be repeated, and Schofferman and Kine have shown that repeated RFN remains effective.29

Sacroiliac joint pain The sacroiliac joint (SIJ) is responsible for the pain in about 2% of patients with FBSS5 and 15–30% of patients with chronic LBP.30 There are many potential inciting events that may lead to the development of SI joint pain. The joint may become painful after acute or cumulative trauma, but the cause is often not known.31 The SIJ is vulnerable to the mechanical stresses of fusion to the sacrum32 and can be injured during bone graft harvesting for fusion.33 There are no data that have specifically examined the symptoms or signs of sacroiliac joint syndrome in patients with prior surgery, but several papers have addressed the problem in the chronic LBP population.15,30 Schwartzer et al. reported that there were no typical symptoms for SIJ pain.30 Others believe there is a pattern with pain experienced in the gluteal regions distal to the posterior superior iliac crest just off the midline. The patient may point directly over the joint when asked to show where the pain is the worst. Pain is worsened during transition from sitting to standing15 and appears to increase with single leg weight bearing. Examination findings are not specific, but there may be tenderness with palpation directly over the SIJ, and when there are three or four other signs, diagnosis is probable.34 As discussed elsewhere, the diagnosis is made by local anesthetic blockade of the SIJ under fluoroscopic guidance. Treatment is multidimensional. It requires strengthening the gluteal muscles, teaching the patient to self-mobilize the joint, and increasing the flexibility of the gluteal and hamstring muscles. This may be supplemented by spinal manipulative therapy. Therapeutic SIJ injection utilizing glucocorticoid can be helpful.35 Very rarely SIJ fusion is necessary.

Epidural fibrosis Epidural fibrosis occurs after most, if not all, posterior lumbar decompressive surgeries. Scar forms in patients with good and bad outcomes alike. There is controversy whether fibrosis can cause pain after lumbar surgery in the absence of other structural disorders or neuropathic pain. Some interventional spine specialists believe fibrosis alone can cause pain, but most spine specialists do not. Although it has been established that fibrosis occurs, that fibrosis may alter neural sensitivity, and that fibrosis may make re-operation more difficult, there is no good evidence that perineural fibrosis itself can cause pain or that treatment directed toward only the fibrosis can improve the pain. There is no proven method to determine whether fibrosis might be a cause of pain, only a somewhat circuitous theoretical construct.36 Finally, even if fibrosis were pathological rather than an innocuous bystander, it would be more likely to cause leg pain rather than LBP. The author believes fibrosis can make other structural problems worse. It traps nerve roots, which are then more susceptible to compression from small disc herniations, foraminal stenosis, or other more primary structural problems.

TECHNICAL FAILURE AND COMPLICATIONS Pseudoarthrosis Pseudoarthrosis is a failure of fusion (nonunion), and was the predominant problem in 15% of the patients of Waguespack et al. with 1131

Part 3: Specific Disorders

FBSS who had prior attempted fusion.4 They did not collect sufficient data to establish the number of patients who had undergone an attempted fusion, and therefore it is not possible to know the clinical relevance of this percentage. Some patients with nonunions have pain, but others do not. Therefore, one cannot assume that the nonunion is the cause of the pain. The author likes this summary poem: If there’s pain and a pseudoarthrosis, It’s usually a disc or spinal stenosis; But think of facet joints or SI – they’re closest. Nerves can be damaged and lose their gliosis And pains can be worsened by depression or neurosis. Rarely an infection can spread by osmosis, But a careful work-up will lead to gnosis. A definitive diagnosis of pseudoarthrosis requires surgical exploration, but radiological findings can be suggestive. Plain radiographs are not reliable to prove fusion is solid, but certainly can be suggestive of nonunion.37 Standing films with sagittal views taken in flexion and extension are useful if there is motion. CT scans that include reformatted curved coronal as well as sagittal and axial images are the most useful test.38 They can visualize the anterior column when there has been attempted interbody fusion (bone or cages), and curved coronal sections extended out to the spinous processes are the best test to visualize the integrity of posterolateral fusions. After interbody fusion with threaded metal cages, a nonunion may be particularly difficult to diagnose.39 There may be no lucency on plain X-rays, no motion with standing X-rays in flexion versus extension, and no lucency on CT scan, and still pseudoarthrosis may be present. The author has noted that patients who are not significantly improved by 6 months after fusion with threaded interbody cages often benefit from a salvage posterolateral fusion.

Instability Some patients who undergo surgery develop instability due to the amount of posterior elements that have been removed. This is referred to as postlaminectomy instability, and implies there is more than 4 mm translation on standing flexion versus extension X-rays or neutral X-ray versus supine cross-table lateral view. The author frequently sees patients who had very slight spondylolisthesis before surgery for disc herniation or spinal stenosis in whom no fusion was done because the slip was so slight. Then some months after surgery, the back pain worsens, and plain X-rays reveal progression of the slip.

Pedicle screw or cage misplacement New leg pain immediately after a lumbar fusion using pedicle screws may be caused by a screw breaching the medial cortex of the pedicle. CT scan may show this, but surgical exploration may be needed. Threaded interbody fusion cages have been used much more frequently recently. At times, one or both cages may either be placed too far laterally and compress or displace a nerve root. This too should be seen on CT scan, particularly on the curved coronal images.

PSYCHOLOGICAL FACTORS IN FAILED BACK SURGERY Psychological disorders are often invoked when evaluating patients with FBSS. Pure psychogenic pain (pain disorder, psychological type) is rare in patients with FBSS.40 It is more likely that if psychological factors are present they make pain worse rather than cause it. More importantly, if psychological problems are present in a patient with FBSS, it is most likely they were present before surgery and did not 1132

just appear afterwards. Psychological issues should always be considered and diagnosed preoperatively. In the author’s opinion, it is not appropriate for a surgeon to invoke a psychological cause of FBSS and, in a sense, ‘blame the patient’ after the surgery. A pain syndrome due to psychological disorders might be defined as LBP with or without leg pain, not attributable to any pathological structural cause or far out of proportion to pain usually produced by that structural abnormality present in the presence of a diagnosable psychological illness by DSM-IV criteria that has been shown to cause or exacerbate pain. Most patients with refractory LBP have symptoms of at least one major psychiatric disorder, most commonly depression, substance abuse disorder, or anxiety disorder. The question is whether a psychological disorder is in fact the primary cause of the FBSS. There are psychological conditions that probably do not impact on surgical outcome as long as one treats them psychiatrically first – major depression, mania, severe anxiety disorder, or active addiction. There are other people who are never going to be good surgical patients, such as borderline personality disorder, antisocial personality, and the addict or alcoholic who is not in recovery.

RADIOLOGICAL EVALUATION OF FAILED BACK SURGERY Herzog discussed the requirements for imaging patients with FBSS and much of the following section is a summary of his presentation.1,38,41 Radiological examination usually includes X-rays and either MRI or CT scan. Standard radiographs with standing flexion and extension lateral views are used to assess alignment, extent of disc space narrowing, instability, and, when fusion has been attempted, perhaps pseudoarthrosis.36 MRI is the optimal examination for most FBSS patients unless the issue is pseudoarthrosis, in which case CT with multiplanar reformations (CT/MPR) is much better.1,37 MRI should be done using a high-field strength (1.0–1.5 Tesla) scanner for maximum information. With MRI, it is necessary that the study be done to visualize left and right extraforaminal zones so as to avoid missing foraminal or extraforaminal pathology. At least one axial sequence should have contiguous stacked images. Angled T2-weighted sections from T12– L1 to L5–S1 through the disc spaces are done to evaluate the crosssectional area of the thecal sac, to evaluate the central canal, and to define the exact relationship of the structural changes to all the neural elements. A coronal sequence is useful to see foraminal and extraforaminal herniations.1,40 In evaluating patients who had surgery for disc herniation, contrast-enhanced MRI became the standard, but with newer equipment and imaging sequences, nonenhanced MRI is frequently adequate if the radiologist monitors the study and administers contrast only if the routine sequences are not adequate. MRI is excellent for spinal stenosis, and can detect hypertrophy of facet joints and ligamenta flava, synovial cysts, or prominence of epidural fat. It will show if decompression was adequate to decompress the nerve root. Arachnoiditis can easily be detected with MRI. In patients with spinal instrumentation using titanium alloys, there should be no significant distortion with a high field-strength MRI if the sequences are optimized for the presence of metal using fast spin echo T2-weighted sequences without fat saturation to reduce artifacts. Short tau inversion recovery (STIR) sequences should be employed if fat saturation is needed. The central canal and neural foramina can be adequately assessed even with the presence of pedicle screws. The artifacts generated by ferromagnetic metal alloys may completely obscure the spinal anatomy and this is one of the few instances that CT myelography may be needed.

Section 5: Biomechanical Disorders of the Lumbar Spine

High-resolution CT/MPR is the optimal study when the integrity of a fusion or the placement of pedicle screws needs assessment.38 It is helpful in a CT examination to perform stacked 1 mm thick sections through the segment containing the cage to detect early loosening or the presence of bridging bone. CT/MPR should employ stacked 2–3 mm sections with sagittal and coronal reformations, and cover several segments proximal and distal to the surgery. There are only rare indications for nuclear imaging studies (e.g. infection, missed malignancy), myelography (pseudomeningocele), or CT myelography in the setting of FBSS.

ROLE OF THE HISTORY The history is the most important part of the evaluation of FBSS. It establishes the differential diagnosis, suggests the emphasis for the physical examination, and provides guidelines for selecting the most appropriate imaging studies and diagnostic injections. With a careful history, the examiner may also be able to discern why things went wrong.

Establishing the structural diagnosis Most often, the history can narrow the potential structural causes of FBSS to a few likely probabilities. The most important elements to this aspect of the history include the location and quality of the pain, and the effects of mechanical changes.

Location of pain It is useful to divide patients into those with predominance of LBP versus those with a predominance of leg pain. In general terms, if LBP is greater than leg pain, the most common causes of FBSS are discogenic pain at the level of prior surgery or adjacent levels, facet pain, SIJ pain, and instability; and if fusion was attempted, pseudoarthrosis. If leg pain predominates, the common causes include foraminal stenosis, recurrent or residual disc herniation, and neuropathic pain. There may be more than one diagnosis present. Pain generally flows down hill. LBP in the midline is often discogenic. Pain 1 or 2 cm off the either side of the midline is often of facet origin. Facet pain is not usually limited to the midline.21 Pain in the gluteal regions is not specific, as the buttocks is a watershed area for pain emanating from most structures in the lumbar spine. Pain directly over the sacral sulcus may indicate the SIJ is the source of the pain. SIJ pain often is referred to the ipsilateral groin. Leg pain is not specific unless it follows a dermatomal pattern.

Quality of pain The words the patient uses to describe the pain is occasionally helpful. Burning pain is often of neurologic origin, particularly neuropathic. Exquisite tenderness to light touch (allodynia) also suggests neuropathic pain. A complaint of numbness in the absence of sensory loss on examination suggests referred pain. Paresthesias and dysesthesia suggest neurologic problems but does not help separate neurogenic from neuropathic pain.

Response to mechanical changes (see Table 103.2) SITTING: LBP or leg pain that increases with sitting and with flexion while standing is more likely due to one or more painful discs or instability (spondylolisthesis). Leg pain that improves with sitting is usually due to spinal stenosis. TRANSITION FROM SITTING TO STANDING: LBP that worsens during the transition from sit to stand suggests disc pain or SIJ and speaks against facet joint pain.15

STANDING: LBP that increases with standing suggests posterior element pathology such as facet joint pain. Leg pain that increases with standing or walking suggests spinal stenosis.

Establishing what went wrong In the author’s experience, it is more likely that FBSS is due to an error in surgical judgment or an incomplete evaluation rather than a technical failure or complication of the surgery itself. Establishing the reason for the failure by the history does simplify the evaluation and may markedly change the treatment. If a patient had the wrong surgery for the preoperative condition, then recommending the patient undergo the correct surgery may be the most conservative and definitive treatment. The history is the key to this aspect of the evaluation of FBSS. It is necessary to compare the current symptoms with the preoperative symptoms and to see if the surgery performed was appropriate for the preoperative symptoms. If the pain before and after surgery share essentially the same location, quality, and response to mechanical maneuvers, this suggests an error in selecting the correct surgery (e.g. laminectomy for LBP) or incomplete surgery (e.g. inadequate foraminal decompression, one-level fusion when there were two degenerated discs). On the other hand, if the symptoms have changed, this suggests new pathology, either as a result of the surgery (e.g. SIJ pain distal to a fusion, disc space collapse after extensive discectomy) or progression of the underlying disease (new disc degeneration).

Mismatch of the surgery performed to the surgery required The judgment error may be straightforward, but requires a baseline understanding of the appropriate surgery for the underlying symptoms and pathology. This underlying premise is that there are surgeries for leg pain (decompression, discectomy) and surgeries for LBP (fusion). If the patient had predominantly LBP but had a leg pain operation, it would not be expected to work. For example, when patients with LBP, even if they have a disc herniation or spinal stenosis, undergo simple depression it is not likely to succeed. In other words, they had a ‘leg pain operation’ when the major problem was low back pain.

Technically inadequate surgery If the surgery was appropriate for the symptoms and pathology, determine whether the technical goals of surgery were accomplished. This usually requires good-quality imaging studies. As described above, residual foraminal stenosis remains a very common problem. There may be three reasons for this: (1) the surgeon did not recognize the degree of the lateral canal stenosis before surgery, often because there is also central stenosis, (2) the surgeon thinks the canal was adequately decompressed, but it remains stenotic in the mid or exit zones, and (3) the surgeon may feel that in order to adequately decompress there would be instability and did not want to fuse.

Technical failure Technical failures that are common include pseudoarthrosis and misplaced instrumentation. At times pseudoarthrosis is obvious, but at other times it is a challenge. There are two common types of fusion: interbody and posterolateral. Interbody fusion can be done via an anterior or posterior approach and can be done with bone or cages. Posterolateral fusions are done with or without instrumentation. Finally there may be combinations. It is reasonably straightforward to diagnose pseudoarthrosis when there is an interbody fusion with bone. It is very useful, but often 1133

Part 3: Specific Disorders

overlooked, to get a Furgeson (angled) view of the L5–S1 interspace to look for lucency. CT scan will often reveal the lucency if plain X-rays are not diagnostic. Posterolateral fusion without instrumentation will usually be seen on CT if there are adequate curved coronal sections taken out to the tips of the transverse processes. If there is instrumentation, nonunion may be difficult to see. Occasionally, oblique radiographs are helpful. The diagnosis of pseudoarthrosis in the presence of interbody fusion with cages presents a real challenge. Plain X-rays and even CT scan may not disclose the nonunion. If one of the author’s patients does well initially after interbody fusion with cages, but then deteriorates, the suspicion is of occult nonunion. However, occasionally the cages can subside into the vertebral bodies and this can be identified by comparing serial X-rays. If the patient is not better by 6 months after surgery, the author will look for other causes, but frequently find none. The author will then offer the patient a salvage posterolateral fusion with instrumentation, and has been gratified with the results (unpublished observation).

Complication If pedicle screws are misplaced medially through the cortex, there can be leg pain in a single dermatome that corresponds to the breach in the pedicle. CT often will suggest this. Complications such as infection usually occur early in the postoperative period but rarely can occur later.41,42

Incomplete evaluation Incomplete evaluation implies that the most obvious structural pathology was addressed surgically, but there may have been additional problems as well. However, a scenario often seen is that there were two or more abnormal discs before surgery but only one was fused. This is an error in judgment due to an incomplete evaluation. The surgeon must determine if any disc that looks abnormal on MRI before surgery is a cause of part or all of the patient’s pain. Some discs that look abnormal cause pain, but others do not. The surgeon can infer from the history if the patient is likely to have discogenic pain, but not which disc is responsible. Discography, although somewhat controversial, is a useful in making this decision when taken in context of the history, examination, and other tests. Discography nihilists can opine that it is not a useful test, but they offer no better alternative to determine whether a disc is a source of pain or not.

CONCLUSIONS Interventional pain specialists evaluate and treat many patients with FBSS. Treatments are most effective when they are matched to the specific cause of the pain. In order to efficiently evaluate the patient, it is very helpful to know and understand the causes of FBSS. In this chapter, the author reviewed the common causes of FBSS and provided the important elements of the history, examination, radiographic studies, and most briefly outlined the roles of injections. Armed with this information, the cause of FBSS should be uncovered in an overwhelming number of patients, and FBSS will no longer be a non-specific and pejorative mystery.

References

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3. Burton CV, Kirkaldy-Willis WH, Yong-Hing K, et al. Causes of failure of surgery on the lumbar spine. Clin Orthop 1981; 157:191–199. 4. Waguespack A, Schofferman J, Slosar P, et al. Etiology of long-term failures of lumbar spine surgery. Pain Med 2002; 3:18–22. 5. Slipman CW, Shin CH, Patel RK, et al. Etiologies of failed back surgery syndrome. Pain Med 2002; 3:200–214. 6. Fritsch EW, Heisel J, Rupp S. The failed back surgery syndrome. Reasons, intraoperative findings, and long-term results: a report of 182 operative treatments. Spine 1996; 21:626–633. 7. Kostuik JP. The surgical treatment of failures of laminectomy. Spine: state of the art reviews 1997; 11:509–538. 8. Fardon DF, Herzog RJ, Mink JH, et al. Contemporary concepts in spine Care. Nomenclature of lumbar disc disorders. North American Spine Society. May, 1995. 9. Merskey H, Bogduk N. Classification of chronic pain. 2nd edn. Seattle: IASP Press; 1994. 10. Slosar PJ, White AH, Wetzel FT. The use of selective nerve root blocks: diagnostic, therapeutic, or placebo? Spine 1998; 20:2253–2256. 11. van Akkerveeken P. The diagnostic value of nerve root sheath infiltration. Acta Orthop Scand 1993; 64:61–63. 12. Freemont A, Peacock T, Goupille P, et al. Nerve ingrowth into diseased intervertebral discs in chronic low back pain. Lancet 1997; 350:178–181. 13. Coppes M, Marani E, Thomeer R, et al. Innervation of ‘painful’ lumbar discs. Spine 1997; 22:2342–2350. 14. Schwarzer A, Aprill C, Derby R, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995; 20: 1878–1883. 15. Young S, Aprill C, Laslett M. Correlation of clinical examination characteristics with three sources of chronic low back pain. Spine J 2003; 3:460–465 16. Walsh TR, Weinstein JN, Spratt KF, et al. Lumbar discography in normal subjects. J Bone Joint Surg 1990; 72A:1081–1088. 17. Derby R, Howard MW, Grant JM, et al. The ability of pressure-controlled discography to predict surgical and nonsurgical outcomes. Spine 1999; 24:364–372. 18. Wetzel FT, LaRocca H, Lowery GL, et al. The treatment of lumbar spinal pain syndromes diagnosed by discography. Lumbar arthrodesis. Spine 1994; 19:792–800. 19. Carragee EJ, Alamin TF. Discography: a review. Spine J 2001; 1:364–372. 20. Barrick W, Schofferman J, Reynolds J, et al. Anterior fusion improves discogenic pain at levels of posterolateral fusion. Spine 2000; 25:853–857. 21. Schwarzer A, Wang S, Bogduk N, et al. Prevalence and clinical features of lumbar zygapophyseal joint pain: A study in an Australian population with chronic low pack pain. Ann Rheum Dis 1995; 54:100–106 22. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–1137 23. Revel M, et al. Capacity of the clinical picture to characterize facet joint pain. Spine 1998; 23:1972–1977. 24. Jackson RP. The facet syndrome: myth or reality? Clin Orthop 1992; 279: 110–121. 25. Helbig T, Lee CK. The lumbar facet syndrome. Spine 1988; 13:61–64. 26. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophyseal joint pain. Spine 2000; 25:1270–1277. 27. van Kleef M, Barendse GA, Kessels A, et al. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine 1999; 24:1937–1942. 28. Leclaire R, Fortin L, Lambert R, et al. Radiofrequency facet joint denervation in the treatment of low back pain. Spine 2001; 26:1411–1417. 29. Schofferman J, Kine G. The effectiveness of repeated radiofrequency neurotomy for lumbar facet pain. Spine 2004; 29:2471–2473. 30. Schwarzer A, Aprill C, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37. 31. Chou L, Slipman CW, Bhagia SM, et al. Inciting events initiating injection-proven sacroiliac joint syndrome. Pain Med 2004; 5:26–32.

1. Schofferman J, Reynolds J, Dreyfuss P, et al. Failed back surgery. Spine J 2003; 3:400–403.

32. Katz V, Schofferman J, Reynolds J. The sacroiliac joint: a potential cause of pain after lumbar fusion. J Spinal Disord Tech 2003; 16:96–99.

2. Farrar JT, Young JP, LaMoreaux L, et al. Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale. Pain 2001; 94:149–158.

33. Ebraheim NA, Elgafy H, Semaan HB. Computed tomographic findings in patients with persistent sacroiliac pain after posterior iliac graft harvesting. Spine 2000; 25:2047–2051.

Section 5: Biomechanical Disorders of the Lumbar Spine 34. Slipman C, Sterenfeld E, Chou L, et al. The predictive value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehab 1998; 79:288–292. 35. Slipman CW, Lipetz JS, Vresilovic EJ, et al. Fluoroscopically guided therapeutic sacroiliac joint injections for sacroiliac joint syndrome. Am J Phys Med Rehab 2001; 80(6):425–432. 36. Schofferman J. Failed back surgery. Response to letter to the editor. Spine J. In press. 37. McAfee P, Boden S, Brantigan J, et al. Symposium: a critical discrepancy – a criteria of successful arthrodesis following interbody spinal fusions. Spine 2001; 26: 320–324.

38. Herzog RJ, Marcotte PJ. Imaging corner. Assessment of spinal fusion. Critical evaluation of imaging techniques. Spine 1996; 21:1114–1118. 39. Heithoff K, Mullin W, Holte D, et al. The failure of radiographic detection of pseudoarthrosis in patients with titanium lumbar interbody fusion cages. Presented at the 14th annual meeting, North American Spine Society. Chicago, IL; 1999. 40. Polatin PB, Kinney RK, Gatchel RJ, et al. Psychiatric illness and chronic low-back pain. The mind and the spine – which goes first? Spine 1993; 18:66–71. 41. Herzog R. Radiological studies in failed back surgery. Presented at the 18th annual meeting, North American Spine Society. Montreal, Canada. October; 2002. 42. Schofferman L, Schofferman J, Zucherman J, et al. Occult infections as a cause of low-back pain and failed back surgery. Spine 1989; 14:417–419.

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PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar

CHAPTER

104

Neural Scarring David W. Chow

INTRODUCTION Of the myriad causes of failed back surgery syndrome (FBSS), neural scarring has been reported to be the cause of failed back surgery syndrome in 6–24% of patients.1–7 In 1996, Ross et al., using a prospective, controlled, randomized, blinded, multicenter methodology, demonstrated a significant association between the gross amount of peridural scar and the occurrence of recurrent radicular pain; those with extensive epidural scarring were 3.2 times more likely to experience recurrent radicular pain than those with less scarring.7 The degree of postoperative scarring relates to the extent and magnitude of the surgery. It is undeniable that the presence of postoperative scar tissue is not solely due to the operative trauma, but is also generated as a reparative response to the herniated disc material as not all patients with scarring are symptomatic.8 Although epidural adhesions are most commonly present following spine surgery, leakage of disc material from a herniated nucleus pulposus or annular disc tear can cause an inflammatory response with fibrocyte deposition and resultant epidural adhesions in the absence of surgery.9,10 There are those who believe that neural scarring such as epidural and/or intraneural fibrosis do not ever cause symptoms. This school of thought is based upon the fact that neural scarring is a normal bodily response to injury and that all postoperative patients will have some degree of scarring, the majority of which are asymptomatic.8 However, just as there are symptomatic and asymptomatic disc protrusions, the same tenet holds true for epidural fibrosis and neural scarring. The fact that not all focal disc protrusions or epidural fibrosis, as demonstrated by magnetic resonance imaging (MRI), are clinically symptomatic does not prove that focal disc protrusions or epidural fibrosis are not pain generators and have no relationship to low back or lower limb pain preoperatively or postoperatively. Such a view is simplistic and is more a function of the lack of an effective clinical pathway in the diagnosis of symptomatic neural scarring. Historically, epidural fibrosis or arachnoiditis was an uncommon clinical entity prior to the introduction of lumbar spine surgery for the treatment of degenerative spine conditions.11 A large number of reports of epidural fibrosis found on repeat surgery led to the association of recurrent symptomatology with perineural scarring.11–13 This chapter will offer a diagnostic algorithmic approach to determine an accurate diagnosis of symptomatic neural scarring. A review of the clinical anatomy of the nerve root and its anatomic relationships is critical to understanding the basis and pathophysiology of symptomatic neural scarring.

Endoneurial sheath

Nerve axon

Perineurial sheath

Axon Finniculus

Finniculus

ANATOMY Sunderland14 described the connective tissue coverings of the nerve fiber. Each axon is surrounded by an endoneurial sheath in which multiple axons or nerve fibers form a funiculi. The endoneurial sheath resists elongation under tension. Each funiculi is invested by perineurial connective tissue. Multiple funiculi are surrounded by the epineurium which consists of alveolar connective tissue. The outer perinerium and epineurium provide some degree of protection from tensile and compressive forces (Fig. 104.1). The portions of the nerve

Epineurial sheath Nerve fiber

Fig. 104.1 Cross-section of nerve fiber and its connective tissue coverings. 1137

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roots which lack this outer sheath are more vulnerable to traction or compression. When there is nerve injury, fibrotic tissue may form perineurally/epidurally or intraneurally. It is important to understand the relationship between the nerve roots and the intervertebral foramen (IVF). Each intervertebral foramen is in the shape of an inverted pear that is bounded laterally by the pedicle, posteriorly by the articular facets and ligamentum flavum, and anteriorly by the intervertebral disc and vertebral bodies.15 The radicular complex of ganglia, nerve roots, spinal nerve, and surrounding sheath accounts for 20–35% of the cross-sectional area of the IVF (Fig. 104.2).15 The remainder of the IVF is occupied by loose areolar or adipose tissue, a radicular artery, and numerous venous channels that often encircle the nerve roots. The depth of the foramen varies from 4 to 9 mm.15 The lumbar nerve root complex is situated toward the upper pole of the foramen. At and beyond the ganglion, the dura loses its identity and forms the outer connective tissue sheath which represents the epineurium and perineurium of the ganglion, anterior nerve root, and the newly formed spinal nerve. The Hofmann ligaments, initially described in 1898, are fine filamentous bands of connective tissue that connect the ventral surface of the dural sac and the exiting nerve roots to the posterior longitudinal ligament and posterior vertebral periosteum (Fig. 104.3).16 The ventral ligamentous attachments within the spinal canal reduce the ability of a nerve root to be dorsally displaced by a disc herniation. The nerve root complex is mobile, but does not have unlimited motion. The lumbar

Fissure in annulus fibrosus

roots undergo an excursion of 0.5–5 mm, depending on the anatomic level.17 There is an average excursion of 3 mm for the intrathecal portion of the L5 nerve root, while for the S1 nerve root this value ranges between 4 and 5 mm.17 Movement is induced by straight leg raising in the lumbosacral roots, nerves, and plexus, and in the intrapelvic section of the sciatic nerve.17 Since the nerve root and its dural sheath are relatively fixed within the spinal canal and the radicular foramen, they cannot easily slip away from a disc protrusion. Fibrosis and adhesions may impair the gliding capacity of the lumbar nerve roots within the radicular canals and increase the vulnerability of the extrathecal intraspinal nerve root to compression. Consequently, the nerve root is stretched and compressed, resulting in edema, ischemia, and radicular symptoms. Postoperative scar tissue formation in the spine can occur within the dura (arachnoiditis) or outside the dura (epidural fibrosis).

ADHESIVE ARACHNOIDITIS Arachnoiditis is inflammation of the pia–arachnoid membrane that covers the spinal cord, cauda equina, nerve roots, or a combination. The extent of scarring varies from mild membrane thickening to severe scarring that can obliterate the subarachnoid space and obstruct cerebrospinal fluid (CSF) flow. The etiology of arachnoiditis is unclear, but typically the intrathecal contents are exposed to an inciting agent such as lumbar spine surgery, intraoperative dural tears, postoperative

Nucleus pulposus Phospholipase A2 Prostaglandins Nitric oxide Metalloproteinases ? Unidentified inflammatory agents

Neovascularization of disc

Inflammatory cell infiltrate (chemical signal for revascularization)

Intervertebral disc Sinuvertebral nerve Nociceptors in annulus fibrosus Pedicle

Ventral rumus

Chemicals may reach nociceptors via fissure to lower threshold for firing. Pain caused by mechanical forces superimposed on chemically activated nociceptors

Intervertebral foramen

Transverse process

Dorsal root ganglion Dorsal ramus

Superior articular process

Spinal nerve root Radicular veins Hoffman’s ligaments

Nerve root–dura interface may be involved by inflammatory process. Chemical factors and compression both contribute to lumbar pain Radicular arteries

Fig. 104.2 Nerve root complex with dorsal root ganglion, nerve root, and its arterial and venous blood supply. 1138

Section 5: Biomechanical Disorders of the Lumbar Spine

Intervertebral disc Posterior longitudinal ligament Sinuvertebral nerve Pedicle Ventral ramus

Dorsal root ganglion Dorsal ramus Spinal nerve root Hoffman’s ligaments and their attachments to the ventral dural sac Thecal sac

infections, intrathecal pharmacologic medications, and injection of oil-based contrast agents. Arachnoiditis is more common in patients who undergo extensive or bilateral surgical procedures, and repeat surgeries.

Pathophysiology Adhesive arachnoiditis causes proliferation of soft tissue leading to filmy adhesions and later to a dense fibrotic matrix. Inflammatory changes are seen microscopically. It is thought that the severity and duration of arachnoiditis is directly correlated to the degree of inflammation and tissue remodeling associated with wound healing. A vascular etiology has also been proposed whereby venous obstruction and dilatation leads to endothelial damage, fibrin deposition, intravascular thromboses, and ultimately fibrosis of the neural elements.18 In the subarachnoid space, the nutritional support of nerve roots is dependent upon its limited vascular supply and the circulation of CSF. The tenuous blood supply and nutrition to the nerve roots within the subarachnoid space can easily be interrupted by neural scarring with subsequent ischemia possible. The exact mechanism of adhesive arachnoiditis is still unknown.

BATTERED NERVE ROOT SYNDROME This entity is frequently discussed in relation to epidural fibrosis as a cause of severe radicular pain postoperatively after a benign immediate postoperative course with incomplete resolution of radicular limb pain. It involves frank nerve root injury, as opposed to reversible nerve root swelling, with worsening of limb pain and associated sensory or motor deficits. Symptoms generally occur over a course of 3–6 months after surgery.

EPIDURAL AND INTRANEURAL FIBROSIS Epidural fibrosis refers to scar tissue formation outside the dura, on the cauda equina or directly on the nerve roots. Epidural fibrosis develops when epidural fat is replaced by the hematoma that typically forms in the path of surgical dissection. The hematoma is gradually absorbed and simultaneously replaced by granulation tissue

Fig. 104.3 Hoffman ligaments connect the ventral surface of the dural sac and the exiting nerve roots to the posterior longitudinal ligament and posterior vertebral periosteum.

that matures into fibrotic connective tissue. Scar tissue development in postoperative patients is not solely due to the operative trauma, but is also a physiologic and reparative response to a herniated disc.8 Epidural scar tissue may constrict the neural elements and cause postoperative pain. Intraneural fibrosis is the formation of scar tissue within the nerve root as opposed to epidural fibrosis, which refers to scar tissue formation outside the nerve root or directly on the nerve root. Intraneural fibrosis cannot be detected by any imaging study and can only be confirmed by pathologic examination under microscopy.

Pathophysiology The pathophysiology of radicular pain caused by epidural or intraneural fibrosis may be the result of inflammation, mechanical compression, or vascular compromise of the spinal nerve roots.

Mechanical compression Nerve fibers encased in collagenous scar tissue suffer an increase in neural tension, impairment of axoplasmic transport, and restriction of arterial supply and venous return. Spinal nerve roots and dorsal root ganglia are particularly sensitive to mechanical deformation due to intraspinal disorders.19 The importance of axonal stretching and deformation in response to a mechanical force and the consequent morphological changes within the nervi nervorum were first described by Horsley et al. in 1883.20 A chronic compressive force decreases blood perfusion causing ischemia and limits CSF circulation which leads to endoneural hyperemia21 and further intraneural damage.22 Since a nerve root lacks a perineurium and has a poorly developed epineurium, it may be more susceptible to compression from intraspinal disorders such as epidural fibrosis or a disc herniation. It has been shown that compression of a peripheral nerve will induce direct mechanical effects on the nerve tissue such as deformation of nerve fibers, displacement of nodes of Ranvier, decreased intraneural microcirculation, and neurophysiologic changes of conduction block. Olmarker et al.19 reported increased permeability of the endoneurial capillaries of the nerve roots resulting in edema from mechanical compression. Intraneural edema may impair capillary blood flow and compromise 1139

Part 3: Specific Disorders

Intervertebral disc Ventral ramus

Dorsal root ganglion Spinal nerve root Thecal sac Facet joint

Clumping of nerve roots Spinous process

nutritional transport, causing ischemia. Compression and edema may lead to intraneural fibrosis. These processes have important implications as intraneural damage causes inflammation and eventual fibrotic tissue formation after healing leading to intraneural fibrosis. Similarly, perineural or epidural fibrotic tissue in response to surgical trauma or part of the normal reparative process, in response to inflammation or vascular compromise, may mechanically compress the nerve roots and initiate the above cascade, leading to intraneural fibrosis. Tension or stretching of nerve segments may lead to similar anatomic alterations. This may occur if a segment of the spinal nerve root is fixed (e.g. intervertebral foramen) or tethered by fibrotic epidural scar tissue (Fig. 104.4.) Ebeling et al.2,23 demonstrated nerve root immobilization as a result of epidural fibrosis causing nerve root impingement from small recurrent disc fragments embedded in fibrotic tissue. This finding occurred in 23% of cases during second operation following lumbar disc surgery in 92 patients.

Inflammatory etiology Marshall24 suggested that leakage of breakdown products from degenerating nucleus pulposus may induce a chemical radiculitis. In animal studies, Bobechko and Hirsch25 demonstrated an autoimmune response to the nucleus pulposus of rabbits. This was confirmed by Gertzbein et al.26 in 1975. Using human nucleus pulposus tested with rabbit sera, they demonstrated the presence of a cellular immune response in 73% of patients whose discs were found to be sequestered at the time of surgery and 26% in those patients whose discs were herniated. McCarron et al.9 showed that there was an inflammatory response to nucleus pulposus injectate in the epidural fat and dura. Saal et al.27 demonstrated that high concentrations of phospholipase A2, the ratelimiting enzyme for the inflammatory cascade of prostaglandins and leukotrienes, were present in human lumbar herniated nucleus pulposus and degenerative discs. Franson et al.28 reported that extracted PLA2 form human lumbar disc has powerful inflammatory activity in vivo. Byrod et al.29 reported that epidural application of substances can have a direct transport route to the axons of the spinal nerve 1140

Fig. 104.4 Lumbar spinal nerve root and dorsal root ganglion tethered by epidural fibrotic adhesions and postsurgical scarring. Thecal sac displaced to the right from postsurgical scar. Left hemi-laminectomy defect.

roots. PLA2 may act to excite nociceptors within the anulus or within the epidural space. Direct contact with a nerve root may cause neural injury either by enzymatic activity on the membrane phospholipids or by production of inflammatory mediators. Human disc PLA2 has been shown to cause perineural inflammation, conduction block, and axonal injury by extrathecal application to animal nerve.30 Leakage of PLA2 or another neurotoxic chemical within the disc may irritate small unmyelinated nerve fibers in the anulus or nearby structures such as spinal nerve roots. It has been suggested that radicular pain results from the ectopic firing within sensory fibers injured by the inflammatory chemical mediators released from degenerated disc tissue.31,32 Perineural inflammation or demyelination induced by phospholipase A2 may be responsible for the hypersensitivity of a nerve root to mechanical stimulation.33 Herniated intervertebral disc material can cause inflammatory changes which may lead to epidural or intraneural fibrosis. It has also been suggested that ventrally located epidural scar tissue that adheres to the dorsal aspect of the disc can create injury via mechanical tension followed leakage of inflammatory enzymes.34

Vascular etiology Disc degeneration has been known to be closely associated with abnormalities in the anatomy and physiology of the adjacent nerve roots. Holt and Yates35 correlated the histology of cervical disc degeneration with adjacent spinal nerve root fibrosis in their cadaver study. Lindahl and Rexed36 demonstrated intraneural fibrosis in 78% of dorsal nerve root biopsies taken at the time of surgery in patients operated on for herniated intervertebral discs. Jayson37 found that there is a statistically significant relationship between the extent of disc degeneration and prolapse with evidence of epidural venous obstruction, perineural/intraneural fibrosis, focal demyelination and neuronal atrophy. A fibrinolytic defect was found in patients with back pain, suggesting that a decreased ability to clear fibrin may be responsible for chronic tissue damage.38 Epidural fibrotic tissue may induce vascular compromise and ischemia with resultant intraneural fibrosis (Fig. 104.5).

Section 5: Biomechanical Disorders of the Lumbar Spine

Intervertebral disc Hoffman’s ligaments Fibrotic adhesions Ventral ramus

Dorsal root ganglion Dorsal ramus

Thecal sac

Post-surgical scarring Fig. 104.5 Nerve root, ventral ramus, dorsal root ganglion, and its vascular supply mechanically compressed by epidural fibrosis.

DIAGNOSIS Imaging Gadolinium-enhanced MRI is the imaging study of choice when evaluating for epidural fibrosis.7,34 Epidural fibrosis can only be seen on MRI performed with gadolinium dye. Gadolinium enhances vascularized fibrotic scar tissue and distinguishes epidural fibrosis from a recurrent disc protrusion in a postoperative spine patient. MRI is the imaging study of choice in diagnosing arachnoiditis and differentiating other causes of FBSS such as epidural fibrosis, retained or recurrent disc protrusion, lateral recess stenosis, and infection.7,34 MRI has demonstrated excellent correlation with CT-myelography

in the diagnosis of adhesive arachnoiditis without the additional risks of an intrathecal injection.39 The characteristic central clumping or clustering of nerve roots within the thecal sac is best seen on axial T2-weighted images (Fig. 104.6).40,41 Peripheral adhesions or severe thecal sac distortion can also be seen. These findings are due to the adhesive nature of the inflamed pia–arachnoid membranes. There is still an occasional role for CT-myelography in a patient with clinically suspected adhesive arachnoiditis and a normal MRI. The ability of CT-myelography to delineate the intrathecal nerve root anatomy may be useful in those patients with limited, localized areas of arachnoiditis involvement.42 It is important to note that findings consistent with arachnoiditis on an imaging study may be clinically asymptomatic.

Intervertebral disc Hoffman’s ligaments Epidural fibrosis and scarring Ventral ramus Radicular artery Dorsal root ganglion

Radicular vein Dorsal ramus Thecal sac Post-surgical scarring Spinal process

Fig. 104.6 Clumping of nerve roots in the thecal sac characteristic of arachnoiditis. 1141

Part 3: Specific Disorders

Clinical assessment The diagnosis of postoperative low back and limb pain due to neural scarring is a diagnosis of exclusion. Any possible cause for the radicular symptoms other than scar formation has to be excluded.43 The common etiologies of FBSS must be algorithmically eliminated. This concept has been discussed by Jerome Schofferman in the preceding chapter. The clinical presentation of radicular pain due to neural scarring is variable. The classically described arachnoiditis patient typically includes a history of postoperative leg pain with or without back pain 1–6 months after a brief pain-free interval. Pain is the consistent complaint. However, the location, character, and frequency of pain complaints vary in each patient. Physical examination may demonstrate sensory and/or motor deficits. Nerve root tension signs such as straight leg raising are typically positive. It is not uncommon for the initial preoperative history and physical examination findings to be unchanged postoperatively. As always, other more treatable conditions such as a recurrent disc protrusion, small lateral disc protrusion, neuroforaminal stenosis, lateral recess stenosis, or spinal stenosis need to be ruled out.

NONSURGICAL TREATMENT Medical rehabilitation and interventional physiatric treatment of FBSS for those patients with recurrent radicular leg pain greater than back pain and with radiologic abnormalities limited to the presence of epidural fibrosis have not shown long-term success.6,44 The majority of the current literature examining FBSS secondary to epidural/intraneural fibrosis has investigated surgical outcomes.6,45–48 Treatment is multidisciplinary. This may include a combination of physical therapy and modalities, pharmacologic agents of various classes, fluoroscopically guided selective nerve root blocks, activity modifications, education, and pain counseling.

Physical therapy Bed rest is not indicated and the patient is encouraged to be as active as possible. Postoperative rehabilitation and physical therapy is necessary to treat the deconditioned lumbar spine stabilizers, pelvic girdle musculature, and lower limb muscles. Although there are no randomized, controlled studies investigating the effectiveness of physical therapy and modalities such as transcutaneous electrical nerve stimulation (TENS) in the treatment of symptomatic neural scarring, current studies to date do show that these patients may show improvement in their overall functional ability and even in their subjective complaints of pain.49 Nerve root glide maneuvers may also be helpful to slacken the tethered nerve roots from fibrotic tissue.

Pharmacologic agents Medications including nonsteroidal antiinflammatory drugs (NSAIDs), neuropathic agents such as tricyclic antidepressants (TCAs) or anticonvulsants, muscle relaxants, and opioid pain medications can be tried. These medications should be given in a step-wise fashion with NSAIDs as first-line treatment. Neuropathic agents are membrane stabilizers and should be initiated if there is a significant component of limb pain with neurogenic symptoms such as dysesthesias, paresthesias, and burning or lancinating pain. Gabapentin, one of the most commonly used agents for neuropathic pain, has been reported to be effective in the management of symptomatic limb pain due to epidural fibrosis.50 Muscle relaxers, as a pharmacologic class, are not consistently effective for the treatment of muscle spasms but may be initiated if the spasms are a primary complaint. Most muscle relaxers are also sedatives and should be best taken in 1142

the evenings. Medications to restore normal sleep cycle are important for those patients with impaired sleep. Opioid pain medications are primarily used for analgesia but do have secondary effects of membrane stabilization. Anxiolytics and antidepressants are indicated for treatment of mood disorders, which are frequent in this population.

Selective nerve root block There are few studies that have examined the nonsurgical outcomes of FBSS secondary to epidural/intraneural fibrosis treated with selective nerve root blocks (SNRB). Devulder51 demonstrated good pain relief in 12 out of 20 patients with FBSS treated with SNRB consisting of local anesthetic diluted in 1500 U hyaluronidase and 40 mg of methylprednisolone. However, this retrospective pilot study lacked stringent inclusion criteria, used only verbal pain scores, and had a follow-up period of only 3 months. Devulder and colleagues52 found no statistical difference between three patient groups treated with SNRB using a combination of either bupivacaine, hyaluronidase, methylprednisolone, or saline in 60 patients with documented fibrosis and a follow-up period of 6 months. Unfortunately, this study also lacked stringent inclusion criteria and used verbal pain scales as the sole outcome measure. A preliminary study by Slipman et al.53 reported epidemiologic data and outcomes of patients with FBSS secondary to epidural or intraneural fibrosis treated nonsurgically with fluoroscopic guided therapeutic selective nerve root blocks using stringent inclusion criteria and multiple outcome measures. The preliminary study reported successful outcomes from the selective nerve root blocks; however, the frequency of a successful outcome was less than 25% in the small sample size of subjects. One of the most effective methods the authors use, and similarly employed at The Penn Spine Center, is the institution of a membrane stabilizer. Typically, the authors use neurontin as a first-line agent. If that is not tolerated then they move on to zonegran, trileptal, keppra and so forth. If symptom reduction is achieved, even only 20% or so, then a therapeutic selective nerve root block is added. These two measures seem to be symbiotic and allow for continued relief that will be maintained provided the patient continues the membrane stabilizing agent. When the side effect of an agent exceeds the benefit obtained then there is a switch to another medication. A therapeutic block is not performed until some symptom reduction is achieved with an oral agent. This approach requires a vigorous scientific trial, which has not yet been conducted. In contrast, several studies have demonstrated the efficacy of fluoroscopically guided transforaminal selective nerve root blocks in the treatment of painful radiculopathy due to a focal disc protrusion. Although selective nerve root blocks may provide reduction of painful lower limb symptoms in the presence of epidural or intraneural fibrosis, the outcomes are much poorer. The injection approach and technique are critical for the successful performance of the selective nerve root block. A fluoroscopically guided SNRB or transforaminal injection is preferably employed instead of an interlaminar or translaminar injection because this facilitates ventral epidural flow to the involved nerve root complex or the posterior surface of the intervertebral discs. The therapeutic agents injected with the posterior translaminar injection approach may remain in the dorsal epidural space without spreading to the affected nerve root or intervertebral disc in the ventral epidural space.54 Furthermore, it is inappropriate to use an interlaminar or translaminar injection technique in patients who have had prior lumbar spine surgery. Surgery alters the normal spinal anatomy with postoperative scar tissue obliterating the normal posterior epidural space and obstructing the flow of contrast dye or medication to the target structures. A transforaminal injection

Section 5: Biomechanical Disorders of the Lumbar Spine Spinal nerve

Intervertebral disc

Pedicle

Ventral ramus

Intervertebral foramen

Spinal needle

circumvents this problem by placing the needle just inside the neural foramen at the disc–nerve root interface in the ventral epidural space (Fig. 104.7). In addition, the needle track of a transforaminal injection, as opposed to an interlaminar injection, will not be impeded by postoperative scar tissue. Confirmation of proper needle position during a fluoroscopically guided diagnostic SNRB occurs when contrast outlines the targeted nerve root and extends extraforaminally without evidence of epidural flow. The rationale for employing an SNRB is that both corticosteroids and local anesthetic agents have been shown to stabilize neural membranes.55–58 Local anesthetic agents also improve intraradicular blood flow.55 These effects may reduce intraneural or epidural fibrosis and/or the endoneurial edema, compression, or ischemia of the nerve roots. Glucocorticoids suppress inflammatory cytokines and inhibit inflammatory cells.59,60 By modulating cytokines controlling proteolytic enzymes such as collagenase, corticosteroids may affect collagen formation and the organization of the epidural or intraneural fibrotic tissue. The combination of an oral membrane stabilizer, a selective nerve root block with corticosteroids, and physical therapy with nerve root gliding techniques may help to reorganize dense fibrotic scar toward looser connective tissue. If such a process occurs, nerve root excursion within the neural foramen may be restored to a more normal state. Due to the sparse literature, no definitive judgment can currently be made regarding the efficacy of therapeutic SNRB for the treatment of radicular pain caused by epidural or intraneural fibrosis. Based upon personal observation and communications with experienced colleagues, these injections typically do not cure the painful symptoms but may relieve these symptoms for varying periods when they are used in isolation.

Minimally invasive procedures Percutaneous lysis of epidural adhesions has been described to be an effective treatment for chronic low back and/or leg pain secondary to epidural fibrosis.10,61–66 Racz initially described the technique involving epidurography, adhesiolysis, and injection of local anesthetic agents, corticosteroids, and hyaluronidase followed by injection of hypertonic saline.10,64,65,67,68 One-year outcome studies reported 25–47% good outcomes.62,64,65 However, there are devastating consequences such as cauda equina syndrome, spinal cord compression, paraplegia, myelopathy, and arachnoiditis if not performed properly.10,69–71 Retinal hemorrhages due to increased intracranial pressure

Fig. 104.7 Position of needle during a selective nerve root block in a postoperative patient. Note Post-surgical scarring the postsurgical scarring that would obstruct (in a post-operative patient) an interlaminar or translaminar epidural steroid Spinal process injection. Superior articular process

from rapid high-volume injections72–76 and catheter shearing with retention in the epidural space have also been reported.10,77 Gabor Racz addresses these issues in much greater detail in Chapter 106. Implantable intrathecal morphine pumps are an option if a patient responds to oral opioid treatment but requires high dosages due to tolerance. The major advantage of a morphine pump is that a small dosage intrathecally can provide the same or better clinical analgesia when compared to oral opioid treatment.78 A drawback to the morphine pump is that the intrathecal agent may act as another insult to the neural elements and worsen arachnoiditis or neural scarring. A detailed discussion of implantable pain pumps including indication, contraindications, and outcomes is covered by Joshua Prager in Chapter 108. The use of TENS units can sometimes reduce painful neurogenic symptoms. Implantable dorsal column stimulators are a more invasive form of TENS, but may provide significant reduction of painful neurogenic lower limb symptoms in carefully selected patients. A more detailed review of this treatment modality is provided by Robert Windsor in Chapter 107.

Education and counseling Concurrent treatment with a psychologist who is adept at addressing the variety of issues confronting the patient with chronic pain is helpful. This will enable a reduction in the subjective component of the patient’s pain threshold. This includes counseling for coping skills, biofeedback, goal setting, reinforcement of activity modifications, and the subjective reduction of pain behavior. Social support from family and friends is important for successful treatment of this difficult entity. Initiating their participation in the overall treatment plan of the patient is important so that they understand the challenging nature of this clinical diagnosis. It should emphasized that psychological counseling is not a categorical requirement. Some patients will respond quite well to the aforementioned therapy, medication and injection cocktail, thereby dramatically diminishing their distress.

ALGORITHMIC APPROACH When approaching a postoperative patient with persistent lower limb pain who has failed a reasonable trial of conservative treatment consisting of physical therapy and medications, one must first determine the location of the lower limb pain and its time course in relation 1143

Part 3: Specific Disorders

to the surgery. The time course characteristically involves onset of radicular symptoms within 1 year of postoperative pain relief. Nerve root pain due to epidural or intraneural fibrosis classically follows a radicular pattern of the involved nerve root and is within all or part of the radicular symptom distribution prior to surgery. The radicular lower limb pain is generally more intensely painful than axial low back pain. Gadolinium-enhanced MRI of the lumbar spine must demonstrate epidural fibrosis around the suspected nerve root without evidence of other pathology such as neuroforaminal stenosis or a recurrent disc protrusion. If the physical examination reveals a new myotomal strength deficit or reflex change correlating with the distribution of radicular pain and MRI findings, a fluoroscopically guided therapeutic selective nerve root block is recommended to treat the involved nerve root. In the absence of these physical examination findings, a positive electrodiagnostic evaluation identifying new acute changes consistent with the involved nerve root level will diagnose the radiculopathy. A therapeutic selective nerve root block is then offered to treat the radiculopathy. An EMG is considered positive when the involved nerve root level has abnormal spontaneous activity at rest in the form of positive sharp waves and fibrillation potentials in the associated paraspinal musculature and in at least two muscles from the same myotomal, but different peripheral nerve innervation with neuropathic recruitment abnormalities.79 Although a positive EMG provides the diagnosis of radiculopathy, a negative EMG does not rule out nerve injury. It is not uncommon for patients with radicular pain to have normal electrodiagnostic findings or instances where only chronic changes are identified.80 If the electrodiagnostic study and physical examination are both negative in the setting of an abnormal imaging study with radicular complaints, a fluoroscopically guided diagnostic selective nerve root block is required.80–82 The diagnostic selective nerve root block is performed only with a small aliquot (1 cc or less) of local anesthetic to directly anesthetize only the suspected nerve root. Care must be taken to ensure that contrast only outlines the nerve root without epidural spread. Otherwise nearby structures in the epidural space will be inadvertently anesthetized, thus comprising the selective nature of this block and removing its diagnostic reliability. If there is at least an 80% or greater reduction of the postblock visual analog scale (VAS) when compared to the pre-block VAS several minutes post-injection, the diagnostic selective nerve root block is positive.81,83,84 This confirms that the radicular lower limb pain is emanating from the suspected nerve root, and a fluoroscopically guided therapeutic steroid selective nerve root block is then offered. The high sensitivity, ranging 99–100%,85,86 and high specificity, ranging 87–100%,85–90 of diagnostic selective nerve root blocks have been well documented by several studies. If the patient fails to improve with a fluoroscopically guided therapeutic steroid SNRB and seeks further treatment for persistent radicular lower limb pain due to epidural fibrosis, percutaneous epidural adhesiolysis under fluoroscopy is recommended by some. A dorsal column stimulator trial is reserved as the last resort if the patient is refractory to the aforementioned treatments.

SURGERY Most authors do not recommend reoperation when fibrosis is suspected to be the only cause of FBSS because the probability of longterm success after reoperation is low.1–7,43–48,91,92 Surgical outcomes have been reported to be between 10% and 30%.6,48 In a prospective case series, Jonssson and Stromqvist47 demonstrated that 62% of patients with FBSS secondary to neural fibrosis after discectomy undergoing reoperation were unchanged or worse. Neurolysis for epidural fibrosis not only yields dismal results and more expansive fibro-

1144

sis, but it also increases the risk of nerve root injury.45,48,93 The overall failure rate for neurolysis has been reported to be 62–83%.91,92,94–96 Outcomes are poor for eliminating scar tissue and significantly reducing pain from adhesive arachnoiditis, and may exacerbate symptoms by further damaging the neural elements.97,98 Exploratory surgery is not indicated in the absence of progressive neurologic deficit nor in patients whose pain can be controlled with nonsurgical treatment. Patients with high-grade arachnoiditis and those with preoperative dysesthesias have a worse prognosis for surgical success.99–102 In recent years, much attention has been focused on various biologic, pharmacologic, and synthetic materials to inhibit neural scarring and its intraoperative applications. Several materials have been used intraoperatively to inhibit scar; however, research related to their efficacy has been via animal models, and clinical results are not convincing. The ideal agent for scar inhibition remains to be identified. Fat free grafts have had the longest history of use and are generally accepted as a way to avoid possible postsurgical fibrosis. Again, its usefulness in epidural and perineural fibroses inhibition is uncertain. Fat graft is readily available with no additional cost, and it can become vascularized, nourishing the dura. The possible disadvantages of using this graft include seroma formation, indentations, and the fact that it is a space-occupying mass that may cause neural compression. The size of the graft is also important. A large graft may possibly result in neural compression, whereas if too thin it may be ineffective as the fat graft shrinks in size over time.103,104 Migration of the graft is also a concern and a few cases of cauda equina syndrome believed to result from migration have been reported.105,106 Generally speaking, surgeons prefer fat grafts, as they are easily available without additional costs and do protect the dura without excessive formation of fibrous tissue. Alternatives to fat grafts include a number of materials. Gelfoam is widely used as a hemostatic agent, but has also been shown to prevent scar adhesion when used in the epidural space after a laminectomy.107 Another gelatin-derived product is ADCONL. It was FDA approved in 1998 for inhibition of postsurgical fibrosis. Several cases of dural tears after use of ADCON-L in posterior lumbar surgeries were reported which has limited the widespread use of this material.108 There are several scar-inhibiting agents that are currently being evaluated in clinical trials.

PREVENTION Outcomes of nonoperative and surgical treatments for neural scarring are poor. Since there is no effective or curative treatment for neural scarring, preventative measures are critical. For example, more recent water-based contrast agents have replaced the oil-based agents for diagnostic imaging studies. In addition, preservative-free local anesthetic solutions are now readily available and are the standard of care when injecting local anesthetic agents into the epidural space. Similarly, with more widespread utilization of pharmacologic agents intrathecally and within the epidural space, minimizing the quantity and duration of these agents in contact with the thecal sac or epidural space and their respective contents is important to reduce the potential risk of neural scarring. From a surgical perspective, meticulous surgical technique can limit the extent of neural scarring by minimizing bleeding, infection, and dural and intrathecal insults.

SUMMARY The pathophysiology of radicular pain caused by epidural or intraneural fibrosis may be the result of inflammation, vascular compromise, mechanical compression, or tension of the spinal nerve roots. An accurate diagnosis of symptomatic neural scarring can be determined with a diagnostic algorithmic pathway incorporating a detailed

Section 5: Biomechanical Disorders of the Lumbar Spine

history, physical examination, electrodiagnostic testing, and fluoroscopically guided diagnostic selective nerve root blocks. Injection of glucocorticoids and local anesthetic agents has been proposed since these agents can indirectly stabilize neural membranes, reduce the local cellular immune response, inhibit inflammatory cytokines, decrease intraneural edema, and increase intraradicular blood flow. Nonsurgical and surgical outcomes for symptomatic neural scarring are poor. Treatment necessitates a multidisciplinary approach that also involves the patient’s social support network.

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56. Cullen BF, Haschke RH. Local anesthetic inhibition of phagocytosis and metabolism of human leukocytes. Anesthesiology 1974; 40:142–146.

83. Anderberg L, Annertz M, Brandt L, et al. Selective diagnostic cervical nerve root block – correlation with clinical symptoms and MRI pathology. Acta Neurochir (Wien) 2004; 146(6):559–565.

57. Hoidal JR, White JG, Repine JE. Influence of cationic local anesthetics on the metabolism and ultrastructure of human alveolar macrophages. J Lab Clin Med 1979; 93:857. 58. Goldstein IM, Lind S, et al. Influence of local anesthetics upon human polymorphonuclear leukocyte function in vitro. J Exp Med 1977; 146:483–494. 59. Takahashi H, et al. Inflammatory cytokines in the herniated disc of lumbar spine. Spine 1996; 21:218–224. 60. Doita M, et al. Immunohistologic study of the ruptured intervertebral disc of the lumbar Spine 1996; 21:235–241. 61. Manchikanti L, Pakanati R, Bakhit CE, et al. Role of adhesiolysis and hypertonic saline neurolysis in management of low back pain. Evaluation of modification of Racz protocol. Pain Digest 1999; 9:91–96. 62. Manchikanti L, Pampati V, Fellows B, et al. Role of one day epidural adhesiolysis in management of chronic low back pain: a randomized clinical trial. Pain Phys 2001; 4(2):153–166. 63. Manchikanti L, Pampati V, Bakhit CE, et al. Non-endoscopic endoscopic adhesiolysis in post lumbar laminectomy syndrome. A one-year outcome study and cost effective analysis. Pain Phys 1999; 2:52–58. 64. Racz GB, Heavner JE, Raj PP. Percutaneous epidural neuroplasty. Prospective oneyear follow up. Pain Digest 1999; 9:97–102. 65. Heavner JE, Racz GB, Raj P. Percutaneous epidural neuroplasty. Prospective evaluation of 0.9% NaCl versus 10% NaCl with or without hyaluronidase. Reg Anesth Pain Med 1999; 24:202–207. 66. Arthur J, Racz G, Heinrich R, et al. Epidural space. Identification of filling defects and lysis of adhesions in the treatment of chronic painful conditions. In: Abstracts, 7th World Congress on Pain. Paris, IASP Publications, 1993:557. 67. Racz GB, Sabaonghy M, Gintautas J, et al. Intractable pain therapy using a new epidural catheter. JAMA 1982; 248:579–581.

85. Haueisen DC, Smith BS, Myers SR, et al. The diagnostic accuracy of spinal nerve injection studies. Clin Orthopaed Rel Res 1983; 198:179–183. 86. Van Akkerveeken PF. The diagnostic value of nerve root sheath infiltration. Acta Ortho Scand 1993; 64:61–63. 87. Dooley JF, McBroom RJ, Taguchi T, et al. Nerve root infiltration in the diagnosis of radicular pain. Spine 1994; 19:1125–1131. 88. Krempen JF, Smith BS. Nerve root injection: a method for evaluating the etiology of sciatica. J Bone Joint Surg [Am] 1974; 56A:1435–1444. 89. Schutz H, Lougheed WM, Wortzman G, et al. Intervertebral nerve-root in the investigation of chronic lumbar disc disease. Canadian J Surg 1973; 16:217–221. 90. Stanley D, McLaren MI, Euinton HA, et al. A prospective study of nerve root infiltration in the diagnosis of sciatica: A comparison with radiculography, computed tomography, and operative findings. Spine 1990; 6:540–543. 91. Ozgen S, Naderi S, Ozek MM, et al. Findings and outcome of revision lumbar disc surgery. J Spinal Disord 1999; 12(4):287–292. 92. Benoist M, Ficat C, Baraf P, et al. Postoperative lumbar epiduro-arachnoiditis. Diagnostic and therapeutic aspects. Spine 1980; 5(5):432–436. 93. Johnston J, Matheny J. Microscopic lysis of lumbar adhesive arachnoiditis. Spine 1978; 3:36–39. 94. Thomalske G, Galow W, Ploke G. Critical comments on a comparison of two series of lumbar disc surgery. Adv Neurosurg 1977; 4:22–27. 95. Johnston J, Matheny J. Microscopic lysis of lumbar adhesive arachnoiditis. Spine 1978; 3:36–39.

68. Racz GB, Heavner JE, Raj PP. Epidural neuroplasty. Semin Anesthesia 1997; 302–312.

96. Grane P. The post-operative lumbar spine. A radiological investigation of the lumbar spine after discectomy using MR imaging and CT. Acta Radiol Suppl 1998; 414:1–23.

69. Aldrete JA, Zapata JC, Ghaly R. Arachnoiditis following epidural adhesiolysis with hypertonic saline report of two cases. Pain Digest 1996; 6:368–370.

97. Quiles M, Machisello PJ, Tsairis P. Lumbar adhesive arachnoiditis: Etiologic and pathologic aspects. Spine 1978; 3:45–50.

70. Kim RC, Porter RW, Choi BH, et al. Myelopathy after intrathecal administration of hypertonic saline. Neurosurgery 1988; 22:942–922.

98. Coventry MB, Stauffer RN. The multiply operated back. In: American Academy of Orthopaedic Surgeons: Symposium on the Spine. St. Louis: CV Mosby; 1999: 132–142.

71. Lucas JS, Ducker TB, Perot PL. Adverse reactions to intrathecal saline injections for control of pain. J Neurosurg 197; 42:557–561.

99. Dolan RA. Spinal adhesive arachnoiditis. Surg Neurol 1993; 39:479–484.

72. Kushner FH, Olson JC. Retinal hemorrhage as a consequence of epidural steroid injection. Arch Ophthalmol 1995; 113:309–313.

100. Johnston J, Matheny J. Microscopic lysis of lumbar adhesive arachnoiditis. Spine 1978; 3:36–39.

73. Ling C, Atkinson PL, Munton CG. Bilateral retinal hemorrhages following epidural injection. Br J Ophthalmol 1993; 77:316–317.

101. Roca J, Moreta D, Ubierna MT, et al. The results of surgical treatment of lumbar arachnoiditis. Int Orthop 1993; 17:77–81.

74. Purdy EP, Ajimal GS. Vision loss after lumbar epidural steroid injection. Anesth Analg 1998; 86:119–122.

102. Wilkinson HA, Schuman N. Results of surgical lysis of lumbar adhesive arachnoiditis. Neurosurgery 1979; 4:401–409.

75. Usubiaga JE, Wikinski JA, Usubiaga LE. Epidural pressure and its relation to spread of anesthetic solution in epidural space. Anesth Analg 1967; 46:440–446.

103. Kanamori M, Kawaguchi Y, Ohmori K, et al. The fate of autogenous free-fat grafts after posterior lumbar surgery: part 1. A postoperative serial magnetic resonance imaging study. Spine 2001; 26(20):2258–2263.

76. Morris DA, Henkind P. Relationship of intracranial, optic-nerve sheath, and retinal hemorrhage. Am J Ophthalmol 1967; 64:853–859. 77. Manchikanti L, Bakhit CE. Removal of torn Racz catheter from lumbar epidural space. Reg Anesth 1997; 22:579–581. 78. York M, Paice JA. Treatment of low back pain with intraspinal opioids delivered via implanted pumps. Orthop Nurs 1998; 17(3):61–69. 79. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley & Belfus; 1997:231. 80. Slipman CW, Chow DW, Whyte WS, et al. An evidenced-based algorithmic approach to cervical spinal disorders. Crit Rev Phys Rehab Med 2001; 13(4): 283–299. 81. Huston CW, Slipman CW. Diagnostic selective nerve root blocks: indications and usefulness. Phys Med Rehabil Clin N Am 2002; 13(3):545–565. 82. Slipman CW, Chow DW. Therapeutic spinal corticosteroid injections for the management of radiculopathies (chapter 12). In: Dillingham TR, ed. Cervical, thoracic,

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84. Slipman CW, Plastaras CT, Palmitier RS, et al. Symptom provocation of fluoroscopically guided cervical nerve root stimulation: Are dynatomal maps identical to dermatomal maps? Spine 1998; 23(20):2235–2242.

104. Kanamori M, Kawaguchi Y, Ohmori K, et al. The fate of autogenous free-fat grafts after posterior lumbar surgery: part 2. Magnetic resonance imaging and histologic studies in repeated surgery cases. Spine 2001; 26(20):2264–2270. 105. Mayer PJ, Jacobsen FS. Cauda equina syndrome after surgical treatment of lumbar spinal stenosis with application of free autogenous fat graft. J Bone Joint Surg [Am] 1989; 71A:1090–1093. 106. Prusik VR, Lint DS, Bruder WJ. Cauda equina syndrome as a complication of free epidural fat-grafting. J Bone Joint Surg [Am] 1998; 70A:1256. 107. LaRocca H, Macnab I. The laminectomy membrane: studies in its evolution, characteristics, and prophylaxis in dogs. J Bone Joint Surg [Br] 1974; 56B: 545–550. 108. Le AX, Rogers DE, Dawson EG, et al. Unrecognized durotomy after lumbar discectomy: a report of four cases associated with the use of ADCON-L. Spine 2001; 26(1):115–117.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar

CHAPTER

105

Postoperative Pseudomeningocele, Hematoma, and Seroma Kenny S. David, Raj D. Rao and Jeffrey S. Fischgrund

PSEUDOMENINGOCELE A pseudomeningocele is an extradural collection of cerebrospinal fluid (CSF) that has extravasated through a dural or arachnoid tear.1–3 Other terms used to describe this condition are ‘meningeal pseudocysts’ and ‘meningeal spurius’.4 Pseudomeningocele was first reported in the literature in 1946 following laminectomy for removal of a neoplasm.5

Epidemiology Among patients undergoing primary decompressive lumbar spine surgery, incidental durotomy occurs at an incidence of 9–12%, making it the most frequently reported complication of lumbar spine surgery.6,7 After cauda equina syndrome, dural tears are the most frequent underlying diagnosis in malpractice litigation involving lumbar spine surgery.8 Pseudomeningoceles are a rare consequence of dural injury. In a review of 1700 laminectomies, Swanson and Fincher reported pseudomeningocele formation in four patients.9 In a group of 400 postlaminectomy patients with persistent back pain and/or radicular symptoms, Teplick et al. found pseudomeningoceles in 8 patients (2%).3 Factors that predispose to a dural tear in surgery are prior surgery or irradiation, congenital spinal malformations, unrecognized dural adhesions, dural calcification contiguous with overlying lamina, and the absence of epidural fat.8,10,11 Severe spinal stenosis and large herniated discs make root dissection and dural retraction more difficult and can predispose to dural tears. Dural injuries and pseudomeningoceles are understandably more frequent with posterior than anterior approaches.

Pathogenesis Pseudomeningoceles generally develop following an intraoperative rent in the dura and arachnoid, but can occur following dural needle puncture procedures, especially after multiple punctures.9 The cerebrospinal fluid leaks dorsal to the lamina, into a space artificially created by dissection of the paravertebral musculature. The fluid cavity is lined by flattened connective tissue cells resting on loose, areolar connective tissue.2,4 An encysted pseudomeningocele refers to a CSF-filled herniation of an arachnoid lined cyst through a small rent in the dura. The narrow opening in the dura acts like a one-way valve leading to an increase in size of the CSF collection and formation of a pseudomembrane.2 The size of the dural defect, pressure of the inflowing CSF, and the resistance of the surrounding soft tissues all influence the size of a pseudomeningocele. Postoperative weakness of paraspinal muscles may be a reason contributing to expansion of the pseudomeningocele.12 Spinal fluid pressure keeps the dural defect open and prevents

healing. Herniation of nerve filaments into the original dural defect may be another factor responsible for keeping the dural opening patent (Fig. 105.1).4 Puncture of the dura can result in escape of large volumes of CSF, leading to intracranial hypotension and a demonstrable reduction in CSF volume. The adult subarachnoid pressure of 15 cmH2O can be reduced to 4 cmH2O or less. The rate of loss of CSF through a dural perforation following puncture with a 25-gauge or larger needle is generally greater than the rate of CSF production.13

Clinical features Cerebrospinal fluid leaks after needle procedures in the lumbar spine classically present with headache. There is evidence that CSF leaks may be inevitable following needle puncture of the thecal sac,14 and it is unclear why only some of these patients are symptomatic. The size of the dural leak has no direct relationship with the occurrence of headache.14 The actual mechanism of headache is also unclear. Some authors suggest that the lowering of CSF pressure following a leak causes traction on the intracranial structures in the upright position. These structures are pain sensitive, leading to the characteristic

Dura mater Arachnoid mater

Posterior longitudinal ligament

Entrapped nerve root Pseudomeningocele

Fig. 105.1 Meningeal layers involved in the formation of a pseudomeningocele, with schematic representation of nerve root entrapment at the site of the dural defect. 1147

Part 3: Specific Disorders

headache.13 Others authors report that the drop in intracranial pressure causes a compensatory intracranial venodilation, which causes the headache. The headache is generally localized to the frontal and occipital regions, with occasional radiation to the neck and shoulders. Other symptoms may include nausea, vomiting, tinnitus, and vertigo. While pseudomeningoceles may be asymptomatic, many present with local swelling, symptoms of CSF leak, or nerve root impingement. Local swelling15 may occasionally be the only suggestion of a pseudomeningocele.12 The swelling may vary in size, depending on whether the patient is standing or recumbent. There is no apparent correlation between the size of the pseudomeningocele, the size of the defect in the dura, and the degree of symptoms.4,16 Postural headache frequently occurs in patients with pseudomeningocele. Miller and Elder4 reported one patient whose postural headache could be increased by manual pressure directly over a large fluctuant meningocele. Back pain, with or without radicular leg symptoms, is commonly associated with pseudomeningocele. In a review of 10 patients with postoperative pseudomeningocele, Miller and Elder found that back pain was a common feature in all patients, with nine having radicular pain radiating into the lower limbs.4 Manual pressure over the paraspinal musculature on the side of the cyst may exacerbate the back pain.16 Coexisting worker’s compensation issues can lead to doubts being expressed as to the authenticity of such complaints in the postoperative patient.16 Radicular findings in patients with pseudomeningocele result from herniation and kinking of the nerve roots in the dural defect,17 adhesion of the nerve roots to the edges of the sac,18 or direct pressure of the pseudomeningocele on an adjacent nerve root. Eismont et al.19 reported a case of persistent postoperative radicular pain along with focal deficits following lumbar disc excision. Myelography revealed a pseudomeningocele involving the left fourth and fifth lumbar nerve roots. Intraoperatively, it was found that the L4 root had buttonholed through the site of the dural tear, while the pseudomeningocele was found to be compressing the L5 root. Ossification of a pseudomeningocele can rarely cause neural compression.20 In many patients an obvious site of nerve root entrapment is not identifiable.4 Asymptomatic meningoceles can become symptomatic after a precipitating event leading to nerve entrapment.21 Radicular pain in a previously asymptomatic patient can be precipitated by maneuvers that increase intracranial and intraspinal pressure, such as coughing, sneezing, or jugular compression.16 Unusual presentations associated with pseudomeningoceles include bone erosion of the posterior vertebral elements22 and chronic meningitis.23

A

1148

B

Investigations Myelography shows a characteristic pattern of dye extruding through the stalk of the pseudomeningocele, and a fluid level may be visible when the opening in the dura is large. Percutaneous injection of contrast material directly into the cyst cavity has been carried out when a palpable or visible mass is present at a surgical site.16 CT-myelography can effectively demonstrate the neck and outline of the pseudomeningocele although nerve root entrapment is not well visualized.18 MRI scans are very sensitive for CSF collections and pseudomeningoceles (Fig. 105.2). Some authors recommend a routine postoperative MRI scan following any repair of a durotomy, even in the absence of symptoms of a pseudomeningocele, in order to ensure that no further leakage is present.24 Digital subtraction myelography may occasionally reveal a pseudomeningocele when plain myelography, CT scan, and MRI show a fluid collection posterior to the dural sac, but no obvious connection between the two.25 In radionuclide cisternography, radionuclide contrast material is injected into the subarachnoid space followed by MRI evaluation. Areas filled with CSF show up as high-signal regions.26

Management of dural tear and pseudomeningocele In an attempt to reduce the incidence of postdural puncture CSF leak, numerous modifications have been made to spinal needles. Newer needle designs with narrow cutting tips and atraumatic bevels have resulted in a lower incidence of postspinal headache, neural irritation,13,27 and CSF leak.28 Spontaneous recovery from postdural puncture headache (PDPH) occurs in over 85% of patients within 6 weeks. Many forms of conservative management have been suggested and practiced, mostly without any scientific evidence to support their efficacy. Bed rest has been historically recommended, but does not lower the incidence of PDPH although it may delay its onset and decrease its intensity.29 Some authors suggest that bed rest may prevent further complications from traction and rupture of meningeal veins caused by intracranial hypotension.30 For severe and persistent headaches epidural blood patch (EBP) injections have been successfully used. Autologous blood is injected into the epidural space, where it forms a clot and seals the dural hole. Although over 90% of PDPH respond initially to EBP injections, a sustained and durable response has been identified in only 61–75%.31 Intraoperative durotomy is managed by primary dural repair, with a watertight suture of the dural defect. The key to prevention of

Fig. 105.2 (A) Parasagittal T2-weighted MRI of postoperative lumbar pseudomeningocele. (B) Axial T2-weighted MRI of the same patient, showing the pseudomeningocele communicating with the thecal sac.

Section 5: Biomechanical Disorders of the Lumbar Spine

postoperative pseudomeningocele is a meticulous primary repair of dural tears detected intraoperatively. Fine suture material such as 5-0 or 6-0 monofilament, braided or coated synthetic is suitable, although leakage of CSF can occur through the needle holes in the dura. A continuous running suture is quickest to perform, but may result in unraveling of the entire suture line if the tension is not perfect or the suture breaks. The use of magnification and coaxial illumination is essential for adequate repair. Local application of fibrin glue greatly reinforces a repair site.26,32 When a CSF leak is noticed postoperatively, surgical treatment is generally recommended for the immediate and definitive management of the lesion.19 Some authors recommend nonoperative management in a patient with a well-healed incision presenting with a soft subcutaneous bulge and no postural headache.33 Waisman and Schweppe treated seven patients by reinforcing the skin suture line, bed rest in the Trendelenburg position, and repeated puncture and drainage of the subcutaneous CSF collection. The CSF leakage stopped immediately after the incision was resutured, the subcutaneous fluctuation disappeared in 10–28 days, and an 8-year follow-up (clinical and ultrasound examination) revealed no pseudocyst formation.34 Eismont et al. reported one case where resuturing the skin stopped the CSF leakage through the incision. A symptomatic pseudomeningocele subsequently developed, and the authors recommends surgical repair of the dura for all dural leaks noted postoperatively.19 Closed subarachnoid drainage is frequently used in the management of CSF leaks33,35 and occasionally for established pseudomeningocele.36 The catheter is positioned in the subarachnoid space using fluoroscopic technique. Epidural catheter placement may be used for drainage of a pseudomeningocele.33 The proximal end of the catheter is connected to a sterile drainage system. The basis of this external CSF drainage is that a reduction of CSF pressure and preferential escape of the CSF through the catheter for 4–5 days generally allows the dural fistula to heal itself. Lumbar peritoneal shunting may play a role in the management of refractory CSF leaks.33,37 The dural opening is surgically repaired when feasible. A catheter is then introduced into the subarachnoid space, and a second catheter left in the meningocele cavity; both catheters are subcutaneously tunneled into the peritoneal cavity, where they are positioned under the diaphragm using laparoscopic assistance. The advantages of this technique including immediate mobilization of the patient, avoidance of complications of external drains and repeated aspirations, and a high success rate. The procedure is not in widespread use due to technically simpler and less invasive options being available. Occasionally, dural tears are lateral or ventral in position and not amenable to direct repair techniques. Thinned out or scarred dura adjacent to segments of thickened extradural scar tissue in the multiply operated back does not readily lend itself to direct repair. Some dural openings are irreparable after intradural procedures when the dura is abnormal or has to be partially resected. In such situations suturing fat, muscle graft, or autologous fascia lata graft over the repaired dural tear may reinforce the dural repair. Graft substitutes including cadaveric dura, silicone-coated Dacron, and bovine pericardium have been used, but are associated with the possibility of disease transmission and immunogenic tissue reaction. In previously irradiated tissue a vascularized myocutaneous flap can be rotated from an uninvolved area to the poorly vascularized defect and sutured to well-vascularized surrounding tissue. Newer techniques such as laser tissue welding are being investigated. Preliminary results show that primary repair combined with laser welding produces a higher leak pressure and tensile tissue strength than either technique used alone, with no evidence of underlying thermal tissue injury.38

Patients with established pseudomeningoceles who are not significantly disabled by their symptoms may be treated with observation alone. Follow-up MRI scans occasionally show complete resolution of small pseudomeningoceles.2 Sustained local pressure has been found to help control some symptoms of pseudomeningoceles. Leis et al.15 reported this form of treatment in a patient who was advised surgery but declined. The patient used a wide belt worn tightly around the waist and a folded towel under the belt so that it applied direct pressure over the swelling. This relieved the postural headache symptoms immediately. Repeat MRI scans done 8 weeks and 6 months after surgery showed progressive decrease in the size of the pseudomeningocele, till there was only a tiny focus of fluid left. The authors suggest a trial of focal compression for symptomatic relief of postural headache from pseudomeningocele. If symptomatic improvement is obtained, a more prolonged trial of mechanical compression may promote dural closure.15 Symptomatic pseudomeningoceles generally require surgical intervention.2,21 The operative procedure usually involves opening of the pseudomeningocele, followed by identification and closure of the dural defect with flaps from the cyst wall or a free graft. Augmentation of the repair with fibrin glue, muscle, fat, and fascial grafts is frequently necessary. Resection of overlying lamina is generally necessary for adequate visualization of the dural defect, and spinal fusion is indicated when excessive bone resection renders the spine unstable.4 Miller and Elder4 reported on the surgical treatment of 10 symptomatic pseudomeningoceles. The authors reported good results in seven patients, satisfactory results in two, and a poor result in one patient. Apart from surgical repair, the only other surgical option for pseudomeningocele is CSF diversion, a technique that is not always successful, especially when spinal fusion implants prevent the normal reapproximation of paraspinal tissues around the collection. In addition, a ball-valve mechanism at the dural fistula site may prevent complete drainage of CSF from the pseudomeningocele. The cavity could persist and reaccumulate CSF after the drain is removed.39 Complications of untreated pseudomeningocele include recurrence of radicular symptoms, the possibility of infection with resultant meningitis,23 ossification of the cyst wall producing canal stenosis and claudication,40 and rarely erosion of the bony vertebral elements from an expansile cyst.22

SPINAL HEMATOMA Introduction The term ‘hematoma’ when used in postoperative spine patients generally refers to a subcutaneous or subfascial incisional hematoma, and must be distinguished from a true spinal hematoma. The frequency of incisional hematomas depends on many factors, including the type and extent of surgery. An incidence of 0.08% (8.7 in 10 000) incisional hematomas was reported among 28 395 patients undergoing lumbar laminectomy,41 whereas rates of up to 12% have been reported following scoliosis surgery.42 True spinal hematomas occur most frequently in the epidural space (Table 105.1). The overall incidence of symptomatic spinal hematomas is very low, with a recent meta-analysis finding only 613 symptomatic patients over the past 170 years.43 Lawton et al.44 reported a 0.1% incidence (12 in 10 500) over a 14-year period comprising 10 500 spine surgery cases at one institution. Smaller asymptomatic hematomas occur more frequently than recognized in postoperative patients. When postoperative MRI is obtained, the reported incidence is 100%, even with procedures such as microdiscectomies.45 1149

Part 3: Specific Disorders

Table 105.1: Distribution of spinal hematomas according to anatomic localization43 Location

Number (n = 604)

%

Epidural

461

76.3

Subarachnoid

96

15.9

Subdural

25

4.1

Intramedullary

5

0.8

Combinations

17

2.8

The incidence of spinal hematoma following epidural/subarachnoid injection procedures is low. In a meta-analysis of 613 patients with spinal hematoma formation, Kreppel et al. reported that 10.3% (63 in 613) of these incidents occurred following lumbar puncture or spinal anesthesia.43 In a literature review of epidural hematomas after needle procedures, Adler et al. reported that 12 of 15 reported cases either had an abnormal bleeding profile or were on anticoagulant therapy.46 A review of subdural hematomas after lumbar injections showed similar results, with 17 of 19 reported patients receiving some form of anticoagulant therapy.46

Etiology In an extensive search of the literature on spinal hematomas, Kreppel et al. found a total 613 case studies reported over the last 170 years. Most cases had a multifactorial etiology, and no etiologic factor could be pinpointed in 29.7% of patients. Idiopathic spinal hematomas represented the most common category among all different age groups analyzed.43 Spontaneous epidural bleeds can arise following fibrinolytic therapy for coronary heart disease.47 Spinal hematomas also spontaneously develop from the lumbar facet joint48 and ligamentum flavum.49 The mechanism in these cases is presumed to be minor injury in the setting of degenerative changes. Arteriovenous malformations are another reported cause of spontaneous hematomas.50 Groen and Ponssen51 reported a spontaneous spinal epidural hematoma following rupture of the internal vertebral venous plexus. Spontaneous hematomas have also been reported in patients with liver disease and autoimmune conditions.52 Spinal hematomas occur rarely following spinal fractures, but are more prevalent with fractures in patients with ankylosing spondylitis.53 Spinal manipulation therapy is known to produce hematomas with resultant neurological deficits.54 Spinal injection procedures such as lumbar punctures, epidural and subdural anesthetic blocks, and therapeutic nerve root injections can lead to spinal hematoma formation. The hematomas are commonly epidural although there are a few reports of subdural hematomas. The common underlying factors in these reports are the coexistence of coagulation disorders, multiple punctures performed during the procedure, the insertion of a catheter, removal of a catheter, prior surgery, fibrosis, undetected spina bifida, and tethered cord syndrome. Preexisting coagulopathy may increase the likelihood of hematoma formation following spinal injection procedures, and the likelihood of back pain and neurologic deficit is also higher in these patients. Spinal hematoma is a recognized cause of postoperative worsening of neurological status in the first 24–48 hours following surgery. Kou et al.52 reviewed factors that predisposed to epidural hematoma formation in 12 patients who underwent lumbar laminectomy over a 10-year period. Multilevel procedures (p=0.037) and a preoperative coagulopathy (p=0.001) were significant risk factors. Age, body mass

1150

index, durotomy, and the use of postoperative drains were not statistically significant risk factors. In multilevel laminectomies, the increased exposure needed may increase the risk for bleeding from the paravertebral muscles. The larger exposures of the epidural space also increase the risk of insidious bleeding from the prominent internal vertebral venous plexus.52 The lordotic posture of the spine postoperatively may have a role in accentuating the pressure effects of a spinal hematoma. Ko and Kakiuchi55 reported on a patient who developed paraparesis 3 hours following decompressive surgery for lumbar spinal stenosis. Flexion of the spine was noticed to relieve the patient’s symptoms. The patient was positioned with the lumbar spine in sustained lumbar flexion and the deficits resolved within 5 days. Subdural spinal hematomas occur less frequently than epidural hematomas, and again are more likely with preexisting coagulopathy or following injection procedures. Accidental subdural spinal injection can occur in patients with postsurgical fibrosis causing obliteration of the epidural space, and mimics the radiographic appearance of epidural hematoma. Spinal subdural hematomas can also track down from a cranial subdural hematoma. The presence of blood within the dura may produce a fibroproliferative reaction of the leptomeninges, resulting in arachnoidal fibrosis and poorer prognosis.

Clinical features The presentation of spinal hematomas varies depending on the precipitating event, size of hematoma, canal dimensions, and location of the hematoma within the spinal column. Small hematomas are generally not evident clinically, and may be a universal phenomenon in the immediate postoperative period. Montaldi et al.56 found computed tomographic changes within the spinal canal suggestive of postoperative spinal hematoma or scar tissue in 84% of asymptomatic patients 1 week after lumbar discectomy. Kotilainen found MRI changes representing hematoma in 100% of asymptomatic patients following lumbar microdiscectomy on the first postoperative day.45 Neurologic deficits from larger spinal hematomas are infrequent. Patients with incomplete deficits fare better than those with complete paraplegia, and the location of the hematoma has a bearing on the clinical presentation as well as outcome. Spinal epidural hematomas at the lumbar cauda equina level usually fare better than hematomas at the spinal cord level. Spontaneous remission has been observed in hematomas at the cauda equina level with minor neurologic deficits.57 Spontaneous resolution has also been reported in two cases where the presentation was rapidly progressive over minutes.58 The symptoms resolved while investigations were being carried out over the next few hours. The authors suggested that while urgent decompression remains the treatment of choice in a symptomatic spinal epidural hematoma, conservative management may be indicated where there are definite signs of neurological improvement in the initial few hours. In patients who develop spontaneous spinal epidural hematomas without preceding trauma, an acute onset of local pain may be followed by radicular paresthesias. Within hours, signs of spinal cord compression can appear, presenting as progressive paraplegia and loss of sensory function. In 61 patients who developed spinal epidural hematomas after epidural puncture for anesthesia, and had been on anticoagulants, Vandermeulen et al. noted muscle weakness was the first sign in 28 of 61 patients, back pain in 23, and sensory deficit in 9.59 Paraplegia was recorded to occur within 14.5±3.7 hours after ending of the anesthetic. The most successful recovery following surgical decompression occurred in patients in whom surgical intervention was performed in less than 8 hours. In another review of five patients with spinal hematomas the authors found that four of five patients complained of acute back pain with paresthesias in both legs,

Section 5: Biomechanical Disorders of the Lumbar Spine

followed by rapidly progressive paraplegia.50 The fifth patient had an incomplete cauda equina syndrome. Slowly accumulating hematomas may result in delayed presentation up to a week following surgery. Long tract symptoms and findings may be seen if the hematoma impinges on the cervical spinal cord, following spinal manipulation or cervical epidural steroid injections. Although the clinical presentation of spinal epidural hematomas is relatively characteristic, other diagnoses need to be considered (Table 105.2)

Investigations Magnetic resonance imaging scanning is the diagnostic method of choice for evaluation of spinal hematomas (Fig. 105.3). MRI scans allow rapid evaluation of large sections of the spinal column and provide accurate information about the size and longitudinal extent of the lesion. Epidural hematomas have an isointense signal on T1weighted images. On T2-weighted images, acute hematomas show low-intensity signal in the periphery with a central high-intensity signal region. Beginning 4–14 days after the hematoma, the signal intensity increases from the periphery to the center due to the presence of methemoglobin derived from erythrocytes. Subdural hematomas can mimic epidural hematomas on MRI, but generally show high-intensity signals on both T1- and T2-weighted images. Preservation of the posterior epidural fat and visualization of the dural outline on axial images provide further clues to the subdural location of the hematoma. Intraspinal compressive lesions such as tumors or abscesses may be differentiated from subdural hematomas by virtue of a rim or uniform enhancement on MRI, whereas subdural hematomas rarely enhance. Some authors describe a 3-pointed star or ‘inverted Mercedes star’ appearance in lumbar subdural hematomas.60 CT scanning, myelography, and ultrasound have all been used to detect spinal hematomas, but do not have the sensitivity or specificity of MRI scanning.

Management An awareness of predisposing factors may substantially lower the incidence of spinal hematoma formation. For patients on anticoagulant therapy and undergoing spinal/epidural anesthetic procedures, the following guidelines may help reduce the occurrence of spinal hematoma:61 (1) atraumatic puncture, (2) a time interval of at least 60 minutes between spinal anesthesia and heparinization (based on the half-life period of heparin), and (3) close monitoring of coagulation parameters. Since the removal of epidural catheters is associated with a high incidence of bleeding complications, Sage62 recommended against the removal of spinal/epidural catheters in the first 2 hours following heparin administration, as many patients develop temporary blood concentration of heparin at this time. Following spine sur-

Table 105.2: Differential diagnosis of spinal epidural haematomas Intradural haemorrhage Spondylosis/disc herniation Infections Inflammatory pathologies Spinal cord infarction Spinal arterio-venous malformation Epidural varices

Fig. 105.3 Axial T2-weighted MRI of 83-year-old male with a thoracic epidural hematoma causing significant anteroposterior flattening of the spinal cord.

gery, most authors recommend at least 12 hours before restarting anticoagulant therapy.63 Although the use of postoperative suction drains following spine surgery is widespread, there is surprisingly limited evidence supporting this practice. In a recent Cochrane review of 21 studies in orthopedic literature on this subject, the authors found no difference in the rate of hematoma formation or other wound complications whether drains were used or not.64 Similar results were noted in a randomized trial on the efficacy of postoperative lumbar drainage on 200 patients after single-level nonfusion lumbar surgery. Patients were randomized into two groups of either receiving postoperative drains for 48 hours, or having no drain inserted. The authors found that no patient in either group developed a significant hematoma/ seroma requiring surgical drainage.65 The management of established spinal hematomas ranges from simple observation to emergency decompression surgery. The decision to treat a hematoma nonoperatively depends on the patient’s presenting symptoms, duration of symptoms, and evidence of clinical recovery in the early hours following onset of neurological deficit. In patients with no neurological deficits, nonoperative measures are reasonable. Even severe deficits have been treated with watchful expectancy and intravenous steroids when there are definite signs of neurologic improvement in the early hours following the onset of symptoms. The more spacious dimensions of the lumbar spinal canal, and the absence of spinal cord in this region lead to less damaging effects of a hematoma in the lumbar region. Younger patients with lumbar spine hematomas showing early evidence of neurological recovery can be considered for close observation. Most spinal hematomas presenting with acute neurological deficits are treated by emergency surgical decompression. The need for decompression of extrinsic cord compression has been demonstrated in experimental as well as clinical studies. Using an animal model, Delamarter et al.66 studied the effects of duration of spinal cord compression. Persistent pressure on the cord for 6 hours led to progressive necrosis within the cord, and neurologic recovery did not occur in this group following decompression. In a clinical review of 55 patients who developed spinal hematomas after spinal or epidural anesthesia and who were treated with emergency decompressive laminectomies, Vandermeulen et al found ‘good’ or ‘partial’ neurological recovery in 77% (10/13) of patients operated within 8 hours, 37.5% (3/8) of those treated within 8–24 hours, and only 17% (2/12) of those decompressed after 24 hours.59 Exceptions to the rule of urgent decompres-

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sion may be made when: (1) a patient presents 48–72 hours after onset of neurologic involvement, and (2) significant recovery is noted in the initial few hours after onset of the deficit. Operative decompression should be carried out along the entire length of a hematoma to ensure adequate evacuation and maximize chances of neurologic recovery. In some cases of extensive spinal hematoma, a limited decompression may obtain similar results without the morbidity of an extensive decompression. Osmani et al. reported limited decompression for a patient who had a hematoma extending from T4 to L5. The authors performed laminectomies from T11 to L5, and then used an arterial embolectomy balloon catheter to extract the more proximally located epidural blood clots. The patient reportedly recovered ‘significant motor power’ at 2 months.67 Another option that may play a role in the future in extensive spinal hematomas is the use of thrombolytic agents locally. Thrombolysis and evacuation of hematoma is achieved by intermittent irrigation of the subdural space with recombinant tissue plasminogen activator (rt-PA), followed by saline lavage.68

SEROMA Introduction The incidence of seromas occurring after lumbar spine procedures varies from 2% to 16%, with higher rates after surgery in the elderly population.69,70 Seromas develop after various posterior spinal procedures, including scoliosis/deformity correction surgery, posterior lumbar interbody fusion, instrumented lumbar fusion procedures, and after paraspinal procedures for the treatment of CSF fistulas. Seroma also occur after implantation of spinal cord stimulators and pain pumps.

Clinical presentation In most cases, seroma formation presents with persistent clear drainage from the surgical suture line noticed in the immediate postoperative period that persists or increases in volume with time. In some cases the drainage appears from a small breakdown in an otherwise healed incision, 3–6 weeks following surgery. Complete wound dehiscence is a potential complication. Rarely, postoperative seromas can cause neural compression with recurrence or worsening of neurological deficits.

Management Attention to surgical technique with prevention of dead spaces during closure is of primary importance in the prevention of seromas. Particular attention needs to be paid to closure of the subcutaneous layer. Interrupted sutures are preferred to a running closure, to avoid the entire closure coming apart if integrity is lost at one site. The skin should not be unnecessarily undermined during the approach, in order to avoid a potential seroma cavity. A postoperative suction drain does not appear to affect the incidence of postoperative seromas.65 Wearing an abdominal binder may help prevent seroma formation after implantation of spinal cord stimulators or pain pumps.71 The diagnosis is self-evident in most cases. MRI signal characteristics of postoperative seromas include relatively well-defined lesions of low or intermediate signal intensity relative to adjacent muscle on T1-weighted images and very high signal intensity on T2-weighted images. Seromas are frequently successfully managed by one or two percutaneous needle aspirations. Sterile technique needs to be used, and the risk of bacterial contamination of the surgical incision makes this option unattractive. Gram-staining of the aspirate is recommended to rule out the possibility of infection, and antibiotic therapy insti1152

tuted if infection is detected. In situations where an infected seroma develops in the subcutaneous pocket housing a pain pump/spinal cord stimulator, antibiotic irrigation of the cavity is advised.71 Open debridement and implant removal need to be considered in all cases with recognized infection.

References 1. Barron JT. Radiologic case study. Lumbar pseudomeningocele. Orthopedics 1990; 13:603, 608–609. 2. Kumar AJ, Nambiar CS, Kanse P. Spontaneous resolution of lumbar pseudomeningocoele. Spinal Cord 2003; 41 470–472. 3. Teplick JG, Peyster RG, Teplick SK, et al. CT identification of postlaminectomy pseudomeningocele. Am J Roentgenol 1983; 140:1203–1206. 4. Miller PR, Elder FW Jr. Meningeal pseudocysts (meningocele spurius) following laminectomy. Report of ten cases. J Bone Joint Surg [Am] 1968; 50A:268–276. 5. Hyndman OR, Gerber WF. Spinal extradural cysts, congenital and acquired. Report of cases. J Neurosurg 1946; 3:474–486. 6. Benz RJ, Ibrahim ZG, Afshar P, et al. Predicting complications in elderly patients undergoing lumbar decompression. Clin Orthop Relat Res 2001; 384:116–121. 7. Silvers HR, Lewis PJ, Asch HL. Decompressive lumbar laminectomy for spinal stenosis. J Neurosurg 1993; 78:695–701. 8. Goodkin R, Laska LL. Unintended ‘incidental’ durotomy during surgery of the lumbar spine: medicolegal implications [comment]. Surg Neurol 1995; 43:4–12; discussion 12–14. 9. Swanson HS, Fincher EF. Extradural arachnoid cysts of traumatic origin. J Neurosurg 1947; 4:530–538. 10. Cammisa FP Jr, Girardi FP, Sangani PK, et al. Incidental durotomy in spine surgery. Spine 2000; 25:2663–2667. 11. Wiesel SW. The multiply operated lumbar spine. Instr Course Lect 1985; 34: 68–77. 12. Rinaldi I, Peach WF. Postoperative lumbar pseudomeningocoele. Report of 2 cases. J Neurosurg 1969; 30:504–506. 13. Turnbull DK, Shepherd DB. Post-dural puncture headache: pathogenesis, prevention and treatment. Br J Anaesth 2003; 91:718–729. 14. Iqbal J, Davis LE, Orrison WW Jr. An MRI study of lumbar puncture headaches. Headache 1995; 35:420–422. 15. Leis AA, Leis JM, Leis JR. Pseudomeningoceles: a role for mechanical compression in the treatment of dural tears. Neurology 2001; 56:1116–1117. 16. Rinaldi I, Hodges TO. Iatrogenic lumbar meningocoele: report of three cases. J Neurol Neurosurg Psychiatry 1970; 33:484–492. 17. O’Connor D, Maskery N, Griffiths WE. Pseudomeningocele nerve root entrapment after lumbar discectomy. Spine 1998; 23:1501–1502. 18. Hadani M, Findler G, Knoler N, et al. Entrapped lumbar nerve root in pseudomeningocele after laminectomy: report of three cases. Neurosurgery 1986; 19: 405–407. 19. Eismont FJ, Wiesel SW, Rothman RH. Treatment of dural tears associated with spinal surgery. J Bone Joint Surg [Am] 1981; 63A:1132–1136. 20. Ishaque MA, Crockard HA, Stevens JM. Ossified pseudomeningocoele following laminectomy: case reports and review of the literature. Eur Spine J 1997; 6: 430–432. 21. Nash L Jr, Kaufman B, Frankel VH. Postsurgical meningeal pseudocysts of the lumbar spine. Clin Orthop 1971; 75:167–178. 22. Lau KK, Stebnyckyj M, McKenzie A. Post-laminectomy pseudomeningocele: an unusual cause of bone erosion. Australas Radiol 1992; 36:262–264. 23. Koo J, Adamson R, Wagner FC Jr, et al. A new cause of chronic meningitis: infected lumbar pseudomeningocele. Am J Med 1989; 86:103–104. 24. Jamjoom AB, Tan JB. Subarachnoid haemorrhage related to a lumbosacral fusion: a case report. J Neurol Neurosurg Psychiatry 1990; 53:174–175. 25. Phillips CD, Kaptain GJ, Razack N. Depiction of a postoperative pseudomeningocele with digital subtraction myelography. Am J Neuroradiol 2002; 23:337–338. 26. Bosacco SJ, Gardner MJ, Guille JT. Evaluation and treatment of dural tears in lumbar spine surgery: a review. Clin Orthop Relat Res 2001; 389:238–247. 27. Sharma SK, Gambling DR, Joshi GP, et al. Comparison of 26-gauge Atraucan and 25-gauge Whitacre needles: insertion characteristics and complications. Can J Anaesth 1995; 42:706–710.

Section 5: Biomechanical Disorders of the Lumbar Spine 28. Cruickshank RH, Hopkinson JM. Fluid flow through dural puncture sites. An in vitro comparison of needle point types. Anaesthesia 1989; 44:415–418.

51. Groen RJ, Ponssen H. The spontaneous spinal epidural hematoma. A study of the etiology. J Neurolog Sci 1990; 98:121–138.

29. Chordas C. Post-dural puncture headache and other complications after lumbar puncture. J Pediatr Oncol Nurs 2001; 18:244–259.

52. Kou J, Fischgrund J, Biddinger A, et al. Risk factors for spinal epidural hematoma after spinal surgery. Spine 2002; 27:1670–1673.

30. Spencer HC. Postdural puncture headache: what matters in technique. Reg Anesth Pain Med 1998; 23:374–379; discussion 384–387.

53. Taggard DA, Traynelis VC. Management of cervical spinal fractures in ankylosing spondylitis with posterior fixation. Spine 2000; 25:2035–2039.

31. Duffy PJ, Crosby ET. The epidural blood patch. Resolving the controversies. Can J Anaesth 1999; 46:878–886.

54. Tseng SH, Chen Y, Lin SM, et al. Cervical epidural hematoma after spinal manipulation therapy: case report. J Trauma 2002; 52:585–586.

32. Shaffrey CI, Spotnitz WD, Shaffrey ME, et al. Neurosurgical applications of fibrin glue: augmentation of dural closure in 134 patients. Neurosurgery 1990; 26: 207–210.

55. Ko Y, Kakiuchi M. Extended posture of lumbar spine precipitating cauda equina compression arising from a postoperative epidural clot. J Orthop Sci 2001; 6: 88–91.

33. Freidberg SR. Surgical management of cerebrospinal fluid leakage after spinal surgery. In: Schmidek HH, Sweet WH, eds. Operative neurosurgical techniques – indications, techniques and results. Philadelphia: WB Saunders; 1995:2049–2054.

56. Montaldi S, Fankhauser H, Schnyder P, et al. Computed tomography of the postoperative intervertebral disc and lumbar spinal canal: investigation of twenty-five patients after successful operation for lumbar disc herniation. Neurosurgery 1988; 22:1014–1022.

34. Waisman M, Schweppe Y. Postoperative cerebrospinal fluid leakage after lumbar spine operations. Conservative treatment. Spine 1991; 16:52–53. 35. Kitchel SH, Eismont FJ, Green BA. Closed subarachnoid drainage for management of cerebrospinal fluid leakage after an operation on the spine. J Bone Joint Surg [Am] 1989; 71A:984–987. 36. Stambough JL, Templin CR, Collins J. Subarachnoid drainage of an established or chronic pseudomeningocele. J Spinal Disord 2000; 13:39–41. 37. Deen HG, Pettit PD, Sevin BU, et al. Lumbar peritoneal shunting with video-laparoscopic assistance: a useful technique for the management of refractory postoperative lumbar CSF leaks. Surg Neurol 2003; 59:473–477; discussion 477–478.

57. Egido Herrero JA, Saldana C, Jimenez A, et al. Spontaneous cervical epidural hematoma with Brown-Sequard syndrome and spontaneous resolution. Case report. J Neurosurg Sci 1992; 36:117–119. 58. Hentschel SJ, Woolfenden AR, Fairholm DJ. Resolution of spontaneous spinal epidural hematoma without surgery: report of two cases. Spine 2001; 26: E525–E537. 59. Vandermeulen EP, Van Aken H, Vermylen J. Anticoagulants and spinal-epidural anesthesia [comment]. Anesthes Analges 1994; 79:1165–1177.

38. Foyt D, Johnson JP, Kirsch AJ, et al. Dural closure with laser tissue welding. Otolaryngol Head Neck Surg 1996; 115:513–518.

60. Johnson PJ, Hahn F, McConnell J, et al. The importance of MRI findings for the diagnosis of nontraumatic lumbar subacute subdural haematomas. Acta Neurochir (Wien) 1991; 113:186–188.

39. McCormack BM, Taylor SL, Heath S, et al. Pseudomeningocele/CSF fistula in a patient with lumbar spinal implants treated with epidural blood patch and a brief course of closed subarachnoid drainage. A case report. Spine 1996; 21:2273–2276.

61. Vandermeulen EP, Vermylen G, Van Aken H. Epidural and spinal anaesthesia in patients receiving anticoagulant therapy. Baillieres Clin Anaesthesiol 1993; 7: 663–689.

40. Shimazaki K, Nishida H, Harada Y, et al. Late recurrence of spinal stenosis and claudication after laminectomy due to an ossified extradural pseudocyst. Spine 1991; 16:221–224.

62. Sage DJ. Epidurals, spinals and bleeding disorders in pregnancy: a review. Anaesth Intensive Care 1990; 18:319–326.

41. Ramirez LF, Thisted R. Complications and demographic characteristics of patients undergoing lumbar discectomy in community hospitals. Neurosurgery 1989; 25:226–230; discussion 230–231.

63. Uribe J, Moza K, Jimenez O, et al. Delayed postoperative spinal epidural hematomas. Spine J 2003; 3:125–129. 64. Parker MJ, Roberts C. Closed suction surgical wound drainage after orthopaedic surgery. Cochrane Database Syst Rev 2001; CD001825.

42. Cummine JL, Lonstein JE, Moe JH, et al. Reconstructive surgery in the adult for failed scoliosis fusion. J Bone Joint Surg [Am] 1979; 61A:1151–1161.

65. Payne DH, Fischgrund JS, Herkowitz HN, et al. Efficacy of closed wound suction drainage after single-level lumbar laminectomy. J Spinal Disord 1996; 9:401–403.

43. Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev 2003; 26:1–49.

66. Delamarter RB, Sherman J, Carr JB. Pathophysiology of spinal cord injury. Recovery after immediate and delayed decompression. J Bone Joint Surg [Am] 1995; 77A:1042–1049.

44. Lawton MT, Porter RW, Heiserman JE, et al. Surgical management of spinal epidural hematoma: relationship between surgical timing and neurological outcome [comment]. J Neurosurg 1995; 83:1–7. 45. Kotilainen E. Microinvasive lumbar disc surgery. A study on patients treated with microdiscectomy or percutaneous nucleotomy for disc herniation. Ann Chir Gynaecol Suppl 1994; 209:1–50. 46. Adler MD, Comi AE, Walker AR. Acute hemorrhagic complication of diagnostic lumbar puncture. Pediatr Emerg Care 2001; 17:184–188.

67. Osmani O, Afeiche N, Lakkis S. Paraplegia after epidural anesthesia in a patient with peripheral vascular disease: case report and review of the literature with a description of an original technique for hematoma evacuation. J Spinal Disord 2000; 13:85–87. 68. Little CP, Patel N, Nagaria J, et al. Use of topically applied rt-PA in the evacuation of extensive acute spinal subdural haematoma. Eur Spine J 2003; 12:12.

47. Harik SI, Raichle ME, Reis DJ. Spontaneously remitting spinal epidural hematoma in a patient on anticoagulants. N Engl J Med 1971; 284:1355–1357.

69. Greenfield RT 3rd, Capen DA, Thomas JC Jr, et al. Pedicle screw fixation for arthrodesis of the lumbosacral spine in the elderly. An outcome study. Spine 1998; 23:1470–5.

48. Nishida K, Iguchi T, Kurihara A, et al. Symptomatic hematoma of lumbar facet joint: joint apoplexy of the spine? Spine 2003; 28:E206–E208.

70. Rhee JM, Bridwell KH, Lenke LG, et al. Staged posterior surgery for severe adult spinal deformity. Spine 2003; 28:2116–2121.

49. Hirakawa K, Hanakita J, Suwa H, et al. A post-traumatic ligamentum flavum progressive hematoma: a case report. Spine 2000; 25:1182–1184.

71. Prager JP. Neuraxial medication delivery: the development and maturity of a concept for treating chronic pain of spinal origin. Spine 2002; 27:2593–2605; discussion 2606.

50. Alexiadou-Rudolf C, Ernestus RI, Nanassis K, et al. Acute nontraumatic spinal epidural hematomas. An important differential diagnosis in spinal emergencies [comment]. Spine 1998; 23:1810–1813.

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Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar

CHAPTER

Epidural Adhesiolysis

106

Miles Day, Rinoo Shah, James Heavner and Gabor Racz

INTRODUCTION Chances are each of us will experience low back pain at some point in our lives. The usual course is rapid improvement, but 5–10% of patients develop persistent symptoms.1 In 1997, the total impact of low back pain on industry in the United States was estimated at US$171 billion.2 The medical treatment of low back pain in 1990 amounted to US$13 billion.3 Treatment varies from conservative therapy with medication and physical therapy to minimally and highly invasive pain management interventions. Surgery is sometimes required in those patients who have progressive neurological deficits or those who have failed other therapies. Surgery is successful in the majority of patients, but an unlucky few continue to have pain and neurological symptoms. A quandary arises as to whether a repeat surgery should be attempted or an alternative intervention should be sought. This is the exact quandary that the epidural adhesiolysis procedure was designed to address. It was developed to break down scar formation, deliver site-specific corticosteroids and local anesthetic drugs directly to the target, and reduce edema with hypertonic saline. Epidural adhesiolysis has afforded patients reduction in pain and neurological symptoms without the expense and sometimes long recovery period associated with repeat surgery, and often prevents the need for surgical intervention.

PATHOPHYSIOLOGY OF EPIDURAL FIBROSIS (SCAR TISSUE) AS A CAUSE OF LOW BACK PAIN WITH RADICULOPATHY The etiology of low back pain with radiculopathy is not well understood. Kuslich and colleagues addressed this issue when they performed 193 lumbar spine operations on patients given local anesthesia. Their study revealed that sciatica could only be produced by stimulation of a swollen, stretched, restricted (i.e. scarred) or compressed nerve root.4 Back pain could be produced by stimulation of several lumbar tissues, but the most common tissue of origin was the outer layer of the anulus fibrosus and posterior longitudinal ligament. Stimulation for pain generation of the facet joint capsule rarely generated low back pain, and facet synovium and cartilage surfaces of the facet or muscles were never tender.5 The contribution of fibrosis (scar tissue) to the etiology of low back pain has been debated.6–8 There are many possible etiologies of epidural fibrosis, including surgical trauma, an annular tear, infection, hematoma, or intrathecal contrast material.9 These etiologies are well documented in the literature. LaRocca and Macnab10 demonstrated the invasion of fibrous connective tissue into postoperative hematoma as a cause of epidural fibrosis, while Cooper and colleagues11 reported periradicular fibrosis and vascular abnormalities occurring with herniated intervertebral discs. McCarron et al.12 investigated

the irritative effect of nucleus pulposus upon the dural sac, adjacent nerve roots, and nerve root sleeves independent of the influence of direct compression upon these structures. Evidence of an inflammatory reaction was identified by gross inspection and microscopic analysis of spinal cord sections after homogenized autogenous nucleus pulposus was injected into the lumbar epidural space of four dogs. In the control group consisting of four dogs injected with normal saline, the spinal cord sections were grossly normal. Parke and Watanabe showed significant evidence of adhesions in cadavers with lumbar disc herniation.13 It is widely accepted that postoperative scar renders the nerve susceptible to injury via compressive phenomena.8 It is natural for connective tissue or any kind of tissue to form fibrous layers (scar tissue) as a part of the process that transpires after disruption of the intact milieu.14 Scar tissue is generally found in three components of the epidural space. Dorsal epidural scar tissue is formed by resorption of surgical hematoma and may be involved in pain generation.15 In the ventral epidural space, dense scar tissue is formed by ventral defects in the disc, which may persist despite surgical treatment and continue to produce low back pain/radiculopathy past the surgical healing phase.16 The lateral epidural space includes epiradicular structures outside the root canals, known as the lateral recess or ‘sleeves’ containing the exiting nerve root and dorsal root ganglia, which are susceptible to lateral disc defects, facet overgrowth, and neuroforaminal stenosis.17 Although scar tissue itself is not tender, an entrapped nerve root is. Kuslich et al.4 surmised that the presence of scar tissue compounded pain associated with the nerve root by fixing it in one position and thus increasing the susceptibility of the nerve root to tension or compression. They also concluded that no other tissues in the spine are capable of producing leg pain. In a study of the relationship between peridural scar evaluated by magnetic resonance imaging (MRI) and radicular pain after lumbar discectomy, Ross et al. demonstrated that subjects with extensive peridural scarring were 3.2 times more likely to experience recurrent radicular pain.18

RADIOLOGIC DIAGNOSIS OF EPIDURAL FIBROSIS Magnetic resonance imaging and computed tomography (CT) scanning are diagnostic tools with 50% and 70% sensitivity and specificity, respectively.14 CT-myelography may also be helpful. None of these imaging techniques can identify epidural fibrosis with 100% reliability. In contrast, epidurography is a technique used with considerable success and it is believed that epidural fibrosis is best diagnosed by performing an epidurogram.19–22 It can detect filling defects in good correlation with a patient’s symptoms in a real-time manner.22 A combination of more than one of these techniques will undoubtedly increase the ability to identify epidural fibrosis. 1155

Part 3: Specific Disorders

INDICATIONS FOR EPIDURAL ADHESIOLYSIS Although originally designed to treat radiculopathy secondary to epidural fibrosis following surgery, the use of epidural adhesiolysis has been expanded to treat a multitude of pain etiologies. These include:23 1. Postlaminectomy syndrome of the neck and back after surgery; 2. Disc disruption; 3. Metastatic carcinoma of the spine leading to compression fractures; 4. Multilevel degenerative arthritis; 5. Facet pain; 6. Spinal stenosis; and 7. Pain unresponsive to spinal cord stimulation and spinal opioids. Contraindications to epidural adhesiolysis include the following absolute contraindications: 1. 2. 3. 4. 5.

Sepsis; Chronic infection; Coagulopathy; Local infection at the site of the procedure; and Patient refusal.

A relative contraindication is the presence of arachnoiditis. With arachnoiditis, the tissue planes may be adhered to one another, increasing the chance of loculation of contrast or medication. It may also increase the chance of spread of the medications to the subdural or subarachnoid space, which can increase the chance of complications. Practitioners with limited experience with epidural adhesiolysis should consider referring these patients to someone with more experience.

Patient preparation Once epidural adhesiolysis has been deemed an appropriate treatment modality, the risks and benefits of the procedure should be discussed with the patient and an informed consent signed. The benefits are pain relief, improved physical function, and possible reversal of neurological symptoms. Risks include bruising, bleeding, infection, reaction to medications used (hyaluronidase, local anesthetic, corticosteroids, hypertonic saline), damage to nerves or blood vessels, no or little pain relief, bowel/bladder incontinence, worsening of pain, and paralysis. Patients with a history of urinary incontinence should have an evaluation by an urologist prior to the procedure to document the preexisting urodynamic etiology and pathology.

Anticoagulant medication Medications that prolong bleeding parameters should be withheld prior to performing epidural adhesiolysis. The length of time varies depending on the medication taken. A consultation with the patient’s primary physician should be obtained prior to stopping any of these medications. Nonsteroidal antiinflammatory drugs (NSAIDs) and aspirin should be withheld 4 days and 7–10 days prior to the procedure, respectively. Although there is much debate regarding these medications and neuraxial procedures, the authors tend to be on the conservative side. Clopidogrel (Plavix®) should be stopped 7 days prior to the adhesiolysis while ticlopidine (Ticlid®) is held 10–14 days prior.24 The warfarin (Coumadin®) withholding period is patient variable, but 5 days is usually adequate.24 Subcutaneous heparin administration should be stopped at a minimum of 12 hours prior to the procedure, while low molecular weight heparin requires a minimum of 24 hours.24 Over-the-counter medications that prolong bleeding parameters should also be withheld. These include vitamin E, gingko 1156

biloba, garlic, ginseng, and St. John’s Wort. In addition, a prothrombin time, a partial thromboplastin time, and a platelet function assay or a bleeding time is obtained to check for coagulation abnormalities. Any elevated value warrants further investigation and postponement of the procedure until those studies are complete.

Preoperative laboratory Prior to the procedure a complete blood count and a clean-catch urinalysis is obtained to check for any undiagnosed infection. An elevated white count and/or a positive urinalysis should prompt the physician to postpone the case and refer the patient to his/her primary care physician for further work-up and treatment. Adequate coagulation status can be confirmed by the prothrombin time, partial thromboplastin time, and a platelet function assay or bleeding time. The tests should be performed as close to the day of the procedure as possible. Tests performed only a few days after discontinuation of the anticoagulant medication may come back elevated, since not enough time has elapsed to allow the anticoagulant effects of the medication to resolve. The benefits of the procedure must be weighed against the potential sequelae of stopping the anticoagulant medication, and this should be discussed thoroughly with the patient.

TECHNIQUE This procedure can be performed in the cervical, thoracic, lumbar, and caudal regions of the spine. The caudal and transforaminal placement of catheters will be described in detail while highlights and slight changes in protocol will be provided for cervical and thoracic catheters. The authors’ policy is to perform this procedure under strict sterile conditions in the operating room. Prophylactic antibiotics with broad neuraxial coverage are given preprocedure. Patients will receive either ceftriaxone 1 g intravenously, or levaquin 500 mg orally in those allergic to penicillin. The same dose is also given on day 2. An anesthesiologist or nurse anesthetist provides monitored anesthesia care.

Caudal approach The patient is placed in the prone position with a pillow placed under the abdomen to correct the lumbar lordosis and a pillow under the ankles for patient comfort. The patient is asked to put his/her toes together and heels apart. This relaxes the gluteal muscles and facilitates identification of the sacral hiatus. After sterile preparation and draping, the sacral hiatus is identified via palpation or fluoroscopic guidance. A skin weal is raised with local anesthetic 1 inch lateral and 2 inches caudal to the sacral hiatus on the side opposite from the documented radiculopathy. The skin is nicked with an 18gauge cutting needle, and a 15- or 16-gauge RX Coude™ (Epimed International®) epidural needle is inserted through the nick at a 45° angle and guided fluoroscopically or by palpation towards the sacral hiatus. Once through the hiatus, the needle’s angle is dropped to approximately 30° and the needle is advanced. The advantages of the RX Coude™ over other needles are the angled tip, which enables easier direction of the catheter, and a less sharp tip. The back edge of the distal opening of the needle is designed to be a noncutting surface that allows manipulation of the catheter in and out of the needle. A Tuohy™ needle should never be used for this procedure as the back edge of the distal opening is a cutting surface and can easily shear a catheter. A properly placed needle will be inside the caudal canal below the level of the S3 foramen on anteroposterior (AP) and lateral fluoroscopic images. A needle placed above the level of the S3 foramen could potentially puncture a low-lying dura. The needle tip should cross the midline of the sacrum towards the side of the radiculopathy.

Section 5: Biomechanical Disorders of the Lumbar Spine

An epidurogram is performed using 10 mL of a non-ionic, watersoluble contrast agent. Confirm a negative aspiration for blood or cerebrospinal fluid (CSF) prior to any injection of contrast or medication. Omnipaque® and Isovue® are the agents most frequently used and are suitable for myelography.25,26 Do not use ionic, non-watersoluble contrast agents such as Hypaque® or Renagraffin® or ionic, water-soluble agents such as Conray®.27,28 These agents are not indicated for myelography. Accidental subarachnoid injections can lead to serious untoward events such as seizure and possible death. Slowly inject the contrast agent and observe for filling defects. A normal epidurogram will have a Christmas-tree pattern with the central channel being the trunk and the outline of the nerve roots making up the branches. An abnormal epidurogram will have areas where the contrast does not fill. These are the areas of presumed scarring and typically correspond to the patient’s back and radicular complaints. If vascular uptake is observed, the needle needs to be redirected. After turning the distal opening of the needle ventrolaterally, insert a TunL Kath™ or TunL-XL™ (stiffer) catheter (Epimed International®) with a bend on the distal tip through the needle. The bend should be 2.5 cm from the tip of the catheter and at a 30° angle. The bend will enable the catheter to be steered to the target level. Under continuous AP fluoroscopic guidance, advance the tip of the catheter towards the ventrolateral epidural space of the desired level. The catheter can be steered by gently twisting the catheter in a clockwise or counterclockwise direction. Avoid ‘propellering’ the tip, i.e. twisting the tip in circles, as this makes it more difficult to direct the catheter. Do not advance the catheter up the middle of the sacrum as this makes guiding the catheter to the ventrolateral epidural space more difficult. Ideal location of the tip of the catheter in the AP projection is in the foramen just below the midportion of the pedicle shadow (Fig. 106.1A). Check a lateral projection to confirm that the catheter tip is in the ventral epidural space (Fig. 106.1B). Under real-time fluoroscopy, inject 2–3 mL of additional contrast through the catheter in an attempt to outline the ‘scarred in’ nerve root. If vascular uptake is noted, reposition the catheter and reinject contrast. Preferably one should not have vascular run-off, but infre-

A

quently secondary to venous congestion an epidural pattern is seen with a small amount of vascular spread. This is acceptable as long as the vascular uptake is venous in nature and not arterial. Extra caution should be taken when injecting the local anesthetic to prevent local anesthetic toxicity. Any arterial spread of contrast always warrants repositioning of the catheter. The authors have never observed intraarterial catheter placement in 25 years of placing soft, spring-tipped catheters. Inject 1500 units of hyaluronidase dissolved in 10 mL of preservative-free normal saline (PFNS). This may cause some discomfort, so a slow injection is favorable. Observe for ‘opening up,’ i.e. visualization, of the ‘scarred in’ nerve root. A 3 mL test dose of a 10 mL local anesthetic/steroid (LA/S) solution is then given. Our institution uses 4 mg of dexamethasone mixed with 9 mL of 0.2% ropivacaine. Ropivacaine is used instead of bupivacaine for two reasons: the former produces a preferential sensory block, and is less cardiotoxic than racemic bupivacaine. Doses for other corticosteroids commonly used are 40–80 mg methylprednisolone (Depo-Medrol™), 25–50 mg triamcinolone diacetate (Aristocort™), 40–80 mg triamcinolone acetonide (Kenalog™), and 6–12 mg betamethasone (Celestone Soluspan™). If after 5 minutes there is no evidence of intrathecal or intravascular injection of medication, inject the remaining 7 mL of the LA/S solution. Remove the needle under continuous fluoroscopic guidance to ensure the catheter remains at the target level. Secure the catheter to the skin using nonabsorbable suture and coat the skin puncture site with antimicrobial ointment. Apply a sterile dressing and attach a 20 micron filter to the end of the catheter. Affix the exposed portion of the catheter to the patient with tape and transport the patient to the recovery area. A 20 minute period should elapse between the last injection of the LA/S solution and the start of the hypertonic (10%) saline infusion. This is necessary to ensure that a subdural injection of the local anesthetic/steroid solution has not occurred. A subdural block can mimic a subarachnoid block but takes longer to establish. If the patient develops a subarachnoid or subdural block at any point during the procedure, the catheter should be removed and the remainder of

B

Fig. 106.1 (A) Catheter tip at the left L4–5 foramen. (B) Catheter in the ventral epidural space at L5–S1. 1157

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the adhesiolysis canceled. The patient needs to be observed to document the resolution of the motor and sensory block and to document the absence of bladder/bowel dysfunction. Ten milliliters of hypertonic saline is then infused through the catheter over 30 minutes. If the patient complains of discomfort, the infusion is stopped and an additional 2–3 mL of 0.2% ropivacaine is injected and the infusion is restarted. Alternatively, 50–100 mg of fentanyl can be injected epidurally in lieu of the local anesthetic. After completion of the hypertonic saline infusion, the catheter is slowly flushed with 2 mL of preservative-free normal saline and the catheter is capped. Our policy is to admit the patient for a 23-hour observation status and do a second and third hypertonic saline infusion the following day. On postcatheter insertion day 2, the catheter is twice injected (separated by 4 hours) with 10 mL of 0.2% ropivacaine without steroid and infused with 10 mL hypertonic saline (10%) using the same technique and precautions as the day 1 infusion. At the end of the third infusion the catheter is removed and a sterile dressing applied. The patient is discharged home with 5 days of oral cefalexin at 500 mg twice a day or oral levaquin at 500 mg once a day in penicillin allergic patients. Clinic follow-up is in 30 days.

Transforaminal catheters Patients with an additional level of radiculopathy or those where the target level cannot be reached by the caudal approach may require placement of a second catheter. The second catheter is placed into the ventral epidural space via a transforaminal approach. After the target level is identified with an AP fluoroscopic image, the superior endplate of the vertebra that comprises the caudal portion of the foramina is ‘squared,’ i.e. the anterior and posterior shadows of the vertebral endplate are superimposed. The angle is typically 15–20° in a caudocephalad direction. The fluoroscope is then obliqued approximately 15° to the side of the radiculopathy and adjusted until the spinous process is rotated to the opposite side. This fluoroscope positioning allows the best visualization of

A

the superior articular process (SAP) that forms the inferoposterior portion of the targeted foramen. The image of the SAP should be superimposed upon the shadow of the disc space on the oblique view. The tip of the SAP is the target for needle placement. Raise a skin wheal slightly lateral to the shadow of the tip of the SAP. Pierce the skin with an 18-gauge needle and then insert a 16-gauge RX Coude™ needle and advance using gun-barrel technique towards the tip of the SAP. Continue to advance the needle medially towards the SAP until the tip contacts bone. Rotate the tip of the needle 180° laterally and advance about 5 mm. As the needle is advanced slowly, a clear ‘pop’ is felt as the needle penetrates the intertransverse ligament. Rotate the needle back medially 180°. Obtain a lateral fluoroscopic image. The tip of the needle should be just past the SAP in the posterior foramen. In the AP plane the tip of the needle should be just medial of the lateral border of the pedicle shadow. Under continuous AP fluoroscopy, insert the catheter slowly into the foramen and advance until the tip is past the medial border of the pedicle shadow (Fig. 106.2A). Confirm the catheter is in the anterior epidural space with a lateral image (Fig. 106.2B). Anatomically, the catheter is in the foramen above or below the exiting nerve root. If the catheter cannot be advanced, it usually means the needle is either too posterior or too lateral to the foramen. It can also indicate the foramen is too stenotic to allow passage of the catheter. The needle can be advanced a few millimeters anteriorly in relation to the foramen, and that will also move it slightly more medially into the foramen. If the catheter still will not pass, the initial insertion of the needle will need to be more lateral. Therefore, the fluoroscope angle will be about 20° instead of 15°. The curve of the needle usually facilitates easy catheter placement. Inject 1–2 mL of contrast to confirm epidural spread. When a caudal and a transforaminal catheter are placed, the 1500 units of hyaluronidase are divided evenly between the two catheters (5 mL of the hyaluronidase/saline solution into each). The LA/S solution is also divided evenly, but a volume of 15 mL (1 mL steroid and 14 mL

B

Fig. 106.2 (A) Transforaminal catheter at L1–2. The tip of the catheter is midline at the shadow of the spinous process. (B) Catheter in the ventral epidural space at L1–2. 1158

Section 5: Biomechanical Disorders of the Lumbar Spine

0.2% ropivacaine) is used instead of 10 mL. Remove the needle under fluoroscopic guidance to make sure the catheter does not move from the original position in the epidural space. Secure and cover the catheter as described above. The hypertonic saline solution is infused at a volume of 7.5 mL per catheter over 30 minutes. It behooves the practitioner to check the position of the transforaminal catheter under fluoroscopy prior to performing the second and third infusions. The catheter may advance across the epidural space into the contralateral foramen or paraspinous muscles or more commonly back out of the epidural space into the ipsilateral paraspinous muscles. This results in deposition of the medication in the paravertebral tissue rather than in the epidural space. As with the caudal approach, remove the transforaminal catheter after the third infusion.

Cervical lysis of adhesions The success of the caudal approach for lysis of adhesions led to the application of the same technique to the cervical epidural space. The indications and preprocedure work-up are the same as those for the caudal lysis technique, but there are a few differences in technique and volumes of medication used. The epidural space should be entered via the upper thoracic interspaces using a paramedian approach on the contralateral side. The most common levels are T1–2 and T2–3. Entry at these levels allows for a sufficient length of the catheter to remain in the epidural space after the target level has been reached. If the target is the lower cervical nerve roots, a more caudal interspace should be selected. We place the patient in the left lateral decubitus position, but use a prone approach in larger patients. A technique referred to as the ‘3-D technique’ is utilized to facilitate entry into the epidural space. The ‘3-D’ stands for Direction, Depth, and Direction. Using an AP fluoroscopic image, the initial Direction of the 15- or 16-gauge RX-Coude™ is determined. Using a modified paramedian approach with the skin entry one and a half levels below the target interlaminar space, advance and direct the needle toward the midpoint of the chosen interlaminar space with the opening of the needle pointing medially. Once the needle engages the deeper tissue planes (usually at 2–3 cm), check the Depth of the needle with a lateral image. Advance the needle towards the epidural space and check repeat images to confirm the Depth. The posterior border of the dorsal epidural space can be visualized by identifying the junction of the base of the spinous process of the vertebral body with its lamina. This junction creates a distinct radiopaque ‘straight line.’ The epidural space is just anterior to this ‘straight line.’ Once the needle is close to the epidural space, get an AP fluoroscopic image to recheck the Direction of the needle. If the tip of the needle has crossed the midline as defined by the spinous processes of the vertebral bodies, pull the needle back and redirect. The ‘3-D’ process can be repeated as many times as is necessary to get the needle into the perfect position. Using loss of resistance technique, advance the needle into the epidural space with the tip of the RX-Coude™ pointed caudally. Once the tip is in the epidural space, rotate the tip cephalad and inject 1–2 mL of contrast to confirm entry. Inject an additional 4 mL to complete the epidurogram. As with the caudal epidurogram, look for filling defects. It is extremely important to visualize spread of the contrast in the cephalad and caudal directions. Loculation of contrast in a small area must be avoided as this can significantly increase the pressure in the epidural space and can compromise the already tenuous arterial blood supply to the spinal cord. Place a bend on the catheter as previously described for the caudal approach and insert it through the needle. The opening of the needle should be directed towards the target side. Slowly advance the catheter to the lateral gutter and direct it cephalad. Redirect the catheter as needed and once

the target level has been reached, turn the tip of the catheter towards the foramen. Inject 0.5–1 mL of contrast to visualize the target nerve root. Make sure there is run-off of contrast out of the foramen (Fig. 106.3). Slowly instill 1500 units of hyaluronidase (Wydase™) dissolved in 5 mL of preservative-free normal saline (PFNS) (6 mL total). Follow this with 1–2 mL of additional contrast and observe for ‘opening-up’ of the ‘scarred-in’ nerve root. Give a 2 mL test dose of a 6 mL solution of LA/S. Our combination is 5 mL of 0.2% ropivacaine and 4 mg dexamethasone. If after 5 minutes there is no evidence of intrathecal or intravascular spread, inject the remaining 4 mL. Remove the needle, and secure and dress the catheter as previously described. Once 20 minutes have passed since the last dose of the LA/S solution and if there is no evidence of a subarachnoid or subdural block, start an infusion of 5 mL of hypertonic saline over 30 minutes. At the end of the infusion, flush the catheter with 1–2 mL of PFNS and cap the catheter. The second and third infusions are performed on the next day with 6 mL of 0.2% ropivacaine without steroid and 5 mL of hypertonic saline using the same technique and precautions described for the first infusion. The catheter is removed and prophylactic antibiotics are prescribed. Clinic follow-up is 30 days.

Thoracic lysis of adhesions The technique for entry into the thoracic epidural space for adhesiolysis is identical to that for the cervical region. Always remember the 3-D technique. Make sure to get a true lateral when checking the depth of the needle. This can be obtained by superimposing the rib shadows upon one another. The target is still the ventrolateral epidural space with the tip of the catheter in the foramen of the desired level. The major difference for thoracic lysis compared to the caudal and cervical techniques is the volumes of the various injectates. Volumes of 8 mL are used for the contrast, hyaluronidase, LA/S, and hypertonic saline.

Fig. 106.3 Cervical catheter and epidurogram. Note run-off of the contrast medium caudally and also out of the foramen. 1159

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Epidural mapping In patients with multilevel radiculopathy and complex pain, it can be difficult to determine from where the majority of the pain is emanating. We have been using a technique, which we have termed ‘mapping,’ to locate the most painful nerve root with stimulation and then carry out the adhesiolysis at that level. There are several references in the literature regarding the use of stimulation to confirm epidural placement of a catheter and for nerve root localization.29 The TunL Kath™ and the TunL-XL™ catheter can be used as stimulating catheters to identify the nerve root(s). After entering the epidural space, advance the catheter into the ventrolateral epidural space past the suspected target level. Make sure the tip of the catheter is pointing laterally towards the foramina, just below the pedicle. Pull the catheter stylet back approximately 1 cm. Using alligator clips, attach the cathode to the stylet and ground the anode on an EKG pad or a 22-gauge needle inserted into the skin. Apply electrical stimulation with a Medtronic® trail stimulating box with a rate of 50 pulses per second, a pulse width of 450 milliseconds, and an internal amplitude of 3 volts, dialing up the amplitude until a paresthesia is perceived. Inquire of the patient as to whether or not the paresthesia is felt in the area of the patient’s greatest pain. This process is repeated at each successive level until the most painful nerve root is identified. Once identified, the adhesiolysis is carried out at that level.

COMPLICATIONS As with any invasive procedure, complications are possible. These include: bleeding, infection, headache, damage to nerves or blood vessels, catheter shearing, bowel/bladder dysfunction, sexual dysfunction, paralysis, spinal cord compression from loculation of the injected fluids or hematoma, subdural or subarachnoid injection of local anesthetic or hypertonic saline, and reactions to the medications used. We also include on the permit that the patient may experience an increase in pain or no pain relief at all.

OUTCOMES Racz and Holubec first reported on epidural adhesiolysis in 1989.30 There were slight variations in the protocol compared to today’s protocol, namely the dose of local anesthetic and the fact that hyaluronidase was not used. Catheter placement was lesion-specific, i.e. the tip of the catheter was placed in the foramen corresponding to the vertebral level and side of the suspected adhesions. This retrospective analysis conducted 6–12 months postprocedure reported initial pain relief in 72.2% of patients (n=72) at time of discharge. Relief was sustained in 37.5% and 30.5% of patients at 1 and 3 months, respectively. Fortythree percent decreased their frequency and dosage of medication use and 16.7% discontinued their medications altogether. In total, 30.6% of patients returned to work or returned to daily functions. At a presentation at the 7th World Congress on pain, Arthur and colleagues reported on epidural adhesiolysis in 100 patients of whom 50 received hyaluronidase as part of the procedure.31 In the hyaluronidase group, 81.6% of the participants had initial pain relief, with 12.3% having persistent relief; 68% of the no hyaluronidase group had relief of pain, with 14% having persistent relief. In 1994, Stolker et al. added hyaluronidase to the procedure, but omitted the hypertonic saline. In a study of 28 patients, they reported greater than 50% pain reduction in 64% of patients at one year.32 They stressed the importance of patient selection and felt that the effectiveness of adhesiolysis was based on the effect of the hyaluronidase on the adhesions and the action of the local anesthetic and steroids on the sinuvertebral nerve. 1160

Devulder and colleagues published a study of 34 patients with failed back surgery syndrome in whom epidural fibrosis was suspected or proved with MRI.33 An epidural catheter was inserted via the sacral hiatus to a distance of 10 cm into the caudal canal. Injections of contrast dye, local anesthetic, corticosteroid, and hypertonic saline (10%) were carried out daily for 3 days. No hyaluronidase was used. Filling defects were noted in 30 of 34 patients, but significant pain relief was only noted in seven patients at 1 month, two patients at 3 months, and none at 12 months. They concluded that epidurography may confirm epidural filling defects for contrast dye in patients with filling defects, but a better contrast dye spread, assuming scar lysis, does not guarantee sustained pain relief. This study was criticized for lack of lesion-specific catheter placement resulting in non-specific drug delivery.34 Heavner and colleagues performed a prospective randomized trial of lesion-specific epidural adhesiolysis on 59 patients with chronic intractable low back pain.35 The patients were assigned to one of four epidural adhesiolysis treatment groups: (1) hypertonic (10%) saline plus hyaluronidase, (2) hypertonic saline, (3) isotonic (0.9%) saline, or (4) isotonic saline plus hyaluronidase. All treatment groups received corticosteroid and local anesthetic. Overall across all four treatment groups, 83% of patients had significant pain relief at 1 month compared to 49% at 3 months, 43% at 6 months, and 49% at 12 months. Manchikanti et al. performed a retrospective, randomized evaluation of a modified Racz adhesiolysis protocol in 232 patients with low back pain.36 The study involved lesion-specific catheter placement, but the usual 3-day procedure was reduced to a 2-day (group I) and 1-day (group II) procedure. Group I had 103 patients and group II had 129 patients. Other changes included changing the local anesthetic from bupivacaine to lidocaine, substituting methylprednisolone acetate or betamethasone acetate and phosphate for triamcinolone diacetate, and reduction of the volume of injectate. Of the patients in groups I and II, 62% and 58% had >50% pain relief at 1 month, respectively, with these percentages decreasing to 22% and 11% at 3 months, 8% and 7% at 6 months, and 2% and 3% at 1 year. Of significant interest is that the percentage of patients receiving >50% pain relief after four procedures increased to 79% and 90% at 1 month, 50% and 36% at 3 months, 29% and 19% at 6 months, and 7% and 8% at 1 year for groups I and II, respectively. Short-term relief of pain was demonstrated, but long-term relief was not. In a randomized, prospective study, Manchikanti and colleagues evaluated a 1-day epidural adhesiolysis procedure against a control group of patients who received conservative therapy.37 Results showed that cumulative relief, defined as relief greater than 50% with one to three injections, in the treatment group was 97% at 3 months, 93% at 6 months, and 47% at 1 year. The study also showed that overall health status improved significantly in the adhesiolysis group. Recently, Manchikanti et al. published their results of a randomized, double-blind, controlled study on the effectiveness of 1-day lumbar adhesiolysis and hypertonic saline neurolysis in treatment of chronic low back pain.38 Seventy-five patients whose pain was unresponsive to conservative modalities were randomized into one of three treatment groups. Group I (control group) underwent catheterization without adhesiolysis, followed by injection of local anesthetic, normal saline, and steroid. Group II consisted of catheterization and adhesiolysis, followed by injection of local anesthetic, normal saline, and steroid. Group III consisted of adhesiolysis, followed by injection of local anesthetic, hypertonic saline, and steroid. Patients were allowed to have additional injections based on the response, either after unblinding or without unblinding after 3 months. Patients without unblinding were offered either the assigned treatment or another treatment based on their response. If the patients in group I or II received

Section 5: Biomechanical Disorders of the Lumbar Spine

adhesiolysis and injection of hypertonic saline, they were considered withdrawn, and no subsequent data were collected. Outcomes were assessed at 3, 6, and 12 months using visual analog scale pain scores, Oswestry Disability Index, opioid intake, range of motion measurement, and P-3®. Significant pain relief was defined as average relief of 50% or greater. Seventy-two percent of patients in group III, 60% of patients in group II, and 0% in group I showed significant pain relief at 12 months. The average number of treatments for 1 year were 2.76 in group II and 2.16 in group III. Duration of significant relief with the first procedure was 2.8 ± 1.49 months and 3.8±3.37 months in groups II and III, respectively. Significant pain relief (=50%) was also associated with improvement in Oswestry Disability Index, range of motion, and psychological status.

EPIDURAL ENDOSCOPIC ADHESIOLYSIS Spinal endoscopy dates back to 1931 when Burman published the first experience with what was to become known as myeloscopy.39 Several more studies were published over the ensuing decades, and a historical review of said studies can be found in an article by Saberski and Brull.40 In 1991, Heavner and colleagues reported endoscopic evaluation of the epidural and subarachnoid spaces in rabbits, dogs, and human cadavers with aid of a flexible endoscope.41 Numerous articles followed over the next decade describing various aspects of spinal endoscopy, including clinical basis, protocol, safety, and costeffectiveness.42–45 Epidural endoscopic adhesiolysis is a minimally invasive technique for adhesiolysis and accurate placement of injectate intended for delivery in the epidural space.45–47 It is based on the premise that the epidural space can be accessed safely by using flexible fiberoptic catheters entering via the sacral hiatus.45 It facilitates three-dimensional visualization of the contents of the epidural space and provides the physician with the ability to steer the catheter toward structures of interest. This procedure allows examination of specific nerve root pathology and treatment by injection of medication onto the nerve root, along with the ability to expand the epidural space with normal saline. Indications and patient preoperative preparation are identical to those for epidural adhesiolysis. The epidural placement of an endoscope is most frequently performed via the sacral hiatus. This is based on anatomy, equipment, and experience.47 A midline entry of the epidural needle through the sacral hiatus is used instead of the usual paramedian approach. An epidurogram with water-soluble, non-ionic contrast is performed to visually assess the nerve roots. Insertion of the endoscope through the sacral hiatus will vary slightly depending on the type of endoscope used, but the Seldinger technique is the method of insertion used most frequently. Once inside the caudal epidural space, the endoscope is advanced using direct video and fluoroscopic guidance. There is a definite learning curve with epidural endoscopy and the operating physician should proceed with caution. In conjunction with gentle irrigation using normal saline, the myeloscope and catheter are manipulated and rotated in many directions to identify structures, namely nerve roots, at various levels. An endoscope with a working channel can facilitate placement of the epidural catheter. After the target level is reached, the epidural catheter is placed through the working channel and once it exits the distal end the endoscope is removed, leaving the catheter at the targeted nerve root (Fig. 106.4). Adhesiolysis is accomplished by the distention of the epidural space with the saline irrigation and by mechanical means using the endoscope and hyaluronidase. The LA/S and hypertonic saline protocol as previously described is then carried out.

Fig. 106.4 Endoscopic epidural adhesiolysis. Note the catheter exiting the working channel of the endoscope.

There is a paucity of literature with regards to epidural adhesiolysis with myeloscopy. Richardson et al. published a prospective case series in 34 patients with severe chronic low back pain.48 All had epidural scar tissue with 14 patients having dense adhesions. Followup over a 12-month period showed statistically significant reductions in pain score and disability. In two separate retrospective studies, Manchikanti and colleagues evaluated the effectiveness of endoscopic adhesiolysis in 85 patients with chronic low back pain with or without history of laminectomy and 60 patients with postlumbar laminectomy syndrome.45,49 In the first study, all 85 patients received significant pain relief (≥50%) in the first month, but this decreased to 77%, 52%, and 21% at 3, 6, and 12 months, respectively. All of the patients in the second study had significant analgesia in the first month which dwindled to 80%, 52%, and 22% at the 3-, 6-, and 12-month follow-up visits, respectively. As with adhesiolysis without endoscopy, short-term relief was afforded.

PHYSICAL THERAPY We routinely have our adhesiolysis patients engage in neural flossing exercises once the procedure is completed. These exercises involve performing repetitive, slow, rhythmic nonpainful distal initiation of dural movements (Fig. 106.5).50 The goal is to restore the normal movement of the involved nerve root in the foramen and to prevent adhesions from reforming. The patient is encouraged to do one set of ten repetitions of each of the three exercises twice a day. The patient is taught these exercises by a physical therapist prior to discharge from our facility.

CONCLUSION Epidural adhesiolysis has evolved over the years as an important treatment option for patients with intractable cervical, thoracic, and low back and leg pain. Studies show that patients are able to enjoy significant pain relief and restoration of function over several months. Manchikanti’s studies show that the amount and duration of relief can be achieved by repeat procedures. Endoscopy offers direct visualization of the affected nerve roots in addition to mechanical adhesiolysis, and may become more mainstream as the technique is 1161

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A

C

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refined. More prospective, randomized, controlled studies need to be performed to further solidify epidural adhesiolysis’s position in the treatment algorithm of patients with intractable pain refractory to previous treatments.

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Fig. 106.5 (A–C) Postepidural adhesiolysis exercises to prevent rescarring.

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39. Burman M. Myeloscopy or the direct visualization of the spinal canal and its contents. J Bone Joint Surg 1931; 13:695–696. 40. Saberski L, Brull S. Spinal and epidural endoscopy: a historical review. Yale J Biol Med 1995; 68:7–15. 41. Heavner J, Cholkhavatia S, Kizelshteyn G. Percutaneous evaluation of the epidural and subarachnoid space with the flexible endoscope. Reg Anesth 1991; 151:85. 42. Saberski L, Kitahata L. Direct visualization of the lumbosacral epidural space through the sacral hiatus. Anesth Analg 1995; 80:839–840.

32. Stolker R, Vervest A, Gerbrand J. The management of chronic spinal pain by blockades: a review. Pain 1994; 58:1–19.

43. Saberski L, Kitahata L. Review of the clinical basis and protocol for epidural endoscopy. Connecticut Med 1996; 60:70–73.

33. Devulder J, Bogaert L, Castille F, et al. Relevance of epidurography and epidural adhesiolysis in chronic failed back surgery patients. Clin J Pain 1995;1 1:147–150.

44. Saberski L. A retrospective analysis of spinal canal endoscopy and laminectomy outcomes data. Pain Phys 2000; 3:193–196.

34. Racz G, Heavner J. In response to article by Drs. Devulder et al. Clin J Pain 1995; 11:151–154.

45. Manchikanti L, Pakanati R, Pampati V, et al. The value and safety of epidural endoscopic adhesiolysis. Am J Anesthesiol 2000; 27:275–279.

35. Heavner J, Racz G, Raj P. Percutaneous epidural neuroplasty: prospective evaluation of 0.9% saline versus 10% saline with or without hyaluronidase. Reg Anesth Pain Med 1999; 24:202–207.

46. Addison R. Spinal endoscopy. Cur Rev Pain 1999; 3:116–120.

36. Manchikanti L, Pakanati R, Bakhit C, et al. Role of adhesiolysis and hypertonic saline neurolysis in management of low back pain: evaluation of modification of the Racz protocol. Pain Digest 1999; 9:91–96.

47. Manchikanti L, Singh V. Epidural lysis of adhesions and myeloscopy. Curr Pain Headache Reports 2002; 6:427–435. 48. Richardson J, McGurgan P, Cheema S, et al. Spinal endoscopy in chronic low back pain with radiculopathy. A prospective case series. Anaesthesia 2001; 56:454–460.

37. Manchikanti L, Pampati V, Fellow B, et al. Role of one day epidural adhesiolysis in management of chronic low back pain: a randomized clinical trial. Pain Phys 2001; 4:153–166.

49. Manchikanti L, Vidyasagar P, Bakhit C, et al. Non-endoscopic and endoscopic adhesiolysis in post lumbar laminectomy syndrome: a one-year outcome study and cost effectiveness analysis. Pain Phys 1999; 2:52–58.

38. Manchikanti L, Rivera J, Pampati V, et al. One day lumbar adhesiolysis and hypertonic saline neurolysis in treatment of chronic low back pain: a randomized, doubleblind trial. Pain Phys 2004; 7:177–186.

50. Sizer P, Phelps V, Dedrick G, et al. Differential diagnosis and management of spinal nerve-root related pain. Pain Practice 2002; 2:98–121.

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Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar

CHAPTER

107

Spinal Cord Stimulation in Chronic Pain Robert E. Windsor, Markus Niederwanger and Steven Lobel

INTRODUCTION Since the first published paper on spinal cord stimulation (SCS) by Shealy in 1967 there have been a total of over 2000 articles, presentations, symposia, and abstracts on the topic of neuroaugmentation.88,92 The long-term results of SCS published in the 1970s were disappointing yet promising.28,30,32,93 Most of the studies published in the 1970s and early 1980s demonstrated success rates of approximately 40%.12 As with many new devices, problems included poorly designed hardware and software, inadequate patient selection criteria, and suboptimal surgical technique. Early on, the hardware typically consisted of a single or dual electrode system that was implanted epidurally. They provided a small electrical field and thus were unable to consistently stimulate the spinal cord. In addition, these systems were implanted via laminectomy or laminotomy with the patient under general anesthesia, thus eliminating the possibility of surgeon–patient interaction. The electrodes were commonly implanted in the high thoracic or lower cervical region for lumbar pain syndromes and patients were not consistently screened for psychological dysfunction, drug habituation, secondary gain issues, pain topography, and quality of pain. All of these factors have considerable impact on the overall efficacy of SCS. Significant advances in SCS have been made in recent years. The hardware is more durable and the electrode size and interelectrode distance have been improved. Improved software allows for more complex programming and multiple, simultaneously operating programs which generally allows for improved coverage and pain relief of difficult pain patterns. The devices may be implanted percutaneously under fluoroscopic guidance, which allows operator–patient interaction and may lead to more accurate positioning of SCS leads. Paddlestyle leads implanted via laminectomy may have certain advantages relating to energy consumption and long-term maintenance of back pain. Three decades of experience have provided improved patient selection criteria. The net result is an improved capacity to control chronic pain.12 This chapter will discuss the clinical indications, outcomes, complications, and other methods of implantation which may positively impact future outcomes and areas of study.

PAIN ANATOMY AND PHYSIOLOGY Pain is an uncomfortable sensation associated with an emotional response.35,106 The International Association for the Study of Pain (IASP) defined pain as ‘an unpleasant sensory and emotional experience associated with actual and potential tissue damage, or described in terms of such damage.’35 It may originate from stimulation of chemical, mechanical, or thermal receptors found in free nerve endings within injured tissue. This is known as afferent pain, and can occur in ligamentous or muscular injuries of the spine.11,47,54,90 Pain can also occur from direct injury to the peripheral nerve, which

results in burning or shooting pain in the distribution of the affected nerve. This is called peripheral deafferentation (neuropathic) pain and is demonstrated in conditions such as complex regional pain syndrome, peripheral neuropathy, or radiculopathy.30,64,65 Central deafferent pain appears after injury to certain structures within the central nervous system, such as the thalamus, that are responsible for the transmission of pain. Peripheral pain signals are transmitted by either thinly myelinated A-delta or unmyelinated C fibers. The A-delta fibers convey discrete, sharp, fast pain at approximately 15 m/sec, whereas the C fibers transmit vague, chronic, burning, slow pain at less than 1 m/sec.25,108 Pain fibers typically enter the spinal cord through the dorsal root and then ascend or descend two to six segments within the dorsolateral fasciculus (Lissauer’s tract)25,108 The A-delta fibers synapse with the dorsal gray horn neurons located in laminae 1, 2, 5, and 10, whereas the C fibers synapse with dorsal gray horn neurons located in laminae 1, 2, and 5. The majority of fibers then cross to the opposite ventrolateral portion of the spinal cord before ascending in the spinothalamic, spinoreticulothalamic, and spinomesencephalic tracts. The lateral spinothalamic fibers terminate in the thalamic ventralis posterolaterales and posteromedialis nuclei, from which fibers are projected into other areas of the thalamus and to the somatic sensory cortex. The medial spinothalamic, spinoreticulothalamic, and spinomesencephalic tracts end in the reticular activating system within the medulla, pons, midbrain, periaqueductal gray, hypothalamus, and thalamic medial and intralaminar nuclei (Fig. 107.1). The thalamus plays the primary role for conscious pain perception, and the cortex is involved in interpreting pain quality and locality. The A-delta fibers convey a distinctive, sharp pain, and C fibers conduct a characteristic diffuse, burning, or aching pain. This is likely a reflection of the A-delta fibers terminating at the cortical level versus C fibers, which end diffusely in the brain stem and diencephalon. In 1965, Melzack and Wall published their ‘gate control’ theory in which they hypothesized that a ‘gate’ system existed for pain modulation located in the dorsal gray horn within the substantia gelatinosa (laminae 2 and 3).60 They proposed that excess tactile signals traveling along the large myelinated A-delta fibers closed the gate, which then inhibited the propagation of pain impulses along the unmyelinated C fibers (Fig. 107.2). Although the pain pathway is still not completely understood, researchers have uncovered important parts of the neuronal system. This includes descending inhibitory influences from the brain, which have been shown to suppress transmission of pain.10,80,86 There is also evidence of an endogenous system of opioids that modulate sensory input.41,89,95 Today, there is a better awareness that the pain experience is not just physiologic but is also influenced by culture, religion, and psychological makeup.29,37,61,62 In order to provide appropriate 1165

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Fig. 107.1 Neuroanatomic pathway for nociceptive pain transmission. (A) Lateral tracts and (B) medial tracts. In: Bonica JJ, ed. The Management of Pain. 2nd edn. Philadelphia: Lea & Febiger; 1990:89.

treatment, all of these factors must be taken into consideration when evaluating patients.

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MECHANISM OF ACTION Gate control L

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Fig. 107.2 Melzack and Wall gate control theory of pain: large-diameter fibers (L), small-diameter fibers (S), substantia gelatinosa (SG), first central transmission cells (T). excitation (+), inhibition (–). From Melzack R, Wall PD. Pain mechanisms: A new theory. Science 1965; 150(699):971–979.

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Although the exact mechanism for pain control from SCS is not entirely understood, it is believed to result from direct or facilitated inhibition of pain transmission.28,30,32,40,60,92 There exist five mechanistic theories for SCS which should be noted: (1) gate control theory – segmental, antidromic activation of A-beta efferents; (2) SCS blocks transmission in the spinothalamic tract; (3) SCS produces supraspinal pain inhibition; (4) SCS produces activation of central inhibitory mechanisms influencing sympathetic efferent neurons; and (5) SCS activates putative neurotransmitters or neuromodulators.40 The gate control theory motivated Shealy et al. in 1967 to apply SCS as a means to antidromically activate the tactile A-beta fibers through dorsal column stimulation.92 Shealy et al. reasoned that sustained stimulation of the dorsal columns would keep the gate closed and provide continuous pain relief. While the theoretical model put forth by Melzack and Wall has been shown not to be

Section 5: Biomechanical Disorders of the Lumbar Spine

precisely accurate, pain gating or pain control has been shown to exist.28,30,32,60 Others believe that pain relief from SCS results from direct inhibition of pain pathways in the spinothalamic tracts and not secondary to selective large fiber stimulation.21 This theory has been supported by Hoppenstein, who showed that the posterolateral stimulation of the spinal cord provided effective contralateral pain relief with substantially less current than posterior stimulation.34 Some investigators speculate that the changes in blood flow and skin temperature from spinal cord stimulation may affect nociception at the peripheral level.11,17,27,54,55 This postulate is further supported in part by data from Marchand et al. who investigated the effects of SCS on chronic pain using noxious thermal stimuli.22,31,36,58,70,87 Since it was discovered that SCS causes vasodilation in animal studies, clinicians have used this modality for the treatment of chronic pain due to peripheral vascular disease and this is one of the leading indications for SCS in Europe today.31,36,40,87,100 The precise methods of action of pain modulation by SCS are still being elucidated. A better understanding of the pain system may lead to continued improvement in SCS hardware and software, implantation techniques, and even improved clinical outcomes.

SPINAL CORD STIMULATION LEADS Only three companies manufacture SCS systems in the United States: Medtronic, Inc. (Minneapolis, MN), Advanced Neuromodulation Systems (Dallas, TX), and Advanced Bionics (Sylmar, CA). Advanced Neuromodulation Systems (ANS) produces several leads for percutaneous placement with four or eight electrodes (Fig. 107.3A). The four-electrode lead has four 3 mm electrodes separated by an interelectrode distance of either 4 mm or 6 mm and spans a distance of either 24 mm or 30 mm. The eight-electrode lead has eight 3 mm electrodes with an interelectrode distance of 4 mm. The notion of spanning a larger distance is to help thwart the effects of possible migratory pain patterns which is thought to be a quality of complex regional pain syndrome type 1 or to provide programming redundancy in case of lead migration. The four-electrode lead spans

A

one average thoracic vertebral body while the eight-electrode lead spans two average vertebral bodies or three average cervical vertebral bodies. ANS also produces several different paddle electrodes for surgical implantation via laminotomy or laminectomy. They have a four-electrode Lamitrode Four, an eight-electrode Lamitrode 44 which has four electrodes side by side, and eight-electrode Lamitrode 8, and a 16-electrode Lamitrode 88 with eight electrodes side by side. ANS recently released curved contour laminotomy leads in dual quad, and dual Octrode configurations. The new curved contour laminotomy leads conform more accurately to the shape of the epidual space in the dorsal spinal canal and potentially provide more consistent service than previous laminotomy leads (Fig. 107.3B). Medtronic also manufactures leads designed for percutaneous or laminotomy implantation. The percutaneously implanted leads have either four or eight electrodes. They have a tough, polyurethane outer covering and a helicoil substrate making the leads very resilient with columnar strength and flexibility. There are three different four-electrode leads and one eight-electrode lead. They each have variable electrode lengths and interelectrode distances. The Pisces Quad Plus has four 6 mm electrodes with an interelectrode distance of 12 mm; the Pisces Quad lead has four 3 mm electrodes with an interelectrode distance of 6 mm; the Pisces Quad Compact lead has four 3 mm electrodes with an interelectrode distance of 4 mm; and the Octad has eight 3 mm electrodes with an interelectrode distance of 6 mm. In addition to these lead configurations, Medtronic has the capability to individually produce a wide variety of four- or eight-electrode leads to accommodate an individual physician’s specifications or to treat complex or difficult pain patterns. In general, the smaller the interelectrode distance, the less risk for rootlet stimulation. Medtronic also produces five electrodes for implantation via laminotomy: the Symmix, the dual-paddle Symmix, the Resume TL, the Resume, and the Specify. The Symmix, Resume TL, and the Resume leads have four electrodes each, the Specify has eight, and the dualpaddle Symmix has two paddles with two electrodes each. The Symmix has four electrodes arranged in a diamond pattern and the

B

Fig. 107.3 (A) Advanced Neuromodulation Systems percutaneous implantable lead types. This picture demonstrates an eight-electrode Octrode lead and two four-electrode leads. The electrodes on all leads are 3 mm long. The eight-electrode and one of the four-electrode leads have an interelectrode distance of 4 mm. The other four-electrode lead has an interelectrode distance of 6 mm. (B) Advanced Neuromodulation Systems laminectomy implantable lead types. This picture demonstrates four paddle-style leads implanted via laminectomy. There are two wide leads and two narrow leads. One of the narrow leads has eight electrodes and the other one has sixteen electrodes. There are two wide leads; one has eight electrodes and the other one has sixteen electrodes. 1167

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the IPG powered system is limited in that at this time it can only power a maximum of eight electrodes at a limited frequency and will require surgical replacement at some point in time. The RF receiver systems have the advantage of being externally powered, thus obviating the requirement for surgical replacement. The ANS receiver also has the capacity to run at a frequency of up to 1500 Hz, thus potentially allowing for a local anesthetic effect on the stimulated nerves.2,50 Both the ANS IPG and receiver have the capacity for complex programming and running several different programs simultaneously, which may have benefits when dealing with complex pain patterns, and has yet to be evaluated in a controlled study (Fig. 107.4).

Specify has a total of eight electrodes with four electrodes arranged side by side. Both of these electrode arrangements facilitate bilateral extremity stimulation. The dual-paddle Symmix has two separate paddles designed to allow implantation over two contact sites on the spinal cord to cover a more complex pain pattern. The Resume lead is the most commonly implanted paddle electrode. Both Medtronics and ANS have internally implanted batteries with pulse generators (internal pulse generator or IPG) and an externally powered radiofrequency (RF) controlled implanted receiver. Both IPG powered systems have the advantage of having the device completely internalized, which makes the system more flexible in that the patient can swim with it on if desired. However,

+

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Fig. 107.4 (A) Advanced Neuromodulation Systems dual lead bipole. This picture demonstrates the electrical field experienced by the posterior spinal cord with a single active electrode on each percutaneously placed Octrode. Note that the bulk of the electrical field is biased to the left side, the cathode. (B) Advanced Neuromodulation Systems dual lead bipole. This picture demonstrates the electrical field experienced by the posterior spinal cord with a single active electrode on each percutaneously placed Octrode. Note that the bulk of the electrical field is biased to the right side, the side of the cathode.

Section 5: Biomechanical Disorders of the Lumbar Spine

+ – +

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Fig. 107.4—Cont’d (C) Advanced Neuromodulation Systems single lead guarded array. This picture demonstrates the electrical field experienced by the posterior spinal cord with a single-lead guarded array. This is a cathode with an anode on either side of it. Note that the bulk of the electrical field is biased in the center adjacent to the cathode. (D) Advanced Neuromodulation Systems transverse guarded array. This picture demonstrates the electrical field experienced by the posterior spinal cord with a transverse guarded array. This is a cathode on one lead with two anodes on the other lead. Note that the bulk of the electrical field is biased to the side of the cathode.

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PATIENT SELECTION CRITERIA – INDICATIONS Proper patient selection is essential to the long-term success of a SCS system. Improper selection criteria were one of the main reasons for suboptimal results reported in the 1970s. During the 1970s and early 1980s, most studies evaluating the long-term efficacy of dorsal column stimulation quoted success rates of approximately 40%. Technical advances leading to improved hardware coupled with improved patient selection, have improved the rate of long-term efficacy to approximately 70%.12,92,93 An SCS system should be considered for patients who have failed all reasonable medical rehabilitation and inteventional spine techniques.12 An ideal patient should be motivated, compliant, and free of drug dependence.56 Psychological screening is recommended but not mandatory to exclude conditions that predispose to failure of the procedure. It is extremely important that the patient and the physician have a discussion regarding probable outcome prior to implantation and that the patient has realistic expectations. If a patient has unrealistic expectations of the intervention, the treating physician should not consider that patient for implantation. Diagnoses that are typical indications for this procedure in the United States include chronic radiculopathy, FBSS, neuropathic pain, and complex regional pain syndrome.8,16,25,43,59 In Europe, SCS is also used for peripheral vascular disease and angina that are not amenable to medical therapy with reportedly excellent results.6,31,36,87,97,100 Other indications for SCS include transformed migraines, perineal pain, and interstitial cystitis.4,83 When considering pain topography, extremity pain responds better than axial pain, and the more distal the extremity pain the greater the clinical response.73,103 Middle and upper lumbar pain as well as thoracic, cervical, and chest wall pain are difficult to adequately control and maintain long term. Pain, due to severe nerve damage superimposed upon cutaneous numbness (i.e. anesthesia dolorosa) is also difficult to treat with SCS. Central pain syndromes do not respond to SCS and are best treated by other modalities. The use of 3–7 day outpatient trials with an SCS system has proved helpful in determining which patients will respond well enough to warrant a permanent implantation.18,19,73,103 Absolute criteria that must be present for a patient to have a positive trial include tolerance of paresthesia, greater than 50% pain relief, and overall patient satisfaction. Relative requirements for a positive trial include improved functional level and reduced usage of pain medication. Long-term goals include reduced use of the medical system.

CLINICAL OUTCOMES Original long-term results of pain control from spinal cord stimulation in the late 1960s and 1970s were disappointing.28,30,32,93,96 This led to widespread disenchantment with SCS. Poor patient selection, inadequate equipment, and failure to perform implantations with the patient awake accounted for the disappointing results. The advent of new technology, careful patient selection, trial implantation, percutaneous placement or strict attention to positioning a paddle electrode in the same place as a percutaneously placed lead during a trial, and active physician–patient interaction during the procedure have all contributed to the success of spinal cord stimulation over the past 15 years. In 1998, Kumar et al. published a case series of 235 patients who had undergone an SCS implantation.44 The follow-up ranged from 6 months to 15 years after implantation with a mean of 5.6 years. One hundred and eighty-nine patients (80%) experienced satisfactory initial pain relief during a trial period of SCS and underwent 1170

a permanent SCS implant. The study population included 150 men and 85 women with a mean age of 51.4 years. Indications for SCS included FBSS (114 patients), peripheral vascular disease (39 patients), peripheral neuropathy (30 patients), MS (13 patients), RSD (13 patients) and other chronic pain etiology (26 patients). One hundred and eleven patients (59%) received satisfactory pain relief and 47 were gainfully employed (as compared with only 22 prior to implantation). Improvements in daily living as well as a decrease in analgesic usage were reported in successful outcomes. The shorter the duration of time to implantation after FBSS, the greater the rate of success. In the group with FBSS there were 101 successful stimulation trials and 13 unsuccessful stimulation trials. In this group, fiftytwo patients received long-term pain relief while 49 patients who underwent permanent implantation were classified as failure. Out of the 235 patients who underwent permanent implantation, 189 had a successful trial SCS and 111 (58.7%) were successful long term. In 2000, Villavicencio et al. published a retrospective nonrandomized case series comparing the long-term effectiveness of SCS using laminectomy-style electrodes versus percutaneously implanted electrodes.105 The etiology of pain was FBSS (n=24), CRPS (n=7), neuropathic pain (n=4) and other (n=6). Mean follow-up after implantation of SCS was 8.6 months for the laminectomy-type electrode and 10.3 months for the percutaneously placed electrodes. Twenty-seven of 41 patients (66%) participating in the trial SCS implantation went on to receive a permanent SCS implantation. The laminectomy-style electrodes were placed under general anesthesia, while the percutaneous ones were placed under local anesthesia. Outcome was measured per VAS scale via phone interview. Visual analogue scale scores decreased by an average of 4.6 points after laminectomy-style electrode stimulation and by 3.1 after percutaneously implanted electrode stimulation. Electrodes placed through laminectomy provided significantly greater long-term pain relief than percutaneously placed ones (p=0.02). Overall, 89% of patients had greater than 50% pain relief. Five of 12 patients in the laminectomy group and seven of 15 patients in the percutaneous group underwent revision due to loss of pain relief. All 3 patients under the age of 65 in the laminectomy group were able to go back to work. Of the four patients working in the percutaneous group, two were able to go back to work, one retired, and one remained disabled due to pain. In 2001, Leveque at al. published the results of a retrospective study involving 30 patients with FBSS who underwent permanent SCS.53 Each patient had had multiple spinal surgeries and was deemed to no longer be a candidate for traditional spine surgery. Each patient had back and leg pain and all patients underwent a screening trial of SCS prior to permanent implantation. Sixteen patients had greater than 50% pain relief during the trial SCS and underwent permanent implantation. Of the 16 patients who underwent permanent implantation, 9 were implanted with percutaneously implanted catheter-style leads and the remaining 7 patients underwent permanent implantation with a paddle-style lead via a laminectomy. Mean follow-up was 34 months with a range of 6–66 months. At last follow-up, 12 of the 16 patients continued to have at least 50% pain relief. All 6 patients who underwent implantation via laminectomy continued to have greater than 50% pain relief with or without narcotics while only 6 out of the 9 percutaneously implanted patients had greater than 50% pain relief with or without narcotics. The authors concluded that SCS is an effective means of treating intractable back pain in the FBSS population. They also suggested that paddle-style SCS leads placed via laminectomy may be superior for long-term efficacy to catheter-style leads placed percutaneously. In 2001, Ohnmeiss and Rashbaum published a retrospective study which evaluated patient satisfaction of SCS for predominant axial low back pain.79 The literature prior to this study does not support

Section 5: Biomechanical Disorders of the Lumbar Spine

the use of SCS for chronic spinal pain that is primarily limited to the low back. The patient sample included 41 patients who underwent SCS for axial low back pain of an average duration of 83 months. Inclusion criteria included failure of aggressive nonoperative care and patients were not considered surgical candidates. Thirty-eight out of forty-one patients had FBSS with back pain greater than leg pain. In all 41 patients, a SCS trial was performed for an average of 5.9 days. Five patients did not receive significant benefit from SCS trial and were not implanted. The remaining 36 patients were implanted with a Medtronics Mattrix system. Of the 36 patients, 4 later had the system removed due to lack of efficacy. The study included a mean follow-up of 10.5 months. Seventy percent of patients implanted reported being satisfied, 78.8% of patients would recommend SCS to others, and 75.8% would have the implantation again. Sixty percent of patients reported improvement, 33% of patients reported no change in their pain. And 6.1% of patients reported being worse off after the implant than before. The authors comment that much of the literature pertains to older devices no longer in use. They report a nonstatistically significant trend towards lower patient satisfaction with greater chronicity of symptoms pre-implantation. An interesting finding revealed in the questionnaire was that some patients dissatisfied with the results were still recommending the procedure to somebody else and would have the procedure done again. This may be due to overly inflated expectations of pain relief after SCS implantation. In 2001, Barolat et al. published a retrospective review of 44 patients who had undergone SCS implantation with a paddle-style electrode and a radiofrequency receiver via a laminectomy for the treatment of intractable low back pain.9 Only patients in whom further lumbar surgery was not indicated or those in whom medical conditions contraindicated surgery underwent implantation. All patients had leg pain in addition to their back pain. The study was a multicenter, prospective study with follow-up at 6, 12, and 24 months. Follow-up data were available in 41 patients. At 6 months, 91.6% of the patients reported fair to excellent pain relief in the lower extremities and 82.7% pain relief in the back. At 12 months, 88.2% of the patients reported fair to excellent pain relief in the lower extremities and 68.8% pain relief in the back. Significant improvement in function and quality of life was reported at both 6 and 12 months using the Oswestry and SIP, respectively. The majority of the patients report that the procedure was worthwhile and no patients considered the procedure not to be worthwhile. The authors concluded the SCS was beneficial in the treatment of intractable low back pain. The authors further opined that paddle-style electrodes may have an advantage over percutaneous catheter-style electrodes due to patient-reported broader coverage of stimulation and lower energy consumption. In 2001, Dario et al. published a five year retrospective analysis (1992–1997) of 49 patients treated for FBSS at the authors’ center.23 Twenty-one patients had predominantly leg pain, 22 had leg pain only, and six had back pain only. Outcome measures include change in VAS, Oswestry Scale, and Pain Disability Index as measured at entry and every three months for a period of 24–84 months with a mean duration of 42 months. The medical therapy was structured and all patients received the same protocol. After 6 months of medical therapy without significant benefit, patients underwent implantation of a Medtronic Itrel 2 or 3 SCS systems. Twenty-two patients had percutaneous leads implanted and 2 patients had laminectomy paddle-type leads implanted. The following measures were evaluated for SCS implanted patients: efficacy of therapy for leg and back pain, return to work status if previously employed, ADL activity if retired, and the concomitant use of medications and dosages after

implant. The results revealed medical therapy improved both back and leg pain with mean VAS decreasing from 76 to 25. Oswestry scale results dropped from 23 to 6, and PDI scores went from 42 to 4. Of the 22 patients who underwent SCS implant, the VAS results were broken down into leg pain only and back pain only. In the leg pain only group, VAS went from 85 to 22, whereas in the back pain only group the VAS went from 45 to 40. The overall SCS groups mean PDI went from 51 to 7 and the Oswestry scoring went from 12 to 9. The authors concluded that neurostimulation only partially resolved the need for chronic medical therapy. In 2002, North and Wetzel selected 26 patients with FBSS to undergo trial SCS.76 Selection criteria included FBSS with leg pain greater than back pain and one or more of the following: recent abnormal diagnostic imaging results, neurological deficit consistent with the patient’s complaints and history, and/or a well-documented history of surgery for appropriate indications. All patients underwent a percutaneous trial with a four-electrode SCS lead. Of the 26 patients trialed, 24 were chosen to undergo a permanent implantation at the same spinal level as the trial lead was placed. Twelve patients were implanted with a percutaneous four-electrode lead similar to the one temporarily implanted for the trial stimulation and the other twelve patients were implanted with an insulated four-electrode lead via laminectomy. The study demonstrated that the laminectomy-placed leads outperformed percutaneously placed leads with better patientreported pain coverage and lower amplitude requirements which should, according to calculations, yield a doubling of battery life. In 2002, Kumar et al. evaluated the overall cost-effectiveness of SCS therapy versus conventional pain therapy for a consecutive series of 104 patients with FBSS.45 Sixty patients with FBSS were treated with SCS versus 44 patients with conventional pain therapies (CPT). Outcome measures utilized included the Oswestry disability questionnaire at enrollment, yearly, and at 5-year follow-up. Cost of treatment was determined based on year 2000 Canadian dollars and expenditures were regulated by the Canadian Healthcare System. Treatment costs included primary care physician and specialist evaluations, imaging studies, surgery and devices for the interventional arm of the study and medication, physiotherapy, chiropractic, massage, and acupuncture for the control arm. The cumulative totals for the SCS arm were $29 123/patient compared to the control arm figure of $38 029/patient. The cost savings of SCS over the CPT group were realized at an average of 2.5 years due to the high initial cost of surgery and the device. After 2.5 years the savings of SCS versus CPT were realized through reduced drug use, reduced use of physical therapy services, and reduced use of the healthcare system in general. It is possible that in the US healthcare system the cost savings would be even greater. A prior study by Bell et al. puts the breakpoint at 2 years based on projected dollar values.13 In 2004, Turner et al. published a systematic review of the literature including the MEDLINE, EMBASE, Scientific Citation Index, Cochrane Controlled Trials Register, and Current Contents bibliographic databases back to their starting dates for articles published on the effectiveness of spinal cord stimulation (SCS) in treating failed back surgery syndrome (FBSS) and complex regional pain syndrome (CRPS) up to May 16, 2003.104 Seven of 583 articles met the inclusion criteria for review of SCS effectiveness (two CRPS, three FBSS, two mixed diagnoses) and 15 others met the criteria for the review of SCS complications. The average number of previous spine surgeries (in the three studies that reported it) ranged from 2 to 3.3. Mean follow-up time was 33.6 months (range 6–60 months) and an average of 72% (range 58–96%) of patients received the permanent implantation after trial implantation. The studies included different SCS implantation methods (percutaneous trial followed by percutaneous implantation, percutaneous trial followed 1171

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by implantation by laminectomy, and direct implantation by laminectomy without trial). Both FBSS studies (Dario23 and Ohnmeiss and Rashbaum79) that reported leg and back pain separately found greater improvement in the leg pain than the back pain with SCS. Due to the study design of the seven publications, no conclusions could be drawn regarding effectiveness of SCS in returning patients to work. There was a suggestion that pain relief after SCS implantation decreases over time; however, no prospective study with a control group was available. Among 40 FBSS patients in an Ohnmeiss et al. study done in 1996, benefit from SCS decreased from 83% after 12 month to 70% after 24 months.78 One large prospective multicenter study published in 1996 by Burchiel et al. with 182 FBSS patients who received a permanent SCS was excluded due to the fact that only 70 completed the follow-up.19 In this study, a one-year follow-up, showed statistically significant pain decrease and improvement in quality of life measures, but not in medication use or work status. However, due to the large number of patients lost in the follow-up, it is unclear if the patients at follow-up were representative of the original sample. Also, in 2004, Mailis-Gagnon et al. performed a systematic review of the medical literature from 1980 to September 2003 regarding the efficacy of SCS in relieving certain types of chronic pain, its complications, and its adverse effects.57 Studies that were only descriptive or observational were excluded. Primary outcome measure was pain relief. Secondary outcomes were indirect statements about pain relief, e.g. well-being, happiness, functional status, etc. A total of 1629 titles and abstracts were screened, 18 papers were retrieved, 16 of those were excluded, and two were included: one by Kemler et al.38 and one by North et al.74 Both studies were randomized, controlled trials but the Kemler et al. study was a truly prospective study while the North et al. study used a cross-over design. The Kemler et al. study evaluated CRPS type I and had 12-month follow-up while the North et al. study evaluated FBSS and had a 6-month cross-over between SCS and operation. Kemler et al. concluded that SCS is more effective and less expensive than standard treatments protocols for chronic CRPS and North et al. concluded that SCS should be considered prior to operation of the spine on a repeat disc herniation at a previously operated segment. The conclusion of Mailis-Gagnon et al. was that there is limited evidence in favor of SCS for FBSS and CRPS type I. Further, they felt that more trials were needed to confirm whether SCS is an effective treatment for certain types of chronic pain. The most common SCS application in North America today is in the treatment of chronic low back and lower extremity pain due to chronic radiculopathy despite surgery.19,46,78,91,95,103 The largest SCS study incorporates 320 consecutive patients who underwent either temporary or permanent implants at the Johns Hopkins Hospital between 1971 and 1990.40 This series included follow-up on 205 patients, the majority of whom had the diagnosis of failed back surgery syndrome. Permanent SCS implants were placed in 171 of these patients. At follow-up (mean interval 7.1±4.5 yrs), 52% of patients had at least 50% continued pain relief, and 58% had a reduction or elimination of analgesic intake. About 54% of patients younger than 65 were working at the time of follow-up; 41% had been working preoperatively. The percentage of patients having long-term pain relief is similar in the majority of large published SCS series of implants for FBSS. The success rate in most of these studies, which is generally reported as 50% or more pain relief, is approximately 50–60%.9,20,23,43,52,53,68,79,81,85 Some studies report success rates as high as 88% and others as low as 37%.39,94 Although these latter studies differ in implantation technique and screening protocols, the success rate for pain reduction generally remains the same. 1172

More recently published reviews have specifically looked at the efficacy of SCS in FBSS for pain control, reduction in narcotic consumption, function, and work status.24,50 69,70,84,105 According to these studies, long-term pain reduction (at least 2 years after implantation) can be expected to range 50–70% in approximately 60% of SCS patients. In 50–90% of individuals, there will be an elimination or reduction in the use of opioids. The return to full employment rate after SCS reported by two studies is 25–59%, which is significant when comparing it to the usual return to work rate in this population of 1–5%.50,70 Reasons for the disparity between pain reduction and return-to-work rates appear to reflect the high percentage of unskilled laborers among this population, the prolonged periods of disability and the attendant socio-behavioral changes tend to take place in chronic pain patients. Despite this disparity, there is a general increase in function and activities of daily living.

COMPLICATIONS There are rarely any serious complications from of SCS implantation.7 In one study, one nonfatal pulmonary embolism and one case of paraplegia lasting 3 months occurred.49 The latter resulted during the laminectomy placement of a paddle-style lead. Other rarely reported complications include sphincter disturbance and gait abnormality.82 Most complications from SCS devices include reduced or altered paresthesia, lead migration, lead fracture, pain at the pocket site or connection site, infection, nerve injury, and epidural hematoma.6,7,25,26,42,66,70,96,99,109 In a comprehensive summary of different publications, lead migration or displacement varied from 3.7% to 69% although most studies reported migration between 16% and 25%.7 Rates of lead fractures were reported in various series from less than 1% to more than 20% and superficial infections occurred in 2–12% of cases. Serious surgical infections were rare as were clinically apparent epidural hematomas. Cerebrospinal fluid leakage was found in one series in 2% of patients. In a more recent study, Kumar et al. published a case series of 235 patients who had undergone a SCS implantation.45 Complications included hardware malfunction (n=8), electrode displacement (n=65, of which 35 were repositioned and 30 were replaced), infection (4% of implanted devices; n=11 of which 8 required removal), CSF leak (n=2, resolved spontaneously), 1 SQ hematoma at the site of the pulse generator, 3 electrical leaks, and 8 electrode fractures. Development of tolerance was thought to be responsible for most of the 79 long-term failures. In 2000, Heideche et al. published a retrospective review of 42 patients with FBSS who had undergone a permanent SCS implantation for the purposes of identifying the types and frequency of hardware failures.33 The patients were followed for 6–74 months. Thirty-five patients had undergone implantation with a single quadripolar SCS lead percutaneously placed and attached to a Medtronic X-trel receiver; three patients were implanted with dual leads attached to a Mattrix receiver; and the other four patients were implanted with a Medtronics Resume lead via laminectomy. In this study, lead breakage or insulation disruption (n=8) was the most frequently encountered hardware failure with receiver leakage being second most common (n=4). In 2004, Turner et al. performed a systematic review of the literature involving SCS and found 583 articles.104 After screening for pertinent articles, they reviewed 21 studies. An average of 34% (range 0–81%) of patients had one or more complications after the implantation of the permanent SCS during the study follow-up period. Complications included superficial infection (mean 4.5%, range 0–12%), deep infection (one case), pain in the region of the stimulator components (mean 5.8%, range 0–40%), and equipment

Section 5: Biomechanical Disorders of the Lumbar Spine

failure (mean 10.2%, range 0–40%). The median rate for equipment failure of 6.5% may be more accurate, since one study in 2002 by Alo et al. had higher than usual equipment failure rates, which may have skewed the rate upwards.5 Other complications include a need for stimulator revision, mostly due to dislodged or displaced electrodes and a need for stimulator removal.5,104

THE FUTURE Authors of several of the current outcome studies have pointed out that older outcome studies bear little relevance to today’s outcomes due to improved patient selection, improved technology, and improved understanding of implantation techniques. In addition, recently published outcome studies have focused on the antegrade placement of percutaneous or paddle leads in the lower thoracic spine for the treatment of chronic back and leg pain. Other methods of lead placement exist that have anecdotally proven effective in the treatment of back and leg pain but that have not yet been subjected to controlled trials. The retrograde placement of percutaneously placed leads has proven effective in the treatment of low back and leg pain (Fig. 107.5).2 This technique typically involves the cephalocaudal advancement of a lead into the lower lumbar or sacral spine via an epidural needle placed at the L2–3 or L3–4 level. Using this technique, the lead may be placed over one or two adjacent nerve roots or actually fed into a particular foramen. This technique allows for a very stable, focused paresthesia along one or a few nerve roots at very low amplitudes. When the lead is entered into a foramen it tends to be very stable and allows for very little positional or activity-related change in paresthesia. Thus, if a patient has a poor result from a SCS trial with a traditionally placed SCS lead, then the placement of a SCS lead via a retrograde approach may be indicated. In selected cases, it is the authors’ experience that by applying this method in lieu of or in addition to a traditionally placed lead, clinical outcomes will improve. Peripheral nerve stimulation (PNS) is a technique that is considered to be very similar to SCS except that the neural elements being stimulated lie outside of the spinal column. This method has

A

Fig. 107.5 Retrograde placement of spinal cord stimulator leads. This picture of a radiograph demonstrates two quadripolar leads percutaneously placed in a cephalocaudal direction. Note that the distal ends of both leads are entering the ipsilateral L2–3 foramen bilaterally. This array succeeded in managing this patient’s low back and bilateral lower extremity pain when two quadripolar leads placed in an antegrade manner failed despite adequate coverage of the patient’s pain pattern with paresthesia.

been successfully applied in the treatment of refractory transformed migraines.5 It has also been successfully applied in an anecdotal manner by the authors and others for the treatment of focal, intense low back pain. This technique involves the placement of an epidural needle immediately beneath the skin peripheral to the center of a focal region of pain (Fig. 107.6A). The needle is then directed into the long axis of the pain so that the distal 5 cm of the needle crosses through the middle of the most intense pain. An eight-channel SCS lead is then advanced into the needle and the needle is removed. The

B

Fig. 107.6 (A) Peripheral nerve stimulation. This picture demonstrates an epidural needle being placed beneath the skin peripheral to a focal region of pain in a patient with a failed back surgery syndrome in preparation for a trial peripheral nerve stimulator. (B) Peripheral nerve stimulation. This picture demonstrates an epidural needle in the L1–2 epidural space with a SCS lead appropriately placed. There is also an epidural needle placed subcutaneously traversing the long axis of a focused region of pain.

(Continued) 1173

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C

D

Fig. 107.6—Cont’d (C) Peripheral nerve stimulation. This picture of a radiograph demonstrates two eight-electrode leads placed subcutaneously along the long axis of a patient’s central low back pain. (D) Peripheral nerve stimulation. This picture of a radiograph demonstrates a hybrid system in which an eight-electrode lead is in the epidural in traditional position and another eight-electrode lead is placed subcutaneously along the long axis of a focused region of pain.

lead is then trialed for efficacy in a manner similar to an SCS trial. This method of PNS provides a very dense, focused paresthesia and is often successful at relieving intense low back pain when SCS alone fails. As a result, when a patient with an intense, focused region of low back pain has a poor result from a trial SCS, a PNS trial should be considered in lieu of or in addition to a traditional SCS trial (Fig. 107.6B–D). The authors have had several anecdotal cases in which a combination of PNS and SCS has succeeded in patients who have had a poor result from the antegrade placement of a percutaneously placed lead despite coverage of the patient’s pain pattern with paresthesia. Studies focused on the combination of PNS and SCS in selected cases may improve long-term success rates.

CONCLUSION Spinal cord stimulation has been demonstrated to be effective at managing pain in selected patients and selected conditions. Hardware, software, and implant technology have improved outcomes and consistency over time. Paddle-style leads implanted via laminectomy may have slight advantage over percutaneously implanted leads when managing back pain over time; however, there does not appear to be a difference in efficacy when managing hip or lower extremity pain. To date, studies have evaluated only leads placed in an antegrade manner either via a laminectomy or percutaneous technique. The efficacy of retrograde lead placement and peripheral nerve stimulation have not been evaluated either alone or in combination with each other or with antegrade lead placement. Finally, the efficacy of complex programming has not been evaluated and may improve consistency and efficacy over time.

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85. Ray CD, Burton C, Lifson A. Neurostimulation as used in a large clinical practice. Appl Neurophysiol 1982; 45(1–2):160–166. 86. Reynolds DV. Surgery in the rat during electrical analgesia induced by focal brain stimulation. Science 1969; 164(878):444–445. 87. Robaina FJ, Dominguez M, Diaz M, et al. Spinal cord stimulation for relief of chronic pain in vasospastic disorders of the upper limbs. Neurosurgery 1989; 24(1):63–67. 88. Robb LG, Spector G, Robb MP. Spinal cord stimulation: neuroaugmentation of the dorsal columns for pain relief. In: Weiner RS, ed. Pain management: a practical guide for clinicians. 5th edn. Boca Raton: St. Lucie Press; 1998:271–293. 89. Ruda MA. Opiates and pain pathways: Demonstration of enkephalin synapses on dorsal horn projection neurons. Science 1982; 215(4539):1523–1525. 90. Saade NE, Tabet MS, Soueidan SA, et al. Supraspinal modulation of nocioception in awake rats by stimulation of the dorsal column nuclei. Brain Res 1986; 369(1–2):307–310.

103. Turner JA, Loeser JD, Bell KG. Spinal cord stimulation for chronic low back pain: a systematic literature synthesis. Neurosurgery 1995; 37(6):1088–1096. 104. Turner JA, Loeser JD, Deyo RA, et al. Spinal cord stimulation for patients with failed back surgery syndrome or complex regional pain syndrome: a systematic review of effectiveness and complications. Pain 2004; 108:137–147. 105. Villavicencio AT, Leveque JC, Rubin L, et al. Laminectomy versus percutaneous electrode placement for spinal cord stimulation. Neurosurgery 2000; 46(2): 399–405. 106. Wall PD, Melzack R. Introduction. In: Wall PD, Melzack R, eds. Textbook of Pain. 2nd edn. Edinburgh: Churchill-Livingstone; 1989:1–18. 107. Yaksh TL. Neurological mechanisms of pain. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. 2nd edn. Philadelphia: JB Lippincott; 1988:791–844.

91. Segal R, Stacey BR, Rudy TE, et al. Spinal cord stimulation revisited. Neurolog Res 1998; 20(5):391–396.

108. Yaksh TL. Anatomy of the pain processing system. In: Waldman SD, Winnie AP, eds. Interventional pain management. 1st edn. Philadelphia: WB Saunders; 1996:10–18.

92. Shealy CN, Mortimer JT, Reswick JB. Electrical inhibition of pain by dorsal column stimulation. Anesth Analg 1967; 46(4):489–491.

109. Young RF. Evaluation of dorsal column stimulation in the treatment of chronic pain. Neurosurgery 1978; 3(3):373–379.

93. Shealy CN, Mortimer JT, Hagfors NR. Dorsal column electroanalgesia. J Neurosurg 1970; 32(5): 560–564.

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94. Siegfried J, Lazorthes Y. Long-term follow-up of dorsal column stimulation for chronic pain syndrome after multiple lumbar operations. Appl Neurophysiol 1982; 45(1–2):201–204.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar

CHAPTER

Neuraxial Drug Administration to Treat Pain of Spinal Origin

108

Joshua P. Prager

INTRODUCTION Advances in neurobiology serve as the basis for current and evolving implantable pain modalities, consisting of neurostimulation and neuraxial drug administration systems. Both neurostimulation and intrathecal drug administration systems are reversible and nondestructive neuromodulatory techniques that can reduce pain of spinal origin. Neurostimulation is preferred over neuraxial drug delivery when the patient’s problem is amenable to both techniques because drug delivery systems require regular medication refills. Neuraxial medication delivery is indicated when side effects of systemic analgesics limit the ability to deliver effective doses of medications. Prager and Jacobs provide a comprehensive review of patient selection for these neuromodulatory techniques.1

RATIONALE The discovery of opioid receptors2,3 provided a rational basis for the delivery of opioid drugs intraspinally. By 1979, reports of epidural4 and intrathecal5 opioid delivery in humans had entered the peerreviewed literature. Intraspinal infusions delivered drugs directly to opioid receptors, limited systemic exposure, and by decreasing the opioid dosage required for pain relief, generally reduced side effects, which facilitated the provision of greater analgesia. The benefits of short-term spinal analgesia, primarily for patients with intractable cancer pain, led to investigation of longer-term continuous subarachnoid opioid infusions for the management of both cancer pain6–17 and noncancer pain, such as that produced by failed back surgery syndrome.18–30 Pain specialists currently are successfully using opioids to treat patients with chronic noncancer pain, noting that such patients can benefit from sustained analgesia and better function without becoming addicted.31 The key to appropriate treatment of pain is proper diagnosis. Pain can be characterized as nociceptive (e.g., somatic pain), neuropathic (pain from nerve injury), or idiopathic. Pure nociceptive pain usually responds well to systemic opioids. Neuropathic pain responds to opioids at higher doses and often is responsive to a large number of antineuropathic medications (Table 108.1). Failed back surgery syndrome (FBSS) pain usually is a mixed type of pain that is both nociceptive and neuropathic. Nociceptive pain arises from disc or bone injury, reaction to hardware or graft harvesting, or reactive spasm. Neuropathic FBSS pain can arise from nerve injury before surgery, chronic compression, chemical irritation, nerve injury during surgery, scar tissue formation, or arachnoiditis. The challenge in treating FBSS pain is that of treating this mixed etiology of pain. Pain from spinal cord injury may be predominantly neuropathic in nature, whereas mechanical pain such as that in the patient with severe osteoporosis is more nociceptive.

In appropriately selected patients, intraspinal therapy has been refined through accumulated experience from treating tens of thousands of cases (more than 25 000 with implantable pumps32), improved drug delivery systems, and new pharmacologic approaches, making it an effective technique for the control of intractable pain.

INTRASPINAL DRUG DELIVERY SYSTEMS Intraspinal drug delivery can be accomplished by a variety of means including percutaneous catheter, percutaneous catheter with subcutaneous tunneling, implanted catheter with subcutaneous injection site, totally implanted catheter with implanted reservoir and manual pump, and totally implanted catheter with implanted infusion pump.33 The choice of the system depends on the indication for intraspinal therapy, the need for bolus versus continuous infusion, the patient’s general medical condition, available support services, ambulatory status, life expectancy, and cost. In general, percutaneous tunneled catheters, external pumps, and implanted passive reservoirs can be more cost-effective when life expectancy is a matter of weeks to months. A fully implanted pump becomes economical if life expectancy is longer than 3 months.34 The first ‘permanent’ catheter for intraspinal drug delivery was developed by DuPen et al.35 in the 1980s. They adapted Broviac catheter technology to create an exteriorized, permanent, three-piece, silicone epidural catheter. The catheter was implanted in 55 cancer patients who had metastatic disease and intractable pain. After 3891 days of catheter use, there were no catheter infections and 18 minor side effects. The rate of hospitalization for pain control was decreased by 90% in these patients. In one series of 350 reported implantations of the DuPen catheter, there were 30 superficial catheter infections, 8 deep catheter infections, and 15 epidural or intrathecal catheter infections, representing a 15.1% infection rate. The DuPen catheter continues to be marketed for use with an external pump. It may represent a cost-effective alternative for patients with a short life expectancy, such as patients with severe metastatic disease to the spine. However, the DuPen catheter and similar external systems have limited applicability in treating noncancer pain of spinal origin. Two types of implantable drug delivery systems are marketed currently in the United States.34,36 The first commercially available implantable pump delivered medication at a fixed rate and consisted of two chambers separated by a flexible bellows in addition to a side port for bolus injections.3 Outflow was regulated by compressed Freon gas, so changes in altitude and temperature affected drug flow. Because the pump ran at a fixed rate, changes in the rate of medication delivery could be accomplished only by emptying the pump and refilling it with a different concentration of medication. This pump was approved by the Food and Drug Administration (FDA) for epidural administration of preservative-free morphine. The original pump has been superseded by a new model,2 which has a single 1177

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Table 108.1: Updated pain treatment interventions and medications32,36 Exercise Meditation, relaxation, yoga, traditional biofeedback and neurobiofeedback Over-the-counter medications (aspirin, traditional nonsteroidal antiinflammatory drugs) and cyclooxygenase inhibitors Antineuropathic adjunctive medications (tricyclic antidepressants, selective serotonin reuptake inhibitors, GABAergic drugs, other antispasmodics, anticonvulsants, local anesthetics, calcium-channel blockers, substance P-depleting amines, α2 agonists, NMDA receptor antagonists, tramadol) and other adjunctive medications: corticosteroids Physical rehabilitation: physical therapy, work hardening, occupational therapy, Pilates Somatic and sympathetic nerve blocks Cognitive and behavioral therapies Opioid medications combined with adjuvants Pure high-potency, time-released opioid medications with breakthrough short-acting opioid medications Spinal cord stimulation if pain is segmental Intraspinal infusion analgesia Neurodestructive procedures

raised septum and no side port. Although essentially the same, the new pump was modified by removing the side port to minimize the potential for overdose. A special needle with a needle shaft aperture and a closed needle tip is used to deliver fluid directly into the catheter rather than the drug reservoir.33 A second and third fixed-rate pump are now available. The third type of implantable delivery system is a programmable electronic pump powered by batteries, which last up to 7 years depending on flow rate.4 Two pumps are FDA approved and contain either 10 or 18 mL collapsible reservoirs, a volume activated valve and a pump or 20 or 40 mL reservoirs, a pressure activated valve and a pump, both of which push medication through a bacteriostatic filter and catheter. Comparison of these pumps is found in Table 108.2. The newer pump, the SynchroMed II has the advantage of having a smaller size with a slightly larger reservoir volume or a vastly greater effective reservoir volume at approximately the same size as its predecessor, the SynchroMed EL. At the time of this writing, both pumps are available for implantation. The SynchroMed II allows for more sophisticated programming, stores more important information, and has a slightly longer battery life expectancy. The newer pump costs approximately 10% more. These pumps are FDA approved for epidural or intrathecal infusion of preservative-free morphine sulfate for chronic, intractable pain, and baclofen for chronic spasticity. Ziconotide was FDA approved for intrathecal use for pain in these pumps in 2004. Both pumps are programmed, using noninvasive telemetry to control medication concentration, volume, and dosage. The programmable feature allows flexible dosing options over time and permits precise dose titration. Both pump types require refilling under sterile conditions at least every several months, depending on flow rate.37 In deciding whether to implant a programmable pump or a fixedrate pump, several factors should be considered, including their specific attributes. Table 108.3 compares the attributes of the two pump types. The programmable pumps provide greater flexibility of medication delivery and are more adjustable. However, a programmable pump is more expensive and needs to be replaced when the battery fails. Hardware is but one component of the entire implantation cost, and when all costs are aggregated, the percentage difference in cost

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diminishes. As a rule of thumb, programmable pumps are implanted when dosage titration and regulation is anticipated, and fixed-rate pumps may provide a cost-effective choice when dosage is expected to be stable. In practical terms for the patient with chronic pain of spinal origin, dosage regulation should be anticipated. Thus, a programmable pump serves the patient better initially. If the patient stabilizes on a regimen, a fixed-rate pump may be considered for replacement to minimize expense. However, the current and future flexibility of programmable pumps make them a superior choice for most important factors, excluding expense.

PATIENT SELECTION AND SCREENING TRIALS The literature is virtually unanimous in emphasizing the importance of appropriate patient selection if intraspinal pain therapy is to be successful.1 Patients with chronic pain are subject to neurophysiologic, emotional, and behavioral influences, which govern their perception of pain and of pain relief. Therefore, treatment of chronic noncancer pain is multidisciplinary, drawing on cognitive and behavioral psychological therapies, functional rehabilitation, orthopedic and neurologic surgery, medications, nerve blockade, neuroaugmentive and sometimes neurodestructive procedures. The pain treatment continuum in Table 108.1 lists these interventions and the antineuropathic medications currently used to treat intractable pain.32 Indications and contraindications for intraspinal opioid therapy appear in Table 108.4.34 Intraspinal drug delivery has been used primarily for patients with nociceptive pain, which has proved to be opioid responsive. Experience in intraspinal treatment of neuropathic pain is more limited, although several studies indicate that neuropathic pain may respond to intraspinal delivery of escalating doses of opioids, or to nonopioid medications.34,38 Finally, a screening trial allows both physician and patient to assess intraspinal drug delivery before committing to pump implantation. Numerous screening protocols exist. Trials can incorporate epidural or intrathecal administration, bolus injection, a series of injections, or continuous infusion, and they can be conducted on an inpatient or outpatient basis. Pure opioid or a mixture containing opioid can be administered. The duration of the trials varies from 24 hours to longer

Section 5: Biomechanical Disorders of the Lumbar Spine

Table 108.2: Comparison of SynchroMed EL with SynchroMed II implantable pumps PUMP COMPARISON SynchroMed EL

SynchroMed II

Reservoir volume

10 mL pumps residual volume 1.2 mL 18 mL pumps residual volume 2.4 mL

20 mL pumps residual volume 1.4 mL 40 mL pump residual volume 1.4 mL

Pump displacement volume

10 mL pumps 107 mL 18 mL pumps 125 mL

20 mL pump 91 mL 40 mL pump 121 mL

Drug stability

Morphine: Lioresal* intrachecal (baclofen injection): FUDRs: Methotrexane:

90 days 90 days 56 days 56 days

Morphine: Lioresal* intrathecal (baclofen Injection): FUDRs: Methotrexane:

180 days 180 days 56 days 56 days

Reservoir fill port

4.75 mm diameter

6.8 mm diameter

Flow rate accuracy

Flow rate accurate until pump reservoir reaches 2 mL

Flow rate accurate until pump reservoir reaches 1 mL

Catheter access port (CAP)

CAP not included on all models. Mesh screen over port allows 25-gauge or smaller needle.

CAP included on all models. Single-hole, funnel design allows 24-gauge or smaller needle.

Pump rollers

Two rollers.

Three rollers. One roller arm has a

Pump tubing volume

Pumps with CAP 0.26 mL to 0.36 mL Pumps without CAP 0.23 mL to 0.32 mL

0.199 mL to 0.289 mL

• Volume-activated valve. • Expanding drug reservoir bellows pulls valve seem onto a metal seat, forming a seal • Upon activation, requires continuous aspiration and time as release.

• Pressure–activated valve. • As pressure diaphragm flatters, a spring pushes valve seem onto a metal seat, forming a seal • Release immediately upon aspiration.

One tone that sounds approximately every 15 seconds when activated.

Critical alarm – louder two-some alarm that indicates:

Alarm indicates:

• Empty reservoir • End of service (EOS) • Motor stall • Stopped pump duration exceeds 48 hours • Critical pump memory error

radiopaque marker.

Reservoir valve

Alarms

• Low reservoir volume reached • Low battery • Pump memory error Can disable (silence) or postpone some alarms.

Non-critical – louder single-tone alarm that indicates: • Low resroir volume reached • Elective replacement indicator (ERI) • Non-critical pump memory error Interval between sounds is adjustable. Some alarms can be silenced once they have sounded. Continued 1179

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Table 108.2: cont’d Comparison of SynchroMed EL with SynchroMed II implantable pumps Warming

Warming to body temperature required before implantation.

No warming required before implantation.

Pump Purge

Pump purge required to confirm pump operation before implantation.

No pump purge before implantation and purge infusion mode not available.

Suture Loops/Mesh Pouch

Suture loops not included on all models.

Suture loops included on all models. Mesh pouch not provided in pump package. May be ordered separately as an accessory (8590–1 Mesh Pouch Accessory).

Mesh pouch provided in pump package for pumps without suture loops. Information Management

The pump stores:

The pump stores:

• Pump model • Patient ID (3 characters) • 1 Drug (5 characters) • Drug concentration • Infusion prescription • Calibration constant

• Patient demographics • Pump information • Catheter information • Drug name (up to 5 drugs, 25 characters each) • Drug concentration (for each drug entered) • Physician notes • Time-stamped event log • Infusion prescription • Calbration constant Notes: Telemetry takes longer because there is more data to transmit between the pump and programmer. A typical session takes 30 seconds for pump interrogation and 30–90 seconds for pump update.

Longevity

Approximately 6.5 years at 0.5 mL per day – determined by battery depletion.

7 years at 0.5 mL per day - determined by a combination of battery depletion, motor revolutions and time.

Radiopaque Identifier

None.

Identifies pump model under fluoroscopy or X-ray.

Battery Composition

Lithium thionyl chloride.

Lithium-hybrid cathode.

Internal Bacterial-retentive Filter

0.22 μm.

0.22 μm.

SynchroMed EL

SynchroMed II

Programmer

Programmer models 8840, 8821, 8820 and 8810 can be used. Magnet accessory required on releme try head of the 8840 N’Vision Programmer.

Only the 8840 N’Vision Programmer can be used. Do not use the magnet accesory on the telemetry head. It will present relemetry with a SynchroMed II pump.

Infusion prescription

Complex continuous infusion mode available.

Flex infusion mode available – has a repeating cycle of 24 hours. Allows 2 different drug delivery pattern over a 7-day week. Can program a bolus to run between flex or simple continuous infusion modes. Bridge bolus can be programmed to-and-from any infusion mode. Minimum rare infusion mode available (non-therapeutic rate of approximately 6 microliters/day).

PROGRAMMING COMPARISON

Periodic bolus infusion mode available. Can program a bridge bolus only with simple continuous infusion mode. Limited bridge bolus duration.

Programmer therapy stop key

1180

Does not obtain pump status before stopping the pump. Programs pump to stopped pump (0 microliters/day)

Obtains pump status before stopping the pump. Programs pump to minimum rate (6 microliters/day)

Section 5: Biomechanical Disorders of the Lumbar Spine

Table 108.3: Comparison of implanted pump characteristics39 Consideration

Programmable pump

Fixed-rate pump

Cost

More expensive hardware* Needs to be replaced† Can change rate without changing medication Requires programmer

Less expensive hardware Can be permanent Rate change requires removal of medications to be replaced with different concentration Larger reservoir can reduce number of refills

Environment factors

Will not run when cold‡

Rate affected by pressure and temperature changes

Flexibility

Can run at multiple rates or deliver periodic boluses Can change rate without changing concentration for short term or long term Can be turned off temporarily

Fixed-rate (some have a fixed rate selectable at time of implantation)

MRI compatibility

Compatible§

Compatible

Reservoir volume

18 mL and 10 mL reservoirs or 20 and 40 mL reservoirs

Can have much larger reservoirs Can be smaller

Other features

Programmer displays pump information (rate, medication, concentration last fill, refill date, etc.) Potential for some patient control for incident pain Potential to collect longitudinal information with programming

* Hardware cost is one component of overall implantation costs. Other costs include operating suite, recovery room, radiology facility and professional fees, anesthesiology professional fees, surgical professional fees, and medications. When considering total cost, hardware cost represents only a small amount. † Battery lifespan is estimated to be up to 7 years. Surgical costs are incurred for replacement. ‡ Only a factor in pump preparation, not at physiological temperatures. § Please see recently distributed guidelines.

Table 108.4: Updated indications and contraindications for intraspinal drug delivery34,36,39 INDICATIONS Chronic pain with known pathophysiology Sensitivity of pain to medication being used Failure of more conservative therapy Favorable psychosocial evaluation Favorable response to screening trial CONTRAINDICATIONS Systemic infection Coagulopathy Allergy to medication being used Inappropriate drug habituation (untreated) Failure to obtain pain relief in a screening trial Unusual observed behavior during screening trial Poor personal hygiene Poor patient compliance

than 1 week. No protocol can be considered superior or definitive on the basis of current research. However, approximating the conditions of long-term therapy during the trial would seem to offer the best chance for assessing efficacy and tolerance. Table 108.5 compares the advantages of each trial technique.39 The choice of protocol is influenced by the patient’s overall condition, the physician’s preference and experience, the available facilities and resources, the practice environment, and the payer coverage. Medicare reimbursement, for example, requires ‘a preliminary trial of intraspinal opioid drug administration … with a temporary intrathecal/epidural catheter.’40 The question of epidural versus intrathecal administration continues to be debated, although no study has directly compared the two routes of administration. Although the epidural route is more convenient, an epidural dose must be roughly 10 times an intrathecal dose to provide equivalent analgesia. Proponents of intrathecal administration argue that the larger epidural dose may induce more severe side effects, deterring some patients from agreeing to intrathecal therapy that might be both beneficial and tolerable. For patients with chronic pain of spinal origin, an intrathecal trial optimizes the chance for uniform drug delivery and simulates actual effect more accurately. Two questions are fundamental. Is the patient’s pain responsive to opioid therapy? Can the patient tolerate the planned drug and dosage?36 The physician and patient should agree in advance on the goals of the trial and on the measures to be used for assessment of the outcome. For example, if returning to work is a goal of long-term intraspinal drug therapy, the patient should be evaluated by a rehabilitation specialist during the screening trial. In general, candidates should not proceed to implantation unless their pain can be reduced by at least 50%.9,41 Behavioral observation during the trial adds to the

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Table 108.5: Comparison of neuraxial trial techniques 39 Epidural Trial Decreased risk of intrathecal infection Lower incidence of post-dural puncture headache (PDPH) No risk of CSF drainage through catheter from disconnect More common for outpatient administration

Intrathecal Trial Most accurately simulates permanent catheter Lower dosage required Smaller needle produces less severe PDPH Even distribution of medication in FBSS

Bolus Trial Ease of administration Does not require pump for trial Decreased trial expense if additional bolus is not necessary

Continuous Infusion Trial Most accurately simulates permanent implant Can be titrated Required by some carriers Does not produce peaks and troughs of medications Facilitates longer trial Fewer side effects by avoiding peaks Can incorporate placebo without need for second procedure Opioid with Adjuvant Medication Trial May more realistically predict long-term administration

Pure Opioid Trial Predicts the effect of pure opioid No need to discern which medication had salutary or untoward effects Inpatient Trial Better monitoring may enhance safety Easier to observe patient Sterile technique more likely

Outpatient Trial More accurately simulates normal activities Facilitates longer trial More opportunity for titration Less expensive per day

Pure Percutaneous Catheter Trail Less procedure-related pain during the trial Simpler to perform Less invasive Twenty-four Hour Trial Less expensive

Tunneled Catheter Trial Decreases chance of CNS infection Facilitates longer trial Decreases chance of catheter dislodgement

Longer Trial Can more accurately simulate normal activities More accurately predicts long-term result Decreases placebo response Withdraw Systemic Medications during Trial Use of Current Systemic Medications during Trial Eliminates possible systemic abstinence syndrome (abstinence symptoms can confound results)

information used for making decisions regarding permanent implantation.42 A psychological interview is valuable during or after the trial to discuss if and how the trial met expectations.

SURGICAL IMPLANTATION Device manufacturers provide recommended surgical procedures, which can be adapted to surgeon and institutional preference. The surgical procedure has two steps: placement of the catheter and implantation of the reservoir or pump. Implantation technique varies widely, even for a single type of pump, as Krames and Chapple43 reported in their review of 202 patients in 22 centers. Most of the catheters were inserted between L2 and L4 (87.2%), introduced through the midline (65.1%), or positioned with their tips at T10 to T12 (64.1%). Also, 95% of the catheters were anchored, 43.8% with a right-angled anchor and 44.8% with a butterfly anchor. Catheter position was confirmed in 94.8% of the cases. Follett et al. analyzed catheter-related complications and determined that paramedian insertion, appropriate anchoring, and placement with redundant loops reduced the chance of complications.44 1182

Can observe the effect and side effects of neuraxial medication without additive effect of systemic medications

DRUG SELECTION Intraspinal drugs must be preservative free. Alcohol, phenol, formaldehyde, and sodium metabisulfite, common drug preservatives, are all toxic to the central nervous system. Any drug packaged in a multidose vial probably contains preservatives and should not be used for intraspinal administration.45 Preservative-free morphine sulfate is the only drug approved by the FDA for intraspinal delivery for pain relief. Its long history of clinical use, long duration of action (12–24 hours), and relative ease of use explain why it remains the gold standard for intraspinal therapy. If morphine is poorly tolerated, other opioids (hydromorphone, meperidine, methadone, fentanyl, and sufentanil) also can be used intraspinally. Care must be taken to ensure that the medication preparation is compatible with the pump tubing, and that the medication is pure and preservative free. Some meperidine preparations have rendered the SynchroMed pump (Medtronic, Minneapolis, MN) inoperable by damaging internal tubing (personal communication with Medtronic personnel). The pharmacokinetic properties of various drugs (their lipid solubility, pH, pKa, molecular weight, and opioid receptor affinity) determine time to onset of

Section 5: Biomechanical Disorders of the Lumbar Spine

action, duration of action, uptake and distribution, and side effects. Lipophilic medications such as sufentanil do not spread more than several neurotomes beyond the delivery site at the catheter tip, whereas hydrophilic medications such as morphine circulate throughout the cerebrospinal fluid (CSF). Furthermore, the site of drug delivery (epidural versus intrathecal) affects distribution. Drugs delivered epidurally must first cross the dura and arachnoid membranes before diffusing to their site of action, whereas drugs delivered intrathecally diffuse passively to the spinal cord. Morphine, which has low lipid solubility and high receptor affinity, diffuses slowly and remains bound for prolonged periods. Unfortunately, the risk of central nervous system side effects (sedation, nausea and vomiting, and respiratory depression) is greater with hydrophilic drugs, such as morphine, than with lipophilic drugs, such as fentanyl or sufentanil. These lipophilic drugs have a rapid onset and prolonged duration of action.32,36,37 Dosing of intraspinal drugs is highly individual and depends on the patient’s pain type, age, previous need for analgesia, and previous use of opioid medication. Usually, patients with neuropathic pain require higher doses of opioids than patients with nociceptive pain if an opioid is the only medication administered. One advantage with the use of continuous infusion or increasing-dose bolus injections during the screening trial is that dosage can be more precisely titrated. Drug admixtures can help patients who experience side effects associated with the increasing doses required to provide analgesia or outright tolerance to opioids. Combining drugs with different mechanisms of action can produce synergy, as in the case of morphine combined with bupivacaine. In theory, synergy reduces morphineassociated side effects by decreasing the opioid dose required for analgesia. One caveat applies: although use of admixtures is increasingly popular and often produces increased analgesia, safety data on many of the combinations are scarce. In fact, there is a paucity of literature even demonstrating the stability of various admixtures in the pump at body temperature up to 3 months. Satisfactory results with a morphine–bupivacaine combination have been reported in several studies of cancer and noncancer pain, although high concentrations of epidural morphine were required and side effects included transient paresthesias, motor blockade, and gait disruption.34 The study of van Dongen et al.46 followed a group of cancer patients treated with intrathecal morphine and bupivacaine through a tunneled percutaneous catheter. Of 17 patients treated with this admixture because morphine alone was insufficient to relieve pain, 10 improved significantly and four moderately. The three patients who experienced no improvement also had clinical signs of severe depression. No serious complications were reported. A more recent study by a similar group found that intrathecal morphine and bupivacaine slowed the progression of morphine dose, as compared with morphine given alone. These authors attributed the diminished morphine dosage to the synergistic analgesic effect of bupivacaine.47 Although bupivacaine is a commonly used adjuvant medication, care should be taken to avoid concentrations greater than 0.75% in noncancer patients because neurotoxicity has been demonstrated at higher concentrations in rats receiving long-term infusions. Lidocaine (a local anesthetic) and clonidine (an alpha-adrenergic agonist) also have been given with morphine. The morphine–clonidine combination seems to be particularly effective for patients with neuropathic or mixed nociceptive–neuropathic pain.32,36 In the mid-1990s, the Epidural Clonidine Study Group evaluated 85 patients with severe cancer pain who were taking large doses of opioids without significant pain relief or suffering from severe side effects. They were randomly assigned to receive 30 μg/ hour of epidural clonidine or placebo for 14 days and had access to rescue epidural morphine. Pain was documented by visual analog score, McGill Pain Questionnaire, and daily epidural morphine use. Successful analgesia was reported by 45% of patients receiving

clonidine, and by 21% receiving placebo. Among the patients with neuropathic pain, 56% receiving clonidine reported successful analgesia, as compared with only 5% receiving placebo. Pain scores were lower at the end of the study for the patients with neuropathic pain who received clonidine rather than placebo, and morphine use was unaffected. Serious hypotension occurred in two patients receiving clonidine and one receiving placebo.48 Clonidine has not yet been approved for intrathecal infusion in the United States, but in European and Australian studies, intraspinal infusion was well tolerated for 6–12 months.49,50 Dexmedetomidine, a highly selective new α2 adrenergic agonist, is known to produce sedation and analgesia in humans.51 Given intrathecally to rats, it is a very potent antinociceptor.52 Alpha-2 agonists also seem to potentiate the analgesic effects of opioids. One study in rats evaluated the interactions between systemically (subcutaneous, intravenous, and intraperitoneal) and spinally (epidural and intrathecal) administered α2 agonists (medetomidine, dexmedetomidine, xylazine, clonidine, and detomidine) and opioids (fentanyl or sufentanil).53 All of the tested α2 agonists potentiated the effects of opioids by reducing the amount of opioid needed to reach specified levels of analgesia and prolonging the duration of analgesia with a fixed dose of opioid. The potentiation appeared to be independent of the route of administration. Dexmedetomidine was second only to medetomidine in its ability to produce deep surgical analgesia when combined with fentanyl. Recent research that elucidates the neurobiology of pain suggests other methods of pain control. Nerve and tissue damage leads to changes in both the peripheral and central nervous system. Drugs specifically targeted at steps in the neuropathologic cascade are being investigated for properties of reducing both pain perception and side effects. One such drug is ziconotide, a highly selective, potent, and reversible blocker of neuronal N-type voltage-sensitive calcium channels that produces antinociception in animals. Ziconotide is the third medication to receive FDA approval for continuous intrathecal administration via a SynchroMed pump. In one study, ziconotide exhibited substantial neuroprotective activity in a model of traumatic diffuse brain injury in rats.54 The effect of intrathecally administered ziconotide and morphine on nociception also has been studied in rats.55 After a 7-day intrathecal infusion, ziconotide enhanced morphine analgesia, but had no effect on ziconotide antinociception. Whereas chronic intrathecal morphine infusion led to rapid tolerance, ziconotide had no loss of analgesic potency during the infusion period. Ziconotide administered with morphine produced a synergistic analgesic effect, but did not prevent morphine tolerance.55 In humans, ziconotide has been administered intrathecally to control acute postoperative pain.56 Mean daily morphine dosage (administered by patient-controlled analgesia) was significantly less in patients receiving ziconotide than in those receiving placebo 24–48 hours after surgery (p>0.040). Patient pain perception (measured by visual analog scale) also was markedly lower in patients treated with ziconotide than in patients treated with placebo. Four of six patients receiving the high dose of ziconotide (7 μg/hour) experienced adverse events including dizziness, blurred vision, nystagmus, and sedation, all of which resolved after drug discontinuation. Ziconotide has also been used to treat cancer and AIDS patients experiencing pain not responsive to opioids.57 Intrathecal ziconotide has demonstrated analgesic efficacy, and the initial reports indicated that adverse events could be controlled with symptomatic treatment. An expert panel convened in July 2000 released clinical guidelines for intraspinal drug selection, dosage, and administration.58 The panel found wide variation in practice patterns on the basis of an Internet survey of physicians using implantable pumps. The guidelines reflect the best available evidence, as judged by experienced clinicians. 1183

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In 2003, a similar meeting was convened and data from the intervening period were reviewed.59 The treatment recommendations are summarized in Figure 108.1. In 2007, a third panel met to review data from the intravening four years.59a The highlights of the new consensus statement include a change in the first line of therapy to include morphine, hydromorphone and ziconotide. The second line of therapy recommendations will also include ziconotide as an adjuvant option along with clonidine and bupivacaine. The panel also ranked other drugs in order of scientific support and clinical utility. A new important component was also developed for the 2007 version of the consensus panel which includes special recommendations for end of life care.59a The panel noted that the extensive preclinical and clinical data obtained as part of a formal drug development program exceeds the data available for other drugs used for intrathecal infusion and will probably lead to placement of ziconotide on an upper line of the algorithm, unless accumulating experience suggests a narrow therapeutic index in practice. Although the FDA approved ziconotide as an intrathecal monotherapy with a starting dose of 2.4 μg/d, a different, but overlapping consensus of experts expect that this medication will be used in conjunction with other intrathecal medications at a significantly lower staring dosage.60

Efficacy Studies on the efficacy of intraspinal morphine report widely ranging success rates for pain relief (Table 108.6).3,4–6,7,9,11–15,18,24,26,30, 31,38,42,57,61–69 In general, pain relief for cancer patients occurred

Morphine

Line 1

a

more frequently (in approximately 80% of cases) and consistently than for noncancer patients. Some studies also included other measures of efficacy, such as improvement in activities of daily living, employment status, and quality of life. In a cancer study, Smith et al. recently compared neuraxial delivery of morphine to maximum analgesic medical therapy in cancer patients and found that in addition to receiving better analgesia, the patients who received intrathecal morphine had greater longevity.69 Several key studies have examined the efficacy and reliability of intraspinal drug delivery. Winkelmüller and Winkelmüller68 investigated the long-term effects of continuous intrathecal infusion for chronic noncancer pain. They followed 120 patients for 6months to 5.7 years, 73 of whom were FBSS patients with mixed nociceptive–neuropathic pain from multiple lumbosacral operations, including spondylolysis. The best long-term results occurred in the management of deafferentation pain and neuropathic pain with pain reduction (measured by a visual analog scale) of 68% and 62%, respectively. The mean morphine dosage was 2.7 mg/d initially, which rose to 4.7 mg/d after an average of 3.4 years. Among 28 patients treated more than 4 years, 18 (64.3%) were maintained on constant doses, and 10 (35.7%) required increases to more than 6 mg/d 1 year after therapy began. Tolerance developed in seven patients, three of whom had the pump removed. During the follow-up period, 74.2% of the patients benefited from intrathecal opioid delivery. The average pain reduction was 67.4% after 6 months and 58.1% at last follow-up examination. Most patients (92%) were satisfied with therapy, and 81% Neuropathic pain

Hydromorphone b

Morphine (or Hydromorphone) + Bupivacaine d

Line 2

c

Morphine (or Hydromorphone) + Clonidine

Line 3

Line 4

* Z i c o n o t i d e

Morphine (or Hydromorphone) + Bupivacaine + Clonidine

e

Fentanyl, Sufentanil, Midazolam, Baclofen f For selected patients only

Line 5

Neostigmine, Adenosine, Ketorolac g

Line 6

Ropivacaine, Meperidine, Gabapentin, Buprenorphine, Octreotide, other**

* The specific line to be determined after FDA review ** Potential spinal analgesics: Methadone, Oxymorphone, NMDA antagonists a. If side effects occur, switch to other opioid. b. If maximum dosage is reached without adequate analgesia, add adjuvant medication (Line 2). c. If patient has neuropathic pain, consider starting with opioid monotherapy (morphine or hydromorphone) or, in selected patients with pure or predominant neuropathic pain, consider opoid plus adjuvant medication (bupivacaine or clonidine) (Line 2). d. Some of the panel advocated the use of bupivacaine first because of concern about clonidine-induced hypotension. e. If side effects or lack of analgesia on second first-line opioid, may switch to fentanyl (Line 4). f. There are limited preclinical data and limited clinical experience; therefore, caution in the use of these agents should be considered. g. There are insufficient preclinical data and limited clinical experience; therefore, extreme caution in the use of these agents should be considered. Fig. 108. 1 Clinical guidelines for intraspinal infusion, 2003.59 (The reader is referred to an updated recommended algorithm for intrathecal polyanalgesic therapies in a forthcoming publication, 2007.59a) 1184

Section 5: Biomechanical Disorders of the Lumbar Spine

Table 108.6: Studies of intraspinal morphine for intractable pain 39 Studies (listed in order of publication)*

Patient population (nonmalignant/ malignant pain)

Route of administration

Efficacy

Side effects

Behar et al.

6

Epidural

3 complete relief 3 >50% reduction in pain

Wang et al.

8

Intrathecal

2 complete relief from separate saline and morphine injections 6 complete relief from morphine alone

Coombs et al.

10 (5/5)

Intrathecal

5 cancer patients: significantly reduced pain 5 noncancer patients: poor pain reduction

Krames et al.

17(1/16)

Intrathecal/epidural

1 noncancer patient: poor pain relief 16 cancer patients: 50–70% reduction in pain

Auld et al.

32

Epidural

66% good 3% side effects

Auld et al.

20 (15 patients with nonmalignant pain)

Epidural

Of 15 patients, 2 had excellent relief, 6 good relief, 1 fair relief, 2 poor relief, 4 no relief

Brazenor

26

Intrathecal

20 had excellent relief, 3 good relief, 1 poor, 1 none, 1 comatose

Penn and Paice

43 (8/35)

Intrathecal

8 noncancer patients: all good or excellent pain relief 35 cancer patients: 80% good or excellent pain relief

Onofrio and Yaksh

53 (0/53)

Intrathecal

67% good or excellent; 19 of 33 improved ambulation Average parenteral opiate doses fell significantly

Hassenbusch et al.

69

Intrathecal

41 patients reduced mean pain scores from 8.6 to 3.4

Follett et al.

37 (2/35)

Intrathecal

35 cancer patients: good pain relief 2 noncancer patients: most good pain relief

Spinal headache (31%), nausea (26%, not necessarily attributable to pump implantation), and lethargy (15%) most common

Kanoff

15

73% good to excellent 40% of patients returned to work

20% catheter-related

Hassenbusch et al.

18

Intrathecal

61% fair to good

33%

Winkelmüller and Winkelmüller

120

Intrathecal

74% 67% had pain reduction at 6 months 58% at last follow-up 92% of patients satisfied with treatment 81% of patients reported improved quality of life

17%

6% complications, mostly catheter-related

Early pump failure problems in 6 units were corrected by device modification

*See original article 39 for references to the studies. Continued 1185

Part 3: Specific Disorders

Table 108.6: cont’d Studies of intraspinal morphine for intractable pain 39 Studies (listed in order of publication)*

Patient population (nonmalignant/ malignant pain)

Route of administration

Efficacy

Side effects

Paice et al.

429 (289/140)

Intrathecal

95% good to excellent 28 patients returned to work

22%

Tutak and Doleys

26

Intrathecal

77% good to excellent

35% catheter-related

Doleys et al.

36

Intrathecal

60.8% subjective improvement 76.7% decreased oral medications 47.8% improved function 83% of patients rated outcome as good or excellent

Nausea was the most frequent side effect (27.8%) 33% catheter problems requiring surgery Three pumps removed, none for mechanical failure

Anderson and Burchiel

30

Intrathecal

50% had at least 25% pain reduction after 24 months Activities of daily living improved for at least 12–18 months

20% device-related

Smith et al.

0/71 compared

Intrathecal

58% achieved 20% pain and toxicity reduction, overall 52% pain reduction. Improved survival compared to conventional medical therapy (54% vs. 37%)

22% device pump to medical Rx

*See original article 39 for references to the studies.

reported improvement in quality of life. Angel et al.70 studied 11 patients (9 with FBSS) referred to a neurosurgery clinic and treated with intrathecal morphine. The patients were observed for up to 3 years. Overall, a good to excellent analgesic response was seen in 73% (8/11) of the patients. Unfortunately, the three patients judged to have poor results all had FBSS. The effective response among all the FBSS patients was 67% (6/9). Bladder dysfunction requiring pump removal occurred in two patients. The authors concluded that intrathecal morphine delivery was a viable alternative in the management of FBSS despite its limitations. They cautioned that it should be a last-choice option. In the most recent study in FBSS patients, The National Outcomes Registry for Low Back Pain collected prospective data on 136 patients with chronic low back pain treated using intraspinal infusion via implanted devices, 81% of whom received morphine. Oswestry Low Back Pain Disability Scale ratings after 12 months improved by 47% in patients with back pain and by 31% in patients with leg pain.71 The largest study, a retrospective, multicenter study, surveyed physicians in the United States regarding intrathecal morphine delivered by the SynchroMed pump.64 In this study, 35 physicians provided 429 case reports detailing screening methods, outcomes, dosing, and adverse effects. Each of the physicians contacted had implanted at least five pumps. Among these patients, 33% were being treated for cancer pain and 67% for noncancer pain. The average length of treatment was 14.6±0.57 months. The patients with somatic pain had the degree of pain relief. After initial dose titration, intrathecal morphine doses increased only twofold, from 5.84±0.65 mg/d to 13.19±1.76 mg/d. The patients being treated for cancer pain had a higher initial dose, which escalated quickly and then reached a plateau. Patients with noncancer pain had a gradual, linear increase in dosage. Adverse

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drug effects were not frequent, but catheter or system malfunction occurred in 21.6% of the cases. Although most implantable drug delivery systems are used to treat nociceptive pain, in the Hassenbusch et al. study38 of intraspinal drug therapy for patients with severe neuropathic pain, 11 of 18 patients (61%) had good or fair pain relief after more than 2 years. Average numerical pain scores declined by 39±4.3%, although long-term pain relief eventually fai™led for 7 of 18 patients (39%). The authors concluded that long-term intrathecal opioid infusions could be effective for treating neuropathic pain, but at higher doses than used for treating nociceptive pain. A recent prospective study examined the long-term safety and efficacy of intrathecal morphine for patients with severe noncancer pain.61 Of 40 patients, 30 experienced pain relief during a screening trial and had an intraspinal delivery system implanted. Patients had mixed neuropathic–nociceptive pain (50%), peripheral neuropathic pain (33%), deafferentation pain (13%), or nociceptive pain (3%). Half of the patients (11/22) reported at least a 25% reduction on the visual analog scale after 24 months of treatment. The results of the McGill Pain Questionnaire and Chronic Illness Problem Inventory showed improvement in sleep, social activities, inactivity levels, and medication use throughout the follow-up period. Device-related problems requiring additional surgery were experienced by 20% of the patients.

COMPLICATIONS The complications of intraspinal therapy fall into several categories: procedure-related complications, drug-related side effects, and equipment-related problems. Immediate drug-related side effects include nausea and vomiting, urinary retention (more common in men with benign prostatic hypertrophy), pruritus, and respiratory

Section 5: Biomechanical Disorders of the Lumbar Spine

depression. Each of these conditions can be managed medically with antiemetics, intermittent catheterization, antihistamines, or naloxone, respectively. Respiratory depression, the most serious of these side effects, is relatively rare in patients already exposed to opioids. Delayed side effects include constipation, myoclonus, edema, arthralgias, facial flushing, and diaphoresis. Clinicians increasingly recognize suppression of the hypothalamic–pituitary axis producing endocrine changes. Examples include decreased testosterone production resulting in decreased libido and suppression of thyroid function resulting in hypothyroidism. For this reason, serum lipids, androgens or estrogens, 24-hour urinary cortisol, and serum IGF-1 levels should be monitored during intrathecal therapy.72 Intraspinal therapy requires conscientious follow-up evaluation, with doses adjusted to balance pain relief against side effects. Many side effects respond to symptomatic treatment.37 Unintentional overdosing can be disastrous. Symptoms of massive morphine overdose include muscle rigidity, severe myoclonus, seizure activity, hypertension, cardiovascular collapse, and severe respiratory depression. Should an overdose occur, the patient should be hospitalized immediately. Replacing some CSF with saline and administering naloxone if signs of respiratory depression occur may help.36 Catheter-related problems are common, occurring in 10–40% of cases. Any abrupt change in pain can signal a catheter problem.34,37 Troubleshooting for equipment problems demands all of a physician’s diagnostic and management skills. A radiograph of the pump and catheter will disclose many catheter problems, but not whether the tip is obstructed or a CSF leak has occurred. Often, surgical inspection and correction are required.36 Meticulous surgical technique can help to prevent some catheter problems. Catheter position can be checked fluoroscopically, CSF flow confirmed at each step during implantation, and the catheter secured with a purse-string suture at the interspinous ligament, and again with a plastic fixation device.34 A recent prospective study of 202 patients in 22 centers in the United States and Europe examined results from the use of a catheter5 modified to overcome some drawbacks of earlier designs.42 The patients in this study were being treated for noncancer pain (60.4%), spinal spasticity (21.8%), cancer pain (12.4%), or other conditions. The catheter implantation technique varied widely with regard to catheter entry site and tip position, spinal introducer position, and catheter anchoring. Based on 3112.8 months of patient use, the overall catheter-caused complication rate was 0.3% per patient per

month. More than 89% of the physicians rated the new catheter as superior to previously available catheters. Table 108.7 lists the nonmedication-related complications associated with this new catheter. Cerebrospinal fluid leaks are inevitable during intrathecal catheter placement, leading to postspinal headache in up to 20% of patients. Persistent CSF leaks should be treated with autologous epidural blood patching. Cerebrospinal fluid hygromas usually resolve spontaneously, but surgical intervention may be necessary if fluid persistently leaks through the suture line after more conservative measures have failed.36 Catheter-tip granulomas, often associated with neurologic sequelae, may develop after intraspinal catheter placement.72 Granulomas are relatively rare. In a survey of 519 US physicians who implanted drug delivery systems, 31 reported a total of 19 cases, 6 of which had not been previously reported in the literature.65 Two reported cases involved patients with FBSS.73,74 Patients with a granulomatous mass may present with new pain, numbness, weakness, or changes in bowel and bladder habits. A recent study analyzed reports of catheter-tip inflammatory masses (granulomas) in 39 patients who received intrathecal morphine or hydromorphone, either alone or mixed with other drugs.75 The authors noted that patients whose mass was diagnosed during the administration of drugs other than intrathecal morphine had probably been exposed to morphine earlier in their clinical course. Subsequently, based on this and preclinical studies, Hassenbusch led a consensus conference that recommended positioning of the catheter tip in the lumbar thecal sac, minimizing opioid dosage and concentration to the extent possible, and providing attentive follow-up of patients to encourage early diagnosis and to reduce the risk of neurological injury.76 This must be weighed against the potential efficacy and reduction of side effects produced by strategic placement of the catheter tip near the level where pain signal enter the cord. If placement of the tip is considered outside the lumbar area, consistent follow-up is essential and unusual neurological symptoms warrant a thorough, immediate evaluation. The diagnosis of granuloma is confirmed by a neurologic examination and MRI. Treatment consists of surgical decompression and removal of the mass and spinal catheter.72 Prevention trumps treatment in the management of surgical infections. Prophylactic cephalosporin or vancomycin administration is recommended, along with strict sterile technique. A wound should never be closed in the presence of uncontrolled bleeding because hematomas are

Table 108.7: Summary of complications related to a new intrathecal catheter72 Complication

Procedure-related

Patient-related

Mechanical

Total

Dislodged

4

5

1

10

Cut during placement

2

0

0

2

CSF leak/hygroma

2

1

0

3

Pain during insertion

1

0

0

1

Occlusion

0

5

0

5

Disconnection

1

1

0

2

Break

1

2

0

3

Kink

0

1

0

1

Pump pocket/site

3

0

0

3

Total

14

15

1

30

Rate per patient month of follow-up

0.45%

0.48%

0.03%

1.0%

1187

Part 3: Specific Disorders

active breeding grounds for infections. Epidural hematoma, diagnosed by MRI or computed tomography (CT), should be treated as an emergency if it impairs neurologic function. Superficial wound infections can be treated with appropriate antibiotics. The implant must be removed if infection invades the catheter or implant pocket. After exploration, the wound should be packed and left open to heal. Intrathecal infections are rare, although many patients spike a fever within the first 3 days after implantation. The most recent information regarding intrathecal granuloma is summarized in the paper from the Polyanalgesic Consensus Conference 200772a. Of note is the fact that the lowest incidence of granuloma is reported with intrathecal fentanyl and baclofen (possibly concentration related). If the complete blood count is normal, the CSF shows only leukocytosis, and the fever falls within 48–72 hours, meningitis probably is not a concern. Untreated epidural infections can abscess and compress the thecal sac, potentially leading to paralysis. Diagnosis relies on clinical signs and symptoms, confirmed by MRI or CT studies. Epidural abscess is treated by removing the pump and catheter and administering antibiotics. Consultation with an infectious disease specialist can be helpful in the selection of antibiotics.36 Many patients notice pump pocket seroma for several months after implantation. The use of postoperative abdominal binders may decrease the incidence and severity of this problem. When seroma persists, fluid can be aspirated for Gram staining if infection is suspected. Intravenous antibiotics and antibiotic irrigation of the pocket can be performed for proven bacterial infection. Patients should be monitored carefully for the spread of infection during treatment, and the device must be removed if the infection does not respond to treatment.36

TROUBLESHOOTING FOR LACK OF EFFICACY When a patient presents with lack of efficacy from a neuraxial drug delivery system, an algorithm for troubleshooting must be used. The clinician must consider possible tolerance to medication or a change in the patient’s back problem as the possible etiology. When these are ruled out, troubleshooting of the system should be initiated. The system can fail to deliver adequate medication when the reservoir volume drops below a critical level, improper programming has occurred, the catheter kinks or obstructs, the catheter becomes dislodged or migrates, the pump malfunctions, or the pump actually stalls. If the clinician approaches troubleshooting in a systematic

A

fashion, the task becomes relatively simple. The first step involves ensuring that the pump has an adequate amount of medication in its reservoir. If the pump is programmable, a scan of the pump should show whether the pump is programmed properly. Once these basics have been covered, the catheter is evaluated. If the pump has a side port, this can be aspirated to determine whether fluid can be obtained from the catheter. Radiography, particularly fluoroscopic radiography, is a valuable tool for evaluating catheter position. If there is any question regarding catheter function after these preliminary steps, a contrast study can be performed by injecting contrast through the side port of pumps so equipped.

Caveat 1 When performing a contrast study through the side port of the pump, the clinician should be careful not to administer a bolus to the patient while medication is contained in the catheter. If it is not possible to aspirate fluid back before injecting, it may not be advisable to inject contrast medium through the catheter.

Caveat 2 When injecting contrast solution into the intrathecal space, the clinician should use contrast medium indicated only for intrathecal administration. Failure to use an appropriate contrast medium can result in adverse events such as seizures and death. Less-severe complications include extreme pain and cramps. Distribution of the contrast solution can demonstrate proper flow within the CSF, verifying catheter function. Pump function (proper pump roller rotation) can be observed under fluoroscopic guidance. Figure 108.2A demonstrates the original position of the pump rotor prior to rotor rotation. Figure 108.2B demonstrates rotation of the rotor. For cases in which conventional contrast radiography leads to a confusing picture, radiolabeled indium can be injected, with the result that serial scans over the ensuing 12–24 hours will show diffusion through the CSF if the catheter is positioned intrathecally.

IMPLANTED PUMPS AND RADIOLOGIC PROCEDURES Patients with FBSS may require diagnostic procedures such as CT or MRI scans. Questions frequently arise regarding the advisability of performing scans for patients with implanted devices. There are no

B

Fig. 108.2 Radiograph of implanted pain pump. (A) Labeled rotor before rotation. (B) Rotor after rotation. Notice the change in the movement of the rotor indication that the pump is turning.39 1188

Section 5: Biomechanical Disorders of the Lumbar Spine

special implications for plain radiographs or CT scans. With modern fixed-rate pumps, exposure of pumps to MRI fields of 1.51 Tesla has demonstrated no impact on pump performance and a limited effect on the quality of the diagnostic information. For patients with implanted programmable pumps, the manufacturer recently released a document stating that the magnetic field of the MRI scanner will temporarily stop the rotor of the pump motor and suspend drug infusion for the duration of MRI exposure. The pump should resume normal operation on termination of MRI exposure. Before MRI, the physician should determine if the patient could safely be deprived of drug delivery. If the patient cannot be safely deprived of drug delivery, alternative delivery methods for the drug can be used during the time required for the MRI scan. If there is concern that suspension of drug delivery during the MRI procedure may be unsafe for the patient, medical supervision should be provided while the MRI is conducted. Before scheduling an MRI scan and on completion of the MRI scan, or shortly thereafter, the pump status should be confirmed using the SynchroMed programmer. In the unlikely event that any change to the pump status has occurred, a Pump Memory Error message will be displayed and the pump will sound a Pump Memory Error Alarm (double tone). The pump should then be reprogrammed and Technical Services notified.66 High doses of radiation can damage a pump’s circuitry. Care should be taken to exclude the pump from the radiation field during radiation therapy.

CONCLUSION Neuraxial medication delivery is now a proven and sophisticated method for managing complex intractable pain, such as that experienced by patients with FBSS. This treatment should be considered when other methods short of neurodestructive procedures have failed. With proper patient selection and medication trial, neuraxial medication delivery is a reversible, nondestructive technique that can benefit patients with FBSS by providing improved pain relief while reducing systemic side effects. Intrathecal medication administration not only can reduce pain while reducing side effects but can play a significant role in functional rehabilitation for the patient with pain of spinal origin. Intraspinal medication delivery has become an effective technique for control of intractable pain in appropriately selected patients seen by spine surgeons.

References 1. Prager J, Jacobs M. Evaluation of patients for implantable pain modalities: medical and behavioral assessment. Clin J Pain 2001; 17:206–214. 2. Hughes J, Smith TW, Kosterlitz HW, et al. Isolation of two related pentapeptides from brain with potent opiate activity. Nature 1975; 258:577–580. 3. Pert CB, Snyder S. Opiate receptors demonstration in nervous tissue. Science 1973; 179:1011–1014. 4. Behar M, Olshwant D, Magor F, et al. Epidural morphine in treatment of pain. Lancet 1979; 1:527–529.

FUTURE CHALLENGES

5. Wang JF, Nauss LA, Thomas JE. Pain relief by intrathecally applied morphine in man. Anesthesiology 1979; 50:149–151.

During the past decade, intraspinal therapy for intractable pain has evolved into a useful clinical treatment. Nevertheless, many challenges remain. Large-scale, well-controlled studies could answer some perplexing questions regarding efficacy in patients with noncancer or neuropathic pain. Patient selection criteria undoubtedly will be refined and validated as more patients are treated. In addition, further investigation of specifically targeted agents or drug combinations for intraspinal use could reduce side effects and expand indications. Basic science is elucidating pain mechanisms, providing a basis for the development of new medications and a rationale for new off-label uses of existing medications. With this in mind, clinicians planning new intrathecal catheter placement should consider a location close to the site where pain information enters the spinal cord so that lipophilic medications can achieve optimal effect. Vigilance must be exercised to observe long- and short-term side effects of medications introduced into the spinal fluid. New combinations of medications provide a huge potential for increased efficacy through additive effects and synergy, but the stability of these admixtures and their neurologic impact must be studied. Microprocessors and miniaturization have enhanced pump development. Programmable pumps are now limited by battery life constraints and size. Improvements in power sources will expand the lifespan of programmable pumps and decrease their size, allowing for larger reservoir volume. At this writing, only one implantable intrathecal system provides an element of patient control and it is not FDA approved for use in the United States. The current pumps are effective in treating baseline pain, but a system that allows patient control for breakthrough pain is essential. Finally, given the contrast in the pharmacokinetics and pharmacodynamics of the various medications that will be used simultaneously in pumps in the future, a system that can deliver different medications at different rates would be desirable. A review of experimental drugs undergoing study can be found in the Intradisciplinary Polyanalgesic Consensus Conference 2007.77

6. Brazenor GA. Long-term intrathecal administration of morphine: A comparison of bolus injection via reservoir with continuous infusion by implanted pump. Neurosurgery 1987; 21:484–491. 7. Coombs DW, Saunders RL, Gaylor MS, et al. Relief of continuous chronic pain by intraspinal narcotics infusion via an implanted reservoir. JAMA 1983; 250:2336–2339. 8. Dennis GC, DeWitty RL. Management of intractable pain in cancer patients by implantable morphine infusion systems. J Natl Med Assoc 1987; 79:939–944. 9. Follett KA, Hitchon PW, Piper J. Response of intractable pain to continuous intrathecal morphine: A retrospective study. Pain 1992; 49:21–25. 10. Harbaugh RE, Coombs DW, Saunders RL, et al. Implanted continuous epidural morphine infusion system. J Neurosurg 1982; 56:803–806. 11. Krames ES, Gershow J, Glassberg A, et al. Continuous infusion of spinally administered narcotics for the relief of pain due to malignant disorders. Cancer 1985; 56:696–702. 12. Onofrio BM, Yaksh TL. Long-term pain relief produced by intrathecal infusion in 53 patients. J Neurosurg 1990; 72:200–209. 13. Penn RD, Paice JA. Chronic intrathecal morphine for intractable pain. J Neurosurg 1987; 67:182–186. 14. Shetter AG, Hadley MN, Wilkinson E. Administration of intraspinal morphine sulfate for the treatment of cancer pain. Neurosurgery 1986; 18:740–747. 15. Spaziante R, Cappabiance P, Ferone A. Treatment of chronic cancer pain by means of continuous intrathecal low-dose morphine administration with a totally implantable subcutaneous pump. J Neurosurg Sci 1985; 29:143–151. 16. Varga CA. Chronic administration of intraspinal local anesthetics in the treatment of malignant pain. Proc Am Pain Soc 1989; 71. 17. Zimmerman CG, Burchiel KM. The use of intrathecal opiates for malignant and nonmalignant pain: Management of thirty-nine patients. Proc Am Pain Soc 1991; 97. 18. Auld AW, Maki-Jokela A, Murdoch DM. Intraspinal narcotic analgesia in the treatment of chronic pain. Spine 1984; 10:777–781. 19. Barolat G, Schwartzman RJ, Aries I. Chronic intrathecal morphine infusion for intractable pain in reflex sympathetic dystrophy. Proc Am Pain Soc 1988; 17. 20. Bedder MD, Olson KA, Flemming BM, et al. Diagnostic indicators for implantable infusion pumps in nonmalignant pain. Proc Am Pain Soc 1992; 111. 21. Burchiel KJ, Johans TJ. Management of postherpetic neuralgia with chronic intrathecal morphine. Proc Am Pain Soc 1992; 136. 22. Goodman RR. Treatment of lower extremity reflex sympathetic dystrophy with continuous intrathecal morphine infusion. Appl Neurophysiol 1987; 50:425–426. 23. Hadley MN, Shetter AG. Intrathecal opiate administration for analgesia. Contemp Neurosurg 1986; 8:1–6.

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Part 3: Specific Disorders 24. Hassenbusch SJ, Stanton-Hicks MD, Soukup J, et al. Sufentanil citrate and morphine/bupivacaine as alternative agents in chronic epidural infusions for intractable noncancer pain. Neurosurgery 1991; 29:76–82. 25. Jacobson L. Clinical note: Relief of persistent postamputation stump and phantom limb pain with intrathecal fentanyl. Pain 1989; 37:317–322.

54. Berman RF, Verweu BH, Muizelaar JP. Neurobehavioral protection by the neuronal calcium channel blocker ziconotide in a model of traumatic diffuse brain injury in rats. J Neurosurg 2000; 93:821–828.

26. Kanoff RBL. Intraspinal delivery of opiates by an implantable, programmable pump in patients with chronic, intractable pain of nonmalignant origin. J Am Osteopath Assoc 1994; 94:487–493.

55. Wang YX, Gao D, Pettus M, et al. Interactions of intrathecally administered ziconotide, a selective blocker of neuronal N-type voltage-sensitive calcium channels, with morphine on nociception in rats. Pain 2000; 84:271–281.

27. Krames ES, Lanning RM. Intrathecal infusion analgesia for nonmalignant pain. Proc Am Pain Soc 1991; 98.

56. Atanassoff PG, Hartmannsgruber MW, Thrasher J, et al. Ziconotide, a new N-type calcium channel blocker, administered intrathecally for acute postoperative pain. Reg Anesth Pain Med 2000; 25:274–278.

28. Krames ES, Lanning RM. Intrathecal infusional analgesia for nonmalignant pain: Analgesic efficacy of intrathecal opioid with or without bupivacaine. J Pain Symptom Manage 1993; 8:539–548.

57. Penn RD, Paice JA. Adverse effects associated with the intrathecal administration of ziconotide. Pain 2000; 85:291–296.

29. Lamb SA, Hosobuchi Y. Intrathecal morphine sulfate for chronic benign pain, delivered by implanted pump delivery systems. Proc Intl Assoc Study Pain 1990; S120.

58. Bennett G, Burchiel K, Buchser E, et al. Clinical guidelines for intraspinal infusion: Report of an expert panel. J Pain Symptom Manage 2000; 20:S37–S43.

30. Prager JP, DeSalles A, Wilkinson A, et al. Loin pain hematuria syndrome: Pain relief with intrathecal morphine. Am J Kidney Dis 1995;25:629–31.

59. Hassenbusch S, et al. Polyanalgesic Consensus Conference 2003: An update on the management of pain by intraspinal drug delivery- report of an expert panel. J Pain Symptom Manage 2004; 27(6):540–563.

31. Portenoy RK. Current pharmacotherapy of chronic pain. J Pain Symptom Manage 2000; 19(1 Suppl):S16–S20. 32. Krames ES, Olson K. Clinical realities and economic considerations: Patient selection in intrathecal therapy. J Pain Symptom Manage 1997; 14:S3–S13.

59a. Deer T, Krames ES, Hassenbusch S, et al. Polyanalgesic Consensus Conference 2007: Recommendations for the Management of Pain by Intrathecal (Intraspinal) Drug Delivery. Report of an Intradisciplinary Expert Panel. In Press 2007.

33. Ferrante FM. Neuraxial infusion in the management of cancer pain. Oncology 1999; 13(5 Suppl 2):30–36.

60. Willis D, et al. Expert Consensus of dosing and use of Ziconotide [Editorial in press]. Neuromodulation June 2005.

34. Levy RM, Salzman D. Implanted drug delivery systems for control of chronic pain. In: North RB, Levy RM, eds. Neurosurgical management of pain. New York: Springer-Verlag: 1997:302–324.

61. Anderson VC, Burchiel KJ. A prospective study of long-term intrathecal morphine in the management of chronic nonmalignant pain. Neurosurgery 1999; 44:289–301.

35. DuPen SL, Peterson DG, Bogosian AC, et al. A new permanent exteriorized epidural catheter for narcotic self-administration to control cancer pain. Cancer 1987; 59:986–993. 36. Krames E. Intraspinal opioid therapy for chronic nonmalignant pain: Current practice and clinical guidelines. J Pain Symptom Manage 1996; 11:333–352. 37. Gianino JM, York MM, Paice JA. Intrathecal drug therapy for spasticity and pain. New York: Springer-Verlag; 1996. 38. Hassenbusch SJ, Stanton-Hicks M, Covington EC, et al. Long-term intraspinal infusions of opioids in the treatment of neuropathic pain. J Pain Symptom Manage 1995; 10:527–543. 39. Prager JP. Neuraxial medication delivery. the development and maturity of a concept for treating pain of spinal origin. Spine 2002; 27:2593–2605. 40. Medicare Conditions for Coverage, Medicare Coverage Issues Manual, February. Transmittal No. 67, Section 40-14, 1994. 41. Caudill MA, Holman GH, Turk D. Effective ways to manage chronic pain. Patient Care 1996; 31:154–166. 42. Prager J, et al. Behavioral evaluation of patients for significant pain interventions. Presented at the American Pain Society Professional Development Course, October, 2000. 43. Krames ES, Chapple I, the 8703 W Catheter Study Group. Reliability and clinical utility of an implanted intraspinal catheter used in the treatment of spasticity and pain. Neuromodulation 2000; 3:7–14. 44. Follett KA, Burchiel K, Deer T, et al. Prevention of intrathecal drug delivery catheterrelated complications. Neuromodulation 2003; 6(1):32–41. 45. York M, Paice JA. Treatment of low back pain with intraspinal opioids delivered via implanted pumps. Orthop Nurs 1998; 17:61–69. 46. van Dongen RT, Crul BJ, DeBock M. Long-term intrathecal infusion of morphine and morphine/bupivacaine mixtures in the treatment of cancer pain: A retrospective analysis of 51 cases. Pain 1993; 55:119–123. 47. van Dongen RT, Crul BJ, van Egmond J. Intrathecal coadministration of bupivacaine diminishes morphine dose progression during long-term intrathecal infusion in cancer patients. Clin J Pain 1999; 15:166–172. 48. Eisenach JC, DuPen S, Dubois M, et al. Epidural clonidine analgesia for intractable cancer pain. Pain 1995; 61:391–399. 49. Hassenbusch SJ. Epidural and subarachnoid administration of opioids for nonmalignant pain: Technical issues, current approaches, and novel treatments. J Pain Symptom Manage 1996; 11:357–362. 50. Krames ES. Intrathecal infusion therapies for intractable pain: Patient management guidelines. J Pain Symptom Manage 1993; 8:36–46. 51. Guo TZ, Jiang JY, Buttermann AE, et al. Dexmedetomidine injection into the locus ceruleus produces antinociception. Anesthesiology 1996; 84:873–881. 52. Kalso EA, Poyhia R, Rosenberg PM. Spinal antinociception by dexmedetomidine, a highly selective alpha 2-adrenergic agonist. Pharmacol Toxicol 1991; 68:140–143.

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53. Meert TF, De Kock M. Potentiation of the analgesic properties of fentanyllike opioids with alpha 2-adrenoceptor agonists in rats. Anesthesiology 1994; 81:677–688.

62. Auld AW, Maki-Jokela A, Murdoch DM. Intraspinal narcotic analgesia: Pain management in the failed laminectomy syndrome. Spine 1987; 12:953–954. 63. Doleys DM, Coleton, Tutak U. Use of intraspinal infusion therapy with non-cancer pain patients: Follow-up and comparison of worker’s compensation vs. nonworker’s compensation patients. Neuromodulation 1998; 1:149–159. 64. Paice JA, Penn RD, Shott S. Intraspinal morphine for chronic pain: A retrospective, multicenter study. J Pain Symptom Manage 1996; 11:71–80. 65. Schuchard M, Lanning R, North R, et al. Neurologic sequelae of intraspinal drug delivery systems: Results of a survey of American implanters of implantable drug delivery systems. Neuromodulation 1998; 1:137–148. 66. Schueler BA, Parrish TB, Lin J-C, et al. MRI compatibility with and visibility assessment of implantable medical devices. J Magn Reson Imaging 1999; 9:596–603. 67. Tutak U, Doleys DM. Intrathecal infusion systems for treatment of chronic low back and leg pain of noncancer origin. South Med J 1996; 89:295–300. 68. Winkelmüller M, Winkelmüller W. Long-term effects of continuous intrathecal opioid treatment in chronic pain of nonmalignant etiology. J Neurosurg 1996; 85:458–467. 69. Smith TJ, Staats PS, Deer T, et al. Randomized clinical trial of an implantable drug delivery system compared with comprehensive medical management for refractory cancer pain: Impact on pain, drug-related toxicity, and survival. J Clin Oncol 2002; 20:4040–4049. 70. Angel IF, Gould HF, Carey ME. Intrathecal morphine pump as a treatment option in chronic pain of nonmalignant origin. Surg Neurol 1998; 49:92–98. 71. Deer T, Chapple I, Classen A, et al. Intrathecal drug delivery for treatment of chronic low back pain: Report from the National Outcomes Registry for Low Back Pain. Pain Med 2004; 5:6–13. 72. Naumann C, Erdine S, Koulousakis A, et al. Drug adverse events and system complications of intrathecal opioid delivery for pain: Origins, detection, manifestations, and management. Neuromodulation 1999; 2:92–107. 72a. Deer T, Krames ES, Hassenbusch S, et al. Management of intrathecal catheter-tip inflammatory masses: an updated 2007 Consensus Statement from an Expert Panel. In Press, 2007. 73. Koulousakis A, Imdahl M, Weber M. Continuous intrathecal application of morphine in cancer pain. Proceedings of the 8th World Congress, 1998. 74. North RB, Cutchis PN, Epstein JA, et al. Spinal cord compression complicating subarachnoid infusion of morphine: Case report and laboratory experience. Neurosurgery 1991; 29:778–784. 75. Coffey RJ, Burchiel K. Inflammatory mass lesions associated with intrathecal drug infusion catheters: Report and observations on 41 patients. Neurosurgery 2002; 50:78–87. 76. Hassenbusch S, Burchiel K, Coffey R, et al. Management of intrathecal catheter-tip inflammatory masses: A consensus statement. Pain Med 2002; 3:313–323. 77 Deer T, Krames ES, Hassenbusch S, et al. Experimental drugs for intrathecal pain management: a review and update from the Interdisciplinary Polyanalgesic Consensus Conference 2007. In press, 2007.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic and Lumbar

CHAPTER

Spinal Ablative Techniques for the Treatment of Chronic Pain Conditions

109

Julius Fernandez and Claudio A. Feler

INTRODUCTION

The diagnosis of pain

The interruption of pathways of the nervous system concerned with pain is a classical approach to the relief of intractable pain disorders, which stems from neurosurgeons having been trained with a primary understanding of anatomy and, to a lesser extent, an appreciation of neurophysiology. While successful when implemented in the correct clinical setting, there have also been significant complications with these procedures, including return of pain and sometimes worsening of pain, and/or the evolution of neuropathic pain syndromes in many patients treated with these procedures. The use of ablative techniques has long been a viable treatment option in many patients; however, today there is reluctance in implementing these procedures in favor of neuromodulation. The latter methods of pain management offer the benefits of reversibility and increased safety. Though many of the alternative ablative techniques have become infrequently used, they can continue to play a role in chronic pain management. The purpose of this chapter is to provide to the reader an overview of chronic pain as well as to revisit neurosurgical ablative techniques in the spinal axis that may be of utility when attempting to manage patients. Procedures to be revisited are: spinal rhizotomies and ganglionectomies; dorsal root entry zone lesioning (DREZ); open and pecutaneous anterolateral cordotomy; midline/ commissural myelotomy; cordectomy; sympathectomy; and facet rhizotomy.

The primary phase in evaluating a patient experiencing pain begins with a targeted history and physical examination. This will lead to a better understanding of the abnormal physiologic and anatomic structures as a first step to appreciating and treating the pathologic state in the patient. The use of vague terms such as ‘failed back surgery syndrome’ or ‘cancer pain’ is of limited use. A full appreciation of taxonomy and classification of painful conditions is required in order to define specific therapy in any given patient. Patients may present to a pain management physician for reasons other than somatic pain. The physician will need to navigate through both psychologic and physical issues that a pain patient may have. The duration of pain is an extremely important issue as this may point to a chronic versus acute condition. Following the chronicity of pain, the location must be noted to help guide the specific intervention as well as occasional subtle elements of those interventions. Treatments aimed at and useful for appendicular pain may not be as useful for midline pain as, for example, unilateral cordotomy. The use of pain descriptors during the targeted history, such as sharp, electriclike, numb, dull, aching, and burning are crucial in focusing on the pain physiology and generators in the patient. Long before the different mechanisms of chronic pain were defined, neurosurgeons distinguished between chronic pain due to cancer and chronic pain of ‘benign’ origin. Currently, a more helpful way to differentiate chronic pain is through physiology: namely, nociceptive and neuropathic pain syndromes. The difference between these two categories is the absence of a continuous nociceptive input through pain receptors in neuropathic pain syndromes. It is key to recognize that a given patient may have features of more than one pain physiology. Weir Mitchell first described and named causalgia as a regional pain disorder associated with both motor and sensory disturbance.9 Since then, many and often confusing terms have been used to describe chronic neuropathic pain syndromes. In 1994, the International Association for the Study of Pain (IASP) adopted the term complex regional pain syndrome (CRPS) to replace the terms reflex sympathetic dystrophy (RSD) and causalgia.10 Complex regional pain syndrome is further divided into type 1 and type 2, representing RSD and causaglia, respectively. CRPS may exist in a state of flux and, regardless of whether the patient suffers from CRPS 1 or 2, there may be sympathetically maintained and independent features involved. While many theories exist, the definitive pathophysiology and etiology of CPRS remains unclear. A correct physiologic diagnosis can only be obtained through detailed history and physical examination. It may be necessary to obtain diagnostic studies such as computed tomography (CT) scan, margnetic resonance imaging (MRI), and electromyogram/nerve conduction velocity (EMG/NCV). Diagnostic spinal procedures such as

Historical aspects of pain management The origin of the word ‘pain’ is the Latin word poena, meaning punishment. The early concept of pain as a form of punishment for sinful activities is as old as humankind.1 Early healers used a wide range of modalities to attempt the control of pain, including herbal medicines and the application of electric fish.2 Decartes’ description of pain conduction from peripheral damage through nerves to the brain led to the first scientific understanding of pain.3 The first plausible surgical management of pain was on an anatomic basis where nerves were cut in attempts to denervate the painful areas of the body. These methods were a direct byproduct of the understanding of pain transmission during the scientific revolution. It was not until the Wall and Melzack Gate Control Theory that a sound scientific basis for pain mechanism was formulated.4 Shortly thereafter, initial efforts were made to modulate pain at peripheral nerve, spinal cord,5,6 and other targets such as brain stem7 and, more recently, the cerebral cortex.8 Despite their long history, destructive pain techniques may continue to fall into disuse as further understanding of the pain system and its physiology becomes more sophisticated.

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selective root blocks, sympathetic blocks, and discography will often further aid the clinician. There is no confirmatory test or procedure for CRPS 1, and this diagnosis can only be attained through a clinical examination. An early and specific refinement of the pain diagnosis is necessary and valuable, as it directs care of the patient.

cated for treating extremity pain in a functional limb, as complete or near-complete functional paralysis will occur because of absence of sensory input. Extensive sectioning of sacral posterior root also needs to be performed with selectivity as interference with sphincter and sexual function can occur.

Preablative therapy evaluation

Pertinent anatomy

Prior to performing an ablative technique on any patient, one should perform a thorough history and physical examination and a review of the available studies before a presumptive clinical diagnosis can be made. A series of diagnostic blocks can then be utilized to further develop a line of reasoning supportive of an ablative technique. It is imperative to distinguish patients experiencing nociceptive pain and those who present with neuropathic pain syndromes. The successful treatment of chronic pain should follow a logical algorithm, beginning with the correct diagnosis. Failure to select the appropriate treatment for a patient will lead to inadequate pain relief and unsatisfactory patient care. Simulation of the ablation can be accomplished through pharmacology and should always precede destructive and irreversible procedures. To best serve a patient, these authors believe that the diagnostic blocks necessary should be performed by the physician who will ultimately perform the definitive ablation so that correct patient selection and therapy can be rendered.

The spinal root anatomy begins with the formation of the anterior roots, which are formed by three to five rootlets emerging from the anterolateral sulcus; the posterior roots are formed by three to ten rootlets which penetrate into the dorsolateral sulcus (Fig. 109.1). The dorsal and ventral roots are separated by the dentate ligaments, though they are grouped together prior to leaving the thecal sac. Microscopic anastomotic branches exist that pass from one rootlet to another. As the roots approach the intervertebral foramen, both the ventral and dorsal roots are situated in a common dural sleeve. In the intervertebral foramen the dorsal ganglion can be identified. At this point the subarachnoid space is sealed by the arachnoid trabeculae and no cerebrospinal fluid (CSF) is contained.19 Distal to the dorsal ganglion and lateral to the foramen, the spinal nerve is formed which will then bifurcate into ventral and dorsal branches.

SPINAL RHIZOTOMIES AND GANGLIONECTOMIES Historical background Dorsal root rhizotomy was first attempted for the relief of intractable pain by Abbe in 1889.11 The operation was based on the concept that afferent signals are conveyed via the dorsal roots while efferent signals are conveyed via the ventral roots.12,13 There now exists a large body of evidence supporting the existence of as much as 30% afferent axons passing through the ventral roots.14–16 Dorsal rhizotomies or ganglionectomies are primarily indicated for treatment of pain syndromes involving the neck, trunk, abdomen, and perineal region. Persistent post-thoracotomy or postlaparotomy pain is a frequent indication for these procedures, as well as treating malignant pain syndromes from pleural based or apical lung lesions. Several variations of spinal root surgery have been developed over the century, though the methods have experienced a long decline due to the disappointing outcomes of most series.17,18 The procedure is contraindi-

Procedure Prior to the procedure, a selective nerve root block may aid in determining if rhizotomy or ganglionectomy may provide any benefit. The operation is performed under general anesthesia with the patient in the prone position and may be performed via an intradural (dorsal rhizotomy) or extradural (ganglionectomy) approach. The desired spinal segments are exposed. In the case of dorsal rhizotomies, laminectomies are performed and a midline dural opening is made. The dorsal rootlets of the desired segments are then sectioned sharply. A technique described by Sindou in 1972 aimed to interrupt selectively small-diameter nociceptive fibers at their radicular entrance into the spinal cord.20 This technique of selective dorsal root rhizotomy allows for preservation of lemniscal fibers that may avoid secondary appearance of pain and leave intact substrates that can be utilized for neuromodulatory procedures.21 For ganglionectomies, foraminotomies are performed to expose the desired dorsal root ganglia. The ganglia are then carefully dissected free from the surrounding tissue and the dorsal root is divided proximal to the ganglion. Following this, the ganglion is gently elevated and the distal connection to the root is sectioned. In most cases, the ventral root can be spared. Important aspects from a purely technical point of view include verification of the level of lamienctomy, root identification by anatomical, radiographic,

Fig. 109.1 Pertinent anatomy. 1192

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and physiological means, selection of roots by stimulation, recognition of anastomoses between roots, and sparing of radicular arteries. Other technical variants exist such as extradural spinal root ganglion resection as described by Scoville in 1966, which avoid the opening of the dura. An alternative to the open surgical technique’s proximal radiofrequency thermocoagulation of primary spinal trunk and ganglion has been described; Uematse et al. proposed a percutaneous technique for lesioning the dorsal root ganglion and rootlets.22

Outcomes The variability of clinical results of posterior rhizotomy and ganglionectomy warrants the cautious use of these denervation interventions and should only be used after nondestructive techniques have been exhausted. For lumbar radiculopathies, there is about a 30% success rate at 1 year.23 The results for postherpetic neuralgia are no better, with success rates at less than 30%.24 And the results for non-specific relief of chronic pain are extremely poor in the long term.25 A review of the literature reveals that results are generally less than 50% for good pain reduction with limited long-term follow-up. Unfortunately, these procedures produce a complete denervation of one or more spinal segments, thus precluding the patient from potential future neuromodulation. Because of this, and the general availability of long-acting opiate analgesics, these procedures are not generally recommended.

DORSAL ROOT ENTRY ZONE LESIONS (DREZOTOMY)

Dorsal root rhizotomy Dorsal root ganglion Spinal nerve

Ganglionectomy

Gray rami communicantes White rami communicantes Thoracic paravertebral sympathectomy Sympathetic trunk Dorsal ramus Thoracic sympathetic ganglion Greater splanchnic nerve Facet denervation

Historical background During the early 1960s, research into pain focused attention on the dorsal root entry zone (DREZ) as the first level of modulation for the cessation of pain.26 What is known of these pathological mechanisms is that the cells in the dorsal root ganglion become hyperactive and send nociceptive impulses via the spinothalamic pathways. Based on this understanding, Sindou performed the first DREZ operation in 1972 for pain caused by Pancoast-Tobias syndrome.27 Others such as Nashold and Ostdahl placed thermal lesions into the substantia gelatinosa of the spinal cord for the treatment of nonmalignant pain.28 In view of the complex anatomy and lack of histological confirmation, the target was referred to as the DREZ. This region in the spinal cord is currently recognized as a sophisticated structure for the modulation of pain and continues to be utilized for ablative techniques, either open or percutaneous.

Pertinent anatomy Using cytoarchitectural criteria, in 1952 Rexed divided the gray matter of the spinal cord of the cat into ten separate cell layers. Similar laminar patterns were confirmed by Schoenen.29 The uppermost lamina (I–V) are pertinent to the DREZ procedure. The major nociceptive input is distributed to layers I, II, and V (layers I and II representing the substantia gelatinosa), with their second-order neurons giving rise to the spinothalamic tract. Neurons in layers III and IV receive non-noxious inputs from the periphery and project to the dorsal column nuclei. Situated dorsolateral to the dorsal horn is the tract of Lissauer, an intersegmental longitudinal spinal tract with multiple collaterals to Rexed layers I and II. This tract plays an important role in the intersegmental modulation of the nociceptive afferents. Its medial part transmits the excitatory effects of each dorsal root to the adjacent segments and its lateral part conveys inhibitory influences to the substantia gelatinosa.30 The DREZ procedure is directed

Lesion locations = Fig 109.2 Thoracic spine anatomy.

at destroying the Rexed layers I, II, and V and the medial portion of the tract of Lissauer which coordinates sensory information.

Procedure The surgical technique of thermal coagulation for DREZ lesions has been described in detail by Nashold and collaborators and extensively published.31 With the patient placed under general anesthesia and in the prone position, laminectomies or hemilaminectomies are performed over the involved regions of the spinal cord. In the cervical region, the localization of the appropriate level is one level rostal to the dermatomal localization, and in the thoracic region two to three veterbral segments rostal to the affected dermatomes (Fig. 109.2). Lumbar and sacral segments are localized through laminectomies at T10 through L1 for exposure of the conus medullaris. The operating microscope is utilized throughout the procedure following the dural opening. Each dorsal root is composed of several small rootlets which enter the cord at the postointermediolateral sulcus at the margin of the dorsal columns. Identification of the root and corresponding cord level can be confirmed with electrophysiologic monitoring. Following the identification of the rootlets of each root, though this may be difficult at the level of the conus, the lesions are made in the dorsal root entry zone. The lesions are created over an additional one to two segments above and below the affected roots to ensure adequate coverage of the painful segments. Bilateral lesioning should be avoided in patients with 1193

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good neurologic function below the lesion, as deterioration in proprioception, motor, or bladder and bowel function can occur. Methods for lesioning include: argon and CO2 laser; radiofrequency; bipolar coagulation; and ultrasound. The authors’ preferred method is radiofrequency (RF) ablation, as it allows for uniform size and depth of lesioning. The electrode used is 2 mm in length and 0.25 mm in diameter. It is typically inserted at a 25° angle; however, the point of exit of each dorsal root and its angulation from the spinal cord is the best guide for introduction of the RF electrode. Lesions are made at 75°C for 15 seconds and are made at 1 mm intervals along the length of the spinal cord and segments. Rapid tissue heating, thermal vaporization of the spinal parenchyma, and tissue scaring at the electrode should be avoided. Care must also be taken not to injure any vasculature of the spinal cord in order to avoid ischemic changes or new neurological deficits that may include weakness.

Outcomes The DREZ procedure has been implemented for a large series of deafferentation pain syndromes. Results from several series report a 54–79% success rate for the procedure.32–34 Probably the single best indication for the DREZ lesioning is pain following brachial plexus avulsion. Long-term pain relief for this procedure for brachial plexus avulsion pain reaches 70%.35 The major complication with thoracic spinal DREZ operation is weakness in the ipsilateral leg due to injury of the corticospinal tract; this is seen in 5–10% of patients,36–38 though this may occur with other sites of DREZotomy. While the DREZ operation has been used in an attempt to treat a multitude of pain conditions, its current indications are very specific. It is best used to treat deafferentation pain (as seen with brachial plexus avulsion), limited cancer pain (as seen with a Pancoast tumor), segmental pain after spinal cord injury, peripheral nerve pain (seen with nerve injuries and phantom limb or stump pain), and postherpetic pain.39 These authors do not utilize this procedure, however, for other than segmental pain following spinal cord injury because neuromodulation is commonly usable in most of the other painful phenomenon listed and neuromodulation has a superior safety profile.

OPEN ANTEROLATERAL CORDOTOMY Historical background In 1889, Edinger40 first described the anatomy of the spinothalamic tracts, though functional correlation was not discovered until Spiller reported his findings in 1905.41 The first anterolateral tractotomy was performed by Martin at the suggestion of Spiller in 1911 for management of pain in man.42 Eventually, both in Europe and America, the surgical cordotomy became a standard neurosurgical procedure for the treatment of pain. Mullan43 developed the technique for percutaneous cordotomy using a radioactive strontium needle in 1963 where the lesion can be made without the necessity of general anesthesia. Rosomoff44 further refined the technique using a radiofrequency needle electrode system. Additional refinements to the procedure have included myelography45 to outline landmarks, CT guidance,46 and electrical impedance monitoring.47 While the operation has remained in essence the same as that introduced by Spiller and Martin, much effort over the decades has continued to be devoted to lesioning the anterolateral quadrant of the spinal cord. Both open and percutaneous techniques will be discussed.

Pertinent anatomy Neuroanatomical and physiological aspects of nociceptive pathways have been extensively studied in animals and humans. Within close proximity to the spinothalamic tract lie many other ascending and 1194

descending tracts, damage to which leads to many of the complications of cordotomy. The corticospinal tract is located posteriorly and injury to it results in ipsilateral weakness. Overlying the spinothalamic tract is the ventral spinocerebellar tract and injury of that pathway may produce an ipsilateral ataxia of the arm. Knowledge of the location of descending respiratory pathways is not just theoretical, as one of the most feared complications of a high bilateral cordotomy is respiratory dysfunction. Typically, the patient is capable of voluntary but not involuntary respiration, and consequently dies during sleep because of destruction of the system for automatic respiration (Ondine’s Curse).48

Surgical cordotomy procedure The basic open surgical cordotomy has not changed much since it was first described by Spiller and Martin in 1912.42 The technique is relatively simple; however, it is important to note that the vertebral and spinal cord segments do not correspond. Functional segments of the spinal cord tend to lie two to three levels lower than the vertebrae. The authors’ practice is to perform open cordotomy at the T1–2 or T2–3 segments. Following the laminectomy, the dura is opened in a semicircular manner paramedian to the midline. In order to facilitate rotation of the spinal cord, a dorsal root may be incised as the dentate ligaments above and below the segment are sectioned. The cut end of the dentate ligament is then grasped and the cord is rotated 45° to allow visualization of the anterolateral surface. The origin of the dentate ligament from the cord is a valid landmark for the dorsal extent of the crossed spinothalamic tract. If necessary, a dental mirror can be used to better identify the anterior spinal artery or the medial limits of the ventral rootlets. A cordotomy knife is then inserted at the origin of the ligament, and an incision is made to a point just medial to the emergence of the most medial fibers of the ventral rootlets. Poletti’s technique has increased safety, as he incises the tough pia with a knife and then completes a tractotomy with a ball hook.49 The incision should be deep enough into the cord to transect a pie-shaped segment of about 90°.

Percutaneous cervical cordotomy procedure Mullan et al., in 1963, introduced a procedure to percutaneously perform an anterolateral cordotomy.43 Since the first description, there are have been few technical advances such as CT guidance17 and impedence monitoring.18 The target in percutaneous cordotomy is the lateral spinothalamic tract, located in the anterolateral part of the spinal cord at the C1–2 level, since the interspace is large enough. The patient is placed in the supine position with the upper cervical spine being kept exactly horizontal. Image guidance may consist of either biplanar fluoroscopy or CT scanning. Following the injection of local anesthetic into the skin, the cordotomy needle is inserted inferior to the tip of the mastoid process in a vertical plane perpendicular to the axis of the spinal cord. The needle is then aimed at the location of the dentate ligament, usually the middle of the C1–2 space halfway between the anterior and posterior bony margins. The needle is then further advanced to perforate the ligamentum flavum and dura. Upon perforating the dura, a contrast medium is injected into the subarachnoid space to outline the anatomy of the cord and dentate ligaments. Originally, strontium radioactive source was used, later modified by Rosomoff50 to incorporate radiofrequency ablation. Many authors currently recommend impedance monitoring. An electrode can be inserted through the needle, and impedance measurements taken to confirm the location as the needle passes from CSF into the spinal cord. Electrical impedance measures about 400 ohms when the electrode is in CSF and rises to about 1000 ohms once the cord is

Section 5: Biomechanical Disorders of the Lumbar Spine

entered. Further physiologic localization can then be performed with stimulation. With appropriate localization, contralateral warm or cold sensory effects are induced at 100 Hz. Ideal placement is generally 1–3 mm anterior to the dentate ligament, with upper extremity fibers tending to be more anterior. A test lesion is then generally made with an electrode tip temperature of 50–60°C. Close monitoring of contralateral motor function must be performed. If no untoward side effects are noted, a permanent lesion is then made at 70–80°C for 60 seconds. It is highly recommended following high cervical cordotomy to monitor these patients’ respiratory status for approximately 5–7 days, as an unintended unilateral lesion may actually represent a bilateral lesion.

Lower cervical cordotomy procedure Lin et al. describe an anterior approach for percutaneous lower cervical cordotomy, thus attempting to avoid phrenic nerve fibers and the dreaded respiratory complications of high cervical cordotomies.51 It involves an anterior transdiscal approach to the lower anterolateral cervical cord, producing a lesion in the spinothalamic tract. This transdiscal technique can be difficult to achieve if the needle should be redirected in the event it does not hit the target. The patient is positioned supine with the neck slightly extended. The needle is then inserted under local anesthetic between the carotid sheath and tracheoesophageal complex. CT or biplanar fluoroscopy is used for guidance. The needle is usually directed towards the C5–6 disc space. Once the needle is passed through the disc space and dura, contrast can be injected into the subarachnoid space. For pain involving the lower extremity, the target is 8 mm lateral and 5 mm anterior to the posterior wall of the canal. For trunk pain, the lesion is 3 mm lateral and 8 mm anterior to the posterior wall. The trajectory is either calculated or determined graphically. As with the high cervical cordotomy, impedance monitoring and stimulation can be performed to confirm physiological localization. The RF lesion is then created as described above.

Outcomes These procedures are not commonly employed for benign chronic pain syndromes, as newer therapies that include long-acting opiates delivered through intraspinal or intraventricular routes or neuromodulation techniques have become first-line therapies. The results for the various cordotomy procedures are fairly similar; however, lower complication rates are seen with the percutaneous approach.52 For open surgical cordotomy, approximately 50% of patients with cancer pain have complete relief and an additional 25% will have significant reduction in pain.20 By 6 months, however, pain will return in half of the initially successfully treated patients.21 After high percutaneous cordotomy, 60–70% have complete relief and 80–90% have significant relief.53–55 As with surgical cordotomy, these results tend to drop at 1 year.28,56 The results for low anterior cordotomy are similar, with 75–80% of patients experiencing significant pain relief.57 Although cordotomy has initially been used to treat all types of pain, it is now reserved for pain of malignant origin. Studies show that 80% of patients undergoing cordotomy have significant relief of their pain, though at 1-year follow-up only 40% have any pain reduction.36,58 The highest level of analgesia that can be reliably and persistently obtained with high cervical cordotomy is the C5 dermatome and is generally not effective for pain due to head and neck cancers. Lesions above C5 may be treated with a mesencephalic tractotomy. Bilateral cordotomy is reserved primarily for midline abdominal and pelvic pain or bilateral lower extremity pain, though not recommend secondary to the risk of Ondine’s Curse.37,59

The complication rates of the various techniques differ, though with surgical cordotomy there is an 8% mortality rate27 and 13% incidence of lower extremity weakness.38 Complications for high cervical cordotomy include a 1–5% mortality rate,60 4–8% incidence of lower extremity paresis or ataxia,34 and a 5% incidence of bladder dysfunction.34 The complications for low cervical cordotomy are similar to the higher posterior approaches with except of the phrenic and respiratory tract injury.32

MIDLINE/COMMISSURAL MYELOTOMY Historical background Midline or commissural myelotomy is a procedure in which the decussating fibers of the spinothalamic tract are interrupted as they cross in the anterior white commissure of the spinal cord. The procedure was conceived as an alternative to bilateral anterolateral cordotomy in patients in whom a bilateral area on analgesia was sought. The procedure was first described by Hitchcock in 1970.61 During a planned percutaneous cervical cordotomy, the electrode was inadvertently inserted into the center of the spinal cord in the upper cervical region. The patient had immediate relief of pain, and the relief lasted when only a small lesion was made at the site. This target was adopted for central myelotomy, and other patients had similar successful relief of pain with this technique. The results tended to be best in those patients with midline or visceral pain. This led some to conclude that a previously undescribed pathway ascends at the center of the spinal cord and carries predominately visceral pain perception. The technique was later refined by Gildenberg and Hirshberg,62 who felt that there was no advantage to making a high cervical lesion for patients with pelvic or perineal pain. Interruption of the central cord at the lumbothoracic level provided similar results. Today, limited myelotomy is most commonly performed for pelvic pain related to rectal or uterine cancer.

Pertinent anatomy On the anterior surface of the spinal cord there can be identified a deep anterior median fissure which penetrates the spinal cord. On the posterior surface, a small posterior median sulcus is continuous with a glial partition. The spinothalamic fibers cross in the anterior white commissure in a decussion that involves several spinal segments and ascend contralaterally. The intent of the myelotomy is to interrupt the paleospinothalamic tract, producing analgesia with preserved ability to localize and discriminate between sharp and dull sensation.63

Procedure It is important to note that the vertebral and spinal cord segments do not correspond. Functional segments of the spinal cord tend to lie two to three levels lower than the vertebrae. With this in mind, the lamina overlying the spinal segments targeted for denervation are identified with the aid of fluoroscopy. Laminectomies are then performed and the dura is opened to expose the spinal cord. The midline can be identified by the vessels diving into the posterior median sulcus between the posterior columns. The pia is then opened sharply and the posterior median septum is identified. The septum is a single fibrous layer that lies between the posterior columns, and one can dissect along either side of it to the central canal area. Dissection continues until the anterior median septum is encountered. This represents the ventral extent of the myelotomy, as further dissection risks injury to the anterior spinal artery. Various other techniques have been reported, including radiofrequency and carbon dioxide laser techniques.64 1195

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Outcomes Midline myelotomy is most effective for pain in the lower portion of the body, especially midline visceral pain. The overall efficacy of midline myelotomy has been reported in the order of 70%.65–67 There are, however, several undesirable side effects of the procedure, such as hyperesthesia, diminished proprioception, parasthesias, and incoordination of gait.68 A reduction in side effects has been reported by performing a limited myelotomy versus the classic midline myelotomy technique. The difficulty with comparing reports stems from the controversy of the depth of cut. Neither the limited and classic myelotomy technique is performed with any frequency, limiting the role of these techniques for chronic pain management.

CORDECTOMY Historical background Armour, in 1916, performed the first cordectomy for pain in a posttraumatic paraplegic.69 Prior to this, cordectomy had been formed for other indications including intramedullary spinal cord tumors, severe spasticity, and post-traumatic syringomyelia.

Procedure The technique for cordectomy is rarely performed, as many of the indications for this procedure have found newer nondestructive therapies. Intrathecal baclofen pumps have rendered cordectomy obsolete for uncontrolled leg spasticity. Shunts have also supplanted the cordectomy for the therapy of syringomyelia. There are several techniques of cordectomy, though the majority of techniques have described multilevel segmental resection of spinal cord at the level of injury. Segments have been reported from 2.5 cm to 21 cm of spinal cord. In the literature there is no standard technique, as the number of cases performed is few.

Outcomes The clinical indications for cordectomy are varied, including posttraumatic syringomyelia, uncontrollable leg spasticity, and post-traumatic spontaneous neurogenic leg pain. The operation of selective spinal cordectomy is rarely performed. Jefferson, in 1983, reported his series of 19 cases of cordectomy with adequate pain relief in traumatic paraplegics.70 Clinical results in the patients with syringomyelia and uncontrollable leg spasticity have been excellent, though cordectomy did not provide permanent relief in the patients with neurogenic leg pain.71

SYMPATHECTOMY Background Surgery on the sympathetic nervous system dates to the late nineteenth century. The functional role of the autonomic nervous system was poorly understood, and early sympathectomies were performed for such varied disorders as epilepsy, vascular disease, and spasticity. By 1930, thoracic and lumbar sympathectomies were being performed for angina, hypertension, and pain.72 While many of these are no longer indications due to the advent of modern pharmaceuticals and surgical techniques, sympathetically maintained pain remains one of the few indications for a sympathectomy other than hyperhidrosis. Currently, sympathetic denervation for pain is carried out for three main sites of pain: the heart, the limbs, and the abdominal viscera. Sympathetically mediated pain includes a wide spectrum of disorders that share in common the factor that the pain can be relieved through sympathetic block or interruption.73 The most common indications for the procedure are reflex sympathetic dystrophy (RSD)/ Sudeck’s 1196

atrophy, causalgia, and ischemic pain states from occlusive vascular disorders. These conditions can be sympathetically mediated pain syndromes and generally respond to sympathetic blocks with local anesthetics. Sympathectomy should not be considered unless there is good relief with the diagnostic block. Often, lasting relief can be achieved with a series of blocks if they are performed early in the progression of the disease. Visceral pain secondary to unresectable cancers of the abdominal visera and painful relapsing chronic pancreatitis are some of the indication for sympathectomy.46,74 Pancreatic afferents travel bilaterally through the splanchnic chain and into the lower thoracic sympathetic ganglia. The biliary tract is supplied by the right splanchnic nerves and each kidney is supplied unilaterally by the nerves on that side. Attempts at chemical sympathectomy of the celiac plexus and splanchnic nerves during exploratory laparotomy, or percutaneously, have had good initial pain relief though poor localization, and the diffuse target make it difficult to assess the completeness of denervation.75

Pertinent anatomy The paravertebral sympathetic trunk extends from the coccyx to the base of the skull. The cervical sympathetic can be divided into three regions: superior, middle, and cervicothoracic (stellate) ganglia. The stellate ganglion is a fusion of the lower cervical and first thoracic ganglia located at the level of the sixth cervical vertebra. The sympathetic innervation to the upper extremity is from preganglionic fibers exiting the T2–10 roots and traveling through the sympathetic chain to the upper thoracic and cervical ganglia. The sympathetic innervation to the lower extremity arises in the lower thoracic cord and travels down the chain into five lumbar ganglia. The splanchnic nerves receive their sympathetic supply from the T4–12 segments, with the lesser splanchnic nerve being mostly from T10–12 and the greater from T4–9. Denervation of the pancreas can be accomplished by bilateral resection of the T9–12 ganglia along with the greater, lesser, and least splanchnic nerves.

Upper thoracic ganglionectomy procedure Sympathetic activity can be interrupted by lesioning the paravertebral sympathetic chain along its course. This can be achieved either by direct/endoscopic surgical resection or through chemical or radiofrequency ablation. Resection of the T2 and T3 ganglia should result in complete sympathetic denervation to the upper extremity.76,77 The most common surgical approach is through a midline incision with the patient in the prone position, which allows for bilateral exposure and lesioning. After a subperiosteal dissection of the muscles, the T3 lamina and rib are identified with the use of fluoroscopy. The transverse process and medial portion of the rib are then resected. The second and third sympathetic ganglia should be found in the paravertebral fat and sectioned at the ganglia; a Horner’s syndrome can generally be avoided. Alternative approaches include the anterior transthoracic, percutaneous radiofrequency, and transaxillary exposure.78 Here, a rib-spreading incision is made low in the axilla between the third and fourth ribs, and the lung must temporarily be collapsed. The thoracic chain can be identified beneath the pleura alongside the vertebrae. Lastly, the procedure can be performed through a supraclavicular approach.48 The lower cervical and upper thoracic sympathetic ganglia can be found in the fatty tissues deep and medial to the sublclavian artery.

Lumbar sympathectomy procedure The operation is performed through a retroperioneal approach through a flank incision.46,79 The external oblique, internal oblique, and transverse muscles are divided in the direction of their fibers in order

Section 5: Biomechanical Disorders of the Lumbar Spine

to reach the retroperitoneal space alongside the psoas muscle. The ureter is identified and carefully elevated from the vertebral column. The sympathetic chain should be encountered between the psoas and vertebral bodies. The ganglia and their rami communicantes can then be segmentally resected. Removal of the L2 and L3 sympathetic ganglion is usually adequate to remove sympathetic tone from the lower extremities. Male patients should be warned that sexual dysfunction may occur with bilateral lumbosacral sympathectomy.

Splanchnicectomy procedure The upper abdominal viscera sends numerous amounts of nociceptive afferents into the spinal cord via the greater and lesser splanchnic nerves. This allows for the effective treatment of pain by denervation of sympathetic tone to the viscera. The patient is positioned prone and an oblique incision is made over the eleventh rib approximately 5 cm from midline. Six centimeters of rib are then resected, starting just lateral to the transverse process. The pleura is carefully stripped away to visualize the lateral aspects of the vertebral bodies. The sympathetic ganglia are identified ventral to the intercostal nerves. The sympathetic chain and T9–12 ganglia, along with the three splanchnic nerves, are then resected. For pancreatic pain, the procedure must be done bilaterally.46,47,80 Further modifications have been reported with the use of endoscopic procedures performed by thoracic surgeons.

Outcomes The indications for open sympathectomy have decreased steadily over the past decades as pharmacological substances have supplanted these aggressive surgical techniques. The results of sympathectomy for pain disorders have yielded modest success. Most authors report sustained pain relief in less than two-thirds of patients at 2 years, and about one-third at 5 years.46,47,51,81,82 The adequate and limited long-term outcomes should give consideration to either repetitive blocks or other neuromodulatory methods that are nondestructive.

RADIOFREQUENCY FACET DENERVATION Historical background Shealy first described the application of radiofrequency to the facet joint for the treatment of spinal pain.83 Prior to Shealy, Goldthwait 84 and others85,86 initiated interest in the neuroanatomy of the facet joint and its origin of nociceptive lumbar pain. In 1971, Rees published a specific method of attempting facet denervation to modulate back pain.87 Others later suggested that the knife that had been used by Rees was, however, too short to have produced a lesion to the innervation of the facet, being long enough to only produce a myofasciotomy.88 In 1979 and 1980, Bogduk and Long went on to describe a more anatomically correct approach to facet denervation, and their approach is the one used today.89,90 The clinical aspects of facet pain are often non-specific, deep aching paravertebral low back pain referred to a nondermatomal distribution. Because of the non-specific symptoms and lack of confirmatory images or examinations, all patients should undergo a diagnostic block.

Pertinent anatomy The facet joint innervation arises from the posterior ramus of multiple nerve roots. The nerve which appears to be most closely associated with the joint is the medial branch of the dorsal primary ramus. The dorsal ramus branches off the segmental nerve immediately after

exiting the foramen. It then continues posteriorly by piercing the intertransverse ligament and subsequently divides into a medial and lateral branch. The medial branch runs caudally and dorsally, lying against the bone at the junction of the root of the transverse process and superior articular process.

Procedure The procedure is performed percutaneously and is usually preceded by temporary pharmacological blocks. The patient is positioned in the prone position with a pillow or foam wedge supporting the lower abdominal region. Fluoroscopy is utilized throughout for adequate anatomic localization of the target. Intravenous sedation is typically employed to remove any anxiety during the procedure. The transverse processes (or sacral ala in the case of L5–S1) of the levels to be denervated are identified. Local anesthetic is then infiltrated into the skin and the introducer cannula is inserted to the superior and medial border of the transverse processes (or into the groove between the ala of the sacrum and the superior articular process at the L5–S1 level). This is performed using anteroposterior fluoroscopy; however, it sometimes may be useful to obtain an oblique image (10–15°) to better visualize the medial border of the transverse process. A lateral fluoroscopic image is obtained to ensure that the cannula is not approaching the foraminal canals. Once the cannula is in correct position, electrical stimulation is performed at 50 Hz. Paresthesia to the back, paravertebral, or hip region should be noted when the medial branches at these levels are stimulated. Adequate stimulation should be noted at less than 1 volt at 50 Hz. Next, electrical stimulation is performed at 2 Hz and lower extremity motor fasiculations should be absent at 3 volts. At this point, 1 cc of local anesthetic is injected through each cannula in preparation for the lesion. Thermal lesions are then created at each level for a duration of 90 seconds at a temperature of 80°C.

Outcomes The only randomized, double-blind study on this topic was conducted by Wedley et al; it demonstrated that lumbar facet denervation is clearly superior to placebo.91 The results from radiofrequency facet denervation series vary greatly; however, most studies report success rates of 45–80%.92–95 The wide range of outcomes is likely due to many factors, including differing techniques and localization of target. Result from facet rhizotomies have a tendency to diminish over time96 and may be explained through the regeneration of the medial branch. This relapse of symptoms may be due to regeneration of the medial branch nerve of the posterior ramus. The most common complications are superficial infections and reactions to local anesthetic, though serious complications with root injury may occur with the malpositioning of electrodes.

CONCLUSIONS A systematic multidisciplinary approach is required to treat patients with chronic pain. While ablative spinal techniques offer pain relief in many patients, the use of these methods should be cautiously utilized. Once destructive therapies have been employed, neuromodulatory procedures may be rendered ineffective. With the sophistication of understanding pain physiology, many of these ablative techniques will likely become historical, although several of the aforementioned techniques can continue to play a role in current pain management. We hope that this chapter has presented a procedurally oriented overview of the spinal ablative techniques for the treatment of chronic painful conditions with a major emphasis on clinical decision-making, indications, and efficacy. 1197

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Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBBS-Cervical, Thoracis, and Lumbar ■ i: Functional Restoration

CHAPTER

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History and Principles of Pain Rehabilitation Hubert L. Rosomoff, Renee Steele-Rosomoff and Elsayed Abdel-Moty

INTRODUCTION Pain rehabilitation is a specific form of rehabilitation medicine applied to the management of chronic pain. To qualify, it is important to distinguish between acute and chronic pain. Acute pain is a self-limiting form of noxious stimulation following tissue injury that persists during that period of time during which the body would be expected to repair itself and recover to its preexistent biological status. Chronic pain is a condition which lasts beyond the reparative phase. Secondary physical and behavioral effects develop that create disability and an inability to function. A variety of adverse events tend to be associated with the development of chronic pain including drug abuse, further decreased function, psychiatric abnormalities, multiple unsuccessful surgical interventions, social and economic isolation, and even suicide.1 Through the early 1970s, the primary medical discipline responsible for the treatment of intractable chronic pain fell mainly to neurosurgeons. Their singular focus entailed the performance of complex ablative surgical procedures to destroy neural pain transmission systems. Anesthesiologists complemented this treatment approach with an assortment of nerve blocks. Ultimately, this paradigm failed to produce successful long-term results. As well, the associated side effects and risks of the procedures were often too adverse to justify their routine use. These failures amplified the crux of the problem which was that no single discipline could manage the multifaceted nature of the problem. Recognition of these issues led to the development of an interdisciplinary approach in 1973–1974 by Bonica and associates at the University of Washington in Seattle, and a multidisciplinary approach by Rosomoff and colleagues in Florida at the University of Miami. Soon afterwards, pain societies were founded and pain medicine evolved, accompanied by the growing science of pain and its clinical applications. The road was difficult, because insurers and governmental agencies were reluctant to pay for treatment regimens or evolving techniques which were then too neophytic to have accumulated the data to support medical necessity. More than a decade passed until Medicare, in 1988, published its Appendix §35-21.1, Coverages Issues – Medical Procedures of Pain Rehabilitation, which set the first standard and, ultimately, criteria which other payors would use for reimbursement. Unfortunately, surgical disciplines confounded this approach by developing more complicated operative remedies for which success was claimed, but whose supportive data base was questionable. The burgeoning world of anesthesiologic interventional techniques also claimed success, again unsupported by scientifically reliable data. The rehabilitation model appears to have produced the most acceptable data and, at least, has equal or better outcome results without the risks attending all interventional applications.2

THE NEUROPHYSIOLOGICAL BASIS OF PAIN REHABILITATION In principle, pain is a signal received by the central nervous system from an anatomical, physiological, or pathological source producing a noxious impulse. Correction and restoration of function will result in diminution and cessation of pain perception. Pain rehabilitation enables patients with chronic pain to return to a productive lifestyle. Pain centers or clinics are facilities where patients are sent for the treatment of chronic pain, after conventional management has failed and no further directed disease-oriented care is deemed appropriate.3 Patients who are considered candidates for pain rehabilitation have chronic pain, illness, disability conviction, and are physically and functionally impaired. Pathological abnormalities must be distinguished from dysfunction. Activation must occur before pain is resolved.4,5 Functional restoration is a keystone to pain rehabilitation. It must be multidisciplinary as compared to single treatments or exercises. Stretching, strengthening, physical modalities, aerobic activities, resistive exercises, education, conditioning, mobilization, pacing, biofeedback, relaxation, and other components are included as treatment individually and in combination. Although a pain rehabilitation program is designed for individuals with measurable functional deficit, it may also be appropriate for either the physically active individual or for someone with severe disability where optimization of residual capacities is needed. Patients with chronic pain present a clinical challenge because of the vast time and the diagnostic and therapeutic resources they consume. The pain management approach must be capable of properly identifying patients’ problems whether sensory, perceptual, psychological, psychosocial, environmental, or biomechanical in nature. Treatment goals are to reduce chronicity, prevent re-injury or disability, and restore function, as well as to return the patient to a productive lifestyle.6 The original concept that nerve root compression from a herniated disc produces pain was challenged decades ago when Rosomoff7 presented a series of observations together with clinical and experimental evidence that supported the contention that alternative nonsurgical methods will provide successful treatment even for manifest disc herniations or lumbar stenosis. Physiologic studies demonstrated that, except for a transient painful impulse when the nerve is first impacted, sustained nerve root compression or ‘pinching’ does not produce pain.8 There could be numbness or loss of function, but this is not a painful event. From inspection of human anatomy, it is inescapably clear that all low back injuries must have associated soft tissue abnormalities. Even if the forces causing the injury reach sufficient magnitude to herniate

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or rupture an intervertebral disc, the force must be transmitted first through the surrounding soft tissue that binds the spine together as a functional unit. These tissues, when injured, undergo a breakdown of the cell membranes to arachidonic acid, from which biosynthesis of prostaglandins and associated products ensues. One important issue in this process is the induction of a state of hyperalgesia, following which a pain signal will evolve when excessive mechanical stimulation occurs or when compounds of reaction to injury, such as histamine or bradykinin, are produced.9 The nerve itself does not originate the pain signal; nociceptors are stimulated to initiate the transmission of the signal. It is our thesis that the disordered musculoskeletal system is responsible for initiating these phenomena.3,7,10 These structures are in the surrounding paraspinal muscles, buttocks, hips, and legs. These peripheral sites are treatable by alternative medical approaches. Treatment will restore function and alleviate pain, often without the need for correcting intraspinal abnormalities that have traditionally been designated as the pain generator. Further, a study carried out in 45 000 patients with low back pain indicated that only 1 in 200 of patients may actually need surgical intervention;11 in our experience the number of patients is 1 in 500. Muscular and fascial abnormalities are called myofascial syndromes. They have been well described by Travell and Simons.12 Abnormal movements of the back, restricted ranges of motion in the hips or legs, or the presence of muscle tenderness and/or trigger points, are

seen with myofascial syndromes. These can perpetuate mechanical dysfunction, continued strain, muscle fatigue, and pain.

ALGORITHM FOR PAIN REHABILITATION Although it can be described in discrete phases, rehabilitation is a continuous process of evaluation, treatment, conditioning, and reevaluations. The intensity and duration of each process depends on a variety of parameters including patient’s response, rate of progress, the presence of comorbidities, and the number and type of objectives to be met. The algorithm is depicted in Figure 110.1 and the elements are described below.

Admission criteria To enter the system, the patient undergoes evaluation over a 3-day period. The rehabilitation team attempts to identify the medical, behavioral, vocational, financial, social, and other significant problems. The approach is comprehensive and holistic. Patient selection criteria are broad. The patient must have the ability to understand and carry out instructions, must be compliant and cooperative, and must not have aggressive or disruptive behavior that would disturb the milieu. Patients with schizophrenia, manic-depression, or other major psychiatric disorders are not precluded as long as they are receiving treatment which renders them stable. The patient, the family, and significant others,

START: EARLY REFERRAL TO A MULTIDISCIPLINARY PAIN CENTER WITH FUNCTIONAL RESTORATION COMPONENT

RESTORATION

Phase I

MEDICAL / PHYSICAL Evaluation by physician (request consults if needed)

FUNCTIONAL

Evaluation by physical & massage therapy, MDE

Evaluation by occupational therapy

BEHAVIORAL / EMOTIONAL

Evaluation by psychology

Evaluation by psychiatry

VOCATIONAL Vocational / ergonomic evaluation (if applicable)

2−3 days Contruct and formalize interdisciplinary plan of treatment. Develop key indicators for each area

Phase II 1−2 weeks

Monitor and supervise treatment plan, address comorbidities

Restore ROM, resolve trigger (TP) points & soft tissue management

Restore functional tolerances. Teach body mechanics, pacing, etc.

Council patient and family in pain impact. Teach relaxation

Taper off narcotic medications

Establish goals with patient & employer

Monitor progress and key idicators. Adjust plan of treatment if necessary

Phase III 1−2 weeks

Interventional procedures for unresolved TP

Strengh and endurance traininng

Implement functional circuits, ADL/ IADL training

Train in stress management. Guide through treatment

Monitor compliance with tapering

Finalize multidisciplinary discharge planning / return to work planning / maintenance program

FINISH: RETURN TO WORK OR PRIOR FUNCTION Fig. 110.1 Algorithm for pain rehabilitation.

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Job simulation, work conditioning, job site visit

Section 5: Biomechanical Disorders of the Lumbar Spine

such as the lawyer, the employer, and the insurer must be accepting of vthe program. Worker compensation, liability cases, multiple surgeries, long histories of invalidism, or drug abuse are not exclusionary conditions. Although integral, the financial, legal, and administrative aspects of patient admission are beyond the scope of this chapter. Upon entry, patients are oriented to the program and are made aware of rules, policies, and expectations. Evaluations and observations are made by the various disciplines in order to: 1. Decide if the patient meets the criteria for inclusion into the program; 2. Determine the appropriate diagnosis based on previous medical records and the additional medical, physical, and psychological assessments; 3. Establish a baseline of abilities, limitations, and goals; and 4. Medication intake, dependence, and use must be determined, particularly as it pertains to narcotics. The multidisciplinary team consists of physicians, psychologists, occupational and physical therapists, massage therapists, ergonomists, nurses, vocational counselors, and biofeedback therapists. Assessment of the injured individual by these disciplines considers not just the injury history but also the patient’s physical and behavioral status and vocational issues, if applicable. The outcome of the exhaustive assessment is a constructed, formalized care plan detailing problem areas, treatment strategies, and expected outcomes. Due to the large number of possible findings upon initial assessment, a set of ‘key indicators’ is used to monitor progress towards the final goals. Key indicators may include (1) pain level; (2) number of hours of sleep; (3) pain medications; (4) lifting, carrying, sitting, standing, walking tolerances; (5) ranges of motion of the neck and trunk; (6) straight leg raise; (7) composite hip range of motion; (8) posture; (9) strength; (10) gait; (11) and key behavioral and vocational problems. These indicators are updated on a weekly basis. Phase I may take 2–3 days for interviews and/or evaluations. A team meeting is then held, findings are discussed, and team recommendations are presented to the Medical Director. In a multidisciplinary conference, the Medical Director discusses the findings with the patient and significant other. Team recommendations, clarification of medical concerns, and diagnosis are addressed. Patient questions,

misconceptions, and expectations are also discussed. Admission to the program is contingent upon the patient’s full consent to participate in the process, including tapering from narcotics or other dependence-producing substances.

Activation and physical restoration During this phase, treatment is initiated. A variety of therapeutic approaches are used to restore ranges of motion, resolve trigger points, taper off narcotic medications, and begin the process of education and relearning. Stretching, physical agent modalities, body mechanics training, and behavioral interventions are used to guide the patients through what is probably the most difficult phase of the program. Patients must surmount hurdles of fear, anger, mistrust, and past misconceptions about diagnosis in order to proceed with confidence and acceptance. Education includes topics such as myofascial pain syndrome, relaxation, stress management, and healthy lifestyles. Simultaneously, the patient’s medication is reviewed and a rigorous management program is initiated and monitored, including tapering from narcotics or other dependence-producing drugs. The use of ice and other modalities to alleviate pain are introduced. A daily treatment schedule is designed to accommodate the various treatments and disciplines. A typical treatment schedule for one patient is shown in Table 110.1. The contents of each patient’s schedule vary on a daily basis depending on the stage (week) in treatment, level of activation, and progress. Treatment is provided on a daily basis including Saturdays. At nighttime, patients are assigned ‘homework’; i.e. evening self-paced exercises determined by the treating therapist and monitored by nursing staff. A very effective tool in this phase is the concept of daily goals, final goal setting, and self-monitoring. Computerized modeling is used to determine optimal pathways a patient should follow during rehabilitation. The model utilizes statistical projection methods, which take into consideration the patient’s initial performance level and the desired goals.13 This nonlinear model derives its coefficients from retrospective data collected from over 1000 patients with chronic pain who successfully completed the 4-week rehabilitation and functional restoration program, and who have returned to a productive lifestyle. Once initial levels of performance have been

Table 110.1: Typical daily treatment schedule Patient name

___________________________________

Time

Activity

8:00–8:30

Movement therapy, warm up, low-impact aerobics

8:30–10:00

Physical therapy, stretching, modalities, back exercises, functional electrical stimulation, active exercises, gait training, flare-up procedures

10:00–11:30

Occupational therapy, body mechanics training, biofeedback, functional circuits, pacing, walking, climbing, lifting, carrying, pushing/pulling, reaching, safety, joint protection, ADL training

11:30–12:00

Psychological counseling, family counseling, stress management, breathing exercises, hypnosis, vocational counseling, vocational preparation, case management

12:00–1:00

Lunch break

1:00–1:30

Strength and cardiovascular training

1:30–2:00

Neuromuscular massage therapy

2:00–3:00

Occupational therapy, upper extremity activities exercises, educational activities, work simulation

3:00–4:00

Group activity, educational sessions

4:00

Evening activities, recreational activities

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measured and treatment goals have been determined, the daily goals are assigned to provide a personalized print-out of the expected ‘daily’ performance. The daily goals program provides daily increments for the patient’s therapeutic activities. The optimal progression printout from initial tolerances to final goals is used by the patient and the treating staff to determine effects needed to achieve the desired daily performance throughout treatment. On a weekly basis or sooner, if necessary, a team conference reviews the patient’s progress and level of participation; and the team determines if the program should be continued, modified, or terminated. Behavioral issues are addressed early. The patient must be in agreement with the treatment plan. The building blocks for the postdischarge maintenance program also start during this phase.

Rehabilitation for lifestyle and work restoration Job simulation is an important concept with respect to return to work. In conjunction with the vocational counselor, job tasks are reviewed with the patient to determine which must be simulated if there is to be a successful return to work. Conferences with the employer and job site visits may be necessary to form the plan. Once the simulation demands are determined, the patient is taught to perform tasks safely to restore confidence and prevent reinjury. This allows the treating physician to certify that the patient can safely handle the job. If a patient’s care plan does not include return to work, functional circuits and realistic lifestyle simulations are utilized to return the patient to those functional levels that will allow comfort and safety.

EVALUATION OF FUNCTIONAL DISABILITY Objective measurements are utilized to determine physical condition, functional abilities, behavioral health, vocational parameters, and other patient attributes relevant to the rehabilitation process. Methods of measuring functional capacity fall under three main categories: (1) patient’s self-report of functional levels, which provides information about the perception of how much the patient believes he can or cannot do; (2) medical examination to provide an estimate of medical impairment; and (3) assessment of abilities or limitations producing quantifiable measures reflecting the level of performance, in comparison with performance levels of healthy subjects (e.g. norms) or the match to job/task demands.

Physician evaluation The entry to evaluation and treatment is through the physician. The physician must obtain a detailed, accurate history. The mechanism of injury and the precise location of the pain at onset are critical. A neurologic examination evaluates reflexes, muscle strength, and sensory status to document the presence or absence of neurologic deficits.14 Although neurologic screening is essential, it is most often not significantly positive. In fact, only 1% of individuals have neurologic dysfunction which is reversible usually and, therefore, should not be considered as a pathological deficit. The soft tissue examination must be sophisticated and thorough.15 All musculoskeletal and myofascial abnormalities must be identified. This is particularly important, since myofascial syndromes may simulate neurological syndromes, particularly radiculopathies. The straight leg raising (SLR) test may produce leg pain considered to be indicative of irritated nerve roots, but this occurs even more regularly with myofascial syndromes. Contractures of the hip musculature, particularly the hip rotators, are common and disabling with standing or walking, so that restricted ranges of motion about the hips are not necessarily an indicator of articular disease. Palpable soft tissue tenderness by itself, again, is thought by some to be less specific or reliable, but, to reiterate, tender/trigger 1204

points and restricted ranges of motion are the hallmark of myofascial syndromes and must be sought so they can be identified and treated. They are, in fact, objective findings. Simple laboratory tests, including blood count and erythrocyte sedimentation rate, are sufficiently inexpensive and efficacious for use as initial tests when there is suspicion of back-related pathology, such as tumor or infection. Lastly, special tests such as radiographs, imaging techniques, electrodiagnostics, thermography, and discography should be reviewed or recommended, if deemed necessary, but should be interpreted with extreme caution.10

Motor dysfunction evaluation This is a method developed to identify and effectively treat ‘motor’ dysfunction in patients with chronic pain conditions.16 This innovative testing utilizes on-line computerized electromyographic (EMG) methods to study recruitment of muscles involved in a chain of motor activities.17 This method may detect functional muscular abnormalities that cannot be identified by clinical examination, even by experienced observers. The EMG signals of the various muscles are examined for baseline activity, symmetry, magnitude, frequency contents, synchrony, timing, and patterns. Patients’ behaviors are also observed. Motor dysfunction evaluation (MDE) findings are then compared to relevant clinical findings. Patient-specific, as well as condition-specific, multidisciplinary approaches are then generated to deal with the problems during daily treatment. The overall objective is to improve function and accelerate restoration. This is accomplished through using EMG and other electrically assisted methods to increase sensory perception of muscles and joints; increase neuromuscular recruitment; increase strength and endurance; and reestablish synchrony, symmetry, pattern, and synergy of muscle activity, thereby increasing functional capacities and reduction of pain.

Physical therapy evaluation This type of evaluation emphasizes the different aspects of the soft tissues and the musculoskeletal system such as muscle tone and strength, ranges of motion, gait, spasm, swelling, pain pattern, etc. Physical examination in this category evaluates muscle strength, which is reported on a scale from 0 (no strength) to 5 (normal strength). While yielding numerical data, these measurements are to some degree subjective. Recently, new technology has enabled the introduction of testing equipment such as electronic goniometers and muscle testing machines that permit quantitative measurement of human functions.

Occupational therapy evaluation Occupational therapy evaluation determines functional levels, such as sitting, standing and walking tolerances; posture, balance and coordination; risk of falling; stair climbing; carrying and lifting, pushing and pulling; self-care, especially activities of daily living, socialization, driving, and other vocational and leisure activities. Descriptive information about the degree of independence, physical tolerances, endurance, speed, and attitude of the patient are established. The assessment of proper body mechanics is key.

Behavioral therapy/psychological evaluation This examination reveals a great deal about the patient’s mental state, behaviors, coping styles, and the effects of pain or injury on personality. Behavioral analysis considers compliance, achievement level before injury, activity level after injury, functional capacities, anxiety, depression, personality disorders, marital status, role reversal, and family dysfunctional states. There are psychological tests designed to elicit

Section 5: Biomechanical Disorders of the Lumbar Spine

responses which can be translated into numerical values and compared with the performance of other persons, such as the Minnesota Multiphasic Personality Inventory and the Millon Behavioral Health Inventory Assessment. These instruments test psychogenic attitudes, such as chronic tension, recent stress, premorbid pessimism, future despair, social alienation, and somatic anxiety. They are not a predictor of outcome, nor should they be used for that purpose. We no longer use these instruments, but depend heavily on individual interview assessments.18 If utilized, it should be for the purpose of finding out how the treating staff can interact with the individual in an effective manner to allow the patient to accept the rehabilitation plan. The patient has to be a partner in the rehabilitative process; otherwise, the effort will fail. Psychological services offer biofeedback, relaxation training, coping skills training, assertiveness, stress management, and self-hypnosis. Group and family therapy deal with social interactions, return to environment, employment, and disability versus wellness with an emphasis on function, not pain. Psychological evaluations are tailored to document these issues. They work with the vocational counselors concerning return to work issues.

Vocational evaluation The objectives of vocational evaluations are: 1. Assessment of education level, training and work history, vocational abilities, transferable skills, job satisfaction, interests, goals, and interpersonal relations at work; 2. Identification of vocational goals and motivation to return to work, same job, modified job, different job and job seeking skills; and 3. Establishment of the role of the significant other, family, employer, attorney as it pertains to return to work issues.1,19

COMPONENTS OF PAIN REHABILITATION (INTERVENTIONS) Pain rehabilitation programs utilize a multimodal, cognitive–behavioral, goal-oriented aggressive physical approach within a supportive environment in which patients learn pain management techniques and work toward clear and achievable goals. Within such a complex paradigm, customization, individualization, communication, collaboration, planning, and flexibility become important characteristics. The program is carried out by experts in pain management and rehabilitation from different specialties. Pain physicians coordinate and oversee the program, including the prescription of medication. Physical medicine and rehabilitation directs the application of all physical medicine modalities and treatments. Nurses trained in rehabilitation and behavior monitor patient progress and education, and reinforce the teachings of all disciplines, provide direct nursing care and medication, manage tapering from narcotics, and serve as case managers. The behavioral division is headed by a psychiatrist; doctorate-level psychologists are assigned to each patient. They do individual and group counseling, administer biofeedback, behavioral modification, stress management, time management, coping methods, self-hypnosis, or other applicable techniques. The vocational rehabilitation division evaluates and directs job readiness, goal setting for job placement, and return to work. The ergonomic division simulates the job and adapts the patient and/or work site while computing daily achievement goals. Functional capacities are measured regularly. The average program will last 4 weeks on an inpatient or outpatient basis or a combination thereof. Inpatient status is preferred for the medically and behaviorally difficult, complicated case, but it is

not always possible, as the healthcare reimbursement system may dictate the circumstances of treatment. In a tertiary referral center, few ‘simple,’ early primary care-type patients are seen. Our program receives the most complex, ‘court of last resort,’ salvage cases.

Medication/narcotics Narcotics have been the first line of treatment for intractable pain since time immemorial. These agents are not particularly effective with chronic pain, even when pursued vigorously as has happened during the past decade. If this statement were not true, then why would patients come to our center, in pain, having been given escalating doses of analgesics, to the daily equivalent of 12 000 mg of morphine? This would seem almost unbelievable, if it were not for the fact this experience has been repeated at our center on numerous occasions. Drug therapy is the primary mode of management for both acute and chronic pain, and conventionally can be classified into three categories: (a) nonopioid analgesics, (b) opioid analgesics, and (c) coanalgesics. Nonopioid analgesics such as salicylates, acetaminophen, nonsteroidal antiinflammatory drugs (NSAIDs) are indicated for pain involving inflammation, although acetaminophen lacks clinically useful peripheral antiinflammatory activity. NSAIDs are both analgesic and antiinflammatory and, therefore, are useful also for the treatment of pain not involving inflammation. NSAIDs differ from morphinetype analgesics in that there is an analgesic dose ceiling above which adverse effects increase, but additional analgesia does not result; NSAIDs do not produce physical or psychological dependence; NSAIDs are antipyretic. The primary mechanism of NSAID action is inhibition of the enzyme cyclooxygenase, inhibiting the formation of prostaglandins which sensitize peripheral nerves and central sensory neurons to painful stimuli. These time-honored agents have been used extensively, but do require caution in that they may produce gastrointestinal side effects such as ulceration or bleeding. Drugs such as ibuprofen, naproxen, ketoprofen, indometacin, ketorolac and others in this group which have their advocates will actually serve good purpose but, in chronic pain, may not produce total relief. The more recent COX-2 group were thought to be more effective, but currently are under scrutiny and have even been banned because of complicating features such as cardiac disease in addition to adverse hematological effects, renal effects, and even occasional central nervous system dysfunction. The opioid analgesics have shown increased use throughout the later decades because of the continuing quest for pain relief in contradistinction to pain control. There have been, and continue to be, opposing views on how these drugs should be used. There are those who take the more standard approach of following the PDR recommendations. Others believe that pain is such an intolerable condition that whatever is required to produce control should be prescribed. Unfortunately, if one carries that thesis to conclusion, it will often turn out that the escalating high-level dose approach will also result in an inability to function because of sedation or other physical side effects and, therefore, prove useless, at least for the noncancer patient. It has always been the philosophy of our center that every effort should be made to taper and discontinue narcotic analgesics in favor of pain rehabilitation. So much of the disability is mechanical in origin as compared to chemical. In fact, throughout the years, there have been very few patients in whom successful tapering and cessation of narcotic use cannot be effected, to the betterment of their physical and psychological status. It would be rare for us to complete our rehabilitation program and prescribe ‘maintenance narcotic.’ This may represent a minority view, but it has been our experience, and it remains our philosophy, unchanged throughout three decades of pain management. 1205

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The coanalgesic group of drugs may be used to enhance the effect of opioids or NSAIDs, have independent analgesic activity in certain situations, or counteract the side effects of analgesics. Neuropathic pain represents 30–40% of this treatment group. This is pain which has a burning, prickling quality which has been called dysesthetic pain as compared to the sharp, toothache-like pain managed with standard analgesics. Included in this group would be the tricyclic antidepressants, the antiepileptic drugs, local anesthetics, glucocorticoids, skeletal muscle relaxants, antispasmodial agents, antihistamines, benzodiazepines, caffeine, phenothiazines, and topical agents.

Physical therapy restoration Physical medicine has the goal of restoring body function to normal or its closest equivalent. Because myofascial contracture is the common denominator in the low back disorders, the first phase of management is muscle stretching and restoration of full range of motion in the joints of the hips, back, and lower extremities. This therapy includes gait retraining because of acquired maladaptive patterns, postural adjustment, proper use of effective modalities, elimination of adaptive equipment when possible, and strength and endurance conditioning with instruction of flare-up management. Modalities, when evaluated as unimodal therapy, may not show clear-cut evidence of effectiveness. However, they appear to be useful in combination which, unfortunately, makes statistical evaluation more difficult. Nonetheless, scientific rationale exists for some. Ice application with lowering of temperature is known to decrease nerve conduction to the point of anesthesia, and the inflammatory reaction is contained with a reduction of chronic changes.20,21 To be effective, the body part must be packed in ice for periods in excess of 30 minutes. Trigger point desensitization is indicated. Liberal use of ice is the preferred method of treatment. Heat does seem to soften muscle preparatory to stretching. An adjunct vapocoolant helps to block the stretch reflex and makes lengthening easier. Mechanical traction is useful for certain specific indications. Conceptually, we apply traction to stretch muscle groups, not to distract the spine or to release nerve entrapment. We do not believe that distraction can be effected with the weights that are used, and the principle of entrapment is not tenable. Therefore, traditional pelvic or leg traction is not employed. Gravity traction is applied for iliopsoas contractures in the patient with a spinal flexion deformity and/or failure to extend the back. Autotraction is an important technique, which allows threedimensional placement of the spine by rotating, flexing, or extending the unit as the patient imposes his or her own body force by pushing and pulling. The self-applied force of autotraction will not exceed that which could be potentially injurious, but it will release tight paraspinal muscles. Autotraction does not decompress the nerve root, as was the concept of its originators.22,23 Most stretching is manual and labor intensive, since it is important that the therapist feels the tissue during treatment. Massage also is used as adjunct treatment to enhance muscle lengthening and supple movement. There are over 200 forms of massage and bodywork. Swedish, shiatsu, rolfing, cranio-sacral release, Alexander technique, sports massage, neuromuscular therapy, seated massage, and Thai massage are several examples. For the purpose of functional restoration and pain reduction, neuromuscular therapy uses advanced concepts in pressure therapy to break the stress–tension–pain cycle. It aims to relax muscle so that the body will return to normal neuromuscular integrity and balance. Neuromuscular massage is essential to resolve trigger points. But trigger point resolution by massage may not be sustained unless progress is made towards restoring normal ranges of motion, flexibility, and mobility. Transcutaneous electrical neural stimulation (TENS) is used infrequently and only with patients who are TENS responders and who

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can be assisted with a difficult drug taper for which TENS may give short-term relief as the drugs are withdrawn. TENS will not be given to the patient beyond this period of time; it has no role in long-term therapy. Conceptually, it is to be emphasized that we are aiming for resolution of the painful disorder by physical restitution, not by an attempt at distraction, masking the pain, or at coping by ‘learning to live with pain.’ Passive, then active ranging of motion is essential, especially about the hips and, in particular, the hip rotators. Hamstring lengthening is another mandate, because hamstring tightness will affect back movement. Full ranges of back motion are the ultimate goal, so flexion and extension exercises are instituted without prejudice for the proponents of either type. Both flexion and extension exercises are needed. A full compendium of exercises is employed, as described in any standard physical therapy textbook, to establish full ranges of motion throughout the lower body with supple muscles and fluid movement. As this is being achieved, muscle strengthening and endurance/cardiovascular conditioning are added to the regimen with monitoring of those patients who have associated medical problems. Movement (dance) therapy is an interesting adjunct, because patients with pain will often perform effortlessly to music when, seemingly, without music, pain will be a limiting factor. It helps to diminish the fear of moving/activation.

Functional electrical stimulation When a specific muscle group is weak, functional electrical neuromuscular stimulation and muscle reeducation are implemented.24,25 This technique can produce rapid and dramatic increases in muscle recruitment patterns and muscle strength; footdrop braces can be discarded. Functional electric stimulation (FES) is used when minimal muscle recruitment or reduced voluntary control are detected upon muscle testing. With FES, muscles can be strengthened ‘passively’ without placing excessive demands on the patient, especially in the presence of pain. FES is the process of applying an external electrical stimulus to a muscle or muscle groups in order to induce muscle contraction. We also use FES successfully to treat conversion-disorders-type paralysis, for electric testing of motor responses, and as a motor dysfunction treatment method. FES allows the induction of maximal muscular contraction without any voluntary effort on the part of the treated individual. This latter aspect is of value for patients with chronic pain whose pain is often aggravated through exercise or who are unable to initiate voluntary effort necessary for muscular conditioning due to disuse. Studies on FES indicate that this passive intervention strategy can be quite effective.25 It should be emphasized here that FES is not a substitute for regular exercise. FES is used to ‘jump start’ the neuromuscular system. Once the patient has gained sufficient power to initiate voluntary movement comfortably, the patient engages in active resistive exercises for strengthening and endurance training.

Motor dysfunction treatment Strategies for treating motor dysfunctions identified upon evaluation (see MDE above) are patient specific, as well as condition specific. The overall objective is to improve functional capabilities. Motor dysfunction treatment (MDT) is incorporated into regular patient treatment to address problems such as depressed muscle activity, increased muscle tension (hyperactivity), significant EMG asymmetry or asynchrony, and nondistinctive EMG activity patterns (work versus rest cycles). For example, in order to restore function to muscle with depressed EMG activity, the MDT protocol will consist of monitoring the target muscle while the patient performs selected therapeutic maneuvers designed to recruit that muscle compared to

Section 5: Biomechanical Disorders of the Lumbar Spine

its contralateral partner. If EMG recruitment is found to be minimal, functional electrical stimulation is used to increase strength and power of the affected muscle. As soon as the patient demonstrates ability to recruit the muscle(s) voluntarily, active EMG interventions using methods of muscle reeducation and biofeedback commence. Motor dysfunction treatment also involves educating the patient as to muscle compensation/isolation, and improving strength, endurance, and muscle tone through progressive resistive training and massage. It also involves increasing kinesthetic awareness in order to reestablish proper motor recruitment patterns. Establishment of proper recruitment patterns becomes essential in order for the patient to perform with proper body mechanics during functional activities and work simulations.

Occupational therapy restoration Occupational therapy concentrates on body mechanics, activities of work and daily living, and on functional circuits. Sitting, standing, walking, lifting, climbing, and reaching tolerances are established and brought to normal levels of function. Pacing of activity and energy-saving techniques are taught. Adaptive equipment is used infrequently and only on specific indication. Posture and gait are corrected, as most patients are found to have poor posture and maladaptive gaits. Proper motor vehicle entry, seating, transfers, and luggage management are taught. Recreational activities are reviewed and eye/hand/ leg coordination and tolerances are established. Vocational goals are set in conjunction with the vocational counselor and ergonomist for job simulation.

Postural correction Awkward postures cause fatigue, strain, and eventually pain; they need to be corrected. Poor postures will result in pain, loss of stability, and falls.26 Faulty posture and poor body alignment develop slowly and may not be apparent to the individual. Poor posture is found with obesity, leading to weakened muscles, emotional tension, and poor body attitudes in the workplace. The incidence of pain increases in predominantly sitting work activities, especially with the use of computers. Ideally, patients do best when they can alternate activities among walking, standing, and sitting.27 It is recognized that when the body is not in correct alignment, static loading on muscles and joints results in awkward positions that are not healthy.26 Prolonged forward bending of the head and trunk, stooped postures, forced postures, and postures causing constant deviation from neutral alignment are but a few examples of poor postures. Even sleeping postures must be assessed.28 Programs must address the factors contributing to poor postures from both the physical as well as the engineering perspective. On the physical level, deficiencies in human structural capabilities can be considered in the design and selection of products and tools. Patients are taught, through practice and the use of biofeedback, to choose proper equipment, to modify their working environment thus encouraging good postural habits, and to alternate activities to avoid postural fatigue.

Body mechanics interventions Proper body mechanics provides the basis for the safest way to perform daily tasks. Corrective training to alleviate and prevent mechanical stressors and improper habits for sitting, standing, walking, lifting,

carrying etc. is provided. Biofeedback may be a helpful adjunct. It is important that body mechanics techniques are taught with sufficient generalization to allow patients to accommodate specific body mechanics technique in the presence of conditions other than pain and as the task demands change. Modification of proper body mechanics must be taught if the task does not lend itself to ideal technique.

Job simulation and work readiness This is the ultimate goal of achievement for the working-aged group, but it does not exclude students or elderly persons, who also require instruction for their needs. The physician, the occupational and physical therapists team with vocational counselors and ergonomists to develop the treatment plan. It is essential that the patient advise the job simulation team of the job activities which provoke the pain. Physical and occupational treatments are highly structured, task-focused to the job requirements, goal oriented, individualized, and multidisciplinary in nature. Patients should not begin this phase of treatment until they possess the necessary tools, such as increased awareness of posture and body mechanics; increased flexibility and mobility; adequate strength and endurance; good stress management skills; good pain control and safety techniques; and positive attitude towards employment, and return to work.

Ergonomic restoration The thrust of the ergonomic approach to injury management and pain rehabilitation is ‘to design effective intervention strategies for the restoration of functional abilities, control of pain, and immediate return to work and productive lifestyle.’ Another objective is to avert further aggravation of an existing condition or injury. This philosophy was adopted by the University of Miami Comprehensive Pain and Rehabilitation Center as early as 1982 when ergonomics was first introduced into a multidisciplinary pain management team. This marked the beginning of a new era for ergonomics research and application in healthcare systems and pain treatment.

Workplace design This type of ergonomic intervention aims at assessing the relationship between human characteristics (e.g. posture, body mechanics) and musculoskeletal stresses with emphasis on work issues.29 The task of the ergonomist is to assist the patient or employer to design or modify the workstation to insure proper engineering design and good body mechanics when performing job tasks. The process of workplace design within a functional restoration program consists of the following components: 1. The patient’s job description, the employee’s job description, and a description of a ‘typical’ work day; 2. Evaluation of essential job tasks is to identify tasks that are potentially stressful/painful. Analysis of video graphic data is used to isolate the critical risk factors; and 3. Intervention phase. Interventions specific to reducing or resolving the risk factors are developed. Ergonomic analysis aims at adjusting, modifying, changing, and/or replacing current heights, layout, equipment, tools, and design characteristics. It is not always necessary to recommend new equipment or adaptive technologies (e.g. cushions, ergonomic chairs, etc.). In most cases, workplaces can be reasonably accommodated to meet ergonomic needs. The patient’s set-up may not be an ‘ideally correct’ setup. It is the responsibility of the ergonomist to teach patient methods of improving safety and comfort without need for expensive adjustments or equipment.

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A tool which we have used in the process of analyzing and recommending workplace adjustments and modifications is Sitting Workplace Analysis and Design (SWAD).30 SWAD is a computer program resembling artificial intelligence. The inputs to the program are workplace user demographics, 16 anthropometric dimensions, workplace dimensions, work tools, and the priority and frequency of use of each work element. SWAD then combines this information with a ‘knowledge base’ of ergonomic principles and guidelines and a set of inference procedures. The output of SWAD is the recommended workplace dimensions, heights, reaches, footrest, chair parameters, VDT parameters, and optimal placement of all work tools. It enables customization of workstation adjustment without trial and error.

Electromyogram biofeedback A carefully processed EMG signal can be a useful tool in the quantitative measurement of muscular performance, for reeducation and in the evaluation of patient’s response to specific treatments.17 Biofeedback is the process of using specialized instruments to give people information about their biological systems (temperature, heart rate, muscle activity, etc.). It is a set of training techniques used to increase awareness and voluntary control of biological conditions and relate them to human physical and emotional well-being. Biofeedback (BF) is useful in the relief of stress, tension, headaches, muscular dysfunction, and for the reduction of muscle tension, which correlates well with a reduction in pain and improvement of muscle strength.31,32 Using EMG biofeedback, patients perform therapeutic maneuvers while affected muscles are monitored. The information is used to facilitate patient awareness of muscular performance. These methods can then be used to improve the patient’s ability to coordinate muscle activity, reestablish proper reciprocal inhibition, reestablish functional synergy including appropriate force couples and sequential contractions, decrease the need for inappropriate muscular or postural compensations, and achieve recruitment levels beyond baseline activity.

Vocational rehabilitation A vocational rehabilitation professional counsels the patient throughout the program to address all vocational issues. The vocational professional will work with the psychologist and ergonomist, and share essential information with the treating team. The vocational counselor is the liaison to outside parties such as case managers, insurers, and employers. The vocational professional addresses the traditional activities such as skills, obstacles to return to work, transferable skills, job readiness, and all skills needed to return to employment. The vocational goal is full functional activity and return to previous employment, when possible. Even the heaviest physical activity capacities have been achievable in most patients. If limitations are inevitable, the counselor works with the patient on possible transferable skills.

Behavioral modification Behavioral management is a key issue. Nearly 20% of Americans suffer one or more emotional disorders, so at the least patients with low back injury may have these disturbances as a preexistent condition. Patients with chronic pain perceive their pain as a disability limiting their functional status. The perception of pain as a disability is such a national problem that the Social Security Administration Commission on the Evaluation of Pain recommended the development of a listing ‘impairment due primarily to pain.’33 An abnormal psychological profile is inherited by the treatment team, insurer, and all others concerned. Our study of pain-population

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patients found 62.5% to have anxiety disorders and 56.2% to have current depression.34 These conditions were comingled with other less prevalent disorders. Only 5.3% of 283 patients were found to have no psychiatric diagnosis. Pure psychogenic pain is probably rare when presented as mental events giving rise to pain. However, all pain, as perceived by the patient, is real, regardless of cause. Most bodily pain is a combination of factors, e.g. physical stimuli and mental events. Abnormal mental and emotional states may arise from a background of past personal experiences with pain, or from personality characteristics. A history of physical abuse is not uncommon in patients with chronic pain. Individual counseling is given when needed, including sexual counseling. Every patient has an assigned doctoral-level psychologist, who monitors daily progress and reinforces the goal of physical restoration. Relaxation training includes coping approaches, muscle reeducation, meditation and distraction, guided imagery, autosuggestion, especially to be used with physical activity, and tape supplements, which enhance ‘live’ therapy. Stress management is incorporated into the behavioral sessions. Hypnotherapy is utilized on selected cases. Weekly family groups explore the goals of the patient with the spouse and/or other family members. How to respond to pain without fear is discussed as well as how to gain control over pain and their lives. Effective communication is an important subject. The roles of the various family members are defined, both as to distribution and as to responsibility. Experiences and frustrations are shared. These sessions facilitate the return to home, hopefully to an environment which will now foster wellness, not disability. The behavioral staff address the ‘fall out’ and behavioral responses to tapering from narcotics. Intense activation will produce endorphin release that helps ameliorate withdrawal.35 Most important of all, we do not teach people how to live or cope with their pain. Our goal is reduction or elimination of pain, and for the patient, to control any painful flare-ups. The pain is thereby no longer catastrophic; hence, it does not control the patient’s life.

Role of psychiatry Patients with chronic pain being treated at pain centers have been reported to suffer a wide range of psychiatric conditions. These include depression, anxiety, drug dependence/abuse, irritability and/ or anger, physical or sexual abuse, suicidal or homicidal ideation, and memory or concentration problems. These data are supported by epidemiological community studies, which indicate a strong relationship between chronic pain and depression.36–39 Depression is not only a potential target for treatment, but coping strategies may differ in depressed patients with chronic pain. Patients with chronic pain may over-rely on passive avoidance coping activities in response to life’s stresses, including pain; these coping activities may be a function of depressed mood.40 Severe depression is an indication for pain treatment facility referral. A facility with on-site psychiatric treatment should be chosen, since levels of anxiety, depression, etc. change rapidly during the treatment program. This necessitates an immediate response. Drug abuse, dependence, and addiction are reported in the range of 3.2–18.9%.41 These diagnoses are reported in a significant percentage of chronic pain patients, but evidence of addictive behaviors is not common. The dependence occurs as a result of the pain, not addiction. At issue is whether patients with physician-perceived drug problems are best treated at a pain treatment facility or at a substance abuse facility. Detoxification in pain treatment facilities where simultaneous pain treatment is available appears to be the

Section 5: Biomechanical Disorders of the Lumbar Spine

better route.37 Detoxification is not realistic unless pain alleviation occurs simultaneously. Management of pain medications and controlled substances should parallel physical and functional restoration.

Role of nursing Nurses are an integral part of the multidisciplinary team. Nurses are involved at every level as programs director, nurse manager, admissions liaison, admitting nurses and staff nurses who work in therapy areas with the patients and team throughout the treatment day. They support the physicians, do crisis management, medication management, monitor underlying medical problems, and provide 24-hour continuity of care when in the inpatient unit. They teach, counsel patients, families and case managers, and are involved with discharge planning. They supervise evening exercises assigned by the therapists.

HEADACHES AND PAIN REHABILITATION Headache is a frequent comorbid condition in patients with chronic pain. These headaches are mostly classified as migraines. However, a considerable number of patients with chronic pain present with injury-related headaches. In one study,42 10.5% of the chronic pain patients had headache interfering with function. Of these, 55.8% related their headaches to an injury and 83.7% had neck pain. Migraine headache was most common (90.3%) with cervicogenic being second (33.8%). Of the total, 44.2% had more than one headache diagnosis. The most frequent headache precipitants were mental stress, neck positions, and physical activity utilizing the neck muscles. Of the total group, 74.6% had a neck tender point. Discriminate analysis found the following symptoms as the most common predictors of headache: (1) onset of severe headache beginning at the neck tender point and numbness in arms and legs; (2) headache brought on by neck positions and arms overhead; and (3) cervical pain with a tender point in the neck. Taut muscle bands and cervical tender/trigger points perpetuate head and neck pain. Successful rehabilitation efforts must address both the headache component through effective medications and physical medicine management of the cervical abnormality.

GERIATRIC PAIN REHABILITATION While generally thought of as a worker compensation injury-related model, the concept of pain rehabilitation applies to patients of all age groups. As American workers age, the number of expected disabled workers is also expected to increase. Older workers and those who do become disabled can respond well to well-designed, customized programs tailored to their levels, goals, and expectations.43 Many studies have reported significant improvement in functional abilities of patients with pain irrespective of their age group.30,44,45 Even when the outcome of return to work in older patients was not achieved (e.g. Mayer and Gatchel4), the consensus is that older patients should not be denied access to pain rehabilitation after onset of injury.30

OUTCOME EVALUATION OF THE PAIN REHABILITATION MODEL Are multidisciplinary pain centers effective? The answer is ‘yes,’ by virtue of increase in functional activity, return to work, decreased use of the healthcare system, elimination of opioid medication, closure of disability claims, pain reduction, and proved cost-effectiveness.46

Evidence from well-designed outcome studies indicates that: (1) multidisciplinary pain facilities do return patients with chronic pain to work; (2) the increased rates of return to work are due to treatment; and (3) the benefits of treatment are not temporary.2,47–49 In one study, our center reported that 86% of all patients treated returned to full activity, with 70% fully employed and another 16% who were physically capable of full employment but could not return to work because jobs were not available.50 Among the 86% who were fully active, there was no clear-cut difference between compensation and noncompensation class cases.14 In a more recent study, the return rate to full function and work was again 86%, albeit the patients had some residual discomfort that eventually remitted or was controlled at a low level of intensity.2 The 14% who failed to return to full function were highly complex patients with major behavioral problems. Treatment at multidisciplinary pain clinics, based on a metaanalysis of 3080 patients, found savings in medical expenditures equal to US$9 548 000, savings in indemnity expenditures equal to US$175 225 000, with a total savings of US$184 772 050! Our data showed a 92% improvement in functional status, a 66% reduction in pain, and a 62% return to employment or a work-ready state. A 93% patient satisfaction rate with treatment is strong testimony to the effectiveness of multidisciplinary pain center treatment. Despite the perceived high cost, multidisciplinary pain rehabilitation programs are cost-effective by reducing long-term utilization of medical services and by returning patients early to employment or previous lifestyle.

SUMMARY AND CONCLUSIONS The problem of chronic pain is a powerful practical example of the complexity of an illness or injury when compounded by patient’s beliefs, cultural aspects, experience, the family, the workplace, the community, as well as the healthcare system. Seen from this perspective, it is predictable that these multifaceted problems are more amenable to a multidisciplinary treatment approach than to a series of single therapeutic interventions. These patients are too complex to be successfully treated by a single discipline. The treatment must be integrated and concurrent. Team communication is essential. The management of back injuries is far from simple, especially for those classified as having non-specific pain. An early referral to a competent pain center may prevent that simple sprain from becoming a catastrophe leading to total disability. The labeled ‘low back loser’ is a victim of the healthcare delivery system. Early multidisciplinary rehabilitation treatment is cost-effective. The healthcare system, therefore, must be capable of identifying the problems early and then dealing with them in a concise, comprehensive, goal-oriented way. We conclude that early referral can prevent the sensory, perceptual, behavioral, psychosocial, biomechanical consequences, and disability that are certain to develop if chronicity becomes established. Although this chapter concentrates on ‘spinal pain,’ pain rehabilitation does not limit its application to musculoskeletal disorders, spinal problems, or work injuries. If one accepts the hypothesis that chronic pain of any etiology produces a dysfunctional state, the mechanical issues of the myofascia loom large as a major contributing factor to the loss of function and its painful consequences. It then becomes clear that pain rehabilitation as described herein would be applicable to all conditions in which myofascial abnormality is found. The holistic, collaborative philosophy of optimizing the physical, functional, behavioral, cognitive, and occupational abilities makes pain rehabilitation the best choice for the patient from the humane, medical, and financial perspective.

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References 1. Rosomoff RS. The pain patient. State of the Art Reviews. Spine 1990; 5(3): 417–428. 2. Cutler RB, Fishbain D, Rosomoff HL, et al. Does nonsurgical pain center treatment of chronic pain return patients to work? A review and meta-analysis of the literature. Spine 1994; 19:643–652. 3. Rosomoff HL, Rosomoff RS. A rehabilitation physical medicine perspective. In: Cohen MJM, Campbell JN, eds. Pain treatment centers at a crossroads: a practical and conceptual reappraisal, progress in pain research and management. Ch. 4, vol. 7. Seattle: IASP Press; 1996: 47–58.

26. Khalil TM, Abdel-Moty E, Rosomoff RS, et al. Ergonomics in back pain. A guide to prevention and rehabilitation. New York: Van Nostrand Reinhold; 1993:81–86. 27. Khalil TM, Abdel-Moty E, Steele-Rosomoff R et al. The role of ergonomics in the prevention and treatment of myofascial pain. In: Rachlin ES, ed. Diagnosis and comprehensive treatment of myofascial pain: handbook of trigger point management. New York: Mosby Year Book; 1993:487–523.

4. Mayer TG, Gatchel RJ. Effect of age on outcomes of tertiary rehabilitation for chronic disabling spinal disorders. Spine 2001; 26(12):1378–1384.

28. Khalil TM, Abdel-Moty E, Steele-Rosomoff R et al. The role of ergonomics in the prevention and treatment of myofascial pain. In: Rachlin ES, ed. Diagnosis and comprehensive treatment of myofascial pain: handbook of trigger point management. New York: Mosby Year Book; 1993:487–523.

5. Rosomoff HL, Fishbain D, Goldberg M, et al. Physical findings in patients with chronic intractable benign pain of the back and/or neck. Pain 1989; 37: 279–287.

29. Khalil TM, Abdel-Moty E, Steele-Rosomoff R, et al. Ergonomic programs in post injury management. In: Karawowski W, Marras WS, eds. The occupational ergonomics handbook. New York: CRC Press; 1999:1269–1289.

6. Rosomoff HL, Rosomoff RS. Comprehensive multidisciplinary pain center approach to the treatment of low back pain. Neurosurg Clin N Am 1991; 2(4):877–890.

30. Abdel-Moty E, Khalil TM, Rosomoff RS et al. Ergonomics considerations and interventions. In: Tollison CD, Satterthwaite JR, eds. Painful cervical trauma: diagnosis and rehabilitative treatment of neuromusculoskeletal injuries. Philadelphia: Williams & Wilkins; 1990:214–229.

7. Rosomoff HL. Do herniated disks produce pain? Clin J Pain 1985; 1:91–93. 8. Wall PD. Physiological mechanisms involved in the production and relief of pain. In: Bonica JJ, Procacci P, Pagni CA, eds. Recent advances on pain: pathophysiology and clinical aspects. Springfield, IL: Charles C. Thomas; 1974:36–63. 9. Vane JR. Pain of inflammation: an introduction. In: Bonica JJ, Lindblom U, Iggo A, eds. Advances in pain research and therapy, vol. 5. New York: Raven Press: 1983:597– 603. 10. Rosomoff HL, Rosomoff RS. Assessment and treatment of chronic low back pain: the multidisciplinary approach. In: Rucker KS, Cole AJ, Weinstein SM, eds. Low back pain: a symptom-based approach to diagnosis and treatment. Boston: Butterworth-Heinemann; 2000:343–362. 11. Spitzer WO, LeBlanc FE, Dupuis M, et al. Scientific approach to the assessment and management of activity-related spinal disorders: a monograph for clinicians. Report of the Quebec Task Force on Spinal Disorders. Spine 1987; 12:51–59.

31. Asfour SS, Khalil TM, Waly S, et al. Biofeedback in back muscle strengthening. Spine 1990; 15(6):510–513. 32. Khalil T, Asfour SS, Waly SM, et al. Isometric exercise and biofeedback in strength training. In: Asfour SS, ed. Trends in ergonomics/human factors, IV. New York: Elsevier Science; 1987:1095–1101. 33. Turk DC, Rudy TE, Stieg RL. The disability determination dilemma: towards a multi-axial solution. Pain 1988; 34:217–229. 34. Fishbain DA, Goldberg M, Meagher R, et al. Male and female chronic pain patients categorized by DSM-III psychiatric diagnostic criteria. Pain 1986; 26:181–197. 35. Carr DB, Bullen BA, Skrinar GS, et al. Physical conditioning facilitates the exerciseinduced secretion of beta-endorphin and beta-hypoprotein in women. N Engl J Med 1981; 305:560–563.

12. Travell JG, Simons DG. Myofascial pain and dysfunction: the trigger point manual. Baltimore: Williams and Wilkins; 1983.

36. Fishbain DA, Cutler R, Rosomoff HL, et al. Chronic pain-associated depression: antecedent or consequence of chronic pain? A review. Clin J Pain 1997; 13:(2) 116–137.

13. Abdel-Moty E, Khalil T, Steele-Rosomoff R et al. Maximizing progress during low back pain rehabilitation. In: V. Nielsen R, Jorgensen K, eds. Advances in industrial ergonomics and safety. London: Taylor & Francis; 1993:331–335.

37. Fishbain DA, Cutler RB, Rosomoff HL, et al. Pain facilities: a review of their effectiveness and referral selection criteria. Psychiatr Manage Pain 1997; 1:(2) 107–116.

14. Rosomoff HL, Green CJ, Silbret M, et al. Pain and low back rehabilitation program at the University of Miami School of Medicine. In: Ng LKY, ed. New approaches to treatment of chronic pain: a review of multidisciplinary pain clinics and pain centers. National Institute on Drug Abuse Research Monograph Series 36. Washington DC: US Government Printing Office; 1981:92–111.

38. Fishbain DA. Somatization, secondary gain, and chronic pain: Is there a relationship? Curr Rev Pain 1998; 6:101–108.

15. Rosomoff H.L, Rosomoff RS. Myofascial pain syndromes. In: Follett KA, ed. Neurosurgical pain management. Philadelphia: WB Saunders; 2004:57–72. 16. Headley B. Assessing muscle dysfunction from active trigger points. Adv Physical Therap 1997; 8:21–22. 17. Khalil TM, Abdel-Moty E, Diaz E, et al. Electromyographic symmetry pattern in patients with chronic low back pain and comparison to controls. In: Karwowski W, Yates JW, eds. Advances in industrial ergonomics & safety, III. London: Taylor and Francis; 1991:483–490. 18. Fishbain DA, Turner D, Rosomoff H, et al. Millon Behavioral Health Inventory scores of patients with chronic pain associated with myofascial pain syndrome. Pain Med 2001; 2:1328–1335. 19. Steele-Rosomoff R, Rosomoff HL, Abdel-Moty E. Vocational rehabilitation and ergonomics. In: Burchiel KJ, ed. Surgical management of pain. New York: Thieme; 2001:171–180. 20. Rosomoff HL. The effects of hypothermia on the physiology of the nervous system. Surgery 1956; 40:328–336. 21. Rosomoff HL, Clasen RA, Hartstock R, et al. Brain reaction to experimental injury after hypothermia. Arch Neurol 1965; 13:337–345. 22. Lind GAM. Auto-traction: treatment of low back pain and sciatica. Sweden: Sturetryckeriet; 1974. 23. Natchev E. A manual on autotraction treatment for low back pain. Folksam Scientific Council Publ, B 1984; 171. 24. Abdel-Moty E, Khalil TM, Rosomoff RS, et al. Computerized electromyography in quantifying the effectiveness of functional electrical neuromuscular stimulation. In: Asfour SS, ed. Ergonomics/human factors, IV. New York: Elsevier Science; 1987:1057–1065.

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25. Abdel-Moty E, Fishbain D, Goldberg M, et al. Functional electrical stimulation treatment of postradiculopathy associated muscle weakness. Arch Phys Med Rehabil 1994; 75:680–686.

39. Fishbain DA, Cutler BR, Rosomoff HL, et al. Comorbidity between psychiatric disorders and chronic pain. Psychiatr Manage Pain 1998; 2:(1)1–10. 40. Weickgerant AL, Slater MA, Patterson TL, et al. Coping activities in chronic low back pain: relationship with depression. Pain 1993; 53:95–103. 41. Fishbain DA, Steele-Rosomoff R, Rosomoff HL. Drug abuse, dependence, and addiction in chronic pain patients. Clin J Pain 1992; 8:77–85. 42. Fishbain DA, Cutler R, Cole B, et al. International Headache Society headache diagnostic patterns in pain facility patients. Clin J Pain 2001; 17:178–193. 43. Khalil TM, Abdel-Moty E, Zaki A M, et al. Reducing the potential for fall accidents among the elderly through physical restoration. In: Kumar S, ed. Advances in industrial ergonomics & safety, IV. London: Taylor & Francis; 1992:1127–1134. 44. Khalil TM, Abdel-Moty E, Diaz E, et al. Efficacy of physical restoration in the elderly. Experimental Aging Research 1994; 20(3):189–199. 45. Cutler RB, Fishbain DA, Lu Y, et al. Prediction of pain center treatment outcome for geriatric chronic pain patients. Clin J Pain 1994; 10:(1)10–17. 46. Turk DC. Efficacy of multidisciplinary pain centers in the treatment of chronic pain. In: Cohen MJM, Campbell JN, eds. Pain treatment centers at a crossroads: a practical and conceptual reappraisal. Progress in pain research and management, vol. 7. Seattle: IASP Press; 1996:257–273. 47. Fishbain DA, Cutler RB, Rosomoff HL, et al. Movement in work status after pain facility treatment. Spine 1996; 21:(2)2662–2669. 48. Fishbain DA, Cutler R, Rosomoff HL, et al. Impact of chronic pain patients’ job perception variables on actual return to work. Clin J Pain 1997; 13:197–206. 49. Fishbain DA, Cutler RB, Rosomoff HL, et al. Pain facility treatment outcome for failed back surgery syndrome. Curr Rev Pain 1999; 3:10–17. 50. Cassisi JE, Sypert GW, Salamon A, et al. Independent evaluation of a multidisciplinary rehabilitation program for chronic low back pain. Neurosurgery 1989; 25:877–883.

Section 5: Biomechanical Disorders of the Lumbar Spine

Further Reading Abdel-Moty E, Fishbain D, Khalil T, et al. Functional capacity and residual functional capacity and their utility in measuring work capacity. Clin J Pain 1993; 9:168–173.

Moty EA, Khalil T, Asfour S, et al. On the relationship between age and responsiveness to rehabilitation. In: Das B, ed. Proceedings of the Annual International Industrial Ergonomics and Safety Conference. Advances in Industrial Ergonomics and Safety 11. Philadelphia: Taylor & Francis; 1990: 49–56.

American Pain Society. Principles of Analgesic Use in the Treatment of Acute Pain and Cancer Pain 2003; 73.

Rosomoff HL, Fishbain DA, Goldberg M, et al. Are myofascial pain syndromes (MPS) physical findings associated with residual radiculopathy? Pain 1990; Suppl 5:S396.

Fishbain DA, Rosomoff HL, Cutler B, et al. Opiate detoxification protocols. A clinical manual. Ann Clin Psychiatry 1993; 5:(1)53–65.

Rosomoff RS, Rosomoff HL. Hospital-based inpatient treatment programs. In: Tollison CD, ed. Handbook of pain management, Ch. 51, 2nd edn. Baltimore: Williams & Wilkins; 1994:686–693.

Fishbain DA, Cutler RB, Rosomoff RS, et al. The problem-oriented psychiatric examination of the chronic pain patient and its application to the litigation consultation. Clin J Pain 1994; 10:28–51. Fishbain DA, Cutler RB, Rosomoff HL, et al. Validity in self-reported drug use in chronic pain patients. Clin J Pain 1999; 15:3184–3191. Fishbain DA, Cutler RB, Rosomoff HL, et al. Does the Conscious Exaggeration Scale detect deception within patients with chronic pain alleged to have secondary gain? Pain Med 2002; 3:139–146. Fishbain DA, Cutler RB, Rosomoff HL, et al. Are opioid-dependent/tolerant patients impaired in driving-related skills? A structured evidenced-based review. J Pain Symptom Manage 2003; 25(6):559–577. Fishbain DA, Cutler RB, Rosomoff HL, et al. Is pain fatiguing? A structured evidencebased review. Pain Med 2003; 4(1):51–62. Gunn CC. Treatment of chronic pain intramuscular stimulation for myofascial pain of radiculopathic origin, 2nd edn. New York: Churchill Livingstone; 1996:165. Khalil TM, Goldberg ML, Asfour SS, et al. Acceptable maximum effort (AME): a psychophysical measure of strength in back pain patients. Spine 1987; 12(4): 372–376. Khalil TM, Asfour SS, Martinez LM, et al. Stretching in the rehabilitation of low-back pain patients. Spine 1992; 17:(3)311–317.

Rosomoff HL, Rosomoff RS, Fishbain D. Chronic low back pain. J Back Musculoskel Rehab 1997; 9(3):201–208. Rosomoff HL, Rosomoff RS, Fishbain DA. Types of pain treatment facilities referral selection criteria: are they medically & cost effective? J Florida Med Assoc 1997; 84:(1)41–45. Rosomoff HL, Steele-Rosomoff R. Surgery for the herniated lumbar disk with nerve root entrapment; are alternative treatments to surgical intervention effective? Curr Rev Pain 1998; 2:121–129. Steele-Rosomoff R, Rosomoff HL. Hospital-based inpatient treatment programs. In: Tollison CD, Satterwaite JR, Tollison JW, eds. Practical pain management, Ch. 53. Philadelphia: Lippincott Williams & Wilkins; 2002:782–790. US Department of Labor, Employment and Training Administration. Selected characteristics of occupations defined in the DOT. Washington, DC: US Government Printing Office; 1981. US Department of Labor, Employment and Training Administration. Dictionary of occupational titles, 4th edn. Washington, DC: US Government Printing Office; 1986. Yeomans SG, Liebenson C. Applying outcomes management to clinical practice. JNMS 1997; 5(1):1–14.

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SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBBS-Cervical, Thoracic, and Lumbar ■ i: Functional Restoration

CHAPTER

Deconditioning

111

Terry C. Sawchuk and Eric K. Mayer

INTRODUCTION Most patients with an episode of low back pain will improve significantly in a relatively short period of time, while others with seemingly minor injuries and often times minimal imaging abnormalities go on to develop chronic low back pain and significant disability. It is believed that there is a reduced level of physical activity associated with their pain leading to a decreased level of fitness or deconditioning. In recent years there has been great interest in why some develop chronic pain and subsequent disability and deconditioning. There is also great interest in what is occurring from a physical as well as a psychological perspective. Deconditioning, or its related terms detraining and disuse, is a multifactorial process that occurs in multiple body systems and is often secondary to an inciting event. Medline lists more than 2.6 million articles published since 1996 related to deconditioning of the heart, vessels, cardiovascular set-points, bone, cognition, affect, and muscles. The common factor for the pathologic change to these varied systems revolves around exercise or, more precisely, a lack of exercise exacerbating pathology. Though deconditioning is a common search term, it is not an entity defined in Steadman's Medical Dictionary. Moreover, existing literature has used the term in various related manners, depending upon whether the investigator is a physiologist, neurologist, physiatrist, or orthopedic surgeon. The favorite terms in the literature associated with deconditioning are: decreased exercise tolerance, decreased VO2 max, decreased ability of adaptation to functional demands, and general decreased performance in occupation and/or activities of daily living. With such an array of connotations and denotations, is it any wonder that the literature is conflicting at times? Since most of those who become disabled are of working age, the costs of their lost productivity and treatment is shouldered by all of society. It now appears evident that chronic low back pain (CLBP) is not merely a function of incomplete healing after an injury. While there certainly may be residual pain, most recover sufficiently to continue working and functioning in daily life. Understanding the reasons behind the development of chronic pain, deconditioning, and disability as well as the physical, psychosocial, and socioeconomic consequences holds significant promise for improved treatment, reduced pain, suffering and disability, and potentially enormous cost savings. A pure physical or anatomic model fails to adequately explain chronic pain and the associated disability and deconditioning. As a result, chronic pain is now conceptualized as a multifactorial phenomenon with biological, psychological, and socioeconomic variables interplaying. Our discussion here will include a review of deconditioning-related physiologic changes such as muscle atrophy, osteoporosis, and obesity as well as deconditioning-related functional changes such as a reduced cardiovascular capacity, a decrease in muscle strength and impaired coordination or motor control in

the presence of CLBP. Psychological variables such as fear-avoidance beliefs and depression and their relationship with CLBP and deconditioning are also reviewed. Chronic low back pain is one of the most costly as well as the one of the most common diseases affecting industrialized societies today. While the incidence of lower back injuries has not changed over time, disability rates have increased sharply over the past 20 years.1 It has been estimated that a percentage as small as 20% of low back pain patients account for 90% of the costs.2 The enormous costs for the treatment including lost productivity and worker replacement has been estimated as high as US$837 billion3,4 secondary to chronic spinal disorders. It has been proposed that with chronic pain there comes inactivity, disuse, and deconditioning. Kottke5 in 1966 stated, ‘The functional capacity of any organ is dependent within physiologic limits upon the intensity and frequency of its activity. Although rest may be protective for a damaged organ it results in progressive loss of functional capacity for normal organs.’ The decrease in function will be proportional to the duration, degree, and type of limitation of activity. Hasenbring et al.6 proposed physical disuse as a risk factor for chronicity in lumbar disc patients. Disuse or disuse syndrome and deconditioning are terms associated with this loss of functional capacity. The disuse syndrome was first described by Bortz in 1984.7 He pointed out how our society had become progressively more sedentary, adhering to an anthropologic law called the Principle of Least Effort. This, stated simply, says when an organism has a task to perform it will seek that method of performance that demands the least effort. Focusing on the long-term adverse consequences of inactivity, he described the identifying characteristics of the syndrome as cardiovascular vulnerability, obesity, musculoskeletal fragility, depression, and premature aging. He did not consider the reasons for inactivity but observed that disuse is physically, mentally, and spiritually debilitating. Mayer and Gatchel8 introduced the term ‘deconditioning syndrome’ in 1988. They felt deconditioning may be a response mediated physically by the injury as well as psychologically by a variety of secondary factors. Some of these include injury-imposed inactivity, neurologically mediated spinal reflexes, iatrogenic medication dependence, nutritional disturbance, and psychologically mediated responses to prior psychiatric distress, vocational adjustment problems, and/or limited social coping resources.9 As a result of inactivity, physical deconditioning represented by muscle inhibition/atrophy, decreased cardiovascular conditioning, decreased neuromuscular coordination, decreased ability to perform complicated repetitive tasks, and musculotendinous contractures ensues. They use the term ‘deconditioning syndrome’ to represent the cumulative disuse changes, physical and psychological, produced in the chronically disabled patient suffering from spinal and other chronic musculoskeletal disorders.

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We will review the physical and psychological consequences of inactivity or disuse in patients with CLBP. Physical measurements have addressed muscle function or strength and endurance isometrically, isokinetically, and isotonically. Methods such as magnetic resonance imaging (MRI), computed tomography (CT) scanning, and electromyography have been utilized to measure changes in muscle composition and function. Cardiovascular capacity and motor control or coordination have also been measured in CLBP patients. Psychosocial issues or variables such as distress, depression, anxiety, and fear-avoidance beliefs and their relationship with CLBP will be reviewed.

DECONDITIONING: A HISTORICAL PERSPECTIVE Original interest in a deconditioning syndrome was prompted primarily by two things. First, as part of the practice of medicine at one time, bed rest was often a prescribed treatment. However, physicians began to realize a multitude of adverse consequences secondary to this imposed immobility. Second, as the space program evolved, astronauts spent longer periods of time in a weightless environment, stimulating further interest on the affects of immobilization. Sixty years ago Dietrick et al.10 studied the effects of immobilization by placing four normal men in plaster casts from the umbilicus to the toes for 6 weeks and then followed them through a 4–6 week recovery period. They and other investigators observed a multitude of physiologic and metabolic changes. While our patients with CLBP certainly have not been immobilized to such a degree, a short review of that literature is enlightening. During exercise, cardiac output, heart rate, and left ventricular function all increase. Even with moderate exercise cardiac output may triple, heart rate may double, and left ventricular effort may more than triple. Oxygen uptake with heavy exercise rises six times higher than that seen at rest. With inactivity, physical fitness decreases rapidly. Resting heart rate was reported to increase by 0.4 beats per minute during an immobilization period.11 Stroke volume decreased by as much as 30% during maximal exercise following a period of immobilization.11 The maximal oxygen uptake (VO2 max) is felt to be the most sensitive measure of physical fitness. A decrease in VO2 max of 21% after 30 days of bed rest was observed by Greenleaf.12 Pulmonary function as measured by total lung capacity, forced vital capacity, forced expiratory volume, alveolar–arterial oxygen tension difference, and membrane diffusing capacity remained unchanged or showed decreases only in proportion to decreases in cardiovascular output and maximal oxygen uptake.10,11 In these studies the immobilization was virtually absolute and cognitive, emotional, and social effects were observed as well as the physiologic and metabolic effects. With immobilization, skeletal muscle obviously undergoes atrophy as well as decreased strength, endurance, and coordination. Muller13 reported strength loss of approximately 3% per day for the first 7 days in the muscle of the upper extremity immobilized in a cast. Little further strength loss was observed with further immobilization. Bone marrow content is lost during immobilization, resulting in osteopenia or osteoporosis.14 This skeletal calcium loss is associated with increased urinary calcium excretion which begins to rise on the second or third day of immobilization.10,14 Decreased physical activity alone without actual confinement to bed may result in skeletal calcium loss.15 Gaber et al.16 have shown that patients with CLBP have an increased incidence of osteopenia and osteoporosis. Another metabolic consequence is a negative nitrogen balance with losses of 29–83 grams during 6–7 weeks of immobilization. This loss reflects the equivalent of 1.7 kilograms of muscle protoplasm.10

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Before beginning our discussion of a deconditioning syndrome as it relates specifically to patients with CLBP, there are several terms should be defined. Verbunt et al.17 defined ‘disuse’ as performing at a reduced level of physical activity in daily life. They described ‘physical deconditioning’ as a decreased level of physical fitness with an emphasis on the physical consequences of inactivity for the human body, whereas Mayer and Gatchel8 included the psychological effects secondary to inactivity or disuse along with the physical consequences as part of their definition of the deconditioning syndrome. Verbunt chose to include the term ‘disuse syndrome’ in their discussion as well. The ‘disuse syndrome’ is defined as a result of long-term disuse, which is characterized by both physical and psychosocial effects of inactivity. Our discussion here will include a review of the literature on disuse or what is actually known about the level of physical activity in daily life of patients with CLBP. We have chosen to utilize the term deconditioning syndrome as defined by Mayer and Gatchel to represent the cumulative changes secondary to disuse, both physiological and psychological, produced in the patient suffering from CLBP. Thus, we can see how disuse leads to the deconditioning syndrome. The assumption is that we can show a significantly reduced level of physical activity resulting in deconditioning in patients with CLBP.

DISUSE In 1946, Young18 described the effects of use and disuse on nerve and muscle. Introducing the term disuse into the medical literature, he described it as not using the musculoskeletal system during periods of immobility. Then Bortz in 1984 referred to the disuse syndrome and included many of the adverse consequences of inactivity in his definition beyond those affecting muscle and nerve. For purposes of this discussion we will define disuse as performing at a reduced level of physical activity.17 We are sure many of us hold the belief that our patients with CLBP are leading a very sedentary existence with an activity level significantly below that of the norm. But, in actuality, what is known about the activity level of these patients? In a group of patients with chronic pain (but not specifically low back pain) the Baecke Total Physical Activity Score was significantly higher in female than in male patients, a finding not observed in healthy controls.19 This study also revealed a statistically significant reduction in a physical work capacity index of 34% in males and only a 17% reduction in found in women, which hardly reached the significance level. The authors concluded that chronic pain may have a greater impact on activity level in male patients than in female patients, whereas Protas20 and Verbunt et al.21 found that physical activity in the daily life of patients with CLBP did not differ significantly from healthy age- and gendermatched controls. The physical activity in daily life expressed as whole-body acceleration measured with a triaxial accelerometer and as the ratio between average daily metabolic rate, measured by the doubly labeled water technique, and resting metabolic rate, measured by ventilated hood, was reported by Verbunt et al.21 Both techniques were used simultaneously for 14 days. They noted that the mean level of physical activity did not differ in CLBP patients when compared with healthy controls. Thus, they could not confirm the presence of disuse in this group of patients. Given that 77% of the patients in this study were employed despite their back problems, it is possible that the patients participating in this study were in relatively better physical condition than other patients with CLBP. Further measurements revealed no difference in percentage of body fat and body mass between patients and controls. They found it remarkable that although patients felt disabled because of

Section 5: Biomechanical Disorders of the Lumbar Spine

their back pain as shown in their Rowland Disability Questionnaire scores, their level of physical activity as actually measured was not decreased in comparison with controls. They also noted there was no correlation between pain intensity and physical activity levels. Several theories as to the reasons for the differing results with regards to the presence or absence of disuse have been offered. Work status may indeed have a significant impact on physical activity levels. On the one hand, in the study by Verbunt et al.21 77% of the CLBP subjects were working, whereas in Neilens and Plaghki's studies19,22,23 only 20–34% of subjects had a paying job. Different methods for assessment of the degree of inactivity have also been employed. While Verbunt utilized physiologic measurements, others used self-reporting to assess physical activity levels. A discrepancy in reported functioning by patients and actual functioning has been reported.24,25 Physical activity levels as reported by patients with CLBP and as reported by their physical therapists revealed that the patients significantly underestimated their level of activity.25 It also has been shown that patients with CLBP have greater difficulty actually estimating their level of exertion during a performance test.24 From these studies, it would appear that self-reporting of activity levels in patients with CLBP is unreliable. In summary, it is surprising that so few studies have been performed on the level of physical activities in daily life or disuse in patients with CLBP. The results have been equivocal and thus, despite what our beliefs may be about the activity level of these CLBP patients, the literature does not support the definitive presence of a reduced activity level. This lack of a decreased activity level particularly seems to be the case, at least in patients with CLBP, who continue to work. The study by Verbunt et al.21 is the most scientifically well designed of these and they were unable to confirm the presence of disuse in a group of CLBP patients. The work status and/or varying methods of reporting activity level may offer some explanation for the inconclusive results reported here.

DECONDITIONING IN CHRONIC LOW BACK PAIN The presence of disuse or a reduced level of physical activity in daily life has not been definitively supported by the literature. However, since deconditioning is felt to be a result of disuse, the presence of deconditioning in CLBP may be used as supportive evidence of a low level of activity. There may be both physiological as well as psychosocial changes associated with the deconditioning syndrome. Physical consequences of inactivity may include decreased cardiovascular endurance, decreased strength and muscular atrophy, impaired coordination, osteoporosis, metabolic changes and obesity. Psychosocial changes may include distress, depression, anxiety, or behaviors consistent with the fear-avoidance model.

Cardiovascular capacity Endurance or cardiovascular capacity in patients with CLBP has been measured utilizing various methods. The most widely accepted measure of cardiovascular fitness is maximal oxygen uptake (VO2 max). The various methods of measurement have included measurement of VO2 max as well as utilizing submaximal exercise testing. Interestingly, the results have not led to a definitive conclusion about the cardiovascular capacity of patients with CLBP. In measuring parameters such as predicted VO2 max utilizing a symptom-limited treadmill test or bicycle ergometer some studies have shown significantly lower levels of cardiovascular fitness in patients24,26–28 whereas Wittink et al.29 and several others have failed to

demonstrate a significantly reduced level of aerobic fitness in patients with CLBP.30–32 A lower cardiovascular capacity was shown for men compared with controls but not for women in some studies.19,22,23 Wittink et al.29 tested a sample of 50 patients with CLBP with a mean duration of symptoms of 40 months. Oxygen consumption (VO2) was measured during a symptom-limited modified treadmill test. Prediction equations were employed to estimate VO2 max. The mean observed VO2 max values for men and women with CLBP were consistent with those found in earlier studies that tested normal subjects. Given these results, they concluded that rather than being a group of significantly deconditioned subjects, at least from an aerobic standpoint, this group of patients with CLBP represented a sample of moderately fit individuals. Furthermore, their data suggest that aerobic fitness levels are independent of diagnosis, duration of pain, pain intensity, work status, or smoking. Previously, Wittink et al.33 had subjects with CLBP perform three symptom-limited maximal exercise tests: a treadmill, an upper extremity ergometer, and a bicycle ergometer test. The treadmill test was found to be by far the best test for measuring aerobic fitness in these patients. Wittink et al.34 went on to show that there is no significant relation between aerobic fitness and pain intensity in patients with CLBP and that a lack of cardiovascular fitness therefore does not contribute to pain intensity in patients with CLBP. In a follow-up sample, patients reported significantly less pain before and after treadmill testing at the end of a functional restoration program compared with their pain intensity with testing before the program. Since their predicted VO2 max had not changed, the authors noted that there had been a decreased pain intensity independent of aerobic fitness levels. Hurri et al.32 measured VO2 max in 245 subjects with CLBP, 81 who were treated as inpatients, 88 treated as outpatients, and 76 controls with a history of CLBP but who were still working. They performed bicycle ergometer tests four times over a 30-month period. The estimated VO2 max of their patients was not significantly different than reference values of healthy persons. Battie et al.30 noted that aerobic fitness did not affect the risk of back injury in a prospective study. He did observe that it might affect the response to the problem and subsequent recovery. Cady et al.,35 in his oft quoted study from 1979 on a group of firefighters, showed a graded and statistically significant protective effect for increasing levels of fitness and conditioning. A criticism of Cady's study was that fitness level included both cardiovascular or endurance parameters as well as strength measures, making it impossible to isolate the benefits of these individually. On the other hand, some investigators have shown what most of us would believe to be true, that indeed there is a significantly decreased level of cardiovascular fitness in CLBP patients. Brennan et al.26 used bicycle ergometry to determine a predicted VO2 max in 40 patients with herniated discs with an average duration of symptoms of 87 days. Comparing these results with those of a matched control group revealed a significantly reduced predicted VO2 max for the patients. Others,24,27 in addition to van der Velde and Meirau,28 have also shown diminished cardiovascular capacity in patients with CLBP. Their original experimental objective was to determine the effects of 6 weeks of exercise on aerobic capacity and on measures of pain and disability in patients with CLBP.28 Baseline measurements determined that the percentile rank of aerobic capacity for the patients with CLBP was statistically significantly lower than those measures for the controls. Patients who completed a 6-week program of aerobic, muscular endurance, and flexibility exercises showed a statistically significant improvement in the mean percentile rank for aerobic capacity. In addition, they showed significant decreases in pain and disability after completion of the exercise program.

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We can see that despite what our preconceived ideas may be regarding a decreased aerobic capacity in patients with CLBP, the literature is inconclusive. Instead, it reveals that a decreased aerobic capacity may or may not actually be present in these individuals. Work status again has been offered as a possible reason why the results have varied so, the thought being that even in the presence of CLBP those individuals continuing to work are more likely to possess a fitness level equal to the norm. Unfortunately, information pertaining to work status is not available for all of the studies considered here. It is notable that in most studies where no difference in cardiovascular capacity was reported, most of the subjects being studied were still working. The cardiovascular capacity was better for CLBP patients who were working compared with those who were not in one study.36 In several studies19,22,23 male subjects had decreased cardiovascular capacity when compared with controls, whereas females did not. Speculation as to why this may be so centered on the idea that when men lose their job there is a greater degree of inactivity, whereas in the case of women they remain more active at home with tasks such as cooking, cleaning, and childcare. This keeps them at an activity level equivalent to that of healthy females.

Muscle changes: composition and performance Skeletal muscle has incredible plasticity associated with it. It can adapt to almost any array of functional demands we place upon it. The level by which muscle function declines with inactivity depends upon the level of training before inactivity began and the duration of inactivity. In discussing muscle, it is important to understand the function of muscle subtypes. Type II (predominantly subtypes a and b) fibers are generally ‘fast twitch.’ They can track fast and are maximally powered by glycolysis, and therefore fatigue quickly. They are usually recruited late when the body needs to exert ‘maximal effort.’ Type I fibers are generally ‘slow twitch.’ They contrast slowly and are metabolically inexpensive, utilizing aerobic metabolism. In the acute period (14–30 days), fiber type is preserved even with activity reduction greater than 75% given the absence of an associated neuromuscular injury (i.e. foot drop such as from an L4 nerve root impingement).37,38 In the subacute period (30–90 days), large progressive shifts of type IIa fibers to type IIb fibers (both fast twitch fibers) occur at a rate of 5–19%.39 This shift can precede fatty replacement of muscle (apoptosis) in animal models. There is also a 15% decrease in the number as well as the size of type I (efficient slow twitch muscle fibers).40 In chronic detraining (90 days to 9 months), power lifters showed oxidative muscle (type I) fibers increased by 1.4 times,41 while type II fibers (fast twitch) decreased by 60% in axial muscles.42,43 It has been noted that the very young (less than 20 years old) may exhibit a certain immunity to fiber-type change in the face of detraining.44,45 A changed fiber cross-sectional area (atrophy) also occurs with deconditioning and detraining. In athletes both type I and type II fibers decreased in size by 9–23% in as little as 6 weeks of detraining.46 In a chronic period (7 months) there can be as much as 37% atrophy across all muscle fiber types.41 Mayer et al.47 noted in CT that CLBP patients (in both operative and nonoperative segments) had significantly decreased muscle bulk with evidence of fatty replacement of muscle. The authors further correlated this observational qualitative finding of atrophy with a quantitative finding of greater than 50% mean reduction in strength testing for the atrophied spinal muscle group compared to age- and gender-matched controls. Several other studies have shown smaller cross-sectional areas of the paraspinal muscles by CT or MRI scanning in subjects with CLBP.48–50 It remains debatable, but some papers have shown that larger muscles (postural 1216

muscles of the back and lower extremities) become atrophic at a faster rate than extremity muscles. Few authors have actually correlated strength performance to atrophy, but generally strength is largely preserved during short periods of convalescence although eccentric strength decreases earlier than other aspects of neuromuscular performance (7–21 days). In the subacute period (4–12 weeks) there are declines in strength, measured by both force and power, of 7–15%.51,52 For chronic periods, decreases in power were 40–60% for trained muscles in the arms and legs, but less dramatic decreases of 15–37% were noted in the contralateral untrained arm.37,53 Muscle endurance times are also decreased with deconditioning. Decreased strength as well as decreased endurance for trunk/spinal musculature was seen in patients with chronic low back pain despite having similar physical activity levels as age- and gender-matched controls.49,54 Mayer et al.55 demonstrated significant strength deficits for both trunk flexors and extensors for a group of CLBP patients utilizing a Cybex prototype sagittal trunk strength tester. Using a dynamic isokinetic lifting device, Kishino et al.56 show significantly decreased isokinetic as well as isometric lifting capabilities for patients with CLBP. Houston et al.37 have noted a capillary density diminution in as few as 15 days after training cessation. However, other authors have noted that even after 90 days of detraining, capillarization remained largely unchanged with only minor decreases in VO2 max.57 Mujika and Padilla, who have analyzed much of the existing data, surmise that capillaries and muscles are preserved in trained athletes and may account for their greater speed to reach previous training levels than in sedentary individuals.58,59 Rapid and progressive reduction in mitochondrial oxidative enzymes creates a rapid decrease in the efficiency of muscle cells to manufacture APT.59 Further, ‘run-time exhaustion’ or subthreshold muscle failure is associated with decreased mitochondrial density and/or efficiency.60 Deconditioned, formerly trained individuals retain higher enzymatic and mitochondrial numbers than sedentary individuals and will reach peak performance levels faster when they resume activity.61 Motor control is also adversely affected in the presence of CLBP. Performing a standardized reach task, postural control in patients with CLBP was more affected in those with severe low back pain compared with moderate pain.62 Patients with CLBP showed a delayed-onset contraction of abdominal muscles during motion of the upper extremities.63,64 Patients with low back pain were shown to have decreased trunk motion patterns while performing a repetitive wheel rotation task.65 Haines66 showed immobility, as well as decreased coordination and balance. Several surface EMG studies have shown reduced recruitment patterns and lower maximum integrated electromyography in paraspinal muscles in CLBP patients.67,68 Moreover, studies of movement patterns have shown the delayed onset of contraction of the transversus abdominis indicating a deficit of motor control, hypothesized to result in inefficient muscular stabilization of the spine.69 Thus, it appears that in the presence of CLBP there is muscular atrophy with a subsequent decrease in strength and endurance. In addition, altered recruitment patterns may affect muscular stabilization of the spine.

Obesity Several studies have addressed the issue of obesity in the presence of chronic pain and deconditioning, some specifically in a population of patients with CLBP. In an experimental study where subjects (not necessarily patients with CLBP) were placed at bed rest, it was shown that lean body mass decreases during 30 days of bed rest whereas body weight did not change.12 This finding suggests that the percentage of body fat will increase as the percentage of muscle mass decreases. During a period of reconditioning, this inverse relationship

Section 5: Biomechanical Disorders of the Lumbar Spine

was confirmed.70 Furthermore, it has been shown that with increasing aerobic fitness there is a significant decrease in the percentage of body fat. Verbunt et al.21 showed that the percentage of body fat of CLBP patients did not differ from controls, which is in agreement with the findings of others.49 Toda et al.71 was able to show that in female patients with CLBP there was an increase in the percentage of body fat when compared to healthy age- and gender-matched controls but were unable to show this same difference in men. Given the study design, it is impossible to state that this information provides definitive scientific evidence that an increased body fat percentage is the result of deconditioning in CLBP. Obesity itself may actually contribute to the occurrence of back pain and was already present before back pain began.

Psychosocial changes Why some patients develop CLBP and significant disability has become an evermore perplexing question. This small percentage of patients with oftentimes seemingly minor injuries and imaging studies comparable to others who recover as expected with little or no disability end up consuming a great majority of the dollars spent on treatment. The fear-avoidance model as an explanation of how and why some individuals with musculoskeletal disorders develop a chronic pain syndrome was first proposed by Lethem et al.72 in 1983. They described how fear of pain and avoidance of it result in the perpetuation of pain behaviors and experiences, even in the absence of demonstrable organic pathology. Fear-avoidance refers to the avoidance of movements or activities based on the fear of increased pain or re-injury. Thus, it is thought to play a role in the development of the deconditioning syndrome. Avoidance is a type of learned behavior which postpones or averts the presentation of an adverse event. Vlaeyen et al.73–75 have proposed a fear-avoidance model with two opposing behavioral responses: confrontation and avoidance, and present possible pathways by which injured patients get caught in a downward spiral of increasing avoidance, disability, and pain. The model predicts several ways that pain-related fear can lead to disability: 1. Negative appraisals about pain and its consequences, such as catastrophic thinking, are considered a potential precursor of pain related fear. 2. Fear is characterized by escape and avoidance behaviors, such that daily activities are diminished, resulting in functional disability. 3. Because avoidance behaviors occur in anticipation of pain rather than as a response to pain, they may persist, resulting in decreasing opportunities to correct them. 4. Longstanding avoidance and physical inactivity have a detrimental impact on the musculoskeletal and cardiovascular systems, leading to disuse and deconditioning. Avoidance also means withdrawal from essential reinforcers, thus increasing mood disturbances such as depression. Depression and disuse have been shown to be associated with decreased pain tolerance.76,77 5. Pain-related fear interferes with cognitive functioning just as other forms of fear and anxiety do, making those affected less able to shift their attention away from pain-related information, at the expense of other important tasks including coping with problems of daily life. 6. Pain-related fear will be associated with increased psychophysiological reactivity when the individual is confronted with situations that are appraised as dangerous. It has been proposed that there is a subgroup of CLBP patients who have a tendency to cope with pain using endurance strategies as opposed to avoidance strategies.6 In this fear-avoidance model of

chronic pain, patients appear to ignore their pain and ‘stick it out’ despite the pain. This ‘stick it out/grit their teeth’ behavior also results in complaints of persistent pain. These individuals are likely to report a physical activity level that fluctuates greatly over time as a reaction to their pain. They will tend to persevere or push on until increasing pain prevents it. This period of increased activity is then followed by a period of rest or reduced activity followed again by resumption of increased activity. This has been referred to as ‘all or nothing’ behavior, representing the so-called ‘overactivity/underactivity’ cycle seen in many chronic pain patients.78,79 What do we know about the effect of pain-related fear on physical performance? A significant correlation was found between painrelated fear and range of motion measured with a flexometer.80 Using a simple task such as lifting a 5.5 kg weight in the dominant arm and holding it until pain or physical discomfort made it impossible to continue, Vlaeyen et al.73 found a significant correlation between lifting time and results from the Tampa Scale for Kinesiophobia (TSK). The TSK was developed as a measure of fear of movement/(re)injury.81 The term kinesiophobia refers to an excessive, irrational, and debilitating fear of physical movement and activity resulting from a feeling of vulnerability to painful injury or re-injury. Using the knee extension–flexion unit (KEF, Cybex 350 system) Crombez et al.82 found a significant association between performance level and pain-related fear, but no relationship between performance and pain intensity in a group of patients with CLBP. They had chosen the knee extension–flexion test specifically because patients believed it put minimal strain on their backs. In a follow-up study utilizing trunk extension–flexion and a weight lifting task, they showed that painrelated fear was the best predictor of behavioral performance.83 They felt the study also supported the idea that pain-related fear is more disabling than pain itself. These studies provide evidence that painrelated fear is associated with escape/avoidance of physical activities, resulting in poor behavioral performance. Somewhat surprising then are the results of Wittink et al.84 who performed a maximal symptom-limited modified treadmill test in patients with CLBP. The Short Form - 36 mental health (MH) scale results were correlated with results from treadmill testing. The results showed that the reason to stop testing and time walked on the treadmill were determined by pain intensity increase and not by low mental health. Although patients with low mental health were more likely than patients with high mental health to stop testing because of pain, the results did not reach statistical significance. How pain-related fear affects daily activities and the development of disability has been studied as well. Waddell et al.85 developed the Fear-Avoidance Beliefs Questionnaire (FABQ) in 1993. It was developed based on theories of fear and avoidance behavior and focused specifically on patients' beliefs about how physical activity and work affected their low back pain. The FABQ is a self-report questionnaire of 16 items where each is answered on a seven-point Likert scale from strongly disagree to strongly agree. Answer analysis indicated a two-factor structure. Factor 1 (FABQ1) concerns fear-avoidance beliefs about the relationship between low back pain and work while Factor 2 (FABQ2) concerns fear-avoidance beliefs about physical activity in general. The two main findings of this study were: first, there was little direct relationship between pain and disability; and the second main finding is the strength of the relationship between fear-avoidance beliefs about work and both work loss and disability in activities of daily living. Waddell et al. concluded that ‘fear of pain and what we do about it is more disabling than the pain itself.’ In a study comparing people matched for pain intensity and duration, fear-avoidance beliefs were found to be an important factor discriminating people with considerable 1217

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sick leave from those with no sick leave.86 Vlaeyen et al.74 have shown that fear of movement (re)injury is a better predictor of selfreported disability levels as measured with the Rowland Disability Questionnaire than either via medical findings or pain intensity levels. Disability was most strongly correlated with the more specific pain-related fear measures as compared to more general measures of anxiety.87 Verbunt et al.88 were able to show that a fear of injury correlated significantly with disability as measured with the Roland Disability Questionnaire. They found no statistically significant association between disability and aerobic fitness or fear of injury and aerobic fitness. Thus, while fear of injury correlated with disability, they were unable to demonstrate that fear of injury leads to physical deconditioning. Prospective studies have attempted to address whether fearavoidance beliefs are a precursor to chronic pain or a consequence of the pain. Work by Klenerman et al.89 supports the idea that pain-related fear is a precursor of disability. In a large prospective cohort study, Linton et al.90 observed that individuals who scored above the median score on a modified version of the FABQ had twice the risk of having an episode of pain during the following year. While not a prospective study, Fritz et al.91 showed that fearavoidance beliefs were present in some patients with acute low back pain of less than 3 weeks' duration. The presence of these beliefs did not explain a significant amount of the variability in the initialdisability levels; however, they were significant predictors of 4-week disability and work status. In a prospective study of 252 patients presenting with low back pain in an effort to isolate risk factors for the development of chronic pain the results did not support the fear-avoidance concept as such a risk factor.92 The information from these studies suggests that there is a subgroup of patients with fear-avoidance beliefs prior to an injury or who develops the beliefs shortly thereafter. Evidence presented in this section suggests that pain-related fear leads to poor physical performance and that these effects also extend to activities of daily life including those in the workplace. In addition, fear-avoidance beliefs may be an important predictor of who may go on to develop chronic low back pain or as a predictor of who is at risk for a pain episode. Fear of injury/re-injury has been shown to correlate significantly with disability. Other psychosocial variables such as distress, depression, and anxiety have been mentioned in the deconditioning syndrome and have been studied in the presence of CLBP. A systematic review of prospective cohort studies in low back pain to evaluate the evidence implicating psychological factors in the development of chronicity in low back pain was recently undertaken by Pincus et al.93 Only six studies met their acceptability criteria for methodology, psychological measurement, and statistical analysis. They concluded that it was not possible to differentiate between psychological distress, depressive symptoms, and depressive mood and therefore chose to use the term distress to represent a composite of these parameters. The most consistent finding was that distress is a significant predictor of unfavorable outcome, particularly in the primary care setting. They also concluded from their review that somatization as well as distress was confirmed as having a role in the progression to chronicity in low back pain. The supporting evidence was felt to be strong for the role of psychological distress/depression and moderate for the role of somatization. They felt the evidence for fear/anxiety is surprisingly scarce in that the single acceptable study that looked at fearavoidance found it had no significant predictive power when analyzed together with other parameters.92 For a group of patients specifically diagnosed with acute radicular pain and a disc prolapse or protrusion, Hasenbring et al.6 looked at various psychological predictors, somatic predictors, and social predictors. Results of multivariate or 1218

regression analysis indicated that depressive mood and specific paincoping strategies are high-risk factors for the development of persistent pain. Relevant coping strategies were extreme tendencies to cope with physical and mental efforts, avoiding behavior on the one hand, extreme tendency to stick it out or to bagatellize on the other, or the nature of communication of the pain experience to others. An example of a maladaptive coping strategy was the tendency toward nonverbal/motoric expressive behavior such as groaning, twisting their faces, or rubbing the painful areas during pain. The extent of disc displacement was the only significant predictor of persistent pain among somatic predictors. Sitting occupation and social status were shown to be high-risk factors of chronicity of pain among the social variables investigated. Polatin et al.94 evaluated 200 patients with CLBP using a structured clinical interview. They reported a 45% point prevalence and a 64% lifetime prevalence of a major depressive episode. They further found that 55% of those who had concurrent major depressive disorder developed it before the onset of the low back pain but 45% became depressed after the onset of their pain.94 In a meta-analysis of studies of chronic pain and depression, 21 of 23 articles related the severity of pain to the degree of depression.95 The authors also concluded that the duration of pain was related to the development of depression in three of three studies of patients with diverse kinds of pain symptoms. They found that depression following the onset of pain was supported in 15 of 15 studies attempting to address this issue but that it preceded the onset of pain in 3 of 13 studies reviewed. Depressed subjects were found to have a reduced work capacity in one study.70 On the other hand, aerobically fit people were found to have reduced psychosocial stress responses in a review of 34 studies on the relationship between physical fitness and stress response.96 Selfreported stress was decreased and scores for subjective health and well-being were improved in 100 healthy police officers following their participation in an aerobic training program which resulted in improved physical fitness.97 Higher levels of physical activity were associated with a better mood, whereas inactive but fit subjects reported a poorer mood than inactive and unfit individuals.98 The authors concluded that the positive relationship between physical activity and mental mood was less mediated by improved fitness and more by participation in the performance of physical activity as a social event. A meta-analysis of the available literature in 1991 concluded that aerobic but not anaerobic exercise was associated with lower levels of anxiety.99 In summary then, it appears that CLBP is associated with increased depression, that depression becomes more common after the onset of pain, and that in the presence of CLBP depression may precede or follow the onset of pain. In addition, it is suggested that an improved level of physical fitness is associated with better mood and less distress while inactivity is associated with increased distress. Depression has been associated with a reduced physical work capacity and a decreased pain tolerance. While treatment is beyond the scope of this chapter and will be covered elsewhere, a brief mention of treatment specifically related to fear-avoidance beliefs seems warranted here. These beliefs and fear of movement/(re-)injury in particular have been shown to be strong predictors of physical performance and pain disability. Given this association, research has begun to be carried out on the effects of treatment specifically aimed at fear-avoidance behaviors. In a small study of six patients Vlaeyen et al.100 showed that improvements in pain-related fear and pain catastrophizing occurred only during a period of exposure in vivo and not during graded activity. Decreases in pain-related fear also concurred with decreases in pain disability and pain vigilance, and an increase in physical activity levels. Further, all

Section 5: Biomechanical Disorders of the Lumbar Spine

improvements remained at 1-year follow-up. Woby et al.101 found that reductions in fear-avoidance beliefs about work and physical activity, as well as increased perceptions of control over pain, were uniquely related to reductions in disability even after controlling for reductions in pain intensity, age, and sex. However, changes in the cognitive factors were not significantly associated with changes in pain intensity in a group of patients with CLBP. In a recent investigation, patients were treated with operant behavioral treatment plus cognitive coping skills treatment or operant behavioral treatment plus group discussion.102 Patients improved with respect to level of depression, pain behavior, and activity tolerance post-treatment and at 12-month follow-up. Treatment also resulted in a short- and long-term decrease in catastrophizing and enhancement of internal pain control. Klaber et al.103 treated patients in an exercise program of eight 1-hour sessions held twice per week designed to encourage movement of the back and strengthen and stretch all the main muscle groups in the body but not focusing on the back. The treatment program also included cognitive–behavioral principles. They compared patients treated with this program versus those allocated to ‘normal general practitioner care.’ High fear-avoiders fared significantly better in the exercise program with behavioral–cognitive principles than in usual general practice care at 6 weeks and 1 year. Those who were distressed or depressed were significantly better off at 6 weeks, but benefits were not maintained at 1 year. In a randomized clinical trial of patients with low back pain of less than 8 weeks' duration, George et al.104 showed that patients who initially had elevated fear-avoidance beliefs appeared to have less disability following fear-avoidance-based physical therapy when compared to those receiving standard physical therapy. However, patients with lower fear-avoidance beliefs appeared to have more disability from fear-avoidance-based physical therapy when compared to those receiving standard physical therapy. The fear-avoidance treatment group also had a significant improvement in fear-avoidance beliefs. There are only a few investigations in this area and conclusions should be drawn cautiously. Given that, it appears as if there is a group of patients possessing fear-avoidance beliefs who may derive greater benefit from treatment programs which address these behaviors.

CONCLUSION It is interesting that when the information available regarding disuse and a deconditioning syndrome in the presence of CLBP is reviewed, a clearer picture does not emerge. Clearly, it has been shown that complete bed rest or immobilization has profound and deleterious affects both physical and psychosocial. Less clear is whether patients with CLBP develop such a condition. With an injury, temporary suppression or cessation of domestic or professional responsibilities may initially be essential to the process of healing. The longer the period of decreased activity or disuse the greater the opportunity to create physical capacity deficits leading to decreased human performance or a deconditioning syndrome. When attempting to objectively confirm the presence of disuse or a decreased level of physical activity, several of the studies reviewed showed no difference between patients with CLBP and matched controls. Methods of activity measurement and working status have been offered as possible explanations for this lack of a discrepancy. If a decreased cardiovascular capacity measured by VO2 max is perceived as the gold standard for deconditioning, the available literature fails to definitively demonstrate its presence in patients with CLBP. Again, work status is proposed as a possible explanation for why results have varied. Muscle atrophy, weakness, and impaired coordination have been demonstrated in the presence of CLBP. As might be expected, there appears to be a significant role for the

presence of psychosocial issues. Particularly interesting appears to be the role of fear-avoidance beliefs. Whether these beliefs precede or follow the onset of pain is unknown and both scenarios may exist. The presence of such behaviors has been demonstrated in the acute phase (0–4 weeks). Their presence acutely has been associated with increased absenteeism from work later. In addition, a high point prevalence and lifetime prevalence of depression has been reported. Clearly, further research regarding disuse and a deconditioning syndrome in the presence of CLBP is needed. Attempts to define and document their presence in patients with CLBP have lead to inconclusive results.

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Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar ■ i: Functional Restoration

CHAPTER

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Functional Restoration Program Characteristics in Chronic Pain Tertiary Rehabilitation Tom G. Mayer

INTRODUCTION After most surgical and nonoperative primary and secondary treatment approaches have been exhausted, the majority of patients with occupational musculoskeletal disorders have returned to work and decreased their health utilization. Depending on the US state or federal workers’ compensation venue and musculoskeletal area, an average of about 10% of patients persist with workers’ compensation disability 3–4 months postinjury. The range is about 5–25%, with a smaller (but growing) group of patients persisting in ‘perpetual limited duty’ (or partial disability) in conjunction with the recent advocacy for ‘keeping patients on the job.’ In time, unless such patients are unable to return to full duty or significantly modified jobs, they too go on to persistent work adjustment problems with employers and increasing disability behaviors. Certain musculoskeletal disorders have a predilection for becoming chronic disabling problems. Spinal disorders, particularly those affecting the low back, usually beginning as ‘sprains and strains,’ are more highly represented among chronic pain/disability workrelated injuries than other musculoskeletal areas. Upper extremity non-neurocompressive complaints, particularly those termed repetitive motion or cumulative trauma disorders (CTD) also have a higher rate of developing chronicity, and CTD claims are known to be 1.8 times more expensive than non-CTD claims.1–7 By contrast, lower extremity injuries, particularly if they involve fractures, tend to resolve more completely within a usual tissue healing period. In many ways, the more subjective the diagnosis and mechanism of injury, the greater the likelihood of symptom persistence. Chronic spinal disorder (CSD) pain is not merely a function of incomplete healing after injury. Traditional medical efforts to treat and rehabilitate chronic back pain have often been met with poor outcomes. Past failed efforts to identify the source of, or treat, CSDs have resulted in the identification of ‘psychogenic’ or ‘functional’ pain, terms attributed to pain for which no physical substrate could be found and, therefore, for which psychological or ‘nonorganic’ causes were suspected. Back pain has been found to be subject to diverse influences including psychological difficulties (e.g. anxiety, substance use, depression), and social losses (e.g. inability to work, family role changes, financial stresses). Turk and Rudy8 set forth the biopsychosocial model of pain asserting that pain is engendered not only by physical insult, but also by cognitive, affective, psychosocial, and behavioral influences. Based on this biopsychosocial theory, CSD treatment considerations now go beyond the physical source of the pain to consider psychological and socioeconomic variables as well. Much controversy exists regarding the development of chronic pain/disability syndromes after work-related musculoskeletal inju-

ries. A variety of psychosocial host factors, secondary gain and socioeconomic predictors have been variably reported in the literature. Clinicians tend to focus on the nonphysiological aspects of pain persistence, regardless of the diagnosis, because of the reasonable assumption that bones, joints, and soft tissues have healed completely, even if imperfectly, in a finite period of time. While there may be persistent bony malalignment, joint degenerative arthritis or soft tissue scar, these changes are deemed ‘set in stone.’ They may result in some degree of permanent impairment. However, while the majority of injured workers (and a perceived greater percentage of patients without compensation) seem to recover in a timely fashion, a disturbingly large and costly group of chronic disability patients remain disabled and refractory to treatment over a substantial period of time. These patients tend to demand a significant preponderance of indemnity and medical costs, and if followed in most federal social systems for 15–20 years, represent the largest number of patients in every industrialized country who become permanently disabled for the longest periods of time. This is because the average age of workrelated musculoskeletal injury developing permanent disability is in the mid-30s, much earlier than any other diagnostic entity producing such disability (with the possible exception of the much less common psychiatric disorders). For these chronic pain/disability patients, repeated passive therapy, manipulation, or surgical intervention has commonly been tried, but has failed to relieve symptoms and overcome disability. These patients tend to produce the most significant cost to society in terms of medical care, disability payments, and loss of productivity. As such, they provoke a great deal of concern and interest. It is this difficult group of patients, failures of ‘conservative care’ and/or surgery, for whom spinal functional restoration is intended. Economic globalization may create dislocations of local economies. In industrialized countries such as the US, these dislocations cause major shifts in demand for workers in different labor-intensive industries. There are pressures on workers to develop skills to shift jobs within the changing job markets. Industry is incentivized to reject those workers unable to make the transition. There are similar incentives to minimize the appearance of unemployment and job dislocations by ‘disappearing’ less flexible employees from the national economy. When chronic disabling musculoskeletal disorders lead to long-term re-employment problems, employers may find it more convenient to convert them to ‘throwaway workers.’ This creates pressure to compensate such patients with public, rather than private financing. Since the 1960s, Social Security Disability Insurance (SSDI), more recently linked to medical benefits through Medicare, has been provided to such individuals under certain circumstances. There has been a recent exponential growth in acceptance of younger and potentially more able-bodied workers onto this 1223

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national insurance scheme, which was initially intended for retirees. Although musculoskeletal problems have decreased as the reason for acceptance onto SSDI rolls, they remain above 35% of all accepted claims. The combination of musculoskeletal and mental health ‘stress claims,’ which are often intertwined, have become the majority of acceptances onto SSDI. Because of the young age (30–45 years) at which many of these workers are accepted for long-term payments, Social Security actuaries have referred to the problem as one of ‘early, early retirement.’ Current costs are US$100 billion/year for SSDI, up 150% since 1980. There are now nearly 9 million ‘disabled’ preretirement Americans on Social Security, more than double the number in 1980.9 There is huge variance from state to state, with twice as many claims accepted in the disability determination process, and three times as many after the administrative hearing process, in the high-acceptance states (New Hampshire, Maine) compared to lowacceptance states (District of Columbia, Texas). The younger the patient accepted, the more likely there is a musculoskeletal basis, and low back pain is the single largest cause of musculoskeletal disability. With disability payments currently representing 5% of the entire US budget, such payments are becoming an increasing drain on the Social Security funds that were initially intended solely for retirees. Failure of tertiary rehabilitation for chronic occupational spinal disorders leads inevitably to patients departing the employment statistics and transitioning to insurance schemes such as SSDI in ever-increasing numbers. Thus, tertiary rehabilitation becomes the leading prevention strategy against permanent loss of productivity and high social cost in US spinal disorder medical care. Because of the multifactorial and subjective nature of chronic pain, traditional therapy has been less than fully effective in treating and rehabilitating CSD patients. As a result, medical approaches have evolved to accommodate this costly and complex phenomenon. There are several risk factors that can be used to guide the treatment of spinal disorders and pain based on the levels of treatment described below. The severity of the dysfunction must be considered. The severity of a musculoskeletal dysfunction is related more to the patient’s chronicity and level of disability than to the presumed causative event. While diagnoses (e.g. degenerative disc disease, facet arthropathy, disc disruption, segmental instability) may be important in identifying surgically treatable pathology, their relevance fades in chronic pain conditions in which patients have generally failed to respond to invasive procedures, or have been deemed unsuitable for surgery. In addition to the psychological factors, inactivity and disuse may play a major role. They may lead to the deconditioning syndrome, in which the injured spinal region becomes a ‘weak link’ connecting the body’s functional units. Deficits of motion, strength, and endurance interfere with physical performance of otherwise unaffected joints and muscles.10–14 While the need for spine surgery is rarely so imminent that a trial of nonoperative therapy is not indicated, there is often a limited understanding of the levels and purposes of such care as a function of the severity of the problem. No one has yet managed to identify the unique structural ‘pain generator’ in the majority of CSD patients. Description of such a site has eluded basic scientists, surgeons, internists, and psychologists, and probably will continue to do so. The obvious reason for this is that pain is a subjective central experience of multifactorial origin. With the source of the pain deeply submerged and inaccessible to visual inspection (similar to headache and chronic abdominal pain) the spine is subject to diverse influences such as psychological difficulty, social losses, and financial uncertainties. These ‘secondary phenomena’ tend to be ignored by the health provider who has no mechanism available to deal with these problems. As a consequence, a critical part of our understanding of spinal disability is lost. Since interdisciplinary experience is not usually part of most physi1224

cian training, lack of conceptualization and resolution in the area of chronic spinal disability is to be anticipated.

Three levels of nonsurgical care The chronologic severity of a spinal disorder can be used as a guidepost in determining the appropriate level of nonsurgical care, which can be organized into three distinct levels. Primary treatment is intended to address acute cases of back and neck pain, usually encompassing treatment of acute pain from an initial or recurrent event to 8–12 weeks after an incident or pain onset. In the majority of individuals experiencing back pain, pain usually resolves spontaneously within this time frame, accompanied only by passive care directed toward symptom control. Treatment modalities include medication (often narcotics, nonsteroidal antiinflammatories, and muscle relaxants), short periods of bed rest, thermal modalities, electrical stimulation, and manipulation techniques. Primary treatment may be supplemented with low-intensity supervised range of motion (ROM) exercise and education. Secondary treatment applies to those individuals (approximately 20–30%) whose pain persists beyond 2–6 months after the initial pain onset (i.e. beyond a reasonable tissue healing period), and who have not responded to primary treatment. More precisely, patients in the postacute phase of injury (and some postoperative patients) are likely to qualify for secondary nonoperative treatment. The secondary level of treatment is geared mainly toward patient reactivation, providing treatment of medium intensity. This intensity level is based on prevention strategies for managing risk factors for developing disability, deconditioning, and chronicity. The secondary level of treatment includes reactivation therapies that involve exercise and education specifically designed to prevent physical deconditioning. The exercise therapy may be supplemented by spinal injections for nerve irritation not requiring surgical decompression (epidural steroids), trigger point injections, or sacroiliac joint injections.15–17 Facet injections may be provided either for pain of facet origin, known as the facet syndrome, or for segmental rigidity noted on physical examination.18–23 Pharmacologic agents may be useful, but trends are away from habituating medication, such as narcotics and benzodiazepine ‘muscle relaxants,’ towards antiinflammatory medications. Exercise and education is usually provided by physical and/or occupational therapists in treatments lasting 1–3 hours several times weekly. Such treatments may also be supplemented by consultative psychological, case management, and physician services in formal programs; such programs are currently termed work conditioning or work hardening, and may involve daily utilization of 4–8 hours/day. The 5–8% of patients whose CSD pain persists beyond 4–6 months after the initial occurrence, and for whom disability predominates, are considered for referral to the tertiary level of treatment. Tertiary treatment at its best is a physician-directed, intensive, interdisciplinary team approach aimed at overcoming chronic pain and disability. The main goal of tertiary treatment is to ameliorate the permanent impairments and prevent the costly permanent disabilities related to CSDs that are the number one causes of total disability payments to claimants under age 45 for federal (public) or long-term (private) disability insurance schemes. Functional restoration programs are typically organized in a fashion similar to the traditional pain rehabilitation clinic, but these are more diverse and eclectic. The Commission for Accreditation of Rehabilitation Facilities (CARF) has guidelines that can be used as a minimum standard for tertiary care programs, currently termed Interdisciplinary Pain Rehabilitation programs. Because of the wide international reach of CARF, such programs may represent functional restoration for occupational injuries (as discussed in this case), or run the gamut to programs that are

Section 5: Biomechanical Disorders of the Lumbar Spine

most involved in cancer care or are mainly an adjunct to pain physician injection therapies and other palliative procedures. Because tertiary care patients have been shown to have a history of psychosocial, as well as functional, disturbances (e.g. substance abuse, affective disorders, limited compliance), tertiary treatment programs address issues of both physical and psychosocial deterioration. Functional restoration is one mode of tertiary treatment that has arisen in response to the poor outcomes associated with the traditional pain clinic, particularly in occupation CSDs.

and guide treatment. In addition to psychosocial problems originating because of persistent pain and disability, latent psychopathology may also be activated by life disruption produced by pain/disability. As such, psychiatric interventions, including use of psychotropic drugs and detoxification from narcotic and tranquilizer habituation, are helpful. Primary and secondary treatment alone may be ineffective in dealing with these multifactorial chronic dysfunctions, so that programmatic care delivered by an interdisciplinary team is desirable, if available.

The site of the disorders: cervical and lumbar

QUANTIFICATION OF PHYSICAL DECONDITIONING

One further consideration in the provision and qualification of CSD treatment is the site of the pain problem or injury. The lumbar and cervical spine have been associated with 60–75% of all musculoskeletal disability cases, while the thoracic spine is a rare problem area. As a result, pondering the similarities and differences between these spinal areas is important. Both the cervical and lumbar spine are characterized by a 3-joint anatomic complex controlling motion, and serving to maximize mobility while protecting neurologic structures. Thoracic motion is limited by a barrel-like rib/spine complex. There is a similarity in the relative size and stabilization of the cervical and lumbar anatomic structures used to support the different loads of the head or trunk, respectively. Compared to the thoracic spine, the lumbar and cervical areas demonstrate lower stability, higher mobility and a greater reliance on soft tissue support. As a result, individuals with injuries in these two spinal areas seem more likely to develop facet and degenerative disc disease, and show a higher rate of developing disabling symptoms associated with disuse, inactivity, and progressive deconditioning. The cervical and lumbar spinal areas also demonstrate characteristic differences. First, cervical disorders occur less frequently than lumbar ones. This region is also associated with ‘whiplash’ injuries and catastrophic neurological injury not found in the lumbar spine. The injuries to the cervical spinal area pose more of an upper motor neuron risk and are affected by sedentary activities, static positioning (e.g. sitting, writing, driving) and upper extremity activities (e.g. reaching, lifting over shoulder height, etc.). Injuries to the lumbar spinal area are exacerbated by the transmission of heavy loads from the hands through the trunk (e.g. lifting from floor while bending or twisting). Cervical spinal motion occurs in three planes (sagittal/coronal/axial) with biomechanical links to the shoulder, whereas lumbar motion occurs primarily in two planes (sagittal/ coronal) with biomechanical links to hip/pelvis. Understanding of these similarities and differences is a key component in designing and implementing an appropriate rehabilitation strategy for specific spinal disorders. The greatest assessment error for most clinicians is the failure to recognize the critical importance of socioeconomic factors in patients with chronic pain. It has been well established over the years that patients being paid for remaining disabled and nonproductive will behave differently from patients who are uncompensated.24–27 Similarly, patients likely to receive a bonus settlement for permanent impairment, even if they are not receiving direct disability indemnity benefits, will likely demonstrate some illness behaviors. Major Axis I psychiatric diagnoses (DSM-IV), such as substance use (often preexisting or iatrogenically abetted), or major depression, may strongly affect treatment progress and ultimate outcomes.28–30 This is particularly true if the clinician fails to recognize, or ignores, these crucial issues, dealing ‘only with the body and not the mind.’ Various treatment interventions have been designed to cope with the psychosocial and socioeconomic factors involved in total or partial disability. Psychosocial assessment is often necessary to identify these factors

While a normal soft tissue, joint, or bony healing period will generally have occurred by the time a patient enters a period of chronic pain/disability, progressive deterioration of physical and functional capacity may still be in an early stage. Deconditioning occurs as a consequence of disuse and fear-related inhibition. The quantitative assessment of function is a vital aspect of developing an effective treatment program for disabling spinal disorders. In the extremities, there is relatively good visual feedback of physical capacity. Joints are easily seen and mobility subject to goniometric measurements, and the muscle bulk is subject to tape measurements. Right/left comparisons between a normal and abnormal side can frequently be made. In the spine, there is inadequate direct visual feedback of physical capacity. Yet, this deficiency has not been generally recognized by clinicians who often continue to rely on subjective self-report or physical measures that are either inaccurate or irrelevant. More accurate methods are necessary for objective quantification.31–34 This information is discussed in greater detail in another chapter. However, for the focuses of this chapter, the author wishes to illustrate several aspects of quantification of function. In Figure 112.1, one sees the dual inclinometer method being used to measure spinal sagittal motion. In Figure 112.2, sagittal spine strength is being tested. The measurements of localized mobility and strength in the injured spinal region is termed physical capacity as it documents the ‘weak link’ deconditioning of an injured or involved area. This is contrasted with the concept of functional capacity, representing whole-person measurements. For whole-person functional measurements, lifting is

Fig. 112.1 Subject being tested for sagittal flexion utilizing the dual inclinometer method. One inclinometer is placed over T12 while the other is placed over the sacrum. 1225

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Fig. 112.2 A trunk extension/flexion (TEF) testing device used to measure sagittal trunk strength isokinetically and isometrically. Computerized calculations from the measurement dynamometer of torques in foot-pounds are generalized, normalized for effective patient comparisons, by age, gender, and body weight.

a useful tool to assess lumbar (floor-to-waist) and cervical (waistto-shoulder) functional regions. The progressive isoinertial lifting evaluation (PILE) test is a simple and inexpensive way to accomplish such measurement as seen in Figure 112.3A.35–37 Figure 112.3B demonstrates isokinetic and isometric (National Institute of Occupational Safety and Health) lift testing being performed.

PSYCHOSOCIAL AND SOCIOECONOMIC ASSESSMENT In a work environment, when injury is associated with compensation for disability, physical problems are rarely the only factor to be con-

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sidered in organizing a treatment program. Many psychosocial and socioeconomic problems may confront the patient recovering from a spinal disorder, particularly if inability to lead a productive lifestyle is associated with the industrial injury. The patient’s inability to see a ‘light at the end of the tunnel’ may produce a reactive depression, often associated with anxiety and agitation. The musculoskeletal injury itself may be associated with emotional distress as expressed by rebellion against authority or job dissatisfaction. Poor coping styles associated with reaction to stress or underlying personality disorders may be manifested in anger, hostility, and noncompliance directed at the therapeutic team. Organic brain dysfunction from age, alcohol, drugs, or a supposedly minor head injury, or limited intelligence may produce cognitive dysfunctions that make patients difficult to manage and refractory to education. Many CSDs exist within an occupational ‘disability system.’ Workers’ compensation laws were initially devised to protect workers’ income and provide timely medical benefits following industrial accidents. In return for providing these worker rights, employers were absolved of certain consequences of negligence, generally including cost-capped liability for any injury, no matter how severe, and set by state or federal statute. Unfortunately, certain disincentives to recovery may emerge. One outcome of a guaranteed paycheck, while Temporary Total Disability persists, is that there may be limited incentives for an early return to work. A casual approach to surgical decision-making and rehabilitation may lead to further deconditioning, both mental and physical, making getting well more problematic. Complicating matters even further is the observation that no group (other than the employer) has a verifiable financial incentive to rapidly return patients to productivity. In consequence, an assortment of health professionals, attorneys, insurance companies, and vocational rehabilitation specialists are involved with limited motivation to combat foot-dragging on the disability issue. Early efforts to distinguish between ‘functional’ (nonorganic) and ‘organic’ pain did not meet with success. The complex nature of chronic pain makes it difficult to categorize component factors as purely physical or psychological. Chronic pain must be understood as an interactive, psychophysiological behavior pattern wherein the physical and the psychological overlap. The focus of psychological

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Fig. 112.3 (A) The progressive isoinertial lifting evaluation (PILE) test uses simple milk cartons, standard-height shelves, and inexpensive weights added to a box with a fixed protocol. (B) A cable lifting device with a dynamometer permitting isometric and isokinetic lift assessment to a full range of motion (or selected ranges) from floor to above shoulder. Again, age, gender, and body weight normalization is common. 1226

Section 5: Biomechanical Disorders of the Lumbar Spine

evaluation of the patient with pain must shift away from ‘functional’ versus ‘organic’ distinctions to the identification of psychological behavioral motivators for each patient. These characteristics impact a patient’s disability and his or her response to treatment efforts. Treatment planning and the prediction of favorable treatment outcome are facilitated by first identifying and then controlling these factors. The assessment goal is to obtain a DSM-IV psychiatric diagnosis, particularly Axis I or II, to assist the interdisciplinary treatment team in understanding and dealing with the preexisting and posttraumatic barriers to recovery. Depression, anxiety, substance use, and stress disorders (Axis I) frequently accompany CSDs, as do preexisting personality disorders (Axis II) and childhood abuse experiences. Socioeconomic factors related to compensation for the injury (or its premature cessation), may be factored in with the variety of problems associated with education, transferable skills or family distress. Multidisciplinary medical treatment may include psychiatric interventions to detoxify and stabilize on psychotropic medication before the interdisciplinary team becomes involved in a treatment approach that requires physical training, education, and counseling as a significant component. Individualizing pain management, stress controls, and education, as well as guidance towards future return to productivity, is a vital outgrowth of the psychosocial assessment.

TERTIARY INTERDISCIPLINARY FUNCTIONAL RESTORATION TREATMENT Sports medicine concepts and physical training The principles of sports medicine have come to be used generally to refer not merely to the rehabilitation of the competitive athlete. Instead, they have been modified to emerge as a conceptual and methodological framework for actively treating all individuals who wish to return to high levels of function. Its component parts are shown in Table 112.1. Much of the initial work was done with extremity injury, but these concepts now involve the spine as well. The physiologic approach to the deconditioning syndrome involves therapeutic exercise to address mobility, strength, endurance, cardiovascular fitness, and agility/coordination. The exercises must progress to involve simulation of customary physical activities to restore task-specific functions. Such exercises must be focused at the specific functional unit that has become deconditioned, and ultimately be generalized to whole-body functions.

Table 112.1: Components of a Functional Restoration Program 1. Quantification of physical capacity and functional capacity 2. Quantification of psychosocial function 3. Reactivation for restoration of fitness 4. Reconditioning of the injured functional unit (weak link) 5. Retraining in multiunit functional task performance 6. Work simulation in common generic tasks 7. Multimodal disability management program 8. Vocational/societal reintegration 9. Formalized outcome tracking 10. Post-treatment fitness maintenance program and monitoring

Dynamic muscle training, which has been shown to be the most efficient method of training, can be employed in CSDs. It involves three basic modes: isotonic, isokinetic, and psychophysical (free weights).38 Isotonic exercises are those in which the same force is applied throughout the dynamic range and is often inappropriately used for exercises in which a changing lever arm actually alters the applied torque. This type of exercise is most often associated with the variable resistance devices, utilizing a cam to equalize muscular demands throughout the dynamic range of motion. Secondary effects of a functional restoration program are also critically important. Physical training appears to have a specific beneficial effect on pain (possibly through increased synthesis of specific neurotransmitters) and has been demonstrated to prevent scarring and adhesions while improving cartilage nutrition. Mobility appears to be the key, which can be done initially through passive and then subsequently through active means. Development of normal to supernormal strength and endurance in muscles acting around a joint may be of benefit in protecting a joint having sustained cartilage damage or instability due to ligamentous incompetence. This development of protective muscular mechanisms is particularly important when a complete return to normal joint architecture can no longer be anticipated. In the early stages of the program, mobility exercise is the most important aspect of physical training. Muscle training requires putting the affected joint (or spinal segment) through a full range of motion to be effective. Endurance training generally accompanies or follows strength training. Stretching of joints as much as possible, sometimes accompanied by use of antiinflammatory medication and/ or corticosteroid injections, is an important first step in the physical rehabilitation process. Yoga-type exercises, with the holding of postures at greater length than many patients are used to, including use of breathing to encourage relaxation, can be an effective tool. It is always a part of lifelong learning as a component of the fitness maintenance program. Strength training is generally done with weight machines. In the functional restoration program at PRIDE (Productive Rehabilitation Institute of Dallas for Ergonomics) the quantification of function using tests described in the previous chapter develops data that are fed into a computer system, which calculates suggested levels of training based on age, gender, body weight, and anticipated activity levels. A stepwise program to increase from the test-determined starting levels, checked periodically with repeat testing, is utilized. In Figure 112.4A, a torso rotation device to strengthen oblique spinal and abdominal musculature is utilized. Figure 112.4B shows a pulldown device for shoulder strength that also affects musculature in the cervical area (paraspinal muscles, trapezii, and scalene muscles). When a fitness maintenance program is developed for patients to continue with what they have learned during their rehabilitation, a Roman chair (Figure 112.4C) may be useful for extensor strengthening of all of the spine muscles from cervical to lumbar area, including the gluteal/hip muscles. In the physical therapy areas, patients train the injured ‘weak link’ area of the spine. This area must be isolated and focused on by the therapists in a supervised environment, because patients are generally inhibited by fear-avoidance or prolonged disuse. Most training devices are therefore specific to a certain injured part of the body (e.g. cervical spine, lumbar spine, knees, etc.). In the occupational therapy area, patients focus on coordinating the injured ‘weak link’ with other body parts to achieve full-person functional activities. The performance of such functional activities predominates, encouraging such capabilities as lifting, bending, reaching, climbing, or twisting. An obstacle course of multiple devices used to demand patient agility in performing functional tasks can be very useful. Figure 112.5A 1227

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B

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Fig. 112.4 (A) A torso rotation strength device using weight stacks with training levels individualized by patient testing scores, age, gender, and body weight. (B) A shoulder pull-down device is used to help strengthen the neck and shoulder girdle musculature. (C) A Roman chair device can be used at home or in a fitness center to help maintain strength of the spinal extensors and gluteal/hip musculature.

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Fig. 112.5 (A) Shows a patient engaged in functional tasks in the occupational therapy gym, combining carrying, lifting, and climbing tasks. (B) Shows patients engaged in upper extremity functional tasks.

Section 5: Biomechanical Disorders of the Lumbar Spine

demonstrates a patient who combines functional tasks, including lifting, carrying, and climbing, with a relatively simple stair device. Figure 112.5B shows wall-mounted devices that can be used to enhance upper extremity motion for patients with cervical CSDs with radicular problems, or associated upper extremity disorders. In the later stages of functional restoration, the occupational therapists supervise a ‘ready room’ allowing actual simulation of work tasks, such as truck driving, clerical work, construction work (carpentry, electrical, plumbing, etc.) and other manual tasks.

patients generally achieve a much higher level of physical and functional capacities, which must be continued in a fitness maintenance program (FMP). The patient is educated on an individualized FMP, based on the training level they have achieved by the program’s conclusion. Follow-up objective physical quantification leads to feedback to the patient on maintenance of physical capacity, which can be correlated with job demands. Relevant pieces of durable medical equipment (DME) (see Fig. 112.4C) or memberships in appropriately equipped fitness centers, may be suggested.

Psychosocial interventions in functional restoration

SUMMARY

The patient undergoing CSD rehabilitation is customarily one who has issues of prolonged disability, associated with longstanding pain. Traditional approaches have focused on ‘pain management’ which is intended to teach patients about coping with pain and modifying self-defeating behaviors. The essential flaw in solely utilizing this approach has been the continued focus on the patient’s self-report of pain, which is ultimately self-serving and unmeasurable. In functional restoration, the physician emphasizes the return to function and the setting of specific goals to achieve this return, recognizing that improved physical capacity, decreased stress and tension, and return of self-esteem and self-confidence will probably reduce the patient’s pain perception. The rehabilitation process itself may be a stressful and physically painful ‘spring training’ experience for the physically and psychologically deconditioned individual. One-half of the program is devoted to education and counseling, and incorporates supportive and inspirational interventions to help the patient to successfully complete rehabilitation.

Individual and group counseling Patients are typically defensive in initial psychological counseling, and resist any interpretation of behavior that does not first acknowledge the validity of their physical complaints. Frustration regarding the pace of training inevitably occurs, making support during the difficult physical and psychological tasks essential, and often takes place on one-on-one individual sessions. In group settings, discussion of difficulties with the process of rehabilitation is encouraged. The use of a ‘buddy system,’ pairing an advanced patient with one who is just getting started, can be helpful. There are group discussions of subjects such as psychological testing, confidentiality, personal responsibility, the work ethic, concerns about returning to work, litigation, fear of pain, and medication/drug use. Depression is presented as a frequent component of chronic pain. Patients are encouraged to discuss their reactions with treatment staff, and are given feedback about their behavior.

Behavioral stress management training Anxiety and accompanying physical tension clearly accentuate the psychophysiological experience of pain. Behavioral stress management is an important component of the treatment program. Biofeedback improves the patient’s ability to relax physically and to gain better self-control over tight and painful muscles. Cognitive behavioral training enables him to relax by gaining control over unwanted thoughts directing his attention away from stressors. Education in stress management teaches him to modulate stress by properly controlled breathing. Group sessions provide discussion of the role of stress in sleep disturbance, stiff joints, tight muscles, and emotional distress, so that patients more clearly understand the importance of a relaxation response when pain and tension increase. The patient’s ultimate socioeconomic outcomes depend on the maintenance of treatment goals. Under treatment supervision,

Chronic spinal disorder pain/disability is a very costly and serious phenomenon in most industrialized countries. Although the majority of individuals will experience back pain in their lifetime, most will see their symptoms remit within a short time. A minority will experience ongoing pain and physical disability well beyond the expected healing time. This minority generates 90% of the cost associated with treating spinal disorders when measured over more than 1–2 decades. Our understanding of CSDs has evolved over the years from a binary classification of pain as either psychogenic or physically based, to a multifactorial model of interlaced phenomena contributing to the pain experience, including biological, social, and psychological influences. As a result of the evolution in our understanding of chronic pain, applicable treatments have also evolved, culminating in the genesis of an eclectic mix of pain clinics across the United States, with treatments geared toward treating the physical substrate of pain as well as addressing psychological and socioeconomic factors. Tertiary treatment is indicated for patients experiencing chronic disability. This level of care involves an intense, interdisciplinary treatment team approach focusing on reestablishing physical function and helping the patient manage the psychological and socioeconomic barriers to recovery. Functional restoration is a form of tertiary treatment which uses objective evaluations of a patient’s physical, functional, and emotional capacity to organize a physician-directed interdisciplinary team-treatment approach whose primary goal is to improve functional status. The functional restoration approach differs from other tertiary chronic pain treatment modalities through an emphasis on physical reconditioning and improved function over the goal of pain relief alone. Traditional chronic pain management programs, however, place pain relief as a primary goal regardless of a patient’s activity level or medication regimen. Patients who fail to respond to both surgical and less invasive levels of nonoperative treatments for CSDs may be referred to functional restoration rehabilitation. In most cases, this is the final level of care before patients reach a medical treatment endpoint, known in most workers’ compensation venues as maximum medical improvement (MMI). This is the point at which all reasonable medical treatments designed to improve or cure the condition have been offered or provided. At this point, it is the patient’s decision whether to return to productivity and decrease health utilization, or to pursue efforts at obtaining compensation for permanent disability through one of the public (SSDI or SSI) or private (LTD) insurance schemes that they may be eligible for. The complex interaction of financial, psychosocial, and physical factors affect the individual’s ultimate decision, and determine the socioeconomic outcomes of a functional restoration program.

References 1. Mayer T, Gatchel R, Polatin P, et al. Outcomes comparison of treatment for chronic disabling work-related upper extremity disorders and spinal disorders. J Occup Environ Med 1999; 41:761–770. 2. Vender M, Kasdan M, Truppa K. Upper extremity disorders: A literature review to determine work-relatedness. J Hand Surg 1995; 20A(4):534–541.

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Part 3: Specific Disorders 3. Association of Schools of Public Health/National Institutes for Occupational Safety and Health. Proposed national strategies for the prevention of leading work-related diseases and injures. Part 1 Washington, DC: Association of Schools of Public Health; 1986:19. 4. Bureau of Labor Statistics. Workplace injuries and illnesses in 1994 (USDL Publication No. 95–508). Washington DC: US Department of Labor; 1995. Available: osh/osnr0001.txt 5. Bureau of Labor Statistics. Workplace injuries and illnesses in 1996 (USDL Publication No. 97–453). Washington, DC: US Department of Labor; 1997. Available: osh/osnr0005.txt 6. Brogmus G, Sorock G, Webster B. Recent trends in work-related cumulative trauma disorders of the upper extremities in the United States: An evaluation of possible reasons. J Occup Environ Med 1996; 38(4):401–411. 7. Webster B, Snook S. The cost of compensable upper extremity cumulative trauma disorders. J Occup Med 1994; 36(7):713–727. 8. Turk D, Rudy T. Toward a comprehensive assessment of chronic pain patients. Behavioral Res Ther 1987; 25:237–249. 9. Charting the future of Social Security Disability Programs: the need for fundamental change, Social Security Advisory Board Report. Washington, DC: Congressional Printing Office; January 2001. 10. Beals R. Compensation and recovery from injury. West J Med 1994; 140: 233–237. 11. Keeley J, Mayer T, Cox R, et al. Quantification of lumbar function, part 5: reliability of range of motion measures in the sagittal plane and an in vivo torso rotation measurement technique. Spine 1986; 11:31–35. 12. Kishino N, Mayer T, Gatchel R, et al. Quantification of lumbar function, part 4: isometric and isokinetic lifting simulation in normal subjects and low back dysfunction patients. Spine 1985; 10:921–927. 13. Mayer T, Smith S, Keeley J, et al. Quantification of lumbar function, part 2: sagittal plane trunk strength in chronic low back pain patients. Spine 1985; 10:765–772. 14. Mayer T, Tencer A, Kristoferson S, et al. Use of noninvasive techniques for quantification of spinal range-of-motion in normal subjects and chronic low-back dysfunction patients. Spine 1984; 9:588–595.

21. Mayer T, Gatchel R, Keeley J, et al. A randomized clinical trial of treatment for lumbar segmental rigidity. Spine; In press. 22. Mooney V, Robertson J. The facet syndrome. Clin Orthop 1976; 115:149–156. 23. Schwarzer A, Aprill C, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–1137. 24. Rainville J, Hartigan C, Wright A. The effect of compensation involvement on the reporting of pain and disability by patients referred for rehabilitation of chronic low back pain. Spine 1997; 22:2016–2024. 25. Greenough C, Fraser R. The effects of compensation on recovery from low back injury. Spine 1989; 14:947–955. 26. Hadler N, Carey T, Garrett J. The influence of indemnification by workers’ compensation insurance on recovery from acute backache. Spine 1995; 20:2710–2715. 27. Sanderson P, Todd B, Holt G, et al. Compensation, work status, and disability in low back pain patients. Spine 1995; 20:554–556. 28. Polatin P, Kinney R, Gatchel R, et al. Psychiatric illness and chronic low back pain: The mind and the spine – Which goes first? Spine 1993; 18:66–71. 29. Dersh J, Gatchel R, Polatin P. Chronic spinal disorders and psychopathology: research findings and theoretical considerations. Spine J 2001; 1:88–94. 30. Dersh J, Gatchel R, Polatin P, et al. Prevalence of psychiatric disorders in patients with chronic work-related musculoskeletal pain disability. J Occup Environ Med 2002; 44:459–468. 31. Gatchel R, Mayer T, Hazard R, et al. Functional restoration: Pitfalls in evaluating efficacy [editorial]. Spine 1992; 17:988–995. 32. Hazard R. Spine update: Functional restoration. Spine 1995; 20:2345–2348. 33. Hazard R, Fenwick J, Kalish S, et al. Functional restoration with behavioral support: A one-year prospective study of chronic low back pain patients. Spine 1989; 14:157–165.

15. Benzon H. Epidural steroid injections for low back pain and lumbosacral radiculopathy. Pain 1986; 24:277–295.

34. Mayer T, Gatchel R, Mayer H, et al. A prospective two-year study of functional restoration in industrial low back injury: An objective assessment procedure. JAMA 1987; 258:1763–1767.

16. Dilkem T, Burry H, Grahame R. Extradural corticosteroid injection in management of lumbar nerve root compression. Br Med J 1973; 16:635–637.

35. Mayer T, Barnes D, Nichols G, et al. Progressive isoinertial lifting evaluation, Part I: A standardized protocol and normative database. Spine 1988; 13:993–997.

17. Weinstein SM, Herring SA, Derby R. Epidural steroid injections. Spine 1995; 20:1842–1846.

36. Mayer T, Barnes D, Nichols G, et al. Progressive isoinertial lifting evaluation, Part II: A comparison with isokinetic in a disabled chronic low back pain industrial population. Spine 1988; 13:998–1002.

18. Dreyfuss P, Dreyer S, Herring S. Lumbar zygapophyseal (facet) joint injections. Spine 1995; 20:2040–2047. 19. Jackson R, Jacobs R, Montesano P. Facet injection in low back pain: a prospective statistical study. Spine 1998; 13:966–971.

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20. Mayer T, Robinson R, Pegues P, et al. Lumbar segmental rigidity: can its identification with facet injections and stretching exercises be useful? Arch Phys Med Rehabil 2000; 81:1143–1150.

37. Mayer T, Gatchel R, Barnes et al. Progressive isoinertial lifting evaluation: an erratum notice. Spine 1990; 15:5. 38. Eriksson E. Sports injuries of knee ligaments. their diagnosis, treatment, rehabilitation and prevention. Med Sci Sports 1976; 8:133–144.

PART 3

SPECIFIC DISORDERS

Section 5

Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar ■ i: Functional Restoration

CHAPTER

113

Tertiary Rehabilitation Program Outcomes Robert J. Gatchel and Tom G. Mayer

Pain is usually broadly defined as either acute, chronic, or recurrent, depending on its time course.1 Acute pain is often indicative of tissue damage, and it is characterized by momentary intense noxious sensations (i.e. nociception). It serves as an important biological signal of potential tissue/physical harm. Some anxiety may initially be precipitated, but prolonged physical and emotional distress usually is not. Indeed, anxiety, if mild, can be quite adaptive in that it stimulates behaviors needed for recovery, such as the seeking of medical attention, rest, and removal from the potentially harmful situation. As the nociception decreases, acute pain usually subsides. Chronic pain is defined as pain that lasts 6 months or longer, well past the normal healing period one would expect for its protective biological function. Arthritis, back injuries, and cancer can produce chronic pain syndromes and, as the pain persists, it is often accompanied by emotional distress such as depression, anger, and frustration. Such pain can also often significantly interfere with activities of daily living. Recurrent pain refers to intense, episodic pain, reoccurring for more than 3 months. Recurrent pain episodes are usually brief (as are acute pain episodes); however, the reoccurring nature of this type of pain makes it similar to chronic pain in that it is very distressing to patients. Such episodes may develop without a well-defined cause, and then may begin to generate an array of emotional reactions, such as anxiety, stress, and depression/helplessness. Often, pain medication is used to control the intensity of the recurrent pain, but it is not usually helpful in reducing the frequency of the episodes that a person experiences. It should also be noted that, many times, patients find it difficult to distinguish between chronic and recurrent pain. Patients will often present with ‘chronic-like’ symptoms from prolonged episodes of, say, headache or back pain. These do not always fit the description of chronic pain, but are usually persistent and can be as disabling. Of course, the above types of pain require different treatment approaches.2 In discussing back pain rehabilitation, for example, primary care is applied usually to acute cases of pain of limited severity. Basic symptom control methods are utilized in relieving pain during the normal early healing period. Frequently, some basic psychological reassurance that the acute pain episode is temporary, and will soon be resolved, is quite effective. There is now evidence for safety, treatment- and cost-effectiveness of evidence-based guidelines for the management of acute low back pain in primary care.3 Secondary care represents ‘reactivation’ treatment administered to those patients who do not improve simply through the normal healing process. It is administered during the transition from acute (primary) care to the eventual return to work. Such treatment has been designed in order to promote return to productivity before advanced physical

deconditioning and significant psychosocial barriers to returning to work occur. At this phase, more active psychosocial intervention may need to be administered to those patients who do not appear to be progressing. Finally, tertiary care requires an interdisciplinary and intensive treatment approach. It is intended for those patients suffering the effects of physical deconditioning and chronic disability. In general, it differs from secondary treatment in regard to the intensity of rehabilitation services required, including psychosocial and disability management.

THE BIOPSYCHOSOCIAL MODEL OF PAIN Before discussing tertiary care, which is a topic of the present chapter, it is important to first review the underlying theoretical model of pain upon which tertiary rehabilitation is based – the biopsychosocial model of pain. Today, this biopsychosocial model is accepted as the most heuristic perspective to the understanding and treatment of chronic pain disorders.4,5 This model views physical disorders such as pain as the result of a complex and dynamic interaction among physiologic, psychologic, and social factors that perpetuate and may even worsen the clinical presentation. Each individual experiences pain uniquely, as the result of the range of psychologic, social, and economic factors that can interact with physical pathology to modulate that individual’s report of symptoms and subsequent disability. The development of this biopsychosocial approach has grown rapidly during the past decade, and a great deal of scientific knowledge has been produced in this short period of time concerning the best care of individuals with complex pain problems, as well as pain prevention and coping techniques. As Turk and Monarch5 and Gatchel and Maddrey6 have discussed in their comprehensive reviews of the biopsychosocial perspective on chronic pain, people differ significantly in how frequently they report physical symptoms, in their tendency to visit physicians when experiencing identical symptoms, and in their responses to the same treatments. Often, the nature of a patient’s response to treatment has little to do with his or her objective physical condition. For example, White and colleagues7 have noted that less than one-third of all individuals with clinically significant symptoms consult a physician. On the other hand, 30–50% of patients who seek treatment in primary care do not have specific diagnosable disorders!8 Turk and Monarch5 also make the distinction between disease and illness in better understanding chronic pain. The term disease is basically used to define ‘an objective biological event’ that involves the disruption of specific body structures or organ systems caused by either anatomical, pathological, or physiological changes. Illness, in contrast, is generally defined as a ‘subjective experience or self-attribution’ that a disease is present. An illness will produce physical discomfort, 1231

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behavioral limitations, and psychosocial distress. Thus, illness refers to how a sick individual and members of his or her family live with, and respond to, symptoms and disability. This distinction between disease and illness is analogous to the distinction made between pain and nociception. Nociception involves the stimulation of nerves that convey information about tissue damage to the brain. Pain, on the other hand, is a more subjective perception that is the result of the transduction, transmission, and modulation of sensory input. This input may be filtered through a person’s genetic composition, prior learning history, current physiological status, and sociocultural influences. Pain, therefore, cannot be comprehensively assessed without a full understanding of the individual who is exposed to the nociception. The biopsychosocial model focuses on illness, which is the result of the complex interaction of biological, psychological, and social factors. With this perspective, a diversity in pain or illness expression (including its severity, duration, and psychosocial consequences) can be expected. The interrelationships among biological changes, psychological status, and the sociocultural context all need to be taken into account in fully understanding the pain patient’s perception and response to illness. A model or treatment approach that focuses on only one of these core sets of factors will be incomplete. Indeed, the treatment efficacy of a biopsychosocial approach to pain has consistently demonstrated the heuristic value of this model.5

THE BIOPSYCHOSOCIAL APPROACH TO TERTIARY PAIN MANAGEMENT Thus, the biopsychosocial approach to tertiary pain management appropriately conceptualizes pain as a complex and dynamic interaction among physiologic, psychologic, and social factors that often results in, or at least maintains, pain. It cannot be broken down into distinct, independent psychosocial or physical components. Each person also experiences pain uniquely. The complexity of pain is especially evident when it persists over time, as a range of psychological, social, and economic factors can interact with pathophysiology to modulate a patient’s report of pain and subsequent disability. The model utilizes physiologic, biologic, cognitive, affective, behavioral, and social factors, as well as their interplay, when explaining a patient’s report of pain. As will be discussed, there have been a number of reviews that have documented the clinical effectiveness of such interdisciplinary treatment of patients with chronic pain.9–12 Interdisciplinary programs are needed for patients with chronic pain who have complex needs and requirements. One variant of interdisciplinary tertiary pain management programs – functional restoration (FR) – has been comprehensively presented in Chapter 112. It has also been described in detail in a number of publications.13–19 The primary goal of this rehabilitation process is to improve function and deal with any potential psychosocial and economic barriers to attaining this goal. As will be noted, these components are amenable to systematic outcome quantification. Indeed, this FR approach to the treatment of low back pain disability has received increasing attention in recent years because of its documented clinical effectiveness. Research has shown that the FR program, when fully implemented, is associated with substantive improvement in various important societal outcome measures (e.g. return to work and resolution of outstanding legal and medical issues) in chronically disabled patients with spinal disorders in a 6-month follow-up study,20 1-year followup studies,21–26 as well as a 2-year follow-up study.27 For example, in the 2-year follow-up study by Mayer et al.,27 87% of the FR treatment group was actively working at 2 years as compared to only 41% of a nontreatment comparison group. Moreover, about twice as many of the comparison group of patients had both additional spine surgery and unsettled workers’ compensation litigation relative to the treat1232

ment group. The comparison group continued with approximately a fivefold higher rate of patient visits to health professionals and had higher rates of recurrence or reinjury. Thus, the results demonstrate the striking impact that an FR program can have on these important outcome measures in a chronic group consisting primarily of workers’ compensation cases (traditionally the most difficult cases to treat successfully). Finally, it should be noted that the original FR program was independently replicated by Hazard et al.23 in this country, as well as Bendix and Bendix24 and Bendix et al.25 in Denmark, Jousset et al. in France,20 Hildebrandt et al.26 in Germany, and Corey et al.28 in Canada. The fact that different clinical treatment teams, functioning in different states (Texas and Vermont) and different countries, with markedly different economic/social conditions and workers’ compensation systems, produced comparable outcome results speaks highly for the robustness of the research findings and utility, as well as the fidelity, of the FR approach. In addition, Burke et al.29 have demonstrated its efficacy in 11 different rehabilitation centers across 7 states. Hazard30 has also reviewed the overall effectiveness of FR. Thus, the clinical effectiveness of FR has been well documented. Indeed, Gatchel and Turk31 and Turk32 have reviewed both the therapeutic- and cost-effectiveness of interdisciplinary programs, such as functional restoration, for the wide range of chronic pain conditions. One of the hallmarks of FR since its development by Mayer and Gatchel16 has been the objective documentation of outcomes, even before it became a requirement in today’s evidence-based medicine environment.

THE IMPORTANCE OF TREATMENT OUTCOMES EVALUATION As Mayer et al.33 have noted, healthcare costs are continuing to increase at an alarming rate in the United States. Therefore, changes in healthcare policy and demands for improved allocations of health resources have recently placed great pressure on healthcare professionals to provide the most cost-effective treatment for pain syndromes and to validate treatment efficacy. As a result, treatment-outcome monitoring has gained new importance in healthcare. Indeed, as highlighted in an Outcomes Symposium sponsored by the American Orthopedic Association, the current outcomes movement has begun to revolutionize clinical research, with the concomitant increased emphasis on the use of well-validated outcome measures.34 Healthcare professionals are now themselves being monitored to determine the effectiveness of the treatments they provide, as well as patient satisfaction with their treatment. Often, a ‘scorecard’ is maintained by third-party payers to monitor practitioners’ efficacy.1 Healthcare professionals also need to monitor such outcomes for quality assurance purposes. In addition, data are also needed that can provide third-party payers with demonstrations of treatment efficacy. This can be an important marketing strategy to highlight the effectiveness of one’s pain management program. Unfortunately, many healthcare professionals do not have a background in conducting program or treatment evaluations because of the requisite experimental methodology and statistical tools needed for such evaluations. One needs to set up a database with appropriate psychometrically sound measures to use at baseline and follow-up evaluations. Such data then need to be statistically analyzed. Fortunately, there are now templates and reviews available for conducting such evaluations. Flores et al.,35 Gatchel,36 and Mayer et al.37 have provided such overviews. These will be discussed below. Morley and Williams38 have also presented a comprehensive review of how to conduct and evaluate treatment outcome studies.

Section 5: Biomechanical Disorders of the Lumbar Spine

It should also be noted that, at an early point in time, Blanchard39 highlighted six important dimensions that one should consider in evaluating clinical applications and effectiveness of therapeutic modalities, using biofeedback as an example. These same six dimensions would similarly be appropriate for the evaluation of various pain management procedures. These dimensions consist of the following: ● ● ● ● ● ●

The percentage or fraction of the treated patient sample that demonstrated significant therapeutic improvement. The degree of clinical meaningfulness of the therapeutic changes that were obtained. The degree of transfer of changes that were obtained in the clinical setting to the patient’s natural environment. The degree of change in the biopsychosocial response for which the treatment was prescribed. The degree of replicability of the results by different clinicians and clinical sites. The extent and thoroughness of the follow-up data for pain.

Each of these dimensions is important, and should be considered when evaluating the therapeutic effectiveness of any pain management intervention. Finally, in any discussion of treatment outcomes monitoring, clinicians now need to be aware of the HIPAA Privacy Rules. These rules establish patients’ rights concerning the use and disclosure of their healthcare information (including when it is being used for research outcomes purposes). Besides the usual informed consent obtained according to each institution’s review board monitoring the safety of subjects involved in any clinical research trial, an additional HIPAA consent form must also be obtained. Healthcare professionals may order HIPAA Privacy Rules from their specialty organizations. For example, HIPAA for Psychologists can be ordered by going to www.apapractice.org.

REVIEW OF OUTCOME MEASURES The article by Flores and colleagues35 reviewed the three broad categories of measures that have been used to objectively evaluate functional improvement in patients with spinal pain disability: physical, psychological and socioeconomic. Moreover, within each of these three categories, some of the major measures utilized were discussed. This review started with the following folk tale: It was six men of Indostan to learning much inclined Who went to see the Elephant (though all of them were blind) That each by observation Might satisfy his mind. The First approached the Elephant And happening to fall against his broad and sturdy side At once began to bawl: ‘Bless me! but the Elephant is very like a wall!’ The Second, feeling of the tusk, cried, ‘Ho! what have we here, so very round and smooth and sharp? To me ‘tis mighty clear This wonder of an Elephant is very like a spear!’ The Third approached the animal, and happening to take the squirming trunk within his hands Thus boldly up and spake: ‘I see,’ quoth he, ‘the Elephant is very like a snake!’ And so these men of Indostan disputed loud and long Each in his own opinion exceeding stiff and strong Though each was partly in the right, and all were in the wrong”! The Blind Men and the Elephant: An Old Indian Folk Tale, version written by John Godfrey Saxe

Just as the blind men in this folk tale viewed and described the ‘whole,’ or the elephant, in quite different terms, depending on what part of it each measured or touched, so too, may functional measures of improvement might be described quite differently depending on what referent or measure of function one decides to touch or quantify. Indeed, when trying to quantify functional change in spinal disorders, there are three broad categories of measures that have been used – physical, psychological and overt behavior (i.e. observable behaviors such as activities of daily living, return-to-work, etc.). Of course, at first blush, they may not appear to be closely related in describing the ‘whole.’ However, upon more careful scrutiny and analysis, they are merely measuring different parts of a whole person’s functional performance. At the outset, though, it should be clearly noted that these three different categories of measures may not always display high concordance with one another in all situations. Such less than perfect concordance among these behavioral referents of a construct such as function or functional improvement is not, however, unique to the area of spinal disorders or rehabilitation medicine in general. For example, it has long been noted in the psychology literature that self-report, overt behavior, and physiological indices of behavior sometimes show low correlations among one another. Thus, if one uses a self-report measure as a primary index of a construct and compares it to the overt behavior or physiologic index of the same construct, direct overlap cannot automatically be assumed. Moreover, two different self-report indices or physiological indices of the same construct may not be as highly correlated as one would desire (Fig. 113.1). In general, what has often plagued the evaluation arena has been the lack of agreement on the wide variation of measures used to document a construct and changes in that construct. Thus, the literature is full with many different measurement techniques and tests of a construct such as function. Recently, though, the literature has begun to demonstrate which measures of function and functional improvement appear to be most reliable and valid. For example, Mayer et al.40 have reviewed the evaluation process of outcomes associated with FR. Because of the emphasis on the return to productivity inherent in FR, socioeconomic outcomes should be evaluated. Some of these outcomes include work status, healthcare utilization, recurrent injury, etc. Such socioeconomic outcomes will be reviewed in greater detail below. Other less objective outcomes that are used, such as validated psychosocial questionnaires, will also be subsequently discussed.

Fig. 113.1 The often low concordance among and within physical, psychosocial, and overt behavior measures.85 From Gatchel 1998,52 with permission of American Pain Society. 1233

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Table 113.1: Major Categories of Measures that can be used to Document Functional Improvement PHYSICAL MEASURES Range of motion Spine strength Lifting capacity Other tests of human performance capability PSYCHOLOGICAL MEASURES Psychological test measures Self-report measures of pain and disability The clinical interview Clinician rating of overt pain behavior SOCIOECONOMIC MEASURES Work status New health utilization Recurrent injury claim Financial claim resolution

Finally, physical assessment as used by the Productive Rehabilitation Institute of Dallas for Ergonomics (PRIDE) involves the evaluation of many variables (such as range-of-motion, strength lifting, and aerobic capacity), normalized to age, gender, or body mass. Once all of these variables are collected, then pre- to postrehabilitation change can be prospectively monitored in order to document improvement. Flores and colleagues also pointed out two major ‘assumption traps’ that clinicians and researchers need to avoid when considering the best measure of function or functional improvement. First, one cannot assume on an a priori basis that one measure will necessarily be more valid or reliable than another measure. In general, the more objectively quantified the measure, the more likely it can be empirically established as a reliable and valid referent or marker. Second, one cannot assume that a physical measure will always be more objective than self-report or psychological measures. As Rudy and Stacey41 had earlier noted, no matter what the level of accuracy or sophistication of a mechanical device used to collect physiological measures, human interpretation must ultimately be used in the understanding of these findings. Moreover, a patient’s performance during a physical assessment protocol may be greatly influenced by fear of pain or injury, instructional set, motivation, etc. With these caveats in mind, Flores and colleagues provided a comprehensive review of the three broad classes of functional measures, which are presented in Table 113.1.

NORTH AMERICAN SPINE SOCIETY’S COMPENDIUM OF OUTCOME INSTRUMENTS FOR ASSESSMENT AND RESEARCH OF SPINAL DISORDERS With the increased scrutiny of healthcare utilization costs and effectiveness by the Federal government and third-party payers, the North American Spine Society42 felt it important to develop a resource for its membership that provided the most reliable and valid measures to utilize for assessment and research purposes. A guiding principle used in selecting the best measures to include in the Compendium was the following quote by Tukey:43 1234

When the right thing can only be measured poorly, it tends to cause the wrong to be measured well. And it is often much worse to have a good measurement of the wrong thing – especially when, as is so often the case, the wrong thing will IN FACT be used as an indicator of the right thing – than to have a poor measurement of the right thing. With this quotation in mind, the Compendium was developed to avoid the many pitfalls often encountered when attempting to measure the right thing (e.g. functional improvement) with good measurements, those that have been reviewed in the Compendium. Table 113.2 presents a summary of the various measures included in this Compendium. It should also be noted that for more comprehensive reviews of the various measures included in the Compendium, as well as other important works, the following are highly recommended: ACC and the National Health Committee,44 Beurskens et al.,45 Deyo et al.,46 Kopec and Esdaile,47 and Turk and Melzack.48 Some of the questionnaires more commonly used to evaluate pain and disability will be briefly reviewed next.

The Oswestry Low Back Pain Disability Questionnaire The Oswestry Low Back Pain Disability Questionnaire49 is the oldest and most thoroughly researched instrument designed to assess functional status and disability.45,50,51 A strength of the Oswestry is that it possesses strong psychometric properties and has been thoroughly investigated.49,52–60 Moreover, a number of studies have shown the Oswestry to be a very responsive self-report instrument in detecting clinically meaningful change.50,61–66 A possible weakness of the Oswestry, though, are studies suggesting a possible floor effect, such that extremely low scores may not be as accurate as more moderate or high scores.50,52,67 Also, as noted by Kopec,52 the majority of currently available disability indices (including the Oswestry) focus primarily on the physical activities of daily living, with only minimal attention given to psychosocial concerns. In fact, no items on the Oswestry directly inquire about one’s emotional or psychological state, despite the fact that research has indicated that psychological factors play an integral role in the development and maintenance of disability.68,69

The Roland-Morris Disability Questionnaire This questionnaire primarily evaluates a person’s physical abilities, such as dressing, walking, and lifting. The Roland-Morris70 was originally intended to be used for research purposes, but it subsequently was found useful in clinical practice.50 The Roland-Morris was derived from the 136-item Sickness Impact Profile,71 which was developed as a generic health status indicator for use in a variety of chronic diseases, but not specifically for back or musculoskeletal injury.72 While the validity and reliability of the Roland-Morris have been proven over time, the responsiveness of the instrument has been the subject of some scrutiny. In fact, it has been shown to be the least responsive measure to clinically meaningful change when compared to other prominent indices of functional status.47,73 In addition, the Roland-Morris is less sensitive at detecting change when disability is classified as severe, likely a shortcoming that can be attributed to the two-level response format of the questionnaire.47,50

The Million Visual Analog Scale This is a 15-item measure designed to assess disability and physical functioning useful primarily in chronic low back pain disorders. Its visual analog scale provides a simple, easy to understand format that causes little difficulty for patients.74 The instrument has been the

Section 5: Biomechanical Disorders of the Lumbar Spine

Table 113.2: Summary of Outcome Measures Included in the Compendium of Outcome Instruments for Assessment and Research of Spinal Disorders MAJOR BIOPSYCHOSOCIAL MEASURES Range of motion Spine strength Lifting capacity (functional measure) Other tests of human performance capacity Psychological test measures Self-reported measures of pain and disability Clinical interview Clinician rating of overt pain behavior PRETREATMENT TO POST-TREATMENT EFFICACY/OUTCOME MEASURES Range of motion, spine strength, lifting capacity and other tests of human performance capacity Self-report measures of pain and disability Psychological measures monitoring functional improvement Socioeconomic measures Treatment helpfulness Gatchel RJ. 2001.42

focus of few studies since its development and, as a result, very little is known about the Million’s psychometric properties outside of the original validation study.53

The SF-36 This is a multipurpose health survey with 36 questions, but was not initially developed with a musculoskeletal pain disability population in mind.75 While it is generally not considered to be a traditional functional status or disability instrument, the SF-36 has been employed as an outcome measure in numerous studies investigating low back pain.62,76,77 Despite the psychometric strengths of the SF-36, its clinical utility as a valuable outcome instrument within the musculoskeletal patient population is uncertain.77 Gatchel and colleagues,77 in an investigation of the SF-36 with a chronically disabled back pain population, found that SF-36 scores demonstrated its utility in documenting group changes over time, but evidenced inadequacies when the instrument was used for individual patient assessment. Furthermore, it was reported that other instruments, such as the Oswestry and the Million Visual Analog Scale, were more useful in providing clinical data on an individual basis. Other studies confirmed these findings.76

Other studies Other less studied indices, such as the Waddell Disability Index78 the Low Back Outcome Score,79 the Quebec Back Pain Disability Scale,52 or the Functional Rating Index,51 show promising beginnings, but have a small research literature relative to the Oswestry and Roland-Morris.45 Furthermore, each primarily assesses activities of daily living, while placing little emphasis on psychosocial factors. Due to the lack of studies investigating these measures, or describing their psychometric properties, an unequivocal statement regarding their utility cannot be made at this point in time.

Pain Disability Questionnaire Finally, one measure developed subsequent to the publication of the Compendium that shows great promise for monitoring change in chronic musculoskeletal disorders is the Pain Disability Questionnaire (PDQ) developed by Anagnostis, Gatchel and Mayer.80 The PDQ was developed as a new measure of functional status. As noted by Anagnostis et al.,80 the measurement of clinical outcomes is an essential element of any musculoskeletal treatment. The PDQ was developed for this purpose, and it yields a total functional disability score ranging from 0 to 150. The focus of the PDQ, much like other health inventories, is primarily on disability and function. Unlike most other measures, however, the PDQ is also designed for the full array of chronic disabling musculoskeletal disorders, rather than purely low back pain alone. Moreover, psychosocial variables, which recent studies have shown to play an integral role in the develop and maintenance of chronic pain disability, formed an important core of the PDQ. The psychometric properties of the PDQ have been found to be excellent, demonstrating stronger reliability, responsiveness, and validity relative to many other existing measures of functional status, such as the Oswestry, Million Visual Analog Scale and SF-36 instruments. In addition, a factor analysis of the PDQ revealed two independent factors that can be evaluated: a functional status component and a psychosocial component. Analyses demonstrated each of these two components to be valid in assessing their theorized constructs.

REVIEW OF OBJECTIVE OUTCOME EVALUATION METHODS Since the development of FR by Mayer and Gatchel,16 its authors have steadfastly held to the belief that the systematic tracking of socioeconomic outcomes was the best approach to documenting the effectiveness of their program. As the approach of FR began to 1235

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receive national and international attention, its authors were routinely approached by other clinical researchers to help in their attempts to objectively evaluate treatment outcomes. In response to these many requests, Mayer and Gatchel published a concise description of their method used at PRIDE.37 Table 113.3 presents the basic dimensions and elements of the objective monitoring of socioeconomic outcomes used in the FR program. In this publication, the ‘nuts and bolts’ of the data collection system are provided, ranging from the actual data coding sheet utilized, to more specific details such as the required structured clinical interviewing skills needed for follow-up evaluations, as well as the best method for tracking patients over a long period of time.

COST-EFFECTIVENESS OF PAIN MANAGEMENT Intimately related to the above reviewed topic of treatment outcomes evaluation is the issue of cost-effectiveness. For example, chronic pain alone is a very expensive healthcare item, with estimates as high as US$125 million annually for healthcare and indemnity costs. Specialized pain management programs are usually expensive, averaging US$8100 for comprehensive treatment programs.81 Thus, if interdisciplinary pain programs are to survive in today’s managed care environment, they will need to demonstrate that they are both clinically effective and cost-effective. Fortunately, there has been systematic evaluations of outcomes related to the issue of cost-effectiveness of interdisciplinary pain management program. For example, Turk and Okifuji82 reported the cost-effectiveness of such programs by calculating differences in pain medication, healthcare utilization, and disability payments. They then compared the outcome of these financial parameters to the most frequently used treatment modalities. Overall, their results demonstrated that pain rehabilitation programs were up to 21 times more cost-effective than alternative treatments such as

surgery. Other publications have also reported such savings.32 It is very worthwhile to provide such scientific data to third-party payers in order to justify the clinical and cost-effectiveness of comprehensive pain management programs. It should also be kept in mind that many treatments for pain involve a wide variety of components delivered in potentially different ways (e.g. individual versus group, inpatient versus outpatient, daily versus weekly), and may also include different healthcare providers. To date, there has been very little research conducted to isolate what features are vitally necessary and sufficient to produce the optimal outcomes. Apparently, third-party payers are insisting that healthcare providers consider cost-effectiveness. The trend for evidence-based medicine requires that we begin to demonstrate the clinical and costeffectiveness of the treatments that are provided.83 In the future, we need to pay better attention to the issue of both what is necessary and also sufficient to produce the best outcomes with specific pain syndromes. As Gatchel and Herring have noted,84 the reasons for monitoring evidence-based outcomes include the following: ●

●

●

To provide objective data to third-party payers in order to document treatment effectiveness. These data can also be used to market the clinical effectiveness of a practice. In order to monitor the quality assurance in one’s own practice. Regular evaluation of treatment outcomes allows the practitioners to ascertain whether there is any ‘slippage’ in the quality of care being provided. For those interested in contributing to the scientific literature, such evidence-based outcomes serve as a foundation for publication or presentation of data at professional meetings.

SUMMARY AND CONCLUSIONS There is now a mandate in today’s evidence-based medicine environment to objectively and reliably monitor treatment outcomes. Fortunately, since its development by Mayer and Gatchel,16 a major

Table 113.3: Major Socioeconomic Outcome Measures used to Evaluate Effectiveness of Functional Restoration RETURN-TO-WORK Work return Work retention (at 1 year) HEALTHCARE UTILIZATION Surgery to injured musculoskeletal area Percentage of patients visiting a new healthcare provider (continued care-and-documentation-seeking behaviors) Number of visits to new healthcare providers RECURRENT (SAME MUSCULOSKELETAL AREA) OR NEW (DIFFERENT AREA) INJURY CLAIMS Percentage with recurrent or new injury claims Percentage with injury claims involving work absence (lost time) CASE CLOSURE Resolution of legal/administrative disputes over permanent partial/total impairment or disability resulting from occupational injury Resolution of related disputes (third-party personal injury or product liability claims) Resolution of financial claims arising from perceived permanent disability (long-term disability, social security disability income, etc.) Mayer TG, Prescott M, Gatchel RJ. 2000.37

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Section 5: Biomechanical Disorders of the Lumbar Spine

hallmark of FR has always been objective quantification of psychological and socioeconomic outcomes. This chapter reviewed these data, as well as the actual process through which such monitoring can be achieved. As a preamble to that review, the biopsychosocial perspective of chronic pain was presented, which serves as the cornerstone of interdisciplinary, tertiary rehabilitation programs such as FR. The distinction was made between disease and illness, with the emphasis that, when dealing with chronic pain conditions, a focus should be on the complex interaction of biological, psychosocial, and social factors in order to fully understand the chronic low back pain patient’s perception and response to illness. A model or treatment that focuses on only one of these core sets of factors will be incomplete. The treatment- and cost-effectiveness of the alternative – interdisciplinary FR – has been consistently demonstrated in the scientific literature. Finally, this chapter reviewed the measures that can be used in documenting outcomes.

Acknowledgments The writing of this chapter was supported in part by Grants No. 5R01 MH046452, K05 MH1107 and 5R01 DE010713 (from the National Institutes of Health) and Grant No. DAMD17-03–1-0055 (from the Department of Defense).

References 1. Gatchel RJ, Oordt MS. Clinical health psychology and primary care: practical advice and clinical guidance for successful collaboration. Washington, DC: American Psychological Association; 2003. 2. Gatchel RJ. Psychological disorders and chronic pain: Cause and effect relationships. In: Gatchel RJ, Turk DC, eds. Psychological approaches to pain management: a practitioner’s handbook. New York: Guilford; 1996:33–52. 3. McGuirk B, King W, Govind J, et al. Safety, efficacy and cost-effectiveness of evidence-based guidelines for the management of acute low back pain in primary care. Spine 2001; 26:2615–2622. 4. Gatchel RJ. Clinical essentials of pain management. Washington, DC: American Psychological Association; In press. 5. Turk DC, Monarch ES. Biopsychosocial perspective on chronic pain. In: Turk DC, Gatchel RJ, eds. Psychological approaches to pain management: a practitioner’s handbook. 2nd edn. New York: Guilford; 2002.

16. Mayer TG, Gatchel RJ. Functional restoration for spinal disorders: the sports medicine approach. Philadelphia: Lea & Febiger; 1988. 17. Mayer TG, Gatchel RJ. Functional restoration for chronic low back pain. Part I: quantifying physical function. Pain Manage 1989; 2:67–75. 18. Mayer TG, Mooney V, Gatchel RJ, et al. Quantifying postoperative deficits of physical function following spinal surgery. Clin Orthopaed Related Res 1989; 244: 147–157. 19. Mayer TG, Polatin PB. Tertiary nonoperative interdisciplinary programs: The functional restoration variant of the outpatient chronic pain management program. In: Mayer TG, Gatchel RJ, Polatin PB, eds. Occupational musculoskeletal disorders: function, outcomes and evidence. Philadelphia: Lippincott, Williams & Wilkins; 2000:639–649. 20. Jousset N, Fanello S, Bontoux L, et al. Effects of functional restoration versus 3 hours per week physical therapy: A randomized controlled study. Spine 2004; 29(5):487–493. 21. Mayer TG, Gatchel RJ, Kishino N, et al. Objective assessment of spine function following industrial injury: A prospective study with comparison group and one-year follow-up. Spine 1985; 10:482–493. 22. Mayer TG, Gatchel RJ, Kishino N, et al. A prospective short-term study of chronic low back pain patients utilizing novel objective functional measurement. Pain 1986; 25(1):53–68. 23. Hazard RG, Fenwick JW, Kalisch SM, et al. Functional restoration with behavioral support: A one-year prospective study of patients with chronic low-back pain. Spine 1989; 14:157–161. 24. Bendix T, Bendix A. Different training programs for chronic low back pain – a randomized, blinded one-year follow-up study. Seattle: International Society for the Study of the Lumbar Spine; 1994. 25. Bendix AE, Bendix T, Vaegter K, et al. Multidisciplinary intensive treatment for chronic low back pain: A randomized, prospective study. Cleveland Clin J Med 1996; 63:62–69. 26. Hildebrandt J, Pfingsten M, Saur P, et al. Prediction of success from a multidisciplinary treatment program for chronic low back pain. Spine 1997; 22:990–1001. 27. Mayer TG, Gatchel RJ, Mayer H, et al. A prospective two-year study of functional restoration in industrial low back injury. An objective assessment procedure [published erratum appears in JAMA 1988; 259(2):220]. JAMA 1987; 258(13): 1763–1767. 28. Corey DT, Koepfler LE, Etlin D, et al. A limited functional restoration program for injured workers: A randomized trial. J Occup Rehabil 1996; 6:239–249. 29. Burke S, Harms-Constas C, Aden P. Return to work/work retention outcomes of a functional restoration program: A multi-center, prospective study with a comparison group. Spine 1994; 19:1880–1886. 30. Hazard RG. Spine update: Functional restoration. Spine 1995; 20:2345–2348.

6. Gatchel RJ, Maddrey AM. The biopsychosocial perspective of pain. In: Raczynski J, Leviton L, eds. Healthcare psychology handbook. Washington, DC: American Psychological Association Press; 2004.

31. Gatchel RJ, Turk DC. Interdisciplinary treatment of chronic pain patients. In: Gatchel RJ, Turk DC, eds. Psychosocial factors in pain: critical perspectives. New York: Guilford; 1999:435–444.

7. White KL, Williams F, Greenberg BG. The etiology of medical care. N Engl J Med 1961; 265:885–886.

32. Turk DC. Clinical effectiveness and cost effectiveness of treatment for patients with chronic pain. Clin J Pain 2002; 18:355–365.

8. Dworkin SF, Massoth DL. Temporomandibular disorders and chronic pain: Disease or illness? J Prosthet Dentist 1994; 72(1):29–38.

33. Mayer TG, Gatchel RJ, Polatin PB, eds. Occupational musculoskeletal disorders: function, outcomes and evidence. Philadelphia: Lippincott Williams & Wilkins; 2000.

9. Gatchel RJ. Perspectives on pain: a historical overview. In: Gatchel RJ, Turk DC, eds. Psychosocial factors in pain: critical perspectives. New York: Guilford; 1999: 3–17.

34. Bourne RB, Maloney WJ, Wright JG. An AOA critical issue: The outcome of the outcomes movement. J Bone Joint Surg 2004; 86(A):633–640.

10. Deschner M, Polatin PB. Interdisciplinary programs: chronic pain management. In: Mayer TG, Gatchel RJ, Polatin PB, eds. Occupational musculoskeletal disorders: function, outcomes and evidence. Philadelphia: Lippincott, Williams & Wilkins; 2000:629–637.

35. Flores L, Gatchel RJ, Polatin PB. Objectification of functional improvement after nonoperative care. Spine 1997; 22(14):1622–1633.

11. Wright AR, Gatchel RJ. Occupational musculoskeletal pain and disability. In: Turk DC, Gatchel RJ, eds. Psychological approaches to pain management: a practitioner’s handbook. 2nd edn. New York: Guilford; 2002:349–364.

37. Mayer TG, Prescott M, Gatchel RJ. Objective outcomes evaluation: Methods and evidence. In: Mayer TG, Polatin PB, Gatchel RJ, eds. Occupational musculoskeletal disorders: function, outcomes and evidence. Philadelphia: Lippincott Williams & Wilkins; 2000.

12. Okifuji A. Interdisciplinary pain management with pain patients: Evidence for its effectiveness. Sem Pain Manage 2003; 1:110–119. 13. Gatchel RJ, Mayer TG. Functional restoration for chronic low back pain, part II: Multimodal disability management. Pain Manag 1989; 2:136–140. 14. Gatchel RJ, Mayer TG, Hazard RG, et al. Functional restoration. Pitfalls in evaluating efficacy [editorial] [see comments]. Spine 1992; 17(8):988–995. 15. Kermond W, Gatchel RJ, Mayer TG. Functional restoration for chronic spinal disorders or failed back surgery. In: Mayer TG, Mooney V, Gatchel RJ, eds. Contemporary conservative care for painful spinal disorders. Philadelphia: Lea & Febiger; 1991:473–481.

36. Gatchel RJ. A biopsychosocial overview of pre-treatment screening of patients with pain. Clin J Pain 2001; 17:192–199.

38. Morley S, Williams AdC. Conducting and evaluating treatment outcome studies. In: Turk DC, Gatchel RJ, eds. Psychological approaches to pain management: a practitioner’s handbook. 2nd edn. New York: Guilford; 2002. 39. Blanchard EB. Biofeedback and the modification of cardiovascular dysfunctions. In: Gatchel RJ, Price KP, eds. Clinical applications of biofeedback: appraisal and status. New York: Pergamon Press; 1979. 40. Mayer TG, McGeary D, Gatchel RJ. Chronic pain management through functional restoration for spinal disorders. In: Frymoyer JF, Wiesel S, eds. Adult and pediatric spine. 3rd edn. Philadelphia: Lippincott Williams & Wilkins; 2004.

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Part 3: Specific Disorders 41. Rudy TE, Stacey BR. The futility of neglecting physical aspects of disability. Am Pain Soc J 1994; 3:200–203. 42. Gatchel RJ. A compendium of outcome instruments for assessment and research of spinal disorders. LaGrange, IL: North American Spine Society; 2001. 43. Tukey JW. Methodology and the statistician’s responsibility for both accuracy and relevance. J Am Statistical Assoc 1979; 74:786–793. 44. ACC and the National Health Committee. New Zealand Acute Low Back Guide. Wellington, New Zealand: 1997. 45. Beurskens AJ, deVet HC, Koke AJ, et al. Measuring the functional status of patients with low back pain: Assessment of the quality of four disease-specific questionnaires. Spine 1995; 20:1017–1028.

65. Burchiel KJ, Anderson VC, Brown FD. Prospective, multicenter study of spinal cord stimulation for relief of chronic back and extremity pain. Spine 1996; 21: 2786–2794. 66. Tandon V, Campbell F, Ross ERS. Posterior lumbar interbody fusion: association between disability and psychological disturbance in noncompensation patients. Spine 1999; 24:1833–1838. 67. Kopec JA, Esdaile JM, Abrahamowicz M, et al. The Quebec Back Pain Disability Scale: measurement properties. Spine 1995; 20:341–352.

46. Deyo RA, Andersson G, Bombardier C, et al. Outcome measures for studying patients with low back pain. Spine 1994; 19:2032S–2036S.

68. Fordyce WE, Roberts AH, Sternbach RA. The behavioral management of chronic pain: A response to critics. Pain 1985; 22:112–125.

47. Kopec JA, Esdaile JM. Functional disability scales for back pain. Spine 1995; 20(17):1943–1949.

69. Turk DC. Assessment of patients reporting pain: An integrated perspective. Lancet 1999; 353:1784–1788.

48. Turk DC, Melzack R. Handbook of pain assessment. 2nd edn. New York: Guilford; 2001.

70. Roland M, Morris R. A study of the natural history of back pain. Part I: Development of a reliable and sensitive measure of disability and low back pain. Spine 1983; 8:141–144.

49. Fairbanks JC, Couper J, Davies JB, et al. The Oswestry low back pain disability questionnaire. Physiotherapy 1980; 66:271–273. 50. Roland M, Fairbank J. The Roland-Morris disability questionnaire and the Oswestry Disability Questionnaire. Spine 2000; 25:3115–3124. 51. Feise RJ, Menke JM. A new valid and reliable instrument to measure the magnitude of clinical change in spinal conditions. Spine 2001; 26:78–87. 52. Kopec JA. Measuring functional outcomes in persons with back pain. Spine 2000; 25:3110–3114. 53. Ohnmeiss DD. Oswestry back pain disability questionnaire. In: Gatchel RJ, ed. Compendium of outcome instruments for assessment and research of spinal disorders. LaGrange, IL: North American Spine Society; 2000. 54. Triano JJ, McGregor M, Cramer GD. A comparison of outcome measures for use with back pain patients: Results of a feasibility study. J Manip Physiolog Ther 1993; 16:67–73. 55. Gronblad M, Hupli M, Wennerstrand P. Intercorrelation and test–retest reliability of the Pain Disability Index and the Oswestry Disability Questionnaire and their correlation with pain intensity in low back pain patients. Clin J Pain 1993; 9: 189–195.

71. Bergner M, Bobbitt RA, Pollard WE, et al. The Sickness Impact Profile: validation of a health status measure. Med Care 1976; 14:57–67. 72. Deyo RA. Measuring the functional status of patients with low back pain. Arch Phys Med Rehabil 1988; 69:1044–1053. 73. Heijden GJ, Beurskens AJ, Koes BW, et al. Traction for back and neck pain: A randomized clinical trial. Design and results of a pilot study. Physiotherapy 1995; 81:29–35. 74. Von Korff M, Jensen MP, Karoly P. Assessing global pain severity by self-report in clinical and health services research. Spine 2000; 25:3140–3153. 75. Ware JE, Sherbourne CD. The MOS 36-Item Short-Form Health Survey (SF-36). I. Conceptual framework and item selection. Med Care 1992; 30:473–483. 76. Gatchel RJ, Mayer TG, Dersh J, et al. The association of the SF-36 Health Status Survey with one-year socioeconomic outcomes in a chronically disabled spinal disorder population. Spine 1999; 24:2162–2170. 77. Gatchel RJ, Polatin PB, Mayer TG, et al. Use of the SF-36 health status survey with a chronically disabled back pain population: Strengths and limitations. J Occup Rehabil 1998; 8:237–246.

56. Fisher K, Johnson M. Validation of the Oswestry low back pain disability questionnaire, its sensitivity as a measure of change following treatment and its relationship with other aspects of the chronic pain experience. Physiother Theory Pract 1997; 13:67–80.

78. Waddell G, Main CJ. Assessment of severity in low back disorders. Spine 1984; 9:204–208.

57. Leclaire R, Blier F, Fortin L, et al. A cross-sectional study comparing the Oswestry and Roland-Morris Functional Disability Scales in two populations of patients with low back pain of different levels of severity. Spine 1997; 22:68–71.

80. Anagnostis C, Gatchel R, Mayer T. The development of a comprehensive biopsychosocial measure of disability for chronic musculoskeletal disorders: The Pain Dysfunction Questionnaire. Spine; In press.

58. Kaplan GM, Wurtele SK, Gillis D. Maximal effort during functional capacity evaluations; An examination of psychological factors. Arch Phys Med Rehabil 1996; 77:161–164.

81. Marketdata Enterprises I. Chronic Pain Management Programs: A Market Analysis. Valley Stream, NY: Marketdata Enterprises; 1995.

59. Ohnmeiss DD, Vanhanaranta H, Estlander AM, et al. The relationship of disability (Oswestry) and pain drawings to functional testing. Eur Spine J 2000; 9:208–212. 60. Gronblad M, Jarvinen E, Hurri H. Relationship of the Pain Disability Index (PDI) and the Oswestry Disability Questionnaire (ODQ) with three dynamic physical tests in a group of patients with chronic low-back pain and leg pain. Clin J Pain 1994; 10:197–203. 61. Beurskens AJ, deVet HC, Koke AJ. Responsiveness of functional status in low back pain: A comparison of different instruments. Pain 1996; 65:71–76. 62. Taylor SJ, Taylor AE, Foy MA, et al. Responsiveness of common outcome measures for patients with low back pain. Spine 1999; 24:1805–1812. 63. Hazard RG, Bendix A, Fenwick JW. Disability exaggeration as a predictor of functional restoration outcomes for patients with chronic low back pain. Spine 1991; 16:1062–1067.

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64. Frost H, Moffett JA, Moser JS, et al. Randomized controlled trial for evaluation of fitness programme for patients with chronic low back pain. Br Med J 1995; 310:151–154.

79. Greenough CG, Fraser RD. Assessment of outcome in patients with low back pain. Spine 1992; 17:36–41.

82. Turk DC, Okifuji A. Treatment of chronic pain patients: Clinical outcomes, costeffectiveness, and cost-benefits of multidisciplinary pain centers. Crit Rev Phys Rehabil Med 1998; 10:181–208. 83. Turk DC, Gatchel RJ. Multidisciplinary programs for rehabilitation of chronic low back pain patients. In: Kirkaldy-Willis WH, Bernard TN Jr, eds. Managing low back pain. 4th edn. New York: Churchill Livingstone; 1999:299–311. 84. Gatchel RJ, Herring SA. Evidenced-based medicine. In: Cole AJ, Herring SA, eds. The low back pain handbook. 2nd edn. Philadelphia: Hanley & Belfus; 2002. 85. Gatchel RJ. Research alert: The need for relevant treatment outcomes. American Pain Society Bulletin 1998; 8:8–11.

PART 4

EXTRA-SPINAL DISORDERS

Section 1

Sacroiliac Joint Syndrome

CHAPTER

Epidemiology and Examination

114

Philip Tasca and Curtis W. Slipman

INTRODUCTION The most current paradigm of interventional spine care admits a multiplicity of potential spine-related sources of axial and appendicular pain. There are 183 anatomic potential sites of spinal pain, including the 23 intervertebral discs, the 50 paired facet joints and most cephalad intervertebral articulations, the 60 paired nerve roots, the 48 paired costovertebral articulations, and the paired sacroiliac joints. The remainder of a myriad of possible symptom generators includes the various ligamentous, tendinous, and supporting structures; the muscles; the various neural elements; and various other interstitial elements. The sacroiliac joints proper represent a solitary pair within this virtual infinitude of potential areas of interest for the interventional spine clinician; moreover, the very fact of their clinical relevance remains controversial. Yet the potential significance of these two structures has been verified by the amount of attention they have received from interested clinicians since they were first ascribed potential clinical importance over a century ago in 1905.1 Confounding factors in the development of rigorous diagnostic and therapeutic guidelines regarding the sacroiliac joints stem not only from the relative numerical minority represented by these articulations and their supporting structures among the spine clinician's vast list of potential painful sites. Variability in epidemiologic and clinically obtainable data also hinders the construction of universally agreed upon clinical pathways and gold standard comparitors. Nevertheless, increasingly detailed anatomic and physiologic data are providing the theoretical foundation for the increasing number of objective clinical observations being made regarding the sacroiliac joints. Armed with these anatomic, physiologic, and clinical facts, the spine clinician may begin to make meaningful assessments and decisions regarding these structures. The validity of such assessments and decisions is the source from which a clinical algorithm draws its success.

EPIDEMIOLOGY Anatomy The anatomic properties of the sacroiliac joints have been well studied, both at the gross and histologic scales. Grossly, the sacroiliac joint is an articulation between the ilium and the sacrum – usually S1–S4 but including the fifth lumbar vertebra up to 5% of the time.2,3 The joint's shape is commonly described as auricular, or L-shaped, with two arms of usually unequal length: the longer arm is dorsocaudally directed, and the shorter arm is dorsocranially oriented.4 The embryologic development of the sacroiliac joint begins in the tenth week and obtains a definitive form by the four month.5 Flat until at least the time of puberty, the articular surfaces eventually become roughened, with numerous and highly variable grooves and protu-

berances on each opposing face.6 In the adult, there is commonly a longitudinal sacral groove at S2 which admits an iliac ridge, although this arrangement may be reversed.4 Gross supporting structures exist anteriorly and posteriorly. Stabilization against anterior motion of the sacral promontory may be aided by the anterior sacroiliac ligament7,8 and the sacrotuberous and sacrospinous ligaments.9,10 Resistance against downward translation of the sacrum may be aided by a posterior structure, the posterior sacroiliac ligament.9 The interosseous ligament, another posterior structure, is thought to be a primary joint stabilizer.10 Anterior and posterior fibrous joint capsule fibers mesh with these structures. In keeping with the somewhat controversial nature of the sacroiliac joint, the histologic characteristics of this structure render strict definitions difficult. The cartilaginous architecture of the sacral and iliac aspects of this joint differ, the sacral face being hyaline with an overall thickness of 1–3 mm, the iliac face composed of columns of fibrocartilage oriented perpendicular to the joint surface and interposed with islands of hyaline cartilage, with a thickness of less than 1 mm.4 The overall histologic architecture of the joint has been postulated to change throughout life, beginning as a diarthrodial joint and progressively losing mobility.6 Further variation is provided by gender: a cadaveric study of 47 specimens by Vleeming found that articular interdigitation was greater in males than in females.11 Thus, the sacroiliac joints have been described as diarthrotic, synarthrotic, and amphiarthrotic.3

Physiology Of physiologic concern is the innervation of the sacroiliac joint, although definitive understanding of this has been elusive. The anterior aspect of the joint is likely innervated by the posterior rami of the L2 through S2 roots, while the posterior portion is likely innervated by the posterior rami of L4 through S3. Innervation is thought to be highly variable, even between two joints in a given individual.12–14 Anterior joint innervation may be further subserved by the obturator nerve, superior gluteal nerve, or the lumbosacral trunk.15,16 Physiologic characterization of the sacroiliac joint, as with all joints, falls under two broad categories: kinetic and kinematic evaluation. The primary kinetic and kinematic considerations of the sacroiliac joints, by definition, involve sacroiliac force transmission and subsequent sacral motion relative to the ilia. In the standing position, superincumbent body weight is associated with an inferiorly directed translatory force acting upon the sacrum.17 An equally important induction of an anteriorly directed rotary force upon the sacral prominence relative to the ilia has been understood since the nineteenth century;18 the axis of this rotary force has been theorized to coincide with the horizontal line connecting the paired iliac tuberosities,2 although other axes of rotation have been postulated, and more than one may exist.19,20 In the standing position these two 1239

Part 4: Extra-Spinal Disorders

forces – one linear and the other rotatory and thus properly termed a torque – should by Newton's first law induce a respective inferior translation and anterior rotation (or flexion, termed nutation) of the sacrum relative to the ilia, unless sacroiliac motion were completely restrained. Likewise, changing positions from standing is accompanied by changes in translatory forces and torques acting on the sacrum, and should therefore induce differing sacral translations and rotations relative to the ilia. The physical parameter that couples the above forces acting on the sacroiliac joint with resultant sacroiliac motion is none other than joint mobility. As sacroiliac mobility has not been well quantified, the effect of sacroiliac kinetics on sacroiliac kinematics has not been well established. The presence of sacroiliac mobility in the pregnant female was suspected by Hippocrates and later by other researchers.2,19 In pregnant women, sacroiliac joint laxity has been quantified using Doppler ultrasound; side-to-side asymmetries in such laxity have been postulated to be associated with pregnancy-related pelvic pain and predictive of postpartum pelvic pain.21 In the nonpregnant patient, however, reported joint range of motion in both the normal and pathologic states varies widely. An early analysis was performed by Mennell, who noted that with a change in position from prone to sitting, the posterior superior iliac spines were displaced apart from each other by 0.5 inch.22 Attempting to verify such sacroiliac motion in normal subjects, Colachis et al. used Kirschner wires to mark bilateral iliac landmarks, and interwire distances were noted in nine different subject positions. Maximal iliac motion was found with trunk flexion from the standing position. The interiliac relationship previously described by Mennell was reversed, however, with greater posterior superior iliac spine approximation found with sitting versus the prone position.19 Subsequent research, in order to maximize sensitivity of detecting sacroiliac motion, has evaluated the extremes of motion about the sacroiliac joint, such as the reciprocal straddle position and other extremes of hip motion. Smidt et al.23 found interinnominate rotation to average 9° around an oblique sagittal axis and 5° around the transverse axis. Similar analyses by Barakatt et al.24 recorded interinnominate motions of up to 36°. Increased detail has been allowed with the use of radiologic studies. In a follow-up cadaveric study utilizing computed tomography, Smidt25 found sagittal sacroiliac motion of up to 17° with hips placed at end-ranges of motion. In contrast to such large values, Sturesson et al., in a roentgen stereophotogrammetric study of 25 individuals diagnosed with sacroiliac disorders, simulated typical motions about the joints and found mean sacral translation of 0.5 mm and usual sacral rotation of less than 3.6°.26 Such minimal amounts of rotation – less than 1.6° – were confirmed by this author in a second study involving six women, five of whom experienced postpregnancy posterior pelvic pain.27 This order of magnitude of rotation echoed similar radiostereometric results obtained by Egund et al.20 The minimal amount of sacroiliac joint mobility described in these latter studies not only contrasts the results of previously noted investigations but also tends to cast doubt on the clinician's ability to detect any related change in joint alignment by physical examination alone. Yet the clinical detectability of sacroiliac joint misalignment has been proposed.28,29

Joint pain Unresolved issues in the anatomic and physiologic characterization of the sacroiliac joint foreshadow the controversy surrounding clinical features associated with putative derangement of this structure. In both historical/epidemiological and clinically observable data, high degrees of variability confound the clinician's ability to reliably diagnose, much less qualify, dysfunction of the sacroiliac joint. The very presence of pain emanating from the sacroiliac joint, the pathologic 1240

factors that cause such pain, the subjective location of such pain, as well as aggravating and alleviating factors, have all been studied to a limited degree, and with limited agreement as to outcome. Pain emanating from the sacroiliac joint may stem from multiple primary and relatively well-defined causes: a list drawing from familiar pathologic categories, such as trauma, infection, tumor, and systemic illness. In the particular case of the sacroiliac joint, these broad categories have been reported specifically as traumatic pelvic ring fracture, intrapartum diastasis, pyarthrosis, metastatic adenocarcinoma, and spondyloarthropathy.12,30,31 Even well-understood pathologies within the sacroiliac joint present with cryptic clinical findings: Bohay reported that in sacroiliac joint pyarthroses the most common symptom and sign was fever. Other common symptoms were also non-specific, including ipsilateral hip, leg, or buttock pain or low back pain. Physical examination focused on the joint is thought to be helpful in timely diagnosis of a suppurative process, and serial Patrick's and Gaenslen's tests and sacroiliac joint compression (described below) are recommended.31 A separate cause of sacroiliac joint pain, intrinsic to and emanating from the joint itself, has been termed sacroiliac joint dysfunction,12,32 and is postulated to stem from an anatomic derangement of the joint. Attempts have been made to characterize this entity,28,29,33–35 although its existence has not been universally accepted in the allopathic medical literature. Within this same body of literature, further clinical analyses have been undertaken, with tacit understanding of the uncertain nature of the underlying pathology of sacroiliac joint dysfunction. These analyses, which are few in number, range from the direct testing of the most basic clinical hypotheses to more advanced, multivariate evaluations. Borrowing from the model set forth by Dwyer and Aprill,36,37 Fortin et al. attempted to derive sacroiliac joint pain referral maps from asymptomatic volunteers. Ten subjects with no history of prior back pain underwent unilateral contrast injection into the sacroiliac joint. This was followed by analyses of the distribution of subsequently produced pain and hypoesthesia. Delineation of area of hypoesthesia was repeated after infusion of Xylocaine into the joint. Hypoesthesia after instillation of an average of 1.6 mL of contrast was noted to comprise one of three patterns: medial buttock inferior to the posterosuperior iliac spine, this area plus the superior greater trochanter, and this last area plus the superior lateral thigh. Areas of provoked pain were found to coincide with these areas of hypoesthesia. Given that the approach used was believed to minimize needle penetration of adjacent potential pain generators, including ligaments and muscle, it was inferred that these referral patterns were derived solely from the sacroiliac joint itself.38 In a follow-up study, Fortin et al. tested the clinical significance of one of the previously derived pain referral zones. Of 54 consecutive patients referred for treatment of lumbar discogenic or facet pain, 16 were tentatively diagnosed with sacroiliac joint-mediated pain based on pain diagrams that indicated maximal discomfort within a region inferior to the posterosuperior iliac spine. All of these patients subsequently demonstrated concordant pain and sensory changes after provocative instillation of contrast into the sacroiliac joint, confirming the diagnosis. Ten of these patients underwent diagnostic evaluation of the lowest two intervertebral discs and lowest two facet joints ipsilateral to their initial pain, and in all cases these structures were deemed not to be pain generators.39 However, subsequent investigation of 100 subjects with and without sacroiliac joint pain, by Schwarzer et al.,40 called into question the clinical validity of sacroiliac pain reproduction by intra-articular contrast injection. Failure to reproduce pain was noted to have some negative predictive value, while pain reproduction was noted to have little positive predictive value. The gold standard here was

Section 1: Sacroiliac Joint Syndrome

pain reduction with subsequent anesthetic injection into the joint. Comparison of historical features of sacroiliac joint versus nonsacroiliac joint-mediated pain yielded only a single statistically significant distinguishing factor: the presence of groin pain with sacroiliac jointmediated pain. No potentially exacerbating or mitigating factors, such as sitting, standing, walking, flexion, or extension, were found to correlate with the presence or absence of sacroiliac joint pain. Following Schwarzer's use of anesthetic instillation into the joint as the diagnostic gold standard for sacroiliac pain, Dreyfuss et al.12 used this injection technique to compare historical features and physical examination findings in patients with and without sacroiliac joint pain. In a group of 85 patients who had been referred for sacroiliac injection, composite preinjection pain diagrams revealed a solitary factor that distinguished sacroiliac joint mediated pain from nonsacroiliac joint pain: the presence of pain above the L5 dermatome in patients without sacroiliac joint pain. Schwarzer's analysis of potentially exacerbating or mitigating factors was modified slightly and extended greatly to include sitting, standing, walking, lying down, coughing/sneezing, defecation, use of heeled footwear, and job activities. Symptom relief with standing was found to be possibly specific for sacroiliac joint pain, although the statistical significance of this finding was not certain. None of the other factors was found to correlate with the presence or absence of sacroiliac joint pain. A similar lack of predictive value was found on analysis of previous response to a variety of therapeutic modalities, including certain classes of oral medication, physical therapy, manipulation, and certain modalities. In a more focused analysis of pain referral zones, Slipman et al.41 studied 50 patients with sacroiliac pain whose diagnosis was tentatively made by means of physical examination maneuvers and confirmed by fluoroscopically guided sacroiliac joint block. Pretreatment interviews were utilized to localize the patients' pain: buttock pain was found to be the most prevalent area of referred pain, occurring in 94% of patients, followed by lower lumbar (72%), thigh (48%), and lower leg pain (28%). Other painful areas included the foot and ankle as well as the groin, upper lumbar region, and abdomen. The greatest prevalence of buttock pain, followed by a descending prevalence of progressively distal lower extremity pain referral, is reminiscent of the previous results of Fortin et al.38,39 Slipman et al. further noted a statistically significant inverse relationship between patient age and the presence of referred pain distal to the knee. The literature thus far, although rather scant, has already yielded some clinical insight into the nature of sacroiliac joint-mediated pain. Firstly, Schwarzer was able to confirm the very presence of such pain by alleviating this symptom with injection of anesthetic into that joint in patients whose symptoms were not relieved by similar injections into neighboring structures.40 The works of Schwarzer, Fortin, and Slipman served to establish and later validate the use of fluoroscopically guided anesthetic injection as the diagnostic gold standard for sacroiliac joint-mediated pain. Although by no means a gold standard, the pain referral zones presented first by Fortin et al. and later by Slipman et al. are at least foundations on which further clinical analyses may be conducted. Assessing possible reasons for the limited clinical usefulness of pain referral zones in the diagnosis of sacroiliac joint pain, Slipman has noted the complexity and variability of this joint's innervation, possible sclerotomal referral patterns, and the proximity of other potential secondary pain generators activated by primary sacroiliac joint pathology. The sacroiliac joint's complex and incompletely understood innervation, described above, may lead to referred pain in the L2–S3 distribution. Sclerotomal referral indicates pain generated in a structure originating from a given embryonic somite being referred to another structure originating from that same somite. As the osseous structures of the spinal column originate from the ventromedial portion of

their respective somites, and the muscles of the trunk and extremity originate from the corresponding posterolateral portions, sclerotomal, or somatic, referral may include a broad swath of the low back, buttock, and lower extremity. A further confounding factor is the proximity of other potential pain generators that may be directly irritated by a putative derangement in the anatomy or mechanics of the sacroiliac joint. An early study by Yeoman, involving sciatica, hints at such a pathologic mechanism,42 which has been further reported more recently.43 In spite of these inherent obstacles, the current literature points undeniably towards continued refinements in the ability to diagnose sacroiliac joint-mediated symptomatology based on historical and epidemiological factors, even if such refinements include further insight into which factors are not clinically useful. In the authors' experience, the above-cited literature has proved useful in helping to determine whether sacroiliac joint syndrome should be present in the differential diagnosis and the relative rank of this syndrome as a possible diagnosis among others. It has been our clinical experience, however, that not only pain location but other qualitative factors are useful as well. One seemingly specific sign is a history of a ‘clunking’ sound emanating from the sacroiliac region. This sound, which is deep, almost resonant, and reminiscent of crepitus, may be experienced audibly by the patient as well as being felt as a ‘clunking’ sensation emanating from deep within the posterior pelvic area. It is to be distinguished from the higher-pitched ‘clicking’ or ‘popping’ sounds and sensations that commonly emanate from other arthritis joints, including the intervertebral disc. It has been our experience that when asked specifically about this ‘clunking’ sound and sensation, with a minimum of explanation and distinction from other sounds on the part of the examiner, patients with sacroiliac syndrome often admit to such a symptom. We have noted that perhaps an even more specific finding associated with sacroiliac joint syndrome is when the patient describes such ‘clunking’ in detail without first being asked specifically about this symptom. Similarly, patients may note a feeling of ‘instability’ in the pelvis, or note frequent occurrences of a sudden pelvic ‘shifting’ sensation. It has been the author' working hypothesis that ‘clunking,’ ‘instability,’ and ‘shifting’ are all manifestations of minute but abnormal sacroiliac joint motions that can be associated with sacroiliac joint syndrome. All three symptoms, which almost always are noted by the patient to occur unilaterally, are almost invariably associated with ipsilateral pain. Yeoman's implication that secondary pain-generating structures may be activated by primary sacroiliac pathology brings to mind a second class of confounding factors in the historical picture of sacroiliac joint dysfunction: other proximate pain generators, unrelated to the sacroiliac joint, which may be the source of symptoms. Each of these extrinsic sources of symptoms has their own associated pain referral pattern; these often overlap the referral zones of the sacroiliac joint. Theoretically, even the most sensitive historical/epidemiologic data set for detecting sacroiliac pain would be of diminished clinical value if specificity were confounded by such external factors. This problem may be mitigated by the standard next step in the clinical algorithm: the physical examination.

PHYSICAL EXAMINATION It is perhaps the increased potential specificity of the physical examination that has led to the greater amount of published research being directed towards this subject rather than towards historical/ epidemiologic data. Such research typically falls under one of two categories: physical findings in sacroiliac joint dysfunction, and provocative maneuvers in sacroiliac joint dysfunction. Along a different axis, studies evaluating physical findings or provocative maneuvers 1241

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in sacroiliac joint dysfunction may also be divided another way: those that aim to determine the predictive value of specific clinical tests and those that aim to determine intertester reliability of such tests.

Physical findings The current peer-reviewed literature contains a relative paucity of inquiry into physical findings associated with sacroiliac joint dysfunction. Excluding by definition provocative maneuvers, such findings are limited to findings obtained by pure patient observation, either through visualization or palpation. Visible signs discussed in the extant literature focus mainly on leg length discrepancy theorized to be secondary to asymmetric innominate tilt, as well as asymmetric hip range of motion. Palpable signs are theorized to detect asymmetry of the bony structures about the sacroiliac joint or abnormal sacral–innominate motion with certain patient movements. Table 114.1 summarizes some physical findings that have been reported to be associated with sacroiliac joint dysfunction.

Study of visible and palpable signs has been performed by Potter and Rothstein,44 in which eight physical therapists – medical professionals whose training specifically addresses the palpation of bony structures – examined 17 patients for whom sacroiliac joint dysfunction was in the differential diagnosis. The methodologies of all 13 tests are well known and had been previously published.45 Eleven of the 13 studied were based on palpation of body landmarks of the sacrum and innominate bones plus or minus evaluation of subsequent changes in these landmarks' relationship to each other with positional changes. These evaluations included the standing flexion test (Fig. 114.1), the sitting flexion test (Fig. 114.2), and the Gillet test (Fig. 114.3), described in Table 114.1. Two of the 13 tests were based on symptom provocation (Table 114.2): the supine iliac gapping test attempts to reproduce pain essentially through the examiner pushing the anterior ilia apart while the patient lies supine (Fig. 114.4), and the side-lying iliac compression test would reproduce pain through the examiner pushing the upward-facing ilium medially in the side-lying patient (Fig. 114.5).

Table 114.1: Visible and palpable physical findings in sacroiliac joint syndrome Visible findings Test name

Procedure

Positive when…

External rotation sign – lying*

Patient is asked to lie supine as comfortably as possible.

Most comfortable position attained includes obvious external rotation of the ipsilateral hip. Passive internal rotation diminishes patient comfort.

External rotation sign – standing*

Patient is asked to stand at rest as comfortably as possible.

Most comfortable position attained includes external rotation and flexion of the ipsilateral hip – often supported by a plantarflexed foot.

Prone knee flexion test

Patient lies prone with hips and knees extended, knees are passively flexed to 90°.

One leg is initially shorter, indicating ipsilateral sacroiliac joint dysfunction. Apparent leg lengthening with knee flexion indicates ipsilateral posterior innominate rotation; shortening indicates anterior rotation.

Supine long sitting test

Patient lies supine with legs fully extended; examiner compares relative locations of both medial malleoli. Patient sits up, flexing hips but leaving knees extended.

Relative position of medial malleoli change with sitting up. Apparent leg length increase is due ipsilateral posterior innominate rotation or contralateral anterior innominate rotation. Apparent leg length decrease is due to opposite rotations.

Palpable findings Gillet test

Patient stands at rest; examiner places one thumb under the PSIS and the other thumb on the adjacent S2 tubercle. The patient maximally flexes the ipsilateral hip and knee.

The PSIS under the examiner's thumb does not migrate inferiorly relative to the adjacent S2 tubercle.

Sitting flexion test

Patient sits at rest; examiner palpates bilateral posterior superior iliac spines. Patient bends trunk forward.

There is asymmetry in the motion of the posterosuperior iliac spines, with increased PSIS motion on the side of joint restriction.

Spring test

Patient supine; examiner repeatedly applies downward pressure to the superior sacrum.

Palpably decreased resistance to motion is noted.

Standing flexion test

Patient stands at rest; examiner palpates bilateral posterior superior iliac spines. Patient bends trunk forward.

There is asymmetry in the motion of the posterosuperior iliac spines, with increased PSIS motion on the side of joint restriction.

Standing/sitting iliac crest palpation

Patient stands/sits at rest; examiner palpates bilateral iliac crests.

The iliac crests are of asymmetric heights.

Standing/sitting posterior superior iliac spine palpation

Patient stands/sits at rest; examiner palpates bilateral posterior superior iliac spines.

The posterior superior iliac spines are of asymmetric heights.

*

1242

Denotes findings noted by the authors.

Section 1: Sacroiliac Joint Syndrome

B

A Fig. 114.1 These evaluations included the standing flexion test.

A

B

Fig. 114.2 The sitting flexion test.

A

B

Fig. 114.3 The Gillet test. 1243

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Table 114.2: Provocative tests for sacroiliac joint syndrome

1244

Test name

Procedure

Positive with pain in…

Gaenslen's test

Patient supine, one leg with hip and knee maximally flexed, the opposite innominate bone and leg is off of side of examination table with hip extended.

Joint on side off of table.

Patrick's test (FABER test)

Patient prone; examiner passively simultaneously flexes, abducts, and externally rotates hip.

Ipsilateral joint.

Posterior shear test

Patient supine, one leg flexed at hip and knee. Examiner exerts downwards pressure on femur of flexed leg.

Joint on side of flexed hip and knee.

Sacral sulcus pressure

Patient prone; examiner exerts pressure just medial to posterior superior iliac spine.

Ipsilateral joint, namely area of palpation.

Sacral thrust

Patient prone; examiner exerts pressure on sacrum.

Ipsilateral joint.

Side-lying iliac compression test

Patient in lateral decubitus position; examiner applies downward pressure to iliac crest.

Topmost joint.

Supine iliac gapping test

Patient supine; examiner pushes anterior superior iliac spines laterally.

Ipsilateral joint.

Fig. 114.4 The examiner pushing the anterior ilia apart while the patient lies supine.

Fig. 114.5 The side-lying iliac compression test would reproduce pain through the examiner pushing the upward-facing ilium medially in the side-lying patient.

It was theorized that anatomic derangement of either or both sacroiliac joints would be accompanied by palpable static or dynamic changes in the relative positioning of the sacrum and the innominate bones, given the ranges of joint motion described previously. The reproducibility of such measurable changes in position was tested by each patient being evaluated in a blinded fashion by two therapists from a pool of eight, who performed all 13 tests on each patient. It was revealed that none of the testing maneuvers that were based on palpating abnormalities in sacroiliac joint positioning achieved intertester reliability of greater than 50%; all of these tests were thus deemed clinically unreliable by the authors. The two provocative maneuvers, supine iliac gapping and side-lying iliac compression tests, in contrast, achieved 94% and 76% intertester agreement, respectively. Of import, however, is the fact that in this study the intertester reliability was evaluated for each test applied in isolation.

Recognizing that no single physical examination finding or maneuver may be diagnostic of sacroiliac joint dysfunction, Cibulka et al.28 utilized the standing flexion test, the prone knee flexion test, the supine long sitting test, and palpation of the posterior superior iliac spine as a single test battery. Twenty-six patients with non-specific low back pain were evaluated by two examiners, and positive results with three of the four maneuvers was deemed sufficient for diagnosis of sacroiliac joint dysfunction. Intertester agreement analysis revealed a Cohen's kappa value of 0.88, considered to represent excellent clinical agreement.46 A pool of only two examiners, who may have been very familiar with each other's technique, effectively diminishes the clinical utility of this study as it applies to the examination maneuvers themselves, potentially as performed by one or more of a pool of many examiners. More recent analysis of the intertester reliability of four testing maneuvers was performed by Riddle and Freburger47 in which paired

Section 1: Sacroiliac Joint Syndrome

examiners were chosen from a pool of 34. Since the ‘subjects’ in this study are not only the patients but also the examiners with their yield of examination data, this larger number of examiners is theorized to better approximate true clinical circumstances by taking into account real-world variations in examination technique. Sixty-five patients with low back pain were examined via the same four tests used by Cibulka.28 It was found that percentage single-test agreement between the paired examiners was between 44% and 63% depending on which test was used. Agreement that three of four tests were positive was between 60% and 69%. This study's usefulness is bolstered by the larger number of included examiners; however, the quality of the patient population perhaps subtracts from the study's utility, as a possibly low prevalence of sacroiliac joint dysfunction in this population is noted by the authors. Turning attention from intertester reliability and towards test specificity, Dreyfuss et al. evaluated the positivity of sacroiliac joint physical findings in 101 asymptomatic subjects. In this blinded study, in which examiners did not know whether or not subjects were symptomatic, the standing flexion test, seated flexion test, and Gillet test were scrutinized. Overall, 20% of asymptomatic subjects had at least one test maneuver that was positive, with single-test false-positive rates of 13% for the standing flexion test, 8% for the seated flexion test, and 16% for the Gillet test. Overall, female subjects demonstrated more such false-positive results than males.32 Other research has focused on hip range of motion as related to sacroiliac joint dysfunction, instead of specific testing maneuvers. Early work by LaBan noted unilateral limitation in hip abduction and external rotation in the presence of sacroiliac joint inflammation.48 Basing itself on the above-mentioned studies, later work by Cibulka et al.49 noted that in subjects with low back pain not attributable to sacroiliac joint dysfunction passive hip range of motion is generally greater for external rotation than for internal rotation. This disparity was found to be increased in a hip joint ipsilateral to a posteriorly rotated innominate bone. In this research, one examiner performed the four sacroiliac joint examination maneuvers used previously by Cibulka28 and designated three of four positive results to be diagnostic of sacroiliac joint dysfunction. Intratester reliability was measured by repeat assessment with these four tests on a different day – with a kappa value of 0.86. A second examiner obtained goniometric measurements of passive hip external and internal rotation and came to the above-mentioned conclusion. If asymmetry in muscle tone is postulated as the intermediary between sacroiliac joint pathology and asymmetry in hip range of motion, it is debatable whether the asymmetry in muscle tone is the cause or the effect of the sacroiliac joint pathology. On the whole, the existing literature on visible and palpable signs of static or dynamic sacroiliac joint derangement seems to indicate that no single test is very reliable, but that certain batteries of tests may be. Technical limitations of such tests are easily imagined given laboratory literature that reports sacroiliac joint ranges of motion on the order of millimeters of translation and less than 5° of rotation and noting that such small motions are to be palpated through skin, fat, and muscle, or observed in the distal lower extremity where such minute changes in configuration may be easily masked by a myriad of other asymmetries. Perhaps more importantly, demonstration of a test's reliability does not imply the validity of that test for the detection of a particular pathology. Lack of proof of validity represents the primary deficiency in the extant peer-reviewed literature on nonprovocative sacroiliac joint examination maneuvers. This lack of evidence-based visible and palpable signs of sacroiliac joint dysfunction has not discouraged many spine care specialists from, as it were, keeping their eyes open in the hopes of discovering some sign that may prove useful.

One such sign that the authors have noted is the presence of seemingly acute, severe pain, attended by obvious discomfort on the part of the patient. Often the patient will grimace with pain, change from sitting to standing frequently, or shift body weight while sitting or standing. Such an appearance of acute pain is all the more impressive when a history is related of longstanding, or chronic, symptomatology. When asked specifically, the sacroiliac joint syndrome patient will frequently admit to being as acutely uncomfortable as presently for months or even years. It has been the authors' further experience that patients with sacroiliac joint syndrome, on standing, tend to place the majority of their body weight on the contralateral lower limb. More specifically, a stereotypical posture is adopted whereby the ipsilateral limb is externally rotated and the hip flexed, this flexion being maintained and assisted by a plantarflexed foot contacting the floor solely distal to the metatarsal heads (Fig. 114.6). Such a posture is assessed when the patient first stands at rest during the initial phase of our physical examination. If the patient does not stand still on his or her own, perhaps due to discomfort alleviated by constantly shifting weight, he or she is asked to stand still in a way that provides maximal comfort. If the above posture is assumed, it is taken as a relatively specific sign of sacroiliac joint syndrome. A relatively less-specific sign can present if the patient does not assume the above posture when asked to stand comfortably: his or her leg is positioned by the examiner as described above, and the patient is then asked if this provides more or less comfort than had been present when initially standing at rest. If the patient states that standing with the ipsilateral hip flexed and externally rotated does indeed provide some relief, we consider it a sign of relief from sacroiliac joint-mediated pain. To be certain, we often adjust the leg into other positions, such as internally rotated, and query the patient as to any pain relief, which in this latter case should not occur. On sitting, the sacroiliac joint syndrome patient often reduces weight bearing on the side of the lesion, sitting in a contralaterally side-leaning position, sometimes with the ipsilateral buttock entirely off of the chair or examination table. A fourth sign that the authors have noted occurs when the patient lies on the examination table at rest in the supine position with both knees fully extended: the ipsilateral leg is externally rotated when the contralateral hip is in neutral rotation This rotation is more than a few degrees – it is obvious even from a distance (Fig. 114.7). On

Fig. 114.6 The flexion being maintained and assisted by a plantarflexed foot contacting the floor solely distal to the metatarsal heads. 1245

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Fig. 114.7 The ipsilateral leg is externally rotated when the contralateral hip is in neutral rotation.

questioning, the patient sometimes will admit to the fact that such external rotation is the usual positioning when lying supine. If the limb is rotated to the neutral position, the patient will admit that this is less comfortable, and may even axially rotate the pelvis contralaterally such that the contralateral leg externally rotates. Conversely and perhaps less specifically, a patient for whom sacroiliac joint syndrome is in the differential diagnosis, if lying supine with both lower limbs neutrally rotated, will often admit to more comfort if the examiner externally rotates the ipsilateral lower limb.

Provocative maneuvers Given the inherent technical limitations of visible and palpable signs of sacroiliac joint dysfunction, another broad category of clinical signs has been described, one that perhaps makes use of the increased subjective sensitivity of the patient to minute internal anatomic derangements that would otherwise go unnoticed by the measurements-from-without described above. These are the provocative maneuvers, designed to reproduce or increase pain emanating from putative pathology within the sacroiliac joint. Like the aforementioned visible and palpable signs of static or dynamic anatomic derangement, these provocative tests have been evaluated with respect to intertester reliability. Moreover, this category of test has found itself being compared to different test methodologies in an attempt to glean not just repeatability but overall validity. More recently, the provocative maneuvers have become the subject of comparison to a newly emerging gold standard: the diagnostic sacroiliac joint injection. Lacking a definitively more accurate method of determining the presence of sacroiliac joint pathology per se, earlier evaluations of provocative maneuvers utilized as a gold standard the more readily diagnosable presence of ankylosing spondylitis. Russell et al.50 prospectively studied just over 100 subjects with low back pain, almost half of whom carried the diagnosis of ankylosing spondylitis based on definite radiologic abnormalities. Provocative maneuvers, in the form of ‘stress tests’ and ‘direct pressure’ tests, were performed. The former category includes Gaenslen's test, in which the supine patient's contralateral hip and knee are flexed and the ipsilateral innominate bone and lower limb hang off the examination table (Fig. 114.8); the sidelying iliac compression test described above; and another test where downward pressure is applied to both ilia in the supine patient. The ‘direct pressure’ tests include direct and forceful palpation over the 1246

Fig. 114.8 Gaenslen's test, in which the supine patient's contralateral hip and knee are flexed and the ipsilateral innominate bone and lower limb hang off the examination table.

sacroiliac joints, the sacrum, or the lower lumbar interspinous areas. Poor correlation was noted between the presence of ankylosing spondylitis and positive examination maneuver results. Along these lines, Blower and Griffin found in a study of 66 low back pain patients that two provocative tests, namely downward bilateral iliac pressure in the supine patient and downward pressure over the inferior sacrum in the prone patient, were each specific for ankylosing spondylitis. More impressive to these authors was the fact that these maneuvers correlated better with the presence of HLA B-27 than with radiologic evidence of ankylosing spondylitis, implying to them that these tests could detect ‘presumptive ankylosing spondylitis’ which does not meet the standard criteria for definitive diagnosis due to insufficient radiologic evidence.51 Assessment of intertester reliability of seven provocative tests was performed by Laslett et al. on 51 patients with low back pain. Tests included the previously described supine iliac gapping test, the sidelying iliac compression test, and Gaenslen's test. Three other tests were assessed as well (see Table 114.2). One was the posterior shear test, in which pressure is transmitted from the examiner through the femur through the flexed hip and into the innominate bone in the supine patient (Fig. 114.9). The sacral thrust test entails direct downward pressure to the sacrum in the prone patient (Fig. 114.10). The cranial shear test involves cranial pressure directed on the sacrum from below the coccyx while the ipsilateral lower limb is pulled in a caudal direction, thus stabilizing the ilium. All examinations were performed by one fixed examiner and another drawn from a pool of five. Paired examinations for all tests demonstrated intertester agreement of at least 78%. Kappa values were lowest for sacral thrust at 0.52 and highest for posterior shear at 0.88. The late 1990s saw the more widespread use in the referred literature of the diagnostic sacroiliac joint block, involving fluoroscopically guided instillation of anesthetic into the joint with subsequent transient symptom relief, become the gold standard for assessing the validity of physical examination provocative maneuvers. Maximizing the presumed ‘gold standard’ status of the diagnostic sacroiliac joint block, Maigne et al. used a double diagnostic block paradigm to more confidently diagnose low back pain as being of sacroiliac origin: 54 patients with symptoms suspicious for sacroiliac joint pathology underwent a fluoroscopically guided

Section 1: Sacroiliac Joint Syndrome

Fig. 114.9 The posterior shear test, in which pressure is transmitted from the examiner through the femur through the flexed hip and into the innominate bone in the supine patient.

Fig. 114.10 The sacral thrust test entails direct downward pressure to the sacrum in the prone patient.

‘screening block’ with instillation into the joint of 2 cc of 2% lidocaine.52 The 19 patients who responded to this injection returned a week later for instillation of 0.5% bupivacaine, a longer-lasting agent that allowed assessment of pain reduction during activities of daily living. Greater than 75% pain relief for at least 2 hours constituted a positive response, present in 10 patients. The following tests were studied: supine iliac gapping, side-lying iliac compression, Gaenslen's, sacral pressure, and Patrick's test. Two other tests included pain provocation with resisted external hip rotation in the prone patient and pressure applied to the pubic symphysis. Unfortunately, this group's emphasis on the assumed value of the diagnostic block was counteracted by their minimal evaluation of the testing maneuvers of interest – response to the double block protocol was compared only to responses to individual tests, a proposition essentially invalidated by Potter and Rothstein.44 Furthermore, the number of examiners is not given; it

is possible that there was only one examiner. Given that the tests themselves are the subject of study, a large number of patients should be accompanied by a large number of examiners to prevent idiosyncratic features of one clinician's examination from skewing the entire data set. A more sophisticated analysis was performed in the previously cited study by Dreyfuss et al.12 Here, 85 patients with low back pain were evaluated in terms of historical features of their symptoms as well as seven provocative maneuvers. These included the Gillet test, the posterior shear test, Gaenslen's maneuver, sacral thrust, and palpation of the sacral sulcus. Another test utilized was Patrick's test, also known as the ‘FABER’ test, in which the ipsilateral hip is passively flexed, abducted, and externally rotated (‘FABER’ is an acronym derived from these three motions). The seventh test, the spring test, involves palpation of motion play at the superior sacrum while the sacrum is pushed in a posteroanterior direction with the patient lying prone. Test results were studied individually and in groups; sacroiliac joint dysfunction was diagnosed based on a stringent 90% symptom reduction with instillation of 1.5 cc lidocaine and 0.5 cc Celestone Soluspan. Intertester reliability was measured between two examiners, a physician and a chiropractor. This was highest, at 87%, for sacral sulcus tenderness, but with a modest associated kappa value of 0.41. The highest kappa value was achieved by the posterior shear test: 0.64, with an associated intertester agreement of 82%. Sacral sulcus tenderness showed the highest individual sensitivity: 0.93 for the physician, 0.84 for the chiropractor. No other test had a sensitivity greater than 0.71 in either clinician's hands. Single-test specificity was even less impressive, never exceeding 0.64 and reaching as low as 0.10 for sacral sulcus tenderness as performed by the physician. Further grouping of tests which were positive for either or both examiners failed to find any particular set of tests that attained clinically useful sensitivity, specificity, or likelihood ratios. The validity of all of the tests was thus called into question, even if intertester reliability was otherwise proven to be good. Slipman et al.41 utilized fluoroscopically guided sacroiliac joint blocks to determine the presence of sacroiliac joint pathology in 50 consecutive patients. Provocative tests studied included Gaenslen's, Patrick's, and Yeoman's tests, pressure application to the sacral sulcus, bilateral pressure to the ilia in the supine patient, side-lying compression, and standing hyperextension. This group concluded that in patients with complaints consistent with sacroiliac joint pathology, including pain over the sacral sulcus, a positive Patrick's test, sacral sulcus pressure test, and at least one more of the other aforementioned provocative tests provided a 60% likelihood of greater that 80% pain relief following a diagnostic sacroiliac joint block with Celestone Soluspan and lidocaine. A positive Patrick's test has been noted by Slipman to include not only ipsilateral pain reproduction but also diminished ipsilateral hip external rotation following flexion and abduction, possibly due to bony block at the sacroiliac joint. These results are in accord with the previous literature utilizing diagnostic blocks to make the definitive diagnosis of sacroiliac joint-mediated pain.

CONCLUSION The peer-reviewed literature of the last two decades bears witness to the conceptual evolution regarding the physical examination of the patient with possible sacroiliac joint-mediated pain. Parameters that were once confidently associated with sacroiliac joint pathology were found to have poor intertester reliability and were discarded. More reproducible tests were sought, and following critical analysis it was found that sets of these tests, not solitary maneuvers, were required to achieve reliability. With the advent of the widespread use 1247

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of the diagnostic sacroiliac injection, the question of external validity was brought to the fore. The validity of single tests was again replaced by the validity of test batteries. Finally, the certainty, bordering on hubris, that characterized the initial, misguided ‘common sense approach’50 to the physical examination in putative sacroiliac joint syndrome was slowly replaced by a mood and clinical tenor far more useful to the spine clinician than certainty: humility. And it is because of this humility, not in spite of it, that it is probable that the clinical assessment of sacroiliac joint syndrome will likely continue to make slow but steady progress. Such humility and caution become the spine clinician in almost all endeavors, as our field is still young and much is left to be learned, uncovered, and understood. For now, the sacroiliac joints, though just a pair out of the multitude of structures of interest, still seem to hold a disproportionate amount of mystery and undiscovered secrets within their appropriately gnarled and crevassed walls.

References 1. Goldwaith JH, Osgood RB. A consideration of the pelvic articulations from an anatomical pathological and clinical standpoint. Boston Med Surg J 1905; 152:593–601. 2. Brunner C, Kissling R, Jacob HAC. The effects of morphology and histopathologic findings on the mobility of the sacroiliac joint. Spine 1991; 16:1111–1117. 3. Solonen KA. The sacroiliac joint in the light of anatomical, roentgenological, and clinical studies. Acta Orthop Scand 1957; 27:1–115. 4. Schunke GB. The anatomy and development of the sacro-iliac joint in man. Anat Rec 1938; 72:313–331. 5. Pilatte R, Vignes H. Articulation sacro-iliague (anatomique et physiologie). Le Progrès Medical [Paris] 1919; 34:479–483. 6. Sashin D. A critical analysis of the anatomy and the pathologic changes of the sacroiliac joints. J Bone Joint Surg 1930; 28:891–910. 7. Kirkaldy-Willis WH, Hill RJ. A more precise diagnosis for low back pain. Spine 1979; 4:102–108. 8. Alderink GJ. The sacroiliac joint: review of anatomy, mechanics, and function. J Orthop Sports Phys Ther 1991; 13:71–84. 9. Kapandji IA. The physiology of the joints, vol. 3. New York; Churchill Livingstone: 1974:54–71. 10. Williams PL. In: Warwick R, ed. Grays Anatomy, 36th edn. Philadelphia: WB Saunders; 1980:473–477. 11. Vleeming A, Stoeckart R, Volers ACW, et al. Relation between form and function in the sacroiliac joint, part I: clinical anatomic aspects. Spine 1990; 15:130–136. 12. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical examination in diagnosing sacroiliac joint pain. Spine 1996; 21:2594–2602. 13. Bogduk N. The sacroiliac joint. In: Bogduk N, ed. Clinical anatomy of the lumbar spine and sacrum, 3rd edn. New York: Churchill Livingstone; 1997:177–186. 14. Bernard TN Jr, Cassidy JD. The sacroiliac joint syndrome: pathophysiology, diagnosis, and management. In: Frymoyer JW, ed. The adult spine - principles and practice, 2nd edn. New York: Raven Press; 1997:2343–2366. 15. Russell A, Maksymowych W, LeClerq S. Clinical examination of the sacroiliac joint: a prospective study. Arthritis Rheum 1981; 12:1575–1577. 16. Slipman CW, Sterenfeld EB, Pauza K, et al. Sacroiliac joint syndrome: The diagnostic value of single photon emission computed tomography. ISIS Newsletter 1994; 2:2–20. 17. Hollinshead WH, Jenkins DB. The bony pervis, femur, and hip joint. In: Hollinshead WH, ed. Functional anatomy of the limbs and back, 5th edn. Philadelphia: WB Saunders; 1981:231–240. 18. Slocumb L, Terry RJ. Influence of the sacrotuberous and sacrospinous ligaments in limiting movements at the sacroiliac joint. JAMA 1926; 87:307–309. 19. Colachis SC, Worden RE, Bechtal CO, et al. Movement of the sacroiliac joint in the adult male: a preliminary report. Arch Phys Med Rehabil 1963; 44:490–498. 20. Egund N, Olsson TH, Schmid H, et al. Movements in the sacroiliac joints demonstrated with roentgen sterophotogrammetry. Acta Radiol Diagn 1978; 19:833–846. 21. Damen L, Buyruk HM, Güler-Uysal F, et al. The prognostic value of asymmetric laxity of the sacroiliac joints in pregnancy-related pelvic pain. Spine 2002; 27:2820–2824. 22. Mennell JB. The science and art of joint manipulation, vol. 2. New York: Blakiston; 1952:24–31.

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23. Smidt GL, McQuade K, Wei S-H, et al. Sacroiliac kenimatics for reciprocal straddle positions. Spine 1995; 20:1047–1054. 24. Barakatt E, Smidt GL, Dawson JD, et al. Interinnominate motion and symmetry: comparison between gymnasts and nongymnasts. J Orthop Sports Phys Ther 1996; 23:309–319. 25. Smidt GL, Wei S-H, McQuade K, et al. Sacroiliac motion for extreme hip positions. Spine 1997; 22:2073–2082. 26. Sturesson B, Selvik G, Udén A. Movements of the sacroiliac joints – a roentgen sterophotogrammetric analysis. Spine 1989; 14:162–165. 27. Sturesson B, Uden A, Vleeming A. A radiostereometric analysis of the movements of the sacroiliac joints in the reciprocal straddle position. Spine 2000; 25:214–217. 28. Cibulka MT, Delitto A, Koldehoff RM. Changes in innominate tilt after manipulation of the sacroiliac joint in patients with low back pain: an experimental study. Phys Ther 1988; 68:1359–1363. 29. Cibulka MT, Delitto A. A comparison of two different methods to treat hip pain in runners. J Orthop Sports Phys Ther 1993; 17:172–176. 30. Humphrey SM, Inman RD. Metastatic adenocarcinoma mimicking unilateral sacroiliitis. J Rheumatol 1995; 2:970–972. 31. Bohay DR, Gray JM. Sacroiliac joint pyarthrosis. Orthop Review 1993; 22(7):817–823. 32. Dreyfuss P, Dreyer S, Griffin J, et al. Positive sacroiliac screening tests in asymptomatic adults. Spine 1994; 19:1138–1143. 33. Beal MC. The sacroiliac problem: review of anatomy, mechanics, and diagnosis. J Am Osteopath Assoc 1982; 81:667–678. 34. Greenman PE. Sacroiliac dysfunction in the failed low back pain syndrome. In: Vleeming A, Mooney V, Snijders C, et al., eds. Proceedings from the First Interdisciplinary World Congress on Low Back Pain and its Relation to the Sacroiliac Joint. San Diego, CA. 1992; 329–343. 35. Cibulka MT, Koldehoff R. Clinical usefulness of a cluster of sacroiliac joint tests in patients with and without low back pain. J Orthop Sports Phys Ther 1999; 29:83–92. 36. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns I: a study in normal volunteers. Spine 1990; 15:453–457. 37. Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal joint pain patterns II: A clinical evaluation. Spine 1990; 15:458–461. 38. Fortin JD, Dwyer AP, West S, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique, part I: asymptomatic volunteers. Spine 1994; 19:1475–1482. 39. Fortin JD, Aprill CN, Ponthieux RT, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique, part II: Clinical evaluation. Spine 1994; 19:1483–1489. 40. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37. 41. Slipman CW, Jackson HB, Lipetz JS, et al. Sacroiliac joint pain referral zones. Arch Phys Med Rehab 2000; 81:334–337. 42. Yeoman W. The relation of arthritis of the sacroiliac joint to sciatica, with an analysis of 100 cases. Lancet 1928; 2:1119–1122. 43. Hiltz DL. The sacroiliac joint as a source of sciatica. Phys Ther 1976; 15:1373. 44. Potter NA, Rothstein JM. Intertester reliability for selected clinical tests of the sacroiliac joint. Phys Ther 1985; 65:1671–1675. 45. Erhard R, Bowling R. The recognition and management of the pelvic component of low back and sciatic pain. Bulletin of the Orthopaedic Section, American Phys Ther Assoc 1977; 2:4–15. 46. Feinstein AR. Clinical epidemiology: the architecture of clinical research. Philadelphia: WB Saunders; 1985:86. 47. Riddle DL, Freburger JK. Evaluation of the presence of sacroiliac joint region dysfunction using a combination of tests: a multicenter intertester reliability study. Phys Ther 2002; 82:772–781. 48. LaBan MM, Meerschaert JR, Taylor RS, et al. Symphyseal and sacroiliac joint pain associated with pubic symphysis instability. Arch Phys Med Rehabil 1978; 59:470–472. 49. Cibulka MT, Sinacore DR, Cromer GS, et al. Unilateral hip rotation range of motion asymmetry in patients with sacroiliac joint regional pain. Spine 1998; 23:1009–1015. 50. Russell AS, Maksymowych W, LeClercq S. Clinical examination of the sacroiliac joints: a prospective study. Arthritis Rheum 1981; 24:1575–1577. 51. Blower PW, Griffin AJ. Clinical sacroiliac joint tests in ankylosing spondylitis and other causes of low back pain – 2 studies. Ann Rheum Dis 1984; 43:192–195. 52. Maigne J-Y, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21:1889–1892.

PART 4

EXTRA-SPINAL DISORDERS

Section 1

Sacroiliac Joint Syndrome

CHAPTER

Sacroiliac Joint Rehabilitation and Manipulation

115

Heidi Prather and Clayton Skaggs

INTRODUCTION The path taken to diagnose sacroiliac joint (SIJ) pain may not be a straight or clearly marked one. Although several studies point to a battery of tests for diagnosing SIJ problems, a standardized protocol has yet to be devised. As a result, the treatment of SIJ pain can be difficult. Similar to many musculoskeletal problems, treatment success with SIJ pain is often varied due to cofactors surrounding each patient. Accordingly, one uniform approach is not likely. Instead, a combination of treatment options that can be applied to varied patient classifications will be more effective. A sacroiliac joint belt with manual therapy may be very successful in one individual and merely provoke pain in another. The treatment must be tailored to the individual. The patient’s history regarding the circumstances around when the pain began is often paramount in selecting treatment and management. For the sake of consistency in this chapter, the authors will use the term posterior pelvic pain to be inclusive of pain related to the sacroiliac joint, but not exclusive to only intra-articular pain. Posterior pelvic pain includes reference to periarticular pain including muscle, fascia, and ligaments around the sacroiliac joint. Patients with pain in the posterior pelvis after a direct fall or trauma to the joint will require management that will resemble treatment of other acute joint injuries. Treatment for a patient with an insidious onset of pain in the posterior pelvis may be directed more towards the spine or hip, depending on where the weak link in the system is thought to occur. Therapeutic intervention should be directed towards reducing tension in pain-generating structures and restoring the mechanics and function of the system complex involving the spine, pelvis, and hip. Limiting treatment only to the site of pain will have limited success.

TREATMENT Initiating treatment often includes testing the healthcare provider’s hypothesis for what caused the breakdown in the system leading to pain. For example, if the posterior pelvic pain began after an episode of lumbar discogenic pain, correcting the motion, loading, and unloading inadequacies in the lumbar spine must be accomplished in order to affect the mechanics at the pelvis and decrease symptoms. In the same fashion, an injury to the ankle may cause a change in gait pattern, giving rise to secondary adaptive changes such as shortening of the hip external rotators. After the ankle injury resolves, this loading and unloading through the hip joint and/or sacroiliac joint may result in posterior pelvic pain. Correcting the muscle imbalances around the hip may be dependent on soft tissue and propriosensory rehabilitation of the lower limb. Determining the site of breakdown in function is important, but recognizing that pain must be diminished first in order to accomplish improved function is essential. For example, if the patient with discogenic low back pain and positive neural tension

signs does not receive medications and education on how to reduce neural symptoms, the appropriate muscle strengthening cannot be accomplished. Neurogenic symptoms can inhibit muscle function. As the pain is reduced, the muscle flexibility and strengthening program can progress. Additionally, the patient should be screened for pain behavior or fear–avoidance behavior that could be perpetuating the neurogenic symptoms. Common examples include self-manipulation or stretching of the joints and soft tissues in the area of pain.

Medication Medications can be very helpful in modifying pain. Choosing a medication involves selecting a medication specific for the problem. For example, the patient with recent trauma that appears to involve the intra-articular and/or periarticular sacroiliac joint related will likely respond well to consistent antiinflammatory medication usage for a set period of time. Conversely, the patient with insidious onset of posterior pelvic pain present for several months may not respond to the same medication. Therefore, the medication should be tailored to the presumed type of pain. Myofascial pain often responds well to tricyclic antidepressants or similar agents such as trazodone and cyclobenzaprine. Antiinflammatories may be helpful and should be tried, but should likewise be discontinued if no added benefit is achieved. Pain that appears to have a neurogenic component can be treated with antiinflammatories in the acute and subacute phases of treatment. Other medications specific for neurogenic pain again include the tricyclic antidepressants, and similar agents including trazodone and cyclobenzaprine. A variety of adjuvant analgesics such as an antiepileptic medication be helpful. These agents have various side effects such as dizziness and sedation that can impair function. Also, some of these medications require monitoring. The complexity of risk–benefit issues need to be taken into consideration when choosing the agent to prescribe. Narcotics and related medications such as tramadol can be helpful in reducing moderate to severe pain, but again, only for a defined duration. The physician should keep in mind that pain not responding well to a narcotic may not need more narcotic, but another agent to address the type of pain. Neurogenic pain commonly does not respond entirely to narcotic medication and an agent that addresses neurogenic pain used with the narcotic may produce more satisfactory pain reduction.

Manual therapy Manual therapies can be used separately or in combination with other pain-reducing modalities. In fact, evidence suggests that decreasing musculoskeletal pain may be one of the most important roles for manual therapy.1,2 In several studies, manual therapy has been shown to be superior to traditional modalities in reducing pain, sometimes even in the absence of change to objective variables, such as range of 1249

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motion.3,4 Accordingly, the authors believe it is important to consider manual therapy as a tool to reduce pain, and to pair it with rehabilitative strategies, such as stabilization exercise, to restore function. Unfortunately, there is a paucity of studies substantiating this position; however, the authors’ collective experiences suggest that this form of treatment can be beneficial. Due to the range of treatments that may be necessary for complete resolution of symptoms, the authors recommend a collaborative approach to care. It is currently recognized that a chiropractor or osteopath will have a better background in manual therapy and a physical therapist or athletic trainer will be more qualified in exercise. However, it is important to recruit and work with practitioners based on their knowledge and skill, and not merely their degrees. Obviously, a practitioner who has abilities and knowledge across a broad range of modalities and therapeutic interventions can be very beneficial.

Therapeutic rehabilitation Once pain has been reduced, participation in a therapeutic rehabilitation program will be more successful. There are many different approaches to a therapeutic program. The authors recommend considering multiple treatment theories and combining types of care according to the individual patient’s needs. This type of comprehensive approach is becoming more popular and will compress the timeline to return to function. There is a vast array of physical therapy approaches to treatment of posterior pelvic pain. One theory proposed by Sahrmann5,6 seeks resolution in symptoms by correcting muscle and joint dysfunction based on specific muscle(s) activation. This theory relies on conscious correction of motor patterns and avoiding activities that promote pain and/or poor movement patterns. A person treated for acute posterior pelvic pain utilizing this treatment method might be instructed to use crutches so as to not develop or enhance a poor gait pattern. In contrast, other theories of treatment develop recommendations based on gross movement patterns. An example is McKenzie’s theory

of systematic treatment for spine dysfunctions.7 Treatment applied is based on specific movement patterns related to spine pathology. A spine stabilization program attempts to combine therapeutic exercises based on deficiencies in spine, abdominal, and hip muscle length and strength. This method also relies on conscious overriding of poor movement patterns. At times, deciding what is acceptable and unacceptable pain while performing exercises in the latter two treatment groups can be difficult for the patient. Another theory proposed by Gray8 recommends using multiple joint movement patterns to improve function but relies on unconscious retraining of movement. The movement patterns are directed either into the restrictive range of movement or away from the restriction. Movement pattern direction is determined by the patient’s pain tolerance. If moving towards the restrictive movement is too painful, applying joint motion, loading, and unloading in the movement pattern and plane tolerated is suggested. As the motion and pain improves, the direction and combination of planes of motion advances. Gray’s approach also incorporates the pelvic floor musculature, an area often omitted from traditional programs. The pelvic floor and diaphragm are thought to play an important role in core or trunk stability. This theory is somewhat ahead of current research validation, but is a growing area of interest in some centers. In general, Gray’s approach to treatment focuses on developing a therapeutic exercise program to resemble the patient’s functional activity requirements. Regardless of what method or combination of methods are used, rehabilitation for posterior pelvic pain must incorporate spine, hip, and pelvic structures and mechanics. Pool-Goudzwaard et al.9 and Vleeming et al.10 have described the importance of the muscle and connective tissue network that assists in the stability of the lumbopelvis and specifically the sacroiliac joint. They have demonstrated through dissection and biomechanical modeling that there is a direct relationship between the tensioning of the dorsal sacral ligament, sacrotuberous ligament, erector spinae muscles, hamstrings, and the movement of the SIJ.11 Additionally, the iliopsoas commonly works in a shortened position. This shortened position can enhance the development of an anteriorly rotated ilium (Fig. 115.1). Hamstring

R

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1250

Fig. 115.1 (A) An anterior view of an anteriorly and (B) posteriorly rotated ilium. This view illustrates the changes that occur at the pubic symphysis and the hip as a result of a change in position of the ilium.

Section 1: Sacroiliac Joint Syndrome

strengthening cannot be accomplished until the iliopsoas is restored to activating in a biomechanically efficient length. An anterior pelvic tilt forces the hamstring to work in a lengthened position. The hamstring is a key muscle in providing stability to the sacroiliac joint because of its direct attachment and/or fascial connections to the sacrotuberous ligament. Other muscles commonly found to be working in a shortened position include the rectus femoris, tensor fascia lata, adductors, quadratus lumborum, latissimus dorsi,12 and obturator internus. Achieving appropriate muscle flexibility may take weeks to achieve. The authors advocate utilizing a stretching program that encompasses all three planes of motion. As muscle length is restored and stiffness reduced, strengthening of muscles inhibited by the biomechanical deficit can be completed. Neuromuscular re-education and facilitation techniques are helpful with this process. Closed kinetic chain strengthening should be attempted first and can then be incorporated into the lumbopelvic stabilization exercises. As trunk strengthening improves, adding multiplanar strengthening exercises will facilitate return to functional activities. Muscles commonly found to be weak include the gluteus medius, gluteus maximus, lower abdominals, and hamstrings. These are merely suggestions that are based on the authors’ experience with respect to muscle patterns of movement proposed by Janda,13,14 and Norris.15,16 As Norris points out,16 these ‘muscle imbalance categorization can usefully assist the astute practitioner, they are not cast in stone.’ Each patient presents with a unique set of circumstances with regards to pain, muscle imbalance, and joint mechanics. The healthcare practitioner must take the patient’s individual set of problems, strengths, and goals into account when creating a treatment program. Manipulation is commonly used to treat posterior pelvic pain related to the sacroiliac joint. Manipulation is a term that may have several definitions. For the sake of discussion in this chapter it will refer to manipulation as treatment that involves manual techniques that restore joint motion. An explanation of the barrier systems utilized to direct manual therapy is useful in understanding the different approaches of manual medicine. The absolute end range of motion within any single plane of motion is referred to as the anatomic barrier (Fig. 115.2). Motion that goes beyond this barrier results in fracture, dislocation, or ligamentous or tendon tear. Within the total range of motion of any joint there are different limits to active and passive range. Active range of motion is limited by a physiological barrier. This barrier is maintained by muscle, ligament, tendon, and capsule. With passive range of motion, increased motion is obtained to the elastic barrier. Again, this barrier is maintained by the previously mentioned soft tissue structures, but at their endpoint of elasticity or length. A restrictive barrier forms as a result of a biome-

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Restrictive barrier Midline neutral Pathologic neutral

Fig. 115.2 Illustration of barriers enhances understanding of the basis of the theory of manipulation.

chanical dysfunction. This barrier reduces the active range of motion and increases the space between available active range of motion and the elastic barrier. A restrictive barrier is created by skin, fascia, long and short muscles, ligament, tendon, and joint capsules. Regardless of the specific type of manipulation used, the goal is to move the restrictive barrier back toward the elastic barrier. There are many techniques that can be used to achieve this goal. The choice of technique is examiner dependent as well as dependent on what is thought to be causing the restriction(s). There are many different techniques used to manipulate a joint to restore motion. Strain–counterstrain developed by Jones,17 an osteopathic physician, is a technique where the healthcare provider palpates for tender points within the restricted area. There are many theories regarding the location and significance of trigger points. Overlap in location is noted in the trigger points identified as Travell’s myofascial trigger points,18 Chapman’s reflex points,17 and acupuncture. Strain–counterstrain utilizes any or all of these identified trigger points to assess and treat the patient. The treatment consists of the examiner monitoring the trigger point while passively positioning the patient until the pain is relieved at the trigger point. Once this position of relief is determined, it is maintained for 90 seconds. The examiner then passively repositions the patient back to a neutral position. In general, the position of comfort is found in the direction away from the restrictive barrier. Pain relief is thought to occur by reducing the inappropriate proprioceptor activity. The inappropriate strain reflex in the painful muscle is inhibited by stretching (counterstrain) the antagonist muscle. This technique is especially helpful to reduce pain related to muscle tone when more active intervention is painful. Muscle energy techniques were first described in osteopathic medicine in the 1960s by physicians T.J. Ruddy and Fred Mitchell, Snr.19 More recently, further expansion has been made by Karel Lewitt and Vladimir Janda. The basic principle involves the healthcare provider passively placing a joint in the position away form the restrictive barrier and the patient then performs an isometric contraction against the force of the healthcare provider. After completing the contraction, the healthcare provider stretches the soft tissues to allow the joint to move through the restrictive barrier. This method of treatment applies both passive positioning and muscle activation to move through a barrier. Lewitt20 has modified this approach and termed it postisometric relaxation (PIR). Importantly, PIR emphasizes a light contraction of the muscle and does not engage the stretch reflex. The procedure is very gentle and usually very comfortable. The doctor identifies the muscle that is overactive and takes the muscle to pathological barrier of functional resistance. The doctor will then ask the patient to lightly contract the muscle being lengthened for approximately 3–5 seconds. After the light contraction, the patient is asked to relax. With relaxation the doctor lengthens the muscle to a comfortable, improved length. This is typically repeated 3–4 times. This approach is particularly beneficial for the acute and subacute patient. The contract relax method of treatment is commonly used by physical therapists and is similar to muscle energy. Patient positioning and isometric contraction are the same, but the examiner’s goal is to improve range of motion to the restrictive barrier while muscle energy attempts to obtain range through the restrictive barrier. Active release therapy (ART) is a (patented) technique used to treat soft tissue problems involving muscles, tendons, ligaments, and nerves. ART is a method of soft tissue mobilization which lengthens hypertrophied or shortened muscles, tendons, ligaments, and connective tissue.21 Preliminary studies with ART have produced encouraging results with a variety of musculoskeletal conditions.22 Once the practitioner has identified the area of tension or adhesion of tissue, a firm manual contact is applied with the thumb or finger to the area 1251

Part 4: Extra-Spinal Disorders

of soft tissue pathology. The practitioner will then shorten the muscle or tissues being treated. While maintaining specific opposition on the area of identified tension or fibrosis, the practitioner will ask the patient to lengthen the muscle and release and/or break up the restrictive tissue. This often promotes better inter- and intramuscular gliding and can improve muscle activation. In cases of posterior pelvic pain, ART can help restore movement for the pelvis by addressing dorsal sacral ligament, sacrotuberous ligament, and hamstrings. This may also be applied to conditions of nerve entrapment by muscles or fascia. Common entrapment sites for posterior pelvic pain include sciatic, gluteal, or lateral femoral cutaneous nerve locations. High-velocity low-amplitude (HVLA) manipulation is the technique often associated with the term ‘manipulation.’ Evidence and international guidelines identifying the efficacy of this type of manipulation for low back pain have flourished since 1986.23–27 This type of manipulation is the form most commonly used by chiropractors. With this technique the patient is moved passively to the restrictive barrier and the examiner then applies an extrinsic force (quick thrust) to move the joint through the restrictive barrier.28 Optimally, one joint is mobilized at a time and restoration of motion at that joint is achieved. The thrust is thought to gap the joint and the gapping is thought to cause the audible pop. While the effects of thrust manipulation remain poorly understood, evidence suggests that the impact is largely a central neurological mechanism.29 Zhu et al.30 demonstrated that decreased pain response after lumbar manipulation was associated with abnormal somatosensory-evoked potentials from paraspinal patients with low back pain. Lehman and McGill,31 in their preliminary investigation, suggested that manipulation could attenuate the muscular response that directly inhibits pain. Suter et al.32 studied the effects of SIJ manipulation on the inhibitory effect of the quadriceps muscle in knee joint pathology. They showed an interaction between manipulation and inhibition of voluntary activity produced by pain. Joint mobilization is a general term coined by physical therapy which is similar in theory to HVLA with one exception. While the goal of HVLA is to move through the restrictive barrier, joint mobilization involves applying grades of pressure to improve motion up to the restrictive barrier but not through it. Lewitt,20 a Czech neurologist, describes several approaches to this type of mobilization for the SIJ. This can include engaging the barrier of resistance and holding or rhythmically springing the barrier. The risk surrounding HVLA for the lower back is often perceived high although it is actually relatively low. Shelkelle33 estimated the serious complication rate for lumbar manipulation at 1 in 100 million manipulations. Haldeman34 revealed that 16 of the 26 cases reported to have complications between 1911 and 1989 had been performed with anesthesia. Therefore, manipulation under anesthesia should be applied with caution. Absolute contraindications to use of manipulation include joint hypermobility and instability, and the presence of inflammatory joint disease, or cauda equina syndrome. Relative contraindications include bone tumors, metabolic bone disease, primary joint disease, congenital or acquired fixed deformities, and vertebral basilar artery insufficiency. Disc herniation and severe spondylosis would also fall in the category of relative contraindications. In these cases with stable neurological findings, manipulation can often facilitate a window of recovery and restoration. Manipulation used for posterior pelvic pain may include any one or combination of the aforementioned techniques. Choosing which to use is usually determined by the practitioner’s skill, experience, and training. When addressing asymmetries in the pelvis, a technique using muscle activation (ART, muscle energy, contract–relax) is often helpful. Utilizing the muscle activation is helpful as the muscles around the hip and pelvis are large, powerful, and have different functions 1252

Fig. 115.3 Example of an iliopsoas stretch that includes three planes of motion: sagittal (hip lunge), frontal (sidebending lumbar spine), and transverse (rotation of the hip) planes.

depending on positioning of the hip. Repositioning can continue until all planes of motion have been addressed. The natural follow-up to the muscle activation treatment is a muscle flexibility and strengthening home exercise program that mimics the manipulation. For example, after a muscle energy technique is applied to reverse a unilateral anterior iliac rotation, the patient should be educated how to perform an iliopsoas stretch encompassing three planes (frontal, sagittal, transverse) of motion (Fig. 115.3). The home exercise program can then facilitate maintaining the improvements made with manipulation. A HVLA treatment might be chosen when muscle activation techniques have failed to provide consistent improvement. There are several sacral thrust maneuvers (Fig. 115.4). In general, a thrust is

Fig. 115.4 One example of a HVLA sacral thrust performed for a diagnosed posterior sacral base dysfunction. The patient extends in a prone position by rising up on elbows. The practitioner places the heel of one hand on lumbosacral junction. The other hand is placed on the lower extremity to stabilize. Pressure is applied on the sacral base until the restrictive barrier is felt. As the patient exhales, the practitioner applies a short thrust anterior.

Section 1: Sacroiliac Joint Syndrome

applied to the sacrum, but is directed in the plane of restriction. The theory is that the applied force will allow a return of improved motion to the joint. Again, the home exercise program should be created to enhance the benefits of the manipulation. For example, the patient who benefits from a sacral thrust performed distally, thereby freeing a unilateral posterior iliac rotation, will likely benefit from a hamstring stretch as part of the home exercise program. Commonly, a practitioner will combine a variety of types of manipulative treatment. Strain–counterstrain or myofascial release might first be used to reduce pain and improve soft tissue elasticity prior to performing a technique involving muscle activation or a thrust. Some practitioner’s skills may lie predominantly with HVLA treatments while others might only use muscle activation treatments. The right combination is the one the practitioner is most skilled at using and allows for maximal patient safety.

Adjunct therapy SIJ belts are often offered as part of the treatment plan for posterior pelvic pain. The belts are used to provide compression to the pelvis (Fig. 115.5). This is particularly helpful in patients with hypermobility at the joint and/or significant muscle weakness. In addition to compression, proprioceptive feedback to the gluteal muscles can assist with neuromuscular re-education. Vleeming35 reported that SIJ belts applied to cadaver models reduced SIJ rotation by 30%. In the clinical setting, Vleeming demonstrated that by stabilizing the ilium, the belts assist with improving hip flexion active range of motion. The healthcare provider must insure that the patient is able to apply the belt appropriately. The SIJ belt should be secured posteriorly across the sacral base and anteriorly, inferior to the anterior superior iliac spines. SIJ belts can dramatically reduce symptoms during walking and standing activities. However, patients with significant pain and weakness may find the belt helpful in reducing symptoms when worn during sedentary activities as well. Recommendations regarding the use of SIJ belts should be individualized, based on the patient’s history and activity goals. Other adjunct treatment considerations include orthotics and shoe modifications. If a leg length discrepancy is noted on physical examination, the examiner should determine if it is a functional or anatomical discrepancy. A shoe lift to correct a functional leg length

Fig. 115.5 Sacroiliac joint belt is worn just below the anterior superior iliac spine.

discrepancy can be helpful in the acute setting to manage pain with weight bearing or ambulating. After the pain with weight bearing has improved, the healthcare provider should determine if the shoe lift should continue to be used. The goal should be to reduce or resolve the functional leg length discrepancy via the therapeutic rehabilitation program. There is some recent evidence that footwear modifications can have systemic effects.36 An inappropriate shoe lift can promote adaptive muscle imbalances, which may initially be asymptomatic. Over time, these changes in force transmission and absorption across the pelvis may become symptomatic. Anatomical leg length discrepancies should be determined as early in treatment as possible so that the appropriate modifications can be completed. SIJ injections can be used as an adjunct to a physical therapy program if the patient’s progress plateaus or the program cannot be advanced because of pain provocation. The injections can also be used diagnostically if done under fluoroscopic guidance. Maigne37 reported 18.5% of 54 patients diagnosed with SIJ pain responded to double SIJ block under fluoroscopic guidance. This study did not control for other treatments given and therefore accurately reports only what an injection alone can improve. Slipman et al. analyzed a cohort of 31 patients who underwent therapeutic SIJ intra-articular injection.38 A minimum follow-up interval of 12 months was used. They found statistically and clinically significant improvement in visual analog scale (VAS) ratings and Oswestry scores. The average VAS rating reduction was in excess of 30 (out of 100). Luukkainen and colleagues39 reported improved visual analog scale and pain index scores at 1 month after a periarticular SIJ steroid injection. This study included 13 patients who received steroid compared to 11 who received saline and lidocaine. The injections were performed by palpation over the painful site at the SIJ region and no control was made for other treatments. In another study, 10 of 12 patients who underwent SIJ steroid injection via MRI guidance reported an improved VAS at 3-month follow-up.40 Again, no control or standardization of other conservative treatment was completed. Though study numbers at this time are small, there is evidence to suggest that SIJ injections should be used as an adjunct treatment in pain management. Recently, studies have reported improvement in chronic SIJ pain treated with radiofrequency ablation (RFA). Ferrante and associates41 reported a 50% reduction in VAS reports for at least 6 months in 33 patients. The authors noted that a positive response to treatment was associated with an atraumatic inciting event, reduction in the area of referred pain on the pain diagram, normalization of SIJ pain provocation tests, and reduction in opioid use with radiofrequency denervations. Although the Ferrante study suggests that RFA was achieved, this conclusion is suspect. The technique used simply entailed placing three probes into the joint. It is more likely that osseous and/or cartilaginous injury resulted from the local heating effect rather than a denervation procedure. Yin and colleagues42 reported a retrospective review of 14 patients who underwent sensory stimulation-guided sacral lateral branch radiofrequency neurotomy for treatment of chronic SIJ pain. Sixty-four percent experienced consistent relief in pain with a 50% reduction in visual integer pain score 6 months after the procedure. Included in these successful outcomes were 36% who had complete relief in their symptoms. In another study, Cohen43 reported choosing radiofrequency ablation candidates for chronic SIJ pain by performing diagnostic blocks at the levels innervating the SIJ (L4–5 dorsal rami and S1–3 lateral branches). Thirteen of 18 patients reported significant relief with nine reporting greater than 50% relief at follow-up. These nine underwent radiofrequency ablation of all branches previously blocked. Eight out of nine (89%) obtained 50% or greater pain relief that continued at 9-month follow-up. Using the same basic theories behind radiofrequency ablation, Calvillo et al.44 reported two cases of chronic SIJ pain treated by 1253

Part 4: Extra-Spinal Disorders

implanting a neuroprosthesis at the third sacral root. The authors reported that the patients continued to use analgesics before and after the procedure, but the patients reported that their activities of daily living were ‘more tolerable.’ These procedures appear to have some promise in the treatment of chronic SIJ pain. More studies are needed to determine long-term outcomes and determine which patients might be good candidates. SIJ hypermobility unresponsive to the above-outlined program is a difficult problem. SIJ arthrodesis45 and percutaneous fixation46 have been utilized for instability. Long-term outcome studies thus far have not been completed and it is unknown what happens to surrounding articulations with the lumbar spine, contralateral SIJ, and hip years after SIJ fusion. Other therapies such as prolotherapy have been proposed as an invasive but less permanent option. Prolotherapy is described as the provocation of the laying down of an increased volume of normal collagen material in ligament, tendon, or fascia in order to restore function of the tissue at a specific site.47 Provocation is achieved by provoking an inflammatory response at the location. A wide variety of agents have been used to provoke local inflammation, including high-concentration glucose solutions to phenol alcohol. Often it is a combination of agents. Though the safety48 and clinical outcomes have been reported,49 no prospective, controlled studies exist to date on the specific use of prolotherapy and SIJ dysfunction.

TREATMENT SCENARIOS Acute phase of treatment for a traumatic injury (1–3 days) Acute injury is often associated with a direct trauma such as a fall or marked increase in intensity, frequency, or duration of a specific activity. Often, sacroiliac joint pain presents as a progressive problem with fluctuations in symptoms. The patient may only experience symptoms during certain activities, including sports or exercise. In the acute setting, antiinflammatory medications and icing are helpful. Relative rest after an acute injury assists with pain management. This includes restricting running or excessive walking as these activities often provoke sacroiliac joint pain. Identifying the activity that may aggravate symptoms is important, especially in those with a progressive onset of symptoms. In general, avoiding activities that require a single-leg stance (activities such as bowling, skating, running, elliptical trainer, and stair stepper) is helpful in alleviating symptoms. In the acute setting, a shoe lift might be used temporarily to help reduce pain associated with weight bearing when a functional leg length discrepancy is present. As pain improves and the leg length discrepancy resolves, the lift can be removed. An SIJ belt may be helpful, especially in patients who complain of clicking or the sense of instability. Many patients find that the belts help reduce pain, especially with walking and standing. Correcting asymmetries in muscle length or stiffness should start as soon as possible and progressed within pain-free limits. Muscle energy techniques are particularly helpful as they require patient activation of muscle groups, and therefore pain tolerance is easily monitored. Joint mobilization and HVLA can be very effective at this stage. Importantly, the ilium or sacroiliac joint opposite the site of pain and inflammation is most commonly the restricted complex. Therefore, joint mobilization and/or manipulation to the side opposite to the pain is indicated and a general guideline for manual therapy. A home stretching and/or self-mobilization program should reinforce the manual techniques used to correct the SIJ dysfunction.

Recovery phase (3 days to 8 weeks) Once pain has been controlled and the injured area has been rested, correction of the functional biomechanical deficit and tissue over1254

load complex50 becomes the focus of rehabilitation. Balancing lower extremity muscle length and strength is important because of direct and indirect force transmission across the ilium and sacrum. Muscle length must be restored to facilitate appropriate joint mechanics at the hip, SIJ, and spine. Again, in this phase of treatment muscle energy and active release techniques are often successful in reducing pain as well as restoring functional motion. In cases where the above techniques have been partially successful or unsuccessful at relieving pain and improving motion, HVLA or mobilization techniques may be helpful. The home exercise program should include selfmobilization exercises to insure carry-over of the manually applied treatment. Once the mobilization has been successful the focus of treatment should turn to maintaining muscle length while improving muscle strength and endurance. Maintaining muscle flexibility with exercises that address all three planes of motion will also reinforce improvements made with the manual techniques. Medications during this time should include nonsteroidal antiinflammatory medications. These medications should be initiated with consistent daily dosage and then weaned as needed and eventually discontinued. If sleep is a problem due to pain, taking advantage of the sedating side effect of muscle relaxers may be helpful by prescribing them for nighttime use. Narcotics and medicines such as tramadol, may be useful but in a limited setting. The goal is to minimize their use. If improvements are plateauing or limited by pain, a therapeutic SIJ steroid injection may be useful with regard to treatment, and a positive response makes one feel more comfortable about the diagnosis. The authors recommend these injections be performed with fluoroscopic guidance to insure accuracy of placement and reduce complications caused by misplacement. The patient should be made aware that the injection is an adjunct treatment utilized to facilitate the progress of physical therapy. As pain improves, the exercise prescription should advance. Muscle flexibility and strengthening exercises should progress to weight bearing, utilizing all three planes of motion. As this improves, the home program should start to incorporate or mimic functional, exercise, or sport-specific activities. Return to unrestricted activities or exercise occurs once the patient is pain free, range of motion and strength have been restored, the patient has demonstrated good technique with activities, and has returned to or initiated an aerobic training program. Education with regards to the importance of a maintenance program should be completed prior to discharge.

Treatment for a nontraumatic injury (1–3 days) The treatment course of a nontraumatic injury should progress similarly to that of a traumatic injury. Initially, the etiology of the problem may not be clear or identified and, as a result, a period of trial and error can often ensue. For example, if the patient began with a segmental restriction at L5–S1 and continues to have posterior pelvic pain that is responding only in part to therapy directed at the SIJ, the restriction at L5–S1 may need to be addressed before further progress can be made. Again, the L5–S1 restriction can be treated with a variety of therapeutic interventions including joint mobilization, manipulation, muscle energy, and contract–relax. Care must be taken to resolve neurogenic pain symptoms. This can be addressed via medications, neuromobilization, and injections. Recurrent or continuous neurogenic pain can inhibit progress being made with muscle flexibility and strength. Clearing hip dysfunction can also be a key factor in progressing a treatment program for posterior pelvic pain. Godges and colleagues51 described this scenario in a case report of a 74-year-old female with posterior pelvic pain thought to be related to the SIJ. They presented a detailed description of successive physical examinations and physical therapy sessions. The iliac and sacral

Section 1: Sacroiliac Joint Syndrome

restrictions resolved within a few sessions of combined manual techniques, neuromuscular re-education, and muscle flexibility and strengthening exercises. Despite these improvements, the patient continued to have pain and activity limitations. Further progress was made once the range of motion (ROM) of the hip on the symptomatic side improved to becoming more symmetrical with the ROM on the asymptomatic side. Adjunct treatments should be instituted in the nontraumatic patient in similar fashion as the traumatic patient. Again, care should be taken to look for areas of dysfunction away from the SIJ if the patient requires prolonged use of medications, or repeated injections. Repetitive manipulation to the SIJ can have long-term side effects of joint hypermobility. Freeing restrictions at the spine and pelvis can be vital in making SIJ manual therapy successful.

Special populations Pregnancy Studies have suggested that between 50–80% of women suffer from low back pain and/or posterior pelvic pain (LBP/PPP) during pregnancy.52–61 Ostgaard and Roos-Hansson62 demonstrated that during pregnancy pain is more commonly attributed to posterior pelvic pain and postpartum is more commonly occurring from dysfunctions within the lumbar spine.63 Of 119 women with pain for more than 2 months postpartum, 27% were thought to have posterior pelvic pain, 18% lumbar spine pain, 39% posterior pelvic and lumbar pain, and in 16% no pain could be provoked on physical examination. Understanding these different etiologies can better direct treatment plans. Treatment for posterior pelvic pain during pregnancy should progress similar to that in the nonpregnant population. Exceptions include the care that should be taken in both examining and applying manual therapy treatments in the pregnant population. Ligamentous laxity promotes joint hypermobility. Overzealous ROM or manipulation can provoke both further pain and dysfunction in this population. On the other hand, SIJ belts can be exceptionally helpful in reducing pain by providing proprioceptive feedback and compression to the gluteal muscles that help provide joint stability. Stabilization exercises should be promoted with care and not all activities should

A

be performed in the supine position. The home exercise program will need to be adjusted as the abdominal girth increases. Instead of lengthening the lever arm with strengthening exercises, it may need to be reduced to adjust for biomechanical inefficiencies. Education is key with regards to activities of daily living, ergonomics of lifting (Fig. 115.6), and position choices during labor when possible. For example, laboring in a side-lying position with the hip in full flexion, abduction and external rotation may further provoke posterior pelvic pain that began during pregnancy. Noren et al.,64 in their study using an education and physiotherapy intervention, calculated a cost savings of US$53 000 for reducing LBP/PPP in pregnancy in 30 women. Education for LBP/PPP in pregnancy has also been studied and proven helpful in reducing the common chronicity seen with these patients.35,61,62,65 These studies all suggest early advice for best results. The authors’ preliminary studies also suggest an important role for assessing and treating the muscles and ligaments of the spine and pelvis in pregnancy-related LBP/PPP.68 While several exercise-directed interventions have been proposed for soft tissue dysfunction in pregnancy-related LBP/PPP,67–72 very little has been studied regarding manual soft tissue intervention.73,74 The procedures the authors utilize most are the muscle energy and ART. While both address muscles, ligaments, tendons, and connective tissue, they are clinically different from traditional massage. PIR is a method of soft tissue mobilization which lengthens shortened muscles that are hypertonic or contain trigger points.20 A few studies on LBP in pregnancy have included manipulation and mobilization in their treatment protocols with encouraging preliminary results.60,75–77 McIntyre and Broadhurst75 and Daly and Rapoza76 showed a 90% success rate in reducing pain in women with pregnancy-related LBP by using thrust manipulation for sacroiliac dysfunction. Berg et al.60 found 70% improvement in women with severe LBP in pregnancy who received specific SIJ mobilization. In a retrospective review, Daikow provided evidence of an 84% success rate in reducing back pain during pregnancy and back labor through manipulation.76 The goal with these procedures is to reduce tension or restricted movement in the pain-generating structures, thereby decreasing the patient’s pain and assisting self-care strategies of activity modification, stretching, and exercise.

B

Fig. 115.6 Review of lifting techniques is important in treating women with low back pain during pregnancy and postpartum. (A) The mother is demonstrating an inappropriate technique of lifting that increases forces to the lumbar spine. (B) The mother demonstrates an appropriate technique to maximize utilization of hip musculature during lifting, allowing the abdominal and gluteal muscles to brace and thereby reduce the risk of sheer forces applied to the lumbar spine. 1255

Part 4: Extra-Spinal Disorders

CONCLUSION Treatment for posterior pelvic pain thought to be related to the SIJ must be approached with the idea that it is likely a variety of therapeutic activities may be required to resolve pain and dysfunction. Care should be taken to determine if coexisting or preexisting dysfunctions in the hip or spine are contributing to the current problem. All must be addressed. Manual therapies can be particularly beneficial in this patient population but should be applied for a specific problem. A home exercise program should then reinforce the manual techniques applied. If multiple manipulations continue to be needed, the practitioner should reevaluate and determine if restrictions outside the SIJ exist and treat them accordingly.

References

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45. Keating JG, Avillar MD, Price M. Sacroiliac joint arthrodesis in selected patients with low back pain. In: Vleeming A, Mooney V, Dorman T, et al., eds. Movement, stability and low back pain. New York: Churchill Livingstone; 1999: 573–586. 46. Lippitt AB. Percutaneous fixation of the sacroiliac joint. In: Vleeming A, Mooney V, Dorman T, et al., eds. Movement, stability and low back pain. New York: Churchill Livingstone; 1999:587–594. 47. Dorman TA. Pelvic mechanics and prolotherapy. In: Vleeming A, Mooney V, Dorman T, et al., eds. Movement, stability and low back pain. New York: Churchill Livingstone; 1999:501–522. 48. Dorman TA. Prolotherapy: A survey. J Orthop Med 1993; 15:2. 49. Ongley MJ, Klein RG, Dorman TA, et al. A new approach to the treatment of chronic low back pain. Lancet 1987; 2:143–146. 50. Herring SA. Rehabilitation of muscle injuries. Med Sci Sports Exerc 1990; 22:455.

Section 1: Sacroiliac Joint Syndrome 51. Godges JJ, Varnum DR, Sand KM. Impairment-based examination of disability management of an elderly woman with sacroiliac region pain. Phys Ther 2002; 82(8):812–821. 52. Fast A, Ducommun EJ, Friedmann LW, et al. Low-back pain in pregnancy. Spine 1987; 11:368–371. 53. MacArthur C, Knox EG, Crawford JS. Epidural anaesthesia and long term backache after childbirth. Br Med J 1990; 301:9–12. 54. Ostgaard HC, Karlsson K. Prevalence of back pain in pregnancy. Spine 1991; 16:549–551. 55. Heckman JD. Musculoskeletal considerations in pregnancy. J Bone Joint Surg 1994; 76A:1720–1730.

65. Mantle MJ, Currey HLF. Backache in pregnancy II: Prophylactic influences of back care classes. Rheumatol Rehabil 1981; 20:227–232. 66. Skaggs CD, Ducar D, Prather H. Musculoskeletal intervention for low back and pelvic pain in pregnancy. 2003. 67. Suputtitada A, Chaisayan P. Effect of the ‘sitting pelvic tilt exercise’ during the third trimester in primigravides on back pain. J Med Assoc Thai 2002; 85:S170–S178. 68. Duffy S. Chronic pelvic pain: defining the scope of the problem. Int J Gynaecol Obstet 2001; 74(Suppl 1):S3–S7. 69. Mens JMA, Stam HJ. Diagonal trunk muscle exercises in peripartum pelvic pain: A randomized clinical trial. Phys Ther 2000; 80:1164–1173.

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PART 4

EXTRA-SPINAL DISORDERS

Section 1

Sacroiliac Joint Syndrome

CHAPTER

Therapeutic Injections and Radiofrequency Denervation

116

Way Yin

INTRODUCTION For more than 70 years, the sacroiliac joint complex has been implicated as a significant and discreet structural source of low back pain. However, of the three major groups of spinal structures identified as contributing to chronic low back pain, the sacroiliac joint complex (SIJC) stands apart from the zygapophyseal joints and intervertebral discs as the least understood from a neuroanatomic, diagnostic, and therapeutic standpoint. The prevalence of low back pain arising from the SIJC has been estimated at 15–30%,1,2 and is likely higher in the older population. The SIJC possesses a unique and complex three-dimensional anatomy with multisegmental sensory innervation. Unlike the zygapophyseal joints and intervertebral discs, the sensory innervation of the SIJC has been described in a detailed fashion only recently, and the definitive gold standard for successful treatment of SIJC pain has not yet been rigorously defined. Numerous studies have demonstrated a lack of pathognomonic historical, symptom, physical examination, or imaging findings specific for the individual diagnosis of zygapophyseal joint, disc, or SIJC pain.1,3–7 The identification of specific structural sources of low back pain must currently be made through validated interventional diagnostic means. A structure-specific diagnosis is ultimately essential for the eventual consideration of appropriate evidence-supported treatment options. A specific structural diagnosis also leads to a definable prognosis, as the long-term outcomes following treatment for zygapophyseal joint pain differ from disc pain, and from SIJC pain as well.8–14 A rational, evidence-based diagnostic algorithm for the identification of the structural source of low back pain is thus invaluable (Fig. 116.1). The area of the SIJC is frequently involved with referred pain patterns associated with other lumbar structures,2,3,15–17 and pain of SIJC origin frequently involves somatic referred pain to various areas of the low back, pelvis, abdomen, and lower extremities,18 with nearly one in seven patients experiencing pain radiating to the foot in a pseudoradicular pattern. Successful implementation of such a diagnostic algorithm is therefore ultimately dependent not only on the physician’s understanding of the technical aspects of diagnostic interventions, but also the overlapping distributions of referred somatic pain arising from different lumbar structures, and the defined sensitivities and specificities of each test considered. The current gold standard for the diagnosis of SIJC pain involves controlled intra-articular anesthetic injections (IAI).1,2,6,7,19 Pain may also arise from the deep interosseous ligament (DIOL), which is exquisitely innervated. The nociceptive potential of the DIOL is supported by anatomic and histologic findings. Although a technique for injection of the DIOL has been described, the clinical overlap in diagnostic sensitivity and specificity between controlled SIJC IAI and DIOL anesthetic injections has yet to be determined,10,20–22 and represents an ongoing area of clinical and anatomical research. Once the

diagnosis of SIJC pain has been established and the presence of other sources of lumbar spine pain excluded, definitive SIJC therapeutic intervention may be considered. A definitive, highly successful, and durable intervention for the treatment of SIJC pain may be just around the corner. Limited reports of the efficacy of surgical fusion23,24 and radiofrequency denervation10,25,26 are available; however, long-term prospective, controlled or comparative studies are currently lacking or are under investigation. This chapter will focus on current evidence supporting therapeutic injection and radiofrequency SIJC denervation.

RELEVANT ANATOMY The sacroiliac joint (SIJ) is the largest syndesmotic joint in the human body. Although possessing a cartilaginous articular surface and synovial component, the sacroiliac joint primarily functions as a stress-relieving joint, insulating the lumbar spine from transmitted shock associated with ambulation. The SIJ is not bounded by capsular tissue like other synovial joints. The joint capsule is composed of ligamentous fibers, and posteriorly, contiguous with the deep interosseous ligament. The joint as a whole is intimately associated with a multitude of surrounding ligaments, which provide structural integrity to the joint complex. The synovial component of the SIJC is composed of two divergent joint planes, a larger lateral (or anterior) pole and the smaller medial (or posterior) pole. Percutaneous access to the medial pole traverses a minimum of ligamentous tissue, whereas access to the lateral pole must traverse the DIOL (Fig. 116.2). The total volume of the synovial component of the SIJC (1.5 mL) is small compared to its surface area.15,27 The ‘capsule’ of the sacroiliac joint is frequently incompetent, even in asymptomatic patients. In one series, 61% of intra-articular injections demonstrated extracapsular extravasation,22 and 25% of asymptomatic volunteers undergoing intra-articular injection demonstrated ventral capsular insufficiencies,27 with contrast extravasating in the region of the traversing lumbosacral plexus. Detailed dissection of the ventral joint capsule in cadavers suggests that these ventral capsular ‘defects’ often appear as small foramina rather than traumatic capsular rents.28

Neuroanatomy of the sacroiliac joint complex Early studies of the sacroiliac joint suggested a combination of ventral and dorsal innervation,29,30 but recent investigation has demonstrated a predominant dorsal innervation in humans21,22 arising from the lateral branches of the L5 dorsal ramus and S1–4 dorsal rami, and composed of a wide range of sensory fiber types.21,30 The lateral branch nerves arise from a lateral dorsal sacral plexus, and divide into multiple smaller branches, some of which enter the DIOL whereas 1259

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Low back pain? Yes

Pain above L5 level?

Yes

Exit algorithm, SIJ pain unlikely, pursue lumbar sources of pain

No Evaluate zygapophysial joints via intra-articular LA injection

Pain completely relieved?

Yes

Exit algorithm, Pt. blinded comparative LA block z-joints

No Evaluate lumbar intervertebral discs with provocative discography

IASP validated discography positive?

Yes

Exit algorithm, consider treatment options for disc pain

No Evaluate SIJ with IAI, IOL LA injection

Yes

Pain completely relieved?

No

Exit algorithm, reassess for other sources of LBP

Pt. blinded comparative local anesthetic block Concordant complete relief?

No Yes

1260

SIJ RF denervation

Fig. 116.1 Sample SIJ diagnostic algorithm flowchart depicts an evidence-supported interventional diagnostic algorithm for the identification and treatment of SIJC pain.

Section 1: Sacroiliac Joint Syndrome

Fig. 116.2 Medial and lateral poles, SIJ. An ipsilateral oblique image of SIJ arthrography, with needle penetrating the posterior joint capsule of the medial pole. The heavy dark line separates the medial from the lateral pole of the joint. Note capsular redundancy of the distal (caudal) medial pole (white arrow), and the small amount of dorsal capsular contrast extravasation (black arrow).

others do not. The segmental location and number of lateral branch nerves innervating the SIJC is extremely variable. On the posterior aspect of the sacrum, these branches are often closely related (Fig. 116.3).20 Unlike the lumbar medial branch nerves of the dorsal rami supplying innervation to the zygapophyseal joints, the complex three-dimensional anatomy of the lateral branch nerves innervating

Left

Right

L5 L5/S1

S1 PSIS S2

LDSIL S3

ST

Fig. 116.3 Dorsal sacral plexus and lateral branch nerves. A representative illustration of the lateral branch nerves supplying sensation to the dorsal sacral joint complex (arrows) from L5 through S3. Note the variability in lateral branch topography between right and left. LDSIL, long dorsal sacroiliac ligament; PSIS, posterior superior iliac spine; ST, sacral tubercle; L5–S1, L5–S1 zygapophyseal joint (superior articular process). (Courtesy of Frank Willard, PhD.)

Fig. 116.4 Incomplete lateral branch staining. Dissection in nonembalmed cadaver of lateral branch nerves, left dorsal sacral plexus following injection of 0.5 mL of colored dye lateral to S1 and S2 dorsal sacral foramina. Note incomplete staining of lateral branch nerves at S2 (black arrows). Unlike similar diagnostic injection techniques to identify painful zygapophyseal joints, it is not possible to selectively anesthetize the lateral branch nerves supplying the sacroiliac joint. (Courtesy of Paul Dreyfuss, M.D. and Frank Willard, PhD, used with permission.)

the SIJC combined with their close proximity to the dorsal sacral foramina renders consideration of selective anesthetic blockade futile (Fig. 116.4).27 The DIOL is richly innervated with nociceptive mechanoreceptors. Sensory fibers must traverse the DIOL to reach the posterior SIJ capsule, and understanding the topographic neuroanatomy of the SIJC becomes invaluable in consideration of the design and performance of diagnostic injection techniques and therapeutic interventions.

DIAGNOSTIC INJECTION TECHNIQUES With the exception of imaging findings on magnetic resonance imaging (MRI) characteristic of sacroiliitis (and in the absence of tumor, fracture, or infection), there are no pathognomonic imaging findings specific for the diagnosis of SIJC pain. As previously discussed, there are also no physical examination findings that accurately identify patients with SIJC pain, although a combination of pain below L5 and localized just medial to the posterior superior iliac spine (PSIS) is suggestive. The diagnosis of SIJC pain therefore rests on a combination of interventional tests to exclude other lumbar sources of pain, and objectively verify the presence of SIJC pain. Once other structures of low back pain have been excluded, consideration of SIJC-specific diagnostic interventions may be entertained. The current gold standard involves blinded, controlled intra-articular local anesthetic injections of the SIJC, or saline placebo-controlled blocks. Because the synovial component of the SIJC is rarely accessed successfully without image guidance, injection of the joint must be performed under fluoroscopy, or possibly computed tomography (CT) guidance.31,32 However, it must be remembered that the sacroiliac joint capsule is frequently incompetent, and extravasation of local anesthetic into surrounding structures, especially from the ventral joint capsule in the region of the traversing lumbosacral plexus, will render such an injection non-specific, and therefore nondiagnostic. Additionally, since the false-positive rate of single anesthetic injections may approach 40%,33–36 no therapeutic decisions regarding ablation or surgery should be made based on a single response to an isolated analgesic test. Patient responses to controlled, comparative or placebo-controlled anesthetic testing must be rigorously assessed and documented. As with any diagnostic procedure, analgesic tests generate negative, indeterminate, and positive results, and have associated false-negative and false-positive rates. Understanding what 1261

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constitutes a negative, indeterminate, and positive result is essential. The methodology of comparative and placebo-controlled analgesic testing has been extensively validated elsewhere, and should be considered mandatory reading for all interventional spine diagnosticians.34,35,37–39 It is further recommended that any analgesic test be performed without sedation. Patient responses in the immediate postprocedural period should be rigorously documented, preferably with a q15 minute or q30 minute pain log. Sedation is an inadequate excuse for poor injection technique. Access techniques for the medial40–44 and lateral poles10,45 of the synovial component of the SIJC have been described, as has a technique for isolated injection of the DIOL.10,45 Any image-guided injection of the SIJC must include the use of radiopaque contrast to obviate vascular uptake, and verify contained distribution of injected local anesthetic. Fluoroscopy offers several intrinsic advantages over CT, including the capability for real-time imaging (and detection of vascular uptake of contrast), although the superior contrast and spatial resolution of CT may offer potential advantages in documenting extracapsular or extraligamentous extravasation patterns. In patients with spinal or pelvic hardware, advanced fluoroscopic imaging technologies, such as digital subtraction algorithm (DSA) imaging permits imaging free of the metallic imaging artifacts common to CT.

THERAPEUTIC INTERVENTIONS Injections of the SIJC have not been demonstrated to have therapeutic value except in the isolated instance of sacroiliitis associated with seronegative spondyloarthropathies.46–50 No structure-specific diagnostic information can be gleaned from steroid injection; if a patient experiences relief beyond the duration of action of local anesthetic, all that can be ascertained is that a steroid response may be present. A prolonged steroid response implies that a component of inflammation may be present, but is not structure-specific; local anesthetic injection in and of itself may also provide prolonged analgesia, well beyond the expected duration of conduction block.37 Once the diagnosis of SIJC pain has been established, therapeutic intervention may be considered. Therapeutic options for SIJC pain may be categorized into surgical interventions, other interventions, and denervation procedures. Surgical intervention for SIJC pain is covered elsewhere in this text. Some religiously advocate other therapeutic options, such as manipulation and proliferative therapies. Regrettably, the efficacy of manual medicine techniques and proliferative treatments remain anecdotal. Several denervation procedures for SIJC pain have described targeting the lateral branch nerves of the dorsal rami at various points between the dorsal sacral foramina and the posterior SIJ capsule. Among the first techniques is that described by Kline, involving the generation of a series of bipolar radiofrequency (RF) lesions along the posterior joint line (Fig. 116.5).51 Recognizing the multisegmental innervation of the SIJC, Kline reasoned that the lateral branch nerves must converge along the posterior joint capsule, and serial lesions along the posterior joint line should effectively denervate the joint. However, a study by Ferrante et al., utilizing uncontrolled single anesthetic diagnostic blocks, found that only 36% of patients experienced more than 6 months of >60% relief, and no patients experienced complete relief.26 A more rigorous evaluation with controlled anesthetic blocks and rigorous postblock assessment may have yielded better results, as initial false-positive block responders would have been eliminated from consideration. Another approach toward denervation of lateral branch nerves at L5 and S1 has been described under CT guidance by Gevargez 1262

Fig. 116.5 Bipolar SIJ RF lesioning technique. Cone down anteroposterior radiograph of bipolar electrode placement over caudal dorsal sacroiliac joint capsule. (Courtesy of Matthew T. Kline, M.D.)

et al.25 Like the Ferrante study, a single anesthetic block was used for patient selection. Thirty-five of 38 patients were followed for 3 months, with 34.2% reporting complete relief, and an additional 32% reporting ‘substantial relief.’ Based on a detailed neuroanatomic study of the dorsal sacral plexus and lateral branch topography, Yin et al. published results of a pilot study utilizing a sensory stimulation-guided approach to select pain-conducting from non pain-conducting lateral branch nerves for subsequent RF denervation.10 Dual analgesic injections of the SIJC DIOL were utilized to identify patients with probable SIJC pain after no relief was reported following anesthetic blocks of the lumbar zygapophyseal joints. In this study, provocative discography was not performed to rule out disc pain. Sensory stimulation-guided localization of the lateral branch nerves was performed to identify painful versus nonpainful nerves. The frequency of painful L5 and S1 lateral branch nerves identified in this group of patients was 100%, with 78% of patients demonstrating a painful branch arising from S2 and 42% with painful S3 branches. Although follow-up was limited to 6 months, preliminary results were encouraging, with 64% of patients experiencing longer than 6 months of >60% relief, and among responders, more than half (36% of total) experiencing 100% relief. No complications were noted. A prospective, long-term follow-up study is currently in progress. Ultimately, prospective, controlled studies will be required to identify a gold standard for the treatment of SIJC pain.

DESCRIPTION OF SENSORY STIMULATION-GUIDED LATERAL BRANCH RADIOFREQUENCY NEUROTOMY TECHNIQUE Background Detailed neuroanatomic examination of the dorsal sacral plexus and associated lateral branch nerves innervating the SIJC demonstrates that these nerves follow a complex and variable course to the DIOL and posterior joint capsule. Penetrating numerous ligaments along their course, the segmental lateral branch nerves are inconsistent with regard to number and location in three dimensions soon after exiting the dorsal sacral foramina (Fig. 116.6).10,28 Because consistent lateral branch contributions to the SIJC have been demonstrated to arise from the S2 and S3 dorsal rami, procedures that only target the lateral branch nerves at L5 and S1 may miss pain-bearing conducting from these lower dorsal rami. A description of the sensory stimulation-guided radiofrequency neurotomy targeting the L5 through S3 lateral branch nerves follows.

Section 1: Sacroiliac Joint Syndrome

Fig. 116.6 Wire study of LB topography. Thin gauge wires have been placed directly overlying lateral branch nerves seen entering the dorsal sacroiliac deep interosseous ligament arising from the dorsal sacral foramina of S1 in this cadaver. Heavier gauge wire has been placed at the dorsal margin of the dorsal sacral foramina. Note the variability or number and location of lateral branch nerves entering the dorsal SIJC.

Patient preparation Prior to surgery, the patient must understand that consistent reporting during sensory stimulation significantly contributes to the success or failure of the procedure. Further, the patient should understand that in order to map the lateral branch nerves, it is not feasible to anesthetize the target area prior to electrical stimulation. Movement and repositioning of the radiofrequency electrode is uncomfortable, but once positioned, the pain associated with electrode movement rapidly extinguishes, permitting detailed recording of patient’s sensory responses. Because consistent and clear communication with the patient is an essential component of any stereotactic surgery, no intraoperative sedation is recommended. A mild preoperative analgesic may be administered (e.g. meperidine 25–50 mg i.m.) if indicated. As the likelihood of infection from a percutaneous dorsal sacral RF procedure is low, no preoperative antibiotics are typically required. Contraindications to the procedure include (but are not limited to): a bleeding diathesis, ongoing infectious process, lack of (or refusal to provide) informed consent, organic or nonorganic pathology that would preclude accurate patient–physician communication during the procedure, or the presence of comorbidities that represent a greater threat to well-being than chronic back pain.

Procedural details The patient is brought to the operating theater and placed in the prone position on a radiolucent operating room table. If unilateral, the side of the procedure is verified with the patient. Anesthetic monitors are applied, and supplemental oxygen is provided, if needed. Although the requirement for intraoperative analgesia or anesthesia is exceedingly rare, the presence of a qualified anesthesia provider is invaluable in the event of a significant vasovagal episode or other unexpected intraoperative occurrence. The patient’s back and buttocks are sterilized with an antiseptic skin preparation (e.g. Betadine) and draped in a sterile fashion. Meticulous aseptic technique is observed. Fluoroscopic imaging is utilized to visualize the sacrum in real time, and the fluoroscope is angled parallel to the ring apophysis of S1. A skin entry site is marked and anesthetized with 1% lidocaine just medial to the posterior superior iliac spine on the operative side. To facilitate subsequent introduction of a blunt radiofrequency electrode, a 1.25", 16-gauge

intravenous catheter is introduced percutaneously, through which a 100 mm, 5 or 10 mm active tip, blunt, curved radiofrequency electrode may be advanced. Through this single entry site, the lateral branch nerves from L5 through S3 may be accessed. Initially, the RF electrode is advanced under fluoroscopic imaging to overlie the superior-medial aspect of the sacral ala, in the region of the medial dorsal ramus of L5. It is often helpful to provide the patient with an initial stimulation sensation that is expected to be nonpainful (and if L5–S1 zygapophyseal joint pain has been adequately excluded, stimulation over the medial dorsal ramus should not result in a painful response). Localization of the medial dorsal ramus of L5 is then achieved with application of stimulation (50 Hz, 1 msec pulse duration) at an initial ‘seeking’ voltage of 0.2–0.4 volts. The L5 medial dorsal ramus has an occasional motor component to the multifidus, but gross tetanic contraction of the multifidus at this level is often not seen, especially in older patients with multifidus atrophy. A strong sensory response to patient-blinded stimulation indicates successful localization of the L5 medial dorsal ramus. Nonpainful responses to stimulation include the sensation of ‘buzzing,’ ‘tingling,’ ‘vibration,’ or ‘pulsing.’ Occasionally patients will describe the sensation as ‘thumping.’ These nonpainful sensations are nearly always clearly differentiated from pain. Painful stimulation is most commonly described as sharp,’ ‘burning,’ ‘aching,’ or ‘stabbing.’ Stimulation threshold is then decreased to a minimum voltage necessary to elicit a sensation, as excessive stimulation of a nonpain-bearing nerve may be incorrectly perceived as painful. Because the proximity of the electrode to the target nerve is inversely (and nonlinearly) proportional to the voltage (or, more accurately, current) required for a sensory response, finely manipulating the electrode to achieve the lowest stimulation threshold will maximize the juxtaposition of electrode to target nerve. Ultimately, this close apposition of electrode to nerve is important for RF lesioning, as the size of an RF lesion is relatively small. To minimize the possibility of a false-positive or false-negative response to stimulation, patient-blinded stimulation, including faux stimulation is performed at the minimum threshold stimulation voltage (ideally <0.2 volts). If patient responses to stimulation are absolutely reproducible, the particular nerve under examination may be considered ‘negative’ if nonpainful stimulation is elicited, and ‘positive’ if painful stimulation is reported. Once the L5 dorsal ramus has been eliminated as a potential source of pain, the lateral branch is localized. The lateral branch of L5 typically lies 5–10 mm lateral to the lateral aspect of the superior articular process of S1 (Fig. 116.7A). The electrode is repositioned along the dorsal sacral ala as described, and stimulation repeated. The electrode is manipulated along the dorsal sacral ala until the lateral branch is identified. The lateral branch of the dorsal ramus of L5 does not have a known motor component, and localization depends solely on sensory findings. Once a potential symptomatic branch has been identified, patientblinded stimulation (with faux stimulation) is performed at the minimum stimulating voltage to determine whether patient responses are consistent. If consistent reproduction of pain is clearly distinguishable from nonpainful stimulation, a radiofrequency thermal lesion is created. Whereas maximum electrical stimulation occurs just proximal to the exposed end of the electrode, the maximum concentration of heat generated with ionic monopolar RF lesioning occurs further proximally along the exposed electrode tip. For this reason, a single thermal lesion at the site of maximum stimulation may not adequately coagulate the target nerve, especially if highimpedance surrounding tissues are present. For this reason, several sequential lesions overlapping the 45° isotherm of the previous lesion are recommended. 1263

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A

C

B

D

Prior to lesion generation, 0.5–1.0 mL of local anesthetic (e.g. 0.5– 0.75% bupivacaine) is injected. As the lateral branch nerves are closely invested within a labyrinthine network of ligaments surrounding the dorsal sacral plexus, injected local anesthetic may not be directed in the area desired; the electrode may have to be rotated in order to achieve diffusion of sufficient local analgesia sufficient to permit painless coagulation. Care should be taken to return the electrode to the exact position where stimulation resulted in pain reproduction prior to lesion generation. The author creates three overlapping 90° C lesions, each of 60 seconds duration, on each symptomatic branch identified. Lesion parameters, including initial temperature and impedance, volts, watts, and milliamperes, should be recorded. Any complaints of pain, especially that which radiates down the lower extremity, should result in the immediate cessation of lesion generation and confirmation of appropriate electrode placement well dorsal to the segmental spinal nerves. Once the L5 lateral branch has been located and mapped, attention is directed towards mapping of the lateral branch nerves arising from the dorsal ramus of S1. As the S1 dorsal ramus supplies the most lateral branch nerves going to the SIJC, care should be taken to map this level carefully. More than one symptomatic branch may be encountered. Because the lateral branch nerves arising from the dorsal sacral plexus are invariably located lateral the cephalocaudad meridian of the foramen, mapping efforts are systematically dedicated to this area (i.e. if the dorsal foramina was viewed as a clock face, between the 12 o’clock and 6 o’clock position) (see Fig. 116.7B). The lateral margin of the sacral foramina is frequently difficult to visualize on fluoroscopy, but can be easily identified by feel as the electrode tip ‘slips over’ the edge of the foramen. Stimulation of the lateral branch nerves or communicating arcade can result in referral of pain to the lower extremity, groin, or abdomen. It is imperative 1264

Fig. 116.7 (A) Typical L5 lateral branch electrode placement. Left SIJC denervation. (B) Typical S1 lateral branch electrode placement. Left SIJC denervation. (C) Typical S2 lateral branch electrode placement. Right SIJC denervation. (D) Typical S3 lateral branch electrode placement. Left SIJC denervation

that such sensation be differentiated from stimulation of the sacral spinal nerves themselves, which may occur if the electrode is inadvertently advanced through the dorsal foramina. If the depth of electrode placement is a concern, nonionic radiopaque contrast may be injected through the electrode and oblique and lateral fluoroscopic imaging used to verify placement of the electrode along the dorsal sacral plate. Any symptomatic branches identified at S1 are lesioned as previously described for the dorsal ramus of L5. In a sequential fashion, the lateral branch nerves of S2 and S3 are mapped. Symptomatic branches are coagulated as described (see Fig. 116.7C,D). At the conclusion of the procedure, the electrodes and introducer catheter are removed. Anecdotally, the author has found it useful to administer a dose of high-potency antiinflammatory corticosteroid at the conclusion of the procedure, which appears to decrease the frequency of early postoperative dysesthesiae. The author follows the practice of Dr. M. T. Kline, who uses a single 10 mg intravenous dose of dexamethasone. The patient’s back and buttocks are cleansed of antiseptic and antibiotic ointment dabbed over the skin puncture site(s). A small adhesive dressing is applied, and the patient discharged to the recovery room. Prior to discharge, most patients experience minimal to no discomfort. A neurological examination is documented prior to discharge.

Postoperative care Prior to discharge, the patient is instructed about expected postprocedural side effects, and counseled on signs and symptoms of infection, acute neurological changes, or other issues that may herald a serious postoperative complication. Typically, the postoperative course is benign, with postoperative discomfort lasting between

Section 1: Sacroiliac Joint Syndrome

1 and 3 weeks. The author has not found it necessary to prescribe opioid analgesics or to escalate existing opioid regimens. If required, one of many nonopioid analgesic agents may be prescribed instead. Occasionally, patients will experience hypoesthesia, focal anesthesia, or dysesthesia affecting a small (i.e. 7.5 × 7.5 cm) region of the buttocks. In the author’s experience, dysesthesiae are self-limited, and resolve 3–6 weeks after surgery. In all of the author’s cases save one, hypoesthesiae and anesthesia have also resolved spontaneously within 3–6 weeks. Return to work may occur as early as the first postoperative day. A return to normal activities is encouraged as quickly as possible. No specific postoperative rehabilitation exercises or regimens are typically required. Routine outpatient follow-up 4–6 weeks after operation is scheduled. Maximum benefit from the procedure may be masked by postoperative discomfort, and may not be obvious for up to 4–6 weeks. If no improvement is seen by 6 weeks after operation, the possibility of a false-positive diagnosis or procedural failure is considered.

REPRESENTATIVE CASE RW, a 55-year-old male, presents with long-standing complaints of right low back and posterior hip pain. He is 20 years status post several lumbar surgeries for low back pain, including two laminectomies, and a noninstrumented posterior fusion. None of his surgeries improved his back pain, and 10 years ago he underwent an instrumented pedicle screw fusion at L5–S1, which he reports markedly worsened his symptoms. He occasionally experiences burning pain that radiates over the hamstring region, usually stopping in the popliteal region, with occasional complaints in the right groin without testicular radiation. His symptoms are worsened with static sitting, prolonged ambulation, and lumbar extension. Typically, his symptoms are severe upon first awakening, improve slightly during the late morning hours, and worsen towards the end of the day proportional to activity. His pain awakens him 3–5 times a night. He rates his pain at 85 mm on a 100 mm visual analog scale (VAS). While living in England over the past 8 years, he underwent a total of 45 caudal epidural steroid injections. Some provided him with incomplete and temporary relief, typically lasting 1–2 weeks. Since relocating to the United States, his family practitioner has prescribed a number of oral neuromodulator agents, muscle relaxants, nonsteroidal antiinflammatory agents, and mild opioid analgesics that have not been helpful. He has undergone numerous therapies over the past decade, including many rounds of physical, massage, acupuncture, and homeopathic therapies, as well as chiropractic and osteopathic manipulations. None of these modalities provided relief. He has been told by a pain psychologist that he must learn to ‘cope with his pain,’ but relaxation, cognitive, biofeedback, and hypnosis techniques have not been successful. Prior urological evaluation of his right groin symptoms demonstrated no abnormalities or hernia. Review of supplied past medical records demonstrates consistent symptom complaints. He works on a full-time basis as a successful oil industry consultant, is married, and has three grown children. He does not smoke cigarettes, but enjoys an occasional cigar. He takes an antihypertensive agent and a cholesterol lowering drug. On examination, the patient is appropriate, well dressed, and exerts excellent effort on physical examination requests; he demonstrates no symptom exaggeration or magnification. His constitutional examination is unremarkable; he is of average height and build. His neurological examination demonstrates no abnormalities, with the exception of a mild decrease in pinprick sensation in the right L5 distribution, extending to the dorsum of the foot. Motor and reflex examinations are normal. Dural traction signs in the lower extremities are absent. Lower extremity vascular examination is normal. His

gait is slightly antalgic to the right, with a minimal amount of pelvic tilt, but tandem heel and toe walking are performed without difficulty. A well-healed midline scar is present between L3 and S1. A well-healed scar consistent with a prior left posterior iliac crest bone graft is present. The patient points to an area just medial to the right PSIS as his primary area of focal discomfort. His lumbar range of motion is decreased in extension, and limited by pain. Forward flexion and thoracolumbar lateral rotation are performed without discomfort, but lateral flexion, especially to the right is painful. On examination by palpation, increased paravertebral muscle tone is present symmetrically in the lumbar spine. There is mild tenderness to palpation in the dorsal midline and paravertebral regions symmetrically at the lumbosacral junction. There is exquisite tenderness to palpation over the dorsal sacroiliac ligaments on the right. No appreciable tenderness is present over the trochanteric bursa, and there is no intrinsic hip joint pain on examination. A seven-view plain film radiographic series of the lumbar spine demonstrates the presence of an instrumented fusion at L5–S1 with pedicle screws and bridging instrumentation. The instrumentation appears intact, and there is no evidence of foraminal intrusion of the pedicle screws. A previous intertransverse bony fusion is evident, with more bony incorporation on the right than left. Bilateral L4 and L5 laminectomy defects are present. Intervertebral disc height is reduced at L4–5 (40%) and at L5–S1 (50%), with moderate anterolateral spondylosis at both levels. Flexion and extension images demonstrate no segmental instability. Marked L4–5 hypertrophic zygapophyseal joint (Z-joint) degenerative changes are seen; the L5–S1 Z-joints appear arthrodesed. A bony defect is present, involving the left posterior ilium. Limited imaging of the sacroiliac joints demonstrates mild degenerative changes, predominantly involving the posterior medial poles on both sides. MRI of the lumbar spine with and without gadolinium enhancement is significant for decreased disc hydration at all lumbar levels, particularly L4–5 and L5–S1. Broad-based disc bulges are present at L3–4, L4–5 and L5–S1. At L4–5, moderate bilateral recess stenosis is present due to a combination of Z-joint hypertrophy and disc bulge, but no clear evidence of central stenosis is present at any level. Sagittal and axial foraminal imaging at L4–5 and L5–S1 is compromised by metallic imaging artifact. Contrast enhanced images demonstrate the present of epidural fibrosis surrounding the thecal sac at L4–5 and L5–S1, circumferentially surrounding the L5 spinal nerves in the lateral recess posterior to the L4–5 disc. Bone scan with SPECT demonstrates no areas of intense focal uptake, although mildly increased uptake is seen in the region of the L4–5 and L5–S1 intervertebral discs, and involving the right acromioclavicular joint. The patient undergoes intra-articular right-sided L4–5 anesthetic injection (0.75% bupivacaine). Z-joint arthrography demonstrates significant intra-articular sclerotic changes, but the joint is competent. The L5–S1 Z-joints are arthrosed, and cannot be accessed. The patient reports no improvement in pain following L4–5 Z-joint anesthetic injection. A right L5 selective spinal nerve local anesthetic injection is attempted via a posterolateral approach, but is not technically feasible, due to previous intertransverse bony fusion. Right S1 selective spinal nerve block is performed, with transforaminal epidural steroid injection. Despite the development of excellent S1 sensory hypoesthesia immediately following injection, the patient notes no anesthetic phase improvement in his pain. For 1 week after injection, he notes that his pain is ‘40%’ better, but rapidly returns to baseline. Provocative rate, volume, and manometrically controlled lumbar discography is then performed at the L2–3 through L5–S1 levels. A posterior transdural midline approach is necessary at L5–S1 due 1265

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to previous posterolateral fusion. Although significant degenerative changes are present at all levels, including frank annular incompetence at L4–5 and L5–S1, provocative discography is painless at all studied levels. Right sacroiliac joint arthrography is successfully performed through a trans-DIOL approach. There is moderate joint sclerosis on arthrography, and a ventral capsular defect is present involving the lateral joint pole. No intra-articular anesthetic is injected. DIOL contrast study demonstrates contained contrast spread, and 2.5 mL of local anesthetic (0.75% bupivacaine) is injected. Post procedure, the patient is observed for 2 hours. The patient notes complete (100%) relief of his pain, despite attempts to exacerbate his pain with prolonged walking, static sitting on a hard chair, and lifting. He is enrolled in a saline placebo-controlled study of the right SIJC DIOL. Following blinded, placebo-controlled injection of the right SIJC DIOL, the patient’s postprocedural analgesic diaries are reviewed. No improvement following saline injection is demonstrated, whereas the patient documents 5 hours of complete relief following bupivacaine injection, with an additional 1.5 hours of near complete (80%) relief, before rapid return to baseline pain. With the diagnosis of right SIJC pain established to the maximum specificity available with validated testing methods, SIJC sensory stimulation-guided RF denervation is recommended. He is told that there is a 65% chance that his symptoms may be reduced by 60%, and an overall 35% chance that his pain may be completely relieved. Intraoperatively, due to previous fusion, the L5 medial PPR and lateral branch cannot be identified. However, two separate painful lateral branches are identified arising from S1, and a single branch identified at S2. No painful branches are identified arising from S3. Multiple nonpainful branches are found with stimulation at the S1–3 levels. RF thermocoagulation is performed over the identified painful lateral branch nerves. The patient tolerates the procedure well and is discharged with a normal lower extremity neurological examination. Nursing follow-up telephone calls on postoperative day one and seven are made. The patient complains of mild postprocedural discomfort, but was able to return to work the day following surgery. He notes no buttock dysesthesiae or hypoesthesiae. At 4-week postoperative clinic follow-up, the patient notes that his procedural discomfort has completely resolved. He complains of no buttock numbness or dysesthesiae. He notes that his posterior hip pain is ‘90% better,’ that he is able to sleep through the night without interruption, and that he no longer has pain with sitting or walking. He notes that his posterior thigh burning pain has completely resolved, as has his groin pain. He is walking 2–3 miles a day, and has started to play golf again. At 8-week postoperative follow-up, the patient notes that his primary presenting pain is ‘100%’ resolved. His low back VAS pain score is 0/100. His neurological examination is normal, including resolution of the mild pinprick deficit in the right L5 distribution. He now primarily complains of right anterior shoulder pain after playing golf. This patient is now 2 years status post SIJ RF at the time of this writing, and remains pain free. Intercurrently, he has been referred to an orthopedic sports medicine specialist who is contemplating right shoulder acromioplasty.

References 1. Maigne J, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21(16):1889–1892.

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4. Schwarzer AC, et al. Prevalence and clinical features of lumbar zygapophyseal joint pain: a study in an Australian population with chronic low back pain. Ann Rheum Dis 1995; 54(2):100–106. 5. Schwarzer AC, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19(10):1132–1137. 6. Dreyfuss P, et al. The value of medical history and physical examination in diagnosing sacroiliac joint pain. Spine 1996; 21(22):2594–2602. 7. Slipman CW, et al. The predictive value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehabil 1998; 79(3):288–292. 8. van Kleef M, et al. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine 1999; 24(18):1937–1942. 9. Dreyfuss P, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophyseal joint pain. Spine 2000; 25(10):1270–1277. 10. Yin W, et al. Sensory stimulation-guided sacroiliac joint radiofrequency neurotomy: technique based on neuroanatomy of the dorsal sacral plexus. Spine 2003; 28(20):2419–2425. 11. Karasek M, Bogduk N. Twelve-month follow-up of a controlled trial of intradiscal thermal annuloplasty for back pain due to internal disc disruption. Spine 2000; 25(20):2601–2607. 12.Karasek M, Karasek D, Bogduk N. A controlled trial of the efficacy of intra-discal electrothermal treatment for internal disc disruption. North American Spine Society, 14th Annual Meeting. 1999; Chicago, IL. 13. Derby R, et al. The ability of pressure-controlled discography to predict surgical and nonsurgical outcomes. Spine 1999; 24(4):364–371; discussion 371–372. 14. Madan SS, Harley JM, Boeree NR. Circumferential and posterolateral fusion for lumbar disc disease. Clin Orthop 2003; 409:114–123. 15. Fortin J, et al. Sacroiliac joint: pain referral maps upon applying a new injection/ arthrography technique. Part I: Asymptomatic volunteers. Spine 1994; 19(13): 1475–1482. 16. Carragee E, Paragioudakis S, Khurana S. Lumbar high-intensity zone and discography in subjects without low back problems. Spine 2000; 25(23):2987–2992. 17. Carragee E, et al. The rates of false-positive lumbar discography in select patients without low back symptoms. Spine 2000; 25(11):1373–1381. 18. Slipman CW, et al. Sacroiliac joint pain referral zones. Arch Phys Med Rehabil 2000; 81(3):334–338. 19. Fortin J, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique. Part II: Clinical evaluation. Spine 1994; 19(13):1 483–1489. 20. Willard F, Carreiro J, Manko W. The long posterior interosseous ligament and the sacrococcygeal plexus. Third Interdisciplinary World Congress on Low Back and Pelvic Pain. 1998. 21. Grob K, Neuhuber W, Kissling R. [Innervation of the sacroiliac joint of the human]. Z Rheumatol 1995; 54(2):117–122. 22. Fortin J, et al. Sacroiliac joint innervation and pain. Am J Orthop 1999; 28(12): 687–690. 23. Giannikas KA, et al. Sacroiliac joint fusion for chronic pain: a simple technique avoiding the use of metalwork. Eur Spine J 2004; 13(3):253–256. 24. Guner G, et al. Anterior sacroiliac fusion: a new video-assisted endoscopic technique. Surg Laparosc Endosc 1998; 8(3):233–236. 25. Gevargez A, et al. CT-guided percutaneous radiofrequency denervation of the sacroiliac joint. Eur Radiol 2002; 12(6):1360–1365. 26. Ferrante FM, et al. Radiofrequency sacroiliac joint denervation for sacroiliac syndrome. Reg Anesth Pain Med 2001; 26(2):137–142. 27. Dreyfuss P, Park K, Bogduk N. Do L5 dorsal ramus and S1–4 lateral branch blocks protect the sacro-iliac joint from an experimental pain stimulus? A randomized double-blinded controlled trial. ISIS 8th Annual Scientific Meeting. 2000; San Francisco, CA, USA: International Spinal Injection Society. 28. Willard F, Carreiro J, Manko W. The long posterior interosseous ligament and the sacrococcygeal plexus. Third Interdisciplinary World Congress on Low Back and Pelvic Pain, 1998. 29. Ikeda R. Innervation of the sacroiliac joint. Macroscopic and histological studies. J Nippon Med School 1991; 58:587–596.

2. Schwarzer A, Aprill C, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37.

30. Solonon K. The sacroiliac joint in light of anatomical, roentgenological, and clinical studies. Acta Orthop Scand [Suppl] 1957; 27:1–127.

3. Schwarzer AC, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995; 20(17):1878–1883.

31. Rosenberg JM, Quint TJ, de Rosayro AM. Computerized tomographic localization of clinically-guided sacroiliac joint injections. Clin J Pain 2000; 16(1):18–21.

Section 1: Sacroiliac Joint Syndrome 32. Hansen H. Is fluoroscopy necessary for sacroiliac joint injections. Pain Phys 2003; 6(2):155–158.

43. Hendrix RW, Lin PJ, Kane WJ. Simplified aspiration or injection technique for the sacro-iliac joint. J Bone Joint Surg [Am] 1982; 64(8):1249–1252.

33. Dreyfuss P, et al. Specificity of lumbar medial branch and L5 dorsal ramus blocks. A computed tomography study. Spine 1997; 22(8):895–902.

44. Dussault RG, Kaplan PA, Anderson MW. Fluoroscopy-guided sacroiliac joint injections. Radiology 2000; 214(1):273–277.

34. Barnsley L, et al. False-positive rates of cervical zygapophyseal joint blocks. Clin J Pain 1993; 9(2):124–130.

45. Yin W. Neuroanatomy of the dorsal sacral plexus: implications for a functional stereotactic approach towards sacro-iliac joint complex radiofrequency neurotomy. 8th Annual Scientific Meeting of the International Spinal Injection Society. 2000. San Fransisco, CA: International Spinal Injection Society.

35. Lord SM, Barnsley L, Bogduk N. The utility of comparative local anesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophyseal joint pain. Clin J Pain 1995; 11(3):208–213. 36. Schwarzer AC, et al. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophyseal joints. Pain 1994; 58(2):195–200. 37. Barnsley L, Lord S, Bogduk N. Comparative local anaesthetic blocks in the diagnosis of cervical zygapophyseal joint pain. Pain 1993; 55(1):99–106. 38. Lord S, et al. Chronic cervical zygapophyseal joint pain after whiplash: A placebocontrolled prevalence study. Spine 1996; 22:1737–1744. 39. Bogduk N, McGuirk B. Medical management of acute and chronic low back pain. An evidence-based approach. Pain research and clinical management. Vol. 13. Amsterdam: Elsevier; 2002:169–185. 40. Haldeman K, Soto-Hall R. The diagnosis and treatment of the sacroiliac condition by the injection of procaine. J Bone Joint Surg 1938; 20:675–685.

46. Bollow M, et al. CT-guided intra-articular corticosteroid injection into the sacroiliac joints in patients with spondyloarthropathy: indication and follow-up with contrastenhanced MRI. J Comput Assist Tomogr 1996; 20(4):512–521. 47. Braun J, et al. Computed tomography guided corticosteroid injection of the sacroiliac joint in patients with spondyloarthropathy with sacroiliitis: clinical outcome and follow-up by dynamic magnetic resonance imaging. J Rheumatol 1996; 23(4): 659–664. 48. Luukkainen R, et al. Periarticular corticosteroid treatment of the sacroiliac joint in patients with seronegative spondyloarthropathy. Clin Exp Rheumatol 1999; 17(1):88–90. 49. Maugars Y, et al. Corticosteroid injection of the sacroiliac joint in patients with seronegative spondyloarthropathy. Arthritis Rheum 1992; 35(5): 564–568.

41. Miskew DB, Block RA, Witt PF. Aspiration of infected sarco-iliac joints. J Bone Joint Surg [Am] 1979; 61(7):1071–1072.

50. Maugars Y, et al. Assessment of the efficacy of sacroiliac corticosteroid injections in spondyloarthropathies: a double-blind study. Br J Rheumatol 1996; 35(8): 767–770.

42. Aprill C. The role of anatomically specific injections into the sacroiliac joint. First Interdisciplinary World Congress on Low Back Pain and its Relation to the Sacroiliac Joint. 1992. San Diego, CA: ECO, Rotterdam.

51. Kline MT. Stereotactic radiofrequency lesions as part of the management of chronic pain. Orlando, FL: Paul M Deutsch; 1992:86.

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PART 4

EXTRA-SPINAL DISORDERS

Section 1

Sacroiliac Joint Syndrome

CHAPTER

Surgery for Sacroiliac Joint Syndrome

117

Michael R. Moore

INTRODUCTION Surgical treatment for sacroiliac pain can be considered when other therapeutic options have failed, and when the patient’s symptoms or functional limitations are of sufficient magnitude to balance the attendant risks. In the course of a general pain or spine practice a relatively small number of patients will be encountered who fall into this group. For patients with recalcitrant symptoms, it is the practitioner’s responsibility to educate patients about all potentially effective treatments, including those that lie outside the scope of a particular physician’s practice. Although not widely appreciated by most practitioners, extensive literature exists that reports satisfactory results from surgical treatment of sacroiliac pain in appropriately selected patients. This chapter will provide a review of the relevant literature and will describe the approaches to surgical treatment of patients with pain of sacroiliac origin.

PATIENT SELECTION As is true for most therapeutic interventions, the most important factor in the ultimate success of surgical treatment of sacroiliac pain is proper patient selection. A patient for whom surgical treatment is a consideration should undergo a thorough evaluation that clearly identifies the sacroiliac joint as a pain generator. As coexistent spinal pathology is not uncommon,1 the preoperative evaluation must include a detailed search for other pain generators that may mimic or overlap symptoms arising from the sacroiliac joint. Plain films and magnetic resonance imaging (MRI) studies of the lumbar spine should be obtained, and additional studies such as provocative discography, selective root blocks, median branch blocks, and other studies described elsewhere in this text should be utilized when appropriate. Physical examination maneuvers alone have been demonstrated to be inadequate in the diagnosis of a sacroiliac origin of pain.2,3 Radionuclide imaging is also of limited usefulness in confirming a diagnosis of sacroiliac-mediated pain, due to its very low sensitivity.4 Diagnosis of pain of sacroiliac origin requires an unequivocally positive result from a flouroscopically or computed tomography (CT)directed injection of local anesthetic into the synovial portion of the sacroiliac joint. False-positive results can be minimized by the use of a double block as described by Maigne et al.5 The author believes that the criteria of Maigne et al. should be modified slightly in that these authors recommended that the patient should report at least 75% reduction of pain for an injection to be considered positive. While percentage reduction of pain is by its nature a very subjective ‘measurement,’ in the author’s experience the response that best predicts a positive outcome from surgical treatment is a response of ‘near complete’ or ‘greater than 90%’ relief of pain. Coexistent pathology can also make any attempt at quantification of pain relief by an intervention that removes only a component of the patient’s symp-

toms very difficult to interpret, as some patients are more able than others to discriminate different components of their pain complaints. Ultimately, clinical judgment plays a crucial role in the assignment of all diagnoses relating to pain generators in any particular patient. The practitioner should, however, avail himself or herself of all diagnostic information necessary to formulate the best conclusions regarding the sources of pain generation before making a recommendation for surgical treatment of any type. Only patients who have failed to improve after undergoing a thorough trial of conservative treatment should be considered candidates for surgical treatment. No consensus exists, however, on what constitutes a thorough trial of conservative treatment. Mooney has described a defined course of physical therapy with demonstrated effectiveness in many patients.6 Prolotherapy has advocates, as does repeated corticosteroid injections. The practitioner should be acquainted with the various alternatives for nonsurgical treatment, and be satisfied that nonsurgical measures have been exhausted before making a recommendation for surgical treatment.

SURGICAL ALTERNATIVES Posterior arthrodesis Historical review Goldthwait and Osgood7 reported on the association of low back pain and sacroiliac laxity in pregnant women. They drew attention to the fact that the sacroiliac joints demonstrate motion in nonpathologic conditions and hypothesized that ligamentous laxity associated with pregnancy might lead to hypermobility and associated pain. Albee8 reported on his dissections of 50 pelvic specimens and drew attention to the fact that the sacroiliac joints were synovial joints and not ‘synchondroses’ as many physicians of that period assumed. Baer9 reinforced the fact that the sacroiliac joints were synovial joints and recommended manipulation under anesthesia as treatment for chronic sacroiliac pain. Gaenslen reported on his surgical treatment first in 1921,10 and later reported on 9 patients’ outcomes at varying intervals after surgery.11 Gaenslen’s operation consisted of a posterior approach to the joint by splitting the ilium to reflect a bone flap with the gluteal musculature attached. A window through the remaining cancellous portion of the ilium was then made to expose the synovial portion of the joint. Curettage of the interior of the joint was carried out. He reported good or very good results in 7 of 9 patients (78%). Smith-Petersen and Rogers12 reported on 26 patients who had undergone sacroiliac arthrodesis for chronic sacroiliac pain (one of whom was Smith-Petersen’s wife). Smith-Petersen’s technique differed slightly from Gaenslen’s technique in that the gluteal musculature was reflected and a transiliac window was made to gain access to the synovial portion of the joint. Decortication of the interior of the joint was carried out with curettes and gouges, and the window 1269

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was replaced and countersunk across the joint after removal of the cartilage and subchondral bone from the window fragment, allowing opposition of cancellous surfaces between the sacrum and ilium. He reported clinical success in 23 of 26 patients (89%), with radiographic union in 95%. Twenty-five of 26 patients (96%) returned to their prior occupation. Willis Campbell13 reported an extra-articular method of fusion, in which the posterior ilium and adjacent sacrum were exposed and decorticated, and bone graft was placed into the gutter dorsal to the joint proper. He reported that five of seven patients had a successful outcome, with two patients being too close to surgery to assess the outcome at the time of his publication. After this series of publications describing differing techniques, all with successful outcomes, there was a surprising absence of publications on both the diagnosis and the surgical treatment of sacroiliac pain. The most likely reason for this was the popularization of the diagnosis of disc pathology and its association with sciatica. Although Mixter and Barr14 are frequently given credit for ‘discovering’ the herniated lumbar disc, several publications discussing both the pathology15,16,17,18 and surgical treatment19 pre-date the Mixter and Barr article. Nonetheless, the influence of the Mixter and Barr article was apparently of sufficient magnitude to largely eliminate the sacroiliac joint from attention of authors in neurosurgical and orthopedic journals. In the 40 years following the Mixter and Barr article, only a handful of publications in the surgical literature make mention of the sacroiliac joint as being a source of low back pain and sciatica, with the exception of papers reporting on septic arthritis and sacroiliitis arising from rheumatoid disorders. Extending the work of Steindler and Luck,20 Haldeman and Soto-Hall21 recommended diagnosis of sacroiliac pain by injection of procaine, although their injection technique involved injecting large volumes (20–30 cc) of 1% procaine into the ligamentous portion of the joint. No mention of surgical treatment was made in their article. Norman and May22 brought attention to the fact that sacroiliac pain could mimic symptoms arising from intervertebral disc lesions, a fact largely unrecognized until the refinement of spinal diagnostic techniques in the 1990s.23 Orthopedic and neurosurgical journals remained silent on the issue of surgical treatment of sacroiliac pain until 1987, when Waisbrod and colleagues reported on 21 patients who underwent posterior uninstrumented sacroiliac arthrodesis for chronic sacroiliac pain.24 Diagnostic evaluation of this cohort included a provocative test, radiographic evaluation with plain films and CT images of the sacroiliac joint, radionuclide imaging, and several psychological questionnaires. The psychological screening was not utilized in the early part of the study period (1981–84). The provocative test consisted of injection of 10% NaCl solution into the ‘dorsocaudal’ portion of the joint. To be considered a positive test, this intervention was required to exactly reproduce the patient’s typical pain pattern. One to 2 cc of local anesthetic was also injected, and presumably this alleviated the previously aggravated symptoms, although the authors were not specific on this point. Follow-up ranged between 12 and 55 months. To be considered for surgery, the patients had to have positive findings on radiographic, nuclear medicine, and provocative testing. Patients with psychological disturbances were excluded regardless of other findings in the later part of the study (1984–86). Patients were divided into satisfactory and unsatisfactory outcomes. A satisfactory outcome required reduction of symptoms of at least 50%, no need for analgesics, and resumption of their preoperative occupation. They reported 50% satisfactory results overall, although this included six patients who would not have been operated upon in the later portion of the study based on psychological exclusion criteria. When they excluded the six patients with psychological disturbances, they concluded that a satisfactory result could be expected in 70% of cases. Moore reported on 13 patients treated with instrumented posterior sacroiliac arthrodesis for chronic 1270

sacroiliac pain at the 1992 North American Spine Society meeting.25 Patients were offered surgical treatment when conservative treatment had failed and the patients had unequivocal relief of their typical symptoms after injection of local anesthetic into the synovial portion of the joint under CT or fluoroscopic guidance. Six of the patients had prior failed lumbar spine surgery. He reported 10 excellent, one fair, and two poor results. This same group of patients was followed up again, with successively larger groups in 1995, 1997, and 1998.1,26,27 In the 1998 review, Moore reported on 59 patients who had isolated sacroiliac joint pain and no coexistent spinal pathology or prior spinal surgery.27 Chart reviews and phone interviews were carried out, and outcome variables included subjective pain relief, satisfaction with outcome, surgical complications, and incidence of pseudoarthrosis. All phone interviews were carried out by an independent research assistant (i.e. the surgeon did not carry out any of the interviews). Of these patients, 53 (89.8%) had a satisfactory outcome, and six (10.2%) were considered failures. Of the six patients who were failures, four had a pseudoarthrosis. The other two patients were clinical failures despite evidence of solid arthrodesis on fine-cut CT scanning. Complications were limited to one superficial wound infection, one intraoperative fracture into the sciatic notch during creation of the transiliac window, necessitating intraoperative repair which healed without incident. One patient required reoperation to retrieve a screw that penetrated the anterior cortex of the sacrum, causing mild radicular dysesthesia. Except for this latter case, there was no incidence of neurologic complications and there were no cases of visceral or vascular injury. Keating et al.29 reported on follow-up of 28 patients who underwent posterior arthrodesis of the sacroiliac joint for chronic sacroiliac pain. Statistically significant improvement between preoperative and postoperative pain was observed and patients remained improved up to the minimum 1 year follow-up period. Berthelot et al.30 reported on posterior sacroiliac arthrodesis in the treatment of two patients with recalcitrant sacroiliitis related to spondyloarthropathy. Both patients were significantly improved at follow-up of greater than 2 years. Belanger and Dall31 reported four patients who underwent posterior instrumented sacroiliac arthrodesis over a 10-year period, all with ultimately satisfactory results. There was one reoperation to remove internal fixation, and no significant complications were reported. In summary, the literature that exits reporting the results of posterior sacroiliac arthrodesis for pain of sacroiliac origin is consistently positive, despite many clinicians’ prejudices to the contrary. The literature supports consideration of posterior arthrodesis in treatment of sacroiliac pain when conservative treatment options have been exhausted and when the diagnosis is clear.

Instrumentation without fusion Lippitt reported on the use of percutaneous screw stabilization of the sacroiliac joint without any attempt to obtain bony fusion.32 In reviewing 43 patients, he reported that 23 patients (53%) had significant or complete relief of symptoms and seven patients (6%) had no improvement at all, with the remaining 13 patient showing varying degrees of partial pain relief. Complications of nerve injuries and RSD were reported, although surprisingly no cases of screw breakage or displacement occurred. The concept of stabilization without arthrodesis has not met with much acceptance at this point and should be considered investigational.

Anterior sacroiliac arthrodesis Although the anterior approach to the sacroiliac joint is one which is familiar to most orthopedic surgeons from their training in the treat-

Section 1: Sacroiliac Joint Syndrome

ment of pelvic ring fractures, it has been associated with significant complications when used in the setting of elective sacroiliac instrumentation and fusion.33 The L5 nerve root is at risk as it crosses the anterior portion of the joint and can be injured during the dissection required to gain access to the interior of the joint and to place internal fixation.34 In addition, it is difficult by this technique to reach the synovial portion of the joint. Achieving compression across the joint by anterior plating alone is problematic as well. The anterior approach may have utility in salvage or revision surgeries, but should be viewed with caution in the primary surgical treatment of sacroiliac pain

Author’s preferred technique: posterior instrumented arthrodesis The surgical technique is a modification of that described by SmithPetersen and Rogers.12 The patient is placed under general anesthesia and a Foley catheter is inserted into the bladder. An image table is used and the patient is placed in a prone position on chest rolls. An image intensifier is used to visualize the joint prior to marking the skin incision. In the anteroposterior projection in this position, the posterior superior iliac spine will usually overlay the midportion of the sacroiliac joint and a curvilinear skin incision is marked centered on this point. The length depends upon the size of the patient, but usually is usually 8–11 cm in length. Dissection is carried through subcutaneous tissue with electrocautery until the fascial attachments to the posterior iliac crest are identified. The fascia is incised and the outer table of ilium is exposed using subperiosteal dissection. It is necessary to divide fibers of the gluteus maximus inferiorly to extend exposure down to the posterior inferior iliac spine. The posterior sacroiliac ligament complex is not divided. The sciatic notch is identified by palpation and the inferior extent of the ilium is visualized. A Taylor retractor is placed deep in the wound to allow visualization of the surface of the ilium overlying the sacroiliac joint. The image intensifier is sterilely draped and brought into the field to visualize the sacroiliac joint. A 3.2 mm drill bit is used to drill channels for internal fixation screws. One is placed across the inferior pole of the joint. Drilling is carried out under intermittent image intensifier control. With experience, very little fluoroscopy time is required. Tactile feedback is used to determine penetration of cortical surfaces. (Tip: if only three cortical surfaces are penetrated, then the drill cannot enter either the pelvis or a sacral foramen.) The image intensifier is used to verify that the drill bit has crossed the sacroiliac joint. This may require manipulation of the C-arm angle into inlet, outlet, or oblique views depending on the shape of the individual joint. After drilling, a depth gauge is used to assess the appropriate length of screw. A 6.5 mm AO cancellous screw or equivalent is placed across the joint with a metallic washer. A similar procedure is carried out at the junction of the middle and superior thirds of the joint. The length of the screws is variable, but the inferior screw will usually be 25–30 mm long and the cephalad screw will be 35–45 mm long. Screws are placed into the ala and it is not necessary to enter the body of S1, due to the stability afforded by the preservation of the interosseous and posterior sacroiliac ligaments. Preparation is then made for creating a transiliac window into the synovial portion of the joint. It is desirable to create as large a window as possible without sacrificing the interosseous ligaments. The boundaries for the window and the thickness of the overlying ilium can be measured on the preoperative CT scan, which should be obtained in every case. The anterior extent of the window can be measured relative to the posterior superior iliac spine. While individual anatomy varies, the preoperative CT scan will show this to be

approximately 5–6 cm anterior to the posterior superior iliac spine. A Midas Rex K-1 dissecting tool is used to score the outer cortex of the ilium. Figure 117.1 shows the approximate location of the window relative to the previously placed screws. The window is completed using straight and curved osteotomes. The thickness of the ilium at this level is greater than most surgeons realize, and for this reason it is important to measure this on the preoperative CT scan. It is helpful to have osteotomes that have centimeter markers on their shafts. A common pitfall is to fail to reach the joint because of not creating a deep enough window. Out of concern for the anterior pelvic structures (iliac artery and vein, lumbosacral plexus, rectum), a surgeon may be reluctant to watch 3–4 cm of osteotome enter the ilium. Many so called ‘failed’ sacroiliac fusions occur because the surgeon never finds the true interior of the joint, and stops short of the joint in making the window, visualizing only subchondral bone on the iliac side of the joint. By following the rectangular outline of the window, the straight and curved osteotomes can be used to fenestrate the subchondral bone and cartilage on the iliac side of the joint, and the window can be removed en bloc, which will allow clear identification of the hyaline cartilage on the sacral side of the joint in the depth of the window. (Helpful hint: when the osteotome reaches the subchondral bone on the iliac side of the joint, a characteristic change of pitch can be heard as the mallet impacts the osteotome, and this is a useful clue in orienting the surgeon as to the correct depth to place the instrument.) If concern exists about the depth to which the osteotome has penetrated, the image intensifier may be used in multiple projections to identify the position of the end of the osteotome relative to the joint surfaces.

Fig. 117.1 Drawing of completed posterior transiliac instrumented sacroiliac arthrodesis. The gluteal musculature has been reflected from the outer table of the ilium. Internal fixation screws are present in the cephalad and caudad positions in the joint. After decortication, the transiliac window has been countersunk across the synovial portion of the joint. 1271

Part 4: Extra-Spinal Disorders

Once the window is created and the sacral side of the joint clearly visualized, decortication of the sacral side of the joint can be carried out using osteotomes and curettes. Angled curettes are useful in expanding the interior dimensions of the window and in removing remaining subchondral bone and cartilage from the synovial portion of the joint. All bone removed is saved and cleaned of cartilage and soft tissue, to be reused as bone graft. Additional bone graft is harvested by osteotomizing the posterior superior iliac spine and using gouges and curettes to retrieve cancellous bone from this area. The cancellous bone is morselized and packed into the lateral margins between the ilium and sacrum in the depth of the window. Subchondral bone and cartilage is removed from the iliac fragment removed in creating the window, and this is countersunk across the joint. A secure interference fit can be achieved by packing additional bone along the margins of the window. Multiple perforations in the facing cortex may then be made with the Midas Rex K-1 dissecting tool to facilitate incorporation. Irrigation is then carried out and the gluteal fascia is reapproximated with #1 Vicryl suture. A Hemovac drain is placed in the subcutaneous space and brought out through a lateral stab wound. Skin closure is in layers. Once the technique is learned, the procedure usually takes approximately 45–50 minutes.

Postoperative care The patient is optimally mobilized on the day of surgery and is kept non-weight bearing on the operated side for 8 weeks. The drain is removed at 24–48 hours. The patient can usually be discharged on the second postoperative day, after demonstrating competence in utilization of crutches and maintaining a non-weight bearing status on the operated side. Patients frequently experience dramatic relief of their preoperative pain in the early (24–48 hours) time period and have to be cautioned against early resumption of weight bearing. At 2 months after surgery crutches are discontinued. Patients are then referred to physical therapy for gluteal strengthening and gait normalization. Patients will tend to have a limp because of gluteal weakness from 2 months of non-weight bearing, and will tend to walk with the hip on the operated side in external rotation. Four to six weeks of physical therapy is usually sufficient to normalize gait and eliminate the limp. Figure 117.1 shows diagrammatically the appearance of the procedure prior to wound closure. Figure 117.2 shows a typical postoperative X-ray.

Fig. 117.2 Radiograph of pelvis after posterior instrumented sacroiliac arthrodesis. 1272

Complications Potential complications of the techniques described above include infection, vascular injury either to the superior gluteal artery or nerve during the approach, visceral, vascular or neurologic injury due to overpenetration of a drill bit, screws, or osteotomes, pseudoarthrosis, as well as systemic complications associated with any operation utilizing general anesthesia, such as deep venous thrombosis, atelectasis, and urinary tract infection. Reported complications, however, have been rare. No cases of vascular, visceral, or permanent neurologic complications have been reported. The most common complication reported has been pseudoarthrosis,26 which occurred in 7 of 77 patients (7/77=9%). Pseudoarthrosis was diagnosed by fine-cut CT scanning. All pseudoarthrosis occurred in smokers. Five patients underwent reoperation in an attempt to repair the pseudoarthrosis. Three patients went on to a solid arthrodesis after the second surgery and had a good result. The other two patients did not heal after a second surgery and continued to have unsatisfactory results. Experience with the technique and requiring that patients quit smoking prior to surgery will minimize the incidence of pseudoarthrosis.

Illustrative cases Case 1 The patient was an athletic 35-year-old female with a complaint of right buttock pain with radiation to the posterior thigh. Symptoms had been present for 6 months and were becoming increasingly severe. Physical therapy had been prescribed and had not improved her symptoms. There was no history of trauma, spondyloarthropathy, or other rheumatologic disorder. Plain films of the thoracic and lumbar spine revealed a mild idiopathic scoliosis and were otherwise unremarkable. An MRI of the lumbar spine demonstrated no disc or neurocompressive pathology (Fig. 117.3). A bone scan showed mild increased uptake in the right sacroiliac joint (Fig. 117.4). The patient described pain when rolling over in bed. She denied using a nonreciprocal gait when ascending stairs. Physical examination showed normal motor strength in the lower extremities as well as normal sensation and symmetric deep tendon reflexes. Waddel’s signs were

Fig. 117.3 MRI of a 35-year-old female with right-sided sciatica. Normal disc and canal anatomy is seen.

Section 1: Sacroiliac Joint Syndrome

Fig. 117.6 MRI of 36-year-old female with bilateral lower back pain and right-sided sciatica. Moderate degeneration is seen at L4–5. She was using morphine for pain control.

Fig. 117.4 Bone scan shows increased uptake in the right sacroiliac region.

negative. The Faber maneuver was negative bilaterally. A CBC was normal. ESR = 7 mm/hr and CRP was within normal limits. The patient underwent a fluoroscopically guided injection of Celestone, 0.5% marcaine, and 1.0% lidocaine into the right sacroiliac joint. The patient’s pain was nearly completely eliminated for approximately 8 hours, at which time it returned and was once again severe. She continued to be unable to pursue normal or recreational activities. She elected to undergo a posterior sacroiliac arthrodesis (Fig. 117.5). Surgery was uncomplicated and she was discharged from the hospital 48 hours after surgery on crutches, non-weight bearing on the right side. The patient was seen at 1 month following surgery and reported complete resolution of her preoperative pain. At 2 months, crutches were discontinued and physical therapy for gluteal strengthening and gait normalization was initiated and continued for 4 weeks. At 6 months post surgery, the patient was seen and reported only 10% pain. At follow-up at 34 months she reported 0% pain, was working in her usual occupation as a cosmetologist without restrictions, and was able to participate in unrestricted recreational activity.

Fig. 117.5 Postoperative X-ray after sacroiliac arthrodesis.

Case 2 The patient was a 36-year-old mother of 4 children with a long history of low back pain that had gotten worse with each of her pregnancies. Her youngest child was 3 years old, and since the time of that delivery her symptoms had become progressively worse. She rated her typical pain as 80–90% in severity, and was using morphine sulfate for pain control. She had many evaluations of the lumbar spine without a clear diagnosis being obtained, and had undergone several courses of physical therapy with no improvement. An MRI of the lumbar spine showed minor degeneration at L4–5 (Fig. 117.6). Provocative discography was carried out and was negative for reproduction of concordant pain (Fig. 117.7). Plain films and CT showed oseitis condensans ilii affecting both sacroiliac joints, right greater

Fig. 117.7 Discography at L3–4, L4–5, and L5–S1 was negative for reproduction of concordant pain. Discography confirms degeneration at L4–5, but was painless on injection.

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Fig. 117.8 CT scan showing oseitis condensans ilii in a 36-year-old female with severe bilateral sacroiliac pain.

Fig. 117.10 Postoperative X-ray after subsequent left sacroiliac arthrodesis. At 2 years, patient reported 10% pain and was using no pain medication.

than left (Fig. 117.8). A flouroscopically guided injection of local anesthetic into the right sacroiliac joint afforded nearly complete relief of her right-sided pain. The patient underwent a posterior instrumented sacroiliac arthrodesis on the right side (Fig. 117.9) At 2 months crutches were discontinued. Physical therapy normalized her gait, and the patient reported complete relief of her right-sided symptoms. She continued, however, to have pain over the left sacroiliac joint. A flouroscopically guided injection of the left sacroiliac joint afforded complete relief of her residual pain. Six months after her index procedure, she underwent a left-sided sacroiliac fusion without complication (Fig. 117.10). At 2-year follow-up from her index procedure, the patient reported 10% pain, was using no pain medication, and had resumed unrestricted activity.

was subjective reduction of pain of 56%, although the patient was still using narcotic medication at follow-up. As of the time of this writing, there have been no other published reports on this mode of treatment.

CONCLUSIONS Surgical treatment of sacroiliac pain should be considered an option for appropriately selected patients who have failed conservative treatment and who have disabling symptoms. Figure 117.11 shows

Clinical suspicion of sacroiliac joint syndrome

Neuroaugmentation Cavillo et al. reported on two patients believed to have bilateral sacroiliac pain after lumbosacral arthrodesis.35 They were treated by bilateral implantation of stimulating electrodes into the third sacral foramina, to treat sacroiliac pain. One patient developed an infection and the electrodes had to be removed. In the other patient, there

Confirmation by double block

Search for coexistent spinal pathology

Positive

Assess priority treat appropriately

Successful

Exit algorithm

Present

Psychiatric evaluation and treatment

Negative Conservative treatment trial Unsuccessful Psychosocial issues, somatoform disorders, secondary gain issues Absent Posterior instrumented sacroiliac arthrodesis Fig. 117.9 Postoperative X-ray after right sacroiliac arthrodesis. Rightsided back pain and sciatica were eliminated after this procedure. She continued to complain of left-sided pain. 1274

Fig. 117.11 Flowchart for evaluation of patient for surgical treatment of sacroiliac joint syndrome.

Section 1: Sacroiliac Joint Syndrome

a flowchart for evaluation of a patient for surgical treatment of sacroiliac pain. The literature supports posterior sacroiliac arthrodesis over other surgical options at this time, although controlled studies are required to further identify the optimum surgical treatment. The best results can be expected in nonsmoking patients with pain of sacroiliac origin and no coexistent spinal pathology.

References 1. Moore MR. Diagnosis and surgical treatment of chronic painful sacroiliac joint dysfunction. In: Vleeming A, Mooney V, Dorman T, et al., eds. The integrated function of the lumbar spine and sacroiliac joint. Rotterdam: ECO; 1995:341–354.

18. Middleton G S, Teacher J H 1911 Injury of the spinal cord due to rupture of an intervertebral disc during muscular effort. Glasgow Med J 76:1–6. 19. Dandy WE. Loose cartilage from intervertebral disc simulating tumor of the spinal cord. Arch Surg 1929; 19:660–672. 20. Steindler A, Luck JV. Differential diagnosis of pain low in the back. Allocation of the source of pain by the procaine hydrochloride method. JAMA 1938; 110:106–113. 21. Haldeman KO, Soto-Hall R. The diagnosis and treatment of sacroiliac conditions by the injection of procaine. J Bone Joint Surg 1938; 20:675–685. 22. Norman GF, May A. Sacroiliac conditions simulating intervertebral disc syndrome. West J Surg Gynecol Obstetr 1956; 64:461–462. 23. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37.

2. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical examination in diagnosing sacroiliac joint pain. Spine 1996; 21:2594–2602.

24. Waisbrod H, Krainick JU, Gerbershagen HU. Sacroiliac joint arthrodesis for chronic lower back pain. Arch Orthopaed Trauma Surg 1987; 106:238–240.

3. Slipman CW, Sterenfeld EB, Chou LH, et al. The predictive value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehab 1998; 79:288–292.

25. Moore MR. Diagnosis and treatment of chronic sacroiliac arthropathy. Orthopaed Trans 1994; 18(1):255.

4. Slipman CW, Sterenfeld EB, Chou LH, et al. The value of radionuclide imaging in the diagnosis of sacroiliac joint syndrome. Spine 1996; 21:2251–2254. 5. Maigne JY, Aivalliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21:1889–1892. 6. Mooney V. Evaluation and treatment of sacroiliac dysfunction. In: Vleeming A, Mooney V, Dorman T, et al., eds. The integrated function of the lumbar spine and sacroiliac joint. Rotterdam: ECO; 1995:393–407. 7. Goldthwait JE, Osgood RB. A consideration of the pelvic articulations from an anatomical, pathological and clinical standpoint. Boston Med Surg J 1905; 152: 593–601. 8. Albee FH. A study of the anatomy and the clinical importance of the sacroiliac joint. JAMA 1909; 53:1273–1276. 9. Baer WS. Sacro-iliac strain. Bull Johns Hopkins Hosp 1917; 28:159–163.

26. Moore MR. Surgical treatment of chronic painful sacroiliac joint dysfunction. In: Vleeming A, Mooney V, Dorman T, et al., eds. Movement, stability, and low back pain. New York: Churchill Livingstone; 1997:563–572. 27. Moore MR. Outcomes of surgical treatment of chronic painful sacroiliac joint dysfunction. In: Vleeming A, Mooney V, Tilscher H, et al., eds. 3rd Interdisciplinary World Congress on Low Back and Pelvic Pain, November 19–21, 1998, Vienna, Austria. Rotterdam: ECO; 1998: 218–226. 28. Moore MR. Surgical treatment of chronic painful sacroiliac joint arthropathy. Poster presentation, 13th annual meeting of the North American Spine Society, San Fransisco, October 28–31, 1998. 29. Keating JG, Avillar MD, Price M. Sacroiliac joint arthrodesis in selected patients with low back pain. In: Vleeming A, Mooney V, Dorman T, et al., eds. Movement, stability, and low back pain. New York: Churchill Livingstone; 1997:573–586. 30. Berthelot JM Gouin F, Glenmarec J, et al. Possible use of arthrodesis for intractable sacroiliitis in spondyloarthropathy. Spine 2001; 26:2297–2299.

11. Gaenslen FJ. Sacro-iliac arthrosesis. Indications, author’s technique and end results. JAMA 1927; 89:2031–2035.

31. Belanger TA, Dall BE. Sacroiliac arthrodesis using a posterior midline fascial splitting approach and pedicle screw instrumentation: A new technique. J Spinal Disord 2001;14:118–124.

12. Smith-Petersen MN, Rogers WA. End-result study of arthrodesis of the sacroiliac joint for arthritis – traumatic and non-traumatic. J Bone Joint Surg 1926; 8: 118–136.

32. Lippitt AB. Percutaneous fixation of the sacroiliac joint. In: Vleeming A, Mooney V, Dorman T, et al., eds. The integrated function of the lumbar spine and sacroiliac joint. Rotterdam: ECO; 1995:371–390.

13. Campbell WC. An operation for extra-articular fusion of the sacroiliac joint. Surg Gynecol Obstetr 1927; 45:218–219.

33. Kim DH, Patel AJ, Brown CW, et al. Arthrodesis of the sacroiliac joint syndrome. Preliminary review of results. Presented at the Annual meeting of the American Academy of Orthopedic Surgeons, February 22, 1996.

10. Gaenslen FJ. Wisconsin Med J 1921; 20:20.

14. Mixter W, Barr J. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934; 211:210–215. 15. Virchow RLK. Untersuchung uber die Entwickelung des Schadelgrund. Berlin: Reimer; 1857. 16. von Luschka H. Die Hallogelenke des menschlichen Korpens. Berlin: Riemer; 1858.

34. Moed BR, Kellan JF, Mclaren A, et al. Internal fixation for the injured pelvic ring. In: Tile M, Helfet DL, Kellan JF, eds. Fractures of the pelvis and acetabulum. 3rd edn. New York: Williams and Wilkins; 2003:249–250. 35. Calvillo O, Esses SI, Ponder C, et al. Neuroaugmentation in the management of sacroiliac joint pain: report of two cases. Spine 1998; 23(9):1069–1072.

17. Goldthwait JE. The lumbosacral articulation: an explanation of many cases of ‘lumbago,’ ‘sciatica,’ and paraplegia. Boston Med Surg J 1911; 164:365–372.

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PART 4

EXTRA-SPINAL DISORDERS

Section 2

Sacral Disorders

CHAPTER

Hip Spine Syndrome

118

Vijay B. Vad, Jennifer L. Solomon and David R. Adin

INTRODUCTION Hip and spine syndrome is a condition in which patients experience hip, buttock, and groin pain that concomitantly originates from pathology involving both the spine and the hip. Symptoms of lumbar spondylosis, stenosis, radiculopathy, and facet arthropathy can cause referral of pain to the groin and anterior thigh. Underlying hip pathology may also present with groin and anterior thigh pain. This leads to the clinical dilemma of determining if the patient’s symptoms originate from the hip, spine, or both. Patients may be misdiagnosed with primary hip pathology leading to ineffective management including total joint arthroplasty. They may also be misdiagnosed with lumbar stenosis as the etiology of their lower limb pain and undergo an unnecessary spinal surgery. Difficulty arises when trying to determine the major source of pathology contributing to the patient’s pain and disability. Consequently, clinicians must evaluate both the hip and the spine as possible sources of lower limb pain and weakness. Lower extremity symptoms can stem from spinal nerve root irritation or compression, particularly at the L3 or L4 nerve roots, which can lead to weakness of the hip flexors and quadriceps, as well as sensory deficits over the anterior thigh. This type of pain will typically have a dermatomal pattern. Lumbar stenosis is a common source of lower limb pain. Approximately 1.2 million people in the United States have back and leg pain that is related to spinal stenosis.1 If lumbar stenosis is the underlying pathology, patients commonly present with complaints of leg pain brought on by standing, walking, or with lumbar extension that increases the lordosis of the spine. They may describe what is termed neurogenic claudication, pain that radiates to the lower extremities and worsens with walking and improves with forward flexion. Severe neurologic symptoms are typically rare.2 Facet arthropathy can cause low back pain with occasional radiation to the buttock, posterior thigh, or knee that worsens with lumbar extension. Pain relief with partial spinal flexion is common.3 Studies carried out by Schwarzer et al. estimate that 15–40% of chronic low back pain is related to facet joint pathology.4,5 In the absence of coexisting pathology, a detailed neurologic examination should be normal. Biomechanical dysfunction such as muscle imbalance secondary to weakness or flexor contractures of the hip can be the cause of low back pain. An abnormality of the hip joint causes abnormal curvature of the sagittal alignment of the spine and can induce low back or lower limb pain.6 Matsuyama et al. examined the total spinal sagittal alignment in patients with bilateral congenital hip dislocations and found that the most common clinical symptom of the lumbar hyperlordosis found in these patients was low back pain and not lower limb pain.7 Additionally, patients with painful hips from synovitis or chronic inflammatory states may develop a biomechanical dysfunction with secondary effects to the spine.

Osteoarthritis of the hip can present in a similar fashion. In general, osteoarthritis has been radiographically reported in more than 80% of individuals older than 55 years.8 Radiographic evidence of osteoarthritis of the hip has been reported in 12% of patients over the age of 80.9 Osteoarthritis of the spine, hip, or both may result in significant impairment and disability and therefore correct diagnosis is essential for approaching the optimal treatment plan. Patients with acetabular labral tears often describe ‘deep’ discomfort, most commonly in the anterior groin but occasionally directly lateral, just proximal to the trochanter or deep within the buttocks. Patients may or may not remember a provoking cause of the hip pain. The general complaint is usually discrete episodes of sharp hip pain triggered by pivoting or twisting.10 Lage et al. reported the incidence of idiopathic and degenerative acetabular labral tears to be 27.1% and 48.6%, respectively.11 Vascular disease is a widely reported phenomenon. It is estimated that up to 12% of the population older than 66 years of age has peripheral vascular disease.12 In many ways, the symptomatology of vascular disease mimics that of hip and lumbar spine pathology. Intermittent claudication secondary to peripheral arterial disease has been commonly described as a pain felt in the calf of the leg. It is brought on by walking, relieved by rest, and described as ‘heaviness,’ ‘cramping,’ or ‘tiredness in the legs.’13 Less frequently, patients may complain of pain in the thigh, buttock, groin, or lower back without associated calf pain as can be seen with common iliac artery obstruction.14 The presence of these symptoms is sometimes coupled with numbness in the foot which results from ischemia of peripheral nerves. The least appreciated symptom associated with severe vascular disease is rest pain.15 It may be intermittent or continuous in nature and it is not made worse with exercise. It characteristically occurs at night when the affected limb is elevated and cardiac output and blood pressure fall. Rest pain is typically relieved when the patient gets up and walks as perfusion improves.16,17

TYPES ‘Simple hip spine syndrome’ occurs when the pain generator is easily determined to be coming from either the hip or the spine exclusively.6 Once the appropriate treatment is instituted, the patient should then have significant relief. ‘Complex hip spine syndrome’ is not as clearly differentiated when both the hip and the spine are contributing to a patient’s discomfort.6 Further differential testing including a comprehensive physical examination as well as other radiologic or interventional diagnostic procedures must be done to find the major structure involved. In ‘secondary hip spine syndrome,’ the hip and spine are not distinct entities, and dysfunction with one causes abnormalities with the other. This syndrome can arise from hip flexor contractures

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placing the spine in excessive hyperlordosis by forward rotation of the pelvis. This increased curvature affects the facet joints, with slippage of the posterior facet joint increasing foraminal stenosis and creating nerve root impingement. Concomitant nerve root involvement with hip osteoarthritis can worsen an already weak hip.6 Difficulty arises when determining the greater offender and the ultimate treatment course.

CLINICAL PRESENTATION The etiology of hip, groin, or lower limb pain can be delineated by a comprehensive physical examination with or without supplemental testing, including imaging and minimally invasive diagnostic studies. Patients must undergo a detailed history and physical examination to establish an appropriate diagnosis and treatment plan. Non-specific diagnoses will lead to poorly directed treatment plans and may compromise patient outcomes. The considerable overlap of referred and radicular pain patterns complicates one’s ability to make a clear diagnosis with any appreciable degree of certainty. This is further confounded with vague symptoms and an incomplete history, which can often be the case. Therefore, a thorough physical examination of a patient with hip, groin, or anterior thigh pain should include an in-depth evaluation of the neurological, musculoskeletal, and vascular systems. The assessment of strength must be performed in a sequential manner, evaluating muscle groups innervated by different peripheral nerves and nerve roots. The strength examination should include the assessment of hip flexors (L1–3), quadriceps (L2–4), tibialis anterior (L4–5), extensor hallucis longus and hip abductors (L5), and the gastrocnemius/soleus complex (S1). Johnsson reported on 163 cases of lumbar spinal stenosis and found that extensor hallicus longus and peroneal paresis were the most common signs.2 L4 nerve root irritation may lead to a diminished patella reflex and can create pain that typically radiates to the anterior knee and not necessarily below the knee. The straight leg raise, sitting root, and femoral nerve stretch tests provide evidence of nerve root irritation. Lower limb symmetry should be carefully assessed, as asymmetric muscle bulk and the presence of muscle fasciculations portend a neurologic component. Asymmetric muscle strength is often subtle in patients with radiculopathies. Single-leg partial squats and single-leg standing heel raises can assess the functional strength of the quadriceps and calf muscles, respectively. Examination of bilateral hip joints is essential. Time should be spent assessing the hip and its function, specifically with passive range of motion and strength testing. Asymmetric decreased range of motion is commonly found in arthritic hips. Pain reproduction with decreased internal rotation of the hip suggests underlying hip osteoarthritis. Patients will typically have decreased hip extension secondary to tight or contracted hip flexors, limited internal and external rotation, and weakness of the quadriceps. Ely’s test can be performed to evaluate for a hip flexion contracture. With the patient prone, the knee is fully flexed. By pushing the heel towards the buttocks, the rectus femoris is stretched, causing the hip to flex and the buttock to rise. Functional testing of the hip abductor strength should be performed with the patient standing on one leg to evaluate for the presence of a Trendelenburg sign. Manual muscle testing of the hip abductors should be performed to elicit subtle differences in muscle strength, which would imply a neurologic component and a probable spinal source of pathology. Anterior acetabular labral tears may be detected by moving the hip from a position of full flexion, external rotation, and abduction to a position of extension, internal rotation, and adduction. Conversely, moving the hip from a position of full flexion, adduction, and internal

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rotation to a position of extension, abduction, and external rotation allows detection of posterior labral tears.18 Hase and Ueo reported that all patients with acetabular labral tears had pain with axial compression upon a 90° flexed and slightly adducted hip.19 Identification of peripheral vascular disease requires blood pressure recordings taken in both limbs, pulses checked on each side, and bruits auscultated for over the major peripheral arteries of both the upper and lower limbs.20 Absence of hair growth on the dorsum of the foot and toes, particularly when it was formerly present, suggests arterial insufficiency.21 Femoral pulses should be palpated and timed with the radial pulses. Other pulses can be assessed and compared in the same manner. Temperature gradients in each limb ought to be assessed. The palm of the hand should be used moving across the limb in a proximal to distal fashion. A cold foot with warm knees is characteristic of popliteal arterial obstruction.14 Simply reporting whether a pulse is present, reduced, absent, or aneurysmal in nature provides less subjectivity than using scales composed of too many gradations. Limb color should be evaluated with the limbs elevated, then with the limbs hanging off the edge of the examination table. A healthy, elevated limb will show mild blanching, whereas an elevated ischemic limb will appear appreciably paler.22 As the limbs are brought into a gravity-dependent position, the ischemic limb will appear redder. Severe ischemic disease will result in dependent rubor. The proximal extent of the rubor is directly related to the severity of the arterial insufficiency.23 Of note, rubor is typically seen in patients with rest pain.14 Assessment of the vascular system after exercise will regularly give rise to an unsuspected diagnosis in patients where there is doubt about the presence or absence of peripheral arterial disease. A poorly perfused limb after exercise will be much paler, with collapsed veins. The patient can exercise the legs by actively dorsiflexing and plantarflexing for 30–60 seconds.21

DIAGNOSTIC AIDS Imaging should begin with plain radiographs that encompass the lumbosacral spine and bilateral hips, looking for degenerative disease or severe arthritis. For further evaluation of the spine, a magnetic resonance imaging (MRI) or computed tomography-myelogram should be performed for better localization of pathology affecting the nerve roots and spinal canal. Plain radiographs have generally been utilized to assess the presence of severe hip osteoarthritis. Plain radiographs in patients with only acetabular labral pathology are typically negative. While arthroscopy is the gold standard for diagnosing acetabular labral tears, MRI arthrography is currently the most sensitive nonsurgical test. MRI alone appears to be less sensitive than arthrography alone for diagnosing acetabular labral tears. Hase and Ueo demonstrated an accurate diagnosis of acetabular labral tears in 37% of their patients tested using arthrography alone. However, they were unable to confirm a tear in any of their patients examined with MRI alone. Arthroscopy was used as the definitive measure to confirm their findings.19 Petersilge et al. found complete correlation between MRI arthrography and arthroscopy in diagnosing acetabular labral tears.24 Electromyography can aid in localizing peripheral neurologic pathology. This becomes particularly beneficial in differentiating between a lumbar radiculopathy versus a lower limb compression neuropathy. Employing minimally invasive diagnostic procedures including epidural nerve root or hip joint injections has proven to be invaluable in assessing the involvement of each area to the patient’s diagnosis. A minimally invasive fluoroscopically guided injection to the hip joint or nerve root can easily and safely be performed with diagnostic and therapeutic benefit. Following the procedure, the patient should be taken through those activities that would normally reproduce or

Section 2: Sacral Disorders

exacerbate their symptoms. A careful assessment of the patient’s response will assist in identifying the area of inciting pathology. Kleiner et al. described the identification of the hip as the source of pain in 88% of cases after injection of 10 mL of bupivacaine HCl to the hip joint.25 If no relief is provided with a hip injection, a closer look should be given to the spine. There are several diagnostic blocks that can be performed to the spine to evaluate and treat the pain etiology. Lumbar facet and medial branch blocks or epidural injections via interlaminar, transforaminal, or caudal approaches can be done. If there is significant relief, the spine is the likely contributor of the pain. When the hip and spine diseases are interrelated, as in ‘secondary’ hip spine syndrome, correction of the hip pathology may amend the symptoms resulting from the lumbar spine. In the setting of ‘complex’ hip spine syndrome where pathology from the hip and spine are both believed to be contributing to pain generation and both areas warrant surgery, hip arthroplasty should probably be considered first. Patient outcomes after this particular surgery tend to be encouraging. Occasionally, the improved gait and longer walking distances after hip arthroplasty can exacerbate spinal pathology. This silent lumbar pathology can become symptomatic, requiring surgery as well. If, on the other hand, hip surgery was performed and the patient still had no relief of their pain, the lumbar spine should then undergo a thorough evaluation. Infrequently, low back and lower limb symptoms may be the result of an occult process. Kleiner et al. reported on 12 cases of misdiagnosis. Ten patients were initially diagnosed with having an L3 and/or L4 or S1 radiculopathy. Two patients were referred with an initial diagnosis of sciatic neuropathy. All patients had failed various therapeutic measures aimed at correcting their initial diagnoses, including two patients who underwent laminectomies without resolution of their symptoms. Further investigation uncovered occult malignancies in nine patients. A hematoma, an aneurysm of the obturator artery, and a neurilemmoma of the sciatic nerve were discovered in the remaining three. The authors note that the most useful means of identifying the correct diagnosis was computed tomography or MRI of the abdomen and pelvis.25

SUMMARY Lumbar spine pathology can create symptoms that mimic those generated by hip joint disease and vice versa. Moreover, pathology of the hip joint and lumbar spine can coexist as well. The impediment to successful treatment has been differentiating the severity each pathologic entity may contribute to the patient’s disability. A detailed, systematic, and exhaustive diagnostic approach may be necessary, as each pathologic process may mandate a separate treatment paradigm. Failure to identify the correct site of disease can result in misdiagnosis of the source of pain, and consequently result in misguided treatment. Unfortunately, many of these patients are identified after the fact when the expected result of treatment is not realized. When faced with hip spine syndrome, a detailed physical examination accompanied by proper diagnostic interventional procedures will usually discern the source. This may spare patients further delay in the correct treatment and speed the process to improved function. Many different pathologies or combination of pathologies can affect the hip and spine as mentioned above. We pointed out some of the diagnoses more commonly identified as the etiologies of pain in the population of patients afflicted with hip spine syndrome. The different diagnoses discussed above are not intended to be exhaustive. Of course, patients can have more discrete and less-known hip and spine diagnoses creating their symptoms. It was our goal to impart

the importance of examining the lumbar spine even though the hip may seem so clearly the source of the patient’s disability and vice versa. As well, it is vital to consider pathology stemming from areas outside the neurologic and musculoskeletal systems.

References 1. Hart LG, Deyo RA, Cherkin DC. Physician office visits for low back pain. Frequency, clinical evaluation, and treatment patterns from a US national survey. Spine 1995; 209(1):11–19. 2. Johnsson KE. Lumbar spinal stenosis. A retrospective study of 163 cases in southern Sweden. Acta Orthop Scand 1995; 66(5):403–405. 3. Dreyer SJ, Dreyfuss P. Low back pain and the zygapophyseal joints. Arch Phys Med Rehabil 1996; 77(3):290–300. 4. Schwarzer AC, Aprill CN, Derby R, et al. The relative contributions of the disc and zygapophyseal joint in chronic LBP. Spine 1994; 19(7):801–806. 5. Schwarzer AC, Wang S, O’Driscoll D, et al. The ability of computed tomography to identify a painful zygapophyseal joint in patients with chronic low back pain. Spine 1995; 20(8):907–912. 6. Offierski CM, Macnab I. Hip-spine syndrome. Spine 1983; 89(3):316–321. 7. Matsuyama Y, Hasegawa Y, Yoshihara H, et al. Hip-spine syndrome: total sagittal alignment of the spine and clinical symptoms in patients with bilateral congenital hip dislocation. Spine 2004; 29(21):2432–2437. 8. Fogel GR., Esses SI. Hip spine syndrome: management of coexisting radiculopathy and arthritis of the lower extremity. Spine J 2003; 3(3):238–241. 9. Lawrence RC, Helmick CG, Arnett FC, et al. Estimate of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum 1998; 41(5):778–799. 10. Fitzgeraled RH. Acetabular labral tears. Diagnosis and treatment. Clin Orthop 1995; 311:60–68. 11. Lage LA, Patel JV, Villar RN. The acetabular labral tear: an arthroscopic classification. Arthroscopy 1996; 12(3):269–272. 12. Pandian G, Hamid F, Hammond MC. Rehabilitation of the patient with PVD and diabetic foot problems. In: Delisa J, Gans BM, eds. Rehabilitation medicine: principles and practice. Philadelphia: Lippincott-Raven; 1998:1517–1544. 13. Zabalgoitia M, O’Rourke RA. Disease of the aorta. In: Stein HL, ed. Internal medicine, 4th edn. St. Louis: Mosby; 1994:285–293. 14. Provan JL, Moreau P, MacNab I. Pitfalls in the diagnosis of leg pain. Can Med Assoc J 1979; 121(2):167–171. 15. Cranley JJ. Ischemic rest pain. Arch Surg 1969; 98(2):187–188. 16. Rutherford RB. Initial patient evaluation. In: Rutherford RB, ed. Vascular surgery, 5th edn. Philadelphia: WB Saunders; 2001:1–13. 17. Craeger MA, Libby P. Peripheral arterial disease. In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001:1457–1484. 18. Huffman G, Safran M. Tears of the acetabular labrum in athletes: diagnosis and treatment. Sports Med Arthroscopy Rev 2002; 10(2):141–150. 19. Hase T, Ueo T. Acetabular labral tear: arthroscopic diagnosis and treatment. Arthroscopy 1999; 15(2):138–141. 20. Braunwald E, Perloff JK. Physical examination of the heart and circulation. In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001:45–81. 21. Arnold GJ. Peripheral vascular assessment: history taking and physical examination of the arterial and venous system. In: Abela GS, ed. Peripheral vascular disease: basic diagnostic and therapeutic approaches. Philadelphia: Lippincott Williams and Wilkins; 2004:37–52. 22. Seidel HM, Ball JW, Dains JE, et al. Mosby’s guide to physical examination, 5th edn. St. Louis: Mosby; 2003. 23. Spittell PC, Spittell Jr JA. Diseases of the peripheral arteries and veins. In: Stein JH, ed. Internal medicine, 4th edn. St. Louis: Mosby; 1994:293–302. 24. Petersilge CA, Haque MA, Petersilge WJ, et al. Acetabular labral tears: evaluation with MR arthrography. Radiology 1996; 200(1):231–235. 25. Kleiner JB, Donaldson WF III, Curd JG, et al. Extraspinal causes of lumbosacral radiculopathy. J Bone Joint Surg [Am] 1991; 73(6):817–821.

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Section 2

Sacral Disorders

CHAPTER

Sacral Insufficiency Fractures

119

Mark A. Harrast

INTRODUCTION Insufficiency fractures of the sacrum are an underrecognized cause of low back pain, particularly in the elderly female. To identify these fractures, the astute clinician needs to consider their possibility when evaluating patients with low back pain. Given that insufficiency fractures are more common in elderly patients, their incidence will likely be increasing dramatically with the aging population. Once such fractures are identified as the source of low back pain, the importance of appropriate treatment cannot be overemphasized. Keeping patients functional with healing insufficiency fractures is the mainstay of treatment in order to limit the cost, disability, and complications of immobility from prolonged bed rest. This chapter is dedicated to exploring sacral insufficiency fractures (SIF), highlighting patient characteristics, etiology and biomechanics, clinical presentation, differential diagnosis, appropriate imaging strategies, treatment, and the rare associated complications. The goal of this chapter is to enhance the index of suspicion of SIF to create a higher rate of recognition of these fractures so that patients may receive appropriate treatment.

NOMENCLATURE Stress fractures are those that occur when the load applied to the bone exceeds the mechanical resistance, typically from repetitive loading of subthreshold forces, as larger forces tend to result in overt fracture rather than stress injuries.1 They are subcategorized into two types: fatigue fractures and insufficiency fractures.2 Fatigue fractures occur in normal, healthy bone from abnormal or repetitive loading. Fatigue fractures commonly occur in the lower extremities of athletes and military recruits, with the most frequent sites being the tibia and metatarsals.3 In contrast, insufficiency fractures occur when the elastic resistance of bone is inadequate to withstand the stresses of normal activity. Insufficiency fractures commonly occur in elderly women with osteoporosis, with the most frequently reported sites being vertebral compression fractures and hip fractures.4 Similarly, pathological fractures occur in weakened bone when the weakening is caused by tumor. Sacral insufficiency fractures were first described in the medical literature by Lourie in 1982.5 He presented the cases of three patients who were hospitalized for severe low back pain within a 4month period in 1981. Two were female and one male, between the ages of 75 and 86 years. All three were diagnosed with SIF by bone scan and confirmed with sacral tomograms. The two female patients did well as they were asymptomatic at their follow-up visits 8 and 10 months later. The male patient died of aspiration pneumonia.

CLASSIFICATION OF SACRAL FRACTURES In 1988, Denis and colleagues described the most uniformly accepted classification system for sacral fractures.6 This system divides the

sacrum into three zones (Fig. 119.1). Zone I fractures are limited to the sacral ala, the most lateral portion of the sacrum (lateral to the sacral foramina). These are typically stable fractures without an associated neurological deficit. Zone II fractures involve the sacral foramina and are present with sacral, or even L5, radiculopathies. Finally, zone III fractures involve the sacral canal and thus can result in cauda equina-type symptoms. The Denis classification system is best reserved for traumatic sacral fractures, as insufficiency fractures rarely extend beyond the sacral alae (Denis zone I).

EPIDEMIOLOGY The true incidence of SIF in the general population is unknown. Most reports in the literature are case reports and case series, typically of patients admitted to the hospital. As of 2003, there have been just over five hundred reported cases in the literature since the first report in 1982.7 Many of these fractures go unrecognized and likely do not require hospital admission. With this in mind, the incidence reported in the literature varies from 0.2% in all patients (male and female) to 4.3% in females.8–10 The vast majority of cases of SIF are in women with over 90% of the reports in the literature being of females.7–9,11 These fractures are seen most commonly in the elderly with the average age of those reported in the eighth decade of life.7,9,11 The most common location of these fractures is in the sacral ala, typically unilaterally, but they do occur bilaterally. The fractures usually extend vertically, in a line parallel to the sacroiliac joints.12 Sometimes, there is a transverse fracture through the sacral body which, on imaging studies, appears to connect the vertically oriented fractures of the sacral alae. SIF is commonly associated with other fractures of the pelvic ring, especially the pubis.7,10,12,13 Pubic fractures are typically more readily diagnosed on plain films and, thus, due to their high clinical correlation, searching for a concomitant sacral fracture is appropriate if warranted by the clinical scenario. In those patients with known osteoporosis, especially those with a prior history of osteoporotic vertebral and/or femoral fractures, a higher index of suspicion for SIF is warranted in those patients who develop low back, buttock, or pelvic pain. In a study of 20 patients diagnosed with SIF, 16 had an associated fracture.9 Nine had pubic rami fractures, one had an iliac fracture, and six had thoracic or lumbar vertebral compression fractures.

ETIOLOGY AND BIOMECHANICS As the definition implies, insufficiency fractures occur in weakened, demineralized bone due to the reduced elastic resistance of that bone. This weakened bone cannot resist the day-to-day stresses; consequently, these fractures can occur spontaneously. Sometimes very 1281

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I

II

III

A

B

C

D

minimal trauma, such as falling from a seated position, is an initiating factor.9 There are multiple factors and associated medical conditions that lead to weakened bone which can result in SIF. The preeminent risk factor is osteoporosis.7,8 Up to three-quarters of patients with SIF have concomitant involutional osteoporosis.11 The second most common risk factor is radiation therapy, primarily for a gynecologic malignancy.8,14 Exposure to radiation weakens bones via many mechanisms.14–16 Radiation can reduce the bony matrix by killing osteocytes, osteoblasts, and osteoclasts. Bony necrosis can occur due to damage of the small feeding arterioles. Radiation-induced insufficiency fractures typically occur about 12 months after radiation therapy.17 Since these patients have a known primary malignancy, the diagnosis of insufficiency fracture is typically delayed, as a pathologic fracture due to tumor recurrence is generally entertained first. Recognizing insufficiency fractures as a possible cause and obtaining the appropriate imaging can save these postmalignancy patients unnecessary bone biopsies. Other predisposing factors (Table 119.1) include metabolic diseases other than osteoporosis (osteomalacia, Paget’s disease, renal osteodystrophy, hyperparathyroidism), corticosteroid therapy, rheumatoid arthritis, and fluoride therapy.8,13,18 Association with solid organ transplantation (liver, lung, heart, and kidney) has been described as well.19–21 Two reports of Tarlov’s cysts as the precipitating etiology for SIF exist.8,22 There are also mechanical causes which may predispose a person to SIF. These include lumbar scoliosis and total hip arthroplasty.18,23,24 1282

Fig. 119.1 Classification of sacral fractures proposed by Denis et al. (A) The three zones classified by Denis et al. Zone I is the region of the sacral ala. Zone II involves the sacral foramina. Zone III involves the central sacral canal. (B) Zone I sacral fracture. (C) Zone II sacral fracture. (D) Sacral fracture extending into zone III.

There has been very limited research into these biomechanical causes. Given the common location of such fractures (vertically extending in the sacral alae, running parallel to the sacroiliac joints, in line with the lateral margins of the lumbar spine) a hypothesis has been developed which suggests that these fractures may be partially caused by weight-bearing loads transmitted through the lumbar spine.12 It is widely recognized that the joints of the pelvis (sacroiliac and pubic symphysis) are strategically placed to buffer the large forces that are transmitted from the lower extremities to the spine during weight-bearing activities. Thus, in a person whose bony elastic resistance is reduced (from osteoporosis, radiation therapy, etc.) the most likely area of bony fracture (when subjected to such large forces) could be predicted to occur in the pubic rami and sacral alae (i.e. areas adjacent to the set of joints designed to buffer the forces).

Table 119.1: Predisposing factors for SIF Osteoporosis

Hyperparathyroidism

Radiation therapy to the pelvis

Rheumatoid arthritis

Corticosteroid therapy

Fluoride therapy

Osteomalacia

Solid organ transplantation

Paget’s disease

Tarlov’s cysts

Renal osteodystrophy

Anorexia nervosa

Section 2: Sacral Disorders

CLINICAL PRESENTATION The clinician needs a high index of suspicion to correctly diagnose SIF since there are no pathognomonic characteristics that can be obtained from the clinical history or physical examination. Most patients are lumped into the diagnostic category of mechanical low back pain, unless the symptoms are severe enough or persistent enough to warrant advanced imaging studies. Most commonly it is an advanced imaging test that provides the information to make the diagnosis. Most patients with a SIF present with low back pain. In addition, some describe buttock and pelvic pain. Rarely are there complaints other than pain.8,25,26 Radicular pain is rare.8 The axial pain is often severe, incapacitating, and mechanical in nature, exacerbated by weight-bearing or physical exertion and relieved with rest.21,27 Some patients are nonambulatory because of the severity of pain.26 There is typically a history of minimal trauma, such as fall from a seated or standing position. Sometimes there is no known trauma. Neurologic abnormalities in patients with SIF are exceedingly rare due to the absence of bony displacement and sacral foraminal compromise in most patients, and thus little or no injury to the sacral roots. There are only a few reports of neurologic complications related to SIF.28–30 The reports include one case of urinary retention and anal sphincter dysfunction in a patient with a markedly displaced fracture28 and one with urinary and fecal incontinence, decreased anal sphincter tone, and lower extremity weakness.29 In another case series of three patients, there were similar findings of urinary incontinence and decreased anal sphincter tone, but also of definite lower extremity motor loss (confirmed by EMG).30 In a 1997, in a meta-analysis of 493 patients with SIF, a total of 12 cases reported neurologic symptoms, a 2% incidence.11 The physical examination of a patient with SIF is generally unrevealing. The most common finding, if any, is sacral tenderness.8 Restricted lumbar spine motion is next most common – a typical finding in the general elderly population.8,10 In general, the neurologic examination is normal, or age appropriate.

DIFFERENTIAL DIAGNOSIS To make an accurate and expeditious diagnosis, one must have a high suspicion for SIF in the elderly patient presenting with low back pain or buttock pain, since plain radiographs are typically normal. Many patients are dismissed with a diagnosis of mechanical low back pain from lumbar spondylosis, stenosis, or myofascial pain. Since lumbar compression fractures are so common in this elderly, osteoporotic population, they must be considered in the differential diagnosis. A pelvic neoplasm should also be entertained. This concept is particularly applicable when an elderly patient provides a history of treatment for a primary tumor, such as uterine, cervical, colon, or prostrate cancer. It is sometimes difficult to rule out a local recurrence manifesting as a pathologic fracture of the sacrum, and thus bone biopsies are sometimes performed to confirm the diagnosis. Finally, since most patients presenting with SIF are women, a separate gynecologic cause should be considered.

on plain films.31 Demineralization of bone in elderly patients also often results in plain radiographs that are difficult to interpret. The most common finding on conventional radiographs that lead one to suspect SIF is areas of vertical sclerosis in the sacral alae. These sclerotic areas represent callus formation. In a case series of 27 patients, 37% of the radiographs had this finding.7 Other studies showed 52–75% of plain sacral radiographs were considered normal, even retrospectively.8,18 Pelvic ring fractures (particularly in the pubic ramus) are more easily seen on conventional radiographs. If these are found, an even higher index of suspicion should be raised for an associated radiographically occult sacral fracture since 47% of patients with SIF had a concomitant pubic insufficiency fracture present in one meta-analysis of 212 patients.8

Scintigraphy Radionuclide bone scanning is the most sensitive technique to detect SIF and thus should be the imaging study of choice when conventional radiographs are inconclusive. In addition to their high sensitivity, bone scans are widely used because they can provide positive detection very early after fracture onset (typically 48–72 hours).32 Sacral fractures are best demonstrated on the posterior view.33 A characteristic scintigraphic finding is the H-shaped (or butterfly) sacral pattern.34,35 This ‘H’ shape has been labeled the ‘Honda’ sign (Fig. 119.2).36 The H-shaped pattern is produced by two vertical bands in both sacral alae interconnected by a horizontal component through the body of the sacrum. This pattern, though pathognomonic for SIF, is not seen in a majority of cases. Reports detailing this scintigraphic appearance are seen 20–45% of the time.8,31 More common sacral patterns include variable parts of the ‘H’ shape: bilateral vertical bars in the sacral alae with partial or no horizontal bar through the sacral body and unilateral alar uptake, again with partial or no horizontal uptake (Fig. 119.3A, B).35,37 This more patchy appearance mimics a primary malignancy or metastatic disease; thus, further evaluation with computed tomography (CT) or magnetic resonance imaging (MRI) is required, especially in patients with a history of previous malignancy.31

Computed tomography Computed tomography of the pelvis is best used to confirm the presence of fracture when one is still not certain after bone scanning. In patients with a history of previous malignancy, CT can often prevent the need for unnecessary biopsy. The appearance of SIF on CT includes bands of bony sclerosis with or without evident fracture

IMAGING STUDIES Conventional radiographs Plain radiographs of the sacrum are generally the first imaging studies used to screen for SIF. Though appropriate as an initial screening tool, they are often falsely negative due to difficulty in interpretation as overlying bowel gas, vascular calcifications, and the normal angulation of the sacrum make the diagnosis of such fractures problematic

Fig. 119.2 Technetium 99 bone scan demonstrating the typical ‘H’ sign that is pathognomonic for sacral insufficiency fractures.

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A

Fig. 119.3 Technetium 99 bone scan of a 68-year-old male with advanced osteoporosis and right buttock pain. These anterior (A) and posterior (B) coronal views of the pelvis show increased radiotracer medial to the right SI joint demonstrating the sacral alar insufficiency fracture confirmed by the MRI in Fig. 119.4.

B

lines within the sacral alae.38 CT is also very helpful in determining fracture displacement and fragmentation as well as bony destruction and soft tissue masses seen in malignancy.32 Reports in the literature demonstrate an 88% detection rate of SIF by CT.7,38 An early finding of SIF on CT, in addition to the sclerosis before the distinct fracture lines develop, is intraosseous gas inclusions in the ventral lateral sacrum.39 As fracture lines can take weeks to months to evolve, these early findings are very useful to make or confirm the diagnosis of SIF.

Magnetic resonance imaging Magnetic resonance imaging is highly sensitive for the diagnosis of SIF but the marrow edema seen is somewhat non-specific, and can also be seen with metastatic disease. The marrow edema seen is of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images and STIR images (Fig. 119.4).33 As with CT, a discrete fracture line may not be evident with MRI and thus marrow edema may be the only finding. An injection of intravenous

* A

B

Fig. 119.4 (A) MRI of the pelvis in a 68-year-old male (same as in Fig. 119.3) with advanced osteoporosis. This is an axial STIR image showing the bone marrow edema surrounding (and obscuring) the right sacral alar (zone I) insufficiency fracture. (B) This is an axial T1-weighted image showing the vertically oriented (small arrows) area of low T1 signal representing the right sacral alar insufficiency fracture. The larger arrows are pointing at the right SI joint. The asterisk is just medial to the right S1 neuroforamen. 1284

Section 2: Sacral Disorders

gadolinium may reveal the fracture line, as it did in the majority of cases in one study where the fracture line was not evident without contrast.40 MR fat suppression sequences also can help to reveal the fracture line.40 There is a delay in MRI findings, with the earliest sign of marrow edema not evident until at least 18 days after the onset of symptoms;37 thus, MRI is used similarly as CT, to confirm the diagnosis made by bone scanning.

*

Imaging recommendations

C Fig. 119.4 Cont’d (C) This is a coronal T1-weighted image showing a different depiction of the same SIF in (B).

Conventional radiographs are an appropriate screening tool for SIF and should be obtained initially. If the plain film is inconclusive, a bone scintigram should be obtained. If increased uptake is not in the pathognomonic H-shaped pattern, CT or MRI should be obtained to differentiate an insufficiency fracture from neoplasm, as primary or metastatic bone lesions do not have a characteristic vertical, linear, or band shape in the sacral alae. 37 With this imaging protocol strategy, unnecessary sacral biopsies should be limited or nonexistent. See Table 119.2 for a flow diagram of a typical clinical scenario with an imaging studies decision tree. Routine follow-up imaging is not necessary to monitor the status of healing. Once the diagnosis is made, treatment decisions are made on a clinical basis. If SIF is the first manifestation of undiagnosed osteoporosis, a DEXA scan should be performed to gather baseline data of the patient’s bone mineralization status.

Table 119.2: Diagnosis of sacral insufficiency fractures: typical clinical paradigm of elderly woman with low back and buttock pain History

Examination

1. Insidious onsıet

1. Sacral tenderness

2. No noted trauma

2. Antalgic gait

3. Pain worse with weight bearing

3. Normal neurologic examination

Imaging

4. Better with rest 5. No radiating symptom 6. No bowel or bladder symptoms

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OTHER DIAGNOSTIC MANEUVERS Serologic evaluation is limited and rarely necessary in making a diagnosis of SIF. Erythrocyte sedimentation rate and alkaline phosphatase may be mildly elevated in certain patients with SIF.8,21,26 However, these findings are not specific to SIF. Bone biopsies were performed more commonly when there were still only a few reports of SIF in the literature, especially in a patient with prior history of malignancy, to rule out recurrence or metastatic disease. With better imaging techniques and a higher awareness of the potential for SIF in the elderly population, bone biopsies should be exceedingly rare. If the bone scan does not demonstrate the typical pathognomonic H-shape, CT or MRI can typically determine fracture versus neoplasm.

TREATMENT There is not one randomized, controlled trial studying treatment efficacy for SIF. Treatment has been based on anecdotal evidence and what intuitively has seemed appropriate. Only recently has one of the main standards of treatment (bed rest) been challenged.41 There are three primary goals of treatment for SIF: pain management, maintaining functional independence, and prevention of complications.

Pain management Adequate pain control is of utmost importance. Without it, patients will not be able to progress toward the other two treatment goals. There are two facets to pain management: analgesics and activity limitation.

Analgesics Analgesics should be used liberally for pain control, but remember that the elderly are more prone to medication side effects and lower tolerance. The routine analgesics for SIF include acetaminophen and a short course of opiates if necessary. Calcitonin nasal spray can be used to treat bone pain and has been reported to have good pain-relieving effects in patients.9,27 Nonsteroidal antiinflammatory drugs (NSAIDs) should be used as second-line treatment since there are some reports implicating NSAID use with delayed fracture healing.42

Activity limitation Bed rest was an early mainstay of treatment and generally quite helpful in initial pain control. However, given the multitude of complications resulting from immobility and bed rest (as amplified in Chapter 111 by Terry Sawchuk and Eric Mayer) and the fact these issues are amplified in the elderly, this strategy must be reconsidered.41 Since these fractures are generally stable, bed rest was used primarily for pain control. A better solution regarding activity level is to instruct the patient to stay mobile and instead use pain as a guide for activity limitations.

Maintaining functional independence Early mobilization, after appropriate pain control for SIF is achieved, is essential to helping elderly patients maintain their functional independence. While managing pain during the early stage of treatment, a physical therapy referral is indicated for instruction on the use of an ambulation aid (cane or walker) to help maintain mobility. To help ensure compliance, remind the patient that the assistive device is only a temporary measure and if he or she was ambulating indepen-

1286

dently prior to the fracture, it is likely that pre-fracture ambulatory status will return. If the patient’s mobility is significantly limited due to pain or other comorbidities, the physical therapy referral can be used to maintain joint range of motion and muscular strength with passive and active movement at all joints and, at minimum, an isometric strengthening program. Inpatient rehabilitation is rarely necessary unless there are profound comorbidities or marked functional disability. An aggressive exercise program is not necessary or appropriate during the early stages of SIF treatment. Maintaining general mobility and function should be the goal of a rehabilitation program at this stage. Once the patient is pain free and the fracture is presumptively healed, a therapeutic exercise program may be beneficial to regain the strength or range of motion lost from the hopefully short period of convalescence. Sometimes, just helping to maintain the patient’s ambulatory status is enough exercise for these frail elderly patients.

Prevention of complications Early ambulation (as opposed to bed rest) decreases the risk of the many complications secondary to immobilization. The effects of immobilization spares virtually no organ system.41 These adverse effects include muscle weakness and strength deficits, deep venous thrombosis, postural hypotension, impaired cardiac function, urinary retention, constipation, and pressure ulcers, all of which can create a higher level of patient disability. The other main group of complications to prevent during this time are those inherently related to osteoporosis and the risk of future fracture. If aggressive osteoporosis management (see Ch. 39 by Joseph Lane et al.) has not already been initiated, it should not be overlooked. Bisphosphonates should be considered, as should a work-up for the etiology of osteoporosis if it is not readily apparent. Preventing a potentially more catastrophic and disabling femoral or vertebral fracture is the goal.

SURGICAL MANAGEMENT Due to the inherent stability of these fractures, lack of neurological complications, the high rate of improvement with conservative measures, and the low rate of nonunion, surgery for SIF is exceedingly rare. Mears and Velyvis authored the only published report examining surgical management for persistent pain and nonunion after SIF.43 They performed in situ fixations in 36 patients with chronic pain and nonunion of sacral alae insufficiency fractures. The surgery was successful in creating pelvic stability and fracture unions; however, subjective reports of patients’ pain and disability were not overwhelmingly positive.

NEW HORIZONS: INTERVENTIONAL TREATMENT There has been recent work to create a technique for SIF analogous to vertebroplasty for compression fractures. Garant44 and Pommersheim et al.45 have published four cases detailing this technique. Since percutaneous polymethyl methacrylate (PMMA) injection has been adapted to treat painful metastatic lesions in the S1 vertebral body,46 the technique has been adapted to treat the pain of SIF. The technique, called sacroplasty, is similar to that used in vertebroplasty. With all four cases, good pain relief and functional improvement after the procedure were demonstrated. However, there are no long-term results to date. Though this technique looks promising, there is no necessary role for invasive procedures with inherent risks in such a relatively benign disease process which has

Section 2: Sacral Disorders

generally excellent long-term outcomes with more conservative management. Its value may be in keeping mobile patients whose pain is uncontrolled by other means.

3. Bennell KL, Brukner PD. Epidemiology and site specificity of stress fractures. Clin Sports Med 1997; 6:179–196.

TREATMENT OUTCOMES

5. Lourie H. Spontaneous osteoporotic fracture of the sacrum. An unrecognized syndrome of the elderly. JAMA 1982; 60:440–452.

Outcomes of SIF treatments are rarely reported but, in general, are quite favorable. The pain, as a rule, resolves typically in the range from 2 weeks to 2 years, with most SIF patients experiencing complete pain relief within 6–12 months.7–9,18,26 Recovery is generally prolonged in patients with associated pubic fractures.8 Most patients do not suffer any prolonged functional loss and most remain independent ambulators. The small minority of patients who do not do as well generally have other confounding medical conditions which limit their mobility and functional status, or suffer other osteoporotic fractures.

6. Denis F, Davis S, Comfort T. Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop 1988; 227:67–81.

COMPLICATIONS Complications from SIF are rare. In general, these are stable fractures with very little risk of complications. The most common complications are seen in those patients treated with bed rest who suffer the consequences of immobility.41 Since these fractures are generally limited to the sacral alae, neurological complications are rare. There have been only a few reports of neurologic damage, to include variants of cauda equina syndrome or sacral radiculopathies.28–30 There is no characteristic of the fracture, such as amount of angulation or displacement, to reliably predict a risk of neurological complications. Finally, as previously mentioned, other complications such as nonunion or persistent pain are also exceedingly rare.

CONCLUSION Sacral insufficiency fractures are more common than once believed. With an increase in aging population, the incidence will no doubt increase. When an elderly patient presents with back, buttock, or groin pain, the diagnosis of SIF should be considered. Conventional radiographs of the sacrum are the first diagnostic study obtained. If these are inconclusive and the index of suspicion is high, bone scanning should be performed. Further diagnostic studies (such as CT or MRI) are necessary only if the bone scan is equivocal and/or there is a concern for malignancy. The hallmarks of treatment are pain management and early mobilization to prevent the complications of bed rest. The natural history and treatment outcomes of SIF are favorable, with most patients being pain free within 6–12 months. Finally, there is a definite need for scientific studies to help determine the most cost-effective diagnostic strategies and most appropriate treatment regimens. General outcome studies are needed to help counsel patients about appropriate treatments, the natural history, and disease course of SIF. All of these studies are lacking in the current medical literature.

Acknowledgment The author thanks John J. Harrast for his insightful review of this manuscript and Nilda Gatchalian for her help in preparation.

References

4. Cummings SR, Melton LJ III. Epidemiology and outcomes of osteoporotic fractures. Lancet 2002; 359:1761–1767.

7. Soubrier M, Dubost JJ, Boisgard S, et al. Insufficiency fracture. A survey of 60 cases and review of the literature. Joint Bone Spine 2003; 70:209–218. 8. Grasland A, Pouchot J, Mathieu A, et al. Sacral insufficiency fractures: An easily overlooked cause of back pain in elderly women. Arch Intern Med 1996; 156( 6):668–674. 9. Weber M, Hasler P, Gerber H. Insufficiency fractures of the sacrum: Twenty cases and review of the literature. Spine 1993; 18:2507–2512. 10. Peh WCG, Khong PL, Ho WY. Insufficiency fractures of the sacrum and os pubis. Br J Hosp Med 1995; 54:15–19. 11. Finiels H, Finiels PJ, Jacquot JM, et al. Fractures of the sacrum caused by bone insufficiency. Meta-analysis of 508 cases. Presse Med 1997; 26(33): 1568–1573. 12. Leroux JL, Denat B, Thomas E, et al. Sacral insufficiency fractures presenting as acute low-back pain. Biomechanical aspects. Spine 1993; 18(16):2502–2506. 13. DeSmet AA, Neff JR. Pubic and sacral insufficiency fractures: clinical course and radiologic findings. Am J Roentgenol 1985; 145:601–606. 14. Bliss P, Parsons CA, Blake PR. Incidence and possible aetiological factors in the development of pelvic insufficiency fractures following radical radiotherapy. Br J Rheumatol 1996; 69:544–548. 15. Henry AP, Lachmann E, Tunkel RS, et al. Pelvic insufficiency fractures after irradiation: diagnosis, management and rehabilitation. Arch Phys Med Rehabil 1996; 77(4):414–416. 16. Libshitz HI. Radiation changes in bone. Semin Roentgenol 1994; 29:15–37. 17. Blomlie V, Rofstad EK, Talle K, et al. Incidence of radiation-induced insufficiency fractures of the female pelvis: evaluation with MR imaging. Am J Roentgenol 1996; 167:120–1210. 18. Gotis-Graham I, McGuigan L, Diamond T, et al. Sacral insufficiency fractures in the elderly. J Bone Joint Surg [Br] 1994; 76(6):882–886. 19. Peris P, Navasa M, Guanabens N, et al. Sacral stress fracture after liver transplantation. Br J Rheumatol 1993; 32(8):702–704. 20. Schulman LL, Addess O, Staron RB, et al. Insufficiency fractures of the sacrum: a cause of low back pain after lung transplantation. J Heart Lung Transplant 1997; 16(10):1081–1085. 21. Aretxabala I, Fraiz E, Perez-Ruiz F, et al. Sacral insufficiency fractures. High association with pubic rami fractures. Clin Rheumatol 2000; 19:399–401. 22. Peh WCG. Tarlov cysts: another cause sacral insufficiency fractures? Clin Radiol 1992; 46:329–330. 23. Cooper KL. Insufficiency stress fractures. Curr Probl Diagn Radiol 1994; 23: 29–68. 24. Cotty PH. Insufficiency fractures of the sacrum: Ten cases and a review of the literature. J Neuroradiol 1989; 16:160–171. 25. Mathers DM, Major GA, Allen L, et al. Insufficiency fractures of the sacrum. Ann Rheum Dis 1993; 52:621–623. 26. Rawlings CE, Wilkins RH, Martinez S, et al. Osteoporotic sacral fractures: a clinical study. Neurosurgery 1988; 22:72–76. 27. Lin J, Lachmann E, Nagler W. Sacral insufficiency fractures: a report of two cases and a review of the literature. J Women’s Health and Gender-Based Med 2001; 10:699–705. 28. Jones JW. Insufficiency fracture of the sacrum with displacement and neurologic damage: a case report and review of the literature. J Am Geriatric Soc 1991; 39:280–283. 29. Lock SH, Mitchell SC. Osteoporotic sacral fracture causing neurologic deficit. Br J Hosp Med 1993; 49:210. 30. Jacquot JM, Finiels H, Fardjad S. Neurological complications in insufficiency fractures of the sacrum: three case reports. Rev Rheum 1999; 66:109–114.

1. Orava S, Hulkko A. Delayed unions and nonunions of stress fractures in athletes. Am J Sports Med 1988; 16(4):378–382.

31. White JH, Hague C, Nicolaou S, et al. Imaging of sacral fractures. Clin Radiol 2003; 58:914–921.

2. Pentecost RL, Murray RA, Brindley HH. Fatigue, insufficiency and pathologic fractures. JAMA 1964; 187:1001–1004.

32. Martin P. The appearance of bone scans following fractures, including immediate and long-term studies. J Nucl Med 1979; 20:1227.

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Part 4: Extra-Spinal Disorders 33. Peh WCG, Khong PL, Yin Y. Imaging of pelvic insufficiency fractures. Radiographics 1996; 16:335–348.

41. Babayev M, Lachmann E, Nagler W. The controversy surrounding sacral insufficiency: to ambulate or not to ambulate? Am J Phys Med Rehabil 2000; 79:404–409.

34. Ries T. Detection of osteoporotic sacral fractures with radionuclides. Radiology 1983; 146:783–785.

42. Giannoudis PV, Macdonald DA, Matthews SJ, et al. Nonunion of the femoral diaphysis. The influence of reaming and non-steriodal anti-inflammatory drugs. J Bone Joint Surg [Am] 2000; 82-B(5):655–658.

35. Schneider R, Yacovone J, Ghelman B. Unsuspected sacral fractures: detection by radionuclide bone scanning. Am J Roentgenol 1985; 144:337–341. 36. Stroebel RJ. Sacral insufficiency fractures. J Rheumatol 1991; 18:117–119.

43. Mears DC, Velyvis JH. In situ fixation of pelvic nonunions following pathologic and insufficiency fractures. J Bone Joint Surg 2002; 84:721–728.

37. Jones DN, Wycherley AG. Bone scan demonstration of progression of sacral insufficiency stress fracture. Australasian Radiol 1994; 38:148–150.

44. Garant M. Sacroplasty: a new treatment for sacral insufficiency fracture. J Vasc Interv Radiol 2002; 13:1265–1267.

38. Chen CKH, Liang HL, Lai PH, et al. Imaging diagnosis of insufficiency fracture of the sacrum. Chin Med J (Taipei) 1999; 62:591–597.

45. Pommersheim W, Huang-Hellinger F, Baker M, et al. Sacroplasty: a treatment for sacral insufficiency fractures. Am J Neuroradiol 2003; 24:1003–1007.

39. Stäbler A, Steiner W, Kohz P, et al. Time-dependent changes of insufficiency fractures of the sacrum: intraosseous vacuum phenomenon as an early sign. Eur Radiol 1996; 6:655–657.

46. Dehdashti AR, Martin JB, Jean B, et al. PMMA cementoplasty in symptomatic metastatic lesions of the S1 vertebral body. Cardiovasc Intervent Radiol 2000; 23:235–241.

40. Grangler C, Garci AJ, Howarth NR. Role of MRI in the diagnosis of insufficiency fractures of the sacrum and acetabular roof. Skeletal Radiol 1997; 26:517–524.

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PART 4

EXTRA-SPINAL DISORDERS

Section 2

Sacral Disorders

CHAPTER

120

Coccydynia Jean-Yves Maigne

INTRODUCTION Although coccygeal pain was first described in relation to a fracture by sixteenth-century French surgeon Ambroise Paré, the term coccydynia was not introduced until 1859 by Simpson.1 The awareness of this condition led to numerous studies, but it has remained poorly understood until recently. The use of dynamic films, described by the author in 1992, has led to a better understanding of the various possible causes of coccydynia and their associated specific symptoms and therefore to a better management.

FUNCTIONAL ANATOMY OF THE COCCYX Very little information is available in the literature regarding coccyx anatomy. According to Gray, the sacrococcygeal joints are very thin intervertebral discs of fibrocartilage and the intercoccygeal joints can be either synovial joints or discs.2 By examining nine aged coccyges from fresh cadavers, the author found that the sacrococcygeal joint was a disc in one case, a synovial joint in four cases and, in the four remaining cases, an intermediate structure composed of a disc containing a fairly extensive cleft, parallel to the endplates, and bordered by annular fibers or synovial cells.3 This intermediate pattern was not found in the intercoccygeal joints. It is unknown if the same distribution is found in young individuals, which raises the question as to whether the cleft extends throughout life as a result of mechanical constraints, with the disc gradually changing to a synovial joint in the same individual. Synovial joints allow more mobility than discs. A fourth type found consisted of complete ossification of the sacrococcygeal joint. A study of two different populations found the frequency of this type to be 22% and 68% of the cases, respectively.4 In some instances, the entire coccyx was ossified. The physiological movements of the coccyx are restricted to flexion and extension. Active flexion (movement in a forward direction) is performed by the levator ani and the external sphincter muscles. Extension (movement in a backward direction) is caused by a relaxation of these muscles and increased intra-abdominal pressure, which occurs during defecation and parturition.5 It is always a passive movement. To the best of the author’s knowledge, the movements of the coccyx in the sitting position have never been reported in the literature. They consist either of flexion (moving forward) or extension (moving backward) or a lack of mobility (rigid coccyx). The angle of incidence determines the direction of sagittal movement of the coccyx. The author has described the coccygeal incidence as the angle at which the coccyx strikes the seat when the subject sits down.6 If the incidence is low, the coccyx will be more or less parallel to the seat surface. The pressure exerted by the seat will push the coccyx forward and upward in flexion. If the angle of incidence is high, the coccyx will be somewhat perpendicular to the

seat surface. The coccyx will then be pushed backward in extension by increased intrapelvic pressure. The incidence is influenced by the shape of the coccyx and the sagittal pelvic rotation.7 Coccyges with more than two vertebrae are often curved and long, and have a low incidence. Conversely, straight, short coccyges have a higher incidence. Four types of coccyx have been described according to the Postacchini and Massobrio8 classification ranging from the straightest (type I) to the most sharply angled coccyx (hooked coccyx, type IV). The coccygeal shape can also be determined by measuring the intercoccygeal9 or sacrococcygeal angle (Maigne), this latter formed by the intersection of the coccygeal and the 4th sacral vertebra axis. A sacrococcygeal angle close to 180° corresponds to a straight coccyx while a curved coccyx will have an angle close to 90°. The incidence is related to another angle; the degree of sagittal pelvic rotation. This angle measures the sagittal rotation of the pelvis when the subject moves from the standing to the sitting position. This rotation is accompanied with reduction of lumbar lordosis. When the sagittal pelvic rotation is high (up to 60°), the incidence is low. This is usually observed in subjects with a normal or low body mass index (BMI). Conversely, when the pelvic rotation is low (less than 30°), the incidence is high. This is the case in subjects with high BMI (>27). It is believed that the pelvic volume in obese subjects restricts the natural movements of pelvic rotation. Other factors can restrict pelvic rotation, including loss of mobility of the lumbosacral junction as a result of degenerative disc changes, sequelae of discectomy and arthrodesis, or, more simply, a high seat. Hyperlaxity of the ligaments and a low seat can also increase rotation. Such factors can affect the occurrence of coccygeal pain. The absence of movement when sitting can be due to ossification of coccygeal joints or the presence of immobile discs. The coccyx is usually less mobile in men than women.

HISTORICAL ASSESSMENT Interviewing the patient with coccydynia should include the following four steps: ● ● ● ●

Confirm the diagnosis. Obtain a detailed history of the symptoms. Identify a cause Assess the potential repercussions.

Confirm the diagnosis: where do you feel the pain? Common coccydynia is primarily characterized by its localization to the coccygeal region, the absence of significant symptom referral, and the fact that the pain may be increased or only present in the sitting position. 1289

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It is therefore essential to ask the patient to turn his or her back toward the examiner and point to the painful area. The identified region must correspond to the coccyx. Diffuse pain or pain present in both the standing and sitting positions does not indicate common coccydynia. Frequent differential diagnoses include pain associated with depression, low back pain radiating to the coccyx, pudendal neuralgia, anal pathology, or certain sacroiliac pains.

Obtain a detailed history of the symptoms: is this acute or chronic coccydynia? It is important to differentiate acute from chronic coccydynia. Initially, coccydynia is acute and by definition becomes chronic after 2 months. Management will depend on how long the patient has been suffering; acute coccydynia usually resolves spontaneously within a few weeks.

Identify a cause Trauma is a classical cause of coccydynia. Sometimes, patients blame a traumatic event sustained several years earlier, although the role of this past event is questionable. Based on the fact that luxation (see below) is the most commonly observed condition after a trauma, it was demonstrated that the interval between the trauma and the onset of coccydynia is a determining factor.7 A very short or nonexistent interval (such as in postpartum coccydynia) is almost certainly indicative of trauma-related pain. Traumatic coccydynia is very likely if the pain occurs within a month of an injury. After 3 months, it is unlikely that trauma is the cause. It is important to know whether the traumatic event is an occupational injury or not, as the treatment results may be less effective when the trauma is work related. In some cases, coccydynia may develop after moderate trauma, as a result of a long car journey, or riding a bicycle or a horse. In obese patients, excess weight in conjunction with the particular way of changing from standing to sitting (see below), and even sitting itself can be considered as repeated microtraumas. Generally, posttraumatic coccydynia is more frequent in straight coccyges that move into extension when the subject sits down than in curved coccyges that move into flexion.7,9 Curved coccyges are actually relatively well protected during the impact of sitting. Thus, contrary to a common opinion, hooked coccyges are less at risk than straight ones regarding post-traumatic coccygodynia. Apart from a possible trauma, it has been shown that other factors such as BMI and the presence of pain when standing up from sitting could have diagnostic value.6 Determining body mass index is essential, as this factor greatly affects coccygeal biomechanics and, therefore, the culprit lesion. Luxation is more frequently observed in the obese population. The obese subject has a low angle of sagittal pelvic rotation when sitting down. As a result, the coccyx is more or less perpendicular to the seat surface, which increases the risk of luxation. In a normal-weight or lean person, the angle of sagittal pelvic rotation is greater, and the coccyx is parallel to the seat and prone to flexion and hypermobility. In lean patients, a spicule may cause significant irritation due to the absence of perineal fat (see below). PAIN ON STANDING UP FROM SITTING The presence of sharp pain on passing from the sitting to the standing position is a sign that suggests a lesion that can be identified with radiologic imaging. These radiographic abnormalities are usually luxation or osseous spicules.7 As with any information gleaned during history taking, this element is of greater value if the patient mentions it spontaneously. LOW BACK PAIN It is essential to know if the back pain was present before or after the onset of coccydynia. If such pain has developed after the onset of coccydynia, it can be due to bad postures adopted 1290

by the patient to avoid or decrease coccygeal pain. If the low back pain occurred before, it may be a key factor in causing coccydynia (see below).

Assessing potential repercussions Pain tolerance is highly variable. Discomfort is best assessed after a car journey, as virtually all patients experience pain in this case. In some cases, any driving may prove to be impossible. Physical requirements of job-related activities also play a role, as patients who can work standing up are less disadvantaged.

Red flags As with any vertebral pain, identifying red flags is essential, as coccygeal pain may rarely reveal a severe pelvic or lumbar condition. It should be noted that information obtained from the patient is generally sufficient and an MRI is requested only if a red flag is observed.

PHYSICAL EXAMINATION The physical examination takes less time than obtaining the history. In addition to the routine comprehensive interventional spine examination some additional elements are added. The patient is asked to assume the prone position, at which time inspection for the presence of a skin pit or a pilonidal sinus in the natal cleft is conducted. Such findings could indicate the presence of a boney spicule. The patient is asked again to point out the painful area. Palpation of the entire coccyx is conducted to determine the most painful area (where pressure results in the most pain), and if the site corresponds to a disc (sacroor intercoccygeal) or to the tip of the coccyx. It is at this time that an osseous spicule may be palpated, jutting out under the skin. Based on the author’s experience, the rectal examination should be optional. Rectal examination is not recommended in patients under the age of 20–25, as it is often poorly accepted. In men, it can be difficult and painful to reach the coccyx by rectal route. In other cases, the rectal examination makes it possible to mobilize the flexible part of the coccyx to see which movement (flexion or extension) best reproduces coccydynia. The rest of the consultation should be focused upon the radiologic procedure and the therapeutic management. An etiologic diagnosis is sometimes possible at this stage. Failing this, it may be possible to identify elements suggesting the presence of a radiologic lesion (Table 120.1).

INITIAL MANAGEMENT Acute coccydynia (less than 2 months) is best treated with nonnarcotic analgesics. Radiographs are not indicated, except in case of severe pain (or pain related to violent trauma). Most acute coccydynia cases heal spontaneously. Conversely, in cases of chronic coccydynia, dynamic radiographs are essential.

Standard radiographs The standard lateral standing film of the coccyx may be sufficient in acute hyperalgic coccydynia. Such films can detect fractures and crystal arthritis. In all other cases, dynamic radiographs are essential.

Fractures Coccygeal fractures are very rare (two in a thousand according to the author’s findings, where the fracture only involved the first coccygeal vertebra). This is easily understood as the weak point of the coccyx is the sacrococcygeal or intercoccygeal joint and not the

Section 2: Sacral Disorders

Table 120.1: Clinical Elements Suggesting the Presence of a Radiologic Lesion on Dynamic Films Versus no Lesion Items Suggesting a Radiologic Lesion

Items Suggesting Normal Radiographs

Local coccygeal pain

Pain radiating to the buttocks and thighs

Pain only in the sitting position

Significant pain also present in the standing position

Pain on standing up from sitting (especially if mentioned spontaneously)

Absence of pain on standing up from sitting

Pain occurring immediately after sitting down

Pain occurring after 30–60 minutes of sitting

Painful sitting position from the beginning of the day

Painful sitting position especially at the end of the day

Pain relieved for at least a month by a steroid injection

Pain unresponsive to a steroid injection

coccyx itself. Luxation is the most common trauma-related injury. However, fractures of the distal portion of the sacrum are slightly more common (1% in the author’s cases). The real figure may be higher, as most of the author’s patients are referred with chronic coccydynia. Fractures are only responsible for acute coccydynia, since they resolve spontaneously, typically within 3 weeks. Pseudoarthrosis seems to be exceedingly rare as this entity has never been observed in the author’s patients.

Calcifications The presence of a small, rounded calcification into a disc is sometimes observed. Calcification appears to have no diagnostic value, although this aspect has not been studied specifically. However, the author had the opportunity to observe five cases of crystal arthritis (probably hydroxyapatite), i.e. a frequency of 0.5%. The clinical pattern is characterized by very intense, permanent pain, appearing suddenly and spontaneously, and which makes any sitting position unbearable. This type of pain usually responds to oral steroid antiinflammatory agents within a few days.

Fig. 120.1 Standard technique for the ‘sitting’ film.

Dynamic radiographs Since coccydynia is more pronounced in the sitting position, it is essential to compare lateral sitting and lateral standing radiographs when evaluating chronic coccydynia. Radiographs should be taken immediately when there is a history of violent trauma or acute pain. The author has termed this examination ‘dynamic exploration.’10 The author has had the opportunity to evaluate in excess of a thousand cases in this manner. The lateral standing X-ray is taken first. In order for the coccyx to be in a neutral position, it is important that the patient avoids sitting for the 5–10 minutes preceding the X-ray examination. Otherwise, in some cases of hypermobility or luxation, there is not enough time for the coccyx to regain a neutral position. Next, the patient sits on a hard stool with the feet on a footrest (if necessary) so that the thighs are horizontal (as in the usual sitting position) until pain is experienced (Fig. 120.1). If necessary, the subject can lean slightly backward to feel the pain. If the pain cannot be triggered after a few minutes, interpretation of the sitting film will be difficult, since it has been taken in a position of no pain. The radiograph must then be taken in the sitting position, the position that regularly provokes the most intense pain for that patient. The two radiographs are read separately to compare the general appearance, number of vertebrae, curves, sacrococcygeal and intercoccygeal joints, and the presence of a possible fracture, or coccygeal spicule. The two films are then superimposed over a bright source of light, with both sacrums superimposed upon each other to compare and measure sagittal movement of the coccyx (Fig. 120.2).

Fig. 120.2 The range of motion of the coccyx is measured in degrees, after superposition of the two radiographs matching the sacrum. This superposition is obtained by pivoting the sitting film through an angle representing sagittal pelvic rotation. The arrow indicates the most mobile disc. 1291

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Angle of mobility It is possible to determine the angle of coccygeal mobility, the apex of which is in the center of the first mobile disc. In two-thirds of cases, coccygeal movement is forward (flexion). Normal values in a control group range from 0° to 25°. An angle of mobility exceeding 30° in women (25° in men) is abnormal.6 In one-third of cases, the coccyx moves backward (extension), resulting in an angle of usually less than 15°. This angle can be increased to 20° only in exceptional cases. As the angle of mobility is the one of greatest importance, it should be measured systematically, except in cases of luxation, which precludes its measurement and is therefore irrelevant. Other angles differ from the angle of mobility, as their significance is purely biomechanical.

Incidence The incidence is the angle at which the coccyx strikes the seat surface. Unfortunately, neither the lateral standing nor the sitting radiograph truly shows the coccyx in this transient position. The solution is to superimpose the two radiographs with both sacra on top of each other. The coccyx of the standing film is then drawn on the sitting film. The angle of this ‘virtual’ coccyx with the horizontal plane is the angle of incidence. The incidence determines the direction in which the coccyx moves.

Sagittal pelvic rotation To superimpose the two sacra, by placing the sitting film on the standing film, the sitting film must be pivoted through an angle representing sagittal pelvic rotation, when the patient passes from the standing to the sitting position (not taking into account the sacroiliac mobility). In a lean subject, the angle of rotation is usually greater than 40°, while in the obese it is usually less than 30°. Sagittal pelvic rotation and incidence are closely associated together (patients with a high pelvic rotation have a low incidence and vice versa). Both are affected by the BMI.

Lesions observed on dynamic radiographs Posterior coccygeal luxation Luxation is the most striking coccygeal lesion (Fig. 120.3). It represents about 20% of the chronic coccydynia cases. Except in very rare

cases of permanent luxation, it occurs only in the sitting position, and spontaneously reduces when the patient stands up. This explains why such a lesion had not been identified prior to the author’s findings. Luxation occurs on straight coccyges, with limited pelvic rotation and a greater angle of incidence. Sacrococcygeal and intercoccygeal discs are equally affected. The coccyx always moves backward. A control-group analysis showed that its displacement had to exceed 20% (based on a measurement method used for spondylolisthesis) to be significant.11 Generally, the backward movement ranges from 50% to 100%, and its implication in pain is almost never an issue. Luxation is by far the most common post-traumatic lesion. Poor pelvic rotation and an increased angle of incidence denotes that the coccyx moves backward if the subject falls, thus increasing the risk of injury if one admits that a fall on the buttocks involves the same pelvic movement pattern as does sitting down. Luxation is also the lesion most often seen in overweight subjects. This is not because obese patients risk more serious injury when falling, but is due to the specific way they sit. Obese individuals have a limited sagittal pelvic rotation (average <30°), which results in a tendency to drop onto the seat to assume the seated position. Coccygeal pain in patients with luxation has two identifying symptoms: pain is triggered as soon as the patient sits, and often occurs when the patient stands up again, which is sometimes the only symptom. The pain is more intense than that provoked by other causes of coccydynia. Due the magnitude of the pain experienced, patients with this etiology present to the spine specialist sooner than for those with other causes of coccydynia.

Hypermobility Hypermobility is defined by coccygeal flexion exceeding 30° in the sitting position.6 It is often associated with impaction of the anterior portion of the two distal vertebrae (Fig. 120.4) and/or a discrete forward displacement of the last vertebra of the coccyx, forming a small step in the sitting position (Fig. 120.5). It is found in 25% of chronic coccydynia cases. Typically, hypermobility is observed in patients with high sagittal pelvic rotation, in which the coccyx (usually curved) faces the seat surface somewhat horizontally, resulting in an incidence of less than 35°. Hypermobility is almost exclusively found in women.

Fig. 120.3 Posterior luxation in the sitting position. 1292

Section 2: Sacral Disorders

Fig. 120.4 Hypermobility in flexion. The arrow indicates a possible friction between joint surfaces in the sitting position.

Hypermobility is more frequent in normal-weighted or lean subjects. It is the particular way the coccyx comes into contact with the seat when these subjects sit down that triggers this disorder. Such patients exhibit a considerable degree of pelvic rotation that pushes the coccyx into a position parallel to the seat increasing flexion forces. Hypermobility is rarely post-traumatic, but can be associated with diffuse ligamentous hyperlaxity. Hypermobility and anterior luxation (5% of cases) are related, as they have the same biomechanical characteristics. Indeed, anterior luxation involves the same type of coccyges and only the most distal coccygeal vertebra is involved. As opposed to posterior luxation, which is always pathological when displacement exceeds 20%, moderate hypermobility (around

30°) is not necessarily so. Although these values were not found in controls, they can exist in patients with asymptomatic hyperlaxity. To ascertain whether hypermobility is the etiological factor, it is necessary that the most painful point upon palpation corresponds to the hypermobile joint and that an intradiscal steroid injection relieves the symptoms for at least 1 month.

Coccygeal spicules The spicule is a bony excrescence that can be palpated at the tip of the coccyx, jutting out under the skin (Fig. 120.6). It can cause irritation to the subcutaneous tissues during sitting. In some instances

Fig. 120.5 Hypermobility in flexion. In the sitting position, the flexion is accompanied by a loss in continuity of the anterior aspect of the coccyx, indicating a severe lesion. 1293

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Fig. 120.6 Coccygeal spicule on the dorsal aspect of the tip of the coccyx on a ‘sitting’ film. It is difficult to detect, even on good-quality radiographs, which explains why it has not been described earlier.

inflammation in the form of a bursitis can develop. It accounts for 15% of all causes of coccydynia. Spicules are more frequent in long and curved coccyges.7 In nearly 80% of cases, there is a skin abnormality over the spicule: a somewhat distinct pit, or, more rarely, a frank pilonidal sinus (Fig. 120.7). A pit or a pilonidal sinus associated with a spicule can be considered as a mirror lesion, indicating an embryologic origin of the malformation, with two poorly separated embryonic layers. Dynamic films show that spicules are most commonly seen in immobile coccyges, in which the pressure from the spicule is made worse by the inability of the coccyx to take evasive action when sitting. The spicule itself is sometimes difficult to visualize. Sometimes, a multiplanar reformatted CT scan is used to visualize the spicule. Currently, MRI is the imaging test of choice when the radiographs are indeterminate (Fig. 120.8).

Fig. 120.8 MRI showing the spicule, prolongated by a connective tract to the cutaneous pit (arrow).

The spicule is potentially present from birth and usually painless. It can also be found in subjects who have never experienced the symptoms of coccydynia. A low BMI may be responsible for the onset of coccydynia, as the spicules become symptomatic in leaner subjects due to the lack of subcutaneous fat. Generally, coccydynia related to spicules develops spontaneously without any inciting trauma. Usually, the symptom manifestation results from an inflammatory process. It should be highlighted that in certain cases the symptoms only develop after psychological trauma. Coccydynia due to spicules is also observed after significant weight loss, for the reasons mentioned above. The diagnosis may be determined with the physical examination. Apart from the presence of a skin pit, the pain is felt at the tip of the coccyx near the anus. Palpation is conclusive, as the sharp excrescence formed by the spicule is readily felt and the pain is easily reproduced by simple pressure. In the case of a frank pilonidal sinus, it is essential to rule out the presence of a discharge or an abscess.

Other causes in the absence of radiologic lesion In one-third of cases, dynamic exploration fails to identify a lesion. The technical quality of the exploration should be questioned first: was pain present when the lateral sitting radiograph was taken?

Dynamic radiographs taken in the absence of pain If pain was absent, two causes can be considered. There could be a slight lesion such as a ‘borderline flexion,’ around 25°, or a slight posterior luxation. Coccygeal displacement may increase with prolonged sitting, especially on an uncomfortable seat, and might be more pronounced when the pain is acutely felt. Therefore, the pain can be perceived only when the patient sits on a particular seat or under certain circumstances, such as car journeys, which add vibrations to the sitting position. If no incipient lesion is visible, the dynamic radiographs should be repeated under better conditions.

Dynamic radiographs taken while pain is present Fig. 120.7 Skin pit or a real pilonidal sinus, and coccygeal spicule often form a ‘mirror-image’ pattern. 1294

If the familiar pain is present, but no abnormality of coccygeal mobility can be documented, then no conclusive etiology can be made from the dynamic films. Nearly half of these patients, i.e. 15% of the total, respond well to intradiscal steroid injection, a fact which tends to substantiate the presence of intradiscal inflammation.

Section 2: Sacral Disorders

Other patients respond to a steroid injection administered at the tip of coccyx, although no spicule is visible on radiographs. Such cases probably reflect apical bursitis on immobile coccyges, where the pain is localized at the tip. However, the injection may not bring any improvement, with the result that the etiology remains unknown. Any coexisting lumbar pain should be assessed first (see below). If the coccyx alone appears to be involved, various sources of pain may be suggested. However, these are only hypotheses and, although plausible, remain to be documented. The pain may originate in the levator ani muscles. In this case, the rectal examination may reveal one or several areas of muscle tenderness (taut bands or trigger points) where the pain is triggered by pressure. The role played by these muscles in coccydynia is poorly understood. In this setting, manual treatment may be effective. Pain may also originate from a muscle or a ligament inserting on the lateral border of the sacrum/coccyx. Careful palpation of the lateral edges of the distal sacrum and the first coccygeal vertebra can reveal focal, unilateral pain, which might correspond to pain from the sacral insertion of fibers of the gluteus maximus muscle or the sacrotuberous ligament. This type of pain is treated with an injection (lidocaine + steroid) at the bone level. Psychological factors, or a dysfunction in the pain pathways can also be considered. Symptoms or history of depression, diffusion of the pain, or pain occurring only after a prolonged sitting, for about an hour for example, with a gradually increasing intensity throughout the day are suggestive of this diagnosis. However, the author believes that depression cannot be the only cause of coccydynia, but it may influence its persistence, due to hypersensitivity or impaired pain memory. For these cases treatment with amitriptyline can be beneficial.

LUMBAR PAIN AND COCCYDYNIA Pain referred from the lumbosacral area A coccygeal pain can be referred from a lumbosacral condition (L4–5 or L5–S1).12 In such cases, the pain in the coccygeal area is exacerbated by lumbar movements (bending over or coughing) rather than sitting. Discogenic low back pain may be felt only in the sitting position and may, thus, be confused with real coccydynia. In these cases, pain in the coccygeal area has developed with or soon after the occurrence of low back pain, but never before. Such pain is a lumbar pain radiating to the coccyx, and is not related to the coccyx itself.

Real coccydynia due to lumbosacral stiffness The authors have described a second mechanism of coccygodynia due to the loss of lumbosacral mobility. This is a frequent condition in patients with chronic low back pain, which increases the risk of coccydynia. If lumbar flexion and extension are restricted, when the subject sits down, the coccyx cannot rotate inside the pelvis. The coccyx is thus more exposed and vulnerable. Coccydynia is common after lumbar arthrodesis, a surgical technique which multiplies the risk of coccydynia by 50 (Maigne, not published), or following discectomy.

TREATMENT OF COCCYDYNIA Treatment should be considered only when the cause of coccydynia has been clearly identified. Three major methods exist: injection, manipulation, and surgery. Other techniques such as the use of special cushions, modifications to seats, may bring additional relief.

Coccygeal injections Pericoccygeal injection had been used long before the author’s studies, and the benefit of this method is significant.13–15 The author has designed a technique for intradiscal injection under fluoroscopic control, and has described how to select the disc to be injected. Intradiscal injections were developed by the author prior to describing dynamic radiographs, based on the hypothesis that the etiology of coccydynia could be similar to that of low back pain. The author suspected that it could be due to sacrococcygeal or intercoccygeal disc involvement. To prove this hypothesis, lidocaine was injected intradiscally under fluoroscopic guidance in 20 patients. If pain was relieved by this simple diagnostic test, a steroid injection was administered. Afterwards, lidocaine was only used for pericoccygeal local anesthesia.

Technique of intradiscal injection This injection can reasonably be conducted only under fluoroscopic control. The patient lies on the left side, hips and knees flexed. The disc that needs to be injected can be identified in two ways. If dynamic films confirm luxation or hypermobility, the responsible disc is obvious to the clinician. Conversely, if moderate hypermobility or no radiologic lesions are uncovered, careful palpation of the coccyx from the lower extremity of the sacrum to the tip of the coccyx will help determine the most painful site. The area is then marked with a paperclip or other radiopaque marker, to verify correct positioning during fluoroscopy. The marker is aligned to rest at the midline of the involved site. A felt pen then marks the intended site of needle puncture. The skin is then carefully disinfected with alcohol and then iodine. A local anesthetic is administered with a thin subcutaneous needle. The center of the disc is then entered with a 23-gauge, 25 mm needle. In obese patients, a 50 mm needle is necessary. The procedure can be difficult sometimes. Small osteophytes can impede advancement of the needle or force it to deviate laterally. Fluoroscopic imaging from the posteroanterior and lateral planes will demonstrate incorrect needle placement. The ideal terminal location is at the center of the symptomatic disc. The needle should not be pushed too ventral as the potential space anterior to the most ventral aspect of the disc is only 5 mm. The approximating structure is the rectal wall. The author usually injects a small amount of dye during coccygeal discography (Fig. 120.9). This allows for confirmation of needle position. In some instances the familiar pain can even be elicited, but the author considers such provocation to be an unreliable indicator of whether the diagnosis is accurate. Examination is completed with the injection of approximately 2 mL of a glucocorticoid. At the next follow-up visit the vast majority of patients describe complete relief of their symptoms. The author has observed no serious complications in over 2000 injections. Despite the safe record, theoretical mishaps must be kept in mind, including iodine allergy, infection, or perforation of the posterior rectal wall.

Injection of the coccygeal tip Injection at the coccygeal tip is indicated in the case of spicule, or when the most painful area corresponds to the tip of coccyx in the absence of radiologic lesion on dynamic films. The method is similar to that for an intradiscal injection. However, following the injection, the area may become sore for a few days.

Results Response to injection is generally slow, especially at the coccygeal tip. The injection benefit is generally assessed 3 weeks later and will persist up to 3 months with good to excellent results in 75% of 1295

Part 4: Extra-Spinal Disorders

Fig. 120.9 Coccygeal discography.

the cases.16 After 3 months, the results may decline, with relapse in one-third of patients. In the case of relapse, a second injection may be performed. If the relief is longer after the second injection, then treatment with local injections may have a good overall outcome. If the relief is shorter, injections are discontinued and another treatment is then considered. At 1 year, treatment by injection is effective in 65% of cases (good to excellent results), a figure which makes it the first line of conservative treatment. The author reserves it for chronic coccydynia (more than 2 months’ duration). Posterior luxations respond less well, with only 50% of good/excellent results. The best results (80%) are obtained in patients with spicules.

Manual treatment Manual treatment is the most ancient treatment of coccydynia. Standard techniques include levator ani massage,17 joint mobilization with the coccyx in extension,18 and levator ani stretching.19 These maneuvers are performed via intrarectal route over three to four sessions within a 2-week interval. A study of manual treatment conducted by the author gave an overall success rate of 25% at 6 months, which remained stable at the 2-year review date.19 A placebo-controlled study, which has not yet been published, reveals slightly better results in patients who had manual treatment than in a placebo group (efficacy was proven in 22% of cases versus 12%, respectively), which confirmed a significant difference between the two groups. Logically, the results of manual treatment vary with the cause of coccydynia. Patients with a rigid coccyx do least well; those with a normally mobile coccyx do best. Patients with luxation or hypermobility have in-between results. Coccydynia resulting from a rigid coccyx is often due to bursitis at the tip of the coccyx, whether a spicule is present or not. Given that such a lesion is inflammatory in nature, it is expected that it would respond to manual treatment.

Surgical treatment Coccygectomy has long been controversial, despite the good results reported in the literature. However, the author feels that the controversy has evolved because of ill-defined selection criteria. Patients 1296

with disabling pain and dynamic radiographs demonstrating coccygeal instability, which includes luxation and hypermobility, represent the objective criteria used for the selection of surgical cases in the author’s study, and the results were excellent.20 In 90% of cases, results were good to excellent. Improvement was experienced in 2–3 months, although it took 6–10 months in some cases. In very few cases, definitive improvement was not described until 1–2 years postoperatively. This fairly long delay could be due to deafferentation pain (phantom limb syndrome). In cases of occupational injury or litigation, the outcome may be negative. A recent review of patients treated by coccygectomy for disabling instability showed that these who have responded positively to an injection (at least for a short period of time, i.e. 4 weeks) had a better outcome than those who failed to respond. The author recently extended the indication for coccygectomy to poorly tolerated spicules, provided that the patient responded to steroid injection at least once (but with a short interval of pain relief). These results are currently being assessed. The method of coccygectomy consists of resecting the unstable portion of the coccyx. In the case of a spicule, the distal extremity of the coccyx is removed as well as any associated pilonidal sinus. Surgery is performed under general anesthesia through a small midline incision in the natal cleft. The posterior aspect of the coccyx is exposed and dissection carried out on contact with the bone. Despite peri- and postoperative aseptic precautions as well as a 48-hour prophylactic antibiotic therapy, the postoperative follow-up was complicated by infection in 2–3% of cases. Infection is the only complication reported in 150 cases and there have been no long-term residual sequelae from any of the infections.

Other treatments Common analgesics are sufficient in acute coccydynia. Tricyclic antidepressants can be useful in idiopathic coccydynia, when not relieved by intradiscal injections, manual therapy, or surgery. Cushions may help in the case of persistent pain, or prevent the occurrence of pain during a long car journey, always a poorly tolerated activity. Patient education may help in avoiding uncomfortable seats. Sport activities such as cycling and horse riding are contraindicated.

CONCLUSION Dynamic radiographs, the core of the author’s research, have led to a better understanding of coccygeal biomechanics and coccydynia. In answer to the question, ‘What is the coccyx for?,’ two important parameters must be taken into account: the shape of the coccyx, including length and curvature, and the movements of the coccyx when sitting down, which consist of either extension, flexion, or absence of mobility. Generally, straight and short coccyges do luxate posteriorly when under heavy mechanical constraints (obesity, trauma), due to their lack of mobility. Conversely, long and curved coccyges move easily into flexion and are better protected against mechanical constraints, as the pelvic rotation tucks them into the pelvis where they will be reasonably well protected against injury. Hypermobility is just an exaggeration of a normal movement of flexion (which luxation is not). An immobile coccyx causes irritation to the subcutaneous tissue when the subject sits down, notably when a spicule is present. Consequently, the ideal coccyx is long, curved and supple, and naturally prolongs the sacral curve. The coccyx is the link between the rigid sacrum and the supple and delicate perineal skin. The coccyx makes the sitting position, which only exists in humans, more comfortable. As anticipated by Howorth,21 the study of coccygeal pathology has shown that the mechanisms of coccydynia are, in their majority,

Section 2: Sacral Disorders

comparable to those encountered in peripheral joint lesions, and not due to hysteria, a diagnosis which is offensive for the patient.

References 1. Sugar O. Coccyx, the bone named for a bird. Spine 1995; 20:379–383. 2. Gray H. Gray’s anatomy. 35th edn. Edinburgh: Longman; 1973. 3. Maigne JY, Molinié V, Fautrel B. Anatomie des disques sacro et inter-coccygiens. Revue de Médecine Orthopédique 1992; 28:34–35. 4. Saluja PG. The incidence of ossification of the sacrococcygeal joint. J Anat 1988; 156:11–15. 5. Smout CF, Jacoby F, Lillie EW. Gynaecological and obstetrical anatomy. 12th edn. Oxford, New-York, Toronto: Oxford University Press; 1969. 6. Maigne JY, Tamalet B. Standardized radiologic protocol for the study of common coccydynia and characteristics of the lesions observed in the sitting position. Spine 1996; 21:2588–2593.

10. Maigne JY, Guedj S, Fautrel B. Coccygodynies: intérêt des radiographies dynamiques de profil en station assise. Rev Rhum Mal Ostéoartic 1992; 59:28–31. 11. Maigne JY, Guedj S, Straus C. Idiopathic coccygodynia. Lateral roentgenograms in the sitting position and coccygeal discography. Spine 1994; 19:930–934. 12. Nelson DA. Idiopathic coccygodynia and lumbar disk disease: Historical correlations and clinical cautions. Perspect Biol Med 1991; 34:229–238. 13. Jurmand SH. Les injections péridurales dans le traitement de la coccygodynie. Rev Rhum Mal Ostéoartic 1976; 43:217–220. 14. Kersey PJ. Non-operative 1(8163):318.

management

of

coccygodynia.

Lancet.

1980;

15. Wray C, Easom S, Hoskinson J. Coccydynia. Aetiology and treatment. J Bone Joint Surg 1991; 73B:335–338. 16. Rouhier B. Résultats des injections coccygiennes dans le traitement de la coccygodynie chronique. Thèse d’université. Paris V, 2003. 17. Thiele GH. Coccydynia and pain in the superior gluteal region. JAMA 1937; 109:1271–1275.

7. Maigne JY, Doursounian L, Chatellier G. Causes and mechanisms of common coccydynia: role of body mass index and coccygeal trauma. Spine 2000; 25:3072–3079.

18. Maigne R. Les manipulations vertébrales. 3rd edn. Paris: Expansion Scientifique Française; 1961:180.

8. Postacchini F, Massobrio M. Idiopathic coccygodynia: analysis of fifty-one operative cases and a radiographic study of the normal coccyx. J Bone Joint Surg 1983; 65A:1116–1124.

19. Maigne JY, Chatellier G. Comparison of three manual coccydynia treatments. Spine 2001; 26:E479–E484.

9. Kim NH, Suk KS. Clinical and radiological differences between traumatic and idiopathic coccygodynia. Yonsei Med J 1999; 40:215–220.

20. Maigne JY, Lagauche D, Doursounian L. Instability of the coccyx in coccydynia. J Bone Joint Surg 2000; 82B:1038–1041. 21. Howorth B. The painful coccyx. Clin Orthop 1959; 14:145–150.

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PART 4

EXTRA-SPINAL DISORDERS

Section 2

Sacral Disorders

CHAPTER

121

Piriformis Syndrome Samir Mehta, Joshua D. Auerbach and Kingsley R. Chin

BACKGROUND In 1928, Yeoman1 ascribed 36% of cases of sciatica to sacroiliac arthritis transmitted via the piriformis muscle. Later articles by Freiberg and Vinkle in 19342 and by Freiberg3 also supported the notion of sciatica secondary to sacroiliac arthritis and compression by the piriformis muscle and fascia. In 1934, Mixter and Barr4 described the herniated disc as a cause of sciatica, which brought into question the original etiologies of sciatica proposed by Yeoman and Freiberg. Despite this compelling new evidence implicating a herniated disc as a major cause of sciatica, the literature continued to reflect the belief that the piriformis muscle can be involved in the etiology of sciatica. In 1936, Thiele5 described piriformis muscle pain secondary to spasm and hypertrophy irritating the sciatic nerve. In 1936, Shordania6 coined the term ‘piriformitis’ based on his observations of 37 women with sciatica. In 1937 and 1938, Beaton and Anson7 ascribed coccydynia to anatomic variations in the sciatic nerve and piriformis muscle. However, it was Robinson8 who, in 1947, first coined the term ‘piriformis syndrome’ and described six associated typical features. Robinson, like his predecessors, reported that the piriformis muscle and fascial tissues could cause sciatica. Despite this historical evolution of the diagnosis and modern advances in techniques of electrophysiologic testing and magnetic resonance imaging (MRI), piriformis syndrome remains a diagnosis of exclusion and is poorly understood and controversial. A recent survey of physiatrists revealed a lack of consensus on whether the diagnosis of piriformis syndrome exists, and if it does exist, how to make the diagnosis.9 Much of the controversy stems from the relative rarity of the diagnosis when compared to the more easily recognized and treatable causes of sciatica stemming from the lumbar spine.10

vertebrae. The piriformis muscle originates from the anterior surface of the sacrum between and lateral to the anterior sacral foramen, capsule of the sacroiliac articulation, the margin of the greater sciatic foramen, and the sacrotuberous ligament. From its point of origin, it passes through the greater notch and dorsal to the sciatic nerve before inserting on the superior-medial aspect of the greater trochanter of the femur (Fig. 121.1). The piriformis muscle is the most proximal of the hip external rotators. With the hip extended, the piriformis muscle externally rotates the hip; however, with the hip flexed, the piriformis muscle becomes a hip abductor.15 Branches from L5, S1, and S2 nerve roots innervate the piriformis muscle. The superior gemellus, inferior gemellus, quadratus femoris, and obturator internus act as synergists with the piriformis muscle (Figs 121.2, 121.3). Many developmental variations of the relationship between the sciatic nerve in the pelvis and piriformis muscle have been observed. The sciatic nerve consists of branches from the L3 to S3 nerve roots and usually courses beneath the piriformis muscle and dorsal to the gemellus

Sacrum

Greater sciatic notch Piriformis muscle

EPIDEMIOLOGY Low back pain and sciatica, described as pain or numbness within the buttock and posterior thigh with occasional radiation into the foot, are common complaints, with a reported lifetime incidence as high as 60–90%.11 The total cost of low back pain and sciatica is significant, exceeding US$16 billion in both direct and indirect costs. Given the lack of agreement on exactly how to diagnose piriformis syndrome, estimates of frequency of sciatica caused by piriformis syndrome vary from rare to approximately 6% of sciatica cases seen in a general family practice.12,13 There is no clear age or gender preference, with reports varying from a 6:1 female-to-male predominance, while others suggest a 1.4:1 male-to-female ratio.13,14

ANATOMY The piriformis muscle is flat, pyramid-shaped, and broadly originates from the ventrolateral surface of the sacrum from the S2–4

Gluteus reflected

Sciatic nerve

Short external rotators (e.g. gemellus muscles)

Fig. 121.1 Posterior view of the piriformis originating from the sacrum, through the greater sciatic notch, and inserting on the superior medial aspect of the greater trochanter. The sciatic nerve is posterior to the piriformis.

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Greater trochanter of femur

Femur A

B

C

Quadrate tubercle of femur

Superior Greater trochanter of femur D

Inferior

E

F

G

Fig. 121.2 Schematic diagram showing the various muscles of the gluteal region. (A) Gluteus maximus (posterior). (B) Gluteus medius (lateral). (C) Gluteus minimus (lateral). (D) Piriformis (posterior). (E) Obturator internus (posterior). (F) Gemelli (posterior). (G) Quadratus femoris (posterior).

muscles after exiting the pelvis through the greater sciatic foramen (Fig. 121.4).16 In approximately 20% of the population, the piriformis muscle belly is split with one or more parts of the sciatic nerve dividing the muscle belly itself. In 10% of the population, the tibial and peroneal divisions of the sciatic nerve are not enclosed in a sheath. Usually, the peroneal portion splits the piriformis muscle belly, while it is rare for the tibial division to split the piriformis muscle belly.16

PATHOPHYSIOLOGY The etiology of piriformis syndrome is unclear but symptoms are likely to occur secondary to neuritis of the proximal sciatic nerve. The piriformis muscle can either irritate or compress the sciatic nerve due to spasm and/or contracture, and this problem can mimic discogenic sciatica (pseudosciatica). 1300

Based on its etiology, piriformis syndrome may be divided into primary or secondary causes (Table 121.1). Primary causes occur from direct nerve compression such as trauma or due to factors that are intrinsic to the piriformis muscle and include anomalous variations in the muscle anatomy, muscle hypertrophy, chronic inflammation of the muscle, and secondary changes from trauma such as adhesions. Secondary causes may include symptoms due to pelvic mass lesions, infections, and anomalous vessels or fibrous bands crossing the nerve, bursitis of the piriformis tendon, sacroiliac inflammation, and possibly myofascial trigger points. Other causes of symptoms may include pseudoaneurysms of the inferior gluteal artery adjacent to the piriformis muscle, bilateral piriformis syndrome due to prolonged sitting during extended procedures, cerebral palsy due to hypertonicity and contractures, total hip arthroplasty as discussed below, and myositis ossificans.

Section 2: Sacral Disorders Posterior superior iliac spine

Superior gluteal nerve Gluteus minimus

Gluteus minimus

Piriformis muscle

Superior gluteal artery and nerve

Pudendal nerve

Piriformis muscle

Sciatic nerve

Inferior gluteal nerve

Gluteus medius

Sacrotuberous ligament Gluteus medius Obturator internus and gemelli Inferior gluteal artery and nerve

Gluteus maximus

Greater trochanter Obturator externus

Fig. 121.4 Posterior view of the hip revealing the course of the sciatic nerve beneath the piriformis muscle but dorsal to the gemellus muscles after exiting the greater sciatic foramen.

Sciatic nerve Quadriceps femoris Gluteus maximus Sciatic nerve

Fig. 121.3 Anatomic relationship of the sciatic nerve as it courses from the sacrum to the lower extremity. Note the position of the piriformis muscle and short external rotators as possible areas of compression.

Table 121.1: Primary Versus Secondary Piriformis Syndrome Primary

Secondary

Trauma

Hematoma

Pyomyositis

Bursitis

Myositis ossificans

Pseudoaneurysm

Dystonia musculorum deformans

Excessive pronation

Hypertrophy

Fibrous bands

Adhesions

Mass lesions

Fibrosis

Anomalous vessels

Anatomic variations

Lumbar hyperlordosis and hip flexion contractures increase piriformis muscle strain and seem to predispose individuals with these to developing symptoms. Altered gait biomechanics has also been theorized to lead to piriformis muscle hypertrophy and chronic inflammation, which can cause piriformis syndrome. Patients with weak abductors or leg-length discrepancies are particularly prone. During the stance phase of gait, the piriformis is stretched as the weightbearing hip is maintained in internal rotation. As the hip then enters the swing phase, the piriformis muscle contracts, aiding in external rotation. The piriformis muscle is under strain during the entire cycle of gait and may be more prone to hypertrophy than other muscles in that region.10,17–19 Any gait abnormality that maintains the affected hip in a position of increased internal rotation or adduction may increase muscle strain even more. Blunt injury may cause hematoma formation and subsequent scarring between the sciatic nerve and short external rotators, which may lead to symptoms. In a study of 15 patients with posttraumatic piriformis syndrome as a result of a direct blow to the buttock, all patients had a release of the piriformis tendon and sciatic neurolysis with return to normal activity 2 months after surgery.20 A lower lumbar radiculopathy also may cause secondary irritation of the piriformis muscle, which may complicate the diagnosis and hinder physical treatment methods, as the treatment for a lower lumbar radiculopathy involves stretching of the lower back and hip musculature which may, in fact, increase the symptoms in a patient with piriformis syndrome. Even though there are case reports linking the superior gluteal nerve to piriformis syndrome, there is insufficient evidence to conclude that this nerve is involved in true cases of piriformis syndrome.21 Furthermore, the superior gluteal nerve usually leaves the sciatic nerve trunk and passes through the canal above the piriformis muscle. 1301

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CLINICAL PRESENTATION The typical patient presenting with piriformis syndrome may complain of cramping or aching in the buttock or hamstring, sciatic leg pain without back pain, and sensory and motor changes in the distribution of the sciatic nerve. Furthermore, the patient may complain of pain that is made worse by bending or stooping, prolonged sitting, arising from a chair, or internal rotation of the thigh. There may also be pain with bowel movements or dyspareunia. However, piriformis syndrome is often a diagnosis made after excluding other causes of sciatica emanating from the lumbar spine or a pelvic mass causing extrinsic compression of the sciatic nerve. Attempts have been made to derive a set of features that could strongly suggest the diagnosis by history and examination. Robinson was the first to do so when he described six typical features: (1) a history of fall on the buttocks; (2) pain in the sacroiliac joint, greater sciatic notch, and the piriformis; (3) acute exacerbations brought on by stooping or lifting; (4) presence of a palpable mass over the piriformis; (5) positive Laseque’s sign; and (6) gluteal atrophy.8 In approximately 50% of patients with piriformis syndrome, there is a history of trauma, with either a direct buttock contusion or hip/ lower back torsional injury. It is likely that the remaining 50% of cases are of spontaneous onset or without an identifiable etiology. Since the diagnosis is difficult to make and the clinical course is often quite protracted for patients with piriformis syndrome, it is often challenging to establish temporal relationships and causality. While there are no pathognomonic tests on physical examination to diagnose piriformis syndrome, there are a number of findings that may aid the diagnosis. In the supine position, the patient may have a tendency to keep the affected leg slightly elevated and externally rotated (positive piriformis sign) (Fig. 121.5).17 Piriformis muscle spasm can be detected by careful deep palpation over the location where the piriformis muscle crosses the sciatic nerve (Fig. 121.6). Locating the midpoint of a straight line drawn between the coccyx and the greater trochanter can approximate this position. Digital rectal examination may reveal tenderness over the lateral pelvic wall that reproduces the syndrome. Reproduction of sciatica-type pain with weakness is noted by resisted abduction/external rotation (Pace test) (Fig. 121.7). The Freiberg test is another diagnostic

Fig. 121.5 Positive piriformis sign in a patient with piriformis syndrome revealing slight elevation and external rotation of the lower extremity on the affected side. 1302

Fig. 121.6 Direct palpation leading to deep buttock pain localized to the region indicated is consistent with piriformis syndrome.

sign that elicits pain upon forced internal rotation of the extended thigh. Beatty described a technique that attempts to distinguish between lumbar radiculopathy, primary hip disease, and pain caused by piriformis syndrome.22 However, it was noted that the Beatty test

Fig. 121.7 The Pace test. Reproduction of sciatica-type pain with weakness is noted by resisted abduction and external rotation.

Section 2: Sacral Disorders Back pain ± buttock pain sciatic nerve findings

Plain films –

+ DJD (spine or hip) Facet disease Stenosis Metastatic lesions Fractures

MRI

HNP Stenosis Endometriosis Tumors Infection Tendon ruptures Fig. 121.8 The Beatty test. The patient is made to lie on his or her side with the affected leg facing up and is then asked to hold the affected knee in the air for several minutes. Deep buttock pain is consistent with piriformis syndrome.

can be positive in patients with herniated lumbar discs or hip osteoarthritis and therefore has a low specificity. The patient is made to lie on his or her side with the affected leg facing up and is then asked to hold the affected knee in the air for several minutes. Deep buttock pain was reported to be consistent with piriformis syndrome (Fig. 121.8). A painful point may be palpated at the lateral margin of the sacrum. On occasion, weak abductors or shortening of the involved extremity may be seen. Careful examination of the ipsilateral foot may reveal that the second metatarsal is longer than the first (Morton’s foot) causing a rocking motion during step-off and increased adduction and hip stress. While in the authors’ experience not one of these physical exam maneuvers is pathognomonic, the authors do feel that a combination of positive findings in a patient with the appropriate history and diagnostic work-up is consistent with piriformis syndrome. It has been described that piriformis syndrome can be distinguished from a herniated intervertebral disc due to a lack of a neurologic deficit in piriformis syndrome.13 This concept was supported by Steiner’s study which stated that lack of a true neurologic deficit was the most important criterion in distinguishing piriformis syndrome from sciatica.23 However, a further examination of the literature reveals eleven of 28 reported cases (40%) where patients had evidence of neurologic deficits on physical examination.9,15,24–28

DIFFERENTIAL DIAGNOSIS Since there is no described pathognomonic sign of piriformis syndrome, a broad differential diagnosis should be considered in patients presenting with sciatica before patients are given the diagnosis of piriformis syndrome (Fig. 121.9). Other possible diagnoses should include but not be limited to lumbar pathology such as herniated disc, degenerative disc disease, and facet arthropathy, sacroiliitis, myofascial pain, and trochanteric bursitis. The diagnosis of piriformis syndrome remains one of exclusion.10 Generally, laboratory studies and imaging have a limited role in diagnosing piriformis syndrome but diagnostic imaging of the lumbar spine and pelvis should be done in all cases to rule out other causes of sciatica. Although there are reports in the literature of nuclear diag-

–

+

Claudication AAA Superior gluteal artery aneurysm

PVR/ABI ± MRA – + Electrophysiologic testing ± diagnostic injection + Piriformis syndrome

– Chronic pain syndrome

Fig. 121.9 Diagnosis algorithm for piriformis syndrome.

nostic imaging and MRI of the pelvis assisting in the primary diagnosis of piriformis syndrome, neither test is considered reliable in making the diagnosis.16 However, future improvements in resolution and image technology may allow visualization of subtle changes in the piriformis muscle signal intensity on MRI or computed tomograms to signify edema or inflammation.29 Electrophysiological testing is a promising area of development to aid in the diagnosis of piriformis syndrome. A 1.86-msec prolongation of the H-reflex with the flexion, adduction, and internal rotation test (FAIR) on the ipsilateral lower extremity has been shown to be a sensitive electrophysiologic criterion for diagnosing pyriformis syndrome.30,31 Some authors have suggested that the H-reflex is an electrically stimulated version of the Achilles reflex. The H-reflex crosses the piriformis muscle twice – in afferent and efferent orthodromic conductions. A growing body of work by Fishman et al.30–32 suggests evidence that piriformis syndrome is a mechanical and functional impingement. However, this methodology is theoretical and far from proven. Further clinical studies and evidence-based methodologies are required to delineate the ramifications of Fishman’s work. Changes in amplitude and latencies of recorded potentials from an epidural electrode inserted into the lumbar spine at L3–4 with stress to the affected leg have also been seen in patients with piriformis syndrome.33 Despite efforts to develop an objective diagnostic test, the diagnosis of piriformis syndrome is still one of exclusion based primarily on a constellation of signs and symptoms stemming from the history, physical examination, and diagnostic tests (Table 121.2). The role of diagnostic injections in the diagnosis of piriformis syndrome has yet to be confirmed. Some authors believe that the diagnosis is based on clinical history and examination findings. Others advocate the use of EMG and fluoroscopically guided lidocaine and/ or corticosteroid injections directly into the piriformis muscle belly and/or tendon. 1303

Part 4: Extra-Spinal Disorders

Table 121.2: Characteristics of Piriformis Syndrome History

Physical examination

Diagnostic tests

Unilateral

Pain

Scintography

Pain

Localized

MRI of piriformis muscle

Buttock

Bending over

Greater trochanter

Lifting

Posterior thigh

Squatting

Prolonged sitting

Limp on affected side

H-reflex

At night

Digital rectal examination

F wave

CT scan of piriformis muscle

Dyspareunia Failed back surgery

Pace test

Trauma

Freiberg test

sound, or electrical stimulation. When these additional techniques are performed prior to the initiation of piriformis stretching, they may allow the hip joint capsule to be mobilized anteriorly and posteriorly and lengthen the muscle belly, thus gaining greater excursion of the piriformis tendon and more effective stretching. A home stretching program must be provided. Frequent and repeated stretching throughout the day is an essential component of the treatment program. During the acute phase of treatment stretching, at a minimum every 6 hours (while awake), is strongly recommended. Prolonged stretching of the piriformis muscle is accomplished in either a supine or orthostatic position with the involved extremity flexed and passively adducted/internally rotated (see Fig. 121.11). Functional and biomechanical deficits that can be addressed via physical therapy include a tight piriformis muscle, tight hip external rotators and adductors, hip adductor weakness, lower lumbar spine dysfunction, and sacroiliac joint hypermobility. Functional adaptations to these deficits include ambulation with the thigh in external rotations, functional limb length shortening, or shortened stride length.

TREATMENT Without a reproducible and accurate method to diagnose piriformis syndrome, current therapeutic treatment regimens are controversial without substantive outcomes data that have been subjected to randomized, blind controlled trials. Despite this fact, numerous treatment strategies exist for patients with piriformis syndrome (Fig. 121.10). The first approach and the mainstay of treatment consists of rehabilitation measures beginning with activity modification and physical therapy. The emphasis of the latter component involves piriformis and hip abductor/adductor stretching and strengthening. Physical therapy aims at stretching the muscle and reducing the vicious cycle of pain and spasm. Stretching several times throughout the day can be complemented with manual techniques, heat, ultra-

Piriformis syndrome

A

Activity modification Non-steroidal anti-inflammatory drugs

Physical therapy Home stretching

Ultrasound Electric stimulation Heat Manual techniques

Injection therapy (Lidocaine ± corticosteroid)

Surgery

1304

B

Fig. 121.10 Treatment algorithm for piriformis syndrome.

Fig. 121.11 Exercises for patients to perform on a regular basis for piriformis syndrome by placing the muscle in a flexed and internally rotated/adducted position. (A) Supine. (B) Sitting.

Section 2: Sacral Disorders

Injection therapy can be incorporated if the situation is refractory to the aforementioned treatment program. Injections are usually applied at the origin of the sacroiliac joint with fluoroscopy, along the course of the muscle belly, or at the insertion of the piriformis.34 For effective injection, the piriformis muscle must be localized, but this can be difficult. Considerations should be given to use image-guided technology such as ultrasound, MRI, computed tomography (CT) scans if available, by a knowledgeable user, or manually by palpation over the point of maximal tenderness or by digital rectal examination. Once localized, the piriformis muscle is injected using a 3.5-inch spinal needle or a longer needle in obese patients. Care is taken to avoid direct injection of the sciatic nerve by asking the patient to report any changes in symptoms during the procedure. Traditional injections have included steroids and/or local anesthetics. Dosages may vary but the authors suggest 2–10 mL of 1% lidocaine and 80 mg of triamcinolone as a mixture or individually. Some researchers believe that there is little to no inflammatory component and, as such, have proposed using only 10 cc of 1% lidocaine followed immediately by piriformis stretching These injections without steroid can be performed on a weekly basis over a period of 4–5 weeks to assess benefit and the need for surgery. It is important to avoid longer-acting anesthetics in case the sciatic nerve is inadvertently injected. Preliminary studies using 12 500 units of botulinum neurotoxin B or a similar dose of botulinum toxin A and physical therapy to treat piriformis syndrome have been conducted. In a few cases patients describe relief for up to 3 months.30,32 Given that nearly 50% of patients suffered side effects including dry mouth and dysphagia, and the lack of compelling scientific evidence proving its efficacy, such treatment remains investigational. Surgical management is the treatment of last resort, but can produce dramatic results. While conservative treatment has been noted to be effective, a review of the 28 reported cases in the literature revealed that 13 (46%) went on to require surgical intervention.9,19,23–27,35,36 Surgery for this condition involves resection of the muscle itself or the muscle tendon near its insertion at the superior-medial aspect of the greater trochanter of the femur.37 The authors’ technique involves a combination of both by first sectioning the tendon from its insertion and then through the muscle belly as it emerges from the greater sciatic notch to remove the muscle and completely decompress the sciatic nerve. The authors believe this offers the best chance to ensure complete decompression and to decrease the likelihood of recurrent compression from scarring of the muscle on the nerve.

Fig. 121.12 Intraoperative photo of a neurovascular bundle (NB) crossing the sciatic nerve (SN). The gluteus muscles have been retracted and the hip has been internally rotated to reveal the piriformis muscle, which was then sectioned.

stant reminder of its presence (Fig. 121.12). The hip is internally rotated and the piriformis tendon is sectioned and used to retract the muscle off the sciatic nerve. The muscle belly is then sectioned to reveal the sciatic nerve more clearly as far back as the greater sciatic notch. The muscle is sectioned at its most proximal location as it emerges from the greater sciatic notch. The sciatic nerve is explored and decompressed to ensure that there are no residual fibrous bands, neurovascular bundles, or other constrictions compressing the nerve (Fig. 121.13). Patients are fully weight-bearing with crutches postoperatively, with physical therapy for abductor/adductor strengthening and gait training. Patients remain overnight in the hospital and may experience dramatic relief the first postoperative day. The authors’ experience with this method is promising as they await longer-term follow-up (Fig. 121.14).

SURGICAL TECHNIQUE The patient is placed on a regular operating room table in the lateral decubitus position with the affected hip facing up. The authors limit their incision to the proximal third of the standard posterolateral incision used for total hip replacements. They believe in a minimally invasive approach and so use a microscope to completely resect the piriformis, in contrast to the endoscopic technique that has been described for releasing the piriformis muscle.38 The approach begins with a 4 cm skin incision that is followed by blunt splitting of the gluteus maximus muscle fibers under the microscope. This should be done slowly and meticulously to avoid injury to the sciatic nerve which can appear unprotected in more distal dissections. A selfretractor system is used to retract the gluteus maximus fibers and the deep adipose tissues are meticulously dissected to locate the piriformis muscle and its tendinous insertion on the greater trochanter. Internal rotation of the hip can facilitate identification of the piriformis tendon as it is placed under tension. The sciatic nerve should be identified and a Penrose drain placed around the nerve as a con-

Fig. 121.13 Cadaveric photo showing fibrous bands (FB) and a neurovascular bundle (NB) crossing sciatic nerve (SN). The gluteus muscles (GM) have been retracted. Exploration and decompression of the sciatic nerve after release of the piriformis muscle and tendon to remove any further constrictions, adhesions, or fibrous bands is essential. 1305

Part 4: Extra-Spinal Disorders 10. Rodrigue T, Hardy RW. Diagnosis and treatment of piriformis syndrome. Neurosurg Clin N Am 2001; 12(2):311–319. 11. Frymoyer JW. Back pain and sciatica. N Engl J Med 1988; 318(5):291–300. 12. Bernard TN Jr, Kirkaldy-Willis WH. Recognizing specific characteristics of nonspecific low back pain. Clin Orthop 1987; 217:266–280. 13. Pace JB, Nagle D. Piriform syndrome. West J Med 1976; 124(6):435–439. 14. Durrani Z, Winnie AP. Piriformis muscle syndrome: an underdiagnosed cause of sciatica. J Pain Symptom Manage 1991; 6(6):374–379. 15. Brown JA, Braun MA, Namey TC. Piriformis syndrome in a 10-year-old boy as a complication of operation with the patient in the sitting position. Neurosurgery 1988; 23(1):117–119. 16. Jankiewicz JJ, Hennrikus WL, Houkom JA. The appearance of the piriformis muscle syndrome in computed tomography and magnetic resonance imaging. A case report and review of the literature. Clin Orthop 1991; 262:205–209. 17. Retzlaff EW, Berry AH, Haight AS, et al. The piriformis muscle syndrome. J Am Osteopath Assoc 1974; 73(10):799–807.

Fig. 121.14 Incision on the left buttock (solid arrow) of a 43-year-old nurse with left-leg sciatica and buttock pain refractory to multiple lumbar injections and physical therapy modalities. MRI of the lumbar spine and pelvis only revealed moderate left L4–5 foraminal stenosis. Patient underwent microscopic piriformis muscle resection and decompression of fibrous bands crossing the sciatic nerve. Patient obtained complete relief of her buttock symptoms and majority of her sciatica. She is currently working as a full-time nurse.

CONCLUSION Piriformis syndrome remains controversial but there is growing literature to suggest that there is a subset of patients who have sciatica secondary to neuritis of the sciatic nerve directly or indirectly related to the piriformis muscle. These patients often benefit from conservative treatment in the majority of cases, but there is another subset of patients who experience dramatic relief after surgical decompression of the piriformis muscle and sciatic nerve. An increased awareness of this disorder and further studies are encouraged between many disciplines within the medical and surgical specialties to enable earlier and improved diagnostic and treatment methods.

References 1. Yeoman W. The relation of arthritis of the sacroiliac joint to sciatica. Lancet 19282:1119–1122. 2. Freiberg AH, Vinkle TH. Sciatica and the sacro-iliac joint. J Bone Joint Surg [Am] 1934; 16:126–136. 3. Freiberg AH. Sciatica pain and its relief by operation on muscle and fascia. Arch Surg 1937;34:337–350. 4. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934; 211:210–214. 5. Thiele GH. Coccygodynia and pain in the superior gluteal region. JAMA 1937; 109:1271–1275. 6. Shordania JF. Die chronische Entzundung des Musculus pirifmoris – die Piriformitis – als eine der Ursachen von Kreuzschmerzen bei Frauen. Med Welt 1936; X:999. 7. Beaton LE, Anson BJ. The sciatic nerve and the piriformis muscle: their interrelation a possible cause of coccygodynia. J Bone Joint Surg [Am] 1938; 20:686–688. 8. Robinson DR. Piriformis syndrome in relation to sciatic pain. Am J Surg 1947; 73:435–439. 9. Silver JK, Leadbetter WB. Piriformis syndrome: assessment of current practice and literature review. Orthopedics 1998; 21(10):1133–1135.

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18. Parziale JR, Hudgins TH, Fishman LM. The piriformis syndrome. Am J Orthop 1996; 25(12):819–823. 19. Barton PM. Piriformis syndrome: a rational approach to management. Pain 1991; 47(3):345–352. 20. Benson ER, Schutzer SF. Posttraumatic piriformis syndrome: diagnosis and results of operative treatment. J Bone Joint Surg [Am] 1999; 81(7):941–949. 21. Rask MR. Superior gluteal nerve entrapment syndrome. Muscle Nerve 1980; 3(4):304–307. 22. Beatty RA. The piriformis muscle syndrome: a simple diagnostic maneuver. Neurosurgery 1994; 34(3):512–514; discussion 514. 23. Steiner C, Staubs C, Ganon M, et al. Piriformis syndrome: pathogenesis, diagnosis, and treatment. J Am Osteopath Assoc 1987; 87(4):318–323. 24. Chen WS. Sciatica due to piriformis pyomyositis. Report of a case. J Bone Joint Surg [Am] 1992; 74(10):1546–1548. 25. Chen WS, Wan YL. Sciatica caused by piriformis muscle syndrome: report of two cases. J Formos Med Assoc 1992; 91(6):647–650. 26. Vandertop WP, Bosma NJ. The piriformis syndrome. A case report. J Bone Joint Surg [Am] 1991; 73(7):1095–1097. 27. Papadopoulos SM, McGillicuddy JE, Albers JW. Unusual cause of ‘piriformis muscle syndrome’. Arch Neurol 1990; 47(10):1144–1146. 28. Tesio L, Bassi L, Galardi G. Transient palsy of hip abductors after a fall on the buttocks. Arch Orthop Trauma Surg 1990; 109(3):164–165. 29. Rossi P, Cardinali P, Serrao M, et al. Magnetic resonance imaging findings in piriformis syndrome: a case report. Arch Phys Med Rehabil 2001; 82(4):519–521. 30. Fishman LM, Konnoth C, Rozner B. Botulinum neurotoxin type B and physical therapy in the treatment of piriformis syndrome: a dose-finding study. Am J Phys Med Rehabil 2004; 83(1):42–50; quiz 51–53. 31. Fishman LM, Zybert PA. Electrophysiologic evidence of piriformis syndrome. Arch Phys Med Rehabil 1992; 73(4):359–364. 32. Fishman LM, Anderson C, Rosner B. BOTOX and physical therapy in the treatment of piriformis syndrome. Am J Phys Med Rehabil 2002; 81(12):936–942. 33. Nakamura H, Seki M, Konishi S, et al. Piriformis syndrome diagnosed by cauda equina action potentials: report of two cases. Spine 2003; 28(2):E37–E40. 34. Foster MR. Piriformis syndrome. Orthopedics 2002; 25(8):821–825. 35. Lam AW, Thompson JF, McCarthy WH. Unilateral piriformis syndrome in a patient with previous melanoma. Aust NZ J Surg 1993; 63(2):152–153. 36. Sayson SC, Ducey JP, Maybrey JB, et al. Sciatic entrapment neuropathy associated with an anomalous piriformis muscle. Pain 1994; 59(1):149–152. 37. Mizuguchi T. Division of the piriformis muscle for the treatment of sciatica. Postlaminectomy syndrome and osteoarthritis of the spine. Arch Surg 1976; 111(6): 719–722. 38. Dezawa A, Kusano S, Miki H. Arthroscopic release of the piriformis muscle under local anesthesia for piriformis syndrome. Arthroscopy 2003; 19(5):554–557.

PART 5

CHAPTER

122

PREGNANCY

Epidemiology of Back Pain in Pregnancy Per O. J. Kristiansson

INTRODUCTION Low back pain is an important and commonly occurring public health problem with high impact to the person, family, and society. Prevalence figures of low back pain vary considerably across studies because of various factors, including case definition. In a prospective Danish study 40% of women, 25–34 years of age, reported low back pain during 1 year with a point prevalence of 20%, regardless of the degree of pain intensity or disability.1 When disability of low back pain was taken into consideration, in a Canadian study, 50% of the population had experienced low-intensity/low-disability low back pain (including the sacral area) and 10% had experienced high disability low back pain in the previous 6 months, with a small age variation. Interestingly, women experienced almost twice the rate of high-disability low back pain compared with men.2

EPIDEMIOLOGY In comparison to the 1-year prevalence of back pain among women from the general population, a reported 9-month prevalence rate of back pain during pregnancy, regardless of its onset, on average about 55% (range, 35.5–89.8%) has been reported.3–16 The 9-month prevalence rate of back pain during pregnancy varies substantially among different studies with a mean prevalence rate within retrospective studies of 54% (range, 36–90%),3,5,6,8,9,11,13,15 and in prospective studies 58% (range, 49–88%) (Table 122.1).4,7,10,12,14,16 A true difference in prevalence of back pain between pregnant and nonpregnant women is strengthened by data from an Australian study where the odds ratio of having low back pain in pregnancy was 3.5 times higher than that of nonpregnant women.12 Thus, it appears that back pain is more common during pregnancy than in the nonpregnant state or in men. When back pain with onset during current pregnancy was considered, prevalence rates of between 61%7 and 88%14 was observed. The onset of back pain during pregnancy was fairly evenly distributed over the pregnancy period in most studies.5,7,8,13–15 The obvious conclusion derived from this information is that most women develop pregnancy-related back pain long before the commencement of abdominal enlargement or postural alterations. Among women developing back pain during pregnancy about 16% had reported a new location of back pain during the first 12 gestational weeks, 67% at 24th gestational week, and 93% at week 36. Thus, the largest proportion of pregnant women were experiencing new low back pain before their fifth month of pregnancy and a smaller proportion of pregnant women develop low back pain during the major growth period of the fetus. Among women with back pain with onset during pregnancy, sacral pain is by far the most common location, reported by about 50% of women, followed in order by lumbosacral, lumbar, and thoracic

pain. Cervical axial pain rarely manifests during pregnancy.7,10 This is in contrast to pregnant women with back pain with onset prior to pregnancy when the lumbar and thoracic pain were the most common.7 Nearly every second women (45.5% and 46.8%) with pregnancy-related low back pain experiences symptoms that refer to the buttocks and thighs, occasionally down the legs,5,6 but only rarely reaching the feet.5 True sciatica with pain below the knee was found in only 1%.10 Regardless of the symptom location in the lower extremity, a duration of 1–3 months is common. However, 5–10% of women report pain duration in pregnancy of more than 5 months where sacral pain is dominating.4,7 Pain intensity among women with onset of back pain during pregnancy significantly increased over the duration of pregnancy. This is reflected by the duration of pain and not simply an increase during the later stages of pregnancy. This means that the longer the duration of back pain related to pregnancy the higher the reported pain intensity. In addition, there is a significant indirect correlation between pain intensity and age in several studies. Younger women reported higher pain scores than older women.3,7,17 Among women with back pain during pregnancy the intensity of pain varied during the day and between days. One study showed that 16% of the pregnant women suffered from pain hourly, 66% daily, and 18% weekly.5 Among women with daily back pain, onethird reported increased pain toward the end of the day and onethird experienced increased pain during the night.5,8 In the study by Mantle et al., nearly half of the women reported most troublesome backache in the morning.8 An explanation of this variation of back pain intensity could be that the intensity of back pain emerges over time during or after strain applied to the spine from various workloads, and then pain is relieved following rest. The specific load on the back initiates pain in susceptible women, leading to the greatest pain intensity later in the day, at night,5,6,13 or the following morning.8 Back pain may result in an impaired sleep pattern as is demonstrated by decreased periods of rapid eye movement sleep.18 About one-third19 of pregnant women arose at night because of a backache, experiencing even more severe pain than during the day.6 Pregnancy-related back pain has a great impact on women, particularly those suffering from high-intensity pain when compared to pregnant women without pain at all. In prospective studies, about 30–35% of women with back pain describe the pain as a severe problem compromising normal, everyday life.7,10 They preferentially describe difficulty with heavy physical work, heavy lifting, running, or physical exercise. They can also experience trouble with walking, sitting for longer than a few minutes, carrying a bag, or activities that require slight forward flexion while in the standing position (such as making the bed). This indicates that back pain during pregnancy causes restricted physical activity over and above that caused by pregnancy itself.7 The impact of pregnancy-related back pain is

1307

Part 5: Pregnancy

Table 122.1: Prevalence of Low Back Pain During Pregnancy in Observational Studies Point Prevalence by Gestational Week Author, Year

Study Design

n = 12 (%)

Mantle, 1977

Retrospective

180

Nwuga, 1982

Retrospective

99

36 (%)

Regardless of Onset (%)

Fast, 1987

Retrospective

200

56

Thomas, 1989

Retrospective

109

87

Fung, 1993

Retrospective

200

54.5

89.8

Orvieto, 1994

Retrospective

449

55

Endresen, 1995

Retrospective

5438

58

Stapleton, 2002

Retrospective

1530

35.5

Berg, 1986

Prospective

862

Bullock, 1987

Prospective

34

Östgaard, 1991

Prospective

855

Pregnancy Onset (%)

48

49 28

62

76

32

32

88.2 49

Kristiansson, 1996

Prospective

200 19

47.3

49.1

76.4

Zib, 1999

Prospective

236

63.3

76.1

76.1

To, 2003

Prospective

326

also highlighted by the fact that among previously pregnant women, one of five from the general population, as well as among women with scoliosis, refrain from becoming pregnant again due to fear of developing back pain during pregnancy.20,21 Back pain related to pregnancy appears to be a global problem that occurs in developed as well as developing countries. High prevalence rates of back pain during pregnancy have been reported in Europe, America, Australia, China, including the mountainous region of Taiwan and Africa’s rural areas as well as among upper-class women in Nigeria.6,7,11–13,22,23 Back pain during pregnancy has been reported from different ethnic groups.5,6,7,9,13,22 Although the distribution of back pain during pregnancy seems to differ among certain ethnic groups, this could, however, be a reflection of socioeconomic status. In a study from Israel9 on consecutive women referred for an antenatal ultrasonographic examination Sephardic women with origin in Africa and Asia had a much higher prevalence of low back pain during pregnancy as compared to those of other origin such as Ashkenazi, mixed, and Arabic (64.5% as compared with 27.5%, 5.5% and 2.5%, respectively). In an American retrospective interview study5 in a maternity ward the ratio of Caucasians was much higher in the back pain group compared with the nonpain group (34% versus 15%). The opposite was true for Hispanics compared to the nonpain group (13% versus 26%). For many mothers, back pain related to pregnancy resolves in the first months after delivery, but for some it may continue for several months or years. In a prospective study, where the onset of pain was not accounted for, the prevalence of low back pain following delivery showed a rapid decline from 65% at 1 month postpartum to 37% at 6 months after delivery. Thereafter, the recovery rate was slow,24 up to the end of study 18 months postpartum when 7% still had persisting serious back problems. This is in agreement with a study of women with onset of back pain during pregnancy, in which women were clinically classified during pregnancy and follow-up. Among those women, 8% were still classified as experiencing daily low back pain 2 years after childbirth.25 1308

24 (%)

9-month Prevalence in Pregnancy

61

76

Characteristics of women with a slow regression of back pain following delivery include longer periods of back pain during pregnancy, high intensity of back pain during pregnancy, older age, and unskilled work during pregnancy.24,25 In addition, women with back pain during previous pregnancies and multipregnant women are more likely to experience persistent back pain following the current pregnancy.24 No association has been identified linking postpartum back pain and mode of delivery or epidural anesthesia.26 Women with continuing back pain after delivery report adverse effects from the pain similar to those during pregnancy. In addition, among women with persisting severe back pain related to pregnancy, 25% changed occupation because of the pain, compared to 3% in the control group.21 Back pain before, and particularly during previous pregnancy, is a strong predictor for the development of back pain in pregnancy.6,9,10,16,21,27 Almost all women with low back pain in an index pregnancy, identified and documented with a neurologic and musculoskeletal examination, developed low back pain during the subsequent pregnancy,21 indicating an extremely high risk for these women. Conflicting results have been reported regarding the possible association between prevalence of back pain in pregnancy and the number of previous pregnancies, the number of previous deliveries, and age. The differences are most likely a consequence of methodological issues. However, the number of pregnancies influenced the duration17 and the number of deliveries the severity of back pain in a subsequent pregnancy.13 In addition, multiparity increased the incidence of back pain after delivery.16 An environmental factor that is associated with pregnancy-related back pain is a heavy workload.10 Among pregnant women in a rural area of Taiwan, 85% of pregnant women who performed very heavy work reported low back pain compared to 49% among pregnant women performing light work.13 Factors that showed no association to back pain in pregnancy were body height and body weight during early pregnancy and weight gain during pregnancy, infant’s birth weight, and postural change. Thus, it appears that back pain emerges more often among women during pregnancy than in the nonpregnant state or in men.

Pregnancy

However, the reason for this is still unclear. During pregnancy there are hormonal, biomechanical, circulatory, and psychosocial changes. Any of these factors, or a combination, may be involved in the pathophysiology of axial back pain. Generally, back pain in pregnancy is assumed to be related to a combination of mechanical stressors and hormone-induced changes in the ligamentous support of the spine. During pregnancy there is a significant change in magnitude of lumbar lordosis and thoracic kyphosis. This change in posture occurs during the fifth and ninth months of pregnancy.14 Yet, no relationship between posture and pregnancy-related back pain has been reported. The absence of any proof of an association between posture and back pain during pregnancy suggests that some factor other than posture must play an important role in pain production.14 Lumbar disc herniation as a cause of back pain in pregnancy is unusual, with an estimated prevalence rate of 1 in 10 000 pregnancies.28 However, a disc bulge or prolapse is common and can occur in as many as every second woman of childbearing age, whether pregnant or not.29 In Chinese pregnant women undergoing magnetic resonance imaging pelvimetry a disc bulge or prolapse was seen infrequently during the last trimester, whereas a significant correlation was shown with current reported low back pain.23 However, as the majority of those women with back pain had no disc bulge this was not the only cause for back pain in pregnancy.23 Interestingly, it was also shown that a higher signal intensity in the uterine cervix correlated with back pain during pregnancy, which may represent indirect evidence for a relationship between pregnancy effects on soft tissue and back pain in pregnancy.23 Furthermore, in general, women experiencing symptoms of a herniated lumbar disc had had more pregnancies resulting in live births than women of similar age without known herniated discs. This observation suggest that a full-term pregnancy may be a cause of radicular pain due to a focal protrusion.30 Women with adolescent idiopathic scoliosis experienced no adverse biomechanical alterations from pregnancy such as progression of the scoliosis curve.20 A progression of scoliosis was not detected in women treated with a posterior spinal fusion or with conservative treatment including wearing an orthosis.20 Furthermore, the rate of complications during pregnancy, including back pain, for women with adolescent idiopathic scoliosis of different degrees was not higher than in the general population.31 The influence of pregnancy on the ligamentous and osseous support of the spine and pelvis, as a cause of pregnancy-related back pain, has been studied in women with congenital defects of collagen synthesis. In a retrospective study of women with osteogenesis imperfecta, a disorder causing fractures and increased fragility of connective tissue, the most common musculoskeletal problem during pregnancy was back pain, while the prevalence of back pain during pregnancy was not higher than among healthy women.32 However, a high proportion of pregnant women reported severe back pain in pregnancy causing a disruption of activities of daily living with no identified cause of the pain in most cases.32 Ehlers-Danlos syndrome is a heterogeneous collection of inherited disorders of the connective tissue. In a retrospective study of previously pregnant women affected by Ehlers-Danlos syndrome as many as 27% were suffering from severe low back pain in the sacral area compared to 7% in a control group of unaffected women.33 Results from several studies indicate that there is an obvious influence of pregnancy on tissue of ligament and bone in the low back region. In anatomic studies, variably deep grooves at the insertions of ligaments at os ilium and os sacrum have been demonstrated. It was also demonstrated that a groove, adjacent to the inferior end of the sacroiliac joint on os ilium, constitutes the insertion of the anterior sacroiliac ligament (Fig. 122.1).34 In radiologic studies, this bone resorption has been demonstrated among 25% of examined women

Fig. 122.1 A relatively deep groove is shown on this anatomic specimen from a 75-year-old parous woman when the anterior sacroiliac ligament and the sacroiliac joint capsule are removed from their insertion on the medioanterior aspect of the iliac bone. (Courtesy of Dale Caville.)

while not present in men.35,36 Furthermore, the deep grooves were displayed only in women with previous deliveries.35 In addition, there was a relationship between the presence of these grooves and osteitis condensans ilii. This latter entity is believed to be a manifestation of bone remodeling in response to stress across the sacroiliac joints associated with a previous pregnancy.35 However, their correlation with back pain has not been studied. Further evidence of the influence of pregnancy on the spine is a doubling of the incidence of degenerative spondylolisthesis in parous women with low back pain compared to men and nulliparous women with back pain.37 Women who had borne children had the highest incidence of degenerative spondylolisthesis (28%), especially at level L4–5, compared to nulliparous women (17%) and men (7.5%).37

CONCLUSION In conclusion, back pain with onset during pregnancy is a global phenomenon that commonly adversely impacts the daily activities of women and their families. The duration of symptoms can be lengthy resulting in important changes to work choices, leisure activities and general well-being. Indeed, in many instances the symptoms persist long after delivery. Despite the scope of this medical problem there is a fundamental lack of knowledge regarding the exact etiology of these painful symptoms. This necessarily means that evidencedbased treatment is in its infancy and that much work needs to be undertaken to elucidate the variety of etiologies of pregnancy-related back pain.

References 1. Biering-Sorensen F. Low back trouble in a general population of 30-, 40-, 50-, and 60-year-old men and women. Study design, representativeness and basic results. Dan Med Bull 1982; 29:289–299. 2. Cassidy JD, Carroll LJ, Cote P. The Saskatchewan health and back pain survey. The prevalence of low back pain and related disability in Saskatchewan adults. Spine 1998; 23:1860–1866. 3. Endresen EH. Pelvic pain and low back pain in pregnant women – an epidemiological study. Scand J Rheumatol 1995; 24:135–141. 4. Berg G, Hammar M, Moller-Nielsen J, et al. Low back pain during pregnancy. Obstet Gynecol 1988; 71:71–75. 5. Fast A, Shapiro D, Ducommun EJ, et al. Low-back pain in pregnancy. Spine 1987; 12:368–371.

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Part 5: Pregnancy 6. Fung BK, Kwong CM, Ho ES. Low back pain of women during pregnancy in the mountainous district of central Taiwan. Chin Med J (Taipei) 1993; 51:103–106.

22. Bjorklund K, Bergstrom S. Is pelvic pain in pregnancy a welfare complaint? Acta Obstet Gynecol Scand 2000; 79:24–30.

7. Kristiansson P, Svardsudd K, von Schoultz B. Back pain during pregnancy: A prospective study. Spine 1996; 21:702–709.

23. Chan YL, Lam WW, Lau TK, et al. Back pain in pregnancy – magnetic resonance imaging correlation. Clin Radiol 2002; 57:1109–1112.

8. Mantle MJ, Greenwood RM, Currey HL. Backache in pregnancy. Rheumatol Rehabil 1977; 16:95–101.

24. Ostgaard HC, Andersson GB. Postpartum low-back pain. Spine 1992; 17:53–55.

9. Orvieto R, Achiron A, Ben-Rafael Z, et al. Low-back pain of pregnancy. Acta Obstet Gynecol Scand 1994; 73:209–214. 10. Ostgaard HC, Andersson GB, Karlsson K. Prevalence of back pain in pregnancy. Spine 1991; 16:549–552. 11. Stapleton DB, MacLennan AH, Kristiansson, P. The prevalence of recalled low back pain during and after pregnancy: A South Australian population survey. Aust NZ J Obstet Gynaecol 2002; 42:482–485. 12. Zib M, Lim L, Walters WA. Symptoms during normal pregnancy: a prospective controlled study. Aust NZ J Obstet Gynaecol 1999; 39:401–410. 13. Nwuga VC. Pregnancy and back pain among upper class Nigerian women. Austr J Physiother 1982; 28:8–11.

26. Breen TW, Ransil BJ, Groves PA, et al. Factors associated with back pain after childbirth. Anesthesiology 1994; 81:29–34. 27. Padua L, Padua R, Bondi R, et al. Patient-oriented assessment of back pain in pregnancy. Eur Spine J 2002; 11:272–275. 28. LaBan MM, Perrin JC, Latimer FR. Pregnancy and the herniated lumbar disc. Arch Phys Med Rehabil 1983; 64:319–321. 29. Weinreb JC, Wolbarsht LB, Cohen JM, et al. Prevalence of lumbosacral intervertebral disk abnormalities on MR images in pregnant and asymptomatic nonpregnant women. Radiology 1989; 170:125–128.

14. Bullock JE, Gwendolen AJ, Bullock MI. The relationship of low back pain to postural changes during pregnancy. Austr J Physiother 1987; 33:10–17.

30. Kelsey JL, Greenberg RA, Hardy RJ, et al. Pregnancy and the syndrome of herniated lumbar intervertebral disc; an epidemiological study. Yale J Biol Med 1975; 48:361–368.

15. Thomas IL, Nicklin J, Pollock H, et al. Evaluation of maternity cushion (Ozzlo pillow) for backache and insomnia in late pregnancy. Aust NZ J Obstet Gynaecol 1989; 29:133–138.

31. Danielsson AJ, Nachemson AL. Childbearing, curve progression, and sexual function in women 22 years after treatment for adolescent idiopathic scoliosis: A casecontrol study. Spine 2001; 26:1449–1456.

16. To WWK, Wong MWN. Factors associated with back pain symptoms in pregnancy and the persistence of pain 2 years after pregnancy. Acta Obstet Gynecol Scand 2003; 82:1086–1091.

32. McAllion SJ, Paterson CR. Musculoskeletal problems associated with pregnancy in women with osteogenesis imperfecta. J Obstet Gynaecol 2002; 22:169–172.

17. Ostgaard HC, Andersson GB. Previous back pain and risk of developing back pain in a future pregnancy. Spine 1991; 16:432–436. 18. Fast A, Hertz G. Nocturnal low back pain in pregnancy: Polysomnographic correlates. Am J Reprod Immunol 1992; 28:251–253. 19. Fast A, Weiss L, Parikh S, et al. Night backache in pregnancy. Hypothetical pathophysiological mechanisms. Am J Phys Med Rehabil 1989; 68:227–229. 20. Betz RR, Bunnell WP, Lambrecht-Mulier E, et al. Scoliosis and pregnancy. J Bone Joint Surg[Am] 1987; 69:90–96. 21. Brynhildsen J, Hansson A, Persson A, et al. Follow-up of patients with low back pain during pregnancy. Obstet Gynecol 1998; 91:182–186.

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25. Albert H, Godskesen M, Westergaard J. Prognosis in four syndromes of pregnancyrelated pelvic pain. Acta Obstet Gynecol Scand 2001; 80:505–510.

33. Lind J, Wallenburg HC. Pregnancy and the Ehlers-Danlos syndrome: a retrospective study in a Dutch population. Acta Obstet Gynecol Scand 2002; 81:293–300. 34. Derry DE. The significance of the sulcus praeauricularis. Anat Anz 1911; 39:13–20. 35. Schemmer D, White PG, Friedmann MB. Radiology of the paraglenoid sulcus. Skeletal Radiol 1995; 24:205209. 36. Gulekon IN, Turgut HB. The preauricular sulcus: Its radiologic evidence and prevalence. Acta Anat Nippon 2001; 76:533–535. 37. Sanderson PL, Fraser RD. The influence of pregnancy on the development of degenerative spondylolisthesis. J Bone Joint Surg [Br] 1996; 78:951–954.

PART 5

CHAPTER

123

PREGNANCY

Low Back Pain and Pregnancy – Examination and Diagnostic Work-up in the Pregnant Patient Colleen M. Fitzgerald and Christina Kerger Hynes

INTRODUCTION Nearly any medical condition that can occur in the nonpregnant state can occur during pregnancy. In fact, because of the pregnant state, women can potentially be at higher risk of misdiagnosis due to the overall general concept that all back pain in pregnancy is somewhat ‘normal’.1 Back pain in pregnancy is common, but when it becomes disabling it demands further diagnostic evaluation. Estimates of incidence are 50–70%.2 One prospective study of back pain in pregnancy showed a prevalence rate of 60%, with 30% of those patients reporting severe limitations in their daily activities.3 Special consideration of postpartum back pain should also be made in the context of the continuum of pregnancy-related pain. The physiologic changes of pregnancy may predispose women to back pain. The increased lumbar lordosis combined with the effects of the hormone relaxin on the joints of the lumbar spine and pelvis with the added weight of the gravid uterus result in a shift of the center of gravity anteriorly and an increased mechanical burden on the low back.2,4 The abdominal wall musculature of the abdominal cavity stretches as the gravid uterus grows. The force–tension curve of the lengthened abdominal muscles restrict their contractile strength while the muscles of the low back work harder to maintain upright posture. The muscles of the pelvic floor will bear the weight of the growing uterus and will eventually allow passage of the fetus. Relaxin is a polypeptide hormone secreted by the corpus lutea and has been identified as the major contributor to joint laxity during pregnancy.4 It is dramatically elevated during the first trimester, declines early in the second trimester to a level that remains stable throughout the pregnancy,4 and then declines sharply after delivery. Widening of the symphysis pubis and increased mobility of the sacroiliac synchondroses begins in the tenth to twelfth week of pregnancy as a result of relaxin.5 The strong sacroiliac ligament which normally resists forward flexion of the ala will become lax with the effects of relaxin.5 Weight gain, maternal obesity, and fetal weight at term have not been found to be related to pregnancy-related back pain.6 Other studies have shown that low back pain prior to or during a previous pregnancy, nulliparity with increased body mass index (BMI), lower socioeconomic status, and placenta with a posterior fundal location were found to be risk factors for back pain in pregnancy.35 A spectrum of clinical symptoms may be produced by the physiologic changes of pregnancy. However, the differential diagnosis of back pain in pregnancy should not be limited to pregnancy-related changes in the musculoskeletal system. Clinical entities implicated as causes of back pain in pregnancy in one review article include: pelvic insufficiency (pain), sacroiliac joint (SIJ) subluxation, sciatica, lumbosacral disc pathology, spondylolisthesis, postural back pain and lumbar lordosis, thoracic back pain and coccydynia.6 Other studies have also included hip pathology, such as osteonecrosis of the femoral head and transient osteoporosis of

pregnancy, as a potential cause of referred back pain.5 Other known causes of back pain include neurologic etiologies such as radiculopathy or plexopathy, vertebral segmental dysfunction, tumor, or fracture of the sacrum or pelvis. There is also growing evidence that the pelvic floor musculature is a pain generator, especially in relation to coccydynia and dyspareunia (Table 123.1).

PELVIC OBLIQUITY The pelvis is a ring comprised of two innominate bones that are connected anteriorly by the pubic symphysis and posteriorly to either side of the sacrum by the SIJ. The pelvis is dynamic or more mobile in the pregnant state as a result of the influence of relaxin on the ligamentous structures. Laxity itself is widespread and does not necessarily result in pain. Asymmetry of any part of the ring will cause dysfunction on the opposite side, i.e. dysfunction of the posterior pelvis will result in asymmetry and dysfunction of the anterior pelvis. They do not occur in isolation. However, there is a clear relation between asymmetric laxity of the SI joints and pregnancy-related pelvic pain (PRPP).8 There is an array of nomenclature to describe a given obliquity. By convention, dysfunction of pelvic ring is named on the hypomobile side. However, anecdotally, in the pregnant state the hypermobile

Table 123.1: Visceral Causes of Low Back Pain in Pregnancy6 GENITOURINARY Urinary tract infection Kidney stones Pyelonephritis Cystitis Urethritis GYNECOLOGIC Ovarian cyst or torsion Uterine dysfunction or placental abnormality Pelvic inflammatory disease GASTROINTESTINAL Constipation Hemorrhoids Irritable bowel syndrome Hernia

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Part 5: Pregnancy

side on physical examination can correlate with the side of pain. Damen et al. studied the prognostic value of laxity in assessing pain postpartum. Asymmetric laxity of the SI joints in pregnancy was believed to increase the presence of pelvic pain postpartum by as much as threefold.9,10 This speaks to treatment of asymmetry of the SI joint and its associated pain during pregnancy to prevent future back pain. In pregnancy, the innominate obliquity is commonly named for the side which gives the patient pain in order to best direct the physical therapy prescription. A number of anatomic landmarks are used to determine pelvic obliquity: the iliac crest, the posterior superior iliac spine (PSIS), the anterior superior iliac spine (ASIS), and the pubic tubercles. The inferior lateral angle of the sacrum (ILA) can also be assessed to further delineate asymmetric sacral positioning in relation to ilial positioning. By measuring the side-to-side difference between these landmarks, the type of obliquity can be determined. A problematic hemipelvis can be rotated anteriorly or posteriorly, sheared superiorly (upslip) or inferiorly (downslip), inflared or outflared. Sacral positioning can be described similarly.11

SACROILIAC JOINT DYSFUNCTION

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and hence should be considered as potential sources of coccygeal pain, especially when the muscles are in a shortened state. All of these muscles together form the pelvic floor which provides support for the intra-abdominal organs and prevents prolapse. Their combined optimal function as a neuromuscular unit is integral to maintaining urinary, flatal, and fecal continence. They also contract during orgasm to provide sexual appreciation. The pelvic floor muscles have a heightened role during pregnancy in maintaining functional support of the changing body habitus. They can be damaged at the time of labor and delivery and remain a persistent cause of pain. When a pelvic obliquity is present, the resulting asymmetry affects the pelvic floor muscles that originate from and that are attached to the pelvic bones. With a pelvic obliquity, the attaching muscles will be either abnormally shortened or lengthened. A force–tension curve of these muscles will be shifted, thereby demonstrating their disadvantageous biomechanical state. As well, it is known that muscle injury and soreness are more selectively associated with eccentric contraction.15a–c An inherently lengthened muscle must also work harder to function properly, and if the external force on the muscular floor is greater than the force the muscles can generate, weakness may eventually develop in addition to or in conjunction with pain.

The sacroiliac joint is a true joint consisting of a synovial component inferiorly. It is auricular-shaped with the thinner sacral side lined with hyaline cartilage and the thicker ilial side with fibrocartilage. Primary innervation to this joint is thought to be from S1. Sturesson, in 1989, described true movement of the SIJ measuring approximately 1–3° of rotation.12 The sacroiliac joint has also been shown to be a potential generator of low back pain.13 In the pregnant patient, the potential for dysfunction is increased secondary to pregnancy-related hormone-induced ligamentous laxity and resultant asymmetry. It is thought that the laxity prepares for and facilitates delivery of the baby at term.14 Ostgaard, in a prospective study of back pain in 855 pregnant women, found an incidence of 19% with sacroiliac pain in week 30 of gestation.15 Additionally, Damen showed that in pregnant patients who were evaluated by Doppler imaging of vibrations there was found to be a definite relationship between asymmetric laxity of the sacroiliac joints and pregnancy-related pelvic pain.8 Patients typically report pain over the sacrum or the sacral sulcus. Transitional motions, particularly while turning in bed and arising from the seated to the standing position frequently triggers or exacerbates the presenting symptoms. Physical examination maneuvers will be discussed later, but posterior pelvic pain provocation test and active straight leg raise testing are well-documented, reliable diagnostic tests to assess pregnancy-related sacroiliac joint pain. The relationship between pelvic obliquity and sacroiliac joint dysfunction is somewhat intuitive. Typically, when a persistent pelvic obliquity exists there is associated SIJ pain and dysfunction due to the anatomic relationship between these structures. The pelvic obliquity, which is secondary to ligamentous laxity, is thought to create the SIJ dysfunction and change in joint mechanics.

Coccydynia (synonymous with coccygodynia and coccyodynia) is defined as pain in and around the coccyx without significant symptom referral. Sitting or arising from the seated to standing position are common exacerbating influences. A prepartum history of coccyx pain or complaints of very low back pain or tailbone pain warrant consideration of this diagnosis in pregnancy. The coccyx is heavily supported by ligamentous structures and serves as the attachment point for pelvic floor musculature. The combination of laxity and asymmetry can create abnormal motion at the level of the coccyx similar to that of the SIJ. It is important to note that coccygeal pain may be secondary to pelvic floor muscle myofascial pain and dysfunction. There is a blatant absence of literature guiding the evaluation of the coccyx in pregnancy; however, it can be easily done via rectal examination. A study by Maigne16 found that body mass index determines the manner by which a subject sits down and that pathologies were different in obese, normal weight, and thin patients. For a detailed description of the analyses in the nonpregnant patient the reader is referred to Chapter 120 by Yves Maigne. Hypermobility of the coccyx defined as coccygeal flexion exceeding 25° when the patient is in the sitting position as evaluated on plain radiograph was also a cause of coccydynia. The pregnant state lends itself to the potential of coccygeal dysfunction and pain with the acute increase of BMI over 9 months as well as ligamentous laxity that accompanies pregnancy as a result of relaxin and estrogen.

PELVIC FLOOR MYOFASCIAL PAIN

STRESS FRACTURE

The pelvic floor is made up of two layers of muscles. The superficial layer of muscles including the ischiocavernosus, bulbocavernosus, and transverse perinei muscles make up the urogenital diaphragm. These superficial muscles provide uretheral support and may be superficial pelvic pain generators. The deep pelvic floor musculature is made up of two large muscles, the levator ani and the coccygeus. The levator ani is actually made up of a combination of three muscles, specifically the pubococcygeus, the puborectalis, and the iliococcygeus. A firm understanding of the anatomy of this region is paramount to fully appreciating the functional significance of these muscles. They are appropriately named for their attachments at the level of the coccyx

Stress fracture is defined as fracture due to repetitive cyclic loading on normal bone, whereas insufficiency fracture occurs when normal forces are applied to abnormal bone. Stress insufficiency fracture occurs when repetitive cyclic loading occurs in the setting of abnormal bone. Any of these fractures at the level of the sacrum, pelvis, or hip may be the cause of back pain in the pregnant patient, similar to the nonpregnant patient. Fractures should be considered in a patient diagnosed with sacroiliac dysfunction which is not improving with medical rehabilitation and interventional spine techniques; in the case of known trauma; or in a patient with a prepartum history of amenorrhea, eating disorder, or known osteopenia (female athletic triad).17

COCCYDYNIA

Pregnancy

Risk factors specific to pregnancy that predispose for sacral fatigue fractures include rapid or excessive weight gain in the third trimester, increased lumbar lordosis, pelvic instability due to relaxin effect, rapid vaginal delivery, and prolactin-induced transient osteopenia. These injuries should also be considered immediately postpartum in the breastfeeding patient. Polatti showed evidence of a progressive decline in bone mineral density (BMD) in lactating women over the first 6 months with increase in BMD following a 1-month weaning period.17a Calcium supplementation during lactation had only a transient effect in minimizing bone loss. The imaging study of choice in pregnancy after the first trimester when there is a high suspicion of stress fracture is magnetic resonance imaging. A comprehensive literature review revealed several reported sacral fractures associated with pregnancy.18,19,19a

PUBIC SYMPHYSIS Symphysitis and symphyseal separation Pubic symphysis motion and asymmetry is seen during pregnancy. Anterior pain can be associated with this increased motion and simultaneously precipitate posterior pelvic or low back pain. Maximum widening of the pubic symphysis during pregnancy is considered to be 10 mm. By definition, pubic symphysis separation is a width greater than 10 mm and is usually seen after a traumatic labor and delivery. Bjorklund et al., in 2000, studied the association between symphyseal distention and pelvic pain and circulating relaxin levels in the pregnant patient.20 They found that severe pelvic pain during pregnancy was strongly associated with an increased symphyseal distention; however, relaxin levels were not associated with the degree of distention or with pelvic pain in pregnancy. Another study showed that the majority of pregnant women with symphyseal pain had an average pubic symphysis width of 9.5 mm or more via sonographic measurement. In comparison, the asymptomatic pregnant patient had an average width of 6.3 mm.21

Osteitis pubis Acute pubic symphysis inflammation, which can begin in pregnancy in association with a pelvic obliquity, can often lead to a chronic, painful, noninfectious inflammatory condition known as osteitis pubis. Osteitis pubis has been described as a complication of various obstetrical and gynecological procedures, including vaginal deliveries.22 Periosteal trauma seems to be part of the initiating event, although there is controversy regarding the true pathophysiological nature of the disorder. One of the first cases cited in the obstetrical literature was a report of a patient with osteitis pubis after a traumatic forceps vaginal delivery. Wiltse and Frantz reported 10 cases associated with the pregnant state.23 As the pubic symphysis becomes more lax to allow passage of the fetus, there is potential for excess movement and trauma. Plain films are the imaging method of choice; however, radiographic findings often lag behind clinical symptoms. Typically, X-ray changes can be seen 4 weeks after the traumatic event, and include loss of smooth cortical bone and reactive sclerosis. Treatment needs to be initiated based on physical examination in the peripartum period to prevent chronic postpartum pain.

LUMBAR DISC HERNIATION Although early studies by LaBan et al. in 198324 suggested that pregnancy was an independent risk factor for the development of a herniated disc, it has been proven in subsequent studies that the actual incidence of lumbar herniated disc is no greater for pregnant women than for the general population.2,4 It is an uncommon etiology of low back pain in pregnancy with an incidence of 1:10 000.24 Risk factors

include prior history of low back pain, increased body mass index, and lower socioeconomic status. Advanced maternal age, birth weight, and primiparity are controversial risk factors. In the last 20 years, the incidence of women aged 30 years and older at delivery has increased from 17.7% to 30.2%.24a Since the inexorable alterations that occur as the degenerative disc cascade proceeds25 will be more prominent as a female ages, it is expected that the probability of pain emanating from degenerative disc disease will be higher in this group. Pain from lumbar degenerative disc disease should be considered in the pregnant and nonpregnant patient alike who complains of back pain, numbness and tingling, or with neurologic findings on examination. A thorough examination is critical to differentiate the symptoms of degenerative disc disease from the radicular pain of a herniated disc from SIJ dysfunction. It is important to note that patients can have SIJ dysfunction concurrently with an S1 radiculopathy. If there is progressive weakness or bowel or bladder incontinence in pregnancy associated with back pain, cauda equina syndrome must be ruled out. Immediate imaging with MRI and surgical referral, even in pregnancy, is warranted.

NEUROLOGIC CAUSES OF BACK PAIN IN PREGNANCY Neurologic sequelae in pregnancy may or may not be related to lumbar pathology. Nerve disorders that occur in the nonpregnant state can occur in pregnancy though they are not well described in the literature. Patients may experience direct nerve trauma or peripheral neuropathy from other disease states such as diabetes. Lateral femoral cutaneous neuropathy, or meralgia parasthetica, is a sensory abnormality of the anterolateral thigh and is the most common nerve injury seen in pregnancy.26 This lesion can be seen in association with a pelvic obliquity (often a left innominate posterior rotation) and consequently in those with concomitant SIJ pain. Hence, early treatment of the pelvic obliquity may influence outcome and improve numbness. Although Wong et al. also described this as the most common immediate postpartum nerve injury, they found low incidences of nerve injuries in general (0.92%) after labor and delivery.27 True sciatic nerve pathology is only seen in 1% of the pregnant population, despite its overuse as a catchall diagnosis for back pain or radiating pain in pregnancy.3 More comprehensive neurologic studies, such as needle electromyography and nerve conduction studies, may need to be done to diagnose a true sciatic nerve lesion versus an S1 radiculopathy or sacroiliac joint pain referred in a neurologic distribution.

CONCOMITANT CONDITIONS Musculoskeletal conditions in pregnancy Hip pathology Osteonecrosis of the hip and transient osteoporosis of pregnancy are two hip conditions that occur in the pregnant state and should be considered in the differential diagnosis. These are relevant to our discussion on back and pelvic pain because they may present with non-specific groin pain, pelvic pain, or low back pain. Osteonecrosis of the hip in pregnancy has not been completely elucidated.5 Cheng postulated that higher adrenocortical activity during pregnancy combined with increased stresses may predispose the pregnant patient to this condition.28 Transient osteoporosis of pregnancy is a rare disorder that occurs typically during the third trimester of pregnancy. Patients typically have hip pain with weight bearing, limited hip range of motion (ROM), and MRI evidence of osteoporosis of the femoral head with preservation of the joint space.29 Early diagnostic imaging is important because persistent weight bearing can lead to stress or occult fracture of the hip or pelvis. 1313

Part 5: Pregnancy

Spondylolisthesis

Core stability examination

Spondylolisthesis is a condition where there is sagittal plane translation or ‘slipping’ of one vertebra on the vertebra below it. This typically occurs when there are bilateral defects in the pars interarticularis, which allows this increase of movement of one vertebra on another. It most commonly occurs with L5 slipping forward on S1. Another form of spondylolisthesis is degenerative in nature and more commonly occurs in women. This form is more likely to occur with the L4 vertebra slipping forward on L5. Saraste, in 1986, found that there was no increase in slippage in women during pregnancy.30 However, Sanderson and Fraser, in 1996, found that women who had children had a higher incidence of spondylolisthesis than women who had never had children.31 In patients with a higher grade of spondylolisthesis, grade III or IV, extra caution should be taken to monitor changes in neurologic examination and increasing back pain in pregnancy.

Testing of core strength is instrumental to overall proper body mechanics. In Akuthota and Nadler’s review of core strengthening in 2004,33 the core is comprised of the diaphragm serving as the roof of the core, the pelvic floor and hip girdle musculature as the floor, the anterior and lateral abdominal musculature including the transversus abdominus and oblique muscles, and the posterior spine stabilizers including the erector spinae and multifidus and gluteals forming the posterior core. The relationship of these muscles is intimate; there is known co-activation of the pelvic floor muscles with transversus abdominus contraction.34 These muscles serve to provide stability to the lumbar spine. In the pregnant state, the growing uterus dictates lengthening of the abdominal musculature, and consequent relative muscle contraction inefficiency. There is an increased demand of the lumbar erector spinae muscles to continually concentrically contract to maintain an erect posture. If the core is weak, this leads to muscle imbalances with compensatory mechanisms which may be contributing to the patient’s pain complaints. Core strength is frequently compromised in the pregnant and postpartum state. Childbirth is directly injurious to the pelvic floor muscles and can create significant transient weakness. Normal pelvic floor muscle strength generally returns within 2 month postpartum.35 Simple tests to evaluation core strength in the pregnant patient include: SUPINE BRIDGING: With the patient laying supine, her hips and knees are flexed and feet are placed flat on the table. Then, the patient lifts her buttocks off the table. Higher-level strength can be assessed by lifting the contralateral leg in a single-leg bridge position. SINGLE-LEG STANCE WITH TRIPLANAR MOTION: Single-leg stance with triplanar reach tests may be an unfair assessment in the pregnant patient due to changes in the center of gravity which naturally compromise balance. Other static core strength tests are more feasible in the pregnant patient as described above. ABDOMINAL MUSCULATURE: Assessment of the integrity of the rectus abdominus is important in the pregnant patient. Diastasis is a common physical finding in pregnancy with increasing growth of the gravid uterus. Although this is typically not a pain generator, a defect anteriorly, especially in conjunction with weakness of pelvic floor muscles, can theoretically lead to muscle imbalance and predispose the pregnant patient to lumbar injury (Fig. 123.1).

EXAMINATION TECHNIQUES Clinical approach When assessing the pregnant patient the physician should attempt to determine the nature, location, duration, precipitating, and alleviating factors of the pain as this may help elucidate the cause. The physical examination is particularly important in the pregnant patient as it is one of the few diagnostic tools safe and available for the physician to use to make a diagnosis. Careful examination of the pregnant patient should be focused on the above-listed differential diagnosis with special emphasis on pelvic alignment and sacroiliac joint examination maneuvers.

Neurologic examination General neurologic examination is imperative in the pregnant patient to evaluate for neurologic disease, specifically to rule out radiculopathy resulting from a herniated nucleus pulposus, lumbosacral plexopathy, or peripheral neuropathy. Neurologic examination should consist of gait examination, lower extremity muscle stretch reflex testing, plantar stimulus response, or evidence of clonus. Strength testing should be done for all muscle groups from the L2 to S1 myotomes including hip flexion, abduction and adduction, knee extension and flexion, ankle dorsiflexion, plantarflexion, eversion and inversion. Sensory examination should be performed in the L1–S5 dermatomes. Dural tension signs are helpful in evaluating for possible nerve entrapment syndromes including the sitting slump test or straight leg raise.

Hip examination Hip range of motion is examined with the patient in supine. The examiner assesses side-to-side differences in range of motion and the patient’s willingness to permit the movement. Pain on any movement is significant. The examiner passively takes the patient’s hip through each movement including flexion (normal 110–120°), hip extension (10–15°), internal (30–40°) and external rotation (40–60°) in neutral and with hip flexion, abduction (30–50°) and adduction (30°) and any restrictions are noted.32

Lumbar spine examination Lumbar spine range of motion is examined with the patient in standing and the examiner sitting behind the patient. The examiner is looking for abnormalities in active range of motion and the patient’s willingness to perform the movement. Pain on any movement is significant. The patient is instructed go through each lumbar range of motion including forward flexion (normal is 40–60°), extension (20–35°), left and right rotation while in extension to elicit any pain, followed by side bending, left and right (15–20°).32 1314

Fig. 123.1 Evaluation of rectus diastasis: place two fingers in the periumbilical region to palpate separation of the rectus abdominus. You may accentuate the separation with an abdominal crunch. Separation is described in centimeters; one centimeter is roughly equivalent to one finger breadth.

Pregnancy

Pelvis and sacroiliac joint examination Physical examination focused on detecting aberrant motion of the SIJ is notoriously unreliable. A study by Dreyfuss et al.36 in 1996 evaluated 12 common testing maneuvers for SIJ pain and found that none of the 12 tests was able to reliably detect SIJ dysfunction in 85 patients. However, this study did not include the pregnant population. Another study by Albert et al.37 in 2000 specifically looked at pregnant patients and found that in patients with sacroiliac joint pain three tests had superior sensitivity: the posterior pelvic pain provocation test, Menell’s test, and FABER test, despite reasonable reliability of several other physical examination maneuvers. In 1994, Laslett concluded that five of seven tests were reliable in predicting the sacroiliac joint as a pain source, and that the remaining two tests were potentially reliable.38 In 2003, Young et al. again validated the significant correlation between clinical examination findings with 3 or more pain provocation tests and SIJ pain.39 In 2003, Laslett et al. further showed that the diagnostic accuracy of the physical examination was superior to sacroiliac joint pain provocation test alone for diagnosing symptomatic SIJ.40 Uniform in all of these studies, intertester reliability is critical. Practice with these tests and performing them consistently each time will help proper diagnosis of sacroiliac joint dysfunction.

Palpation and mobility testing of the sacroiliac joint ALIGNMENT: Iliac crest, PSIS, ASIS: With the patient standing, the examiner notes the heights of both iliac crests and each PSIS. The ASIS may be assessed in standing or supine. If the anterior and posterior iliac spines are at the same level, the pelvis is considered to be in proper alignment. If not, the pelvis is misaligned – either anteriorly rotated, posteriorly rotated or sheered superiorly or inferiorly.37 PALPATION OVER THE SIJ: Positive test is if there is sacral sulcus tenderness immediately medial to the posterior superior iliac spine.36 Palpation in this area approximates the sacroiliac joint line. GILLET’S TEST: The examiner has the patient stand with his or her feet 12 inches apart, while the examiner sits behind the patient and palpates the bilateral posterior superior iliac spines. The patient then flexes the knee and hip on the side to be tested (Fig. 123.2). ‘Stand on one leg and bring the other leg to your chest,’ is often the direction given. The test should show movement of the PSIS inferiorly or a ‘drop’ of the PSIS is seen on the ipsilateral side of the lifted leg. If there is no drop, the test is positive for hypomobility on that side, but is not correlated to the side of pain.36 PALPATION OF PUBIC SYMPHYSIS: With the patient lying supine, the pubic symphysis is palpated gently. If palpation causes pain, that is a positive sign for pubic symphysis tenderness.37

Fig. 123.2 Gillet’s test to assess left SIJ motion.

GAENSLEN’S TEST: With the patient lying supine and on the edge of the examination table, one hip and knee are flexed and held by the patient, while the other hip is extended off the side of the table. Overpressure exerted on the extended knee is applied to force the

Provocative testing of the sacroiliac joint FABERS TEST: With the patient lying supine, the patient’s hip is Flexed, ABducted and Externally Rotated so that the heel rests on the opposite kneecap. Pain may be experienced in the inguinal region, which suggests hip joint pathology. Pain may also be experienced in the back or SIJ, suggesting SIJ dysfunction.37 This test is also known as the figure-4 test and Patrick’s maneuver. FORCED FABER’S TEST: This is another maneuver more specific for SIJ pathology. With the patient in the same position as above, anterior to posterior force is placed on both the externally rotated leg at the knee and on the opposite ASIS (Fig. 123.3). This test is positive with production of pain in the SIJ.32

Fig. 123.3 Faber’s maneuver to test right-sided SIJ dysfunction.

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sacroiliac joint to its end range.38 This test can be performed in the side-lying position with the patient holding the lower leg flexed against the chest while the uppermost leg is extended.32 MENELL’S TEST: With the patient lying supine, one hip is moved into 30° abduction and 10° flexion. It is then first pushed into, then pulled out from the pelvis causing sagittal movement. Pain is considered positive for this test.37 POSTERIOR PELVIC PAIN PROVOCATION TEST (OR AP GLIDE): With the patient lying supine, the hip is flexed to be perpendicular with the table at 90° and the knee is flexed at 90°. A gentle force is applied to the femur in the direction of the examination table, from anterior to posterior (Fig. 123.4). The test is positive when the patient experiences pain in the gluteal region of the tested leg.37,41 ACTIVE STRAIGHT LEG RAISE (ASLR) TEST: This test is performed with the patient supine with both legs extended on the table. The patient raises one leg at a time to 30° of hip flexion without flexing the knee. The test is considered positive when the patient has pain in the back with the leg raised, or describes a heaviness or difficulty in performing the task.42,43 In the second part of the maneuver, posterior compression is applied and the patient is then asked to actively perform a straight leg raise (Fig. 123.5). If there is less pain upon compression or greater ease in motion this is considered a positive provocative test. COMPRESSION TEST: With the patient supine, pressure is placed on both sides of the pelvis at the ASIS with force applied inward by the palms of the examiner’s hands.38

Fig. 123.5 Active straight leg raise with compression to test right-sided SIJ dysfunction.

Although there is no literature describing its use as an aid in examination, the use of an SIJ belt may be helpful. Similar to the compression test described above, the SIJ belt can be applied to provide a compressive force about the pelvis. The ASLR is then repeated to see if the patient’s pain is reduced. If these tests are positive, it suggests the SIJ may be the putative pain generator. This will then help guide prescription and application of an SIJ belt in treatment of SIJ pain.

Pelvic floor and coccyx examination

Fig. 123.4 Posterior pelvic provocation test (AP glide) to test right-sided SI joint dysfunction. 1316

A vaginal manual examination of the pelvic floor musculature is not recommended in the pregnant patient as this may potentially induce contractions or introduce infection in the region of the cervix. However, rectal examination to evaluate the coccyx and pelvic floor is an option.44 The examination can be done using several techniques reviewed in detail in an article by Maigne.45 Most commonly, the examination is performed with the patient in the side-lying position. A finger is inserted into the rectum and the coccyx can be palpated by gradually pushing the finger posteriorly until contact is made with the coccyx. This technique allows for simultaneous palpation of the pelvic floor because the coccyx is the anatomical insertion for most of these muscles, including the iliococcygeus, pubococcygeus, and coccygeus. Palpation of the coccyx can be performed in this manner and any pain elicited with palpation or mobility is noted. Mobilization of the coccyx using Mennell’s technique46 can be performed by grasping the coccyx between the external thumb and the internal index finger while flexion, extension, and rotation are applied to the coccyx. The intrarectal finger can be used to palpate the pelvic floor musculature. In the nonpregnant patient, pelvic muscle assessment is done using a one-finger technique both vaginally and rectally. This should be considered, especially in the postpartum patient with persistent pain at the sacral sulci. Pelvic floor muscle tone, strength, conditioning, coordination, tender/trigger points, anatomic deficits such as prolapse, and pelvic descent are evaluated. Tightness, tenderness, and the presence of trigger points are evaluated at the 12, 3, 6, and 9 o’clock positions. By convention, the 12 o’clock position is at the underside of the pubic symphysis and 6 o’clock represents the posterior coccyx. General contractile strength is evaluated, including 10-second isometric holds to evaluate endurance slow-twitch muscle fibers and ‘quick flicks’ to evaluate fast-twitch muscle fibers.47 The obturator

Pregnancy Low back pain (LBP) in pregnancy

Absent reflex + Slump sit + Flexion based LBP +/– SI joint provocative tests

+ AP glide + Pelvic obliquity + Fabers with posterior pain + ASLR

Rule out lumbar disc pathology

LBP wth radiation No neurologic findings

SI joint referred pain or Pelvic obliquity with pubic symphysis dysfunction

Sl joint dysfunction

+ Fabers with anterior pain Pain with hopping or weight bear Pain with hip ROM

Rule out transient osteoporosis of pregnancy, pelvic fracture or hip avascular necrosis

Physical therapy SI joint belt

Physical therapy

If no better or progressive neurologic change: MRI

If not improving

MRI pelvis R/o stress/ insufficiency fracture

FUTURE U/S guided SI joint injections

Pelvic floor myofascial pain or dysfunction

Fig. 123.6 Algorithm for low back pain in pregnancy.

internus can also be palpated by internal examination and is activated with hip external rotation. As the patient’s knee presses against the examiner’s external hand, the internal hand can appreciate ipsilateral obturator internus muscle contraction.

DIAGNOSTIC WORK-UP In 1997, the National Council on Radiation Protection and Measurements (NCRP) evaluated the effects of all types of radiation on reproduction. Many articles were presented which discussed the effects of irradiation on the developing fetus, including congenital malformation, growth retardation, pregnancy loss, and mental retardation.48,49 Although there is argument over the amount of irradiation that would produce such effects, it is generally thought that avoidance of such exposures for the pregnant patient is the rule. However, the failure to correctly diagnose maternal medical problems may pose a much greater risk to the fetus. One paper proposed guidelines for single radiographic image of the abdomen or pelvis with the fetus in field of view as well as estimated fetal dose for CT of the abdomen or pelvis with the fetus in field of view.50 Despite these guidelines, practitioners generally associate exposure to roentgenograms or abdominal CT with high risks to the developing fetus.51 Ultrasound, on the other hand, has been used clinically as an effective diagnostic tool in pregnancy for many years. To date, there is no documented evidence of fetal harm from ultrasound.51 Technological advances have significantly improved, intra-abdominal, intrapelvic and fetal assessments, but because sonography cannot penetrate bone, intra-osseous, epidural, intrathecal and discogenic disease cannot be adequately evaluated. It is limited in its ability to diagnose more sinister etiologies of back or pelvic pain in pregnancy.

Magnetic resonance imaging does not use any ionizing radiation and therefore is thought to be safe for use in the pregnant patient. Until recently, MRI in the pregnant patient was used in the evaluation of adnexal masses, pelvimetry, hydroureteronephrosis of pregnancy, and placenta accreta and to evaluate fetal anomalies such as arachnoid cysts and ventriculomegaly.53 Fast MRI has essentially done away with the need for sedation of the mother and fetus to prevent fetal movement artifact.54 Fast MRI taken during suspension of maternal breathing removes this artifact and results in excellent images with high resolution.55 Gadolinium is not recommended during pregnancy because of its ability to cross the placental barrier and potentially cause harm to the fetus.55 Although MRI appears safe in pregnancy, the International Radiation Protection Association takes the position that MRI should be postponed until after the first trimester and should be limited to cases where unique diagnostic information can be obtained.55 Fast MRI has expanded its usefulness to evaluate and diagnose nonpregnancy-related conditions in the pregnant patient such as lumbar disc herniations and pelvic stress fractures. It can also be used in patients with both posterior and anterior pelvic pain postpartum. One study demonstrated increased T- weighted signal change consistent with edema of the pelvic joints in those with pain.56 Ultrasound would seem to be an excellent tool to use diagnostically to evaluate the SIJ in the pregnant patient; however, there are no published studies to date. SIJ injections have been used as a diagnostic tool for potential sacroiliac joint-mediated pain. There is literature suggesting a low success rate of blindly placing medications intra-articularly within the sacroiliac joints.57 In contrast, there is evidence that medications can be successfully placed within the SIJ using CT guidance58 or fluoroscopic guidance.59 It has been shown that sacroiliac joint injections are 1317

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clinically effective for the diagnosis and treatment of SIJ syndrome. Because the pregnant population should not undergo fluoroscopy or CT, Pekkafal, in 2003, studied SIJ injections performed under sonographic guidance.60 Of the 60 sonographically guided SIJ injections they performed, 76% were successfully placed intra-articularly and 23% were missed. More importantly, the last 30 injections that were performed had a success rate of 94%, suggesting a significant training effect. Although these were not performed specifically in the pregnant population, the use of ultrasound during pregnancy is known to be safe and the obvious utility of this intervention is important. Future studies should be aimed at the use of ultrasound guided intraarticular SIJ injections for both the diagnosis and treatment of SIJ dysfunction in the pregnant women. Needle electromyography and nerve conduction studies can be used in pregnancy for evaluation of a radiculopathy. There are no data that such testing is contraindicated in pregnancy.

CONCLUSIONS Disabling back pain in the pregnant patient warrants meticulous and detailed physical examination and appropriate diagnostic workup in light of limited radiographic options. Differential diagnoses include disorders commonly seen in the nonpregnant population with an emphasis on pelvic obliquity and associated SIJ dysfunction. Subsequent therapeutic options are based on comprehensive assessment (Fig. 123.6). Low back pain in pregnancy is manageable and treatable if a proper and timely diagnosis is reached.

References 1. Johnson D, Coley S. Back pain in pregnancy. J R Soc Med 1998; 91(6):344. 2. Ireland ML, Ott SM. The effects of pregnancy on the musculoskeletal system. Clin Orthop 2000; 372:169–179. 3. Kristiansson P, Svardsudd K, et al. Back pain during pregnancy: a prospective study. Spine 1996;21(6):702–709. 4. Heckman JD, Sassard R. Musculoskeletal considerations in pregnancy. J Bone Joint Surg [Am] 1994; 76(11):1720–1730.

17a. Polatti F, Capuzzo E, Viazzo F et al. Bone mineral changes during and after lactation. Obstet Gynecol 1999; 94(1):52–56. 18. Thienpont E, Simon JP, et al. Sacral stress fracture during pregnancy – a case report. Acta Orthop Scand 1999; 70(5):525–526. 19. Rousiere M, Kahan A, et al. Postpartal sacral fracture without osteoporosis. Joint Bone Spine 2001; 68(1):71–73. 19a. Parrish KM, Holt VL, Easterling TR et al. Effect of changes in maternal age, parity, and birth weight distribution on primary cesarean delivery rates. JAMA 1994; 271(6):443–447. 20. Bjorklund K, Bergstrom S, et al. Symphyseal distention in relation to serum relaxin levels and pelvic pain in pregnancy. Acta Obstet Gynecol Scand 2000; 79(4):269–275. 21. Schoellner C, Szoke N, et al. [Pregnancy-associated symphysis damage from the orthopedic viewpoint – studies of changes of the pubic symphysis in pregnancy, labor and post partum]. Z Orthop Ihre Grenzgeb 2001; 139(5):458–462. 22. Lentz SS. Osteitis pubis: a review. Obstet Gynecol Surv 1995; 50(4):310–315. 23. Wiltse LL, Frantz CH. Non-suppurative osteitis pubis in the female. J Bone Joint Surg [Am] 1956; 38A(3):500–516. 24. LaBan MM, Perrin JC, et al. Pregnancy and the herniated lumbar disc. Arch Phys Med Rehabil 1983; 64(7):319–321. 24a. Schmid L. Pfirrman C, Hess T, et al. Bilateral fracture of the sacrum associated with pregnancy: a case report Osteoporosis International 1999; 101(1): 91–93. 25. Kirkaldy-Willis WH, Wedge JH, et al. Pathology and pathogenesis of lumbar spondylosis and stenosis. Spine 1978; 3(4):319–328. 26. Aminoff MJ. Neurological disorders and pregnancy. Am J Obstet Gynecol 1978; 132(3):325–335. 27. Wong CA, Scavone BM, et al. Incidence of postpartum lumbosacral spine and lower extremity nerve injuries. Obstet Gynecol 2003; 101(2):279–288. 28. Cheng N, Burssens A, et al. Pregnancy and post-pregnancy avascular necrosis of the femoral head. Arch Orthop Trauma Surg 1982; 100(3):199–210. 29. Beaulieu JG, Razzano CD, et al. Transient osteoporosis of the hip in pregnancy. Clin Orthop 1976; 115:165–168. 30. Saraste H. Spondylolysis and pregnancy – a risk analysis. Acta Obstet Gynecol Scand 1986; 65(7):727–729. 31. Sanderson PL, Fraser RD. The influence of pregnancy on the development of degenerative spondylolisthesis. J Bone Joint Surg [Br] 1996; 78(6):951–954. 32. Magee D. Orthopedic physical assessment. Philadelphia, PE: WB Saunders; 2002.

5. Ritchie JR. Orthopedic considerations during pregnancy. Clin Obstet Gynecol 2003; 46(2):456–466.

33. Akuthota V, Nadler SF. Core strengthening. Arch Phys Med Rehabil 2004; 85(3 Suppl 1):S86–S92.

6. MacEvilly M, Buggy D. Back pain and pregnancy: a review. Pain 1996; 64(3):405–414.

34. Sapsford RR, Hodges PW, et al. Co-activation of the abdominal and pelvic floor muscles during voluntary exercises. Neurourol Urodyn 2001; 20(1):31–42.

7. Orvieto R, Achiron A, et al. Low-back pain of pregnancy. Acta Obstet Gynecol Scand 1994; 73(3):209–214. 8. Damen L, Buyruk HM, et al. Pelvic pain during pregnancy is associated with asymmetric laxity of the sacroiliac joints. Acta Obstet Gynecol Scand 2001; 80(11):1019–1024. 9. Damen L, Buyruk HM, et al. The prognostic value of asymmetric laxity of the sacroiliac joints in pregnancy-related pelvic pain. Spine 2002; 27(24):2820–2824. 10. Damen L, Stijnen T, et al. Reliability of sacroiliac joint laxity measurement with Doppler imaging of vibrations. Ultrasound Med Biol 2002; 28 (4):407–414. 11. Isascs E, Mark B. Bourdillon’s spinal manipulation. 6th edn. Boston, Butterworth Heinemann 2002. 12. Sturesson B, Selvik G, et al. Movements of the sacroiliac joints. A roentgen stereophotogrammetric analysis. Spine 1989;14(2):162–165.

35. Peschers UM, Schaer GN, et al. Levator ani function before and after childbirth. Br J Obstet Gynaecol 1997; 104(9):1004–1008. 36. Dreyfuss P, Michaelsen M, et al. The value of medical history and physical examination in diagnosing sacroiliac joint pain. Spine 1996; 21(22):2594–2602. 37. Albert H, Godskesen M, et al. Evaluation of clinical tests used in classification procedures in pregnancy-related pelvic joint pain. Eur Spine J 2000; 9(2):161–166. 38. Laslett M, Williams M. The reliability of selected pain provocation tests for sacroiliac joint pathology. Spine 1994; 19(11):1243–1249. 39. Young S, Aprill C, et al. Correlation of clinical examination characteristics with three sources of chronic low back pain. Spine J 2003; 3(6):460–465.

13. Schwarzer AC, Aprill CN, et al. The sacroiliac joint in chronic low back pain. Spine 1995; 20(1):31–7.

40.Laslett M, Young SB, et al. Diagnosing painful sacroiliac joints: A validity study of a McKenzie evaluation and sacroiliac provocation tests. Aust J Physiother 2003; 49(2): 89–97.

14. MacLennan AH. The role of the hormone relaxin in human reproduction and pelvic girdle relaxation. Scand J Rheumatol Suppl 1991; 88:7–15.

41. Ostgaard HC, Zetherstrom G, et al. The posterior pelvic pain provocation test in pregnant women. Eur Spine J 1994; 3(5):258–260.

15. Ostgaard HC, Andersson GB, et al. Prevalence of back pain in pregnancy. Spine 1991; 16(5):549–552.

42. Mens JM, Vleeming A, et al. The active straight leg raising test and mobility of the pelvic joints. Eur Spine J 1999; 8(6):468–473.

15a. Friden J. Muscular pain after physical training [Swedish]. Lakartidningen. 1984, 81(18):1825–1826.

43. Mens JM, Vleeming A, et al. Validity of the active straight leg raise test for measuring disease severity in patients with posterior pelvic pain after pregnancy. Spine 2002; 27(2):196–200.

15b. Friden J. Changes in human skeletal muscle induced by long-term eccentric exercise. Cell & Tissue Research 1984; 236(2):365–372. 15c. Friden J, Lieber RL. Structural and mechanical basis of exercise-induced muscle injury. Medicine & Science in Sports and Exercise. 1992; 24(5):521–530. 16. Maigne JY, Doursounian L, et al. Causes and mechanisms of common coccydynia: role of body mass index and coccygeal trauma. Spine 2000; 25(23):3072–3079.

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17. Nattiv A. Stress fractures and bone health in track and field athletes. J Sci Med Sport 2000; 3(3):268–279.

44. Thiele G. Coccydynia and pain in the superior gluteal region. JAMA 1937; 109:1271–1275. 45. Maigne JY, Chatellier G. Comparison of three manual coccydynia treatments: a pilot study. Spine 2001; 26(20):E479–E483; discussion E484. 46. Mennell J. The science and art of joint manipulation. London: Churchill; 1952.

Pregnancy 47. Theofrastous JP, Swift SE. The clinical evaluation of pelvic floor dysfunction. Obstet Gynecol Clin North Am 1998;25(4):783–804.

54. Nagayama M, Watanabe Y, et al. Fast MR imaging in obstetrics. Radiographics 2002; 22(3): 563–580; discussion 580–582.

48. Brent RL. Utilization of developmental basic science principles in the evaluation of reproductive risks from pre- and postconception environmental radiation exposures. Teratology 1999; 59(4):182–204.

55. Amin RS, Nikolaidis P, et al. Normal anatomy of the fetus at MR imaging. Radiographics 1999; 19 Spec No:S201–S214.

49. Schull WJ, Otake M. Cognitive function and prenatal exposure to ionizing radiation. Teratology 1999; 59(4):222–226. 50. El-Khoury GY, Madsen MT, et al. A new pregnancy policy for a new era. Am J Roentgenol . 2003; 181(2):335–340. 51. Ratnapalan S, Bona N, et al. Physicians’ perceptions of teratogenic risk associated with radiography and CT during early pregnancy. Am J Roentgenol 2004; 182(5):1107–1109. 52. Ziskin MC. Intrauterine effects of ultrasound: human epidemiology. Teratology 1999; 59(4):252–260. 53. Levine D, Barnes PD, et al. Obstetric MR imaging. Radiology 1999; 211(3): 609–617.

56. Wurdinger S, Humbsch K, et al. MRI of the pelvic ring joints postpartum: normal and pathological findings. J Magn Reson Imaging 2002; 15(3):324–329. 57. Rosenberg JM, Quint TJ, et al. Computerized tomographic localization of clinically guided sacroiliac joint injections. Clin J Pain 2000; 16(1):18–21. 58. Pulisetti D, Ebraheim NA. CT-guided sacroiliac joint injections. J Spinal Disord 1999; 12(4):310–312. 59. Slipman CW, Lipetz JS, et al. Fluoroscopically guided therapeutic sacroiliac joint injections for sacroiliac joint syndrome. Am J Phys Med Rehabil 2001; 80(6): 425–432. 60. Pekkafahli MZ, Kiralp MZ, et al. Sacroiliac joint injections performed with sonographic guidance. J Ultrasound Med 2003; 22(6):553–559.

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CHAPTER

124

PREGNANCY

Treatment of Low Back Pain in Pregnancy – Special Considerations Adriana S. Prawak, Brinda S. Kantha and Larry H. Chou

INTRODUCTION The occurrence of back pain in pregnancy ranges from 42% to 81%.1–7 In retrospective studies among young and middle-aged women with chronic low back pain, 10–25% reported the first episode of back pain during pregnancy.8,9 It is therefore important that effective treatment be pursued. Back pain during pregnancy is variable but can be classified into low back pain (LBP) or posterior pelvic pain (PPP). Differentiating between these two may be difficult. Low back pain is pain in the lumbar region with or without radiation to the legs whereas posterior pelvic pain is in the sacroiliac (SI) region with or without radiation into the thighs.10 Treatments for both types of pain include patient education, exercise, modalities, orthoses, medications, alternative treatments such as acupuncture, manipulation, massage, injections, and lastly, surgery. Close monitoring by, or contact with, the obstetrician is essential for appropriate medical management. No longer should bed rest be prescribed since it has been shown to make no difference in decreasing pain, but increases sick leave and disability in low back pain patients.11 Exercise as well as activity in patients with low back pain, in contrast, has been shown to decrease pain and improve function.10

EDUCATION Patients who are provided with individual back care education that reviews anatomy and prognosis of back pain have a reduction in symptoms and sick leave time4,12,13 Several authors have also recommended additional guidance, including orthoses (such as a customized lumbar corset), use of a lumbar roll while sitting and Ozzlo pillow while lying, maintenance of proper upright posture, frequent rests when symptoms increase, changing of positions frequently, use of stress management techniques, training in work and home ergonomics, and a self-directed home exercise program. These recommendations have generally been found to reduce back pain and improve activities of daily living.4,12,14,15 Activities that should be avoided are also part of the education. These activities include high-impact, weight-bearing movements that asymmetrically load the body (such as twisting and lifting, single-leg stance postures, climbing stairs) and frequent motions at the endrange of low back and hip motions.

EXERCISE General principles Pregnant females should always consult with their physicians before making any decisions regarding participating in an exercise program. Although this disclaimer is frequently stated, many spine physicians

are not well versed in the pregnancy and exercise literature. Women who regularly exercised before pregnancy were found to have a decreased risk of pregnancy-related back pain.4 Exercise during pregnancy can have a protective effect and does not appear to be detrimental to the unborn child.16 Those females who exercise do not have shorter or easier labors but it may enable them to tolerate it better. Exercise may help prevent as well as treat gestational diabetes since the utilization of large muscle groups improves insulin sensitivity.17 A major concern with exercise is fetal injury, which may potentially occur during the second and third trimester. It is therefore recommended that sports with a high risk of collision and contact sports be avoided. Fetal heart rate may increase during maternal exercise between 10 and 30 beats per minute; however, the clinical significance is unknown. Tachycardia may be due to hypoxia; however, blood flow to the uterus during exercise is maximal at its attachment to the placenta, thereby minimizing any potential hypoxic effects.18 There is a small decrease in the average birth weight of babies born to women who exercised intensively during pregnancy, yet there are no reported cases of adverse outcome in pregnancy. No cases of premature labor due to maternal exercise have been reported. Hyperthermia is also a concern since it has been shown to possibly cause neural tube defects in animals, though not in humans. Since the neural tube closes approximately 25 days after conception, hyperthermia should be avoided in pregnant females during the first few weeks of pregnancy. Since only minimal increases in core temperatures occur with moderate levels of exercise under normal environmental conditions, this level of activity should be safe in the pregnant female.19 Risks to the pregnant woman include an increase in musculoskeletal injuries such as low back pain and hypotension, which can occur as a result of lying in the supine position or with prolonged standing. Contraindications for exercise in pregnant females are as listed in Table 124.1. If the pregnant woman was exercising before pregnancy, barring any pregnancy-related abnormalities or complications, she can safely continue without increasing complication risks to the unborn fetus. There is, however, a tendency for the mother to gain less weight and deliver smaller babies than sedentary women.21 She should be prepared to modify the intensity and duration of her regimen if she experiences severe discomfort and as the pregnancy progresses, usually around the sixth month. Sedentary pregnant women should not initiate high-intensity exercise programs, yet moderate exercise should be encouraged. As pregnancy progresses into the third trimester the adverse effects of supine exercises need to be taken into consideration.22 The Sports Medicine Australia position statement indicates that moderate exercise for pregnant females is safe. It also indicates that studies have shown that it may be possible for trained athletes to exercise at a higher level than is recommended by the American

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Table 124.1: Contraindications to exercise in pregnant females ABSOLUTE CONTRAINDICATIONS MATERNAL RELATED Congestive heart failure Active myocardial disease Rheumatic heart disease Active infectious disease Thrombophlebitis Recent pulmonary embolism Restrictive lung disease Severe hypertensive disease PREGNANCY RELATED No prenatal care Persistent uterine bleeding Ruptured membranes Placenta previa after 26 weeks of gestation Preeclampsia/pregnancy-related hypertension Intrauterine growth retardation Suspected fetal distress Severe isoimmunization Any risk for premature labor Incompetent cervix/cerclage Multiple gestations RELATIVE CONTRAINDICATIONS MATERNAL RELATED Severe anemia Unevaluated maternal cardiac arrhythmia Chronic bronchitis Poorly controlled seizure disorder Poorly controlled hyperthyroidism Poorly controlled hypertension Poorly controlled diabetes mellitus Heavy smoker Essential hypertension Thyroid disease Blood disorders Sedentary lifestyle Excessive obesity or underweight PREGNANCY RELATED Breech presentation in last trimester Adapted from American College of Obstetricians and Gynecologists committee opinion, Exercise During Pregnancy and the Postpartum Period.20

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College of Obstetricians and Gynecologist. No adverse effects have been seen with resistance training with moderate weights and submaximal isometric contractions in pregnant women.23 There are general guidelines published by the American College of Obstetricians and Gynecologists and the American College of Sports Medicine for exercise in pregnancy.20,24 Some highlights are listed below: 1. Thirty or more minutes of moderate exercise a day most days of the week, if not all, is safe unless contraindicated or advised by the physician. 2. Sports that include direct contact, trauma, or risk of falling are to be avoided, such as most court sports and downhill skiing. 3. Scuba diving should be avoided for the duration of the pregnancy due to the risk to the fetus of decompression sickness, since the fetal pulmonary circulation is unable to filter bubble formation.25 4. Exertion at altitudes below 6000 feet appears to be safe; however, above 10 000 feet the risks significantly increase.26 5. Supine activities are to be avoided after the third or fourth month of gestation, as well as prolonged motionless standing, due to potential venous return obstruction and subsequent decreased cardiac output.20,27

Prevention of back pain Patients who regularly exercised before pregnancy are less likely to develop low back pain during pregnancy.16 In a study by Mantle et al.,3 there was no evidence linking backache during pregnancy with height, weight, obesity index, weight gain, or the baby’s weight. There were differences, however, between LBP in pregnancy and ‘mechanical’ LBP in the nonpregnant patient. This finding is consistent with Kristiansson.28 Pregnant patients attending antenatal physical therapy had slightly less LBP reported, but no clear evidence of a protective effect was established. Smoking, however, has been shown not only to be detrimental to fetal growth, but in the nonpregnant population it has been correlated with disc herniation and the severity of low back pain.29 Weight and weight gain were not associated with LBP in pregnancy. Focusing on weight loss or minimizing weight gain is not likely to be beneficial at preventing or treating back pain.3,30 A prospective study has shown that the functional pattern of back extensors is related and can predict future back pain, including in pregnancy. Dysfunction in the relaxation of the lumbar extensors was directly related to current and future pain levels, and back muscle activity level was inversely related to disability.30

Strength and resistance training According to the American College of Sports Medicine’s guidelines, an exercise program for pregnant females is somewhat unique in that stretching is recommended only to relieve muscle soreness and not to lengthen muscle because of concern with overstretching connective tissue.24 Relaxin is a polypeptide hormone secreted by the corpora lutea of mammalian species during pregnancy. It is thought to facilitate the birth process by remodeling pelvic connective tissue via softening and lengthening of the pubic symphysis and cervix during pregnancy. Kristiannson et al. noted that there was an increase in serum relaxin levels that occurred, with peak value at the twelfth week followed by decline until the seventeenth week. Thereafter, it remained stable around 50% of peak value. By 3 months postpartum, serum relaxin was no longer detectable. They noted that there was a strong correlation between mean serum relaxin levels during pregnancy and symphyseal or low back pain during late pregnancy by medical history or pain provocation tests. Although this information

Pregnancy

is very interesting, it is currently not only impossible to determine the exact role of relaxin, but it is currently unalterable.31 Chan et al. found that soft tissue laxity may be more important as a cause of low back pain than disc prolapse or bulge in pregnancy.32 Before the hazards of radiation to the unborn fetus were known, earlier anatomical studies showed an increase in amount of articular fluid within the sacroiliac joint. This was thought to decrease friction and increase stability of the SI joints.33–35 In 2001, Damen et al. found that SI joint laxity was not associated with pregnancy-related pelvic pain since laxity was found in all pregnant women. The patients who experienced symptoms of PPP had an asymmetric laxity of the SI joints.36 Treatment recommendations including a nonelastic sacroiliac joint belt,4,37 as well as strengthening the muscles that stabilize the SI joint,38 are discussed in more detail below. Kristiansson et al. found that a provocative examination may be more useful than history and range of motion testing in identifying back pain in pregnancy. Since low back pain in pregnancy seems to have several pain generators because of the involvement of numerous ligaments forming a functional unit, this may have therapeutic implications.28 Mens et al. showed less LBP and pelvic pain following cesarean section. Other risks with a positive correlation for LBP and PPP include: twin pregnancy, first pregnancy, higher maternal age, and larger weight of the baby, forceps or vacuum extraction, and fundus expression, prolapse, and flexed position of woman during childbirth. They hypothesized that peripartum pelvic pain is caused by strain of ligaments in the pelvis and lower lumbar spine due to combination of new or previous ligamentous injury, hormonal effects, muscle weakness, and weight of the fetus. Of all the predisposing factors, only muscle weakness and parturition position can be adequately addressed.39 Franklin and Conner-Kerr took measurements in 12 pregnant females in the first and third trimesters and showed that there was a significant increase in low back pain and hyperlordotic posture; however, there was no correlation between magnitude of change in posture and low back pain. There was no conclusive evidence that postural changes leads to increased LBP. It may call into question the appropriateness for posture-correcting exercises in pregnancy.40 In a study by Foti et al., a gait analysis was done on 15 pregnant women whose gait remained relatively unchanged throughout pregnancy, with no evidence of the ‘waddling gait.’ The maximum anterior pelvic tilt increased a mean of 4 degrees during gait, but there was a wide variability noted in test subjects. Significant increases in hip and ankle gait parameters resulted in increased demands placed on hip abductors, hip extensor, and ankle plantarflexor muscles during pregnancy. Perhaps strengthening these muscle groups should be emphasized. It should be emphasized that this study was not done on pregnant females with low back pain.41 As well, Ostgaard et al. concluded that biomechanical factors, such as abdominal sagittal diameter, transverse diameter, and depth of lumbar lordosis, could not alone explain back pain in pregnancy.42 When the sacroiliac joint is thought to be the cause of back pain in pregnancy, using an SI joint belt (see below) and addressing the surrounding musculature may be helpful. The strengthening of muscles that create a force that is perpendicular to the SI joint and surrounding muscles, such as the internal and external abdominal obliques, the latissimus dorsi, multifidus (part of the erector spinae) and the gluteus maximus, could stabilize the SI joint via force closure.43–45 Mens et al. studied persistent pelvic pain after delivery. Although 63.6% of patients noted improvement after 8 weeks of treatment, they found no difference in outcomes between the experimental group and both control groups. Participants in all three groups received an information video describing causes of peripartum pelvic pain, prognosis, and treatments in addition to recommendations on

activity modifications and instructions on the use of a pelvic belt. The treatment group received additional nonindividualized training of the external and internal abdominal oblique and gluteus maximus muscles, while one control group was taught strengthening exercises for the rectus abdominus, the longitudinal components of the erector spinae, and the quadratus lumborum. The other control group did no exercises. Twenty-five percent of the treatment group developed increased fatigue and pain when strengthening the hip extensors and had to cease training. The development of pain and the training cessation may have offset any benefit that they might have otherwise appreciated.38 The goal of exercise is not always to strengthen the surrounding musculature around the sacroiliac joint. Mooney et al. found symptomatic patients with SI joint pain had electromyographic evidence of hyperactivity in the ipsilateral gluteus maximus and contralateral latissimus dorsi. When those patients underwent a rotary strengthening exercise program, there was not only improvement in strength and myoelectric activity but also a decrease in pain.43 Vleeming and colleagues reported tension not only in the gluteus maximus but also in the hamstring muscles further decreases the mobility of the SI joint.37 The abdominal muscles are weakened during pregnancy. Fast and colleagues found that 16.6% of pregnant women had difficulty performing a single sit-up whereas all nonpregnant women could do a single sit-up. Although the abdominal muscles become insufficient during pregnancy, there is no statistically significant correlation with abdominal muscle weakness, specifically sit-up performance, and occurrence of LBP.46,47 In a cross-sectional analysis by Mens et al. performed in patients with posterior pelvic pain after pregnancy (PPPP) it was concluded that hip adduction strength can be used to measure disease severity. The apparent decrease in strength, however, appeared to be caused by the inability to activate the hip muscles rather than by true neurologic weakness.48 Therefore, correcting the muscle inhibition would, in theory, decrease PPPP. Another exercise that could potentially decrease back pain is the ‘sitting pelvic tilt exercise.’ In a prospective, randomized, single-blinded study evaluating primigravidas treated during the last trimester, it was found that the ‘sitting pelvic tilt exercise’ could decrease back pain without complications to the mother or unborn child.49

Aquatic therapy Water therapy is used to aid in the treatment of many musculoskeletal disorders. In a prospective, randomized, controlled trial of pregnant women, with 129 patients treated with water gymnastics in the second half of pregnancy and 129 patients in the control group, water gymnastics was found to reduce the intensity of LBP and number of days on sick leave. Back pain invariably increased with pregnancy, but there was no excess risk of LBP, or urinary or vaginal infections in the water gymnastics group, indicating this method of treatment is safe in pregnancy. The water temperature ranged 32–34°C, and the program consisted of exercises recommended by the Swedish Swimming Society performed 17–20 times (once a week during the second half of the pregnancy). The duration of the class was one hour: 30 minutes of physical training and 30 minutes of relaxation.50

Self-directed versus formal physical therapy Should the patient undergo a formal physical therapy treatment program or simply receive instructions and/or perform exercises on an individual basis? Noren et al. compared the effects of an individualbased education and training program to no treatment in pregnant females who had peripartum pelvic pain. They found that the intervention group had a decrease in sick leave in comparison to the no 1323

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treatment group.12 In another study, Mantle et al. noted that when back care advice (as used in low back pain schools) was given to primiparous women as early as possible, patients experienced significantly less ‘troublesome and severe backache’ than the control group, who were not advised.51 In a randomized trial, Ostgaard et al. evaluated 407 pregnant patients.4 Sick leave was reduced in patients who had undergone an individualized program that consisted of back school education and training program, whereas the control group participants did not fair as well.

Summary Stuge et al. performed a systemic review of prospective, controlled clinical trials assessing the effectiveness of physical therapy interventions for the prevention and treatment of pregnancy-related back and pelvic pain. Three high-quality studies were found. Two showed no difference in pain intensity and functional status between the exercise and control groups. The third study found a significant reduction in sick leave in patients participating in water gymnastics compared to the control group. Strong evidence supporting the effectiveness of physical therapy in preventing and treating pregnancy-related back and pelvic pain is lacking.52

MODALITIES Modalities can provide patients autonomous management of fluctuating painful symptoms. Such modalities normally include the use of hot and cold packs, ultrasound, and transcutaneous electrical nerve stimulations (TENS). The use of these modalities is modified, and sometimes contraindicated, in pregnant women. Although there is no significant literature on the use of heat or ice for analgesia in the pregnant patient, these options are widely available and easily utilized. They may be safe when used appropriately and cautiously in the forms of warm and cold packs placed over the low back. In the nonpregnant patient, therapeutic ultrasound is a common modality used during physical therapy. However, this option is not recommended in a gravid patient over or near the fetus since cavitation in the amniotic fluid could harm the fetus.10 TENS use during labor seems to be safe53 but evidence for improvements in pain is weak.54 A randomized clinical trial performed by van der Ploeg et al.55 reveals that TENS does not appear to decrease the intensity of pain or preclude the use of other forms of analgesia during labor. Similar results were seen in a study by Labrecque et al. of 34 patients during labor with the use of TENS to mitigate intensity of back pain.56 Analgesic TENS used over the abdomen during pregnancy is not recommended by the FDA owing to a lack of safety data.10 In general, the use of modalities in treatment of pain is targeted toward temporary symptomatic relief and should be included as part of a comprehensive treatment regimen.

ORTHOSES Lumbosacral binder Maternal weight gain and an enlarging uterus changes the center of gravity for the pregnant woman, causing subtle changes in posture and gait that can lead to muscle fatigue and strain on weight-bearing joints.41 The use of maternity support binders could offer a safe, lowcost, and accessible comfort measure for the many women affected by back pain during pregnancy. Carr studied the acceptability and effectiveness of a maternity support binder for the relief of LBP in women in the second and third trimesters of pregnancy.57 The study included 40 women with self-reported LBP of at least a ‘medium’ level and no history of prior back pain or disc disease. The orthosis 1324

used was the Loving Comfort® lumbosacral orthosis, which is a wide belt that supports the low back and lower abdomen. It fastens under the abdomen with hook and loop fastener straps, and an optional narrow, stabilizing belt used across the top of the uterus. The binder is advertised to provide low back support, stabilize the pelvis, and support the lower abdomen. It is approved by the Food and Drug Administration and covered by some insurance companies. Over a 2-week period, the intervention group had significantly fewer days of pain and significantly fewer hours of pain than the control group. Interview data revealed a high level of acceptance of the back support. The woman’s size, weight, or obesity did not affect the fit of the binder, but height appeared to be a challenge. Short women (under 62 inches) and women with short torsos complained that the belt rolled in the back and buckled with sitting. The sample group’s size was small, and more studies need to be performed with randomized and diverse populations. However, the modest price, its ease of fitting, and lack of side effects holds promise for the lumbosacral binder’s use in pregnancy.

Sacroiliac belt Ostgaard et al. studied the efficacy of nonelastic sacroiliac belts.4 The belts were found to reduce PPP during ambulation in a large majority of women studied. Posterior pelvic pain is differentiated from low back pain in its distribution and etiology as defined earlier in the chapter. Most of the 59 women studied wore the belt daily and found that they were able to increase their walking distance. None of the women experienced pain reduction at work or at rest, and visual analog scales were unchanged. Physical fitness alleviates symptomatic patients with low back pain, but has less of a demonstrable beneficial effect for those with PPP. Nonetheless, the use of a low nonelastic SI belt is a cost-effective and safe tool for alleviation of posterior pelvic pain in many women during ambulation. The mechanism of action of the SI belt is still unclear. It may have an effect on muscle forces or muscular insertions on the posterior pelvis. Lowering vertical load transmission to the SI joints is unlikely but not entirely unreasonable.

Pelvic and lumbar belts Pelvic belts are another type of supportive device that have been studied in pregnant women. They appear to be effective in the treatment of peripartum pelvic pain (PPPP),39 defined as pain in the pelvic region that started during pregnancy or within the first 3 weeks after delivery and for which no clear diagnosis is available to explain the symptoms. PPPP is prominent around the sacroiliac joints and symphysis. There is a striking incidence of increased PPPP during pregnancy which parallels the increase of movement of the sacroiliac joints during pregnancy observed in anatomic and radiographic studies.58,59 The belts have been beneficial in patients during pregnancy, and even more so following delivery. According to Mens et al., the beneficial influence of a pelvic belt supports the notion that PPPP results from strain of the muscular and osteoligamentous complex in the pelvis and lower parts of the spine.39 To further evaluate the biomechanical effect of a pelvic belt, 12 cadaveric sacroiliac joints of six human pelvis–spine preparations were sagittally rotated via bidirectional forces at the level of the acetabula.37 The sacroiliac joints were tested without the belt, with a nonelastic pelvic belt of 50 N tension, and with a nonelastic belt of 100 N tension. In seven out of 12 joints, application of the 50 N loaded pelvic belt caused a significant decrease in sagittal rotation. The average reduction in rotation was 29.3%. A comparable result was obtained with the 100 N belt, and the differences between the 50 N and 100 N belts were not statistically significant. Larger tensile forces on the belt did not yield better results. These results are

Pregnancy

concordant with a previous biomechanical study, in which the efficacy of a pelvic belt was determined by the site of application and not by the amount of tension.60 Wearing the belt just above the greater trochanter braced the pelvis and improved pain. The exact position must be adjusted according to the patient’s demands and comfort. In addition, the authors do not advise use of the pelvic belts as a monotherapy. Simultaneous muscle training, especially the internal pelvic musculature and gluteus maximus, has been recommended. The use of large lumbar belts may be difficult due to the growing size of the abdomen. The belts may fit poorly and many women worry about pressure on the fetus from the belt. In considering the safety of lumbar supports on the hemodynamics of a mother and fetus, a study was conducted by Beaty et al. that included 25 healthy women between 24 and 36 weeks’ gestation.61 No significant changes were seen in the fetal heart rate baseline or variability during use of the support. The maternal mean arterial blood pressures were unaffected, as were the right- and left-sided cardiac outputs. They found that the women studied reported improvement in back discomfort with the use of a lumbar support while sitting and standing. Therefore, this option should not be entirely excluded when considering orthotic devices that are available to the patient and are potentially beneficial in treating low back pain.

Bracing for scoliosis Danielsson and Nachemson looked at the progression of scoliotic curvature during pregnancy and childbirth, as well as the incidence of LBP in women with scoliosis, as part of their study published in 2001.62 The frequency of low back pain during pregnancy was 36% for patients surgically treated for adolescent idiopathic scoliosis with Harrington rods and 43% for patients who had been treated with Milwaukee or Boston braces. These numbers are similar to the incidence of pain in the nonscoliotic pregnant control group whose prevalence was 49% for back pain.7 As well, the curve type did not appear to influence back pain during pregnancy. The rate of complications in women with scoliosis during pregnancy, including back pain and number of cesarean sections, was no higher than in the general population. The severity of the scoliotic curve did not seem to be affected by the number of pregnancies or the age at first pregnancy. This suggests that corrective interventions during pregnancy are not necessary other than for cosmesis.

Ozzlo pillow The Ozzlo pillow is a hollowed out, nest-shaped pillow which appears to provide better pain relief than a standard pillow in pregnant women. It is probably most helpful to women who suffer back pain at night. A review article by Young and Jewell87 describes results

of a study by Thomas utilizing the Ozzlo pillow for relief of back pain in pregnancy. A crossover randomized trial64 included 109 women comparing the efficacy of a specially designed pillow (Ozzlo pillow) for supporting the pregnant abdomen to a standard hospital (Tontine) pillow. Of the 92 women who completed the 2-week study, 63 women obtained moderate or better improvement in sleep using the Ozzlo pillow and 47 women rated it as at least moderately useful for back pain as compared to only 31 who reported decreased low back pain using a standard pillow versus no pillow. Although there is a plethora of articles specifically citing and evaluating the Ozzlo pillow, it is no longer being manufactured. Women can attempt to form their own version of the Ozzlo pillow until orthotic companies consider remanufacturing this product.

MEDICATIONS When opting to utilize drug therapy, clinicians should begin by assessing the potential for harm to the mother, the fetus, and to the course of pregnancy.65 The period of fetal development, known as organogenesis, occurs during the fourth through tenth weeks of pregnancy. Prior to organogenesis, drug exposure has an all-or-nothing effect: either the fetus does not survive or develops without abnormalities. Administration of medications during this period should be performed with extreme caution to avoid potential complications. Certain drugs may have an impact on fetal development during organogenesis, leading to potential intrauterine growth retardation, multiple organ failure,66 or spontaneous abortion. Other medications may adversely affect the course of pregnancy. The United States Food and Drug Administration (FDA) has implemented a 5-category labeling system which rates the potential risk for teratogenic or embryotoxic effects for all drugs approved in the United States (Table 124.2). The labeling system is based on the available scientific and clinical evidence.

Acetominophen (Tylenol) Acetaminophen seems to be a safe and effective first-choice drug in the pregnant patient. It provides similar analgesia without the antiinflammatory effects of the nonsteroidal antiinflammatory drugs (NSAIDs). It has no known teratogenic properties, and does not inhibit prostaglandin synthesis or platelet function.66 If persistent pain demands use of a mild analgesic, acetaminophen is a safe choice.

Nonsteroidal antiinflammatories The results of the Collaborative Perinatal Project suggest that firsttrimester exposure to aspirin does not pose appreciable teratogenic risk.67 However, aspirin-induced inhibition of prostaglandin synthesis

Table 124.2: FDA classification for pregnancy risk of pain management medications Category A

Controlled human studies have been performed with no apparent risk to fetus.

Multivitamins

Category B

Animal studies either do not show fetal risk or animal studies do show risk but human studies do not.

Acetaminophen, fentanyl, hydrocodone, methadone, oxymorphone, ibuprofen, naproxen, prednisolone, prednisone, fluoxetine

Category C

No controlled studies have been performed in animals, or animal studies indicate teratogenic risk, but no controlled studies have been done in humans.

Aspirin, ketorolac, codeine, propoxyphene, gabapentin, lidocaine

Category D

There is evidence of human fetal risk, but the benefits of the drug may outweigh the risks.

Amitriptyline, imipramine, diazepam, phenytoin, phenobarbital, indomethacin

Category X

Evidence of significant fetal risk exists.

Ergotamine

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may result in prolonged gestation and protracted labor.68 Low-dose aspirin therapy (60–80 mg/day) has not been associated with maternal or neonatal complications, but larger doses seem to increase the risk of neonatal intracranial hemorrhage before 35 weeks of gestation.66 Even in a full-term newborn, platelet function can be inhibited for up to 5 days after birth.69 Furthermore, aspirin’s platelet-inhibiting properties may increase the risk of peripartum hemorrhage, placing both the mother and child at risk. NSAIDs have been known to delay onset of labor as well as increasing neonatal risk for pulmonary hypertension. The use of the NSAID, indometacin, has been linked to premature antenatal closure of the fetal ductus arteriosus.68 Ibuprofen and naproxen have not been linked to congenital defects; however, their use during pregnancy may result in a reversible and mild constriction of the fetal ductus arteriosus.70

Opioid analgesics There is no evidence to suggest a relationship exists between exposure to opioid agonists or agonist–antagonists during pregnancy and major or minor malformations. The Collaborative Perinatal Project monitored over 50 000 mother–child pairs, 563 of which had firsttrimester exposure to codeine and 686 of which had first-trimester exposure to propoxyphene.67 No evidence was found to link either drug to large categories of malformations. Codeine was associated weakly with respiratory defects, genitourinary defects, Down syndrome, tumors, and umbilical and inguinal hernias in a total of 35 cases. Only the association with respiratory malformation was found to be statistically significant. The possible associations with individual defects following propoxyphene exposure included microcephaly, persistent ductus arteriosus, benign tumors, and clubfoot in a total of 41 cases. None of these associations reached statistical significance. Thus, data from large surveillance studies have pointed to possible associations with individual defects, but the incidence is not statistically greater than that in the general population with the exception of respiratory malformations and codeine. Both codeine and propoxyphene are labeled Risk Category C by the FDA. Caution is advised with administration of fentanyl to the mother immediately before delivery, as this drug may lead to respiratory depression in the newborn.71 Maternal administration of fentanyl or other opioids has been shown to depress the normal variability in fetal heart rate, which signals fetal hypoxemia. Hydrocodone, meperidine, methadone, morphine, oxycodone, fentanyl, hydromorphone, oxymorphone, butorphanol, and nalbuphine are all labeled Risk Category B by the FDA.

Muscle relaxants Benzodiazepines are frequently prescribed as skeletal muscle relaxants in patients with chronic pain.72 First-trimester exposure to benzodiazepines may be associated with an increased risk of congenital malformations. Diazepam may be associated with cleft lip and palate,

as well as congenital inguinal hernia.73 This is mentioned as a possible risk even though the incidence of cleft lip and palate remained stable after the introduction and widespread use of diazepam.73 Benzodiazepine use immediately prior to delivery carries the risk of fetal hypothermia, hyperbilirubinemia, and respiratory depression.74 There have been no extensive studies determining the risks associated with other commonly prescribed muscle relaxants such as tizanidine, cyclobenzaprine, and methocarbamol.

Anticonvulsants Women who were receiving phenytoin, carbamazepine, or valproic acid for epileptic seizures were found to have twice the risk of bearing a child with a congenital defect than the general population.75 While inadequate maternal folate absorption associated with anticonvulsant use during pregnancy may contribute to neural tube defects, epilepsy itself may be partially responsible for fetal malformations.76 It is plausible that pregnant women taking anticonvulsants for chronic pain may have a lower risk of fetal malformations than those taking the same medications for seizure control. Nonetheless, women taking anticonvulsants for neuropathic pain should strongly consider discontinuation of anticonvulsants during pregnancy, particularly during the first trimester. A prospective and retrospective study by Montouris77 collected data involving 51 fetuses from 39 women with epilepsy and other disorders exposed to gabapentin during pregnancy. The results of this study showed that the rates of maternal complication, cesarean section, miscarriage, low birth weight, and malformation were less than or similar to those seen in the general population or among women with epilepsy. Gabapentin exposure during pregnancy did not lead to an increased risk for adverse maternal and fetal events in this study. Animal studies have shown gabapentin to be toxic to fetuses in rodents and to be associated with increased postimplantation fetal loss in rabbits. These adverse effects occurred at varying doses, some of which were equivalent to human doses. Because of the small number of patients examined in the Montouris study, additional data from more pregnancies and outcomes are needed. In summary, acetaminophen (Tylenol) is the safest medication for pain control during all three trimesters of pregnancy. Other drug treatments for the control of pain must be closely evaluated, with risks and benefits to the patient and unborn child considered carefully.

Breastfeeding considerations while taking medications The typical neonatal dose of most medications obtained through breastfeeding is 1–2% of the maternal dose.75 Even with minimal exposure via breast milk, neonatal drug allergy and slower infant drug metabolism must be considered. The American Academy of Pediatrics has classified recommendations for maternal medication use during lactation (Table 124.3).

Table 124.3: American Academy of Pediatrics classification of maternal medication use during lactation

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Category 1

Medications that should not be used during lactation due to serious adverse effects on the nursing infant.

Ergotamine

Category 2

Drugs that should be used with caution since their effects on infants are unknown.

Amitriptyline, desipramine, fluoxetine, trazodone, diazepam, lorazepam, midazolam

Category 3

Medications compatible with breast feeding.

Acetaminophen, ibuprofen, indomethacin, naproxen, caffeine, lidocaine, codeine, fentanyl, methadone, morphine, carbamazepine, phenytoin, valproic acid

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Salicylate transport into breast milk is limited, in part due to its high degree of protein binding and its highly ionized state. It would be prudent, however, to limit long-term or frequent aspirin use, as neonates tend to eliminate salicylates very slowly.78 Both ibuprofen and naproxen are also minimally transported into breast milk and are considered compatible with breastfeeding.75 Indomethacin should be avoided during lactation, based on case reports of neonatal seizures and nephrotoxicity.79 Acetaminophen does enter breast milk, although maximal neonatal ingestion is considered less than 2% of a maternal dose.80 Acetaminophen is considered compatible with breastfeeding.67 Opioids are excreted into breast milk. Breast milk concentrations of codeine and morphine tend to be equal to or greater than maternal plasma concentrations.81 Fortunately, morphine undergoes glucoronidation via first-pass metabolism, converting the drug to its inactive metabolites. The American Academy of Pediatrics considers morphine, and other opioid analgesics including codeine, fentanyl, methadone, and propoxyphene, compatible with breastfeeding. Meperidine, on the other hand, undergoes N-demethylation to normeperidine, an active metabolite, whose prolonged half-life and subsequent accumulation results in risks of neurobehavioral depression and seizures in the newborn.66 Diazepam and its metabolite desmethyldiazepam can be detected in infant serum for up to 10 days after a single maternal dose due to the slower metabolism in neonates.82 Clinically, infants who are nursing from mothers receiving diazepam may show sedation and poor feeding.82 It seems prudent to avoid any use of benzodiazepines during lactation. In summary, ibuprofen, naproxen, acetaminophen, and some opioids are considered compatible with breastfeeding. Colostrum production and secretion is minimal for the first few days postpartum, so medications received during the delivery period pose little risk to the newborn via breast milk. All other medications should be discontinued or used with caution.

ALTERNATIVE TREATMENTS Acupuncture Properly performed acupuncture appears to be a safe procedure. As used in pregnancy, it is theorized to activate endogenous opioid mechanisms. Functional magnetic resonance imaging has suggested region-specific and quantifiable effects of acupuncture on relevant brain structures. Acupuncture may also stimulate gene expression of neuropeptides. It has been shown to be effective for pregnancyassociated nausea, yet there has been equivocal and contradictory results for chronic pain, back pain, and headache.83 In an unblinded, controlled study done by Kvorning et al., acupuncture was found to relieve pelvic and LBP in pregnancy. It was safe with no serious adverse effects in treatment group (n=37) to either mother or infant. The treatment sessions occurred 1–2 times a week until delivery or recovery of LBP. Pain on visual analog score (VAS) decreased in 60% of the acupuncture group versus 14% in control group, and 43% of the treated group noted improvement with activities compared to only 9% of the controls.84 Forrester documented a case report of a 24-year-old primigravida at 24 weeks of gestation who was incapacitated by severe low back pain. After serious organic causes were excluded, acupuncture was performed to control her pain and improve function, with good success.85 Wedenberg et al. compared the efficacy of acupuncture to physical therapy. There were 60 patients involved in the study. In comparing the mean morning and evening VAS, the acupuncture group scores were statistically significantly lower in comparison to the physical therapy group. The values of the Disability Rating Index had

also significantly decreased in the acupuncture group in 11 out of 12 activities whereas in the physical therapy group there was little change.86 These differences, however, could be explained by the fact that the acupuncture group received individual attention.87

Manipulation Low back pain in the general population is often treated with chiropractic or osteopathic manipulations. Daly et al. diagnosed 11 out of 23 pregnant women with ‘sacroiliac subluxations.’ Of those 11, 10 had relief of pain after rotatory manipulations to the SI joint with no adverse clinical side effects.88 A similar study by McIntyre and Broadhurst found that low back pain in pregnancy from clinically diagnosed SI joint dysfunction can be successfully treated with SI joint manipulation and home exercises. Of 20 pregnant women with back pain, they identified pain emanating from the SI joint in 17. After these patients were treated for three visits, 15 had no pain, and the other two had more than 50% improvement.89 Osteopathic treatments are also often used in pregnancy; however, their role, especially the cranial–sacral techniques, is somewhat unknown.63 Their role will hopefully be better delineated as new research becomes available.

Massage Field et al. noted that pregnant women benefited from massage and had less anxiety, improved mood, better sleep, and less back pain by the last day of treatment in comparison to the relaxation therapy group. The level of norepinephrine, considered a urinary stress hormone, was less in the massage group, and they had fewer complications during labor and less prematurity. Both groups underwent 20-minute sessions twice a week and reported less anxiety and leg pain.90

Psychosocial treatment Well-being can be defined as adequate physical and mental functioning.91 During pregnancy, shifts occur in a couple’s interactions, as well as relationships among friends and colleagues. Moreover, ability to perform daily and occupational tasks may be challenged. Until recently, little attention has been paid in the literature to the genuine pregnancy-related complaints, such as fatigue, nausea, and back pain. Nevertheless, it can be deduced that pregnancy-related complaints may reflect some aspect of an individual’s psychosocial well-being. The aim of the study by Paarlberg et al. was to examine the potential of psychosocial variables as predictors of well-being and of pregnancy-related complaints.91 Over 400 pregnant, nulliparous women were used in this study, none of whom had psychological or psychiatric illnesses requiring hospitalization. Correlations were found in all trimesters between depression and the independent variables age, work satisfaction, and degree of satisfaction with received support. A high correlation was found between depression and number of daily stressors. Incidence of back pain showed a consistent correlation with age and professional and educational level. As to the predictive value of psychosocial factors with regards to pregnancyrelated complaints, back pain complaints were predicted by lower educational level, younger age, increased number of daily stressors, and with depression. Of note, the mean physical workload was calculated for women with low, middle, and high education levels. The observed higher mean physical workload reported by women with a low educational level was significant. Another study which correlated with the above findings was conducted by Orvieto et al.13 It was conducted to assess the frequency, manifestation, and the contribution of various factors to the development of LBP during pregnancy. One factor found to be 1327

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significantly associated with an increased risk of developing LBP during pregnancy was low socioeconomic class, apparently because these women are exposed to more strenuous physical work, including repetitive lifting and bending. This is consistent with previous reports.92 In contrast, another report shows a much higher incidence of LBP among Caucasian women of a higher socioeconomic class and an ‘easier life.’93 Several studies show a connection between high back pain intensity, decreased functional ability, and an increased number of days on sick leave.7,94 Pregnant women with back pain were found to rate significantly higher on the Disability Rating Index (DRI), and on The Nottingham Health Profile (NHP) for assessing health-related quality of life.93 Several investigators7,93 found that work factors, younger maternal age, and low educational level were the most important predictors of back pain. Work factors that increase risk include twisting, forward bending, standing work posture, and inability to change posture or take breaks. Twisting or bending many times per hour emerged as significant in the regression analyses for low back pain performed by Endresen.92 The correlation matrix showed that working hours were inversely correlated with LBP. This agrees with other studies that show that, on the whole, women who work ‘short part-time’ suffer most. Short part-time work is often associated with occupations that are physically demanding, such as sales work, nursing assistants, service work, etc.95 A significant positive correlation was found between back pain and physical workload, and an inverse correlation was found between work satisfaction and back pain. In a study performed in Sweden, 135 working pregnant women were divided into an intervention group and a control group, with evaluation of the effects of individual education as well as individualized therapy on pain and number of sick days. Five visits were offered at physical therapy centers. After back pain assessment, an individually designed program was started. Patients were taught anatomy, body posture, vocational ergonomics, gymnastics, pelvic floor training, and relaxation training. An individual exercise program, including back muscle strengthening exercises, was designed according to pain type and intensity. With this intervention, pain intensity was significantly reduced, and sick days were reduced from an average of 53.6 days for the control group to 30.4 days for the intervention group. Furthermore, the economical gain was considerable in the intervention group despite the cost of physical therapy, as determined by The Social Insurance Office in Boras, Sweden.12 A controlled trial by Ostgaard et al. was aimed at reducing back pain during pregnancy by determining whether particular preventive measures can impact occupational exposures.4 It was found that individual instruction, not classes, reduced sick leave during pregnancy. In the study by Orvieto et al., back care advice early in pregnancy, such as appropriate posture and lifting technique, was subjectively reported to significantly reduce LBP occurrence and intensity.13 Public health nurses, family physicians, and obstetricians advised these women on how to prevent LBP. Pregnancy health, including LBP, was found to improve with increasing power to control work pace, in both manual and nonmanual work.96 This suggests increased individual control over work pace as a prime target for job adjustment during pregnancy.

INJECTIONS There is a serious lack of research investigating interventional procedures for back pain in pregnancy. For obvious reasons, fluoroscopic guidance cannot be used. This leaves local injections, and blind caudal and interlaminar epidurals. Myofascial pain can cause low back pain in pregnant women. Tsen and Camann describe a case report of 1328

a primiparous woman who continued to have low back after epidural infusion for labor analgesia. She was found to have trigger points that were successfully treated with simple local analgesic injections.97 The authors have had excellent anecdotal success with ultrasound-guided SI joint injections for SI joint-mediated pain in pregnant women, though there are no scientific studies supporting this contention.

SURGERY Only in rare cases of back pain does the pregnant patient require surgery. In the pregnant patient population, lumbar disc herniations are rare and can be treated conservatively. However, for progressive neurological deficits, cauda equina syndrome, or for incapacitating pain, surgery could be considered. Garmel et al. reported three cases wherein lumbar surgery was performed on pregnant women, and the patients did well, with decrease in their pain postoperatively and no adverse consequences to the pregnancy. Their results were not significantly different than in the nonpregnant population.98 Van Zwienen et al., in a single-group prospective study, evaluated postsurgical functional outcome of 58 pregnancy-related severe low back and pelvic pain patients. These patients were diagnosed with SI jointmediated pain, had severe disability, failed conservative treatments, and were evaluated by Majeed score as well as with endurance tests of walking, sitting, and standing. Surgery consisted of symphysiodesis and bilateral percutaneous placement of sacroiliac screws under fluoroscopy. The average follow-up was 2.1 years, and improvement of more than 10 points on the Majeed score was achieved in 69.8% and 89.3% of the patients at 12 and 24 months, respectively. Complications included irritation of nerve roots (8.6%), nonunion of the symphysis (15.5%), failure of the symphyseal plate (3.4%), and pulmonary embolism.99 A spontaneous epidural hematoma of the spine during pregnancy is rare and may present as acute low back or neck pain with or without progressive neurological deficit. Even rarer is the subacute presentation. Prompt identification of the hematoma and surgical evacuation should be performed prior to the onset of neurologic signs.100 Carroll et al. reported a case of a 26-year-old primigravida who developed acute onset of back pain and neurological symptoms from an acute spontaneous extradural hematoma with successful outcome following prompt surgical evacuation.101

SPECIAL CONSIDERATIONS The most common feature of osteoporosis in pregnancy is back pain, which may be severe. Although uncommon, it can occur during pregnancy or in the immediate postpartum period. It is usually self-limited, and recurrence is unusual. Osteoporosis should be suspected if the pain is unrelieved with simple analgesics, or there is a noticeable loss of height. Plain films in the postpartum period can reveal osteopenia and even vertebral fracture. A majority of cases occur during the first pregnancy. Since bone mineral density decreases in the postpartum as well, breastfeeding should be discouraged. In a minority of cases, symptoms can last months or years.102 In a study by Smith et al., 24 cases of pregnancy-related osteoporosis were followed for up to 24 years. The most common symptom was back pain in late pregnancy or postpartum, followed by hip then ankle pain. Most symptoms occurred in the first pregnancy and improved shortly after delivery. X-rays demonstrated vertebral body collapse or hip osteoporosis, with evidence of edema on MRI. Bone mineral density of the spine was low by DEXA scans. Overall, the long-term prognosis is good with low recurrence in subsequent pregnancies.103,104 In a case study by Jensen and Mortensen, a 26-year-old female with LBP developed thoracic spine compression fractures 4 months after delivery.

Pregnancy

She was diagnosed with pregnancy-related osteoporosis after bone biopsy and collagen analysis failed to reveal any other explanation. The patient was treated with calcium and vitamin D postpartum, with resolution of the osteoporosis after 3 years.105 There are also rare cases of sacroiliac joint infections. Treatment should be tailored to the specific organism and continued for 3–6 weeks.106

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30. Sihvonen T, et al. Functional changes in back muscle activity correlate with pain intensity and prediction of low back pain during pregnancy. Arch Phys Med Rehab 1998; 79(10):1210–1212. 31. Kristiansson P, Svardsudd K, von Schoultz B. Serum relaxin, symphyseal pain, and back pain during pregnancy. Am J Obstet Gynecol 1996; 175(5):1342–1347. 32. Chan YL, et al. Back pain in pregnancy – magnetic resonance imaging correlation. Clin Radiol 2002; 57(12): 1109–1112. 33. Albinus, Hunter. The pelvic articulations during pregnancy, labor and the puerperium. Surg Gynecol Obstet 1920; (30):575–80. 34. Brooke R. The sacroiliac joint. J Anat 1924; (58):299–305. 35. Sashin D. A critical analysis of the anatomy and the pathological changes of the sacroiliac joints. J Bone Joint Surg 1930; (12):891–910.

2. Bjorklund K, Nordstrom ML, Bergstrom S.Sonographic assessment of symphyseal joint distention during pregnancy and post partum with special reference to pelvic pain. Acta Obstet Gynecol Scand 1999; 78(2):125–130.

36. Damen L, et al. Pelvic pain during pregnancy is associated with asymmetric laxity of the sacroiliac joints. Acta Obstet Gynecol Scand 2001; 80(11):1019–1924.

3. Mantle MJ, Greenwood RM, Currey HL. Backache in pregnancy. Rheumatol Rehabil 1977; 16(2):95–101.

37. Vleeming A, et al. An integrated therapy for peripartum pelvic instability: a study of the biomechanical effects of pelvic belts. Am J Obstet Gynecol 1992; 166(4):1243–1247.

4. Ostgaard HC, et al. Reduction of back and posterior pelvic pain in pregnancy. Spine 1994; 19(8):894–900. 5. Ostgaard HC, Roos-Hansson E, Zetherstrom G. Regression of back and posterior pelvic pain after pregnancy. Spine 1996; 21(23):2777–2780. 6. Ostgaard HC, Zetherstrom G, Roos-Hansson E. Back pain in relation to pregnancy: a 6-year follow-up. Spine 1997; 22(24):2945–2950. 7. Ostgaard HC, Andersson GB, Karlsson K. Prevalence of back pain in pregnancy. Spine 1991; 16(5):549–552. 8. Kristiansson P, Svardsudd K, von Schoultz B. Back pain during pregnancy: a prospective study. Spine 1996; 21(6):702–709. 9. Svensson HO, et al. The relationship of low-back pain to pregnancy and gynecologic factors. Spine 1990; 15(5):371–375. 10. Carlson HL, et al. Understanding and managing the back pain of pregnancy. Curr Women’s Health Reports 2003; 3(1):65–71. 11. Deyo RA, Diehl AK, Rosenthal M. How many days of bed rest for acute low back pain? A randomized clinical trial. N Engl J Med 1986; 315(17):1064–1070. 12. Noren L, et al. Reduction of sick leave for lumbar back and posterior pelvic pain in pregnancy. Spine 1997; 22(18):2157–2160. 13. Orvieto R, et al. Low-back pain of pregnancy. Acta Obstet Gynecol Scand 1994; 73(3):209–214. 14. Hainline B. Low-back pain in pregnancy. Adv Neurol 1994; 64:65–76. 15. Rungee JL. Low back pain during pregnancy. Orthopedics 1993; 16(12):1339–1344. 16. Brown W. The benefits of physical activity during pregnancy. J Sci Med Sport 2002; 5(1):37–45. 17. Hartmann S, Bung P. Physical exercise during pregnancy – physiological considerations and recommendations. J Perinat Med 1999; 27(3):204–215. 18. Clapp JF, Capeless EL. Fetal heart rate response to sustained recreational exercise. Am J Obstet Gynecol 1993; 168:198–206. 19. Artal R. Exercise during pregnancy and postpartum. Cont Obstet/Gynecol 1995; 40:62–90. 20. Committee on Obstetric. ACOG committee opinion. Exercise during pregnancy and the postpartum period. Number 267, January 2002. American College of Obstetricians and Gynecologists. Int J Gynecol Obstet 2002; 77(1):79–81. 21. Bennell K. The female athlete. In: Pike C, ed. Clinical sports medicine. Sydney: McGraw-Hill; 2000:674–699. 22. Lumbers ER. Exercise in pregnancy: physiological basis of exercise prescription for the pregnant woman. J Sci Med Sport 2002; 5(1):20–31. 23. Anonymous. SMA statement the benefits and risks of exercise during pregnancy. Sports Medicine Australia. J Sci Med Sport 2002; 5(1):11–19. 24. American College of Sports Medicine. ACSM’s guidelines for exercise testing and prescription, 6th edn. Philadelphia: Lippincott, Williams Wilkins; 2000. 25. Camporesi EM. Diving and pregnancy. Sem Perinatol 1996; 20(4):292–302. 26. Jensen GM, Moore LG. The effect of high altitude and other risk factors on birthweight: independent or interactive effects? Am J Public Health 1997; 87(6):1003–1007. 27. Practice ACO. ACOG Committee opinion. Number 267, January 2002: exercise during pregnancy and the postpartum period. Obstet Gynecol 2002; 99(1):171–173. 28. Kristiansson P, Svardsudd K. Discriminatory power of tests applied in back pain during pregnancy. Spine 1996; 21(20):2337–2343; discussion 2343–2344. 29. Ernst E. Smoking, a cause of back trouble? Br J Rheumatol 1993; 32(3):239–242.

38. Mens JM, Snijders CJ, Stam HJ. Diagonal trunk muscle exercises in peripartum pelvic pain: a randomized clinical trial. Physical Ther 2000; 80(12):1164–1173. 39. Mens JM, et al. Understanding peripartum pelvic pain. Implications of a patient survey. Spine 1996; 21(11):1363–1369; discussion 1369–1370. 40. Franklin ME, Conner-Kerr T. An analysis of posture and back pain in the first and third trimesters of pregnancy. J Orthopaed Sports Phys Ther 1998;28(3):133–138. 41. Foti T, Davids JR, Bagley A. A biomechanical analysis of gait during pregnancy. J Bone Joint Surg [Am] 2000; 82(5):625–632. 42. Ostgaard HC, et al. Influence of some biomechanical factors on low-back pain in pregnancy. Spine 1993; 18(1):61–65. 43. Mooney V, et al. Exercise treatment for sacroiliac pain. Orthopedics 2001; 24(1):29–32. 44. Vleeming A, et al. The posterior layer of the thoracolumbar fascia. Its function in load transfer from spine to legs. Spine 1995; 20(7):753–758. 45. Vleeming A, et al. The function of the long dorsal sacroiliac ligament: its implication for understanding low back pain. Spine 1996; 21(5):556–562. 46. Fast A, et al. Low-back pain in pregnancy. Abdominal muscles, sit-up performance, and back pain. Spine 1990; 15(1):28–30. 47. Fast A, et al. Low-back pain in pregnancy. Spine 1987; 12(4):368–371. 48. Mens JM, et al. Reliability and validity of hip adduction strength to measure disease severity in posterior pelvic pain since pregnancy. Spine 2002; 27(15): 1674–1679. 49. Suputtitada A, Wacharapreechanont T, Chaisayan P. Effect of the ‘sitting pelvic tilt exercise’ during the third trimester in primigravidas on back pain. J Med Assoc Thailand 2002; 85(Suppl 1):S170–S179. 50. Kihlstrand M, et al. Water-gymnastics reduced the intensity of back/low back pain in pregnant women. Acta Obstet Gynecol Scand 1999; 78(3):180–185. 51. Mantle MJ, Holmes J, Currey HL. Backache in pregnancy II: prophylactic influence of back care classes. Rheumatol Rehab 1981; 20(4):227–232. 52. Stuge B, Hilde G, Vollestad N. Physical therapy for pregnancy-related low back and pelvic pain: a systematic review. Acta Obstet Gynecol Scand 2003; 82(11):983–990. 53. Cluett E. Analgesia in labour: a review of the TENS method. Professional Care of Mother & Child 1994; 4(2):50–52. 54. Carroll D, et al. Transcutaneous electrical nerve stimulation in labour pain: a systematic review. Br J Obstet Gynaecol 1997; 104(2):169–175. 55. van der Ploeg JM, et al. Transcutaneous nerve stimulation (TENS) during the first stage of labour: a randomized clinical trial. Pain 1996; 68(1):75–78. 56. Labrecque M, et al. A randomized controlled trial of nonpharmacologic approaches for relief of low back pain during labor. J Family Pract 1999; 48(4):259–263. 57. Carr CA. Use of a maternity support binder for relief of pregnancy-related back pain. J Obstet Gynecol Neonat Nurs 2003; 32(4):495–502. 58. Abramson D, et al. Relaxation of the pelvic joints in pregnancy. Surg Gynecol Obstet 1934; (58):595–613. 59. Brooke R. Discussion on the physiology and pathology of the pelvic joints in relation to childbearing. Proc Roy Soc Med 1934; (17):1211–1217. 60. Vleeming A, et al. Relation between form and function in the sacroiliac joint. Part II: biomechanical aspects. Spine 1990; 15(2):133–136. 61. Beaty CM, et al. Low backache during pregnancy. Acute hemodynamic effects of a lumbar support. J Reprod Med 1999; 44(12):1007–1011.

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Part 5: Pregnancy 62. Danielsson AJ, Nachemson AL. Childbearing, curve progression, and sexual function in women 22 years after treatment for adolescent idiopathic scoliosis: a casecontrol study. Spine 2001; 26(13):1449–1456. 63. Sullivan C. Introducing the cranial approach in osteopathy and the treatment of infants and mothers. Complement Ther Nursing Midwif 1997; 3(3):72–76. 64. Thomas IL, et al. Evaluation of a maternity cushion (Ozzlo pillow) for backache and insomnia in late pregnancy. Aust NZ J Obstet Gynaecol 1989; 29(2):133–138. 65. Rathmell JP, Viscomi CM, Ashburn MA. Management of nonobstetric pain during pregnancy and lactation. [see comment]. Anesth Analges 1997; 85(5):1074–1087. 66. Briggs GG, Yaffe SJ. Drugs in pregnancy and lactation. Baltimore: Williams and Wilkins; 1990. 67. Heinomen OP, Shapiro S. Birth defects and drugs in pregnancy. Littleton: Publishing Science Group; 1977. 68. Moise KJ Jr, et al. Indomethacin in the treatment of premature labor. Effects on the fetal ductus arteriosus. N Engl J Med 1988; 319(6):327–331.

86. Wedenberg K, Moen B, Norling A. A prospective randomized study comparing acupuncture with physiotherapy for low-back and pelvic pain in pregnancy. Acta Obstet Gynecol Scand 2000; 79(5):331–335. 87. Young G, Jewell D. Interventions for preventing and treating pelvic and back pain in pregnancy [update of Cochrane Database Syst Rev. 2000;(2):CD001139; PMID: 10796248]. Cochrane Database of Systematic Reviews 2002(1): CD001139. 88. Daly JM, Frame PS, Rapoza PA. Sacroiliac subluxation: a common, treatable cause of low-back pain in pregnancy. Family Pract Res J 1991; 11(2):149–159. 89. McIntyre IN, Broadhurst NA. Effective treatment of low back pain in pregnancy. Aust Family Phys 1996; 25(9 Suppl 2):S65–S67. 90. Field T, et al. Pregnant women benefit from massage therapy. J Psychosomat Obstet Gynecol 1999; 20(1):31–38.

69. Stuart MJ, et al. Effects of acetylsalicylic-acid ingestion on maternal and neonatal hemostasis. N Engl J Med 1982; 307(15):909–912.

91. Paarlberg KM, et al. Psychosocial factors as predictors of maternal well-being and pregnancy-related complaints. J Psychosomat Obstet Gynecol 1996; 17(2): 93–102.

70. Hennessey LE. The incidence of ductal constriction and oligohydramnios during tocolytic therapy with ibuprofen. Am J Obstet Gynecol 1992; (166):324.

92. Endresen EH. Pelvic pain and low back pain in pregnant women – an epidemiological study. Scand J Rheumatol 1995; 24(3):135–141.

71. Rayburn W, et al. Fentanyl citrate analgesia during labor. Am J Obstet Gynecol 1989; 161(1):202–206.

93. Olsson C, Nilsson-Wikmar L. Health-related quality of life and physical ability among pregnant women with and without back pain in late pregnancy. Acta Obstet Gynecol Scand 2004; 83(4):351–357.

72. Dellemijn PL, Fields HL. Do benzodiazepines have a role in chronic pain management? Pain 1994; 57(2):137–152. 73. Rosenberg L, et al. Lack of relation of oral clefts to diazepam use during pregnancy. N Engl J Med 1983; 309(21):1282–1285. 74. Scanlon JW. Effect of benzodiazepines in neonates [letter]. N Engl J Med 1975; 292(12):649–650. 75. Anonymous. American Academy of Pediatrics Committee on Drugs: The transfer of drugs and other chemicals into human milk. [see comment]. Pediatrics 1994; 93(1):137–150.

94. Cherry N. Physical demands of work and health complaints among women working late in pregnancy. Ergonomics 1987; 30(4):689–701. 95. Central Bureau of Statistics. Working Conditions 1989. NOS C9, Oslo 1992. 96. Wergeland E, Strand K. Work pace control and pregnancy health in a populationbased sample of employed women in Norway. Scand J Work Environ Health 1998; 24(3):206–212. 97. Tsen LC, Camann WR. Trigger point injections for myofascial pain during epidural analgesia for labor. Regional Anesthesia 1997; 22(5):466–468.

76. Yerby MS. Pregnancy, teratogenesis, and epilepsy. Neurol Clin 1994; 12(4): 749–771.

98. Garmel SH, et al. Lumbar disk disease in pregnancy. Obstet Gynecol 1997; 89(5 Pt 2):821–822.

77. Montouris G. Gabapentin exposure in human pregnancy: results from the Gabapentin Pregnancy Registry. Epilepsy Behav 2003; 4(3):310–317.

99. van Zwienen CM, et al. Triple pelvic ring fixation in patients with severe pregnancy-related low back and pelvic pain. Spine 2004; 29(4):478–484.

78. Levy G, Garrettson LK. Kinetics of salicylate elimination by newborn infants of mothers who ingested aspirin before delivery. Pediatrics 1974; 53(2):201–210.

100. Steinmetz MP, et al. Successful surgical management of a case of spontaneous epidural hematoma of the spine during pregnancy [erratum appears in Spine J 2004 Mar-Apr; 4(2):following table of contents Note: Chahlavi A [corrected of Chalavi A]]. Spine Journal: Official Journal of the North American Spine Society 2003; 3(6):539–542.

79. Dailland P. Analgesia and anaesthesia and breast feeding. In: Reynolds F, ed. Effects on the baby of maternal analgesia and anaesthesia. London: WB Saunders; 1993:268. 80. Notarianni LJ, Oldham HG, Bennett PN. Passage of paracetamol into breast milk and its subsequent metabolism by the neonate. Br J Clin Pharmacol 1987; 24(1):63–67. 81. Findlay JW, et al. Analgesic drugs in breast milk and plasma. Clin Pharmacol Ther 1981; 29(5):625–633.

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85. Forrester M. Low back pain in pregnancy. Acupuncture in Med 2003; 21(1–2): 36–41.

101. Carroll SG, et al. Spontaneous spinal extradural hematoma during pregnancy. J Maternal-Fetal Med 1997; 6(4):218–219. 102. Topping J, et al. Osteoporosis in pregnancy: more than postural backache. Professional Care of Mother & Child 1998; 8(6):147–150. 103. Smith R, et al. Osteoporosis of pregnancy. Lancet 1985; 1(8439):1178–1180.

82. Erkkola R, Kanto J. Diazepam and breast-feeding. Lancet 1972; 1(7762): 1235–1236.

104. Smith R, et al. Pregnancy-associated osteoporosis. Q J Med 1995; 88(12): 865–878.

83. Kaptchuk TJ. Acupuncture: theory, efficacy, and practice [see comment]. Ann Internal Med 2002; 136(5):374–383.

105. Jensen JE, Mortensen G. [Pregnancy associated osteoporosis]. Ugeskrift for Laeger 2000; 162(27):3865–3866.

84. Kvorning N, et al. Acupuncture relieves pelvic and low-back pain in late pregnancy. Acta Obstet Gynecol Scand 2004; 83(3):246–250.

106. Egerman RS, et al. Sacroiliitis associated with pyelonephritis in pregnancy. Obstet Gynecol 1995; 85(5 Pt 2):834–835.

PART 6

CHAPTER

125

INTERVENTIONAL SPINE IN SPORTS

Biomechanics of the Spine in Sport Lisa M. Bartoli and Robert S. Gotlin

INTRODUCTION The spine is a complex design of bony and soft tissues, allowing the human form to move through various ranges of motions and positions. It serves both to transfer forces between the upper and lower extremities and to actively generate forces.1,2 Both the biomechanical design of the spine and the biomaterial composition of the various tissues determine its response to external stressors and forces generated within the body. The design and composition also provide an incredible ability to adapt to these stressors; however, there is a finite amount of adaptation that can occur before structural failure and injury can result.3 The epidemiology and biomechanical analysis of sports-related spinal injuries has allowed for the identification of the precise mechanism of various spinal injuries. This has resulted in sporting rules changes, equipment modifications, and changes in skill techniques, all of which have lowered the incidence of catastrophic spinal injury.4–7

FUNCTIONAL ANATOMY The osseous spine consists of 7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral vertebrae and the coccyx. The ligaments, muscles, and intervertebral discs connect the vertebrae to form the four curves of the spine: the two lordotic curves of the lumbar and cervical spine and the two kyphotic curves of the thoracic spine and sacrum. This structural property helps the spine absorb forces of compression and also contributes to the coupled motions that occur in the spine.1,3 The functional spinal segmental unit is defined as two adjoining vertebrae, the disc between them, and their surrounding soft tissues.1,3,8,9 The functional spinal segment, however, may be further divided into anterior and posterior segments. The anterior segment consists of the anterior longitudinal ligament, the vertebra, the disc, and the posterior longitudinal ligament. The anterior segment with its osseous vertebral body serves as the primary load-bearing portion of the spinal segment.1,3 The posterior segment contains the neural arch, beginning at the pedicles and extending posteriorly to the spinous process. This area is responsible for guiding and restraining the motion that occurs between the spinal segments.3 The vertebral bodies of the anterior motion segment are composed of cancellous bone, surrounded by a thin layer of cortical bone. Various studies have shown that cancellous bone contributes as much as 50% to the strength of the bone during compression. The surrounding cortical bone provides approximately 10% of the strength.1,9 As the spine progresses from C3 to L5, the size of the vertebral bodies increase in size and mass. This is an adaptation of the spine to allow for more load-carrying capacity in the lower lumbar segments. The loss of cancellous bone seen in osteoporotic patients explains the high incidence of fractures occurring with increases in compressive loads.1,3

Specific to each area of the spine are the zygapophyseal joints (Z-joints) and their orientation in space. The Z-joints are located in the posterior functional segment and restrict motion at each spinal segment. Their orientation determines the amount and direction of movement that can occur in each segment of the spine. In the cervical vertebrae (C2–7), the Z-joints are oriented 45 degrees from the horizontal axis (x axis) and parallel to the vertical axis (y axis).3,9 The exception in the cervical spine occurs with the atlas and axis, which have the Z-joints oriented nearly parallel to the horizontal axis.9 In the thoracic spine the Z-joints are oriented 60 degrees from the horizontal plane and 20 degrees from the vertical axis. The lumbar spine Z-joints are oriented 90 degrees from the horizontal axis and 45 degrees from the vertical axis. The inferior articulating processes of lumbar spine Z-joints are convex while the superior articulating processes have a concave surface.9 Articulations with the skull, ribs, and sacrum also influence motion in the spine. The cervical spine (C3–7) can move through flexion, extension, lateral flexion, and rotation. Motion in the thoracic spine consists mostly of transverse plane rotation, lateral bending, and a smaller component of flexion and extension. The lumbar spine allows a small amount of rotation, but a much larger amount of flexion, extension, and side-bending. Slightly more rotation occurs at the lumbosacral junction due to the more obliquely oriented Z-joints at this segment.3,9 To summarize, the majority of flexion and extension occurs in the cervical, lower thoracic, and lumbar spine. The majority of rotation occurs in the upper thoracic and cervical spine, and lateral flexion is greatest in the cervical spine.3,9 The combination of the orientation of the Z-joints with the spinal curves results in ‘coupled motions’ occurring at the spinal segment.1,3,9 Assuming a neutral position, cervical lateral flexion will cause rotation of the spinous process towards the convexity of the curve. For example, cervical side-bending left causes the spinous process to rotate towards the right. The same is true in the upper thoracic spine, but not in the lumbar spine. In the lumbar spine, lateral flexion causes rotation of the spinous process towards the concavity of the curve, i.e. side-bend right, rotation of the spinous process right.1,3,9 The exceptions to this motion occur between C1 (atlas) and C2 (axis). The skull articulates with C1, which lacks a vertebral body, and because it has superiorly oriented Z-joints, it is limited to flexion and extension of approximately 10–15 degrees between the occiput (C0) and C1 and approximately 8 degrees of side-bending.3,9 There is almost no rotation at this segment. Rotation occurs at the C1–2 articulation.3,9 Approximately 40 degrees of axial rotation occurs at the C1–2 articulation. This constitutes approximately 50% of total axial plane rotation seen in the cervical spine. The curves of the thoracic and sacral spine are fairly rigid in comparison to the more flexible curves of the cervical and lumbar spine. It is the transition points of the spine, the cervicothoracic,

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thoracolumbar, and lumbosacral junctions, where the spine is subjected to the greatest amount of stress. This is due to the differences in mobility that occur at these transitions.1 In general, the cervical spine demonstrates the greatest amount of range of motion in all planes and consequently is less stable and more vulnerable to injury. Also vulnerable to injury are the cervicothoracic and thoracolumbar transition regions. The combination of relatively mobile cervical and lumbar spines with the relatively immobile thoracic spine causes these transition zones to experience more torque. Because the spinal cord is located at both these levels, the potential for catastrophic spinal cord injury is of great concern.1 The biomaterial make-up of the spine is an important consideration when attempting to understand spinal biomechanics. The bony structures, especially the cancellous bone, is very strong when compressive forces are applied, while the ligaments are stronger in tension and buckle under compression.1,3,9 The ligaments of the spine provide stability and store energy during motion. The primary ligaments of the spine are the anterior and posterior longitudinal ligament, the supraspinous ligament and the interspinous ligament. These ligaments have high collagen content, whereas the ligamentum flavum has high elastin content. The capsular ligaments of the Z-joints contribute to their stability.3,9 The ligaments protect the spine by restricting motion to physiologic ranges, as well as helping to absorb external forces applied at high speeds.9 The ability of the ligaments to withstand deformation and their energy-absorbing characteristics were found to diminish with age.9 The high elastin content of the ligamentum flavum bestows a protective effect on the spinal unit. The elasticity allows for rapid flexion–extension motions and prevents permanent deformation of the ligamentum flavum, thereby limiting subsequent impingement of the spinal cord.9 When looking at injuries to the different spinal ligaments, one can identify the likely direction of the motion which caused the injury. For example, a hyperflexion motion would likely cause disruption to the supraspinous ligament. Axial rotation of the spine can cause damage to the capsular ligaments; rotation right would injure the right capsular ligament.9 The ligamentum flavum is stressed with lateral bending. If the intervertebral disc is degenerated, the ligaments are at higher risk for injury.9 The function of the intervertebral discs is to resist compression, help distribute some of the compressive load placed on the vertebral column, and to resist tensile and torsional loads as well.3,9 The disc is composed of an outer covering of fibrocartilage, the anulus fibrosus. The anulus is organized in concentric layers, with the fibers oriented ±30 degrees to the horizontal axis, and 120 degrees to the adjacent layer. The inner layers are attached to the cartilaginous endplates of the vertebral body, while the outermost layers, known as Sharpey’s fibers, attach directly to the osseous tissues. This outer vertebral attachment is stronger than the attachment to the vertebral endplate.1,3,9 The anulus fibrosus surrounds the nucleus pulposus. It is composed of glycosaminoglycans, which have a high water-binding capacity. Approximately 80–90% of the nucleus pulposus is water, which desiccates with age.10 Flexion and rotation of the spine results in tension, compression, and shear stress to the disc.9 When loads are applied slowly over a long period of time, adequate time is allowed for deformation to occur. With degeneration of the disc its viscoelastic properties are reduced, thereby decreasing its ability to absorb loads.9 Compression forces cause bulging of the discs and increased tensile stress in the anulus. Studies have shown that pure axial compression caused deformation of the disc, but no actual herniation of the disc. The vertebral endplate was more likely to fracture, with herniation of the disc into the vertebral body (Schmorl’s node).1,11 1332

In flexion, the posterior portion of the disc is subjected to tensile stresses, while the anterior portion experiences tension while in extension. In a study evaluating disc injury, a side-bending motion with hyperflexion caused increased tension in the posterolateral aspect of the anulus, opposite to the induced side-bending; a sudden compressive load was then applied which resulted in disc prolapse in a posterolateral direction.1,9,12,13 The spine consisting only of ligaments, discs, and bony vertebrae, and absent of any musculature can only resist 20 N before collapse.1,9,14 The rib cage acts to strengthen and stiffen the spine as well as provides energy absorption during trauma.9 When the rib cage is added only 70 lb can be supported.1,9 It is the addition of the spinal musculature which provides additional strength, stability, and movement of the spine and protection from large externally applied forces (i.e. football tackles).9,15 The stability of the spine comes from the osseous and ligamentous structures, which provide a more passive stiffness, as well as the dynamic or more active stiffness provided by the muscles.16 The muscles of the spine can be divided into two basic groups. Those located posterior to the spine are primarily responsible for extension of the spine, and those located anterior to the spine are primarily responsible for flexion of the spine. The anteriorly located spinal flexors consist of the deeply located psoas, and the more superficial abdominal muscles: the internal/ external abdominal obliques, transversus abdominis, and the rectus femoris.9,16,17 The posteriorly located spinal extensors can be divided by location into deep and superficial muscles. The deep muscles include the rotators, intertransversari, multifidi, semispinalis thoracicis, cervicis, and capitis. The superficial muscles include the more laterally located iliocostalis and the medially located longissimus and spinalis.9,16 McGill has identified the muscles attaching directly to the vertebra as most important in spinal stabilization: the multifidi, the quadratus lumborum, the longissimus and the iliocostalis. The abdominal muscles also have an important role in spinal stabilization.18 Richardson et al. have divided the muscles into either local muscles or global muscles. The local muscles act at the spinal segmental level and function as postural or segmental stabilizers. These muscles are the multifidi, quadratus lumborum, the lumbar portions of the iliocostalis and longissimus posteriorly, and the psoas, transversus abdominis, internal oblique and the diaphragm. The global muscles are dynamic and have greater torque-production capabilities. These consist of the rectus abdominis, external oblique, internal oblique (anterior fibers) and iliocostalis (thoracic portion).19 A term used often in rehabilitation of the lumbar spine is ‘core strengthening.’ This is an approach which strengthens the muscles about the spine in order to provide better dynamic stabilization, or muscular control, on the core. This core consists of the abdominals anteriorly, the paraspinals and gluteals posteriorly, the diaphragm above and the pelvic floor musculature and hip muscles below.16,19 The thoracodorsal fascia is an important structure with regards to lumbar stabilization and maintenance of correct spinal mechanics.2,16,20 This fibrous connective tissue encases the spinal extensors and is made up of three layers. These have been identified as the anterior, middle, and posterior layers. It extends inferiorly from the posterior thoracic spine, to the sacral and ilial attachments of the hip musculature. It also expands anteriorly to enmesh with the fibers of the internal oblique, and transversus abdominus, and extends superiorly to the serratus posterior inferior.2,16,20–22 The superficial laminae of the posterior layer have fibrous connections with the latissimus dorsi and the gluteus maximus. This is a key link between the upper and lower extremities.16,20,23 This posterior layer is the most important layer with regards to providing support to the lumbar spine and abdominals.16 The two lamina

Interventional Spine in Sports

of the posterior layer have fibers which are directed inferiomedially and laterally. The middle and deep layers of the thoracolumbar fascia form connections with the transversus abdominus.2,16,19,20 The thoracolumbar fascia functions as a site of muscular attachment and aids in trunk rotation. It also works with the spinal ligaments to increase stiffness of the spine.20,21 The thoracolumbar fascia is not the only fascia present in the spine. The dorsal fascia of the cervical spine extends from the ligamentum nuchae, forming attachments to the spinous process of the cervical spine, with attachments made to the sternocleidomastoid, trapezius, acromion, scapular spine, and even as far anterior as the manubrium.20 This forms a functional connection between the head, neck, and shoulder girdle.20,24 The quadratus lumborum has three fascicles, the inferior oblique, superior oblique, and the longitudinal fascicles. The inferior oblique works isometrically to stabilize the spine and laterally flex the spine.16,18 The other fibers of the quadratus lumborum actually work during stabilizing the twelfth rib.16 The abdominal muscles, internal/external obliques, transversus abdominus, and rectus abdominus make up the anterior portion of the ‘core.’ The act of ‘hollowing out’ the abdomen selectively activates the transversus abdominus, while isometrically bracing the abdomen activates the transversus abdominis, and external/internal obliques. The pelvic floor muscles also fire with activation of the transversus abdominis.16,18 The rectus abdominus is activated by doing curl-ups of the trunk, and in essence flexes the lumbar spine. The obliques work with the transversus abdominis to increase intra-abdominal pressure. The connection of these muscles with the thoracolumbar fascia, as noted previously, transfers contractile stresses in a ‘hooplike’ direction about the trunk, thereby increasing stability to the lumbar spine.16,17 The external oblique helps to prevent anterior pelvic tilt, and eccentrically controls lumbar extension and torsion.16 The diaphragm and pelvic floor serve as the roof and floor of the core, respectively. Akuthota and Nadler noted poor muscular coordination in both in those individuals with sacroiliac pain. As noted earlier, firing of the transversus abdominis also causes activation of the pelvic floor, and may be a way to improve muscular control of the pelvic floor. Instruction in diaphragmatic breathing may be a way to improve recruitment of the diaphragm.16 Regarding the cervical musculature, the muscles responsible for flexion of the cervical spine when firing bilaterally are the longus colli, scalenes, and the sternocleidomastoid. The muscles of extension, again firing bilaterally, are the splenius capitis, semispinalis capitis and cervicis. Muscles producing lateral flexion are the iliocostalis cervicis, longissimus capitis and cervices, splenius capitis and cervicis, trapezius, sternocleidomastoid, and the scalenes. Rotation is

produced by the unilateral action of the rotators, semispinalis capitis and cervicis, the multifidi, and the splenius cervicis.9,24 In general, the muscles posterior to the spinal column are stronger than those located anteriorly (Table 125.1).25

BIOMECHANICS OF SPINAL INJURY Denis derived a functional system to predict spinal vulnerability to injury. In this system, the spine is seen as divided into three columns, the anterior, middle, and posterior columns. The anterior segment extends from the anterior longitudinal ligament posteriorly through two-thirds of the vertebral body and intervertebral disc. The middle column extends from the posterior one-third of the vertebral body/ discs to the posterior longitudinal ligament. The posterior segment extends from the lamina posteriorly to the spinous process.26 Haher et al. have described the contributions the columns make to resistance of axial loading and compression. If two of the three columns are disrupted, the structural integrity of the spine, specifically its ability to resist axial loading, is severely compromised by as much as 80% (Fig. 125.1).1 As much as two-thirds of the disc is located in the anterior column. This characteristic accounts for the fact that destruction of the anterior anulus can result in as much as 90% loss of rigidity or a decrease in resistance to torque (Fig. 125.2).1 Haher et al. describe the center or axis of rotation of the spine as having no anatomic location. This is because its position is not static, but instead changes depending on the motion induced. The properties of the various spinal materials, as well as pathologic changes such as fractures and ligament sprains and muscle strains, also influence and alter the location of the axis of rotation.1 Because the axis of rotation is changing on a moment-to-moment basis, Haher et al. refer to it as the ‘instantaneous axis of rotation’ (IAR).1 The location of the spinal structures in relation to the IAR determines the amount of torque these structures will produce or resist. A two-dimensional study of the location of the IAR in the cervical spine revealed its location to be anterior to the neural canal in both flexion and extension. In the lumbar spine, this was observed to be located in the inferior disc of the observed vertebra.27 With injury to one of the columns, the IAR moves yet again. Haher et al. examined the effects of destruction of two of the three columns on the location of the IAR. Destruction of the anterior and middle column caused the IAR to move inferior and posterior with flexion (Fig. 125.3). When the posterior and middle columns were destroyed the IAR moved inferior and anterior during extension (Fig. 125.4).1 The disc has been shown to be important in resisting rotation or torsional forces, and consequently when damaged, limits the lumbar

Table 125.1: A summary of the cervical paraspinal muscles based on location Anterior cervical muscles

Posterior cervical muscles

Lateral cervical muscles

Longus colli

Superficial

Trapezius

Longus capitis

Splenius capitis and cervicis

Sternocleidomastoid

Rectus capitis anterior and lateralis

Longissimus capitis and cervicis

Scalenes – anterior, middle, and posterior

Iliocostalis cervicis Deep Semispinalis cervicis and capitis Rotatores

1333

Part 6: Interventional Spine in Sports Axial compression 60%

Fig. 125.1 The contribution of the three columns of the spine to axial loading. The associated numbers reflect the loss of stability as a result of the destruction of the corresponding structure. From Haher TR, Felmy WT, O’Brien M. Diagnosis and treatment of spinal fractures. In: Bridwell KH, DeWald RL, eds. Treatment of surgical spine disease. Philadelphia: JB Lippincott; 1991; with permission.

20%

A

M P

30% 70%

Loss of rotational stability (@ 5⬚)

Fig. 125.2 The contribution of the three columns of the spine to torsional rigidity. The associated numbers reflect the loss of rigidity as a result of the destruction of the 0% corresponding structure. From Haher TR, Felmy WT, O’Brien M. Diagnosis and treatment of spinal fractures. In: Bridwell KH, DeWald RL, eds. Treatment of surgical spine disease. Philadelphia: JB Lippincott; 1991; with permission.

Anterior 2/3 of disc

90%

Middle

35%

P

30%

I A -AM

Fig. 125.3 The effect of the three columns of the spine on the axis of rotation in flexion. With anterior and middle column destruction, the instantaneous axis of rotation (IAR) migrates posteriorly. From Haher T, Bergman M, O’Brien M, et al. The effect of the three columns of the spine on the instantaneous axis of rotation in flexion and extension. Spine 1991; 16: S312–S318; with permission.

spine’s ability to resist those forces.1 Haher et al. noted the importance of the anulus to resist rotation was greater than that of the Z-joints alone.1 They also noted that damage to the posterior and middle column resulted in a loss of rotational stability of 35% while damage to the anterior column resulted in a loss of rigidity to torsion by as much as 90% (Fig. 125.2). Disc disease or damage to the structures located anteriorly would significantly alter the ability of the lumbar spine to resist torsional forces.1,28 Haher et al. also notes the importance of the disc to resist lateral flexion as well. The importance of the zygapophyseal joints seems to be in the coupled motions, which occur at the spinal segments.1 1334

I

-P

Fig. 125.4 The effect of the three columns of the spine on the axis of rotation in extension. With middle and posterior columns destruction, the instantaneous -PM axis of rotation (IAR) migrates anteriorly and inferiorly.

The location of the IAR and its change in position with injury to the various columns is clinically relevant. The muscles farthest from the IAR have the greatest mechanical advantage in various planes of movement. The knowledge of the IAR location as well as the anatomical location of various muscle groups can help to direct the training and rehabilitation of the spine to protect from overload of the various structures.1 Haher et al. describe the use of this knowledge in optimizing athletic performance. If spinal rotation is limited or compromised, changing an athlete’s technique may not be beneficial, while physical therapy to restore rotation would be.1

BIOMECHANICS OF SPORTS-SPECIFIC INJURIES The specific demands of individual sports place increased loads on different aspects of the spine, making some athletes more prone to certain injuries than others. Sports can be broken down into categories according to the types of motions required of the spine. It follows, then, that these motions can help to identify which aspect of the spine is most vulnerable to injury.

The cervical spine Injuries to the cervical spine from athletic activity have been estimated to account for 5–10% of the 10 000 annual cervical spine injuries in the United States.4 Higher-risk sports are football, wrestling, gymnastics, diving, ice hockey, downhill skiing, and rugby.4,9,25

Fractures, dislocation, spinal cord injury Cervical spine injuries can result in fracture dislocation of the vertebrae, ligament disruption, disc injury, nerve root injury, and spinal hemorrhage. Spinal hemorrhages from sports-related trauma have only been reported in the cervical spine, and not in the thoracic or lumbar spine.25 All cases of quadriplegia, without spinal stenosis, reported by the National Center for Sports Injury Research, were the result of fracture dislocation of the cervical spine.25 This fact emphasizes the need for proper on-field management of suspected cervical spine injuries in order to prevent further damage from an unstable spine.25 The predominant mechanism of cervical spine injury in American football has been identified by Torg, in conjunction with the National Football head and neck injury registry, as one of axial loading.4,5,29 Axial loading has also been implicated as the primary mechanism of injury in the cervical spine for other sports such as diving and ice hockey.5–7 In diving this generally occurs with diving in shallow water,

Interventional Spine in Sports

while in hockey it often occurs with being checked from behind into the boards. Work done by other researchers evaluating the ability of hyperflexion and hyperextension movements to cause cervical spine fractures failed to show an occurrence of cervical spine fracture and dislocation.5 Axial loading occurs when a force is directed through the vertex of the head. In football, when the cervical spine is flexed 30 degrees, the energy-absorbing lordotic curve is eliminated (Fig. 125.5). The cervical spine is then unable to absorb the sudden axial load from the player in motion striking another player or object. The momentum of the player’s head must then be rapidly decelerated, while at the same time the player’s body continues its forward momentum. This results in the compression of the straightened cervical spine between the decelerated head and the forward momentum of the body. Ultimately, the cervical spine’s integrity fails, resulting in buckling of the cervical spine in a flexion direction with the end result being fracture and/or dislocation, most often at C4, C5, or C6, with subsequent spinal cord damage.4,5,9,29 The normal cervical spine can withstand loads up to 4450 Newtons before compression failure occurs.4 In 1976, rules were changed to ban the high-risk methods of spear tackling and head butting. This has decreased the incidence of quadriplegia from 35 per year to 1–6 incidents per year.4 In the rugby scrum, eight players bind together in prescribed positions to oppose an identical formation of the opposing team. In this situation, the mechanism of axial compression combined with flexion and rotation was shown to result in fracture dislocations at the C4–5 and C5–6 levels.30,31 As with football, the governing bodies of various rugby associations have made recommendations to depower the scrum and

Fig. 125.5 With the neck in 30 degrees of flexion, the normal lordotic curve is lost and the spine becomes a segmented column. If an axial load is applied the spine will buckle, most often at C4–5 or C5–6.

to control the point of engagement. This has resulted in decreased cervical spine injuries in the most vulnerable front row players. The fracture pattern resulting from axial loading is one of a teardrop fragment (fracture off the anterior inferior corner of the vertebral body). Torg notes that if this fracture occurs in isolation, permanent neurologic sequelae usually do not occur. If, however, the teardrop fracture occurs with a sagittal vertebral body fracture and fractures of the neural arch, permanent neurologic involvement is often present.9,29 Initially the forces in axially loaded segments can be absorbed by the discs, vertebrae, and paravertebral muscles.29

Transient quadriplegia or cervical cord neurapraxia Neurapraxia is a temporary paralysis which occurs after a collision with either another player or the ground. The symptoms resolve quickly, often within 10–15 minutes but occasionally as long as 24–36 hours later, but there is no residual impairment.5 The symptoms associated with this phenomenon include both sensory and motor findings. Sensory symptoms include burning pain, numbness, tingling, and loss of sensation. Motor findings can range from weakness to complete paralysis. Athletes so affected do not have cervical pain at the time of injury and radiographs are without evidence of fracture or subluxation.29 This injury has been associated with a group of athletes with developmental spinal stenosis.4,25,29 Torg et al. identified the association of cervical neurapraxia with developmental stenosis in an evaluation of 32 patients with this phenomenon; all had cervical stenosis at one or more levels.29 Herniated nucleus pulposus and spondylosis can also narrow the anteroposterior (AP) diameter of the spinal canal. In a hyperflexion or hyperextension injury, the cord can be transiently compressed. In hyperextension the posterior inferior portion of the superior vertebral body and the lamina of the vertebra below create a ‘pincer’ effect on the cord. The same can occur with hyperflexion, although in this instance the lamina of the superior vertebra and the superior aspect of the vertebra below approximate to compress the cord.4,29,31,32 Torg et al. introduced the concept of the ‘Torg ratio’ in 1986 as a way to identify developmental stenosis. This was based on plain radiographs in which the AP diameter, measured at the midpoint of the posterior aspect of the vertebral body to the nearest point on the spinolaminar line, is divided by the sagittal diameter of the vertebral body. A ratio of 0.80 or less was considered to be a developmentally stenotic canal.33 Since the original description of the Torg ratio, studies by Cantu et al. and Herzog et al. have shown a high percentage of false-positive Torg ratios in asymptomatic football players. This was attributed to the larger vertebral bodies noted in larger athletes.34,35 The use of magnetic resonance imaging (MRI) to directly evaluate the spinal canal and available space has led to the description of functional stenosis. Cantu notes that computed tomography (CT)myelogram or MRI can be used to assess the normal ‘functional reserve’ or the space surrounding the cord. This space contains the cerebrospinal fluid (CSF), which provides a protective cushion around the cord.34 Cantu’s use of MRI evidence of functional stenosis and increased risk of catastrophic neurologic injury has not yet been demonstrated in a population-based study. Nonetheless, it has been suggested that the presence of functional stenosis in an athlete with a prior episode of transient quadriparesis is a strong contraindication to further participation in collision sports.34,36 Researchers have also noted that in those athletes with spinal stenosis who sustained a fracture dislocation injury, there was no instance of complete neurologic recovery, while in athletes without spinal stenosis and fracture dislocation there have been instances of complete recovery.34 1335

Part 6: Interventional Spine in Sports

Spear-tacklers spine This refers to a collection of findings, which include developmental cervical spinal stenosis, loss of cervical lordosis, and evidence of prior cervical spine injury (i.e. disc bulges/herniations, healed compression fracture and evidence of spinal instability). The combination of these findings combined with an illegal spear-tackling technique increases the risk of neurologic injury.4

Burners or stingers Burners or stingers were thought to occur from cervical nerve root neuropraxia.4,25,37 Needle electromyographic studies have also shown injuries to the cords and trunks of the brachial plexus as well as injuries to peripheral nerves.34,38 Symptoms can include a transient occurrence of lancinating burning-type pain radiating down the involved upper extremity with or without muscle weakness. The muscles most often involved are the deltoid, biceps, supraspinatus, and infraspinatus.4,25 This can last for minutes or several days and only occurs unilaterally.4,25,37,38 This phenomenon is estimated to occur in as many as 50–65% of all college football players per year.4,37 The football players most vulnerable to burners are defensive backs.38 There are two mechanisms of injury noted. The first involves a traction injury to the brachial plexus, which usually occurs from a combination of lateral neck flexion away from the involved side and shoulder depression: for example, lateral neck flexion left with depression of the right shoulder.4,25,37,38 The second mechanism of injury involves a compression of the nerve root within the foramen, most often from the head and neck in an extended and side-bent position, while being driven down toward the ipsilateral shoulder.25,37,38 This results in pinching of the nerve root within the foramen.4,25,37,38 Levitz et al. looked at a group of athletes with chronic, recurrent burners which they defined as having ‘1) a chronic, recurrent neurapraxia or axonotmesis or both of a nerve root associated with prolonged weakness, 2) time loss from practice and games, and 3) recurrence.’37 The mechanism of injury in these individuals is one of cervical spine extension and lateral deviation towards the involved side.37 In their study, Levitz et al. also noted a high incidence of cervical canal stenosis, reversal of the normal cervical lordosis, disc disease, and foraminal narrowing secondary to osteophyte formation. They further suggest that while acute burners may well be due to a brachial plexus traction injury, chronic burners are more likely due to nerve root or dorsal ganglion compression within the foramen secondary to disc changes.37 Meyer et al. confirmed a similar finding. They noted that in athletes sustaining chronic stingers, the predominant mechanism was one of extension with lateral compression towards the ipsilateral shoulder. Their findings also demonstrated a higher incidence of cervical canal narrowing in symptomatic versus asymptomatic football players.39 The mechanism of injury for the younger player appears to be one of traction or stretch injury to the brachial plexus. In the older collegiate or professional players the mechanism is a pinching of the nerve root within the neural foramen.25,37,38 In athletes with chronic or repeated stingers, persistent proximal arm weakness and pain may develop. In these individuals the use of a cervical roll and or high shoulder pads in conjunction with retraining in proper tackling and blocking techniques should be instituted. If symptoms persist despite these interventions, a change of position or complete stoppage of play may be necessary.4,25

The lumbar spine Low back pain in the athlete is a fairly common occurrence, with studies noting an overall incidence of low back pain in 27% of 1336

collegiate football players and 50% of football interior lineman.28,38 The lifetime incidence of low back pain in football players is 10–15% during participation years.28 In intercollegiate sports, the injury rates for low back pain over a 10-year period were highest for the sports of football and gymnastics. Low back pain can result from muscle strains, ligament sprains, spondylolysis with or without spondylolisthesis, disc disease, radiculopathy, facet syndrome synovitis, sacroiliac joint dysfunction, and myofascial pain syndromes.38,40–42 These injuries are the result of excesses of axial compression, tension, rotational torque, or shear forces. Examples of sports involving high compressive loads are football, rugby, and weightlifting. Baseball, golf, tennis, basketball, soccer, and boxing are associated with high rotational or shear forces. Tensile or bending stresses are associated with swimming, gymnastics, and rowing.42,43 In general, hyperextension will tend to result in posterior element injury, while flexion causes increased stress to the Z-joints posteriorly or the disc anteriorly.41 Injuries to the lumbar spine can occur with acute compressive loads or with repetitive microtrauma.41,44 Lumbar strain/sprain injuries involve injury to the lumbar muscles and ligaments, respectively. These can occur from repetitive muscular contraction41 or from a sudden extension–contraction to the unprepared spine resulting in muscle and ligament disruption.40 Athletes who undergo a sudden change in training intensity or duration, or change in skill technique, may be at increased for these types of injuries.41

Fractures Fractures of the lumbar spine are most often compression-type fractures as a result of sudden axial loading.9 This has been noted in snowmobiling and tobogganing.1,9,45 These injuries will often occur at the T12 and L1 vertebrae. In snowmobiling, these injuries have occurred following a sudden drop into a hole or hitting a bump.9,45 A burst fracture of the thoracolumbar spine can occur from a vertical impact from below.8 Compression fractures of the thoracic and lumbar spine have also occurred in football players.28 Fractures of the spinous process and transverse process can occur as well. Transverse process fractures may occur from sudden forceful contraction of the quadratus lumborum or psoas. Fracture of the spinous process may occur from a direct blow to the area.45 Both of these fractures have occurred in football players.28 Vertebral endplate fractures with subsequent herniation of the nucleus pulposus into the vertebral body may occur in the younger athlete. This is due to the relative weakness of the endplate versus the disc in the skeletally immature athlete. With a rapid compressive load, the young disc can better withstand compression than the endplate, and ultimately the endplate fails.1,9,28,40 This endplate defect is referred to as a Schmorl’s node. This can be seen in weightlifters and football players.40

Lumbar disc disease Lumbar disc disease and herniations can occur with a flexion and lateral bending preload followed by rapid compression load.1 These types of movement can be seen in football, rugby, skiing, and weightlifting.1 Tears to the anulus without disc herniation were noted with flexion and torsion motions.1,12,41 The anterior lumbar intervertebral disc resists rotation and torque. An annular tear significantly compromises the disc’s ability to resist these motions.1,41 In sports requiring increased rotational stress, such as tennis and baseball, repetitive loading of the disc with both rotational and hyperextension motions results in fissuring and weakness of the anulus.1,41,45

Interventional Spine in Sports

Hainline describes three theories to explain lumbar disc pathology in tennis players. The first possibility involves excess fatigue in either underconditioned or overworked lumbar paraspinal muscles with subsequent transfer of kinetic stress to the ligaments. Because of the ligament’s limited ability to withstand these stresses, the loads are consequently transferred to the discs. Inadequate stability from weakened muscles and ligaments imparts an increased shearing effect on the caudal lumbar discs. The second explanation speaks to the nature of the serve, which requires repetitive rotational forces combined with hyperextension. This can result in excess annular shear forces and subsequent tears. Finally, he notes that tennis players who have experienced these injuries may have a hereditary predisposition to them.41 Football imparts a series of repetitive flexion, extension, and torsion movements coupled with axial loading moments to the lumbar spine.28 A study of interior lineman showed higher levels of disc degeneration compared to other positions.28 Gatt et al. studied offensive lineman while they were hitting a blocking sled, and evaluated loads at the L4–5 segment. The blocking sequence imposes compression, shear, and lateral bending forces to the lumbar spine. The Gatt et al. study found extraordinary compressive forces averaging 8679 N±1965 N.28,46 To reiterate, the lumbar disc is the prime stabilizer to rotational forces and is more important than the Z-joint in resisting rotation. Damage to the lumbar disc compromises its ability to resist rotation, leading to instability as well as placing more weight-bearing load on the Z-joints.1,27,41

Spondylolysis Spondylolysis is a defect of the pars interarticularis, either congenital or acquired.28,38,40,44,47,48 Higher rates of spondylolysis have been noted in gymnastics, football, power/weightlifting, tennis, figure skating, and hockey,38,47,48 while another study reported higher rates occurring in weightlifting, judo, rugby, and football.43 The incidence of spondylolysis has been estimated to be 3–6% in the general population,38,47,48 with males affected 2–3 times as often as females.48 As well, higher incidences are noted in athletes overall.47,48 In football 15% of high school and college players had spondylolysis, while interior lineman had incidence rates as high as 50%.28 While this defect was initially thought to be congenital, current theory now is one of acquisition from either a single sudden overload event or more commonly with repetitive loading.45,47,48 It is felt by many that the repetitive demands of various sporting activities places increased stress on the lumbar spine, thereby causing the higher rates of spondylolysis seen in athletes.44,47–49 The mechanism of repetitive lumbar flexion and extension causes excess load at the L5–S1 level with stresses greatest at the pars interarticularis.28,47,48 It is this repetitive loading which makes the pars more vulnerable to fatigue fractures under lower loads.47,48 The L5 vertebra is the most common level to sustain a spondylitic defect, with 85–95% off defects occurring at this level. The L4 level sustains 5–15% of such defects.47,48 The sports of gymnastics, diving, football (especially offensive lineman), rugby (forwards or players involved in the scrum), weightlifting, and hockey involve repetitive lumbar flexion and extension motions, and consequently exhibit the highest rates of spondylolysis.

Spondylolisthesis Spondylolisthesis is defined as a sagittal plane translation of one vertebra over another. Anterolisthesis and retrolisthesis are terms frequently used to describe the direction of slippage of the superior

vertebral body relative the one immediately below. It most often occurs at the L5–S1 junction and is a result of the loss of continuity of an intact pars articularis or a bilateral spondylolysis.9,38,40 The mechanism most often attributed to the development of spondylolisthesis is a fatigue fracture or stress fracture occurring bilaterally at the pars interarticularis with resultant forward slippage of the superior vertebra on the one below. The risk of progression of forward slippage has been studied and has been noted to be fairly small. In a study of 47 patients under the age of 16 with either symptomatic spondylolysis or spondylolisthesis over a 7-year period, only two individuals had a slip progress to more than 20%. Various studies of adolescents have shown the percentage of slip progression greater than 20% was 3–4% in these individuals with spondylolysis or low-grade spondylolisthesis.48 Also of note was that the increased tendency towards forward slippage was greatest in adolescents during their growth spurt. No specific increased risk for slip progression was noted with sports participation.48 The sports most often associated with this injury are the same as those associated with spondylolysis. Those sports with repetitive lumbar flexion and extension motions have higher rates then other sports. The body mechanics associated with spondylolysis and spondylolisthesis is one of hyperlordosis in the lumbar spine with excessively tight hamstrings.28,48 Increased lumbar lordosis has been associated with tight hip flexors, tight thoracolumbar fascia, thoracic kyphosis, weak abdominals, and genu recurvatum.28,49 In general, injuries to the lumbar spine can occur from 1 of 3 forces occurring either alone or in combination. These are compression, tension, or torque (either shear or rotational).40,42 Compression or axial loading can lead to vertebral endplate fracture or ultimately vertebral body compression fracture. Sports associated with these forces are football and weightlifting.50,51 Running has been shown to produce compressive forces sufficient to decrease intervertebral disc height. Because the lumbar discs are dynamically loaded during running the decrease in disc height is greater than with static loading.52 Axial loading in combination with hyperextension places increased shear stress on the posterior elements, ultimately leading to a higher risk of spondylolysis and spondylolisthesis.40,42,47 Sports associated with these motions are football (offensive linemen),28,40,42,43,47,48 gymnastics,40,42,44,48,49 weightlifting, diving, volleyball,40,42,49 the throwing field events of track and field,40 high jumping, and pole vaulting.40 Rotational forces are associated with baseball and softball batting, throwing, golf, and tennis.2,20,40,42,43 Rotation forces initially place increased stress on the disc, but with continued rotation this shifts to the Z-joints.42

SUMMARY Proper management of spinal pain and injury requires a comprehensive understanding of both the biomechanics of the spinal segment and the biomechanics of the skill involved in the injured athlete’s sport. Prevention and rehabilitation of spinal injuries involve application of these principles to the rehabilitation program. For example, restoration or correction of normal spinal curves helps the spine to absorb and disperse loads.4,5,9 Therefore, prior to return to play from an injury, athletes with cervical spine injuries should have restoration of normal cervical lordosis.4 Correction of hyperlordosis in the lumbar spine by addressing lack of flexibility in the hip flexors, thoracolumbar fascia, and weakness of the abdominal muscles can help prevent additional overload of the posterior elements.28 Proper strengthening of the cervical spine via cervicothoracic stabilization is important in both the rehabilitation and prevention of cervical spine injuries. 1337

Part 6: Interventional Spine in Sports

These include scapular stabilization exercises as well as strengthening of the cervical intrinsic musculature.4,53 Strengthening of the trunk, lumbar spine, hip girdle muscles, and the lower extremity is important to ensure the transfer of forces from the lower extremities through the lumbar spine. Moreover, it prevents overload of structures due to a weak link in the kinetic chain. Core strengthening for sporting activities should involve training in three planes: sagittal, frontal, and transverse.16 Triplanar core strengthening accomplishes more than just simple muscular strengthening, but involves muscle reeducation, improvement of muscular endurance, and improvement in balance and proprioception.16 Finally, coaches and physicians should work together to instruct athletes on safe training techniques and proper skill mechanics in order to prevent injury, enhance performance, and prolong playing careers. When necessary, physicians should work with sporting officials and governing bodies to implement rules changes to decrease injury to players. This has helped to dramatically decrease the number of spinal cord injuries seen in football29 and rugby.6,7,30,31

References 1. Haher TR, O’Brien M, Kauffman D, et al. Biomechanics of the spine in sports. Clin Sports Med 1993; 12:449–464. 2. Young JL, Casazza BA, Press JM, et al. Biomechanical aspects of the spine in pitching. In: Andrews JR, Zarins B, eds. Injuries in baseball. Philadelphia: LippincottRaven; 1998:23–35. 3. Wells MR. Biomechanics: an osteopathic perspective. In: Ward RC, et al., eds. Foundations for osteopathic medicine, 2nd edn. Philadelphia: Lippincott Williams & Wilkins; 2003:63–89. 4. Kim DH, Vaccaro AR, Berta SC. Acute sports-related spinal cord injury: contemporary management principles. Clin Sports Med 2003; 7:22. 5. Torg JS, Vegso JJ, O’Neill, J, et al. The epidemiologic, pathologic, biomechanical, and cinematographic analysis of football-induced cervical spine trauma. Am J Sports Med 1990; 18:50–57.

23. Vleeming A, Pool-Goudzwaardmaard AL, Stoeckart R, et al. The posterior layer of the thoracolumbar fascia. Its function in load transfer from spine to legs. Spine 1995; 2:753–758. 24. Moore KL. Clinically oriented anatomy, 3rd edn. Baltimore, MD: Williams & Wilkins; 1992:323–372. 25. Proctor MR, Cantu RC. Head and neck injuries in young athletes. Clin Sports Medicine 2000; 19(4):693–715. 26. Denis F. The three-column spine and its significance in the classification of the acute thoracolumbar spinal injury. Spine 1983; 8:817–831. 27. Haher T, Bergman M, O’Brien M. Effect of 3 columns on the instantaneous axis of rotation in flexion and extension. Spine 1991; 16:312–318. 28. Gerbino PG, d’Hemecourt PA. Does football cause an increase in degenerative disease of the lumbar spine. Curr Sports Med Rep 2002; 1:47–51. 29. Torg JS, Thibault L, Sennett B, et al. The pathomechanics and pathophysiology of cervical spinal cord injury. Clin Orthopaed Rel Res 1995; 321:259–269. 30. Milburn PD. Biomechanics of rugby union scrummaging. Sports Med 1993; 16: 168–179. 31. Silver JR, Stewart D. The prevention of spinal injuries in rugby football. Paraplegia 1994; 32:442–453. 32. Silver JR. Injuries of the spine sustained during rugby. Br J Sports Med 1992; 26:253–258. 33. Torg JS, Pavlov H, Genuario SE, et al. Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg [Am] 1986; 68(13):54–70. 34. Cantu RC. Stingers, transient quadriplegia, and cervical spinal stenosis: return to play criteria. Med Sci Sports Exerc 1997; 29(Suppl 7):S233–S235. 35. Herzog RJ, Wiens JJ, Dillingham MF, et al. Normal cervical spine morphometry and cervical spinal stenosis in asymptomatic professional football players. Spine 1991; 16(Suppl 6):S78–S86. 36. Cantu RC. The cervical spinal stenosis controversy. Clin Sports Med 1998; 17: 121–127. 37. Levitz CL, Reilly PJ, Torg JS. The pathomechanics of chronic, recurrent cervical nerve root neurapraxia. The chronic burner syndrome. Am J Sports Med 1997; 25:1.

6. Wetzler MJ, Akpata T, Albert T, et al. A retrospective study of cervical spine injuries in American rugby, 1970–1994. Am J Sports Med 1996; 24:454–458.

38. Sherman AL, Young JL. Musculoskeletal rehabilitation and sports medicine. Head and spine injuries. Arch Phys Med Rehab 1999; 80:S40–S49.

7. Wetzler MJ, Akpata T, Laughlin W, et al. Occurrence of cervical spine injuries during the rugby scrum. Am J Sports Med 1998; 26:177–180.

39. Meyer SA, Schulte KR, Callaghan JJ, et al. Cervical spinal stenosis and stingers in collegiate football players. Am J Sports Med 1994; 22:158–166.

8. Sances A, Myklebust JB, Maiman DJ, et al. The biomechanics of spinal injuries. Crit Rev Biomed Eng 1984; 11:1–76.

40. Alexander MJL. Biomechanical aspects of lumbar spine injuries in athletes: a review. Can J Appl Sport Sci 1985; 10(1):1–20.

9. White AA, Panjabi MM. Clinical biomechanics of the spine, 2nd edn. Philadelphia: Lippincott Williams & Wilkins; 1990.

41. Hainline B. Low back injury. Clin Sports Med 1995; 14:241–265.

10. Panagiotacopulos ND, Pope MH, Block R, et al. Water content in human intervertebral discs, Part II. Viscoelastic behavior. Spine 1987; 12:918.

42. Montgomery S. Haak M. Management of lumbar injuries in athletes. Sports Med Feb 1999; 27:135–141.

11. Hochschuler S. The spine in sports. Philadelphia: Hanley and Belfus; 1990.

43. Ichikawa N, O’Hara Y, Morishita T, et al. An aetiological study on spondylolysis from a biomechanical aspect. Bri J Sports Med 1982; 16:135–141.

12. Adams M, Hutton WC. The relevance of torsion to the mechanical derangement of the lumbar spine. Spine 1981; 6:247–248.

44. Hall SJ. Mechanical contribution to lumbar stress injuries in female gymnasts. Med Sci Sports Exer 1986; 18:599–602.

13. Adams MA, Hutton,WC. Prolapsed intervertebral disc. A Hyperflexion injury. Spine 1982; 7(3):184.

45. Bowerman JW, McDonnell EJ. Radiology of athletic injuries – football. Radiology 1975; 117:33–36.

14. Crusco JJ, Panjabi MM. Euler stability of the human ligamentous lumbar spine. Part 1 Theory. Clin Biomechan 1992; 7:19–26. Part II, Experiment. 1992; 7:27–32.

46. Gatt CJ, Hosea TM, Palumbo RC. Impact loading of the lumbar spine during football blocking. Am J Sports Med 1997; 25:317–319.

15. Granata KP, Orishimo KF. Response of trunk muscle coactivation to changes in spinal stability. J Biomechanics 2001; 34:1117–1123.

47. Letts M, Smallman T, Afanasiev R, et al. Fracture of the pars interarticularis in adolescent athletes: A clinical-biomechanical analysis. J Pediatr Orthoped 1986; 6:40–46.

16. Akuthota V, Nadler SF. Core strengthening. Arch Phys Med Rehab 2004; 85:Suppl 1.

48. Standaert CJ, Herring SA. Spondylolysis: a critical review. Br J Sports Med 2000; 34:415–422.

17. McGill SM, Low back disorders: evidence based prevention and rehabilitation. Champaign, IL: Human Kinetics; 2002. 18. McGill SM. Low back stability: from formal description to issues for performance and rehabilitation. Exerc Sport Sci Rev 2001; 29(1):26–31. 19. Richardson C, Jull G, Hodges P, et al. Therapeutic exercise for spinal segmental stabilization in low back pain; scientific basis and clinical approach. Edinburgh: Churchill Livingstone; 1999.

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22. McGill SM, Norman RW. Potential of lumbodorsal fascia forces to generate back extension moments during squat lifts. J Biomed Eng 1988; 10:312–318.

49. Gerbino PG, Micheli LJ. Back injuries in the young athlete. Clin Sports Med 1995; 14:3. 50. Garbutt G, Boocock MG, Reilly T, et al.. Physiological and spinal responses to circuit weight training. Ergonomics 1994; 37(1):117–125. 51. Granhed J, Jonson R, Hansson T. The loads on the lumbar spine during extreme weight lifting. Spine 1987; 12:146–149.

20. Young JL, Herring SA, Press JM, et al. The influence of the spine on the shoulder in the throwing athlete. J Back Musculoskel Rehab 1996; 7:5–17.

52. Ahrens SF. The effect of age on intervertebral disc compression during running. JOSPT 1994; 20:1.

21. Bogduk N, Anat D, Macintosh JE. The applied anatomy of the thoracolumbar fascia. Spine 1984; 9:164.

53. Cross KM, Serenelli C. Training and equipment to prevent athletic head and neck injuries. Clin Sports Med 2003; 22:3.

PART 6

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126

INTERVENTIONAL SPINE IN SPORTS

On-the-field Assessment of the Cervical Spine-Injured Athlete Jonathan A. Drezner

INTRODUCTION Physicians caring for athletes during sports competition must be prepared to evaluate and treat injuries to the cervical spine. While most injuries are mild and self-limiting, injury to the spinal cord resulting in temporary or permanent neurologic injury is a rare but potentially catastrophic event. The medical team at sporting events must be prepared to assess, stabilize, and transport athletes with suspected cervical spine injuries. Cervical spine trauma is most common in contact or collision sports such as American football, rugby, and ice hockey.1–6 Other sports such as gymnastics, skiing, wrestling, and diving also carry a higher risk of injury.1,7,8 American football has provided the largest population of athletes to follow with serious cervical spine injuries. The National Center for Catastrophic Sports Injury Research reported a total of 223 spinal cord injuries in American football between 1977 and 2001, with an incidence of cervical spinal cord injury in high school football of 0.52/100 000 participants, 1.55/100 000 participants in college football, and 14/100 000 participants in professional football.9 Cervical spinal cord injuries were also the most common catastrophic football injury and the second leading cause of death attributable to football.9 The objective of this chapter is to review the on-the-field assessment of an athlete with a suspected cervical spine injury. A thorough understanding of the mechanism and spectrum of injuries to the cervical spine during athletic participation is essential for a physician to properly evaluate an injured athlete. A detailed review of the literature regarding cervical cord neurapraxia, cervical spinal stenosis, and return to play recommendations after an episode of transient cervical cord injury is included.

A NOTE ON ATHLETIC BRAIN INJURY AND CONCUSSION While a detailed discussion of athletic head and brain injury is beyond the scope of this chapter, physicians treating spine-injured athletes must be conscious of the potential for a concurrent head injury. Injuries to both the brain and cervical spine usually result from a similar mechanism, i.e. traumatic blows to the head, and the medical team must always suspect injury to both in the assessment of an injured athlete. Severe closed head injuries include diffuse axonal injury, intracerebral hemorrhage, intracerebral contusion, subdural hematoma, and epidural hematoma. Concussion is the most common sports-related head injury and is defined as a transient post-traumatic alteration in neural functioning. Concussive symptoms include confusion, dizziness, headache, visual disturbance, nausea, equilibrium disturbance, difficulty concentrating, post-traumatic amnesia, and loss of consciousness. Many classifications of concussion have attempted to grade the severity

of concussion based on clinical presentation and duration of symptoms.10,11 Recent research involving neuropsychological testing preand post-concussion has better delineated which symptoms correlate with severity and the time needed for full recovery.12 Collins et al.12 showed that the presence of amnesia, not loss of consciousness, is the best predictor of concussion severity and neurocognitive deficits. For the sideline evaluation, no athlete with a concussion should be allowed to return to play if still symptomatic. Several references are available which summarize recent advances and recommendations in the management of athletic concussion.13–15

MECHANISM OF INJURY Understanding the mechanisms of cervical spine injuries will assist the physician to properly evaluate and manage an injured athlete. For the on-site medical team, direct observation of the mechanism of injury is the first step in the evaluation of an injured player and is helpful in assessing the likelihood of significant injury.

Axial loading The mechanism of injury to the cervical spine and associated anatomic risk factors that lead to serious neurologic injury have been the subject of active interest and debate within the sports medicine and spine surgery communities. Early research suggested that serious cervical spine injuries occurred from forced hyperflexion2–7,16 or hyperextension.17–20 However, more recently axial loading has been defined as the most likely mechanism for catastrophic injury to the cervical spine during sports competition. Axial loading occurs when a player strikes another player with the top of the head as the point of initial contact (so-called ‘spear tackling’). Axial loading places the cervical spine at a biomechanical disadvantage and makes it particularly susceptible to severe injury. Typically, most forces from a traumatic load to the cervical spine are dissipated through controlled spinal motion, the paravertebral muscles, and the intervertebral discs. When the top or crown of the helmet is used for initial contact, the neck is typically flexed approximately 30° and loses its normal cervical lordosis and ability to properly distribute force (Fig. 126.1). In this position the cervical spine assumes the characteristics of a segmented column and forces are transmitted along the longitudinal axis of the spine (Fig. 126.2).21 In athletes with cervical spinal stenosis, axial loading followed by forced hyperextension or hyperflexion can cause transient or permanent sensory and motor changes. Penning19 described a ‘pincer mechanism’ with compression of the spinal cord between a vertebral body and the spinolaminar line of an adjacent vertebra. Compression of the spinal cord occurs in hyperextension when the distance between the posteroinferior margin of the superior vertebral body and the anterosuperior aspect of the spinolaminar line 1339

Part 6: Interventional Spine in Sports Flexion Extension

A

B

Fig. 126.1 (A) In the normal upright anatomical position, the cervical spine is slightly extended with a natural cervical lordosis. (B) When the neck is flexed to approximately 30°, the cervical spine is straightened and loses its ability to properly distribute force.

of the subjacent vertebra decreases (Fig. 126.3). With hyperflexion, the anterosuperior aspect of the spinolaminar line of the superior vertebra and the posterosuperior margin of the inferior vertebra approximate. Eismont et al.20 also noted that hyperextension causes narrowing of the anteroposterior diameter of the spinal canal and can compress the spinal cord. Torg et al.22 described an axial load input with subsequent hyperextension and indentation of the ligamentum flavum with compression of the spinal cord. In each of these mechanisms, the anteroposterior diameter of the spinal canal decreases, resulting in compression of the spinal cord. Transient or permanent cervical cord injury can occur and usually involves a contusion of the spinal cord with temporary restriction of blood flow and a focal area of ischemia.8 While advances in helmet materials and equipment used in American football lead to a decrease in head injuries, it also contributed to the development of dangerous playing techniques using the top of the helmet as the initial point of contact. Torg et al.23 compared the total number of head and neck injuries in the National

Fig. 126.3 Hyperextension ‘pincer mechanism’ as described by Penning.19 During hyperextension, the distance between the posteroinferior aspect of the superior vertebral body and the anterosuperior aspect of the spinal laminar line of the subjacent vertebra decreases, and the cord is pinched between the two vertebral bodies.

Football League between 1971 and 1975 with previous work done by Schneider24 analyzing injuries between 1959 and 1963. The major difference between these time periods was the type and quality of helmet worn during competition. The study found a reduction in intracranial hemorrhages of 66% and deaths due to intracranial injury of 42%. However, the study also found a 204% increase in cervical spine fractures, subluxations, and dislocations and a 116% increase in the number of cases of permanent quadriplegia. The majority of cases of permanent quadriplegia that occurred were due to direct compression when a player struck another player with the top of his helmet. Delineation of the axial load mechanism as the major cause of catastrophic cervical spine injury in American football resulted in rule changes that caused a sustained decrease in the rate of cervical spine injuries and quadriplegia. In 1976 the National Collegiate Athletic Association banned ‘spearing,’ defined as intentionally striking an opponent with the crown of the helmet, as well as other tackling techniques in which the helmet is used as the initial point of contact. In 1976, the rate of cervical spine fracture, subluxation, and dislocation was 7.72/100 000 and 30.66/100 000 in high school and college athletes, respectively. In 1987, this had decreased to 2.31/100 000 and 10.66/100 000 serious injuries to the cervical spine in high school and college athletes, respectively.21 Injuries resulting in permanent quadriplegia also significantly decreased as a result of the rule changes. In 1976, the rate of quadriplegia was 2.24/100 000 and 10.66/100 000 in high school and college athletes, respectively. In 1977, only 1 year after the rule changes, these rates decreased to 1.30/100 000 and 2.66/100 000 in high school and college athletes, respectively, and have continued to remain low.21 In 1990 Torg and colleagues25 further confirmed axial loading as the mechanism in catastrophic cervical spine injury by review of actual game films and videotapes. Analysis of films allowed an accurate determination of the mechanism of injury in 85% of cases, and axial loading was found to be the mechanism in every case.

INJURIES TO THE NECK AND SPINAL CORD A

B

C

D

E

Fig. 126.2 (A) Spear-tackler’s spine involves loss of the normal cervical lordosis and an axial load. (B) The straightened cervical spine assumes the characteristics of a segmented column and forces are transmitted along the longitudinal axis of the spine, first compressing the intervertebral discs. When maximum compression is reached the spine flexes and fails (C) with potential fracture, subluxation, or dislocation (D,E).

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Before discussing the on-the-field management of cervical spine injuries, it is necessary to review the spectrum of cervical spine injuries that occur. The medical team must be aware of the conditions they will need to recognize and treat. Athletic neck injuries can occur to any of the soft tissue, bony, or neurologic elements of the cervical spine – including muscle strains, peripheral nerve injuries, central cord injury, fractures, and dislocations.

Interventional Spine in Sports

Strains and sprains Soft tissue injuries to the cervical spine, such as muscle or tendon strains and ligament sprains, are probably the most common sportsrelated neck injuries. These injuries are typically mild and self-limiting and present with minor neck pain and without any neurologic symptoms. Indicators of a more significant spine injury include significant cervical muscle spasm, tentative active range of motion, and severe pain. Evaluation of the athlete includes active cervical spine range of motion and strength testing of the neck and upper extremities. Manual compression and axial load to the cervical spine (Spurling’s maneuver) should not cause pain or radicular symptoms and is helpful in ruling out more significant injury. The athlete can return to play when full pain-free range of motion and normal strength of the cervical spine are restored. It is important that no symptomatic athlete returns to competition. Occasionally, more significant ligamentous injury may go unrecognized but should be suspected if persistent muscle spasm and limited range of motion lasts days or weeks following the injury. In this case, flexion and extension radiographs of the cervical spine should be taken to rule out instability.

Stingers ‘Stingers’ or ‘burners’ are descriptive terms used to characterize transient unilateral upper extremity pain and paresthesias following a blow to the neck or shoulders. Because of confusion with a potentially more serious central cord injury called ‘burning hands syndrome,’26 use of the term ‘stinger’ rather than ‘burner’ is encouraged. Stingers are very common and are reported in up to 50–65% of college football players.27,28 Stingers are peripheral nerve injuries, not spinal cord injuries, and are considered a transient neurapraxia of the cervical nerve roots or upper trunk of the brachial plexus, usually involving the C5 and/or C6 distribution. Because the dorsal root ganglion is positioned within the neural foramen, symptoms may be purely sensory and in a dermatomal distribution. Stingers are characterized by burning dysesthesias that typically begin in the shoulder region and radiate unilaterally into the arm and hand. Weakness, numbness, or both are sometimes associated with the burning pain. Initially, there can be a great deal of posterior cervical tenderness because the posterior primary ramus of the nerve innervates the skin in that area and comes directly off the dorsal root ganglion. Stingers usually result from one of two mechanisms: tensile overload or compression overload.29 While either mechanism is possible in any athlete, the mechanism of injury is more likely depending on the age of the athlete. In most high school athletes, the mechanism involves a tensile or stretch injury when the involved arm and neck are stretched in opposite directions. This occurs as the neck is forcibly stretched away while the ipsilateral shoulder is depressed (Fig. 126.4). In the older college or professional athlete with a higher likelihood of degenerative changes of the cervical spine, a compressive mechanism is more likely. This involves a compression or ‘pinch’ of the cervical nerve root within the neural foramen as the neck is forcibly flexed in a posterolateral direction towards the symptomatic upper extremity (see Fig. 126.4).30 Stingers must be differentiated from spinal cord injuries. The key distinguishing feature is that stingers result in unilateral upper extremity impairment. Spinal cord injury results in multiple limb involvement, i.e. bilateral upper extremities or both upper and lower extremities. Stingers typically resolve in minutes. Sideline evaluation of an athlete with a stinger involves a complete neck and upper extremity neurologic examination. As the symptoms improve, the athlete will demonstrate improved cervical spine range of motion. Athletes with transient stingers are safe to return to play when

Tensile load

Compression load

Fig. 126.4 ‘Stingers’ result from either a tensile or compression load. A blow to the neck producing lateral neck flexion with ipsilateral shoulder depression causes a traction or tensile load to the cervical nerve roots and upper trunk of the brachial plexus. Forceful flexion of the neck in a posterolateral direction causes compression of the nerve roots within the neural foramen.

symptoms have fully resolved, the athlete can demonstrate normal cervical neck range of motion, Spurling’s maneuver is negative, and neurologic and strength examinations are normal. Recurrent stingers are more common in the presence of cervical degenerative disc disease. Levitz et al.30 studied 55 athletes with recurrent stingers. The mechanism of injury was extension combined with ipsilateral compression in 83% of patients, and 70% had a positive Spurling’s sign. Eighty-seven percent of patients had evidence of disc disease by magnetic resonance imagimg (MRI), and 93% had disc disease or narrowing of the intervertebral foramina. The authors concluded that nerve root compression in the intervertebral foramina secondary to degenerative disc disease was the likely cause of recurrent or chronic stinger syndromes in collegiate and professional athletes. Athletes with more than one stinger can be placed in a protective neck collar that limits lateral neck flexion and hyperextension. Rarely, more significant nerve injury and axonotmesis occurs causing chronic symptoms. Patients usually demonstrate persistent weakness in the distribution of the upper trunk of the brachial plexus, and muscle atrophy may be present in severe cases. Electromyography will assess the distribution and degree of injury and should be performed if symptoms have lasted more than 3 weeks. Most cases of axonotmesis have a high likelihood of recovering within 1 year.27

Cervical cord neurapraxia and transient quadriplegia Injury to the spinal cord can be complete or be neurapraxic – a reversible injury with motor and sensory function returning within 24–48 hours. Neurapraxia of the cervical spinal cord is characterized by an acute, transient sensory and/or motor change to more than one extremity. Symptoms include burning pain, numbness, tingling and loss of sensation with or without motor changes of paresis or complete paralysis.31 Several other terms have been used to describe cervical cord neurapraxia and have been used interchangeably, including ‘transient quadriplegia,’31 ‘central cervical spinal cord syndrome,’32 and ‘spinal cord concussion.’33 1341

Part 6: Interventional Spine in Sports

The most typical pattern of incomplete spinal cord injury is the central cord syndrome. This involves weakness of the upper extremities in excess of lower extremity findings secondary to the lamination of the corticospinal tracts and selective damage to fibers serving arm and hand function. ‘Burning hands syndrome’ described by Maroon26 is characterized by burning dysesthesias of the hands and associated weakness of the upper extremities and is a variant of central cord syndrome. Transient quadriplegia is a temporary paralysis characterized by loss of motor function, with or without sensory disturbances.31 Episodes of cervical cord neurapraxia are transient by definition and complete recovery usually occurs in 10–15 minutes, although in some patients gradual resolution occurs over 1–2 days. Except for burning paresthesia, the athlete does not experience neck pain, and there is complete return of motor function and full, pain-free range of motion of the cervical spine. Torg et al.34 studied 110 patients with transient cervical cord neurapraxia and found that 40% presented with plegia (complete motor weakness), 25% with paresis (incomplete motor weakness), and 35% with only paresthesia and sensory symptoms. The neurapraxia resolved in 74% of patients within 15 minutes and lasted more than 24 hours in 11% of patients. Eighty percent of patients had symptoms in all 4 extremities, 15% in the upper extremities only, 2% in lower extremities only, and 3% with symptoms in the ipsilateral upper and lower extremities. Of 110 patients, 109 had a complete neurologic recovery, with one patient having a residual hemiplegia following operative intervention. For those athletes who did return to football, the recurrence rate for transient cervical cord neurapraxia was 56% with no athlete experiencing permanent neurologic injury, although the follow-up period was only 3 years and some athletes chose to retire from collision sports.

Cervical spinal stenosis Cervical spinal stenosis is an important factor in the occurrence of cervical cord neurapraxia and the severity of neurologic injury following cervical spine trauma. Cervical spinal stenosis is a congenital or developmental narrowing of the cervical spinal canal defined by the midsagittal diameter or cross-sectional area. A diminished anteroposterior diameter of the spinal canal can be caused by congenital narrowing of the spinal canal, developmental spinal stenosis from degenerative changes, cervical instability, or intervertebral disc protrusion. The method to best determine spinal stenosis in an athlete has been the subject of considerable debate. Early definitions used the absolute anteroposterior canal diameter to detect spinal stenosis – measured from the posterior aspect of the vertebral body to the most anterior point on the spinolaminar line. In general, a canal was considered normal if the diameter between C3 and C7 was >15 mm, and spinal stenosis was present if the diameter was <12 mm.35 Torg et al.31 and Pavlov et al.36 described a measurement to detect spinal stenosis using a spinal canal to vertebral body ratio (known as the ‘Torg ratio’). The ratio uses the anteroposterior diameter of the spinal canal and the anteroposterior width of the midpoint of the vertebral body (Fig. 126.5). The measurements are made at the level of the third through the sixth vertebral body on a routine lateral radiograph of the cervical spine. The ratio method eliminates error caused by magnification factors or differences in target-to-film distances. A spinal canal-vertebral body ratio of <0.8 indicates significant spinal stenosis. In Torg’s study,31 a ratio of <0.8 was recorded at one or more levels in 24 athletes with cervical cord neurapraxia, compared to a ratio of 1.0 or more in 49 age-matched controls with no neurologic complaints. Eismont et al.20 also observed that a smaller-diameter spinal canal measured by plain film significantly correlated with neurologic injury 1342

a b

a ratio = — b

Fig. 126.5 The Torg ratio is the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the spinolaminar line (a) divided by the anteroposterior width of the vertebral body (b).31

in 98 patients with cervical spine traumatic fracture-dislocations. Others studies have further documented the association of a small sagittal diameter of the spinal canal with the severity of neurologic injury following cervical spine trauma.37,38 The Torg ratio has been the subject of considerable scrutiny, and its usefulness in sports and spine medicine questioned. Herzog et al.39 found the ratio to have a high sensitivity (92%) but a low positive predictive value (12%) for detecting cervical spinal stenosis in a cohort of professional football players. In their study, 49% of professional football players had a Torg ratio <0.8 at one or more levels, but only 13% had true spinal stenosis documented on advanced imaging. Herzog et al. concluded that the Torg ratio was a poor predictor of true functional spinal stenosis and may yield many false-positive results, and the low positive predictive value of the ratio precludes its use as a screening tool for determining eligibility of an athlete for participation in contact sports. Several problems exist which limit the usefulness of the Torg ratio in determining spinal stenosis. Most concerning is that the ratio does not account for the size of the spinal cord and define the anatomic relationship of the spinal cord within the spinal canal. In addition, the ratio does not identify soft tissue pathology that may be impinging on the spinal canal. Resnick40 stated that roentgenography alone failed to assess the width of the cord and account for stenosis which results from ligamentous hypertrophy or disc protrusion. Cantu41 also argued that spinal stenosis cannot be defined by bony measurements alone and that normal canal size on a lateral radiograph does not rule out the possibility of ‘functional spinal stenosis.’ He defines ‘functional spinal stenosis’ as a loss of cerebrospinal fluid (CSF) around the cord or deformation of the spinal cord, as documented on computed tomography (CT), MRI, or myelography.42 The term ‘functional’ refers to the functional reserve or protective cushion of the CSF around the spinal cord. While the Torg ratio has its limitations, Torg and colleagues31,36 should be credited with their efforts to define a measure used to assess cervical spinal stenosis and the risk of cervical cord injury. In addition, it should be noted that the Torg ratio was created at a time when MRI was not widely available. In the setting of an athlete with a history of cervical cord neurapraxia or transient quadriplegia, an evaluation with MRI, myelogram, or contrast-positive CT should be performed. If the Torg ratio is measured early in the diagnostic evaluation, an abnormal ratio is a strong indicator to pursue advanced imaging.41

Interventional Spine in Sports

Whether congenital or acquired, the relationship of cervical spinal stenosis to serious neurologic injury is well established. The National Center for Catastrophic Injury Research has reported cases of quadriplegia in the absence of a spine fracture only when functional spinal stenosis is present, and conversely reported cases of complete neurologic recovery after spine fracture or dislocation only in the absence of functional spinal stenosis.42 In addition, the presence of cervical spinal stenosis places the athlete at higher risk to require surgery after a cervical disc herniation, for potential paralysis without a fracture-dislocation, and to develop paralysis and a greater degree of paralysis after fracture-dislocation.20,42–46

Return to play after cervical cord neurapraxia Return to play after an episode of cervical cord neurapraxia is a frequently discussed and controversial area in sports medicine and spine surgery. Torg et al.47 compared cohorts of asymptomatic college and professional football players with no history of transient neurapraxia, with a cohort of 45 high school, college, and professional athletes with an episode of transient neurapraxia, and 77 patients with permanent quadriplegia as a result of high school or college football. The Torg ratio was found to have a sensitivity of 93% for the detection of transient neurapraxia, but a low specificity and low positive predictive value. None of the 77 patients with permanent quadriplegia had an episode of transient neurapraxia before catastrophic injury to the spinal cord, and none of the 45 athletes with transient neurapraxia became quadriplegic. Developmental narrowing of the spinal canal in the quadriplegic group was also absent. The authors concluded that the occurrence of transient neurapraxia of the spinal cord and permanent quadriplegia were unrelated, and that developmental narrowing of the spinal canal in the absence of instability is not a predisposing factor for permanent neurologic injury. Therefore, congenital cervical spinal stenosis should not preclude an athlete from participation in contact sports. Torg et al.34 further characterized the relationship of the spinal cord to the spinal canal by analyzing MR images in 110 athletes with cervical cord neurapraxia. The disc-level canal diameter was measured as the shortest distance between the intervertebral disc and the osseous posterior elements and the transverse cord diameter determined. The MRI measurements were compared to the spinal canal–vertebral body ratio measured on lateral radiograph. The study found using

both methods of measurement that the probability of recurrent cervical cord neurapraxia was inversely correlated with spinal canal size. Using logistic regression analysis, plots were generated to calculate the risk of recurrent neurapraxia that could be used in counseling athletes with a history of cervical cord neurapraxia about their individual risk of a recurrent episode. The authors concluded that: (1) cervical cord neurapraxia is a transient neurological phenomenon and individuals with uncomplicated neurapraxia may be permitted to return to their previous sport without an increased risk of permanent neurological injury; (2) congenital or degenerative narrowing of the sagittal diameter of the cervical canal is a causative factor; (3) the overall recurrence rate after return to play is 56%; and (4) the risk of recurrence is strongly and inversely correlated with sagittal canal diameter and is useful in the prediction of future episodes of cervical cord neurapraxia. Although controversial, Torg et al.21 do not believe that athletes who experience an episode of uncomplicated transient cervical cord are at risk of incurring permanent neurologic sequelae and should not be disqualified from participation in contact or collision sports. Other experts strongly disagree. Cantu41 contends that cervical spinal stenosis increases the risk of permanent neurologic injury and asserts that a history of transient quadriplegia and functional spinal stenosis is an absolute contraindication to return to contact or collision sports. Table 126.1 contrasts return to play recommendations following cervical cord neurapraxia by Torg et al.21 and Cantu.41 Several reported cases draw support of Cantu’s concept of functional spinal stenosis and raise concern regarding Torg’s recommendations. Firooznia et al.43 reported three cases of permanent quadriplegia in patients with marked spinal stenosis after only minor trauma. Matsuura et al.38 also described the association of cervical canal stenosis and neurologic injury and found that the shape of the bony spinal canal as measured by thin-cut CT was critical in determining residual neurologic injury following traumatic spinal cord injury. In addition, Cantu41 reported a case of a high school football player with transient quadriplegia who had abnormal Torg ratios by lateral radiograph, but was allowed to return to play and later suffered a permanent spinal cord injury with resultant spastic quadriplegia. After the second injury, CT and MRI revealed functional cervical stenosis, a posterior disc herniation of C3–4 with displacement of the cord and thecal sac, and edema within the spinal cord from C2 to C5. Brigham and Adamson33 also reported a case of permanent neurologic

Table 126.1: Guidelines for Return to Play After Transient Cervical Cord Neurapraxia Torg21

Cantu41

No restriction

No history of CCN and spinal canal–vertebral body ratio ≥0.8

One episode of TQ with full recovery and normal work-up without functional spinal stenosis

Relative restriction

One episode of CCN and spinal canal–vertebral body ratio ≤0.8 One episode of CCN with intervertebral disc disease or degenerative changes One episode of CCN with MRI evidence of cord deformation

One episode of TQ as a result of minimal contact One episode of TQ and evidence of disc bulging or herniation without functional spinal stenosis

Absolute contraindication

CCN with ligamentous instability, neurologic symptoms >36 hours, and/or more than one episode CCN and MRI evidence of cord defect or edema

TQ with functional spinal stenosis documented by myelography, CT, or MRI Any permanent neurologic injury, ligamentous instability, or spinal cord contusion following cervical spine trauma

CCN, cervical cord neurapraxia; TQ, transient quadriplegia.

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injury in a professional football player with congenital spinal stenosis. This player presented with tingling in all four extremities upon neck flexion. Initial MRI demonstrated congenital cervical spinal stenosis without degenerative changes. Two years later he sustained an axial load to the neck and experienced immediate numbness in all four extremities, severe burning, and painful dysesthesias in both arms. MRI immediately after this injury was normal, but 3 months later repeat MRI demonstrated a focus of increased signal within the spinal cord at C5 likely representing an area of diffuse axonal injury. The patient continues to experience mild, bilateral upper extremity dysesthesias. In athletes who experience transient cervical cord neurapraxia, the criteria for return to play are controversial and must be individualized. The reported cases of permanent neurologic injury following cervical cord neurapraxia in the setting of functional spinal stenosis are concerning.33,41 This author believes that the presence of functional cervical spinal stenosis in an athlete with a history of cervical cord neurapraxia is an absolute contraindication for the athlete to return to play in contact or collision sports. Mild disc bulging without functional spinal stenosis in an athlete with a history of transient cervical cord neurapraxia is a relative contraindication to return to play.

Spear-tackler’s spine Torg and colleagues22 described a group of athletes who are at a particularly high risk for the development of cervical spinal cord injuries because of developmental narrowing of the cervical canal and the use of spear tackling or head-first playing techniques. In 15 patients who used spear-tackling techniques, permanent neurologic injury occurred in four patients from axial loading. Each of the four patients with permanent injuries had the following combination of findings on cervical spine radiographs: (1) developmental cervical canal stenosis (defined by a spinal canal–vertebral body ratio of <0.8); (2) straightening or reversal of cervical lordosis; and (3) preexisting minor post-traumatic evidence of bone or ligamentous injury. Some experts regard speartackler’s spine as an absolute contraindication to participation in collision sports.21 Other experts believe that return to collision sports is permitted if normal cervical lordosis is restored and the athlete refrains from further spear-tackling techniques.41

Fractures and dislocations Axial loading to a straightened cervical spine results in compressive deformation and subsequent failure in a flexion mode with the potential for fracture, subluxation, or facet dislocation.25 The axial load ‘teardrop’ fracture is characterized by a triangular fracture fragment at the anteroinferior corner of the cervical vertebral body with a sagittal fracture through the vertebral body and the posterior arch (Fig. 126.6). These fractures occur most commonly at C5 but can also occur at C4 and C6. In a series of 55 patients with this

Fig. 126.6 The axial load ‘teardrop’ fracture is characterized by a triangular fracture fragment at the anteroinferior corner of the cervical vertebral body, a sagittal vertebral body fracture, and a fracture through the posterior arch. 1344

C1

C2

C3

Fig. 126.7 Hangman’s fracture involves bilateral fractures of the pars interarticularis of C2 with or without anterior subluxation (arrow).

injury from the National Football Head and Neck Injury Registry, 49 patients had a three-part, two-plane fracture including a sagittal fracture of the vertebral body, with resultant quadriplegia in 90% of patients.48 Isolated fracture of the anteroinferior corner occurred in 11% of cases and usually without neurologic sequelae. Anterior subluxation and unilateral and bilateral facet dislocations are infrequent but severe injuries with a high risk of permanent quadriplegia. Torg et al.49 identified the C3–4 level as the most common dislocation in football resulting in quadriplegia. Anterior subluxation usually involves rupture of the posterior longitudinal ligament and ligamentum flavum. Prompt recognition and reduction in a controlled environment have led to more favorable results. Contrast-enhanced CT or MRI of the cervical spine should be obtained before fracture reduction to rule out the presence of a retropulsed interveterbral disc.41 Other potential injuries include a Jefferson fracture of the ring of C1, ‘Hangman’s fracture’ involving bilateral fractures of the pars interarticularis (Fig. 126.7), zygapophyseal (facet) fractures, and rupture of the atlantoaxial transverse ligament with atlantoaxial dislocation. Most fracture-dislocations of the cervical spine require surgical stabilization. Some fractures such as isolated spinous process fractures require minimal treatment with short-term immobilization in a cervical collar. In general, stable fractures that have healed completely allow the athlete to return to play the following season. These fractures include chip, minor wedge, isolated laminar, and spinous process fractures. Athletes with cervical spine fractures or dislocations that require reduction and surgical stabilization are not considered safe to return to contact sports. Even after fracture healing, these athletes are thought to have insufficient spinal strength and altered biomechanics and motion in surrounding spinal segments and are at high risk of future sports-related injury.41,50 Thus, any injury requiring internal stabilization is suspect in its ability to withstand further stresses from contact or collision sports. Cervical fusions at the C4 level or above and multilevel fusions are also a contraindication to return to contact or collision sports.

ON-THE-FIELD EVALUATION Adequate preparation is required for the assessment of the cervical spine-injured athlete. Anticipation of required personnel and equipment and a well-designed emergency response are critical to the management of catastrophic neck injuries. The medical team should develop and review emergency plans including predetermination of who will be on the field (i.e. certified athletic trainer

Interventional Spine in Sports

and team physician), who will conduct the initial evaluation, what special equipment should be brought onto the field, and when the emergency medical system (EMS) should be contacted. Emergency equipment such as a spine board, cervical collar, and devices used to remove protective gear safely and quickly should be readily available. In 2001, the Inter-Association Task Force for Appropriate Care of the Spine-Injured Athlete established guidelines for the prehospital care of the spine-injured athlete.44 Experts from a range of disciplines including athletic training, sports medicine, rehabilitation medicine, orthopedic surgery, neurosurgery, and emergency medical technicians contributed to the recommendations, and the guidelines should be regarded as the standard of care in the evaluation of a spine-injured athlete.

Table 126.2: Glasgow Coma Scale

Eyes open

Best motor response

Response

Points

Spontaneously

4

To verbal commands

3

To pain

2

No response

1

Obeys commands

6

Localizes pain

5

Withdrawal to pain

4

Flexion (decorticate) to pain

3

Initial assessment

Extension (decerebrate) to pain

2

The care of an injured athlete begins with observation of the event that leads to the potential injury. The medical team at sporting events should make every attempt to closely view all plays, as direct observation of the mechanism of injury is helpful in assessing the likelihood of significant injury. The initial assessment of an injured athlete begins with a basic assessment of the ABCs – airway, breathing, and circulation – and level of consciousness. If any concerns regarding basic life support are present the EMS should be activated immediately. Any athlete suspected of having a spinal injury should not be moved and should be treated as if a spinal injury exists. Unconscious athletes are presumed to have unstable spine injuries until proven otherwise. All participants on the field including coaches, officials, and teammates must be aware of the dangers of moving a player with a suspected spinal injury before appropriate stabilization of the cervical spine. If the athlete is not breathing, an adequate airway must be established. The jaw thrust maneuver allows opening of the airway while maintaining the cervical spine in a stable position. If spontaneous respiration does not resume, assisted ventilation may be necessary. In an unconscious athlete, an oral airway should be used to assist proper bagvalve-mask ventilation until endotracheal intubation can be performed in a controlled setting. High cervical spine injuries can cause apnea, ineffective breathing patterns, and paralysis of the phrenic nerve. Although rare, prolonged hypoxemia can lead to cardiac arrest. Once adequate ventilation and circulation are established, the level of consciousness should be further assessed. The conscious athlete is questioned regarding person, place, situation, the presence of neck pain, and sensory or motor disturbances in any body part. A screening neurologic examination is performed to assess sensation and strength in all four extremities. In the unconscious athlete or athlete with altered mental status, the Glasgow Coma Scale may be a useful prognostic indicator of cerebral function (Table 126.2).10 In the conscious athlete, it may be possible to clear the cervical spine on the field. The athlete must be alert, oriented, and without neck pain, neurologic symptoms, or distracting injury to the extremities. A brief four-extremity neurologic examination should be normal, and palpation of the cervical spine should be without tenderness. Active cervical spine range of motion should be pain free and without the development of neurologic symptoms and can be tested by asking the athlete to flex the chin to the chest and then rotate the head from side to side. If a cervical injury has been excluded, then the athlete can be assisted to the sitting position. If stable in the sitting position, the athlete can be helped to a stand, walked off the field, and further observed. If there is any suspicion for the presence of a cervical spine injury, it is better to err on the side of safety, and immobilize the cervical spine and transport the athlete for more definitive evaluation.

No response

1

Best verbal response

Oriented

5

Confused

4

Inappropriate words

3

Incomprehensible sounds

2

No response

1

The Glasgow Coma Scale is scored between 3 and 15 (3 being the worst and 15 the best). A score of 13 or higher correlates with mild brain injury; a score of 9 to 12 correlates with moderate brain injury; and a score of 8 or less represents severe brain injury.

Equipment management Protective equipment used in sports such as football and hockey can make the management of a spine-injured athlete more difficult. Each member of the medical team should be familiar and practiced in the operation of emergency equipment. Practice with the tools required for face mask removal of the catastrophically injured athlete is essential. The face mask should be removed as soon as possible before transportation and regardless of respiratory status, even if the athlete is conscious.44 In football, the face mask is secured to the helmet with four or more plastic loop-straps that can be cut or removed. Several tools for removing the loop-straps have been described including screw drivers and various cutting tools such as knives, scissors, pruning shears, the Trainer’s Angel (Fig. 126.8), and the Face Mask Extractor.51–53 Because moisture can rust the screws making screwdrivers unreliable,

Fig. 126.8 The Trainer’s Angel. A tool specifically made for removing the loop-straps of the facemask from a football helmet. 1345

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and injuries to other rescuers have been documented while using cutting instruments such as knives, scalpels, or box cutters, these tools are not recommended as the primary tool for loop-strap removal.54 The most widely used tool specifically made to remove loop-straps is the Trainer’s Angel. However, this tool may cause more head movement than other available devices. The face mask removal should be performed in the shortest time possible with the least amount of head and neck movement. The anvil pruner, commonly used for gardening, has been shown repeatedly to be the most efficient tool for removal of the loop-straps and is recommended by the InterAssociation Task Force.44,54 Athletic trainers or another designated member of the responding medical team should have the appropriate removal equipment available and be familiar with its use before an emergency occurs. Football helmets and chin straps should be left in place with few exceptions. If the athlete is wearing shoulder pads, football helmets hold the head in a position of neutral spinal alignment. If the helmet is removed from a down player wearing shoulder pads, the athlete’s head will hyperextend and may result in secondary injury to the cervical spine. The Inter-Association Task Force recommends removal of a helmet on the field under the following circumstances: (1) if the face mask cannot be removed in a reasonable period of time to gain access to the airway; (2) if after removal of the face mask the airway and ventilation cannot be adequately controlled; (3) if the helmet and chin straps do not hold the head securely such that immobilization of the helmet does not also immobilize the head; and (4) if the helmet prevents immobilization in an appropriate position.44 If the helmet needs to be removed, spinal immobilization and alignment must be maintained. Removal of a football helmet in a suspected spine-injured athlete should be performed cautiously. Internal helmet padding should be removed or air padding deflated while an assistant manually stabilizes the chin and the back of the neck. A stiff flat-bladed object such as a tongue depressor can be used to pry the padding away from the helmet. Air padding can be deflated with a large-gauge hypodermic needle. The helmet should slide off the occiput with slight forward rotation or traction of the helmet. In contrast, motorcycle helmets are not as snugly fit to the head and are worn without shoulder pads. Removal of a motorcycle helmet before transportation achieves neutral spine alignment and allows better stabilization of the injured motorcyclist. If removal of the helmet or shoulder pads is required, the helmet and shoulder pads should always be removed simultaneously

A

or neutral spine alignment will be lost.55,56 Football shoulder pads elevate the torso of a supine athlete to the same height as a helmeted head. The front of the shoulder pads can be opened to allow access to cardiopulmonary resuscitation and defibrillation if needed without actually removing the shoulder pads. Indications to remove the shoulder pads include: (1) the helmet is being removed; (2) injuries require full access to the shoulder area; and (3) ill-fitting shoulder pads preclude adequate spinal immobilization.44 To remove football shoulder pads, cut the jersey and other shirts from neck to waist and from midline to the end of each sleeve, cut all straps used to secure the pads to the torso, and cut the laces or straps over the sternum. Cervical stabilization is maintained by placing one’s forearms on the athlete’s chest while holding the maxilla and occiput. With assistance on both sides, the patient is lifted and the shoulder pads removed by spreading apart the front panels and pulling them around the head.44

Immobilization and transportation The medical team should be prepared to immobilize and transport an injured athlete if indicated. Every situation should be evaluated on an individual basis. When uncertainty exists, it is better to err on the side of caution and immobilize the patient until further diagnostic work-up can be performed. In general, any athlete with significant neck or spine pain, diminished level of consciousness, or significant neurologic deficits should be prepared for transport to a predetermined medical facility capable of definitive diagnostic and therapeutic neurosurgical procedures. Manual stabilization of the head, neck, and shoulders should be performed as the athlete is being assessed. If transport is indicated, the athlete will need to be immobilized to an appropriate immobilization device, usually a standard spine board. To transfer a supine athlete to a spine board, the Inter-Association Task Force recommends a six-plus-person lift technique of the athlete onto a rigid long spine board.44 One person is responsible for stabilization of the head and neck and will lead the team through all commands to lift the athlete and then lower onto the backboard. The rescuer’s hands should be placed palm-up underneath the shoulder pads, with the athlete’s head resting between the rescuer’s forearms. To transfer an athlete who is prone or face down, a log-rolling technique is recommended (Fig. 126.9). This is performed with a minimum of four persons with one designated to maintain stabilization of the head and neck. If the prone athlete is not breathing, the athlete

B

Fig. 126.9 The log-rolling technique is used to transfer a prone athlete with a suspected cervical spine injury and requires a minimum of four persons. The lead rescuer stabilizes the head and cervical spine by using a cross-arm technique and applying slight traction (A). Three assistants are positioned at the shoulders, hips, and knees and roll the patient towards themselves supine onto a spine board (B). 1346

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should be log-rolled immediately. The athlete can later be lifted a second time onto the spine board for immobilization as described above. If the athlete is conscious, the log-roll should be delayed until the backboard is available. To immobilize the patient, the head and spine should be maintained in a neutral position at all times. Again, in most cases, the helmet and shoulder pads are left in place, and the face mask removed prior to transport. After removal of the face mask and with the chin strap in place, the helmeted head is secured to the spine board by adhesive tape or straps. Standard straps secure the body, pelvis, arms, and legs. Filling any gaps with rolled towels or rigid foam will further stabilize the patient. The straps should be applied firmly so the athlete does not move if rolled onto his/her side in response to vomiting. Transport of a spine-injured athlete should be directed to a trauma center or facility with diagnostic and surgical capabilities for spine injury.

Prevention of secondary injury The pathophysiology of irreversible spinal cord injury involves not only the primary injury but also a cascade of secondary injury including neuronal edema, hypoxia, and aberration of cell membrane potential. Spinal cord resuscitation in an attempt to prevent secondary injury is recommended and supported by the National Acute Spinal Cord Injury Study.57,58 This includes respiratory and hemodynamic support to facilitate spinal cord perfusion, prompt relief of spinal cord deformation through controlled realignment and stabilization, and intravenous administration of corticosteroids.57,58 Intravenous methylprednisolone is given with a loading dose of 30 mg/kg body weight over 1 hour and is recommended as soon as possible, preferably within the first 4 hours after injury. This is followed by a subsequent dose of 5.6mg/kg body weight administered over the next 23 hours.

Education The major risk factor for permanent neurologic injury in athletics is the use of spear-tackling techniques where the head is used as the initial point of contact producing axial compression and subsequent failure of the cervical spine. Prevention of cervical spine injuries through the teaching of proper tackling technique is the key intervention to decrease catastrophic cervical spine injuries. Educational programs emphasizing a ‘see what you hit’ technique of blocking and tackling should be implemented on a regular basis. Changes in equipment, rules, strengthening, and conditioning may also be helpful.

CONCLUSION Catastrophic spine injuries in sport usually occur from an axial load to the cervical spine. All unconscious athletes following a collision, and conscious athletes with any sign or symptom that suggests cervical spine trauma, must be treated as if they have a cervical spine injury. Bilateral neurologic symptoms after contact injury should alert the physician to a possible spinal cord injury. The athlete’s airway, breathing, circulation, neurologic status, and level of consciousness must be assessed, and EMS activated if necessary. When it becomes necessary to immobilize and transport an athlete, the head, neck, and trunk must be stabilized and moved as a unit. Proper management of a spine-injured athlete can prevent secondary damage from occurring and expedite definitive treatment. An episode of cervical cord neurapraxia in an athlete found to have functional cervical spinal stenosis on advanced imaging represents an absolute contraindication to return to play. Any athlete with a permanent neurologic injury, fracture-dislocation requiring surgical stabilization, and high

cervical fusions should also be prohibited from further participation in collision sports.

References 1. Cantu RC, Mueller FO. Fatalities and catastrophic injuries in high school and college sports. Phys Sports Med 1999; 27:35–50. 2. Funk FF, Wells RE. Injuries to the cervical spine in football. Clin Orthop 1975; 109:50–58. 3. Carvell JE, Fuller DJ, Duthie RB, et al. Rugby football injuries to the cervical spine. Br Med J (Clin Res Ed) 1983; 286:49–50. 4. Silver JR. Injuries to the spine sustained in rugby. Br Med J (Clin Res Ed) 1984; 288:37–43. 5. McCoy GF, Piggot J, Macafee AL, et al. Injuries of the cervical spine in schoolboy rugby football. J Bone Joint Surg [Br] 1984; 66:500–503. 6. Tator CH, Edmonds VE. National survey of spinal injuries to hockey players. Can Med Assoc J 1984; 130:875–880. 7. Wu WQ, Lewis RC. Injuries to the cervical spine in high school wrestling. Surg Neurol 1985; 23:143–147. 8. Ghiselli G, Schaadt G, McAllister DR. On-the-field evaluation of an athlete with a head or neck injury. Clin Sports Med 2003; 22:445–465. 9. Cantu RC, Mueller FO. Catastrophic spine injuries in American football. 1977–2001. Neurosurgery 2003; 53:358–362. 10. Cantu RC. Return to play guidelines after head injury. Clin Sports Med 1998; 17:45–59. 11. Quality Standards Subcommittee. Practice parameter: the management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee. Neurology 1997; 48:581–585. 12. Collins MW, Iverson GL, Lovell MR, et al. On-field predictors of neuropsychological and symptom deficit following sports-related concussion. Clin J Sport Med 2003; 13:222–229. 13. Collins MW, Hawn KL. The clinical management of sports concussion. Curr Sports Med Rep 2002; 1:12–22. 14. Lovell MR, Collins MW. New developments in the evaluation of sports-related concussion. Curr Sports Med Rep 2002; 1:287–292. 15. McCrea M, Guskiewicz KM, Marshall SW, et al. Acute effects and recovery time following concussion in collegiate football players: the NCAA Concussion Study. JAMA 2003; 290:2556–2563. 16. Schneider RC. Serious and fatal neurosurgical football injuries. Clin Neurosurg 1964; 12:226–236. 17. Burke DC. Hyperextension injuries of the spine. J Bone Joint Surg [Br] 1971; 53: 3–12. 18. Edeiken-Monroe B, Wagner LK, Harris JH Jr. Hyperextension dislocation of the cervical spine. Am J Roentgenol 1986; 146:803–808. 19. Penning L. Some aspects of plain radiography of the cervical spine in chronic myelopathy. Neurology 1962; 12:513–519. 20. Eismont FJ, Clifford S, Goldberg M, et al. Cervical sagittal spinal canal size in spine injury. Spine 1984; 9:663–666. 21. Torg JS, Guille JT, Jaffe S. Injuries to the cervical spine in American football players: current concepts review. J Bone Joint Surg [Am] 2002; 84:112–122. 22. Torg JS, Sennett B, Pavlov H, et al. Spear tackler’s spine. An entity precluding participation in tackle football and collision activities that expose the cervical spine to axial energy inputs. Am J Sports Med 1993; 21:640–649. 23. Torg JS, Quedenfeld TC, Burstein A, et al. National football head and neck injury registry: report on cervical quadriplegia, 1971 to 1975. Am J Sports Med 1979; 7:127–132. 24. Schneider RC. Head and neck injuries in football. Mechanisms, treatment, and prevention. Baltimore: Williams and Wilkins; 1973. 25. Torg JS, Vegso JJ, O’Neill MJ, et al. The epidemiologic, pathologic, biomechanical, cinematographic analysis of football-induced cervical spine trauma. Am J Sports Med 1990; 18;50–57. 26. Maroon JC. ‘Burning hands’ in football spinal cord injuries. JAMA 1977; 238: 2049–2051. 27. Clancy WG, Brand RL, Bergfeld JA. Upper trunk brachial plexus injuries in contact sports. Am J Sports Med 1997; 5:209–215. 28. Sallis RE, Jones K, Knopp W. Burners. Offensive strategy in an underreported injury. Phys Sports Med 1992; 20:47–55.

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Part 6: Interventional Spine in Sports 29. Watkins RL. Nerve injuries in football players. Clin Sports Med 1986; 5:215–246. 30. Levitz CL, Reilly PJ, Torg JS. The pathomechanics of chronic, recurrent cervical nerve root neurapraxia. The chronic burner syndrome. Am J Sports Med 1997; 25:73–76. 31. Torg JS, Pavlov H, Genuario SE, et al. Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg [Am] 1986; 68:1354–1370. 32. Schneider RC, Reifel E, Crisler HO, et al. Serious and fatal football injuries involving the head and spinal cord. JAMA 1961; 177:362–367. 33. Brigham CD, Adamson TE. Permanent partial cervical spinal cord injury in a professional football player who had only congenital stenosis. A case report. J Bone Joint Surg [Am] 2003; 85A:1553–1556. 34. Torg JS, Corcoran TA, Thibault LE, et al. Cervical cord neurapraxia: classification, pathomechanics, morbidity, and management guidelines. J Neurosurg 1997; 87:843–850. 35. Wolfe BS, Khnilnani M, Malis L. The sagittal diameter of the bony cervical spinal canal and its significance in cervical spondylosis. J M Sinai Hosp 1956; 23:283– 292. 36. Pavlov H, Torg JS, Robie B, et al. Cervical spinal stenosis: determination with vertebral body ratio method. Radiology 1987; 164:771–775. 37. Kang JD, Figgie MP, Bohlman HH. Sagittal measurements of the cervical spine in subaxial fractures and dislocations. An analysis of two hundred and eighty-eight patients with and without neurological deficits. J Bone Joint Surg [Am] 1994; 76:1617–1628. 38. Matsuura P, Waters RL, Adkins RH, et al. Comparison of computerized tomography parameters of the cervical spine in normal control subjects and spinal cord-injured patients. J Bone Joint Surg [Am] 1989; 71:183–188. 39. Herzog RJ, Wiens JJ, Dillingham MF, et al. Normal cervical spine morphometry and cervical spinal stenosis in asymptomatic professional football players. Plain film radiography, multiplanar computed tomography, and magnetic resonance imaging. Spine 1991; 16(6Suppl):S178–S186. 40. Resnick D. Degenerative disease of the spine. In: Diagnosis of bone and joint disorders. Philadelphia: WB Saunders; 1981:1408–1415. 41. Cantu RC. Cervical spine injuries in the athlete. Semin Neurol 2000; 20:173–178. 42. Cantu RC. Functional cervical spinal stenosis: a contraindication to participation in contact sports. Med Sci Sports Exerc 1993; 25:1082–1083. 43. Firooznia H, Ahn JH, Rafii M, et al. Sudden quadriplegia after a minor trauma. The role of preexisting spinal stenosis. Surg Neurol 1985; 23:165–168. 44. The Inter-Association Task Force for Appropriate Care of the Spine-Injured Athlete. Prehospital care of the spine-injured athlete. Dallas, TX, National Athletic Trainers Association, March 2001.

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45. Cantu RV, Cantu RC. Guidelines for return to contact sports after transient quadriplegia. J Neurosurgery 1994; 80:592–594. 46. Cantu RC. Transient quadriplegia: to play or not to play. Sports Med Digest 1994; 16:1–4 47. Torg JS, Naranja RJ Jr, Palov H, et al. The relationship of developmental narrowing of the cervical spinal canal to reversible and irreversible injury of the cervical spinal cord in football players. J Bone Joint Surg [Am] 1996; 78:1308–1314. 48. Torg JS, Pavlov H, O’Neill MJ, et al. The axial load teardrop fracture. A biomechanical, clinical, and roentgenographic analysis. Am J Sports Med 1991; 19:355–364. 49. Torg JS, Truex RC Jr, Marshall J, et al. Spinal injury at the level of the third and fourth cervical vertebra from football. J Bone Joint Surg [Am] 1977; 59: 1015–1019. 50. Bailes JE, Hadley MN, Quigley MR, et al. Management of athletic injuries of the cervical spine and spinal cord. Neurosurgery 1991; 29:491–497. 51. Swartz EE, Norkus SA, Armstrong CW, et al. Face-mask removal: movement and time associated with cutting of the loop straps. J Athl Train 2003; 38:120–125. 52. Angotti DD, Hoenshel RW, Kleiner DM. The most efficient technique to using the Face Mask Extractor. J Athl Train 2000;3 5(Suppl 2):S60. 53. Kleiner DM, Knox KE. An evaluation of techniques used by athletic trainers when removing a facemask with the Trainers Angel. J Athl Train 1995; 30(Suppl 2):7. 54. Knox K, Kleiner DM. The efficiency of tools used to retract a football helmet face mask. J Athl Train 1997; 32:211–215. 55. Swenson TM, Lauerman WC, Blanc RO, et al. Cervical spine alignment in the immobilized football player: radiographic analysis before and after helmet removal. Am J Sports Med 1997; 25:226–230. 56. Gastel JA, Palumbo MA, Hulstyn MJ, et al. Emergency removal of football equipment: a cadaveric cervical spine injury model. Ann Emerg Med 1998; 32:411–417. 57. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med 1990; 322:1405–1411. 58. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA 1997; 277: 1597–1604.

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Epidemiology of Injuries Mark D. Tyburski and Joel M. Press

INTRODUCTION Back pain is one of the most common reasons patients seek medical care. Low back pain is the second leading cause for primary care office visits, with an estimated lifetime prevalence of 60–90% and an annual incidence of 2–5%.1,2 In the general population, back pain is the number one cause of disability in patients younger than 45 years of age, and the number three cause for those older than age 45. Although there has been recent debate as to whether athletes are protected from back pain or more susceptible to back pain, it remains a common complaint in the athletic population. Back pain etiology in the athlete varies from mild lumbar muscle strain to traumatic fracture dislocation of the cervical spine with associated cord compromise. However, the most common etiology of athletic back injury mirrors that of the general population – injury to soft tissue structures including muscle, ligaments/capsule, and fascia. Past studies have reported the inability to identify a specific pain generator in up to 85% of cases of low back pain. Despite these historical findings, correct identification and treatment of biomechanical deficits leading to back pain can prevent injury from recurring and progressing to a chronic phase. From a radiographic standpoint, degenerative disc disease and spondylolysis are the most commonly associated structural abnormalities seen in athletes. In fact, numerous studies have shown an increased prevalence for degenerative spine changes in athletes when compared to nonathletes.3,4 The assessment and management of back- and spine-related pain in the athlete presents many unique challenges to the clinician. Issues specific to athletes are numerous, including: elevated pain tolerance, ‘no pain, no gain mentality,’ secondary gain presenting as nonreporting of injuries due to fear of lost playing time or altered monetary compensation, expectation for return to prior high functional level, and the need for rapid return to play. Thus, it is essential to establish an accurate diagnosis and concrete treatment plan in a timely manner. To this end, a functional understanding of the biomechanical demands of the particular sport involved is imperative for understanding the mechanism of injury, the mode of rehabilitation, and the measure to prevent re-injury. Return to play criteria will need to mesh the understanding of spinal kinematics and load transfer with sport-specific activity.

kinetic chain in injury etiologic mechanisms. They are the framework for many athletic injuries. In the following sections, the authors will present the differentiation of sport injury categorized by age group and spinal region. When available, information regarding technique, position, and competition level specific factors will be presented within the subsequent sections of sport-specific epidemiologic data.

The degenerative cascade model as an etiologic predictor of back pain Virtually all athletes are subjected to repetitive end range forces on the spine, grueling competitive schedules, rigorous training routines and, depending on the sport, significant contact forces with other players. The result is an accelerated progression through the degenerative cascade of spinal motion segments. The degenerative cascade model based upon the work of Kirkaldy-Willis5a is currently a comprehensive model of back pain (Fig. 127.1). It describes three basic stages of degeneration found in spinal motion segments due to the effects of trauma and repetitive stress. At each stage, the

Facet joints

Stage

Other annulus tears

Synovial reaction

Meniscal tear

Disc

Dysfunction End-plate separation

Cartilage destruction

HNP

Nuclear peripheralization

Disc resorption

Capsular laxity Instability Subluxation

Loss of disc height

GENERAL ETIOLOGIC FACTORS The etiology and precipitating factors of most episodes of back pain in athletes retain a common functional and structural basis. They may be predicted by several characteristics including: patient age, sport type, position played, improper technique, training routine, and level of competition. Before evaluating sport-specific data, the reader should have a basic understanding of the degenerative cascade model of spinal motion segment dysfunction, as well as the role of the

Enlargement of facet and osteophytes

Fixed deformity (stenosis)

Osteophytes form

Fig. 127.1 Overview of the degenerative cascade. (Adapted from Selby D, Saal JS: Degenerative Series. CAMP Healthcare, with permission.5) 1349

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classification system outlines the pathoanatomical and pathophysiologic changes that occur throughout the motion segment, which can be used to predict etiology of spine-related pain. It is an important process to understand when examining etiology and epidemiology of back pain in athletes. A basic overview of the degenerative cascade is as follows: Stage I – Dysfunction: Zygapophyseal joint (Z-joint) synovitis and subluxation, annular tears, release of inflammatory mediators, local ischemia, sustained segmental muscle hypertonicity, ligamentous strain, and discogenic pain. Stage II – Instability: Progressive Z-joint cartilaginous degeneration and laxity, increased rotational movement in physiologic range, increased frequency of nuclear and annular disruption leading to herniation, increased translational forces on motion segments, annular laxity, and increased ligamentous stress and dysfunction. Stage III – Stability: Intra- and extra-articular fibrosis, hypertrophy and spurring of Z-joints, disc resorption and fibrosis, joint space narrowing, nuclear degeneration, endplate irregularities, vertebral body osteophyte formation, central and lateral canal stenosis, ligamentum flavum hypertrophy and calcification, nerve root scarring, loss of segmental mobility, and stenotic pain.

The role of the kinetic chain While the degenerative cascade model attempts to describe the pathoanatomical and pathophysiological changes that occur over time within spinal motion segments, one needs to understand the relationship between sporting activity and injury to the spine. The spine and trunk function as a dynamic link between the upper and lower extremities. The hip joint and pelvis act as the link between the lower extremities and the trunk, while the scapulothoracic and scapulohumeral joints serve as the link between the upper extremities and the trunk. In order to achieve a specific action such as swinging a golf club, throwing a ball, or blocking an opposing player, the spine takes on significant stress by performing three important functions. These include force generation, force transfer, and force re-acquisition. This coordinated activation of body segments and sequential force transfer is described as the kinetic chain. Failure of a single link in the kinetic chain can lead to increased load and stress transfer to the remaining functional links, including the spinal motion segments. Thus, when approaching the complaint of back pain in the athlete, the associated functional links of the kinetic chain above and below the injured segment must also be considered in the evaluation and plan of treatment.

secondary gain issues and are more likely to have a pathologic etiology for their pain. Therefore, a high index of suspicion and a low threshold for the utilization of diagnostic imaging and evaluation techniques should be applied to this population.7 Red flag signs and symptoms such as night pain, constitutional symptoms, non-specific onset, failure of pain remittance with rest, weight change, skin rash, and multiple joint or organ involvement should prompt further investigation and appropriate referral. This young population also deserves special attention because some causes of back pain may be related to the growth process itself. The distribution of spine-related causes for back pain in sports can be organized by anterior element, posterior element, and soft tissue etiologies.

Anterior element Disc disease accounts for 10% of back pain in athletes under the age of 21, and 2% of all disc herniations are attributable to this age population. The most commonly involved sports include: weight lifting, rowing, football, and wrestling.8 Scheuermann’s disease, a progressive thoracic kyphosis due to anterior wedging of at least 5° in three or more consecutive vertebral bodies, occurs in 0.4–8.3% of the population. The most common age group is 13–17 years, and increased prevalence has been noted in sports such as waterskiing.9 Thoracolumbar Scheuermann’s has been reported in weightlifting, football, gymnastics, and wrestling.10,11 Infection presenting as idiopathic infectious discitis is more common in younger patients with an average age of 6 years; however, reports span the entire pediatric and adolescent age group. Vertebral osteomyelitis, benign and malignant tumors, scoliosis, and rheumatologic disease are also more prevalent in this younger population than in adults.

Posterior element Posterior element injuries are more common in sports requiring repetitive hyperextension such as gymnastics, football, figure skating, diving, and dance.4,6,12 Spondylolysis has been reported to account for up to 47% of low back pain in adolescent athletes.13 Spondylolisthesis is usually associated with a pars interarticularis defect or elongation, and most slip progression tends to occur during the growth spurt in preadolescence.6,14 Incidence is reported from 11% in gymnastics to 63% in diving.15,16 Lumbar facet syndrome (Z-joint synovitis) is also reported in this population, and is associated with the first stage of the degenerative cascade.

Soft tissue

THE EFFECT OF AGE ON ETIOLOGIC DISTRIBUTION OF BACK PAIN Most epidemiological reviews of sports-related back pain and injury divide athletes into two discrete populations: young (pediatric and adolescent) and adult. This division principally exists because of the unique back pain etiologies specific to the pediatric and adolescent age groups. While the adult population is usually described as a single entity, it is best suited to division into young adult and older adult athletes. This division reflects the predominance of later-stage degenerative segment disease etiology in the older adult population as predicted by the degenerative cascade model of back pain.

Pediatric and adolescent athletes Back pain and back injury occurs in 10–15% of all young athletes.6 The prevalence of specific injury types is related to sport played as well as position within that sport. When compared to their adult counterparts, pediatric and adolescent populations have fewer 1350

During the adolescent growth spurt, the disproportionate growth of soft tissue and bone may lead to tight lumbodorsal fascia, thoracodorsal fascia, or hamstrings. This may lead to back, pelvis, hip, and knee pain. Another growth-related disorder is that of endplate fracture and nucleus pulposus herniation. Children have a disproportionately stronger nucleus pulposus compared to the vertebral endplate, which may result in endplate fracture and herniation of the nucleus into the vertebral body with resultant Schmorl’s node formation.

Spinal cord injury It is noteworthy to mention the high risk of cervical spine injury in the pediatric population associated with trampoline use and diving accidents. In 1998, more than 6500 trampoline-associated cervical spine injuries occurred in pediatric patients. Although most were minor injuries, there were reports of death and quadriplegia. This represented a fivefold increase over a 10-year period at the time of report.17 Increased risk for serious spinal trauma due to diving in uncontrolled environments is also prevalent in this population.

Interventional Spine in Sports

Young adult athlete The repetitive multiplanar nature of sport-specific training regimens (rotation, flexion–extension, and axial loading of the spine), high number of hours spent in training, and the general use of weight training for overall strength and conditioning may lead to earlier evidence of stage I (dysfunction) and stage II (instability) degenerative change in the spine compared to nonathletes. This is supported by radiographic evidence as well as the types of injury commonly encountered in this population.3,4 As with other age groups, the most common cause of back pain in this population is soft tissue injury that is usually manifest as muscle strain or ligament sprain in the low back. Segmental hypertonicity of overlying paraspinal musculature is commonly seen in many degenerative related disorders. These injuries include annular tears (symptoms may be confused for muscle strain), disc herniation, and Z-joint synovitis. Bony injury such as spondylolysis (gymnastics) and mild compression fractures (weight lifting, football) also occur in this age group. This population also carries an increased risk for serious spinal trauma and spinal cord injury manifest by diving and trampoline injury as mentioned in the above section on pediatric/adolescent athletes.

Older adult athlete As the general population ages, the number and age of those participating in sporting activities continues to increase. There will be approximately 70 million people age 65 or older in the United States by the year 2030.18 The spinal motion segments in this subset of the population are more likely to be further along in the degenerative cascade (instability and stabilization phases of degeneration).

In addition, medical comorbidity and age-related changes including diminished bone density, general loss of strength and muscle mass, changes to the vestibular, visual, and somatosensory systems, as well as decreased joint flexibility may play a role in back injury.19 In addition to the etiologies described for the young adult athlete, considerations in the older recreational athletic population include discogenic pain due to annular tears (30–40 year old age group), Zjoint capsular laxity with or without subluxation, central canal and lateral foraminal stenotic etiologies (50–60 year old age group), nerve root scarring, and compression fractures.

EPIDEMIOLOGIC DATA AND BIOMECHANICAL FACTORS FOR SELECTED SPORTS Table 127.1 summarizes the basic biomechanical etiologic factors associated with common spine injuries in sports.

Baseball/softball Overview Between 1995 and 1999, back injuries accounted for approximately 5% of all disabled list (DL) days in major league baseball. Overall, back pain accounted for the fifth highest number of injuries per anatomic region reported. In 1999, the number of DL days attributable to back injury reached 1490 days, which even outnumbered the 1348 days for wrist and hand injury.20 Severe injury to the cervical spine, while uncommon, is typically associated with head-first sliding. These neck hyperextension injuries

Table 127.1: Basic Biomechanical Etiologic Factors of Common Spine Injuries in Sports Injury Classification Spinal Region

Biomechanics

Injury

Sport

Sacral

Repetitive axial loading, plyometrics, jumping

Sacral stress fracture, sacroiliac joint dysfunction

Running sports (especially long distance), volleyball

Lumbar

High weight/flexion–extension/ lever arm effect

Soft tissue sprain/strain, disc herniation, radiculopathy, vertebral compression fracture, spondylolysis, spondylolisthesis, transverse/spinous process fracture Soft tissue sprain/strain, Z-joint arthropathy, spondylolysis, spondylolisthesis Soft tissue sprain/strain, annular disruption, disc herniations, Z-joint arthropathy

Weight lifting, football, rugby, basketball

Low weight/end range/extension based/repetitive Torsional forces

Thoracic

Torsional forces Repetitive flexion based loading

Cervical

Acute axial loading, lateral neck flexion with shoulder depression, hyperextension/rotation Repetitive flexion/extension/rotation

Spinal cord

Flexion based axial load

Z-joint arthropathy, annular disruption Scheuermann’s kyphosis, thoracolumbar Scheuermann’s

Gymnastics, ballet, diving, cycling Golf, tennis, baseball, basketball, soccer

Baseball, tennis, golf Weight lifting, football, gymnastics, wrestling, water-skiing

Stretch or compression to nerve root or brachial plexus with resultant neurapraxia, axonotmesis, or neurotmesis (Stinger/burner), fracture, subluxation Soft tissue sprain/strain, disc herniation ± radiculopathy, annular disruption

Football, rugby, hockey

Acute spinal cord injury, transient quadriparesis, quadriplegia

Football, rugby, diving, trampoline

Soccer, football, rugby, boxing, hockey, cycling

1351

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range from ligamentous disruption to vertebral fracture and quadriplegia. The mechanism involves rapid deceleration against a stationary base or opposing player. However, the incidence of cervical spine injury has decreased since the advent and widespread use of breakaway bases.21 Other cervical spine injuries, which may be observed in pitchers, include those to the Z-joints and cervical discs. Lumbar spine injury in baseball and softball is commonly attributed to hitting. Frequent participation in batting practice produces repetitive rotational movement that accelerates the progression of degenerative changes in spinal motion segments. The most common etiology of pain in this population is soft tissue in nature, while less common injuries include disc herniation, Z-joint arthropathy, spondylolysis, and spondylolisthesis.22,23

Fast-pitch softball According to the NCAA Injury Surveillance System data from 1997/1998, 5–15% of all traumas in fast-pitch softball were due to injury to the thoracic, back, and abdominal regions. Low back injury accounted for 7% of these injuries. Back injury is most commonly associated with overuse injuries and contusions.24

Functional considerations Frequent batting practice subjects the lumbar spine to repetitive stress injury. Watkins recorded surface EMG data from 18 professional baseball players to evaluate hitting mechanics and determined that the erector spinae and abdominal oblique were the most important muscles involved in trunk stabilization and rotation for smooth power transfer throughout the kinetic chain. They also noted that hamstring and lower gluteus maximus contributed most to the ‘stable base’ and ‘power-of-the-thrust’ form that the torso ‘uncoils’ during the swing.22 As predicted by the kinetic chain model of biomechanics, coordinated transfer of muscle activity occurs from the lower extremities to the trunk to the upper extremities. Any isolated weakness along the kinetic chain places undue stress on isolated functional segments and may eventually lead to overuse injury. Kinetic chain dysfunction is also observed in injuries sustained by pitching. According to Casazza and Rossner, the baseball pitch may be the most dynamic motion executed in sports. Acceleration of the upper extremity is driven by an initial anteroposteriorly directed ground force that is transformed into a rotational force at the hip that continues through the spine to the shoulder, culminating in forceful internal rotation to accelerate the arm. The spine also plays a crucial role in the attenuation of forces during the deceleration phase of throwing. Overload of the Z-joints and the intervertebral discs may occur if the thoracolumbar fascia is unable to dissipate the forces from the spinal motion segments.25 Restricted or excessive range of motion and poor coordination at specific segments along the chain may be as important, or more important, than relative weakness of isolated segmental musculature. Thoracic injuries are commonly seen in sports that involve throwing or hitting motions causing torsional forces on the spine. High thoracic pain is typically associated with upper extremity mechanics, and thoracolumbar junction pain is associated with lower extremity dysfunction. The thoracolumbar junction is at risk due to the stabilizing effect of the ribcage on the thoracic spine, and the Z-joint orientation at the transition from the thoracic (coronal Z-joints) to lumbar (sagittal Z-joints) region.

Basketball Overview In basketball players, thoracic and lumbar spine injuries are more common than those to the cervical spine. Overall, the most common injuries to the spine are lumbosacral soft tissue strains and 1352

sprains, as opposed to discogenic or bony abnormalities. Traditional ‘weekend warrior’ athletic injuries commonly arise as a consequence of diminished physical condition combined with participation in intensely competitive pick-up games. These injuries are usually soft tissue in nature; however, a predisposing spinal abnormality such as degenerative disc disease or spondylolisthesis may complicate the diagnostic picture. Competitive athletes at the high school, college, and professional levels are usually well conditioned but may ignore core strengthening and therefore also tend to suffer from soft tissue injuries to the low back.26 Meeuwisse et al. analyzed collegiate varsity basketball injuries as reported through the Canadian Intercollegiate Sports Injury Registry (CISIR) over a 2-year period. A total of 215 injuries accounted for 1508 sessions of time loss. Injury to the lumbar spine and pelvis accounted for 4.7% of injuries with 50.5 total sessions lost and average time loss of 5.05 days per injury. Injury to the thoracic spine and ribs accounted for only 1.9% of injuries with 7 total sessions lost and an average time loss of 1.75 days per injury.27 Other studies have reported a higher incidence of lumbar/hip-directed injuries. Hickey et al. reviewed injuries among female basketball players at the Australian Institute of Sport. Of the 49 elite female players followed, a total of 223 injuries over the time period of 1990 to 1995 were reported. Injury to the lumbar spine was the third most frequently injured region of the body with an incidence of 11.7%, with the most frequent diagnosis being mechanical low back pain (4.5%).28 Henry et al.28a retrospectively reviewed injuries in professional men’s basketball players over a period of 7 years, and found that back and hip injuries accounted for 11.5% of all injuries. The majority of these injuries were diagnosed as contusions. Only 1% of injuries occurred to the neck, and all were described as contusions or strained muscles. Although less common, discogenic injury, spondylolisthesis, and fractures of the spine have been reported in basketball players. Fracture types include vertebral body compression, spondylolysis, spinous process fractures, and transverse process fractures. The prevalence of spondylolysis is reported to be as high as 9%.26,29,30

Functional considerations Basketball injuries commonly occur in the setting of mechanical overload associated with severe hyperextension or hyperflexion combined with rotation and side-bending of the spine. The typical example is the airborne player in this position who encounters a blow to the back or neck region and experiences an awkward landing. Discogenic back pain may present as localized pain occurring in the dysfunction and instability phases. Nerve root irritation may eventually arise in the stabilization phase of the degenerative cascade. Spinal stenosis may occur more frequently in taller athletes than in the general population26 and may play a contributing factor. Older players with existing degenerative disc disease presenting in the stabilization phase may develop nerve root irritation and radicular symptoms. Common fractures at the lumbar spine include transverse and spinous process, pars interarticularis, and vertebral endplate. Vertebral body compression fractures are rare in basketball, but may occur due to supramaximal axial loading of the spine.26 Spondylolysis, spondylolisthesis, and pars interarticularis injury represent a spectrum of pathologic dysfunction as described by the degenerative cascade. High-grade spondylolisthesis is rare in high-level athletes. Low-grade spondylolisthesis can occur as a consequence of pars stress fracture, which is usually isthmic in origin, but may also be traumatic or rarely pathologic in nature. These injuries are frequently accompanied by lumbar spine pain and associated with tight hamstrings and the functional adaptation complex of loss of the lumbar lordosis. Degenerative

Interventional Spine in Sports

forms of this injury are more common in women and elderly populations. Slip rarely progresses beyond 33%.31

Football

Diving

Football is a violent, high-contact sport. Injuries to the spine account for approximately 40% of all traumatic injuries reported. Cervical spine injuries account for approximately 7–8% of all injuries to high school football players.36 Compared to other sports, football and rugby have the highest rate of cervical spine-related injury. These injuries range from transient cord neurapraxia to cervical spine fracture resulting in permanent quadriplegia. The significant amount of traumatic injury in football results from the unexpected deforming loads that occur during high-velocity collisions between players, frequently with the use of the helmet and head for spearing, tackling, and blocking.37 Major etiologic factors for low back injury in football include the heavy focus on weight training and strength development, as well as repetitive, intense player-to-player contact during game play and practice drills.

Overview Recreational diving accidents are the fourth most common cause of spinal cord injury following motor vehicle accidents, gunshot wounds, and falls. They have caused more cases of quadriplegia than all other sports combined.32,33 In comparison, there are only two reports of fatalities in international competition in the literature, both of which occurred during platform diving. In the United States, there has been no reported fatality or catastrophic injury during supervised training or competition in over 80 years. Factors related to catastrophic injury in diving include lack of formal training, insufficient water depth, lack of supervision, and alcohol consumption. Cervical strains and sprains, as well as brachial plexus stretch injuries can occur but are thought to be uncommon due to the protective effect of arm position during entry to the water.34 Low back pain is common in competitive divers, and in many cases may be related to spondylolysis, spondylolisthesis, or Z-joint arthropathy. Rossi performed a radiographic study of 1430 athletes, including 30 divers, and found a 63% incidence of spondylolysis in divers compared to an overall incidence of 16.7% for all athletes. This was the highest incidence of all sports in the study.16 Within the sport of diving, a higher incidence of lumbar spondylosis has been noted in platform diving when compared to springboard diving.35

Functional considerations There are three main elements of a dive at which the diver can sustain injury to the spine: takeoff, flight, and entry. Cervical spine injuries are relatively uncommon due to the protective effects of the overhead arm position on water entry. A high degree of mobility as well as stability is required by the lumbar spine during all components of the dive; thus, weakness, limited flexibility, or incorrect technique may lead to either flexion- or extension-based injury. Increased loading of the intervertebral disc occurs during the press phase of takeoff, the pike position in flight, and upon entry, especially if the diver is in a flexed position. Increased loading of the spinal elements is thought to occur during board work on the springboard as compared with the platform. This is because a greater component of the axial stress is absorbed by flexion of both the hips and knees on the platform. Extension-based injuries, however, are more common according to the literature. Stress on the posterior elements occurs during maximal lumbar extension and extension combined with rotation. These extension and rotational forces occur during takeoff for backward or reverse dives, as well as upon nonvertical entry of the water. Hyperextension is a common technical error that occurs in two main situations. The first involves backward rotating dives that achieve inadequate rotation and end up short of the vertical upon water entry. The second scenario results from forward rotating dives that are over-rotated and finish beyond the vertical upon water entry. Inward and reverse dives pose high risk in competitive diving. The angular momentum for the somersault is derived from the horizontal takeoff force of the diver’s feet while pushing off the board. Inappropriate direction of this force in too vertical a line will lead to the diver’s head striking the board. In a reverse dive, if the angular momentum is initiated by the diver pulling the head and shoulders backward instead of pushing off with the feet, adequate horizontal force will not be produced, placing the head and neck at risk of injury.

Overview

Cervical spine Hagel et al. evaluated rates of acute injury among football players in the Canada West Universities Athletic Association over the time period of 1993–1997. The incidence of head and neck injuries was found to be 1.59 injuries and 15.06 injuries per 1000 athletic exposures for practice and game play, respectively.38 While cervical spine trauma is rare, injuries that occur can be devastating. Reports from the National Football Head and Neck Injury Registry (NFHNIR) from 1971 to 1988 revealed the following distribution of midcervical spine injury. At the C3–4 level, there were four intervertebral disc herniations, four anterior subluxations of C3 upon C4, six unilateral articular process dislocations, seven bilateral articular process dislocations, and four fractures of the C4 vertebrae.39,40 In addition, flexion teardrop fractures have also been reported in football players. These rare injuries may or may not be associated with neurologic sequelae. Spear-tacklers spine is a clinical entity defined as (1) developmental narrowing of the cervical canal (Torg ratio of <0.8), (2) reversal of the normal cervical lordosis, and (3) post-traumatic radiographic abnormalities in (4) a player who has been seen utilizing spear-tackling techniques. Recommendation has been made that this population of patients be precluded from all collision sports and activities that expose the cervical spine to axially directed force input. The implementation of rules against spearing at both the high school and college level have resulted in significantly decreased incidence of cervical quadriplegia from 34 events in 1976 to only four events in 1995. In addition, the incidence of both fracture-subluxation and dislocation of the cervical spine has also seen a significant decrease in high school and college athletes. The incidence dropped from 7.72 and 30.66 per 100 000, respectively, in 1976, to 2.31 and 10.66 per 100 000 in 1987 according to NFHNIR records. ‘Stingers’ or ‘burners’ are common clinical entities that occur in high-contact sports such as football, rugby, and hockey. They represent a spectrum of nerve injury severity as described by Seddon: neurapraxia, axonotmesis, and neurotmesis. Cervical cord neurapraxia has an estimated prevalence of seven injuries per 10 000 participants.41 Clinical manifestations include transient loss of function, burning, and lancinating pain in the trapezius and shoulder regions extending down the arm in a dermatomal distribution. Symptoms typically last up to 10–15 minutes, and some trace neurologic deficit may last for months. More detailed information on sports-related cervical spine injuries can be found in Chapter 126.

Lumbar spine Mechanical low back pain is common in football players. A high incidence is reported at the beginning of training camp, and is most 1353

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notable in offensive linemen in conjunction with blocking drills. Repetitive forced extension of the lumbar spine may lead to Zjoint pain, spondylolysis, and spondylolisthesis.42,43 The reported incidence of spondylolysis in football players varies greatly, and has been reported to be as high as 50%.44 McCarroll et al. followed 145 freshman football players through their careers at Indiana University from 1978 to 1983 and reported the overall incidence of spondylolysis to be 15.2%, with 2.4% acquiring the diagnosis during the study period. The incidence of spondylolisthesis in this group was 4%. Of 31 players presenting with low back pain during the study period, 42% had radiographic findings of spodylolysis.45 A study by Shaffer et a.l46 examined, via physician survey, the prevalence of known isthmic spondylolisthesis in elite football players. Interviewing the team physicians of all 28 NFL teams and the top 25 NCAA teams as determined at the end of the 1993–1994 season, they found that 21 NCAA players and 20 NFL players were reported as known to have spondylolisthesis. This accounts for an estimated prevalence of 0.9% for NCAA players, and 1.5% for NFL players. Approximately half of the affected players were linemen (48% of NCAA and 50% of NFL). The most common level affected was L5–S1 (76%), and of all known cases 86% of NCAA and 75% of NFL were grade I slips. Six players in total had grade II slips, and two players had grade III slips. Other authors have reported the incidence of spondylolisthesis to be as high as 21%.47 These reports are contrasted with a 3–6% incidence of spondylolysis and 2–7.7% incidence of spondylolisthesis in the general population.46,48 However, these prevalence rates by Shaffer et al. are likely to be artificially low, as this report only included athletes with known spondylolisthesis and did not utilize evaluation of diagnostic imaging procedures. Other lumbar injuries include acute transverse process and spinous process fractures, disc injuries, radiculopathy, and tears in the thoracodorsal and lumbodorsal fascia. Tewes et al.49 reviewed all lumbar transverse process fractures that were known to have occurred in the NFL during the period of 1983 to 1991. Of the 29 cases, 27 were attributed to impact-related injuries, while two cases were thought to be secondary to a torsional mechanism. The fractures were fairly well distributed in regard to position played. Football players also have an increased incidence of lumbar degenerative disc disease. Studies have shown that weight training and hyperextension play a significant role in the production of intervertebral disc injury and degenerative disease in football players.50–52

Functional considerations Axial loading of the cervical spine is the primary mechanism of injury to the cervical spine in football. On analysis of videotape of actual injuries causing permanent quadriplegia, Torg et al. found that axial loading was the mechanism in every case.53 When the cervical spine undertakes a compressive force in its neutral position of lordosis, the forces are dissipated by the cervical paravertebral musculature, ligaments, and intervertebral discs. When the neck is flexed to 30°, the cervical spine becomes straight and the forces created by an axial load are no longer dissipated by the supporting soft tissue structures. The spine becomes compressed by the decelerated head and the accelerating trunk. The end result of this structural failure may be fracture, subluxation, or Z-joint dislocation. This compressive deformation leading to failure may occur in as little as 8.4 msec.54 Stingers or burners are typically the result of one of four major etiologic mechanisms causing stretch or compression of a nerve root or plexus. These mechanisms include (1) pure axial compression, (2) contralateral lateral neck flexion with ipsilateral shoulder depression, (3) hyperextension with ipsilateral side-bending of the cervical spine, and (4) a direct blow to the brachial plexus at Erb’s point (located 1354

in the supraclavicular region). Axial loads may cause unilateral arm pain, bilateral arm pain, or even transient quadriparesis secondary to cervical stenosis. Contralateral neck flexion coupled with ipsilateral shoulder depression injury may result in longer-lasting pain and dense paresthesia secondary to brachial plexus traction injury. Hyperextension with ipsilateral side-bending injuries usually result in radicular pain in dermatomal pattern secondary to functional narrowing of the neural foramina.55,56 Lumbar injuries range from lumbodorsal fascia or muscle strain to spinous process fracture or disc pathology. Repetitive extension movements combined with blows to the lumbar spine, especially when in a position of sudden off-balance rotation, may contribute to pars injury, Z-joint pain, and spinous or transverse process injury. This mechanism also contributes to the degeneration of specific vertebral motion segments. Disc degeneration and spondylolysis is prevalent in offensive linemen due to the repetitive hyperextension combined with rotation under load as they block opposing players. Football linemen sustain an average peak compression force of 8679±1965 N at the L4–5 motion segment when hitting a blocking sled. The average peak and shear forces are 3304±1116 N and 1709±411 N, respectively. The magnitude of these forces generated during blocking drills is greater than that which was determined during fatigue studies to cause pathologic changes in the disc and pars interarticularis.43 Core strength for adequate lumbar stabilization becomes an essential component to injury prevention in these athletes.

Golf Overview Golfers have the highest incidence of back injury of all professional athletes.57 A recent study of 703 professional and amateur golfers58 found that back injuries were the first and second most common injuries, in the respective groups. Back pain accounted for 34.5% of all professional injuries and 24.7% of all amateur injury reports. The lumbar spine was most commonly affected (62%) followed by the cervical (33%) and thoracic (5%) regions. In 92% of reported back problems, excessive play was blamed, as opposed to single traumatic events. The considerable rotational and compressive forces to the spine imposed by the golf swing subject players to myofascial pain, lumbar disc disease, spondylolysis, Z-joint arthropathy,59 and vertebral compression fractures.60 Injuries to the thoracic and lumbar spine are associated with greater time loss than injuries to all other anatomic regions except the elbow. When examining available gender data, there is no significant difference between men and women for number, severity, or distribution of injury.58

Functional considerations The repetitive nature of the sport lends itself to the development of degenerative changes in the spine. Studies have noted increased prevalence of injury when players hit more than 200 range balls or play four or more rounds per week.58 During the golf swing, the lumbar spine is subject to significant rotational and compressive forces. Many golfers use what is referred to as the ‘modern swing’ in which their hips slide from side to side, rather than rotating, to increase torque in the back and shoulders in attempt to increase angular club head speed. The endpoint of this swing positions the golfer in a reverse C stance that places the lumbar spine in extreme hyperextension. In attempt to hit the ball further, many players exaggerate this position, leading to increased force through the spine. In order to decrease the forces acting on the spine, an ‘athletic swing’ (also termed ‘classic swing’) that utilizes the larger muscles of the lower extremity and trunk to dictate the swing is advocated. The

Interventional Spine in Sports

athletic swing follows the principles of the kinetic chain to sequentially load and then unload each successive joint complex, with hip rotation coupled to that of the shoulders. The result is a more efficient swing with increased power and decreased rotational stress through the lumbar spinal motion segments. At the end of the swing, the player maintains a more upright posture. Nonswing-related factors are also important in the development of back pain in golf. A statistically significant association between low back pain and range of motion deficits in lumbar spine extension, lead hip internal rotation, and lead hip FABER’s distance (knee to table distance with the subject supine and hip flexed, abducted, and externally rotated) has been documented in professional golfers.61 Golfers who carry their bag on a regular basis also have a significantly higher incidence of low back injury.58 It has been demonstrated that significant shrinkage and decreased shock absorbance of the intervertebral disc occurs after carrying a golf bag over a distance of only nine holes.62

Gymnastics Overview There is a high prevalence of low back pain in gymnasts. Review of the literature reveals a range 12–85% depending upon the study population and definition of injury.3,63–66 In women’s gymnastics, floor exercises account for the majority of injuries, followed by balance beam, uneven bars, and vaulting.67 While there is a wide variance of injury to the spine in gymnasts, soft tissue injury is the most common etiology of back pain, as it is in most sports.67,68 Symptoms include myofascial pain, tenderness to palpation, and range of motion limitations. Other important causes of back pain in gymnasts include muscle strains, ligament sprains, degenerative disc disease, disc herniations, Scheuermann’s disease, compression fractures, Schmorl’s nodes, spondylolysis, spondylolisthesis, Z-joint chondromalacia, and spinous or transverse process avulsion. Spondylolysis is the classic spine-related injury associated with gymnastics. This is thought to be due to the repetitive hyperextension and rotational forces that gymnastic maneuvers place upon the lumbar spine. Compared to the estimated prevalence of 3–6% in the general population,48,69 the reported incidence of spondylolysis in gymnasts is significantly higher, ranging from 11% to 32%.9,16 While back pain in gymnasts is commonly associated with injury to the posterior elements, there is also a high incidence of anterior and middle column disease. A prospective study of spinal injury in 33 top level gymnasts by Goldstein et al.70 revealed MRI evidence of disc abnormality in 24%. In the 12 athletes with MRI-documented degenerative lumbar spine changes, there was a trend of increased degenerative change with increased skill level. The distribution of degenerative change was 1 of 11 pre-elite, 6 of 14 elite, and 5 of 8 Olympic-caliber gymnasts. Also noted in this series was a positive correlation of abnormal MRI findings with the average number of training hours per week and the age of the gymnast. As witnessed in the study by Goldstein et al., gymnasts who train for more than 15 hours per week may be at risk for accelerated degenerative changes of the lumbar motion segments (adjacent vertebrae, intervening disc, paired Z-joints and capsules, ligamentous components, lateral neural foramina). Supporting this study is the work of Sward which evaluated 24 elite male gymnasts. He found a higher prevalence of disc degeneration in male gymnasts (75%) compared to nonathletes (31%).71 Jackson et al. state that the most limiting lumbar disc pathology in the gymnast involves posterior and posterolateral disc herniation with associated nerve root irritation or compression. In these cases, epidural corticosteroid injections have been shown to be helpful in 40% of athletes with more chronic radicular symptoms.72

Bony abnormalities such as compression fractures and Schmorl’s nodes are reported pain generators in gymnasts. Superior or inferior herniation of the nucleus pulposus through the growth plates of vertebral bodies, commonly referred to as a Schmorl’s node, may occur in skeletally immature gymnasts. These injuries have been linked to hyperflexion and are most commonly seen at the thoracolumbar junction.63,66,73

Functional considerations The most frequently performed gymnastic skills include front and back walkovers, front and back handsprings, and the handspring vault. These maneuvers all require significant lumbar hyperextension for proper performance. This repetitive hyperextension, which is often coupled with torsional movement at end range of motion, results in repeated loading of the pars interarticularis and may eventually lead to spondylolysis. With continued stress, the associated spinal motion segments are placed at risk for spondylolisthesis. Spondylolisthesis occurs most frequently at the L5–S1 level. Developing adolescent gymnasts are at risk for both isthmic and traumatic subtypes of spondylolisthesis. From a clinical standpoint, these injuries are often associated with increased lumbar lordosis and tight hamstrings. When associated with nerve root irritation, patients may present with radicular pain. The problem of repetitive hyperextension movements has been recognized by the international governing body of rhythmic sportive gymnastics, The Federation International Gymnastics, and they have begun to limit the number of extension elements in a given routine to a single element.68 In addition to repetitive lumbar hyperextension, gymnasts also perform maneuvers producing repetitive torsion coupled with flexion. This may explain the cases of herniated nucleus pulposus reported in adolescents. These injuries most often occur at the L3–4 and L4–5 levels but have also been reported at the thoracolumbar junction.66,74 Improving range of motion at other sites along the kinetic chain, such as the hips and thoracic spine, may allow the athlete to achieve similar positions with less stress placed upon the extended lumbar spine.

Soccer Overview There are no comprehensive reviews in the literature dedicated to back injury in soccer. Soccer is a contact sport that involves highspeed collisions, dribbling, feigning, heading, throw-ins, and acrobatic movements in the air involving flexion, extension, and rotation of the trunk. Spinal injuries in soccer have been reported in both the cervical and lumbar regions. Trauma to the cervical spine has been reported as the sequelae of a bicycle kick. In 1978, a player of Nantes, France, landed on his occiput following a bicycle kick and sustained a bilateral fracture-dislocation of C5–6.75 Other acute cervical injuries reported in the literature include disc herniations.76 Lumbar spine injuries are the most common back injuries reported. Ekstrand et al. documented injuries over the course of a year in an amateur division consisting of 12 teams and 180 players. They recorded 256 total injuries in 124 players. Twelve of the 256 injuries (5%) were localized to the back region.77 Schmidt-Olsen et al. followed a cohort of 496 youth players aged 12–18 for 1 year and found that back injuries accounted for 14% of all injuries suffered.78 They proposed that back problems in youth players may be associated with growth. In addition, they noted that few players included prematch warm up routines that focused on the lower back. While acute vertebral fractures are rare, there is anecdotal evidence that there may be an increased incidence of pars stress fractures.79 Supporting this claim is a recent study of 28 soccer players with activity-related low back pain that utilized SPECT imaging techniques to find that 82% 1355

Part 6: Interventional Spine in Sports

of patients had evidence of increased scintigraphic uptake in the posterior elements of the lumbar spine. Of the 35 instances of spondylolysis, 25 were reported to be complete fractures, while 10 were noted to be incomplete.80 Ostenberg and Roos followed 123 female players from eight teams of different levels during one season. Injuries to the back accounted for 11% of all injuries that resulted in absence from at least one practice or game.81 Kibler82 logged injury data from 480 games and 74 900 player-hours over a 4-year period from the Bluegrass Invitational Soccer Tournament that included male and female players aged 12–19. He found a 10.9% incidence of injury to the torso, which included the abdomen, spine, and genital areas, and an 8% incidence of injury to the head and neck.

Functional considerations Traumatic spine injuries in soccer are rare. While the majority of spine-related injuries are attributed to lumbar strain, the cervical spine is also susceptible to injury. Soccer is a unique sport in that the head is used in a functional capacity to pass, trap, and shoot the ball. Heading requires quick thrusts of neck flexion and extension, often combined with rotation and side bending. It has been suggested that soccer players are at a higher risk for development of cervical degenerative disc disease when compared to nonsoccer players of the same age group.83 There is also a high amount of asymmetric impact to the trunk which is frequently combined with torsional motion. This can lead to muscle strain, annular rupture, and Z-joint capsular injury. Quick lateral and torsional movements of the spine and rapid hip internal and external rotation occur when the player uses feigning maneuvers in attempt to evade an opposing player. These rapid changes in direction and speed may hasten lumbar motion segment degeneration. In addition, throw-ins involve significant lumbar hyperextension followed by a whipping motion during the rapid transition to forward flexion. The use of the hands overhead creates a long lever-arm, and may accelerate degenerative disease in the lumbar spine.

Cycling Overview Studies indicate a high incidence of spine-related pain in cyclists. Although the majority of research focuses on traumatic injuries, there is a small amount of literature describing overuse injuries in both road and off-road cycling. In addition, cycling is a common component to various other endurance sports such as triathlons, cyclocross, and adventure racing. In regard to neck pain, a population survey of 4500 individuals found that regular cycling was a strong independent risk factor for persistent neck pain (OR 2.0–2.4).84 Weiss evaluated 132 riders who completed an 8-day bicycle tour over a distance of 500 miles. He found that 20.4% of all participants reported neck and shoulder pain.85 An even higher prevalence of neck pain was found in a questionnaire based study of 294 male and 224 female recreational cyclists. Forty-nine percent of cyclists reported neck pain, which was the most common anatomic site of complaint. In addition, females were found to be 1.5 times more likely to develop neck complaints than males.86 The prevalence estimates of low back pain in cyclists range from 2.7% to 60%, depending upon the type of cycling and skill level involved.18,86–89 In a study of 92 Japanese triathletes, low back pain was reported by 32% of athletes during the previous year and accounted for 28% of all injuries reported. Cycling was believed to be a major risk factor for development of low back pain in this population.88 Kronisch and Rubin surveyed 265 mountain bikers in the United 1356

States and reported complaints of back pain in 37% of respondents.87 In 1996, Callaghan and Jarvis investigated musculoskeletal injuries in over 500 elite British Cycling Federation cyclists. They found that low back pain was the most frequently encountered problem in this population, accounting for 60% of complaints.89

Functional considerations The lumbar spine and the pelvis represent a significant point of support from which the power derived from the lower extremities is transmitted to the pedals. In the racing position, the lumbar spine is placed into a kyphotic position with increased pressure on the intervertebral discs. However, it appears that using the upper limbs to support the body decreases intradiscal pressure by distributing load.90 Mountain biking, on the other hand, places the lumbar spine of the rider in a more neutral position, but consequently allows for increased axial load to the spine due to the more upright position. They are also subject to repetitive vibrational exposure that may lead to acceleration of the degenerative process in the lumbar spine. The customization of the bicycle setup for the individual athlete is of utmost importance. Handlebar position that is too high may lead to accentuated lumbar lordosis and increased stress on the posterior elements of the spine. Handlebar position that is too low, increases lumbar flexion and increases the load upon the intervertebral disc. Too long of a stem will cause the rider to be stretched out too far and necessitate holding the neck back, placing stress upon the neck and shoulders. Alterations in bike seat positioning also cause changes in the biomechanics of the lumbar spine. High seats cause the rider to laterally flex the lumbar spine toward the pedal. The incline of the saddle alters the amount of lumbar lordosis and may be adjusted to relieve back pain. In addition, good flexibility of the hamstrings will allow the lumbar spine to achieve a more lordotic position.91–93

Racquet sports Overview Overuse injuries of the low back are common in tennis players, but there are few data available that analyze the incidence and distribution of specific pain generators in back injury. According to Saal, the most common injuries appear to be soft tissue injury to the thoracic and lumbar regions, upper lumbar and thoracolumbar Z-joint injury, and disc disease.94 Chard and Lachmann studied 631 injuries occurring during racquet sports and found a 12% incidence of back injury.95 Another study evaluated professional men tennis players and found that approximately 38% reported missing at least one tournament due to lumbar pain.96 A recent study by Saraux et al. comparing recreational level tennis players to controls found no significant difference between the two groups when comparing reports of low back pain or sciatica during the week prior to survey.97

Functional considerations Tennis players and athletes involved in other racquet sports subject the spine to repetitive hyperextension and rotational movements. Compared to other strokes in tennis, the serve and overhead volley place the highest load through the spinal motion segment. During the service toss, the spine is initially subject to hyperextension, rotation, and lateral flexion. This represents a loading phase through the kinetic chain. Upon striking the ball, force transfer occurs from the lower extremities through the spine to the shoulder joint, and finally the racquet. Inappropriate technique or weakness at any level of the kinetic chain may increase stress upon subsequent segments due to uncoupling of the pelvic and shoulder rotation. Improper location of toss often leads to hyperextension of the spine in order to

Interventional Spine in Sports

make racquet contact. During the forehand and two-handed backhand strokes, the lumbar spine is subject to approximately 90° of axial rotation. Limited range of motion in the hips or uncoordinated rotation of the pelvis with the shoulders will place greater stress on the spinal motion segments. Alternatively, the one-handed backhand requires less rotation of the lumbar segments, decreasing the stress placed upon the lumbar spine.

CONCLUSION The spine is a common source of pain in athletes. In particular, the lumbar spine is the most common site of athletic spine injury, just as it is for spine injury in the general population. However, diagnosis and treatment of athletes requires special consideration due to the unique needs of the athlete, including rapid return to play. Special attention must be given to young athletes, as the chronic complaint of back pain is more likely to be associated with a pathologic etiology than it is in adults. The etiology of spine injury is related to multiple factors and can be predicted by sport type, position played, technical skill, training routine, and age. Knowledge of the degenerative cascade, the motions and demands of the particular sport, and the role of the kinetic chain are paramount when treating athletes with back pain, as they provide a conceptual framework utilized for both the diagnosis and functional rehabilitation necessary for rapid return to play and prevention of injury recurrence.

References 1. Herring SA, Weinstein SM. Assessment and nonsurgical management of athletic low back injury. In: Nicholas JA, Hershman EB, eds. The lower extremity and spine in sports medicine. St Louis: Mosby; 1995:1171–1197. 2. Trainor TJ, Wiesel SW. Epidemiology of back pain in the athlete. Clin Sports Med 2002; 21(1):93–103. 3. Sword L, Hellstrom M, Jacobsson B, et al. Disc degeneration and associated abnormalities of the spine in elite gymnasts. A magnetic resonance imaging study. Spine 1991; 16:437–443. 4. Ong A, Anderson J, Roche J. A pilot study of the prevalence of lumbar disc degeneration in elite athletes with lower back pain at the Sydney 2000 Olympic Games. Br J Sports Med 2003; 37:263–266.

17. Brown PG, Lee M. Trampoline injuries of the cervical spine. Ped Neurosurg 2000; 32:170–175. 18. Standaert CJ, Herring SA, Cole AJ, et al. The lumbar spine in sports. In: Cole AJ, Herring SA, eds. Low back pain handbook. Philadelphia: Hanley and Belfus; 2003:385–404. 19. Mazzeo RS, Cavanaugh P, Evans WJ, et al. Exercise and physical activity for older adults: American College of Sports Medicine position stand. Med Sci Sports Exerc 1998; 30:992. 20. Conte S, Requa RK, Garrick JG. Disability days in major league baseball. Am J Sports Med 2001; 29(4):431–436. 21. Kane SM, House HO, Overgaard KA. Head-first versus feet-first sliding: A comparison of speed from base to base. Am J Sports Med 2002; 30(6):834. 22. Watkins RG. Baseball. In: Watkins RG, ed. The spine in sports. St. Louis: Mosby; 1996:436–455. 23. Koichi S, Katoh S, Sakamaki T, et al. Three successive stress fractures at the same vertebral level in an adolescent baseball player. Am J Sports Med 2003; 31(4): 606–610. 24. Meyers MC, Brown BR, Bloom JA. Fast pitch softball injuries. Sports Med 2001; 31(1):61–73. 25. Casazza BA, Rossner K. Baseball/lacrosse injuries. Phys Med Rehabil Clin N Am 1999; 10(1):141–157. 26. Herkowitz HN, Paolucci JP, Abdenour MA. Basketball. In: Watkins RG, ed. The spine in sports. St. Louis: Mosby; 1996:430–435. 27. Meeuwisse WH, Sellmer R, Hagel BE. Rates and risks of injury during intercollegiate basketball. Am J Sports Med 2003; 31:379–385. 28. Hickey GJ, Fircker PA, McDonald WA. Injuries of young elite female basketball players over a six-year period. Clin J Sport Med 1997; 7(4):252–256. 28a. Henry JH, Lareau B, Neigut D. The injury rate in professional basketball. Am J Sports Med 1982; 10(1):16–18. 29. Rossi F, Dragoni S. Lumbar spondylolysis: occurrence in competitive athletes. J Sports Med Phys Fitness 1990; 30:450–452. 30. Herskowitz A, Selesnick H. Back injuries in basketball players. Clin Sports Med 1993; 12(2):293–306. 31. Viere RG. Special populations and problems: elderly patients. In: Cole AJ, Herring SA, eds. Low back pain handbook: A guide for the practicing physician. Philadelphia: Hanley and Belfus; 2003:437–452. 32. Lebwohl NH. Diving. In: Watkins RG, ed. The spine in sports. St. Louis: Mosby; 1996:391–396. 33. Kim DH, Vaccaro AR, Berta SC. Acute sports-related spinal cord injury: contemporary management principles. Clin Sports Med 2003; 22:501–512.

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40. Torg JS, Sennett B, Vegso JJ, et al. Axial loading injuries to the middle cervical spine segment. An analysis and classification of twenty-five cases. Am J Sports Med. 1991; 19:6–20.

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41. Torg JS, Pavlov H, Genuario SE, et al. Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg [Am] 1986; 68:1354–1370.

12. Cirillo JV, Jackson DW. Pars interarticularis stress reaction, spondylolysis, and spondylolisthesis in gymnasts. Clin Sports Med 1985; 4:95–110.

42. Watkins RG. Lumbar spine injuries in football. In: Watkins RG, ed. The spine in sports. St Louis: Mosby; 1996:343–348.

13. Micheli L, Wood R. Back pain in young athletes. Arch Pediatr Adolesc Med 1995; 149:15–18.

43. Gatt Jr CJ, Hosea TM, Palumbo RC, et al. Impact loading of the lumbar spine during football blocking. Am J Sports Med 1997; 25:317–321.

14. Lament LE, Einola S. Spondylolisthesis in children and adolescents. Acta Orthop Scand 1961; 82:45.

44. Ferguson RJ, McMaster JH, Stanitski CL. Low back pain in college football linemen. Am J Sports Med 1974; 2:63–69.

15. Jackson DW, et al. Stress reaction involving the pars interarticularis in young athletes. Am J Sports Med 1981; 9:304.

45. McCarroll JR, Miller JM, Ritter MA. Lumbar spondylolysis and spondylolisthesis in college football players. Am J Sports Med 1986; 14:404.

16. Rossi F. Spondylolysis, spondylolisthesis and sports. J Sports Med Phys Fitness 1978; 18:317.

46. Shaffer B, Wiesel S, Lauerman W. Spondylolisthesis in the elite football player: an epidemiologic study in the NCAA and NFL. J Spinal Disord 1997; 10: 365–370.

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73. Sward L, Hellstrom M, Jacobsson B, et al. Back pain and radiologic changes in the thoraco-lumbar spine of athletes. Spine 1990; 15:124.

48. Beutler WJ, Fredrickson BE, Murtland A, et al. The natural history of spondylolysis and spondylolisthesis: 45-year follow-up evaluation. Spine 2003; 28(10):1027.

74. Saal JA. Lumbar injuries in gymnastics. In: Hochschuler SH, ed. Spine – state of the art reviews: spine injuries in sports. Philadelphia: Hanley and Belfus 1990: 426–440.

49. Tewes DP, Fischer DA, Quick DC, et al. Lumbar transverse process fractures in professional football players. Am J Sports Med 1995; 23(4):507–509. 50. Day AL, Friedman WA, Indelicato PA. Observations on the treatment of lumbar disc disease in college football players. Am J Sports Med 1987; 15:72. 51. Virgin HW. Football injuries to the skeletal system. Compr Ther 1985; 11(1):19.

76. Tysvaer AT. Cervical disc herniation in a football player. Br J Sports Med 1985; 19(1):43–44.

52. Gerbino PG, d’Hemecourt PA. Does football cause an increase in degenerative disease of the lumbar spine? Curr Sports Med Rep 2002; 1(1):47–51.

77. Ekstrand J, Gillguist J. The avoidability of soccer injuries. Int J Sports Med 1983; 4:124.

53. Torg JS, Vegso JJ, O’Neill MJ, et al. The epidemiologic, pathologic, biomechanical, and cinematographic analysis of football-induced cervical spine trauma. Am J Sports Med 1990; 18(1):50–57.

78. Schmidt-Olsen S, Jorgensen U, Kaalund S, et al. Injuries among young soccer players. Am J Sports Med 1991; 19:273–275.

54. Torg JS, Guille JT, Jaffe S. Injuries to the cervical spine in American football players. J Bone Joint Surg [Am] 2002; 84A(1):112–122. 55. Weinberg J, Rokito S, Silber JS. Etiology, treatment, and prevention of athletic ‘stingers.’ Clin Sports Med 2003; 21:493–500. 56. Dossett AB, Watkins RG. Stinger injuries in football. In: Watkins RG, ed. The spine in sports. St. Louis: Mosby; 1996:337–342. 57. Watkins RG. Lumbar disc injury in the athlete. Clin Sports Med 2002; 21(1): 147–165. 58. Gosheger G, Liem D, Ludwig K, et al. Injuries and overuse syndromes in golf. Am J Sports Med 2003; 31(3):438.

79. Kraft DE. Low back pain in the adolescent athlete. Pediatr Clin North Am 2002; 49(3):643. 80. Gregory PL, Battand ME, Kerslake RW. Comparing spondylolysis in cricketers and soccer players. Br J Sports Med 2004; 38:737–742. 81. Ostenberg A, Roos H. Injury risk factors in female European football: A prospective study of 123 players during one season. Scand J Med Sci Sports 2000; 10(5):279. 82. Kibler WB. Injuries in adolescent and preadolescent soccer players. Med Sci Sports Exer 1993; 25(12):1330–1332. 83. Sortland O, Tysvaer AT. Brain damage in former association football players: An evaluation by cerebral computed tomography. Neuroradiology 1989; 31(1):44–48.

59. Hosea TM, Gatt CJ. Back pain in golf. Clin Sports Med 1996; 15(1):37–53.

84. Hill J, Lewis M, Papageorgiou AC, et al. Predicting persistent neck pain: a 1-year follow-up of a population cohort. Spine 2004; 29(15):1648–1654.

60. Ekin JA, Sinaki M. Vertebral compression fractures sustained during golfing: report of three cases. Mayo Clin Proc 1993; 68(6):566–570.

85. Weiss BD. Nontraumatic injuries in amateur long distance bicyclists. Am J Sports Med 1985; 13(3):187–192.

61. Vad VB, Bhat AL, Basrai D, et al. Low back pain in professional golfers: The role of associated hip and low back range-of-motion deficits. Am J Sports Med 2004; 32(2):494–497.

86. Wilber CA, Holland GJ, Madison RE, et al. An epidemiological analysis of overuse injuries among recreational cyclists. Int J Sports Med 1995; 16(3):201–206.

62. Wallace P, Reilly T. Spinal and metabolic loading during simulations of golf play. J Sports Sci 1993; 11:511. 63. Oseid S, Evjenth G, Evjenth O, et al. Lower back trouble in young female gymnasts: Frequency, symptoms and possible causes. Bull Phys Educ 1974; 10:25–28. 64. Dixon M, Fricker P. Injuries to elite gymnasts over 10 years. Med Sci Sport Exerc 1993; 25:1322–1329. 65. Garrick JG, Requa RK. Epidemiology of women’s gymnastics injuries. Am J Sports Med 1980; 8:261–264. 66. Katz DA, Scerpella TA. Anterior and middle column thoracolumbar spine injuries in young female gymnasts: Report of seven cases and review of the literature. Am J Sports Med 2003; 31:611. 67. Kurzweil PR, Jackson DW. Gymnastics. In: Watkins RG, ed. The spine in sports. St. Louis: Mosby; 1996:456–464. 68. Hutchinson MR. Low back pain in elite rhythmic gymnasts. Med Sci Sports Exercise 1999; 31(11):1686. 69. Bono CM. Low back pain in athletes. J Bone Joint Surg [Am] 2004; 86A(2): 382–396. 70. Goldstein JD, Berger PE, Windler GE. Spine injury in gymnasts and swimmers: An epidemiologic investigation. Am J Sports Med 1991; 19:463. 71. Sward L. The thoracolumbar spine in young elite athletes. Current concepts on the effects of physical training. Sports Med 1992; 13(5):357–364. 72. Jackson DW, Rettig A, Wiltse LL. Epidural cortisone injections in the young athletic adult. Am J Sports Med 1980; 8:239.

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87. Kronish RL, Rubin AL. Traumatic injuries in off-road bicycling. Clin J Sports Med 1994; 4(4):240–244. 88. Manninen JS, Kallinen M. Low back pain and other overuse injuries in a group of Japanese triathletes. Br J Sports Med 1996; 30(2):134–139. 89. Callaghan MJ, Jarvis C. Evaluation of elite British cyclists: the role of the squad medical. Br J Sports Med. 1996; 30(4):349–353. 90. Usabiaga J, Crespo R, Iza I, et al. Adaptation of the lumbar spine to different positions in bicycle racing. Spine 1997; 22(17):1965–1969. 91. Mellion MB. Neck and back pain in bicycling. Clin Sports Med 1994; 13(1): 137–164. 92. Mellion MB. Common cycling injuries. Management and prevention. Sports Med 1991; 11(1):52–70. 93. Salai M, Brosh T, Blankstein A, et al. Effect of changing the saddle angle on the incidence of low back pain in recreational bicyclists. Br J Sports Med 1999; 33(6): 398–400. 94. Saal JA. Tennis. In Watkins RG, ed. The spine in sports. St. Louis: Mosby; 1996: 499–504. 95. Chard MD, Lachmann MA. Racquet sports-patterns of injury presenting to a sports injury clinic. Br J Sports Med 1987; 21(4):150–153. 96. Marks MR, Haas SS, Wiesel SW. Low back pain in the competitive tennis player. Clin Sports Med 1988; 7(2):277–287. 97. Saraux A, Guillodo Y, Devauchelle V, et al. Are tennis players at increased risk for low back pain and sciatica? Revue de Rhumatisme (English Edition) 1999; 66(3):143–145.

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128

INTERVENTIONAL SPINE IN SPORTS

Acute Intervention and Return to Play Wesley Smeal and Joel Press

INTRODUCTION As a team physician, one has an opportunity to work with and treat athletes. Being a team physician requires a vast fund of knowledge, including familiarity with trauma protocols, musculoskeletal injuries, and medical conditions that affect the athlete. The team physician must be prepared, have an appropriate knowledge base of the sport, and be flexible enough to deal with a multitude of situations that may unexpectedly or emergently arise.1 The principal responsibility of the team physician is to provide for the athlete’s overall well-being, allowing all to maximize their potential. The team physician must take the responsibility of making medical decisions regarding the participant’s safety, and communicate effectively with coaches, athletic trainers, healthcare providers, the parents, and the athlete.1 Preparation is critical to effective and efficient management of sports-related injuries. With the appropriate equipment available, the proper personnel present, and a chain of command in place, each injury can be properly evaluated and appropriate medical decisions can be made to optimize the health and safety of the athlete. With each injury, a condition-specific medical history and physical examination, along with appropriate medical tests and consultations, help establish an accurate diagnosis to best direct treatment and ultimately make a decision regarding the athlete’s safe return to athletic participation.2,3 The purpose of this chapter is to outline how to evaluate and manage the injured athlete on the field, to highlight conditions that can occur during or as a result of active athletic participation, and to review current guidelines for decision-making regarding safe return to play for specific injuries. This information is also discussed in Chapter 127 (Epidemiology of Injuries) and in Chapter 126 (On the Field Assessment).

ON-FIELD EVALUATION Proper preparation, which includes a chain of communication, education of medical personnel, easy access to emergency equipment and tools, and ambulance availability eases anxiety in the potentially tense situation of an athletic injury.4 Preparation enhances efficient and optimal management of the injured athlete. A comprehensive list of recommended on-site medical equipment is available in the Sideline Preparedness Consensus Statement.2 For spinal injuries, it is imperative to have a spine board with appropriate attachments, a semirigid collar, and a face mask removal tool, such as a screwdriver or bolt cutter.4,5 Other necessities besides ACLS equipment and medications include equipment for an urgent neurological evaluation, such as a flashlight, a reflex hammer, and a sharp object for sensory testing.4 On-field evaluation and management of neck or head injuries can be separated into five categories: (1) preparation for any neurological injury,

(2) suspicion and recognition, (3) stabilization and safety, (4) immediate and possible secondary treatment, and (5) evaluation for return to play.6 When an injury occurs after an acceleration–deceleration impact to the head or neck, medical personnel must immediately evaluate the athlete for the possibility of a head injury, a spinal cord injury, or both.7 Indications of possible cervical spine or spinal cord injury include neck pain, numbness, or dysesthetic pain. Bilateral involvement or neurological deficits in the upper and lower extremities also suggest a possible spinal cord injury. In any case that a spinal cord injury cannot be ruled out, the athlete should have his or her neck immobilized, be positioned on a spinal board, and be transported to the nearest trauma center for further physician and radiological evaluation.8 The most important principle of injury management is to prevent further injury.9 If an athlete is downed and not moving, the athlete should be treated as though a brain injury and spinal cord injury have occurred,8 and immediate assessment of the ABCs (airway, breathing, and circulation) of trauma should ensue. Although the ABCs are of highest priority, extreme caution should be taken to avoid movement of the athlete in order to prevent further neurological injury. The head and neck of the athlete should immediately be immobilized in a neutral position.4,5,7 As standard trauma protocol management of the ABCs occurs, evaluation of the athlete’s level of consciousness should be undertaken. Neurological evaluation should consist of level of consciousness, pupil response, pain response, weakness, abnormal posturing, rigidity, or flaccidity.4,5 If the athlete is unconscious, the individual needs to be moved safely to a supine position to facilitate emergency management. If an athlete is face down and unconscious, he or she should be logrolled to a face-up position while the neck is maintained in a neutral position.4,7 Ideally, the individual is log-rolled by four members of the medical team, with the leader controlling the head and neck and issuing the commands. The leader should maintain neck immobilization with slight cervical traction and employing the cross-arm technique to ease positioning throughout the roll. Each of the other three team members should control a specific region of the body, either the shoulder, hips, or the lower leg, as the athlete is rolled toward them. A fifth member can help with carrying and positioning as necessary (Fig. 128.1).4,10 If the injured athlete is wearing a helmet or shoulder pads, neither should be removed until the person has been transported to a trauma facility where appropriate clearance can be provided after a proper physician examination and radiological evaluation have been performed.4,10 When positioning a helmeted athlete on the backboard, the positioning of the head and neck must be done cautiously, as further injury can be caused if the helmet unintentionally causes flexion of the cervical spine.11 The spine should be maintained in a

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A

B

C

D

Fig. 128.1 Demonstration of a four person log roll of a potentially spine-injured athlete. (A) The leader ideally employs the cross-handed technique to control the head and maintain the position of the cervical spine. The three assistants control the shoulders, hips, and lower leg to roll the athlete toward them onto the spine board. The leader provides verbal commands. (B) The leader and three assistants maintain body alignment during the roll. (C) The athlete is positioned on the spine board. (D) Straps and rolls are used to maintain proper positioning of the athlete on the board in anticipation of lifting the athlete for transfer.

straight line during any movement or positioning. Once the player is on the board, straps and pads are used to secure the position.5 If the downed athlete is not breathing, the mouthpiece and face mask should be promptly removed to expedite airway access and cardiopulmonary resuscitation (CPR) management. A screwdriver, Trainer’s Angel, Face Mask Extractor, or bolt cutter should be used to remove the face mask while maintaining proper positioning of the neck. The jaw thrust maneuver is the preferred method of opening the airway in an individual with a potential cervical spine injury.4 The Inter-Association Task Force for Appropriate Care of the Spine Injured Athlete has outlined four situations in which the athletic helmet and chin strap may need to be removed on the field: (1) if the helmet and chin strap do not hold the head securely, meaning that immobilization of the helmet does not immobilize the head; (2) if because of the design of the helmet and chin strap the airway is unable to be maintained even after the removal of the face mask; (3) if the face mask cannot be removed in a reasonable time period; and (4) if the helmet prevents immobilization of the head in an appropriate position for transport.6,12,13 Emergency Medical Service (EMS) personnel may be more familiar with Advanced Trauma Life-Support (ATLS) protocols designed more specifically for motorcycle helmets, so communication among those managing an injured, helmeted athlete is critical.14 In cases in which the helmet has to be removed on the field, the athlete’s head must be supported at the occiput and the cervical spine kept in straight alignment. While the occiput is supported, the chin strap is removed and the team leader spreads the ear flaps and pulls the helmet off in a straight line with the spine.4 Efforts to maintain absolute immobilization should be continued until comprehensive evaluation at a trauma center can be completed.

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INJURIES AND RETURN TO PLAY As a physician involved in the care and treatment of athletes, one of the most challenging responsibilities is determining when an athlete is safe to return to competition. The physician needs to explain to the athlete the severity of the injury and the risk for reinjury or more severe injury. The physician must have a depth of knowledge about the sport, the nature of the injury and its course, and the potential sequelae to best counsel the athlete.1,15 Guidelines are available to help direct decision-making, but each case must be evaluated on an individual basis. Ultimately, the athlete, and when appropriate the coach and parents, must be given recommendations regarding return to play that are in the athlete’s overall best interest.3 Cervical spine injuries that are a result of athletic competition have been classified into three broad categories based on duration of symptoms or radiographic findings. The classification provides a general framework to develop an initial expectation for return to play (Table 128.1).5,15,16 Type I injuries are those in which the athlete acquires a permanent spinal cord injury. This class includes complete, and four variations of incomplete, spinal cord injury. The four types of incomplete spinal cord injury are Brown-Sequard, anterior spinal cord syndrome, central cord syndrome, and mixed-type of spinal cord injury. Furthermore, evidence of spinal cord pathology on radiographic studies also is classified as type I. Thus, evidence of spinal cord injury, whether clinical or radiographic, is an absolute contraindication to return to play in contact or high-velocity sports.5,16 Injuries that are classified as type II are those with neurological changes that are transient, resolving in minutes to hours, and without abnormalities on radiographic evaluation. Examples of type II injuries

Interventional Spine in Sports

Table 128.1: Classification of cervical spine injuries Type I

Type II

Type III

Permanent Spinal Cord Injury Complete spinal cord injury Incomplete spinal cord injury Brown-Sequard Anterior spinal cord syndrome Central cord injury Mixed-type spinal cord injury

Transient Neurological Changes Transient quadriparesis Burning hand syndrome

Radiographic Abnormalities Only Fracture Fracturedislocation Herniated disc Ligamentous injury

From Warren and Bailes.11,15,16

are transient quadriparesis and a variation of central cord syndrome known as burning hands syndrome (Fig. 128.2). Those athletes with type II injuries are not absolutely contraindicated from returning to play, but each case must be thoroughly evaluated on an individual basis. There is controversy regarding type II injuries and safe return to play. Certain criteria must be met for each specific type II injury before an athlete may return to play.5,16 There is a condition in which spinal cord injury occurs though there is no evidence of fracture or osseous malalignment on either radiographs or computed tomography (CT). This condition has been termed ‘spinal cord injury without radiographic abnormalities’ (SCIWORA). This condition has largely been reported in the pediatric population, though it has also been described in the adult population.17 Because of the predilection for the pediatric population, SCIWORA has also been referred to in the literature as ‘pediatric syndrome of traumatic myelopathy without demonstratable vertebral injury.’18 SCIWORA has been theorized to occur more frequently in the pediatric population due to anatomical and biomechanical properties. Suggested reasons for increased incidence in the pediatric population include the following: (1) more horizontal orientation of facet joints in the pediatric population, (2) anterior wedging of the superior aspects of the vertebral bodies, and (3) more ‘elastic’ ligaments and joint capsules.17 These differences in the pediatric population, which are typically apparent until 16–18 years of age, allow for more intersegmental motion, potentially leading to neurological injury without apparent osseous or ligamentous injury. SCIWORA, which typically results from a flexion–extension-type injury, may be the result of a spinal cord infarction due to temporary occlusion of either the vertebral arteries or the anterior spinal artery.18 Fortunately, magnetic resonance imaging (MRI) now allows better evaluation of the soft tissues of the spine. Thus, even when patients presenting with a spinal cord injury have no apparent osseous abnormality, MRI can delineate extradural lesions such as disc herniations and ligamentous injuries, as well as intradural lesions such as spinal cord hematomas and edema. Furthermore, these MRI findings have been determined to correlate well with the clinical presentation and are also of prognostic significance.17 Type III injuries are based solely on radiographic abnormalities, including fractures, fracture-dislocations, herniated discs, and ligamentous and soft tissue injuries. This class encompasses a vast range of injury severity and must also be evaluated on a case-by-case

Athlete presents with severe motor +/– sensory deficits

(Variable length of symptoms – minutes to hours)

Initiate on-field treatment as though SCI has occurred

If no movement by athlete, immobilize and transfer to trauma center

If symptoms rapidly resolve and athlete moving, perform on-field screening evaluation

Athlete should not RTP until completion of a diagnostic work up

Determine if need for immobilization and transfer or if able to move to sideline for further evaluation

Proceed with radiographic evaluation (AP/lateral/ oblique/open mouth views)

If radiographs inconclusive, proceed with CT of cervical spine to rule out osseus abnormality

If no radiographic abnormality on initial radiographs, consider flexion− extension views

If radiographs + for abnormality, consider further imaging (MRI or CT) and refer to spine surgeon

Proceed with MRI to evaluate for functional cervical stenosis

Regardless of work-up RTP is controversial after TQ

If MRI + for functional cervical stenosis in athlete with history of TQ

If MRI – for functional cervical stenosis in athlete with history of TQ

May be considered an absolute contraindication to RTP in contact/collision sports, but ultimately should be decided on an individual case basis

May consider RTP on an individual basis if symptoms have completely resolved and strength, sensation, and ROM are all normal

SCI = spinal cord injury; RTP = return to play; AP = anterior−posterior; TQ = transient quadriparesis-not transient good diagnosis; CT = computed tomography; MRI = magnetic resonance imaging; ROM = range of motion Fig. 128.2 Algorithm of transient quadriparesis. Information primarily from Wilberger11 and Allen and Kang.27

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basis. An important aspect of each type III injury is determining the stability of the injury in order to assess the potential for return to play.5,16 Surgical stabilization alone does not mean that the athlete can return to play. The level and type of surgical repair, as well as the sport in question, must all be considered before a decision on safe return to play can be made.9,19 More specific return to play guidelines will be further outlined in the discussion of each respective injury.

Return to play

CERVICAL SPINE INJURIES

Due to the severe nature of spinal cord injuries, athletes who sustain a spinal cord injury have an absolute contraindication to return to contact or high-velocity sports.11

Spinal cord injury

Spinal cord injury variant

Epidemiology Acute spinal cord injuries are relatively infrequent, but are an inherent risk of collision and high-velocity sports. With an incidence of 4 per 100 000 population per year, approximately 10 000 new spinal cord injuries occur annually in the United States.16 Between 5% and 10% of these spinal cord injuries occur during athletic activity, both organized and recreational.11 Spinal cord injuries occur most frequently in tackle football (1.87 per 100 000 players per year) among organized sports and in diving among recreational activities.5 While severe spinal cord injuries in sports are usually rare accidents, other sports with documented spinal cord injuries, in addition to American football, include gymnastics, wrestling, ice hockey, rugby, snow skiing, snowboarding, surfing, and soccer among others.4,20,21 With a conscious focus on better understanding the pathomechanics of the injuries that lead to acute sports-related spinal cord injuries, particularly in organized sports such as football, various interventions have led to a decrease in the occurrence of spinal cord injuries over the past 30 years.5,21 Changes in rules, advances in protective equipment, and adjustments in proper playing techniques have all contributed to the decrease in the incidence of spinal cord injuries in organized sports. Because so many circumstances are variable and uncontrollable in recreational activities, it has been far more difficult to impact the frequency of spinal cord injuries in those situations.5,21

Pathomechanics According to the National Center for Sports Injury and Research, almost all of the cases of sports-related cervical spinal cord injury resulted from cervical spine fractures/dislocations, unless spinal stenosis was present.22 The mechanism of permanent spinal cord injury is thought to be from a tremendous axial load to the vertex of a player’s head that is then absorbed in the cervical spine, which is overwhelmed. This load leads to a structural failure of the spinal column and a resulting spinal cord injury. The structural failure is more likely to occur when the neck is in slight forward flexion, negating the seemingly protective natural lordosis of the cervical spine, and establishing a more uniform column which absorbs the axial load rather than dissipating it.7,23 The primary neurological injury occurs at the time of the impact. The secondary neurological injury, involving a cascade of edema and hemorrhage, occurs after the primary injury and can be minimized with the proper immediate care of the injured athlete.5

Evaluation and management An individual with a spinal cord injury may present with no movement, complaints of pain, particularly in the neck, or with complaints of sensory changes.11 When a spinal cord or other severe acute neurological injury is thought to have occurred, the ABCs (airway, breathing, circulation) of the standard trauma protocol must be initiated immediately. 1362

It is critical that every unconscious athlete be treated as though a spinal cord injury has occurred.15 While the ABCs are the highest priority, the downed athlete should have the cervical spine stabilized as soon as possible, as previously discussed, and prepared for transport to a medical facility for further evaluation and management.

Burning hand syndrome is a type of spinal cord injury. A variant of central cord syndrome thought to preferentially affect the spinothalamic tracts, burning hand syndrome is classified as a type II cervical spine injury. Athletes with burning hand syndrome present with a burning sensation in the bilateral hands and fingertips, often in the absence of neck pain or limitation. Weakness may or may not be noticed and occasionally the dysesthesias are noted in the lower extremities. If an athlete is suspected of having burning hand syndrome, he or she must be removed from competition, as with any spinal cord injury, until a full physical examination and radiographic evaluation determines the nature and extent of the injury. While there may be no detectable cervical spine abnormality, at least 50% of the cases of burning hand syndrome will have evidence of a fracture or soft tissue injury.7,24,25

Transient quadriparesis and cervical stenosis Epidemiology Transient quadriparesis is a relatively rare cervical spine injury that, by definition, is not permanent. Thought to be a temporary dysfunction of the spinal cord, transient quadriparesis has also been referred to in the literature variably as transient neurapraxia, cervical cord neurapraxia (CCN), and spinal cord concussion (SCC).26–28 Because the pathophysiology of this temporary phenomenon is not completely understood, the more descriptive terminology of transient quadriparesis is often used. Transient quadriparesis occurs most frequently in American football, but has also been described in athletes injured in boxing, hockey, basketball, and wrestling. The incidence of this type of injury has been estimated to be 1.3 episodes of sensorimotor deficits per 10 000 athletes and 6 episodes per 10 000 athletes in sensory disturbance alone.29 Athletes with an episode of transient quadriparesis may report a sensory change, a functional motor change, or a combined sensorimotor syndrome. Transient quadriparesis is not permanent; however, the athlete may complain of sensory changes or demonstrate motor deficits anywhere from a few minutes to several days later, though usually it is less than 48 hours.11,27 The vast majority of cases resolve in 10–15 minutes.23 Transient quadriparesis may present as a sensory change, motor weakness, or complete paralysis and can affect the bilateral arms or legs, the ipsilateral arm and leg, or all four extremities. Episodes of transient quadriparesis can be classified into three grades, based on the time frame of symptoms. Grade I injuries last less than 15 minutes. Grade II episodes last anywhere from 15 minutes to 24 hours. Grade III injuries last greater than 24 hours, but less than 48 hours. The vast majority of cases are grade I quadriparesis.28,30

Pathomechanics Transient quadriparesis is a result of contact, typically axial loading with the neck in either flexion or extension.23 When first described, transient quadriparesis was considered a ‘concussion’ of the cervical

Interventional Spine in Sports

spinal cord.26,27 Though still not completely understood, several mechanisms have been proposed, including spinal cord edema or local ischemia. However, these two mechanisms do not correlate with the immediate onset and rapid resolution of the symptoms. A mechanism of transient quadriparesis that is often described is a functional disturbance of the axonal membrane without disruption of the structural integrity.26 Though the nerve itself is not disrupted, there may be prolongation of the absolute refractory period of the long-tract axons of the spinal cord. Ultimately, the prolonged refractory period may lead to a lengthened period of time in which the axons do not respond normally to subsequent stimulation.26,27 The term neurapraxia is often used to describe the proposed phenomenon that leads to transient quadriparesis27,28 because neurological symptoms occur, but the integrity of the long-tract axons of the spinal cord is thought to be preserved. However, the term neurapraxia is classically used to refer to peripheral nerve dysfunction.31 Thus, the distinction between involvement of a spinal cord axon and a peripheral nerve axon may have different implications. The term neurapraxia may misrepresent the pathophysiology of this central nervous system lesion compared with the more common neurapraxia of the peripheral nervous system. The current understanding of the mechanism of transient quadriparesis is consistent with the ‘pincer mechanism’ as described by Penning.28,32 A combination of axial loading and hyperextension is thought to be the primary cause. With hyperextension, the spinal canal is maximally narrowed and the cord can be compressed between the posteroinferior aspect of the superior vertebral body and the anterosuperior aspect of the spinal laminar line of the subjacent vertebral body. The degree of compression is dependent on the sagittal diameter of the canal, the degree of extension, and the amount of infolding of the soft tissues such as the ligamentum flavum and posterior longitudinal ligament.27,32 Extreme flexion with axial loading is another potential cause of transient quadriparesis. With hyperflexion, the spinal canal is also significantly reduced, potentially resulting in compression of the spinal cord. The compression occurs because the distance is reduced between the spinal laminar line of the superior vertebral body and the posterosuperior aspect of the inferior vertebral body.27,30

Evaluation and management The presentation of transient quadriparesis can be dramatic, as the athlete may have severe motor deficits, even to the point of complete paralysis of both the upper and lower extremities. Sensory changes include sensory loss, burning dysesthetic pain, numbness, and tingling. The episode is temporary, resolving in minutes to hours. Even though the athlete often experiences dysesthesias, neck pain is generally not present immediately after the incident.27 Any athlete who has an episode of transient quadriparesis requires a thorough history and physical examination. During the history, attention must be focused on the type and length of symptoms, prior episodes of transient quadriparesis, and any prior neck injuries or pain, and a description of the events prior to and during the event. The physical examionation should focus on the musculoskeletal and neurological aspects in order to best document subsequent recovery.27 Thorough radiographic evaluation must be performed to evaluate for fracture, dislocation, instability, cervical stenosis, spondylosis, or congenital abnormalities. Radiographic evaluation typically begins with plain films, including anteroposterior (AP), lateral, oblique, and open-mouth odontoid views. If parts of the cervical spine are not adequately visualized, including the T1 vertebra, axial CT may help delineate any structural problems.27 Dynamic flexion and extension films are important in evaluating ligamentous instability once the patient can actively perform the maneuvers without pain.

Those athletes with a history of transient quadriparesis or persistent neurological abnormalities should have an MRI performed to rule out ongoing extrinsic cord compression, nerve root compression secondary to a herniated disc, intrinsic cord abnormalities, or evidence of ligamentous injury.11,27

Return to play Athletes with transient quadriplegia typically have rapid and complete recovery, often with no identified spine or spinal cord injury on plain radiographs.11,33 An individual who has had an episode of transient quadriparesis should be evaluated for underlying cervical stenosis. There is ongoing controversy regarding the potential increased risk of severe, permanent neurological injury in an athlete after an episode of transient quadriparesis and also the relationship of cervical spinal stenosis to transient quadriparesis.11,27 Thus, cervical stenosis can be the determining issue in the return to play question.

Cervical stenosis The issue of cervical spinal stenosis in an athlete, regardless of whether he or she has suffered a prior cervical injury, and return to play decisions remains controversial. The definition of cervical stenosis itself is debatable and has changed with advances in radiographical techniques. Opinions vary on whether the presence of cervical stenosis makes an athlete more susceptible to permanent neurological injury or transient quadriparesis.11,22,27,30,34 Originally, cervical stenosis was determined by measurements made from plain lateral cervical spine radiographs. From the lateral films, measurements were made from the posterior aspect of the vertebral body to the most anterior aspect of the spinal laminar line to establish the anteroposterior diameter of the spinal canal. Between C3 and C7, an anteroposterior canal measurement of 15 mm or more is considered normal, whereas a measurement of less than 13 mm is defined as cervical stenosis.27,35,36 Variations in technique, magnification, positioning, and body size all potentially affect the accuracy of the measurements on plain radiographs, and ultimately, the diagnosis of cervical spinal stenosis.37,38 In an attempt to eliminate the effect of some of the variables, Torg and Pavlov developed a ratio to better qualify cervical stenosis. The Torg ratio compares the sagittal diameter of the spinal canal to the sagittal diameter of the midbody of the vertebral body at the same level. A normal Torg ratio was designated as 1:1 and the criteria for significant cervical spinal stenosis was determined to be a ratio of less than 0.80.19,27 The Torg ratio was determined to be highly sensitive, but had a low positive predictive value in determining significant spinal stenosis.27 In fact, in some cases, the absolute diameter of the canal is greater that 15 mm, but the Torg ratio is less than 0.80 because of large vertebral bodies.39 The clinical value and cost-effectiveness of using the Torg ratio as a screening technique to determine who should undergo more advanced radiographic evaluation of cervical stenosis is also debated in the literature (Fig. 128.3). With widespread use and access of MRI, the concept of functional spinal stenosis has been established. Functional spinal stenosis is defined by the loss of the normal cerebrospinal fluid (CSF) cushion around the spinal cord or an apparent compression of the cord itself. In this case, functional refers to the functional reserve of CSF that provides the protective cushion around the spinal cord in a nonstenotic canal.34,35,39 Determination of functional spinal stenosis can be done with MRI, CT, and myelography. Thus, the amount of space available to the spinal cord is more important that the absolute size of the spinal canal.11 Most MRI of the cervical spine is performed with the patient in the neutral position. However, in a hyperexten1363

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b

b

a

a

Ratio = a– b

Fig. 128.3 Torg ratio. The Torg ratio = a/b: a is the distance from the midpoint of the posterior surface of the vertebral body to the midpoint of the corresponding spinolaminar line; b is the distance from the midpoint of the anterior aspect of the vertebral body to the posterior aspect.

sion position, which can often occur during athletic participation, the spinal canal diameter can be compromised as much as 30%.35 Therefore, some might argue the need for dynamic MRI to better assess functional stenosis. Controversy persists regarding cervical stenosis and the incidence of neurapraxia, recurrent neurapraxia, and permanent neurological injury. Torg et al. have done extensive investigation into the relationship of cervical stenosis and whether it predicts or contributes to permanent neurological injury. One study included 77 athletes who sustained permanent quadriplegia as a result of tackle footballrelated injuries, and all denied a prior history of transient quadriparesis. With an average canal size of 18.9 mm and a Torg ratio of greater than 0.90, cervical stenosis was not thought to be a contributor to the resulting permanent neurological deficits. Another

study of 110 athletes with transient quadriparesis concluded that 56% had a recurrence of symptoms, and those who experienced a recurrence had a smaller Torg ratio. Thus, cervical stenosis was proposed to be a contributor to transient quadriparesis, but not necessarily to permanent neurological injury.27,40 Torg and Ramsey-Emrhein proposed the following guidelines for return to play. No contraindication for an asymptomatic athlete with a finding of a Torg ratio less than 0.80. Relative contraindication for an athlete with one episode of transient quadriparesis less than 36 hours in duration and a Torg ratio of less than 0.80 as well as for an athlete with an episode of transient quadriparesis and evidence of disc disease or degenerative changes. An athlete with an episode of transient quadriparesis and MRI evidence of a cord defect has a relative or absolute contraindication to return to play based on other variables in the specific case. Athletes with multiple episodes of transient quadriparesis, a single episode lasting more than 36 hours, or evidence of ligamentous instability have an absolute contraindication to return to play.27,40,41 Others argue that cervical spinal stenosis predisposes one to transient quadriparesis and permanent neurological injury. Though relatively few in number, there are reports of athletes with cervical stenosis and a prior episode of transient quadriparesis who subsequently incurred a permanent neurological injury without a fracture or dislocation.27,42 Moreover, the recovery of neurological deficits in those athletes with a fracture or dislocation is thought to be better in those athletes with normal-sized spinal canals. Thus, some authorities recommend an absolute contraindication to return to play in contact sports for athletes with cervical stenosis. Those with an episode of transient quadriparesis but without evidence of cervical stenosis or instability may return to play when symptoms are completely resolved and strength and sensation are intact.27,42

Spear-tackler’s spine Epidemiology Spear-tackler’s spine is a condition found in American football players. Torg identified a class of athletes who are at high risk of permanent cervical quadriplegia (Table 128.2). Through an evaluation of the National Football Head and Neck Injury Registry and identification of those individuals who sustained severe cervical spinal cord injuries, a condition called spear-tackler’s spine

Table 128.2: Spear-tackler’s spine Spear-tackler’s spine A condition in which an athlete repeatedly uses a spearing technique for tackling Risk factors 1. Developmental narrowing of the cervical spinal canal (Torg ratio < 8.0) 2. Persistent straightening or reversal of normal cervical lordotic curve on lateral radiographs 3. Radiographic evidence of preexisting post-traumatic cervical spine abnormalities Return to play issues May consider return to play on an individual basis if: Loss of cervical lordosis is reversed and Athlete is able to learn to tackle with proper (nonspearing) technique From Torg,41 Wilberger,11 and Allen and Kang.27

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was established.43 These athletes were noted to repeatedly use the spearing technique, which incorporates a head-first approach to tackling with the vertex of the helmet used to initiate contact with a competitor. Other risk factors identified by Torg in the classification of spear-tackler’s spine include: (1) developmental narrowing of the cervical spinal canal (Torg ratio 0.8 or less), (2) persistent straightening or reversal of the normal cervical lordotic curve on lateral radiographs, and (3) radiographic evidence of preexisting posttraumatic cervical spine abnormalities, such as wedge fractures, disc bulges, and disc herniations.7,43

Pathomechanics Typically, the cervical muscles, which actively flex, extend, and lateral side-bend the neck, dissipate the forces of axial loading from the cervical spine. The ability to absorb axial loading is thought to be maximal when the neck is in anatomical position, with slight extension and a normal cervical lordosis. With neck flexion of approximately 30 degrees or loss of the normal cervical lordosis the cervical spine becomes a straight, segmented column and the axial load is transmitted directly to the bones, discs, and ligaments rather than the muscles.19,23 If the tremendous axial load is absorbed only by the segmented column, the spine may buckle, leading to fractures, dislocations, and potentially catastrophic neurological injury.37 This situation is thought to occur in the athlete who initiates a tackle with the vertex of the helmet and sustains a spinal cord injury.

Evaluation and management The diagnosis of spear-tackler’s spine is made when an athlete has been seen using a spearing technique with tackling and demonstrates the three aforementioned radiographic findings.

Return to play Athletes with the four risk factors of spear-tackler’s spine are generally considered to have an absolute contraindication to participating in contact sports. If the loss of the cervical lordosis is reversed, and the athlete is trained to incorporate proper tackling techniques without spearing, a return to play may be considered on an individual basis.11,27,43

Stingers Epidemiology The stinger syndrome, also known as a burner, is a common injury in contact sports, especially tackle football. The incidence of stingers is likely higher than reported because in many cases the symptoms are so short in duration that they are never reported. It has been estimated that 50–65% of college football players will incur a stinger during a 4-year collegiate career.44 Athletes with a stinger usually have an immediate, unilateral, radiating shoulder or arm pain along with burning dysesthesias after a collision. Athletes may also have associated ipsilateral arm weakness, especially of the biceps, deltoids, supraspinatus, and infraspinatus muscles leading to limited shoulder abduction, elbow flexion, and external rotation.45,46 Often the athlete is seen trying to ‘shake it off ’ or to support the injured arm with the other, noninjured upper extremity. In the overwhelming majority of cases, the symptoms are transient, usually lasting only seconds to minutes. In some cases, stingers last longer than 2 minutes.47 In more unusual situations, weakness may not be apparent until days to week after the injury.46 Stingers do recur (up to 57% in one study) and they may recur frequently in some athletes.44

Pathomechanics Though still debatable, the specific cause of stingers is thought to be trauma to either the cervical nerve roots or the brachial plexus. Both compression and stretch injuries have been theorized as the mechanism of injury. Current hypotheses for stingers include the following: (1) nerve root compression in the neural foramen (extension–axial compression), (2) stretch or tensile injury to the cervical nerve root–spinal nerve complex, (3) traction or stretch injury to the brachial plexus, particularly the upper trunk, and (4) direct blow or compression to the brachial plexus.48 In a traction injury, a direct blow to the head causes a contralateral neck lateral flexion and ipsilateral shoulder depression. In the compression mechanism, the direct blow causes ipsilateral lateral flexion and acute narrowing of the ipsilateral neural foramen.46 The anatomy and components of the brachial plexus, particularly the plexiform design and the presence of perineural tissue, makes it more resistant to both compressive and traction forces in comparison to the nerve root–spinal nerve complex.45,48 At the high school and lower amateur level, especially in tackle football, stingers are typically a result of a brachial plexus stretch injury. At the more elite levels of competitive sports, particularly college and professional tackle football, stingers are thought to be due to compression of the nerve root in the neural foramen (Fig. 128.4).39 Stingers can be graded into three classes based on Seddon’s criteria.31,46 Grade I is a neurapraxia, involving a temporary motor or sensory deficit without structural disruption of the axon. With a grade I stinger, full recovery is expected within 2 weeks. Grade II is axonotmesis, in which there is disruption of the axon but the outer protective epineurium is intact. The neurologic deficit or symptoms typically last longer than 2 weeks but less than 1 year. In grade II stingers, findings on electromyographic (EMG) studies of axonal injury may be seen 2–3 weeks postinjury. Grade III injuries are consistent with neurotmesis, with total disruption of the axon and its supporting structures. The symptoms persist longer than 1 year with no significant clinical improvement.46

Evaluation and management As with any injury, the first step is observation. In the case of a stinger, the athlete will complain of unilateral burning pain, upper extremity weakness, or both. Stingers are peripheral nerve injuries and not spinal cord injuries. If the symptoms are present in the bilateral upper extremities, the athlete has likely suffered a spinal cord injury and the appropriate precautions and care for a spinal cord-injured patient must be enacted. Burning hand syndrome, discussed previously, is a spinal cord injury with bilateral upper extremity involvement that should not be confused with a stinger.24,25,48 In the case of a stinger, the athlete typically maintains a flexed posture of the cervical spine, which helps reduce the pressure on the nerve root. Often the ‘shoulder abduction relief sign’ will be observed, in which the athlete instinctively elevates the shoulder or arm of the involved limb to reduce tension on the nerve roots or brachial plexus.45 A thorough musculoskeletal and neurological examination of the cervical spine and upper extremities should be performed, including evaluation of range of motion, strength, sensation, and reflexes. After palpation of the cervical spine is performed to evaluate for deformity, spasm, swelling, pain, or tenderness, the athlete should then be directed to perform active range of motion, including flexion, extension, rotation, and side-bending within tolerance to pain. Passive range of motion is contraindicated on the sideline if the patient is symptomatic, as cervical fracture needs to be ruled out. If cervical

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Traction

A

Compression

B

Fig. 128.4 Pathomechanics of a stinger. (A) Depiction of a traction injury caused by contralateral neck flexion and ipsilateral shoulder depression. (B) Injury to the side opposite of contact caused by contralateral compression.

range of motion is not restricted or painful, a Spurling maneuver can be performed to assess for radicular symptoms.45 In the upper extremities, the fifth, sixth, and seventh myotomes, because of their anatomic positioning, must be tested and compared to the uninvolved side as they are most likely to be affected by a stinger. Grip strength alone is inadequate, as those muscles are innervated by the seventh and eight cervical nerves. To properly assess the fifth, sixth, and seventh myotomes, the supraspinatus, infraspinatus, deltoids, biceps, brachioradialis triceps, serratus anterior, wrist flexors, and wrist extensors must all be evaluated.49 If symptoms persist 2 weeks or longer, further diagnostic evaluation should ensue, including radiographic and electrodiagnostic testing.

Other guidelines suggest that in cases of a recurrent stinger, the athlete should be withheld from sports activities for the number of weeks that correspond to the number of that stinger in a given season. Thus, if an athlete has his or her second stinger of the year, he or she should be withheld from practice and competition for 2 weeks.49 If three or more episodes of a stinger occur in a season, serious consideration must be given to ending the athlete’s season, and full diagnostic work-up should be performed.49 The rationale for increasingly prolonged avoidance of participation is that significant impairments are thought to be more likely with recurrent episodes (Fig. 128.5).

Return to play

Evaluation of return to play after a stinger with prolonged symptoms or a repeated episode during the same season should include a thorough, and often repeated, neuromuscular physical examination as well as an appropriate imaging evaluation. Another aspect of the evaluation is electrodiagnostic testing. Electrodiagnostic testing can be performed as early as 7–10 days following the onset of symptoms, but ideally is done 2–4 weeks after the injury. Needle electromyography (EMG) is generally more effective that nerve conduction studies (NCS) in evaluating stingers and the possibility of axonal loss. On EMG, stingers usually show a mild degree of axonal injury and a variable degree of neurapraxia (conduction block). Indicators of membrane instability, including positive sharp waves and fibrillation potentials, suggest axonal disruption. Positive sharp waves alone may be a result of muscle trauma, and without the presence of clinical weakness should not preclude a return to play. A moderate degree of fibrillation potentials, or a mild degree of fibrillation potentials with clinical weakness, should indeed prevent a return to play. In these cases, serial EMGs should be performed. A normal EMG is not required for return to play as long as the athlete has returned to normal clinically and the EMG findings suggest re-innervation.48,49

Many athletes who suffer stingers return to play or continue to play without reporting the problem because of the brevity of the symptoms. The athlete may not leave the field or even realize the problem. Several guidelines exist for returning athletes who have reported a stinger phenomenon to participation. An individual who has a first-time stinger or who has had fewer than three prior stingers with symptoms of less than 24 hours may return to play if symptoms have completely resolved and the patient has full and painless active range of motion of the cervical spine as well as intact bilateral upper extremity strength.46 Some guidelines suggest that the symptoms should resolve and the athlete should demonstrate full clinical recovery within 15 minutes in order to return to the same game.49 An athlete who incurs a stinger that does not resolve on the sideline should not return to play until the symptoms have completely resolved and a thorough physical examination and radiographic work-up have eliminated any potential causative pathology.46 Other guidelines suggest that after a first-time stinger that lasts 48–72 hours before full recovery, an athlete should not return to participation for 1 week.49 Relative contraindications to return to play include a stinger that persists longer than 24 hours or if it is the third (or more) episode of a stinger in a season. In these situations, evaluation for causative factors must be thoroughly explored.46 1366

EMG in stinger evaluation

Radiographic evaluation Thorough radiographic analysis is also important in the evaluation of an athlete with a stinger. Plain films with flexion and extension

Interventional Spine in Sports Stinger guidelines

Recurrent stinger in same season

1st stinger

Symptoms resolve <15 minutes

May RTP same day if no weakness, pain, or ROM

Full clinical recovery in 48–72 hours

May RTP (practice or game) in 1 week if no weakness, pain, or ROM

RTP = retun to play; ROM = range of motion.

Symptoms persist more than 72 hours RTP only considered after further diagnostic assessment

If more than 3 stingers

If <3 stingers

As a general rule, if symptoms completely resolve with no residual weakness, pain, or ROM, may RTP after sitting out the number of weeks that correspond with the number of that stinger

Strongly consider ending the athlete’s season

Confirm that diagnostic work-up has been comprehensive

Decision for RTP should be individualized based on length of symptoms and findings on diagnostic workup. The athlete's position and personality may also be taken into consideration.

views allow evaluation of zygapophyseal joint arthropathy, alignment, and hypermobility. MRI can provide more detailed evaluation of neuroforaminal stenosis and disc abnormalities such as herniation and degenerative changes. An acute herniated disc must be ruled out before an athlete can return to play.48

Cervical disc disease Epidemiology Cervical disc disease is another spine condition that can affect the athlete and potentially limit athletic participation. Cervical disc disease is more common in people in their mid-30s or older, but can occur in the younger athlete as well. In the younger athlete, cervical disc disease is seen most commonly in individuals who participate in tackle football and wrestling.50,51 Cervical disc disease is diagnosed by a combination of the history, physical examination, and radiographic findings (Fig. 128.6). Cervical disc disease is often a forerunner of chronic, degenerative changes of cervical spondylosis. Acute disc herniations occur most frequently at the C5–6 level followed by the C6–7 and C4–5 levels. Most disc herniations occur posterolaterally.51

Pathomechanics Cervical disc disease can be acute or chronic in nature, and in the literature is often classified as either soft disc or hard disc disease. Soft disc disease is associated with acute herniation of the nucleus pulposus into or through anulus fibrosus. Individuals with soft disc disease often have an identifiable event which corresponds with the onset of acute neck pain and paraspinal muscular spasm. In the absence of a specific incident, soft disc disease may be an early indicator of degenerative disc disease.51

Fig. 128.5 Algorithm of stinger. Information primarily from Weinstein and Herring.49

Hard disc disease is the more common type, occurring as a result of progressive degeneration of the disc, often concomitant with spondylosis. The progressive nature of hard disc disease results from changes in the components of the intervertebral disc, which then leads to secondary changes. These secondary changes include loss of disc space height, bulging or frank herniation, and ultimately, osteophytosis and changes at the zygapophyseal joint. The gradual changes in the anatomy lead to alterations in the kinematics, which often results in symptoms of pain and stiffness.51

Evaluation and management Athletes with an acute disc herniation will present similarly to a nonathlete.50 The individual typically experiences severe, posterior neck pain, and, depending on the level, may also have referred pain to the shoulder, arm, or hand. The athlete may also complain of dysesthesias or muscular weakness. Disc herniations at C4–5 and below affect the corresponding nerve root and may cause radicular symptoms. The individual may present with muscular weakness, reflex or sensory changes, as well as pain. In rare cases, cervical disc herniations that occur posterolaterally may lead to spinal cord injury. The history must include questions related to lower extremity weakness, gait disturbance, or changes in bowel or bladder function to further assess for cervical myelopathy.51,52 As with other potentially neurologically based injuries, in addition to a thorough history, the neuromuscular physical examination is critical in diagnosing the injury or ordering the proper sequence of diagnostic tests. A careful assessment of posterior cervical tenderness and range of motion is obligatory in a patient with neck and/or shoulder pain. Because of the potential for myelopathy, it is necessary to test strength and reflexes (muscle stretch, Hoffman, and Babinski) of both the upper and lower extremities. The examination 1367

Part 6: Interventional Spine in Sports Athlete presentation: +/– Neck pain +/– Pain referring/radiating to shoulder, arm, or hand +/– Muscle pain/weakness of upper extremities +/– Dysesthesia

Perform thorough history and physical examination with an emphasis on questions regarding neurologic status and bowel and bladder function and the examination focused on motor control and strength of the extremities, and gait

Obtain appropriate radiographic evaluation: AP/lateral/oblique and odontoid views of cervical spine

If + , treat accordingly

May consider MRI/CT myelogram if indicated

If negative or inconclusive, consider further radiographic imaging

If concern about cervical spine instability, obtain lateral flexion and extension views

Proceed with MRI of cervical spine (or CT myelogram if MRI contraindicated or need to better define osseous anatomy)

If physical exam and MRI do not suggest a progressive neurological deficit, proceed with non-surgical management • Activity modification • Traction • Antiinflammatory • Epidural steroid medications injection if • Modalities radicular symptoms • Physical therapy

If findings suggest a progressive neurological deficit, referal to spinal surgeon

Fig. 128.6 Algorithm of cervical disc disease. Information primarily from Scherping51 and Jackson.52

should also include an assessment of shoulder and scapulothoracic motion as potential sources of the pain. Provocative tests such as head compression, Spurling maneuver, and shoulder abduction are valuable in the assessment of radiculopathy and cervical disc disease.51,52 Initial radiographic evaluation should include a set of plain films, ideally including anteroposterior, lateral, oblique, and odontoid views, to assess for disc space narrowing, spondylosis, congenital abnormalities, tumor, or infection. If these films are unremarkable for spinal instability or significant osseous pathology, dynamic flexion and extension views should be obtained to better assess spinal stability. If neurological findings are appreciated on physical examination or the plain films are inconclusive, MRI should be performed to better evaluate the intervertebral discs and soft tissue structures. If MRI is contraindicated, the best alternative is myelography with postcontrast CT. It must be reiterated that not all herniated discs seen on MRI are symptomatic. Thus, the radiographic findings must be correlated clinically.51 1368

Unless the patient presents with progressive neurological changes or myelopathy, initial management of cervical disc disease should be conservative. The initial, conservative treatment entails activity restrictions including at least temporary removal from competition, antiinflammatory medications, immobilization with a soft collar, modalities such as heat, and in selected cases, traction. As the initial symptoms dissipate, a therapeutic program emphasizing range of motion and cervical muscle strengthening should be implemented. Selective nerve root injections may be an option if the pain persists to confirm the diagnosis and provide therapeutic relief.50,51 Surgical evaluation must be pursued if there is progressive neurological decline or rapid change in neurological function. Surgery is often considered on a case-by-case basis, usually after 6–8 weeks, if the symptoms and pain persist or gradually worsen despite a comprehensive conservative approach.50,51

Return to play As with many spine injuries, established guidelines for return to play after a cervical disc disorder are lacking and the topic remains controversial. Athletes without contraindication to return to play include those who were treated conservatively, had complete resolution of pain and neurological symptoms, and demonstrate full, painless range of motion and strength.50 However, if the disc herniation leads to spinal stenosis, the severity of the spinal stenosis becomes the overriding issue in determining appropriate return to play recommendations.51 Operative management of cervical disc disease often determines the contraindication to return to play. The type and approach of the surgery and how it affects recovery and return to play is also a debatable topic. An individual who has a one-level anterior cervical discectomy and fusion or a posterior approach and laminoforaminotomy below C3–4 may return to contact sports after complete resolution of neurological deficits, strength, and range of motion have fully returned, and radiographs demonstrate a solid fusion.51,53 In general, athletes with a single-level fusion in the upper cervical spine, especially C2–3 (and some argue C3–4) will have a relative contraindication to return to play.51 A relative contraindication also exists for those athletes who have a two- or three-level anterior or posterior fusion. Others would argue that a fusion of three levels or more should result in an absolute contraindication to return to contact sports.51,53 As mentioned previously, a spinal cord injury is an absolute contraindication to return to play. Thus, if a disc herniation occurs centrally and causes a spinal cord injury, the athlete has an absolute contraindication to return to play.

Minor cervical injuries Fortunately, while medical personnel at athletic events must be educated and prepared to manage catastrophic spinal cord injuries, the majority of cervical spinal cord injuries are minor. Most of the spine injuries are ligamentous sprains, muscles strains, or soft tissue contusions as a result of soft tissue trauma. These injuries typically heal with proper management and without long-term sequela.50

Sprains, strains, and contusions Sprains, strains, and contusions are common sports-related neck injuries, which often occur concomitantly as the result of a single traumatic incident. Sprains are defined as a stretch injury to the ligamentous structures, and range from mild pain without instability to gross ligamentous disruption with resulting instability. Strains are defined as stretch injuries to the muscle or at the musculotendinous

Interventional Spine in Sports

junction. Contusions are blunt force trauma to the soft tissues, usually over taut, contracted muscles.50 Individuals with a cervical sprain, strain, or contusion usually present with painful, limited cervical motion and tenderness in the area. These athletes must have radiographic evaluation of the entire cervical spine, from the occiput to the first thoracic vertebrae, to rule out instability or fracture. Radiographic evaluation of the cervical spine is performed to evaluate for fracture, dislocation, and instability. Radiographic signs of instability include the following: interspinous widening, vertebral subluxation, vertebral compression fracture, and loss of cervical lordosis.50,54 Objective measurements to evaluate for cervical spine instability include horizontal displacement of 3.5 mm or more on lateral plain radiographs or angular displacement of 11 degrees or more.50,55 Muscles spasms may prevent the detection of cervical instability on initial radiographs, even flexion and extension views. Thus, patients with muscles spasms should be maintained with cervical immobility

until the spasms resolve and repeat films, including flexion–extension, are performed to rule out ‘subacute’ instability.50,54

Compression fractures Isolated compression fractures of the cervical spine, though less frequent than compression fractures in the thoracolumbar spine, often occur as a result of a hyperflexion position. Because of the type of mechanism, injuries to the posterior structures often occur concomitantly and must be carefully evaluated if a compression fracture of the cervical spine is detected. Cervical compression fractures are usually treated for 8–10 weeks with a semirigid cervical collar for immobilization, which also serves as a proprioceptive reminder of the injury and to limit activity. When the collar is removed, flexion and extension radiographs are performed to evaluate for instability and ligamentous injury.50

Player down

Assess ABCs

Responsive

Assess level of consciousness

– Neck pain

+ Neck pain

Unresponsive

Possible TBI and/or SCI

– Numbness/tingling or weakness

+ Numbness/tingling or weakness

– Numbness/tingling or weakness

+ Numbness/tingling or weakness

Perform on-field screening exam (neuro-MSK)

Perform on-field screening exam (neuro-MSK)

Perform on-field screening exam (neuro-MSK)

Perform on-field screening exam (neuro-MSK)

Determine if 1 need to immobilize and transfer or 2 if can continue evaluation on sideline

Determine if 1 need to immobilize and transfer or 2 if can further evaluate on sideline

As possible SCI/TQ immobilize and transfer to trauma center

+ In one upper extremity

+ In more than one extremity

Possible stinger or shoulder pathology

Possible SCI (Burning Hands or TQ)

Possible – Cervical spine fracture – Cervical disc disease/herniation – Cervical muscle contusion or strain

Perform sideline evaluation and repeat as needed

Treat as SCI, immobilize athlete and transfer to trauma center

If + neck pain, ROM, or abnormality on screening exam, no RTP

Initiate principles of basic trauma management

If regaining consciousness, determine if need to immobilize and transport or if can further evaluate on sideline

See responsive algorithm

No regaining of consciousness

– Avoid movement – Immobilize head/neck – Position on spine board – Remove face mask but leave helmet on if athlete was wearing – Carefully monitor airway and cardiovascular status

Transfer to trauma center by ambulance

MSK = Musculoskeletal; SCI = Spinal cord injury; TQ = Transient Quadriparesis; TBI = Traumatic brain injury; Rom = Range of motion; RTP = Return to play

Fig. 128.7 Summary algorithm of downed player. 1369

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Spinous process fractures Spinous process fractures can also occur in isolation and are usually relatively minor, with a good long-term prognosis. These fractures are more likely to occur in the lower cervical or upper thoracic region. These injuries typically result from an avulsion, either from a significant contraction of the trapezius and rhomboid muscles or by the supraspinous or interspinous ligament during a hyperextension or hyperflexion injury. Spinous process fractures are typically treated with 4–6 weeks of immobilization with a cervical collar. Spinous process fractures usually heal without any long-term sequelae. After the period of immobilization, flexion and extension films are obtained to rule out instability. If the films are negative for instability, the athlete can gradually resume range of motion and strengthening exercises in anticipation of return to play.50

PREVENTION Prevention of initial injury or recurrence is an important aspect of the management of athletes. Prevention is best achieved through rules designed for the athlete’s safety, teaching of proper techniques, effective and properly fitting equipment, and adequate functional strength and mobility for the sport.56 Cervical strength and range of motion are critical aspects in the prevention of injuries to the neck, just as they are in the treatment of cervical injuries.46 Cervical strength can be invaluable in dissipating the force in a collision that affects the cervical spine. In addition to properly fitting helmets and shoulder pads, accessory equipment has been designed for the purpose of reducing cervical spine injuries and stingers. If appropriately chosen, cervical orthoses, such as neck rolls, cowboy collars, and butterfly restrictors, can be effective in decreasing stingers in tackle football players.56 Though beyond the scope of this chapter, the proper selection of accessory equipment is essential.

CONCLUSION Practitioners with an understanding of sports and associated injuries can provide valuable care, education, and recommendations to injured athletes. Preparation, knowledge, and experience are essential in efficiently managing the acutely injured athlete and minimizing potential complications. Athletic injuries range from severe and life-threatening to minor and nagging. Understanding the diagnosis, evaluation, and management of these injuries is important not only in guiding the injured athlete on returning to play at a point that is in the athlete’s overall best interest, but also in making recommendations to prevent injuries or recurrences (Fig. 128.7).

8. Warren WL, Bailes J, Cantu RC. Guidelines for safe return to play after athletic head and neck injuries. In: Cantu RC, ed. Neurologic athletic head and spine injuries. Philadelphia: WB Saunders; 2000. 9. Torg JS. Management guidelines for athletic injuries to the cervical spine. Clin Sports Med 1987; 6(1):53–60. 10. Magee DJ. Emergency sports assessment. In: Orthopedic physical assessment, 4th edn. Philadelphia: WB Saunders; 2002. 11. Wilberger JE Jr. Athletic spinal cord and spine injuries. Guidelines for initial management. Clin Sports Med 1998; 17(1):111–120. 12. Waninger KN. Management of the helmeted athlete with suspected cervical spine injury. Am J Sports Med 2004; 32(5):1331–1350. 13. Kleiner D, Almquist J, Bailes J, et al. Inter-Association Task Force For Appropriate Care of the Spine. Indianapolis, IN: Inter-Association Task Force for Appropriate Care of Spine; 1998. 14. Roberts WO. Helmet removal in head and neck trauma. Physician Sportsmed 1998; 26:7. 15. Warren WL Jr, Bailes J. On the field management of athletic head and neck injuries. In: Cantu RC, ed. Neurologic athletic head and spine injuries. Philadelphia: WB Saunders; 2000. 16. Maroon JC, Bailes JE. Athletes with cervical spine injury. Spine 1996; 21(19): 2294–2299. 17. Gupta SK, Khosla VK, Sharma BS, et al. Spinal cord injury without radiographic abnormality in adults. Spinal Cord 1999; 37:726–729. 18. Ergun AOW. Pediatric care report of spinal cord injury without radiographic abnormality (SCIWORA): case report and literature review. Spinal Cord 2003; 41:249–253. 19. Wilberger JE. Acute cervical spinal cord and spine injuries. In: Cantu RC, ed. Neurologic athletic head and spine injuries. Philadelphia: WB Saunders; 2000. 20. Davis PM, McKelvey MK. Medicolegal aspects of athletic cervical spine injury. Clin Sports Med 1998; 17(1):147–154. 21. Cooper MT, McGee KM, Anderson DG. Epidemiology of athletic head and neck injuries. Clin Sports Med 2003; 22(3):427–443, vii. 22. Cantu RC. Head and spine injuries in youth sports. Clin Sports Med 1995; 14(3):517–532. 23. Torg JS, Guille JT, Jaffe S. Injuries to the cervical spine in American football players. J Bone Joint Surg [Am] 2002; 84(1):112–122. 24. Maroon JC. ‘Burning hands’ in football spinal cord injuries. JAMA 1977; 238(19):2049–2051. 25. Wilberger JE, Abla A, Maroon JC. Burning hands syndrome revisited. Neurosurgery 1986; 19(6):1038–1040. 26. Zwimpfer TJ, Bernstein M. Spinal cord concussion. J Neurosurg 1990; 72(6): 894–900. 27. Allen CR, Kang JD. Transient quadriparesis in the athlete. Clin Sports Med 2002; 21(1):15–27. 28. Castro FP Jr. Stingers, cervical cord neurapraxia, and stenosis. Clin Sports Med 2003; 22(3):483–492. 29. Torg JS, Pavlov H, Genuario SE, et al. Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg [Am] 1986; 68(9):1354–1370. 30. Torg JS, Corcoran TA, Thibault LE, et al. Cervical cord neurapraxia: classification, pathomechanics, morbidity, and management guidelines. J Neurosurg 1997; 87(6):843–850. 31. Seddon H. Three types of nerve injury. Brain 1943; 66(4):238–286.

References 1. Herring SA, Bergfeld JA, Boyd J, et al. Team physician consensus statement. Med Sci Sports Exerc 2000; 32(4):877–878. 2. Herring SA, Bergfeld JA, Boyd J, et al. Sideline preparedness for the team physician: a consensus statement. Med Sci Sports Exerc 2001; 33(5):846–849. 3. Herring SA, Bergfeld JA, Boyd J, et al. The team physician and return to play issues consensus statement. Med Sci Sports Exerc 2002; 34(7):1212–1214. 4. Vegso JJ, Lehman RC. Field evaluation and management of head and neck injuries. Clin Sports Med 1987; 6(1):1–15.

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32. Penning L. Some aspects of plain radiography of the cervical spine in chronic myelopathy. Neurology 1962; 12:513–519. 33. Ladd AL, Scranton PE. Congenital cervical stenosis presenting as transient quadriplegia in athletes. Report of two cases. J Bone Joint Surg [Am] 1986; 68(9):1371–1374. 34. Cantu RC. The cervical spinal stenosis controversy. Clin Sports Med 1998; 17(1):121–126. 35. Cantu RC. Functional cervical spinal stenosis: a contraindication to participation in contact sports. Med Sci Sports Exerc 1993; 25(3):316–317.

5. Warren WL Jr, Bailes JE. On the field evaluation of athletic neck injury. Clin Sports Med 1998; 17(1):99–110.

36. Cantu RC. Cervical spinal stenosis: diagnosis and return to play issues. In: Cantu RC, ed. Neurologic athletic head and spine injuries. Philadelphia: WB Saunders; 2000.

6. Ghiselli G, Schaadt G, McAllister DR. On-the-field evaluation of an athlete with a head or neck injury. Clin Sports Med 2003; 22(3):445–465.

37. McAlindon RJ. On field evaluation and management of head and neck injured athletes. Clin Sports Med 2002; 21(1):1–14, v.

7. Kim DH, Vaccaro AR, Berta SC. Acute sports-related spinal cord injury: contemporary management principles. Clin Sports Med 2003; 22(3):501–512.

38. Herzog RJ, Wiens JJ, Dillingham MF, et al. Normal cervical spine morphometry and cervical spinal stenosis in asymptomatic professional football players. Plain film

Interventional Spine in Sports radiography, multiplanar computed tomography, and magnetic resonance imaging. Spine 1991;16(6 Suppl):S178–S186. 39. Cantu RC, Bailes JE, Wilberger JE Jr. Guidelines for return to contact or collision sport after a cervical spine injury. Clin Sports Med 1998; 17(1):137–146. 40. Torg JS, Ramsey-Emrhein JA. Management guidelines for participation in collision activities with congenital, developmental, or post-injury lesions involving the cervical spine. Clin Sports Med 1997; 16(3):501–530. 41. Finnoff JT, Mildenberger D, Cassidy CD. Central cord syndrome in a football player with congenital spinal stenosis: a case report. Am J Sports Med 2004; 32(2): 516–521. 42. Cantu RC. Stingers, transient quadriplegia, and cervical spinal stenosis: return to play criteria. Med Sci Sports Exerc 1997; 29(7 Suppl):S233–S235. 43. Torg JS, Sennett B, Pavlov H, et al. Spear tackler’s spine. An entity precluding participation in tackle football and collision activities that expose the cervical spine to axial energy inputs. Am J Sports Med 1993; 21(5):640–649. 44. Sallis R, Jones D, Knopp W. Burners: offensive strategy for an underreported injury. Physician Sportsmed 1992; 20(11):47–55. 45. Feinberg JH. Burners and stingers. Phys Med Rehabil Clin N Am 2000; 11(4): 771–784. 46. Weinberg J, Rokito S, Silber JS. Etiology, treatment, and prevention of athletic ‘stingers.’ Clin Sports Med 2003; 22(3):493–500, viii. 47. Shannon B, Klimkiewicz JJ. Cervical burners in the athlete. Clin Sports Med 2002; 21(1):29–35, vi.

48. Weinstein SM. Assessment and rehabilitation of the athlete with a ‘stinger.’ A model for the management of noncatastrophic athletic cervical spine injury. Clin Sports Med 1998; 17(1):127–135. 49. Weinstein S, Herring SA. Assessment and rehabilitation of the athlete with a stinger. In: Cantu RC, ed. Neurologic athletic head and spine injuries. Philadelphia: WB Saunders; 2000. 50. Zmurko MG, Tannoury TY, Tannoury CA, et al. Cervical sprains, disc herniations, minor fractures, and other cervical injuries in the athlete. Clin Sports Med 2003; 22(3):513–521. 51. Scherping SC Jr. Cervical disc disease in the athlete. Clin Sports Med 2002; 21(1):37–47, vi. 52. Jackson RJ. Treatment of disk and ligamentous diseases of the cervical spine. In: Winn HR, ed. Youmans neurological surgery, 5th edn. Philadelphia: WB Saunders; 2004. 53. Morganti C. Recommendations for return to sports following cervical spine injuries. Sports Med 2003; 33(8):563–573. 54. Herkowitz HN, Rothman RH. Subacute instability of the cervical spine. Spine 1984; 9(4):348–357. 55. White AA 3rd, Johnson RM, Panjabi MM, et al. Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop 1975; 109:85–96. 56. Cross KM, Serenelli C. Training and equipment to prevent athletic head and neck injuries. Clin Sports Med 2003; 22(3):639–667.

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INTERVENTIONAL SPINE IN SPORTS

Spondylolysis Frank Lagatutta

INTRODUCTION

DIAGNOSIS

Spondylolysis is a devastating injury to a young athlete. It is the most frequent lumbar spine injury in the adolescent population. Sixty percent of all adolescent athletes experience low back pain of some sort, but only 6% are diagnosed with an acute spondylolysis.1–3 An acute spondylolysis is a stress fracture of the pars articularis or a complete breakthrough of the pars articularis. Most patients who suffer from spondylolysis have low back pain on extension, but the pain may radiate into the legs as it worsens. If the patient is placed in a lumbosacral corset, there may be immediate relief of the pain with almost complete relief of the pain within 5 days; yet if the athlete returns to the activities, the pain will return immediately. This chapter’s goal is to explore the biomechanics, diagnostic work-up, and treatment for spondylolysis.

Patients who present with symptomatic spondylolysis describe pain in their back. If they are evaluated very quickly in a training room setting, they may only have back pain with extension and may also have a positive stork sign. This maneuver is accomplished by asking the patient to stand on one leg and extend the spine. It is believed that the ipsilateral side will hurt more than the contralateral side if there is a unilateral pars lesion. If the patient has pain in the back and continues to perform his or her activity, the pain will not only be in the back but will begin to radiate into both legs and will mimic a disc injury. If one side is worse than the other, that side will exhibit symptoms compatible with sciatica and leg pain that can be severe. Not only will there be pain with extension movements, but there will similarly be pain with standing, walking, or running. In fact, the pain initially presents during standing or running, and occurs in sitting at a later date. Pain with lying down usually will not be present unless the patient is resting in the prone position. There may be paresthesia radiating into the legs in a myotomal pattern, which depends upon how much sympathetic overflow is present in the individual. It is unusual for bowel/bladder symptoms to be described, though it is possible in an adolescent in a high-pressured position attempting to please her parents. In the latter situation, any type of symptom may be described. When this occurs the clinician will have to sort out the actual injury and simultaneously tease out any psychosocial problems that may be also present, but not the source of the pars injury. After the history is taken, the physical examination will consist of a complete spinal evaluation, most importantly range of motion of the lumbar spine with extension being more painful than flexion and the extension on the ipsilateral leg or stork test being positive. In many cases, there are tight hamstrings, which were probably present premorbidly. There may be a diminished ankle reflex secondary to pain, not necessarily due to a nerve injury itself. The motor and sensory examination should be normal. Palpation may elicit tenderness over the posterior elements or facet joints themselves. Often, the presence and/or degree of sensitivity is directly correlated to the acuteness of the injury and whether any exacerbating activities were continued. Other physical tests include the Patrick test and reverse Thomas test. The latter maneuver will be positive, pointing to the facet joints. Straight leg raising will hurt in the spine but not in a radicular pattern. Sacroiliac joint pain could be seen in patients with early ankylosing spondylolysis, some other inflammation secondary to Crohn’s disease, or ulcerative colitis, or ever rheumatoid arthritis itself. The initial diagnostic test should be a plain radiographic examination of the lumbar spine including anteroposterior (AP), lateral, and oblique views. The AP perspective can rule out scoliosis. The obliques are done to look for a ‘Scottie dog’ fracture of the neck or the pars (Figs 129.1, 129.2A,B) A pars defect can be

ANATOMIC CONSIDERATIONS The lumbar vertebra is made up of an anterior portion, the vertebral body, and the posterior elements, which are made up of the pars as well as the facet and joints and spinous process. The lamina connects them together. When a normal person performs most activities, it is either in the standing or sitting position. The bulk of these pressures on the spine are on the vertebral body and very little is on the posterior elements, i.e. the pars and facet joints. When athletes do extension and rotation, such as winding up to pitch a baseball, back flips in gymnastics, or kicking in soccer, extra force and weight are placed on the posterior elements, which can cause one of two things to happen. The most common result is that the facet joints of the posterior elements become inflamed and develop an overuse syndrome, termed facet joint synovitis.4,5 The other result of overuse becomes a stress fracture or spondylolysis. The only way to differentiate between facet synovitis and spondylolysis is with radiographic testing, which will be described later in this chapter.6 The partes themselves are the thinnest parts of the neural arch and are the most susceptible for a fracture within the posterior elements. A recent study by Chosa et al. demonstrated this in a three-dimenstional, mechanical study of the lumbar spine.7 Their study showed that the stress in the pars intra-articularis was least with compression alone but stronger under compression with lateral bending along with rotation and extension. It was the highest with extension and rotation. Consequently, repetitive extension with rotation should be considered a relatively high-risk factor for the development of spondylolysis.8 This is no surprise to the practitioner who sees most of these injuries in the athletes who perform extension–rotation movements, such as offensive linemen in football, wind-up players in cricket, as well as pitchers in female softball and male hardball.

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Superior process (facet) Transverse process

Fig. 129.1 Spondylolytic defects of the Collar (spondylolytic pars interarticularis defect of pars are evident on oblique interarticularis) X-rays as collars on a ‘Scottie dog.’ 1993; Spinous 21(3):182–194] (From process Brotzman S, Brent, Wilk KE. Clinical orthopedic Inferior rehabilitation, 2nd edn. process (facet) Philadelphia, Elsevier Inc. 2003.)

detected in the lateral view, but its primary benefit is to identify spondylolisthesis.9 Plain radiographs may be normal when there is only a stress reaction and not frank fatigue leading to fracture or when the spondylolysis has only recently occurred. The next step would be to perform a single-photon emission computed tomography (SPECT) multiplanar bone scan. If the SPECT scan and plain films are positive, the evidence suggests a stress fracture. When the plain films are negative and the SPECT scan is positive then a stress reaction is the likely diagnosis. If the SPECT scan and plain films are negative the diagnosis is probably not spondylolysis.10,11 The third test of choice for this condition is a computed tomography (CT) scan (Fig. 129.3). A recent study by Stretch et al. showed that the CT scan was very sensitive in showing nonunion and healing6. Using thin-slice CT, they were able to show with repeat studies of the CT scans complete healing in 8 out of 9 injured athletes. Magnetic resonance imaging (MRI) is not of much benefit, even using bone windows. In a recent study Sherif and Mahfouz attempted to place the epidural space in an anterior position between the dura mater and spinous process to diagnose spondylolysis.12 This allows for different tissues to contrast with each other to brighten the bone views. Unfortunately, the MRIs were not very beneficial even with the new technique.12 Additionally an MRI might identify if there is concurrent disc disease or spinal cord pathology (Fig. 129.4). This obviously will not be observed with X-ray or SPECT scan. The CT scan may show some disc disease, but not to the same degree as MRI. If the X-ray is negative, either CT or SPECT scan can be perfomed. If negative, either CT or SPECT scan can be performed. If a bone scan is performed and is positive, the patient can be treated symptomatically. At the end of the treatment, the patient can have a CT scan.13 If the CT scan shows complete union, then no further treatment is necessary. Other testing that may be needed for adolescents with back pain are a rheumatoid work-up with CBC and sedimentation rate, HLA-B27 and C-reactive protein looking for spondylitis, which could mimic the pain of spondylolysis. If there is a question with

A

B

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Fig. 129.2 (A,B) An oblique radiograph demonstrates spondylolytic defect in the pars interarticularis of L4 (arrow). Note the intact neck in the ‘Scottie dog’ outline in the L3 vertebra. (From DeLisa JA. Rehabilitation medicine: principles and practice, 2nd edn. Philadelphia: JB Lippincott; 1988:365.)

Fig. 129.3 Spondylolisthesis L5–S1 and spondylolysis L5. Horizontal undulating defects (white arrows) in pars interarticularis sclerotic 45 degrees obliquely oriented facet joints (black arrows). (From Atlas SW. Magnetic resonance imaging of the brain and spine, 3rd edn. Philadelphia, Lippincott Williams & Wilkins. 2002.

Interventional Spine in Sports

Fig. 129.4 Horizontally oriented pars defect seen as low-intensity band (black arrow) whereas facet joints (white arrow) are oriented obliquesagittally above and below nerve root (open arrow) compromised by narrow neural foramen on parasagittal spine echo image. (From Atlas SW. Magnetic resonance imaging of the brain and spine, vol. 11, 3rd edn. Philadelphia, Lippincott Williams & Wilkins. 2002.

continued symptomatology without much relief from the current treatment, diagnostic injections, under fluoroscopy, of the medial branch nerve or the pars itself would be of benefit and give enough information to identify the source of the pain. For patients needing to return to play immediately, this is definitely a treatment option for short-term activity, but not for a long-term solution.

TREATMENT The treatment of choice is as follows. Symptom abatement is the most accurate indication of healing. Initially, the patients should be banned from exacerbating activities and put into a lumbosacral corset (Fig. 129.5).14 Fifteen years ago, patients were placed in plastic thoracolumbosacral orthosis (TLSO) with a thigh cuff to achieve spine extension (Fig. 129.6). There were compliance problems with this bulky brace. The pain subsides so the patient will not wear it. These

A

braces were not only uncomfortable but unsightly, leading to poor compliance. A more simple solution involves the use of a lumbosacral corset with metal stays or the new lumbosacral corsets that are now available (Fig. 129.7). The brace should be worn 24 hours a day or at least while awake. The patients should become asymptomatic within 4 weeks. If pain relief is achieved, an aggressive stretching and strengthening program involving the upper back muscles, abdominal muscles, hip, and the lower limbs (Table 129.1), as well as a stretching program is begun (Table 129.2).15 Back extension activities or even flexion activities are prohibited for the first 8 weeks, which allows time for the pars to heal. During the 8 weeks when they are resting, the patients can do upper body strengthening, and possibly some lower extremity strengthening. They may be able to use an exercise bike or perform any other type of aerobic activity (Table 129.3) as long as the brace is on and the back has no flexion or extension movements. If the bone scan was positive and the X-rays and CT are negative, the patients can return to activity within 4 weeks. If the CT scan is positive, it would be wiser to wait 8–12 weeks before returning to activities, although there have been no studies that show if there is any correlation between rest and return to activity in healing of the pars itself.16 The authors performed SPECT scans on patients at the time of the injury, 3 months afterwards, and up to a year later. This study showed that there was no correlation between healing on the SPECT scans and their symptoms. It was found that one-third of patients were asymptomatic despite having positive bone scans. No patients were symptomatic with a negative bone scan. A recent study with the CT scan as previously mentioned showed that 40% of the people were asymptomatic completely, with 60% asymptomatic and 40% still with some pain when they returned to activities with normal CT scans. These findings indicate that the symptoms will improve faster than the radiographic findings. With no studies proving that resting for 3 months, 6 months, 1 year, or even 2 years has any improvement on the CT scan healing, the standard of care is to treat the patient symptomatically. If it is during the season relevant to the patients’ activities, return the patients to their activity as soon as they are asymptomatic, with a strengthening program and some type of lumbar support that reduces extension. If some pain lingers, the patients are to rest completely for 8 weeks after the season is

B

C

Fig. 129.5 The patients should be taken out of activities and put in a lumbosacral corset. 1375

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A

B

A

B

D

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Fig. 129.6 Fifteen years ago, patients were placed in plastic TLSO with a thigh cuff to achieve extension.

C

Fig. 129.7 The new lumbosacral corsets that are now available.

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Table 129.1: Strengthening Strengthening Lumbar stability examination Hip flexion, extension, abductors, adductors Rotational extensors exercise Closed kinetic lower extremity strengthening exercises Sport-specific exercises Initially, lumbar stabilization exercises are performed with the addition of the hip muscles finally leading to more advanced exercises.8

Table 129.2: Flexibility Flexibility Hamstring muscles

guidance is very important as the children may refuse to wear the braces. When they feel better, and without the deformity seen in scoliosis, it is much more difficult to persuade patients to wear the braces. In patients who have an X-ray that shows permanent pars fracture already present or a break in the neck, a bone scan with SPECT scan should be performed. If the bone scan with the SPECT is negative, this indicates it is an old lesion and that the pain is either coming from the lesion or from the joints themselves. Such patients should be first placed in a corset for 4–8 weeks, but many continue with activities and perform a strengthening program. If they continue to have pain, they are the candidates for injection directly into the pars, or medial branch blocks to relieve the pain. In most of these cases, a CT scan will show the lesions. If the bone scan is positive, these patients will need to be braced and given a CT for diagnosis of injury and another CT scan 3 months later. At this time, if the CT scan is showing healing, they should be ready to continue activities. If, at 3 months, the CT scan shows no change from the original CT scan, this would indicate it is a permanent pars lesion and that treatment is completely based on symptomatology, and therapy and injections would be the primary treatment. Surgery is a last resort.

Iliopsoas muscles Abdominal muscles Hip extensor muscles The above muscles may have restrictions which need to be resolved to achieve proper biomechanics and relieve the stress on the pars.7

Table 129.3: Aerobic exercises Aerobic non-loading Swimming Bike Jog in pool

SURGICAL INTERVENTION AND INJECTIONS If a patient has continued pain, a treatment with medial branch block would be diagnostic as well as therapeutic. If two blocks are done, a medial branch neurotomy may be contemplated. If this gives relief from pain, the patient can return to play. If this doesn’t work, fusion may be performed or direct repair of the pars may be undertaken.17 There is literature showing that this is of benefit. Obviously, when patients are adolescents with a fusion, there is a risk that the level above the fusion will become degenerative much sooner, causing early degenerative disc disease.18–20 Therefore, surgery should only be performed in cases of severe pain causing a patient to be unable to attend school or obviously in a case of spondylolysis deteriorating into spondylolisthesis and spondylolisthesis going beyond grade 1 to grade 3 or 4.21

Minor loading Walking Stair climbing Elliptical Early exercises including non-loading aerobic are listed above with graduation to minor loading exercises.7

ended, and before they start to work out in the following season. Figures 129.5–129.7 show the different types of corsets available. Other treatments besides rest, corsets, and strengthening program include medications. These should include antiinflammatory medications, which do nothing directly for healing but may help the patient’s pain. In this population, the analgesic medication tramadol should be used; it has a 6-hour duration unlike the short-acting opiates, which only have 4 hours’ duration. The opiates have more side effects such as constipation, addiction, and mental status changes. Muscle relaxants may play a role early on but once the brace is worn all the spasm symptoms will be gone within the first week or two. Modalities such as massage, electrostimulation, and ultrasound are all of benefit. If they make patients feel better, so that they may attend class and perform other activities, these modalities may be encouraged although they have no effect on healing. Parental

CONCLUSION In conclusion, spondylolysis is the most common, serious injury in the lumbar spine in adolescents. This will be seen primarily in repetitive trauma situations although it may be seen in one-event instances. In this case, it may be brought about by employment and involve worker’s compensation. Diagnoses are made primarily with an examination showing extension and rotation pain, positive X-rays, bone scan with SPECT or CT scan. Treatment includes rest for 4–8 weeks, a lumbosacral corset that the patient will wear up to 23 hours a day, a stretching program for the hamstrings and alignment of the lower limbs, and strengthening of the hips as well as the abdomen and back muscles. Injections are the second to last chance, and surgery is the treatment of last resort.

References 1. Gregory PL, Batt ME, Kerslake RW. Comparing spondylolysis in cricketers and soccer players. Br J Sports Med 2004; 38(6):737–742. 2. Kraft DE. Low back pain in the adolescent athlete. Pediatr Clin North Am 2002; 49(3):643–653. 3. Lundin DA, Wiseman DB, Shaffrey CI. Spondylolysis and spondylolisthesis in the athlete. Clin Neurosurg 2002; 49:528–547. 4. DePalma MJ, Slipman CW, Siegelman E, et al. Interspinous bursitis in an athlete. J Bone Joint Surg [Br] 2004; 86(7):1062–1064.

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Part 6: Interventional Spine in Sports 5. Miller SF, Congeni J, Swanson K. Long-term functional and anatomical follow-up of early detected spondylolysis in young athletes. Am J Sports Med 2004; 32(4): 928–933. 6. Stretch RA, Botha T, Chandler S, et al. Back injuries in young fast bowlers – a radiological investigation of the healing of spondylolysis and pedicle sclerosis. S Afr Med J 2003; 93(8):611–616. 7. Chosa E, Totoribe K, Tajima N. A biomechanical study of lumbar spondylolysis based on a three-dimensional finite element method. J Orthop Res 2004; 22(1):158–163. 8. Mihara H, Onari K, Cheng BC, et al. The biomechanical effects of spondylolysis and its treatment. Spine 2003; 28(3):235–238.

15. Stasinopoulos D. Treatment of spondylolysis with external electrical stimulation in young athletes: a critical literature review. Br J Sports Med 2004; 38(3):352–354. 16. Iwamoto J, Takeda T, Wakano K. Returning athletes with severe low back pain and spondylolysis to original sporting activities with conservative treatment. Scand J Med Sci Sports 2004; 14(6):346–351. 17. Lundin DA, Wiseman D, Ellenbogen RG, et al. Direct repair of the pars interarticularis for spondylolysis and spondylolisthesis. Pediatr Neurosurg 2003; 39(4):195–200.

9. Reitman CA, Gertzbein SD, Francis WR Jr. Lumbar isthmic defects in teenagers resulting from stress fractures. Spine J 2002; 2(4):303–306.

18. Debnath UK, Freeman BJ, Gregory P, et al. Clinical outcome and return to sport after the surgical treatment of spondylolysis in young athletes. J Bone Joint Surg [Br] 2003; 85(2):244–249.

10. Van der Wall H, Storey G, Magnussen J, et al. Distinguishing scintigraphic features of spondylolysis. Pediatr Orthop 2002; 22(3):308–311.

19. McNeely ML, Torrance G, Magee DJ. A systematic review of physiotherapy for spondylolysis and spondylolisthesis. Man Ther 2003; 8(2):80–91.

11. Watanabe O, Hashimoto M, Tomura N, et al. [Evaluation of usefulness of bone SPECT for lumbar spondylolysis] (Japanese). Nippon Igaku Hoshasen Gakkai Zasshi 2002; 62(8):423–429.

20. Ranawat VS, Heywood-Waddington MB. Failure of operative treatment in a fast bowler with bilateral spondylolysis. Br J Sports Med 2004; 38(2):225–226.

12. Sherif H, Mahfouz AE. Epidural fat interposition between dura mater and spinous process: a new sign for the diagnosis of spondylolysis on MR imaging of the lumbar spine. Eur Radiol 2004; 14(6):970–973. 13. Campbell RS, Grainger AJ, Hide IG, et al. Juvenile spondylolysis: a comparative analysis of CT, SPECT and MRI. Skeletal Radiol 2005; 34(2):63–73.

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14. d’Hemecourt PA, Zurakowski D, Kriemler S, et al. Spondylolysis: returning the athlete to sports participation with brace treatment. Orthopedics 2002; 25(6):653–657.

21. Beutler WJ, Fredrickson BE, Murtland A, et al. The natural history of spondylolysis and spondylolisthesis: 45-year follow-up evaluation. Spine 2003; 28(10): 1027–1035; discussion 1035.

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INTERVENTIONAL SPINE IN SPORTS

Return to Competition Following Prolonged Injury Brian Krabak and Evan Minkoff

INTRODUCTION Athletes can experience a variety of spinal injuries depending upon the nature of the sporting activity. Most injuries are relatively benign in nature, typically involving muscle strains. These injuries can be treated in a brief period of time with limited resources, allowing the athlete to quickly and safely return to competition. More serious or chronic injuries, including fractures, radiculopathies, or spondylolysis, may require an extensive evaluation and treatment plan prolonging the athlete’s recovery period. With a prolonged recovery comes the potential for deconditioning, further delaying the athlete’s return to competition. The challenge to the physician involves balancing the prompt recognition and treatment of the spine injury against the pressure to return quickly to competition and potential for recurrent injury. This chapter will assess the basic principles pertaining to returning an athlete to competition after a prolonged injury. Specifically, it will attempt to utilize the current literature to support or refute the use of specific interventions in the treatment of the athletes. Though the main focus involves cervical and lumbar injuries, the same principles could be utilized for individuals with thoracic spine injuries.

EPIDEMIOLOGY It is important to understand which sports have an increased risk for more severe injuries. Overall, it has been estimated that cervical spine injuries account for 2–3% of all athletic injuries.1 Fortunately, severe or catastrophic cervical spine injuries are rare. Typically the mechanism of injury involves cervical hyperflexion with concurrent axial loading. In football players,2 cervical hyperflexion, as may occur with spear tackling, has been proposed as the primary mechanism of cervical spine injury leading to spinal cord neurapraxia3 and cervical fractures. Similar cervical flexion-type injuries have been noted in athletes involved in gymnastics, diving,4 ice hockey, wrestling, trampoline, somersaulting, rugby,5 cheerleading, and motor sports. Fortunately, the use of protective equipment and improvement in equipment design in some sports has helped decrease the incidence of cervical spine injuries.6 Similar to cervical spine injuries, the incidence of low back injuries varies depending on sports and mechanism of injury. Several studies have suggested that lumbar spine injuries represent 10–15% of competitive sports injuries.7 Compared to cervical spine injuries, the mechanism of injury is more variable, relating to hyperflexion, hyperextension, and rotatory motions. Hyperflexion injuries can typically occur in football, ice hockey, and rowing. Gymnasts have been shown to have a higher incidence of spondylolysis compared to nonathletes, most likely due to repeated hyperextension and axial loading of the lumbar spine.8 Twisting and rotatory motions can contribute to lumbar pain in racquet sports and golf. It has been

estimated that 10–30% of tour golf players experience lumbar spine pain.9 As with cervical spine injuries, lumbar spine injuries with neurologic compromise are rare, representing less than 1% of all sports injuries.9

ASSESSMENT Proper management of an athlete’s spine injury requires a thorough and comprehensive evaluation of the athlete. A full discussion regarding a comprehensive evaluation is beyond the scope of this chapter, but several principles are unique to the management of an athlete’s injuries. A complete discussion should occur with the athlete and coach, as appropriate, regarding the athlete’s goals and expectations. One should understand the athlete’s training and competition schedule for the year in order to plan an appropriately timed treatment program. The physician should have a thorough understanding of the biomechanics of the sport and demands placed on the athlete to perform at the highest level possible. Finally, a comprehensive history will include the mechanism of injury and prior spinal injuries which might contribute to a prolonged recovery. Examination of an athlete with a spine injury requires a fundamental knowledge of the underlying functional anatomy in relation to the rehabilitative process. The initial priority should include the assessment of spinal stability. A more aggressive evaluation of the spine may occur only once the physician is 100% certain there is no underlying spinal instability. The reader is referred to the previous chapters in this textbook for a complete discussion relating to the clinical evaluation of the cervical and lumbar spine. In addition, resources such as the PASSOR Musculoskeletal core competency list will provide a more detailed outline of the various physical examination tests.10 Finally, radiographic imaging of the spine will depend upon the working diagnosis. Plain radiographs in multiple planes, including active flexion–extension films, are needed in the acute assessment of spinal injuries whenever one needs to rule out an underlying fracture or concerns for spinal instability. Further testing including computed tomography (CT) scans, bone scans, and magnetic resonance imaging (MRI) may be necessary to delineate the potential causes of the spine pain when the source is still uncertain. Follow-up imaging may be warranted to assess the healing process and prognosticate about the athlete’s return to competition. Of note, injuries in children are of particular concern due to the inherent ligamentous laxity. Cervical radiographs should be interpreted with caution as spinal cord injury can be seen without radiographic abnormality. Beck et al. concluded that children and adolescents who have neurological deficits and spinal cord injuries without radiographic abnormalities (SCIWORA) require close following of their deficits and further evaluation to define structural pathology and often require prolonged therapy.11 1379

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GENERAL TREATMENT PRINCIPLES An appropriate treatment plan will depend upon the etiology and severity of, and secondary maladaptations associated with, the spinal injury. After an acute injury, the focus is on inflammation and pain control with the goal of promoting tissue healing. After prolonged injury, treatment interventions should be utilized in a systematic manner focusing on: (1) pain control, (2) correction of inflexibilities and strength deficits, (3) maintenance of cardiovascular stamina, (4) assessing any psychological barriers, and (5) reintegration into sports-specific activities. The general treatment outline is summarized in Table 130.1.

Pain control Pain control interventions include activity modification, medications, physical therapy modalities, and/or injections into the muscle or spinal structures. Any of these interventions may be used during the acute phase of injury where they may assist with inflammation. However, during a prolonged injury, the utility of these interventions most likely relates to assisting with pain control to facilitate rehabilitative functional recovery. Muscular strains and ligamentous sprains usually occur as a blow to the head or body creates rotary, sidebending and flexion–extension forces to the spine. Trying to maintain the head and neck in normal alignment by strong eccentric contraction creates muscle and

Table 130.1: General Principles for Recovery from Prolonged Spine Injuries I. INITIAL PHASE: PAIN CONTROL Activity modification Antiinflammatory medication Physical modalities Peripheral or axial injections II. RESTORATIVE PHASE: CORRECTING FLEXIBILITY AND STRENGTH DEFICITS Truncal and extremity stretching Soft tissue mobilization Cervical or lumbar stabilization strengthening exercise Maintenance of cardiovascular fitness III. INTEGRATIVE PHASE: FUNCTIONAL ADAPTATIONS Normalization of spine mechanics Progression towards sports-specific activities IV. RETURN TO COMPETITION Pain free Pain-free range of motion Pre-injury strength Ability to perform sports-specific maneuvers

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ligamentous tearing by overcoming their tensile strength.12 It is during the acute pain period that the athlete may learn protective compensatory posturing, resulting in abnormal posture, thus leading to a chronic pain mechanism. The head protruded forward is commonly seen in those with poor posture secondary to habit or body habitus. A cycle of biomechanical derangements occurs, resulting in an alteration of the normal anatomy and alignments. Muscles meant to stabilize come to function as movers of the spine, leading to a further pattern of chronic myofacial pain syndrome. In general, injury to a musculoskeletal structure such as a muscle or ligament will lead to a systematic process of degradation and repair. During the initial inflammatory phase, micro/macro tears and localized hematoma formation give way to phagocytosis and enzymatic degradation with subsequent tissue necrosis. Modalities to control the inflammatory process may play a role in limiting the extent of tissue damage during the initial stages. During the reparative phase, the body attempts to repair the injured area through collagen formation. However, the reparative process will lead to disorganized fibrous tissue without the appropriate applied stressors. Prolonged pain symptoms will inhibit the rehabilitative process by limited the amount of stress one can tolerate during the recovery process. Therefore, adequate pain control is imperative during the management of an athlete with prolonged injury. It is the basis for early mobilization and is the reason why soft tissue is not immobilized for a prolonged period, unless absolutely indicated by the injury.13 Unfortunately, evidence supporting the use of specific pain modalities in the athlete is lacking. In the general population, there is strong evidence that prolonged bed rest is detrimental to the functional recovery of individuals with acute low back pain without radiculopathy.14 It could be surmised that the principle of relative rest and the avoidance of bed rest in athletes will also facilitate earlier functional recovery. Fellander-Tsai et al.15 suggested some benefit from the use of modalities for pain relief in individuals with spondylolysis, including activity modification and electrical stimulation. However, the study had several design flaws including small sample size and selection bias. Various studies provided conflicting support as to the efficacy of interventional spinal injections.16,17 Finally, O’Sullivan et al.18 showed a signification reduction in pain intensity and utilization of pain medication at 30-month follow-up in a treatment group that underwent a 10-week exercise treatment program compared to controls. Future, randomized, controlled studies are need to better support or refute the utilization of these various modalities in managing a specific spinal injury in athletes.

Correction of inflexibilities and strength deficits Spinal flexibility Correction of spinal inflexibilities has been advocated as an important component of rehabilitation of the spine. In theory, prolonged injury and pain lead to muscle spasms and pain avoidance patterns. Continuation of this viscous cycle will lead to abnormal remodeling of the injured area and alteration of the normal biomechanics of the spine. Eventually, there is a loss of spine flexibility and altered biomechanics of the spine and limbs. The resultant altered biomechanics may lead to chronic pain, decreased performance, and prolonged recovery. However, evidence is limited as to the role of spine flexibility and injuries in athletes. In addition, a review of the literature pertaining to nonathletes yields conflicting reports as to the role of spine flexibility and range of motion in the treatment of spine injuries. Several recent studies outlined below have suggested that there is no correlation between spinal flexibility and disability or function. Kuukkanen et al. suggested that flexibility does not play an important role in the

Interventional Spine in Sports

functional ability of individuals with back pain that is not severe in nature.19 Similarly, Sullivan et al. studied the relationship of active lumbar spine range of motion and disability. Using the Roland-Morris Back Pain Questionnaire and therapist assessments, they suggested that active lumbar spine flexion should not be used as a treatment goal.20 In contrast, Magnusson et al.21 studied a group of patients’ with chronic low back pain. The study suggested that increased trunk motion could be achieved by participation in a 2-week, full-time rehabilitation program. The authors suggested that motion was of ‘greater magnitude and was done at an increased velocity.’ In addition, patients who demonstrate a pain avoidance behavior can achieve the confidence to recover in spite of their pain. More comprehensive randomized, prospective studies are needed to better assess the role of spinal flexibility in the recovery process in athletes. Despite these limitations, the authors still advocate that athletes work on correcting any loss of spinal flexibility or range of motion. These flexibility exercises may be initiated at the beginning of the recovery period and in combination with the strength training once the pain is controlled. A flexion- or extension-based program will depend upon the specific limitations as per the physical examination.

Strength deficits Addressing strength deficits is another primary focus of spine rehabilitation. Similar to the previous discussion of spinal flexibility, prolonged injury and pain can lead to muscle atrophy, altered spine biomechanics, and decreased athletic performance. There are a variety of spine exercise programs including spine stabilization exercises, McKenzie exercises, and Williams’ flexion exercises which are utilized to treat spine injuries based upon the etiology of the spine pain.22 However, there is limited study of the utility of these programs in the management of prolonged spine injuries in athletes. The following is a review of the various studies that have attempted to analyze the role of the spine muscles in supporting the spine, anatomical changes which occur from an exercise program, and efficacy in treating individuals with prolonged spine injuries. In the lumbar spine, the superficial and deep truncal muscles are strengthened to assist with the control of the lumbar spine. Various studies have yielded conflicting results as to changes involving the superficial muscles of the lumbar spine. In contrast, the multifidus muscles are believed to be important in maintaining stiffness and strength of the lumbar spine.23,24 Zhao et al. suggested that functional inactivity may contribute to selective type 2 atrophy of the multifidus muscles in patients with lumbar disc herniations.25 Antigravity postural muscles have been shown to atrophy to a greater extent than lower extremity muscles in microgravity simulation models.26 Changes in muscle composition in healthy subjects who stopped normal repetitive low-level activity patterns is thought to result in transformation of the muscle towards a more fatigable type of muscle fiber.26,27 The implication is that muscles situated on the trunk and lower extremities are affected most by prolonged inactivity and deconditioning. Fortunately, it is believed that these changes are reversible with adequate therapy. Various studies have looked at the anatomical changes in spinal muscles after a treatment exercise program. Hides et al. attempted to assess the recovery of lumbar multifidus muscles after treatment with an exercise program consisting of isometric contractions of these muscles with cocontraction of the abdominal muscles compared to medical treatment only for individuals following a nonradicular acute lumbar spine injury.28 These authors noted a more rapid and complete recovery of the multifidus muscles as measured by an improvement in the muscle symmetry. Sung studied the endurance of multifidus muscles and functional status of chronic low back pain patients after

participation in a 4-week spinal stabilization program.29 Although the authors believed it was difficult to measure the isolated effect on the multifidus alone, they suggested the evidence did show a change in the multifidus strength in conjunction with other spinal extensor muscles. Finally, Danneels et al. analyzed effect of three different 10-week exercise training programs on the cross-sectional area of the paravertebral muscles in individuals with chronic lumbar spine pain.30 The authors suggested that a lumbar stabilization program combined with dynamic resistance training was necessary to restore the size of the paravertebral muscles. These studies would suggest that a structured lumbar exercise program can lead to anatomical improvement in the lumbar multifidus muscles. Other studies have attempted to define the functional efficacy of a structured strengthening exercise program in the management of individuals with chronic lumbar spine pain. Unfortunately, there are few prospective, randomized studies. O’Sullivan et al.18 compared a treatment group utilizing strengthening of the deep abdominal muscles with coactivation of the lumbar multifidus to a control group in individuals with chronic low back pain and spondylolisthesis. The treatment group showed a significant improvement at 30 months in regards to pain, function, range of motion, and abdominal muscle recruitment. Mannion et al.27 performed a prospective study of three active exercise treatments (active physical therapy, muscle reconditioning on devices, and low-impact aerobics) over a 3-month period for individuals with chronic lower back pain. All three treatment exercises showed a similar increase in isometric strength in all lumbar planar movements, increase activation of the erector spinae during extension testing, and increased endurance testing as measured by the Blering-Sorensen test. The authors concluded that significant muscle performance was observed in all three exercise groups. Though these studies were not specific to athletes, they would suggest that a structured strengthening program may be efficacious in the management of chronic spine injuries. In the lumbar spine, the program should focus on strength training of the deep intrinsic spinal muscles, such as the lumbar multifidus, with cocontraction of the abdominal muscles (Fig. 130.1). Indeed, many of today’s spinal rehabilitation programs incorporate control and strengthening of these ‘core’ muscles of the spine (Fig. 130.2). However, more comprehensive randomized, prospective studies are needed to better assess the efficacy of spinal strengthening exercises in treatment of athletes.

Fig. 130.1 Spine stabilization exercise with use of balance ball for lumbar strengthening and balance. 1381

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Fig. 130.2 Spine stabilization exercise with use of balance ball for cervical/thoracic strengthening and balance.

Maintenance of cardiovascular stamina For the athlete, prolonged recovery can have a significant impact on cardiovascular fitness. Intuitively, maintenance of cardiovascular fitness during the recovery process will allow the athlete to return to their peak performance in a shorter period of time. Prolonged recovery or decreased cardiovascular exercising will lead to deconditioning within a few weeks. In addition, aerobic exercise may assist in the management of pain, decreasing the need for medication which might have adverse side effects. Therefore, most rehabilitation treatment programs utilize some form of aerobic exercise depending upon the etiology of the spinal injury. Such interventions have included swimming, cycling, elliptical trainers, and water running. Despite the rationale for cardiovascular fitness during the recovery process, there are no definitive studies to suggest the effectiveness of a fitness program in athletes after a spinal injury. Wittink et al. noted in a prospective case series that patients with chronic low back pain had comparable level of aerobic fitness with those of healthy subjects.31 Though the authors suggested that aerobic fitness level was independent of diagnosis, duration of pain, pain intensity, or work status, they felt aerobic fitness training was a useful treatment modality. Sulco et al. studied low back pain patients who underwent a 10-week aerobic fitness training regimen. In the short term, improvements in mood profile were noticed, but not in pain levels. However, at 2.5year follow-up, the exercise group received fewer pain medication prescriptions, was given fewer physical therapy referrals, and showed an improved work status in exercising patients.32 Future prospective studies are needed to better define the amount and efficacy of aerobic fitness training for athletes with specific diagnoses. Despite this need, maintenance of aerobic fitness should be part of a rehabilitation treatment program.

burnout can cause the athlete to regress during rehabilitation, which should put the training and medical staff on notice to look for the symptoms while following the athlete’s recovery.33 Therefore, the physician must be aware of these issues and the patient’s goals to develop a complete treatment program. The impact on recovery of the manifestation of the psychological issues has been studies in both athletes and nonathletes with chronic low back pain. A few studies have found a relation to psychological distress and the development chronic back pain in workers.34,35 Sports psychology, while generally relating to a much different population, can, in some ways, draw parallels with regards to anxiety and fears of pain. If the athlete’s focus falters, a negative cycle can develop which can evolve into increased tension. It is important for the support team to help the athlete maintain high self-esteem and concentration. As noted above, burnout can occur from overtraining and erode the self-confidence and motivation of the athlete. A stepwise approach with directed goals will help with maintaining a positive outlook for the athlete as he or she reaches for new levels of achievement during the course of rehabilitation. Fear of re-injury can be an inhibitory consequence of having low back pain. Patients often will not attempt certain activities due to a belief that it will worsen their condition. Obviously, this can be quite detrimental to progression in a therapeutic program. In patients with chronic low back pain, it has been shown that if they believe that their pain will worsen, significant disability and depression will be encountered.36 For these reasons, it is sometimes important to employ a sports psychologist to facilitate rehabilitation and ensure a smooth progression to eventual return to activity, as appropriate.

Reintegration in sports-specific activity The final steps in the rehabilitation process involve integrating the athlete back into their sports-specific activity (Fig. 130.3). Progression from the basic flexibility and strengthening exercises of the spine will depend upon the athlete’s symptoms and performance needs. Athletes should begin these sports-specific motions under the guidance of the trainer or therapist. Such supervision will allow the trainer or therapist to review any biomechanical abnormalities which might impede the recovery process. In addition, the athlete should be pain free and without surgical restriction. Any asymmetry in muscle strength would limit the athlete’s progress toward the sports-specific activity.

Psychosocial issues All athletes, whether amateur or professional, may experience psychosocial issues, which may affect their recovery from a prolonged injury. For most athletes, this may pertain to the frustration of not being able to return to a specific sport in a certain period of time. For elite athletes, the issues may be more complex due to the many stakeholders including agents, trainers, and coaches. In addition, 1382

Fig. 130.3 Open kinetic chain resistance throwing exercise.

Interventional Spine in Sports

The progression from basic to more complex motions will depend upon the subsequent forces placed on the spine. As an example, athletes participating in tennis should simulate a basic forehand or backhand swinging motion in a plane parallel to the ground. The motion should initially begin without any contact with the tennis ball or resistance measures, such as Therabands. Contact or resistance is then added in a linear plane with progression toward reaching in multiple planes as would occur in competition. Overhead volleys and serves should be avoided until the athlete is able to perform the above motions with fluidity and without pain. The athlete is then progressed to overhead serves and volleys which will place a greater amount of stress on the spine. Again, the motions should initially occur without any ball contact. The athlete can then progress from low-speed to high-speed motions with increased power as tolerated. A final decision allowing return to full activity should occur in the context of a complete medical recovery from the injury with the hopeful prevention of any future injury.

RETURN TO COMPETITION The eventual return of the athlete to competition requires a balance of various factors. The physician must be sure the athlete has had adequate time to recover from the medical injury with a relative assurance that the athlete will not sustain a recurrent injury. The athlete must demonstrate a return to the pre-injury proficiency in athletic performance. The level of proficiency will vary depending upon the level of competition, external pressure from coaches, peers and agents, and timing of competition. In general, the athlete should be pain free, exhibit pre-injury range of motion and pre-injury strength. In addition, the athlete should be able to perform sport-specific maneuvers involving such movements as running, cutting, or jumping motions without any significant abnormal motions (Fig. 130.4).

Cervical spine Several authors have suggested an algorithmic approach for treating injuries to the cervical spine. Wang el al.37 attempted to study the effectiveness of an algorithmic approach for treating different etiologies of cervical pain. Patients were grouped according to symptoms, including radicular arm pain or neck pain, referred neck or arm pain, cervicogenic headaches, and neck pain only. Treatment approaches included range of motion, traction, postural exercise, and joint mobilization. Based on the results, the authors determined that there was a place for individualized treatment approaches using such an algorithm. Beazell et al. suggested specific exercises for the cervical region to correct dysfunctional motion and restore posture.38 Exercises to facilitate proper posture include stretching of the pectoralis minor and the posterior shoulder depressors in addition to the trapezial and cervical paraspinal muscles. Other muscles that can be targeted to prevent muscle inhibition include the longus colli and lower trapezius. Maintenance of proper posture during reconditioning is emphasized to facilitate normal neuromuscular patterns that can carry over to sport-specific exercises. Scapular strengthening will help with stabilizing the shoulder in order to aid in maintaining cervical alignment. Prior to returning to sport, the athlete should be able to demonstrate appropriate cervical posture. As previously noted, criteria for return are pain-free range of motion, no abnormal neurologic signs, spinal stability, normal strength, and no provocative signs. Torg and Ramsey-Emrhein39 proposed criteria for clinicians to use to help patients understand the risks of collision activities and to help make sound recommendations regarding participation in competition. The following are brief summarizations, and the reader is directed to the references for a full discussion of the recommendations. Congenital conditions such as odontoid anomalies and atlanto-occipital fusion are complete contraindications, while Klippel-Feil anomaly depend on the type and confounding pathology. Developmental cervical

Prolonged injury

Chronic pain Interventions Activity modification Anti-inflammatory Physical modalities Medications Injections

Inflexibility/strength

Deconditioning

Psychologic issues

Interventions Spine sretching exercises (bias: flexion vs extension) Spine strengthening exercises

Intervention Pain limited cardiovascular training

Interventions Counseling

Intergration phase Normalization of spine biomechanics Progress to sports specific activities

Return to play criteria No pain Pain free range of motion Pre-injury strength Ability to perform sports specific maneuvers Adequate aerobic fitness Psychological readiness

Fig. 130.4 Algorithm of return to play criteria. 1383

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stenosis without evidence of instability does ‘not predispose athletes to permanent catastrophic neurologic injury’ and should not disallow the athlete from playing. However, athletes with a loss of ‘functional reserve’ as defined by obliteration of the protective cerebrospinal fluid around the spinal cord on MRI imaging should not participate in contact or collision sports.40 Those athletes with uncomplicated cervical cord neurapraxia or ‘stingers’ can be allowed to play without risking more serious neurologic injury.39 Spear-tackler’s spine as seen in athletes with developmental stenosis, straightening of the cervical column and post-traumatic radiographic abnormalities, is an absolute contraindication. There are no contraindications for athletes with single-level stable cervical fusions. However, athletes with 2–3-level fusions present a relative contraindication and those with more levels are absolutely contraindicated.

Lumbar spine Similar to the cervical spine, a variety of algorithms have been recommended to treat lumbar spine injuries. Despite the need for more prospective, randomized, controlled studies, most physicians will utilize a spine program which incorporates lumbar stretching and assessment of lower extremity inflexibilities. The main focus of lumbar strengthening involves control of the ‘core’ muscles of the spine, including the abdominal and lumbar multifidus muscles. Prior to returning to competition, the athlete should exhibit pain-free range of motion, normal strength, and sport-specific activities. As an example, the treatment of lumbar spondylolysis and time to return to competition will vary depending upon the physician’s beliefs and preference. Standaert et al.41 recommended that athletes may return to competition if they are asymptomatic after 4–6 weeks with a mature corticated fracture on CT scan. If the CT scan shows an earlier-stage lesion with either a stress reaction or minimal separation with noncorticated or cystic margins, the athlete should rest for 12 weeks and no extensive physical activity beyond that associated with normal daily activities. After a gradual rehabilitation program and no symptoms, the athlete can progressively return to the sport. Cogeni recommended that athletes can return to competition if they are pain free during therapy, at rest, with lumbar hyperextension motions and specific athletic activity after 8 weeks from the diagnosis.42 Omey and Micheli recommend the application of a rigid brace for 6–9 months for athletes with early spondylolytic lesions before returning to sport.43 Despite the variation in treatment times, the overall goal is to allow adequate healing of the pars defect, relieving pain, and optimizing function. In each case, the athlete should not be allowed to return to play until demonstration of painless range of motion and relief of hamstring spasm, if present. The goal of physical therapy is to increase spinal stability, whether implemented in a brace or without a brace. However, prolonged brace use will require reconditioning. Physical therapy exercises have varied, but focus on targeting the deep abdominal muscles and lumbar multifidi.18,44 With time, most athletes will eventually return to competition. For a more complete discussion, the reader is referred to the earlier chapter on spondylolysis.

SPECIFIC CONCERNS FOR VARIOUS SPORTS Specific injuries involving the spine will vary depending upon the specific sport and competitive level of the athlete. Although a comprehensive discussion of all sports is beyond the scope of this chapter, several sports will be highlighted to review the unique factors and areas of focus which may contribute to or assist with the man1384

agement of spine injuries. Each sport listed below incorporates the biomechanical and technical issues of the sport. A comprehensive rehabilitation program focusing on the unique biomechanical issues in the setting of the previously outlined basic principles will allow the physician to facilitate an appropriate and efficient recovery for the athlete.

Running sports Running athletes are less likely to experience back pain injuries compared to injuries involving the lower extremity. However, back pain injuries may represent approximately 2–11% of all running injuries.45 The majority of these injuries involve lumbar strains. Less common injuries that may lead to prolonged injury include lumbar radiculopathy, lumbar spondylolysis, lumbar spondylolisthesis, and lumbar stress fractures. Fortunately, the majority of lumbar spine injuries can be managed with medical rehabilitation and rarely require surgical intervention In general, the compressive forces and flexion–extension moments generated in the spine during running are not believed to place the spine at an increased risk for injury. However, any biomechanical abnormalities that may increase the forces on the spine may contribute to lumbar spine injuries.45 During the running gait cycle, there appears to be coordinated movements for: (1) flexion–extension of the lumbar spine and anterior–posterior pelvic tilt, and (2) lateral bending of the lumbar spine and obliquity of the pelvis.46 The lumbar extensor muscles appear to exhibit significant muscular activation at the time of heel strike, assisting with truncal deceleration and stabilization of the pelvis. At the same time the peak compressive forces range from 2.5–5.7 times body weight at heel strike.47 Any lower extremity abnormality, such as excessive pronation, may increase internal tibial rotation placing increased stress on the lumbar spine. In athletes with chronic lumbar spine injuries, the physician should assess for extrinsic and intrinsic factors which may contribute to the prolonged lumbar pain. Extrinsic factors include assessment of the athlete’s running shoes, frequency and distance of running, terrain (pavement, trails and treadmill, flat versus hills) and weekly progression of time or mileage. Most athletes experience injuries when they attempt to abruptly change one of the above extrinsic factors. Intrinsic factors relate to the anatomical alignment, inflexibilities, and strength of the athlete. The physician should assess for lumbar spine and lower extremity range of motion and alignment including any increased lumbar lordosis, anterior pelvic tilt, excessive tibial rotation, or excessive foot pronation. Areas of inflexibility common to runners include hip flexors (iliopsoas), hip abductors (iliotibial band), and lower extremity (hamstring and gastrocnemius muscles). Strength deficits may involve the lumbar paraspinal muscles (erector spinae), abdominal muscles, and pelvic stabilizers, including the gluteal muscles. Finally, maintenance of cardiovascular fitness is essential in the recovery of running athletes. Aquatic running is quite useful and alleviates some of the biomechanical forces on the lower extremity and spine.

Golf Golfers experience one of the highest incidences of back pain for all sports. The incidence varies for amateur and professional athletes depending upon the study. The incidence in amateur athletes incidence ranges 25–46%, and in professional athletes range 30–40%.48 In the amateur golfer, the majority of golf injuries are due to technical error or biomechanical deficiencies.49 In professional golfers, the majority of injuries are due to overuse.50 In both types of athletes, the most common injury involves the lumbar spine including lumbar strains, lumbar radiculopathy, and lumbar spondylolysis.

Interventional Spine in Sports Trapezius Levator scapulae

70

Rhomboids 60

Serratus anterior

Percent mmt

50 40 30 20 10 0 Take away

Forward swing

Acceleration

Early followthrough

It has been suggested that poor swing mechanics may lead to an increased injury of the lumbar spine. Hosea and Gatt noted that compressive, rotatory, lateral flexion and anterior–posterior traction forces are applied to the lumbar spine during the golf swing.51 The spine may be particularly at risk during the take-away or back swing and late follow-through phases of the golf swing due to the compressive forces placed on the spine. The erector spinae and abdominal oblique muscles exhibit increased muscle activity throughout the golf swing. The erector spinae assist with stabilization, while the abdominal muscles contract for truncal flexion and rotation.52,53 For the scapular stabilizers: (1) the trapezius is active in the trailing arm during take-way and during the leading arm during acceleration, (2) the levator scapulae and rhomboid muscles are active in the leading arm during the forward swing and acceleration phases and the trailing arm during take-away, and (3) the serratus anterior is constantly active in the leading arm and mainly during the acceleration and early followthrough phase in the trailing arm (Kao, 1995) (Figs 130.5, 130.6).54 In any technical error in the golf swing, spinal inflexibility or truncal strength deficits could contribute to subsequent injury. A comprehensive rehabilitative program will focus on all components of flexibility, strength, and endurance conditioning, as well as

Late followthrough

Fig. 130.5 Scapular muscle activation in the leading arm during the phases of the golf swing.

poor swing biomechanics. Potential areas of inflexibility include limited lumbar spine mobility in any plane, limited hip motion, tight hamstrings, and tight pectoralis muscles. Strengthening exercises should focus on the lumbar paraspinal muscles (erector spinae), abdominal muscles (rectus and oblique), latissimus dorsi, and scapular stabilizers (rhomboid, serratus anterior and trapezius). Finally, a thorough review of all phases of the golf swing is essential to improve any potential technical flaws. Specific areas of focus may include: straightening of the back posture during the swing, proper positioning of the feet to allow equal distribution of weight and appropriate weight transfer during the swing, and speed control during trunk rotation.48

Cycling Cervical and lumbar spine injuries are quite common in the sport of cycling. The injury will vary for amateur verses professional riders and road verses off-road cycling. In addition, traumatic injuries are more likely to lead to head injuries or spinal fractures, which are beyond the scope of this discussion. For atraumatic injuries, cervical spine injuries include cervical and trapezial muscle strains, Trapezius Levator scapulae

60

Rhomboids 50

Serratus anterior

Percent mmt

40 30 20 10 0 Take away

Forward swing

Acceleration

Early followthrough

Late followthrough

Fig. 130.6 Scapular muscle activation in the trailing arm during the phases of the golf swing. 1385

Part 6: Interventional Spine in Sports

while lumbar spine injuries are typically lumbar strains secondary to the various positions of the cyclist. The incidence of low back pain has ranged from 10% to 17% of competitive cyclists.55 Other common injuries include radiculopathies and spondylosis in the older athlete. The position of the road cyclist for prolonged period of times may predispose the athlete to injury. The cyclist rides with the cervical spine hyperextended and the lumbar spine hyperflexed for aerodynamic stability. The position may be exaggerated when the cyclist utilizes the drop handlebars or aerobars. Cervical and upper back injuries are probably secondary to the increased load on the arms and shoulders while riding.56 An electromyographic study suggested increased activity in the thoracic muscles depending upon head position and aerodynamic positioning.57 Lumbar spine injuries are probably secondary to an increased stretch to the lumbar paraspinal muscles and increased pressure to the lumbar disc in the hyperflexed position. In addition, lumbar extensor muscle activity appears to be proportional to pedal cadence.57 Management of cervical or lumbar spine injuries requires a thorough assessment of the bicycle for proper fit to the athlete. Factors to include in the assessment of the fit of a bicycle include the frame size, seat height, fore and aft saddle position, saddle angle, handlebar reach, handlebar height and amount of rotation in the pedals. In addition, review of how the athlete pedals and utilizes gearing to overcome resistance is imperative. Physical assessment of the cyclist may often reveal decreased cervical or lumbar spine range of motion as well as hip flexor, iliotibial band, or hamstring tightness. Strength deficits may involve cervical paraspinal, trapezial, lumbar paraspinal, gluteal, and hamstring muscles. A comprehensive program should focus on correcting the biomechanical deficits of the athlete and improper fit of the bicycle.

Rowing Injury rates among rowers are relatively low when compared to other traumatic sports. However, a fair number of injuries involve the lumbar spine, with an incidence of 15–20% among elite and club level rowers.58,59 Fortunately, the majority of injuries relate to muscle strains from overuse and subsequent fatigue. Rowers must repetitively cycle though four distinct phases: the finish, recovery, catch, and drive. It has been hypothesized that alterations in flexibility or strength may lead to subsequent injury due to fatigue. A study of 20 elite rowers reveals greater mobility in the lower lumbar spine region and less in the pelvic region in rowers with no history of lower back pain. In contrast, rowers with chronic lower back pain were noted to have hypomobility in the lower spine and compensatory increased motion in the upper lumbar or pelvic regions.60 Over the rowing time period, there was an increase in the lumbar flexion and the electromyographic activity of the lumbar muscle including the multifidus, iliocostalis lumborum. and longissimus muscles.61 In theory, this may lead to subsequent injury. The rehabilitation of spinal injuries involves a restoration of the spinal mobility and endurance training of the core lumbar muscles. Rowers will benefit from stretching exercises focusing on the hamstring and iliopsoas muscles to increase lumbar flexion and synchronize the lumbopelvic motion.60,61 Strengthening exercises should focus on endurance concentric and eccentric exercises of both the abdominal and lumbar extensor muscles. In addition, exercises should strengthen the gluteal muscles, which assist with developing the explosive forces during the drive phase of rowing. Maintenance of the lumbar flexibility and strength should assist with the prevention of subsequent injuries.

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CONCLUSION A variety of spinal disorders can lead to prolonged injury in the athlete. A structured rehabilitation treatment program should focus on pain control, correction of inflexibilities and strength deficits, maintenance of cardiovascular stamina, and assessment of psychological barriers. The athlete may progress to sports-specific activities and eventual return to competition once pain free. Future prospective, randomized, controlled studies are needed to better define the efficacy of the various treatment interventions to allow the athlete the quickest return to competition.

References 1. Maroon JC, Bailes JE. Athletes with cervical spine injury. Spine 1996; 21(19): 2294–2299. 2. Torg JS, Guille JT, Jaffe S. Injuries to the cervical spine in American football players. J Bone Joint Surg [Am] 2002; 84A(1):112–122. 3. Torg JS, Pavlov H, Genuario SE, et al. Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg [Am] 1986; 68(9):1354–1370. 4. Bailes JE, Herman JM, Quigley MR, et al. Diving injuries of the cervical spine. Surg Neurol 1990; 34(3):155–158. 5. Webb JK, Broughton RB, McSweeney T, et al. Hidden flexion injury of the cervical spine. J Bone Joint Surg [Br] 1976; 58(3):322–327. 6. Marshall SW, Waller AE, Dick RW, et al. An ecologic study of protective equipment and injury in two contact sports. Int J Epidemiol 2002; 31(3):587–592. 7. Maxwell C, Spiegel A. The rehabilitation of athletes after spinal injuries. In: Watkins R, ed. The spine in sports. Philadelphia: Hanley and Belfus; 1990:281–292. 8. Garrick JG, Requa RK. Epidemiology of woman gymnast injuries. Am J Sports Med 1980; 8:260. 9. Tall RL, DeVault W. Spinal injury in sports: Epidemiologic considerations. Clin Sports Med 1993; 12:441–448. 10. Smith J, et al. PASSOR musculoskeletal physical examination core competencies. 2003; http://www.aapmr.org/passor/attachmt/msk.pdf 11. Beck A, Gebhard F, Kinzl L, et al. Spinal cord injury without radiographic abnormalities in children and adolescents: case report of a severe cervical spine lesion and review of literature. Knee Surg Sports Traumatol Arthrosc 2000; 8(3):186–189. 12. Press JM, Herring S, Kibler WB. Rehabilitation of musculoskeletal disorders. In: Press JM, Herring SA, Kibler WB, eds. The textbook of military medicine. Borden Institute, Office of the Surgeon General; 1998. 13. Laskowski ER, Concepts in sports medicine. In: Braddom RL, Buschbacker RM, Dimitru D, et al, eds. Physical medicine and rehabilitation. Philadelphia: WB Saunders; 2000:957–983. 14. Deyo RA, Diehl AK, Rosenthal M. How many days bed rest for acute low-back pain: a randomized clinical trial. N Engl J Med 1986; 315:1064–1070. 15. Fellander-Tsai L, Micheli LJ. Treatment of spondylolysis with external electrical stimulation and bracing in adolescent athletes: a report of two cases. Clin J Sport Med 1998; 8(3):232–234. 16. Karppinen J, Ohinmaa A, Malmivaara, A, et al. Cost effectiveness of periradicular infiltration for sciatica: subgroup analysis of a randomized controlled trial. Spine 2001; 26:2587–2595. 17. Carette S, Leclaire R, Marcoux S, et al. Epidural corticosteroid injections for sciatica due to herniated nucleus pulposus. N Eng J Med 1997; 336:1634–1640. 18. O’Sullivan PB, Phyty GD, Twomey LT, et al. Evaluation of specific stabilizing exercise in the treatment of chronic low back pain with radiologic diagnosis of spondylolysis or spondylolisthesis. Spine 1997; 22(24):2959–2967. 19. Kuukkanen T, Malkia E. Effects of a three-month therapeutic exercise program on flexibility in subjects with low back pain. Physiother Res Int 2000; 5(1):46–61. 20. Sullivan MS, Shoaf LD, Riddle DL. The relationship of lumbar flexion to disability in patients with low back pain. Phys Ther 2000; 80(3):240–250. 21. Magnusson ML, Bishop JB, Hasselquist L, et al. Range of motion and motion patterns in patients with low back pain before and after rehabilitation. Spine 1998; 23(23):2631–2639. 22. Young JL, Press JM, Herring SA. The disc at risk in athletes: perspectives on operative and nonoperative care. Med Sci Sports Med 1997; 29(7):S222–S232. 23. Hodges PW. Core stability exercise in chronic low back pain. Ortho Clin North Amer 2003; 34(2):245–254.

Interventional Spine in Sports 24. Wilke HJ, Wolf S, Claes LE, et al. Stability increase of the lumbar spine with different muscle groups: A biomechanical in vitro study. Spine 1995; 20:192–198.

42. Congeni J, McCulloch J, Swanson K. Lumbar spondylolysis. A study of natural progression in athletes. Am J Sports Med 1997; 25(2):248–253.

25. Zhao WP, Kawaguchi Y, Matsui H, et al. Histochemistry and morphology of the multifidus muscle in lumbar disc herniation: comparative study between diseased and normal sides. Spine 2000; 25(17):2191–2199.

43. Micheli LJ, Hall JE, Miller ME. Use of modified Boston brace for back injuries in athletes. Am J Sports Med 1980; 8(5):351–356.

26. St. Pierre D, Gardiner PF. The effect of immobilization and exercise on muscle function: a review. Physiother Canada 1987; 39:24–36. 27. Mannion AF. Fiber type characteristics and function of the human paraspinal muscles: normal values and changes in association with low back pain. J Electromyogr Kinesiol 1999; 9(6):363–377.

44. Blanda J, Bethem D, Moats W, et al. Defects of pars interarticularis in athletes: a protocol for nonoperative treatment. J Spinal Disord 1993; 6(5):406–411. 45. Gatt CJ. Back pain in running. In: Guten G, ed. Running injuries. Philadelphia: WB Saunders; 1997:47–60. 46. Schache AG, Blanch P, Rath D, et al. Three-dimensional angular kinematics of the lumbar spine and pelvis during running. Human Movement Sci 2002, 21:273–293.

28. Hides J, Richardson C, Jull G. Multifidus muscle recovery is not automatic after resolution of acute, first-episode low back pain. Spine 1996; 21:2763–2769.

47. Capozzo A. Force actions in the human trunk during running. J Sports Med 1983; 23:14–22.

29. Sung P. Multifidi muscles median frequency before and after spinal stabilization exercises. Arch Phys Med Rehabil 2003; 84:1313–1318.

48. Theriault G, Lachance P. Golf injuries: An overview. Sports Med 1998; 26(1): 43–57.

30. Danneels L, Vanderstraten G, Cambier, et al. Effects of three different training modalities on the cross-sectional area of lumbar multifidus in patients with chronic low back pain. Scand J Sports Med 2001; 35:186–191.

49. Theriault G, Lacoste E, Gaboury M, et al. Golf injury characteristics: a survey from 528 golfers. Med Sci Sports Exerc 1996; 28(5):565–571.

31. Wittnick H, Michel TH, Wagner A, et al. Deconditioning in patients with chronic low back pain: fact or fiction? Spine 2000; 25(17):2221–2228.

51. Hosea TM, Gatt Jr CL. Back pain in golf. Clin Sports Med 1996; 15:37–53.

50. McCarroll JR. The frequency of golf injuries. Clin Sports Med 1996; 15:1–7.

32. Sulco AD, Paup DC, Fernhall B, et al. Effects of aerobic exercise on low back pain patients in treatment. Spine J 2001; 1(2):95–101.

52. Pink M, Perry J, Jobe FW. Electromyographic analysis of the trunk in golfers. Am J Sports Med 1993; 21(3):385–388.

33. Ahern DK, Lohr BA. Psychosocial factors in sports injury rehabilitation. Clin Sports Med 1997; 16(4):755–768.

53. Watkins RG, Uppal GS, Perry J, et al. Dynamic electromyographic analysis of trunk musculature in professional golfers. Am J Sports Med 1996; 24(4):535–538.

34. Gatchel RJ, Polatin PB, Mayer TG. The dominant role of psychosocial risk factors in the development of chronic low back pain disability. Spine 1995; 20(24): 2702–2709.

54. Kao JY, Pink M, Jobe FW, et al. Electromyographic analysis of the scapular muscles during a golf swing. Am J Sports Med 1995; 23(1):19–23.

35. Croft PR, Papageorgiou AC, Ferry S, et al. Psychologic distress and low back pain. Evidence from a prospective study in the general population. Spine 1995; 20(24):2731–2737. 36. Verbunt JA, Seelen HA, Vlaeyen JW, et al. Disuse and deconditioning in chronic low back pain: concepts and hypotheses on contributing mechanisms. Eur J Pain 2003; 7(1):9–21. 37. Wang WT, Olson SL, Campbell AH, et al. Effectiveness of physical therapy for patients with neck pain: an individualized approach using a clinical decision-making algorithm. Am J Phys Med Rehabil 2003; 82(3):203–218. 38. Beazell JR, Magrum EM. Rehabilitation of head and neck injuries in the athlete. Clin Sports Med 2003; 22(3):523–557. 39. Torg JS, Ramsey-Emrhein JA. Management guidelines for participation in collision activities with congenital, developmental, or postinjury lesions involving the cervical spine. Clin J Sport Med 1997; 7(4):273–291. 40. Cantu RC. Functional cervical spinal stenosis: a contraindication to participation in contact sports. Med Sci Sports Exerc 1993; 25(3):316–317.

55. Burke ER. Cycling. In: Watkins RG, ed. The spine and sports. St Louis: Mosby; 1996:592–596. 56. Mellion MB. Common cycling injuries: Manag Prevent Sports Med 1991; 11(1): 52–70. 57. Usabiaga J, Crespo R, Iza I, et al. Adaptation of the lumbar spine to different positions in bicycling racing. Spine 1997; 22(17):1965–1969. 58. Hickey GJ, Fricker PA, McDonald WA. Injuries to elite rowers over a ten year period. Med Sci Sports Exer 1997; 29:1567–1572. 59. Bahr R, Anderson SO, Loken S, et al. Low back pain among endurance athletes with and without specific back loading: a cross-sectional survey of cross-country skiers, rowers and orienteerers and nonathletic controls. Spine 2004; 29(4):449–454. 60. MacGregor A, Anderson L, Gedroyc W. The assessment of interspinal motion and pelvic tilt in elite oarsmen. Med Sci Sports Exerc 2002; 34(7):1143–1149. 61. Caldwell J, McNair PJ, Williams M. The effects of repetitive motion on lumbar flexion and erector spinae muscle activity in rowers. Clincal Biomechanics 2003; 18:704–711.

41. Standaert CJ, Herring SA, Halperin B, et al. Spondylolysis. Phys Med Rehab Clinic North Amer 2000; 11(4):785–803.

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PART 7

NEW FRONTIERS

CHAPTER

Disc Replacement

131

Richard D. Guyer and Donna D. Ohnmeiss

INTRODUCTION Maintaining motion has long been the quest in the treatment of painful spinal disorders. Movement of the neck and trunk is a large part of everyday life. Limitations due to pain or surgical intervention are frustrating for patients with back pain and can be related to significant loss of work and reduced quality of life. Beginning in the 1980s, clinically useful lumbar disc replacements were introduced. Today, there are several such devices available for use. Although these devices hold great promise for improving the long-term care of patients with back pain, they are certainly not a cure-all, and the basics of any spine surgery still apply with respect to the importance of proper patient selection. The purpose of this chapter is to discuss the indications and diagnostic work-up for patients who may be candidates for total disc replacements, describe the basics of the surgical procedure for implanting these devices, and review the clinical results and complications reported to date.

HISTORY The first patent for disc replacement was issued in 1956 to van Steenbrugghe in France.1 This was just one of many devices described in his patent application. The first clinically useful artificial disc was simply stainless steel spheres implanted into the disc space following discectomy.2,3 This procedure was first performed in 19624 and reported in 1966 by Fernström of Sweden, who implanted the spheres into 133 patients, 125 lumbar disc levels and eight cervical disc levels. Among the lumbar implants, in follow-up of 6–30 months, there were only two complications: one sphere displaced into the epidural space and one case of temporary paresis of the peroneus. Clinically, Fernström noted that patients receiving the sphere had a better result than patients undergoing discectomy alone. In 1971, Fernström reported the 4–8-year follow-up on 142 patients.4 He found that among the patients operated for disc prolapse, 65% had no pain and were able to work full duty. An additional 28% had reduced pain and were able to work in some capacity. These results were more favorable than those from a series of control patients undergoing discectomy without the placement of a sphere. In 1995, McKenzie reported follow-up of 10–20 years on 67 patients who had received the spheres described by Fernström.5 He noted a high success rate, 83% among patients with disc herniations and 75% among those with degenerative disc. Prosthesis removal was required in only one of 155 patients who received the implant. The author reported that although more than 90% of patients were not working prior to surgery, 95% were working after receiving the sphere. The author also reported that 95% of the patients felt that the procedure was worthwhile. In 1982, Drs. Kurt Schellnack and Karin Büttner-Janz in East Germany at the Charité Hospital began the development of an

artificial disc based on careful biomechanical analysis of the motion and properties of a normal lumbar disc. The design was a three-piece implant consisting of two metallic endplates and a sliding polyethylene core. The design concept was tested in the laboratory, and the first SB Charité artificial disc prosthesis was implanted in September 1984 in Berlin.6 There were problems with subsidence with this device. In 1985, a second design was introduced that had ‘wings’ on two sides of the circular endplates to increase the contact surface area between the metallic endplates and the vertebral body. This design had problems with fracture between the core and the wings. A third design was introduced in 1987. This design proved to be reliable and remains in use today (Fig. 131.1). In the late 1980s, Thierry Marnay in France designed the ProDisc. It also allows motion through articulation between a concave and convex surface. The original design was anchored by two keels on each of the superior and inferior metallic endplates. The current design of this device has one keel in the center of each of the endplates (Fig. 131.2). In the last several years there have been numerous other designs, including metal-on-metal discs such as the Maverick (Medtronic-Sofamor-Danek) and the FlexiCore (Stryker). These four discs are currently being studied in IDE FDA studies with the Charité having achieved FDA clearance October 26, 2004. There are two additional devices that are being used outside of the US called the Mobidisc (LDR Medical), consisting of metal and polyethylene, and SpinalMotion’s Kineflex™, which is of similar design.

Indications As with any surgical procedure, much of the success of total disc replacement is dependent upon the selection of patients being treated. There are indications that apply to any elective spine surgery procedure. These include the failure to achieve acceptable pain relief after an appropriate nonoperative course of treatment. In general, appropriate nonoperative management should include medication, active physical rehabilitation, education, activity modification, and often injections with at least 6 months of nonoperative care. As with any patient, careful and comprehensive history and physical examination are crucial to patient evaluation. These findings are then reviewed with respect to image findings. Most patients who have failed nonoperative management have had a magnetic resonance imaging (MRI) scan. This is reviewed to evaluate the disc, facets, bony structures, and to rule out pathologies such as spinal tumor. In most patients being evaluated for symptomatic disc degeneration, it is recommended that further evaluation be undertaken using discography. This evaluation is used as a confirmatory test to determine if the disc(s) appearing as abnormal on an MRI is the source of the patient’s symptoms. This is particularly important in view of the reports of the high rates of disc abnormalities seen on MRI scans made on individuals with no back pain.7 Also, the discogram can be 1389

Part 7: New Frontiers

A A

B B

C

Fig. 131.2 Model and radiographic images of the ProDisc lumbar device. Motion at the implanted level can be seen when comparing the flexion (B) and extension (C) views.

C Fig. 131.1 Model and radiographic images of the Charité Artificial Disc. Motion at the implanted level can be seen when comparing the flexion (B) and extension (C) views.

used to better assess the condition of the discs adjacent to the suspect level. Discography should be undertaken with the patient awake and responsive. If the patient is too heavily sedated the pain response cannot be adequately evaluated. The patient should be asked the location of the pain provoked, if any, its location with respect to the location of their usual symptoms, and the intensity of the pain. If pain is provoked that is not concordant to the usual symptoms, the discogram is not considered to be a positive test. 1390

Another important aspect in the evaluation of possible surgical candidates is psychological screening. While imaging studies are closely related to anatomical findings during surgery, psychological testing is more strongly related to surgical outcome.8 The presurgical psychosocial screening instrument has been found to have a high correlation to surgical outcome.9,10 Patients with a significant psychological component to their pain experience are likely to do poorly following surgery and should generally not undergo an elective procedure. Another important component to achieving a favorable surgical outcome is the establishment of realistic expectations. This may be addressed during the psychological screening. It can also be addressed during preoperative patient education. Patients must understand that results are not guaranteed and there is a very good chance that they will continue to have some level of pain or painful flare-ups following any spine surgery. The goal is to significantly reduce their pain and allow for improved function. Being totally and permanently pain free is not a realistic goal. Patients also need to understand that they play a major role in accomplishing these goals and must be willing to comply with a postoperative rehabilitation plan.

TOTAL DISC REPLACEMENT IN THE LUMBAR SPINE The primary indication for total disc replacement is symptomatic disc degeneration or disruption at one or two disc levels unresponsive

New Frontiers

to nonoperative management. This condition is best diagnosed by the combined use of MRI and discography. Other diagnostic observations include disc space narrowing. The patient may have complaints of back pain with or without leg pain.

Bertagnoli and Kumar described what they defined as an ideal candidate for total disc replacement.13 Such patients have singlelevel disc degeneration, a disc space height of at least 4 mm, no facet joint changes, intact posterior elements, and no degeneration at the adjacent segments.

Contraindications

Obesity

The contraindications for total disc replacement are very similar to those traditionally applied to anterior lumbar interbody fusion since the approach to the spine is the same. Details of inclusion and exclusion criteria have been discussed.11 One should screen patients for the number of types of previous abdominal surgery. If there have been several procedures, or surgery in the immediate vicinity of the painful disc, the patient may not be a good candidate. There is a risk of significant vascular injury related to scarring from previous surgery. One must evaluate the preoperative imaging studies to rule out patients with significant calcification of the vessels. This could result in significant vascular complications. As with any arthroplastic procedure, active infection is a contraindication for disc replacement. Patients should also be asked if they have any known allergy to metal or any other material in the artificial disc implant. Diseases affecting bone quality, such as osteoporosis, Paget’s disease, and osteomalacia, are contraindications for total disc replacement. There is the risk of the device subsiding into osteoporotic bone, particularly if the positioning and size of the implant used are less than ideal. There may also be an increased risk of fracturing the vertebral body during, or after, surgery if the patient is osteoporotic. Poor bone quality may also negatively influence the anchoring of the device to the vertebral bodies. Vertebral body fracture following implantation of a total disc replacement into a patient with osteopenia has been reported.12 The role of nerve root compression in the patient’s symptoms must be carefully evaluated. If the compression is related only to a bulging disc, this can be addressed by the prosthesis, which generally increases disc space height. However, if symptoms are related to nerve root compression caused by a migrated, extruded disc fragment, this cannot be addressed by disc replacement and such patients are not considered good candidates for disc replacement. Spondylolisthesis of greater than a 3 mm slip is a contraindication for total disc replacement. A severe slip will likely make it difficult, or impossible, to correctly place the device in alignment with the vertebral bodies. This may also lead to an increased chance of device failure due to altered loading or displacement of the device. Disc degeneration is often associated with degenerative changes of the facet joints. One must carefully assess the condition of the facets prior to undertaking total disc replacement in the lumbar spine. If the facets are compromised, the motion allowed by the disc prosthesis may eventually lead to facet joint pain. This is particularly true if the implant is not ideally positioned or not of the ideal size, altering the natural loading pattern on the facets. Also, severe facet joint degeneration can cause stenosis. This condition may not be addressed by total disc replacement. Previous surgery at the painful level is not an absolute contraindication for total disc replacement, but does require special consideration. The primary concern is the condition of the posterior elements. Unlike fusion, the disc is designed to allow motion of the segment. If the posterior elements have been compromised by previous surgery, the patient should not receive a total disc replacement. If the patient has undergone a percutaneous discectomy or a minimally invasive microdiscectomy, he or she may be a viable candidate for disc replacement.

As with anterior lumbar interbody fusion, accessing the spine is more difficult in an obese patient. There is also the possibility that additional weight may alter the biomechanical properties of the implant, leading to subsidence or displacement.

Procedure The surgical approach for total disc replacement is the same as for anterior lumbar interbody fusion. The mini ALIF retroperitoneal approach has been described in detail elsewhere.14,15 In this chapter, we will provide an overview of the general approach to the anterior lumbar spine. The exact approach may vary by surgeon preference or design of the device to be implanted. In our practice, a general surgeon initiates the procedure to provide access to the spine and remains available in the event of a vascular injury or other difficulty. A radiolucent table is necessary, since imaging is needed during the surgery. It is helpful if a table is used that allows the spine to be put into a slightly extended position to aid during device implantation. Another alternative is to have an inflatable device under the level to be operated that can be inflated to create extension when desired during the implantation. During the rest of the procedure, this positioning is not needed. The skin is prepped and draped in the usual fashion. A small incision of approximately 4–6 cm is made either transversely or vertically. Imaging is used to identify the lumbar levels. This imaging also verifies that the spine is positioned with the pedicles on the same horizontal plane and perpendicular to the spinous processes. The anterior rectus sheath is incised over the disc space to be operated. The left rectus muscle is released and mobilized laterally, taking care not to injure the inferior epigastric vessels. The posterior sheath is incised to reveal the peritoneum. Using one’s fingers, a plane is defined between the peritoneum and the internal oblique and transversus muscles. This allows entry into the retroperitoneal space. The psoas muscle is identified. As the peritoneum is moved away from this muscle, the ureter is revealed. Although rare, damage to the ureters can occur during anterior spinal surgery. The peritoneum is mobilized further and a retractor is used to hold the peritoneum while further dissection is performed. The ascending iliolumbar vein is often ligated during exposure of the L4–5 disc space. During exposure to the disc space, injury to the left sympathetic trunk may occur, resulting in a warm leg. Fortunately, this condition is usually temporary. One must be cautious not to injure the superior hypogastric plexus at the L5–S1 level, which can result in retrograde ejaculation. Fortunately, this is a relatively rare complication and usually resolves by 6 months after surgery. However, the problem does not resolve in some cases. When operating above L5–S1, the vessels are gently mobilized. At the L5–S1 level, the disc space may be accessed under the bifurcation of the vessels. Once access to the spine has been safely achieved, the midline of the disc space is marked with a small screw into the vertebral body or an osteotome is used to mark the vertebral endplate, depending on the type of prosthesis being implanted. The disc tissue is removed. The spine may be placed into a slightly extended position to widen the access to the disc space. Preoperative templating can be used to estimate the size of the endplates and polyethylene core needed. However, the final determination of device size is 1391

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made intraoperatively. The prosthesis size should be selected to fit within the disc space but cover as much of the vertebral body endplates as possible. This will help prevent subsidence. Obliquelyshaped endplates are selected to match the lordosis of the spine at the level to be implanted. If the vertebral endplates have a relatively posterior lip, it may be beneficial to remove them with a Kerrison ronguer or burr to increase the amount of contact area between the vertebrae and the metallic endplates of the device, allowing for a firmer fit. The disc space is temporarily distracted to make space for the device. Prior to finalizing the device placement, the spine is returned to a neutral position, rather than the slightly extended position. Once the device is implanted, images are taken to make sure that the prosthesis is properly positioned. In the anteroposterior (AP) view, the prosthesis should be centered in the disc space. On the lateral view, the prosthesis should be centered in the disc space or placed approximately 2 mm posteriorly for the Charité. Cinotti et al. have reported that optimal prosthetic sizing and positioning are related to outcome.16 Coverage of at least 80% of the vertebral body endplates by the device endplates was related to the amount of motion at the operated segment at follow-up. These authors also found that prostheses positioned anteriorly to midline were related to decreased motion at follow-up. Lemaire reported that implantation of the prosthesis of more than 4 mm anterior to the center was related to posterior facet pain.17 After verification of proper device positioning, the retractors are removed and the layers of fascia are closed with absorbable sutures. The patient is usually hospitalized for 1–3 days. A light brace or corset is worn for 2–6 weeks. Although the indications and surgical approach for total disc replacement are similar to those for anterior lumbar interbody fusion, the postoperative rehabilitation is quite different. There is no need to have a period of significantly reduced activities to allow the formation of bone to create a solid fusion. With respect to activities, one must keep in mind that many of these patients have become deconditioned during the months of symptoms leading to surgical intervention. After surgery, rehabilitation can be helpful in increasing strength, through core stabilization exercises, and general fitness. Also, these programs will hopefully help modulate symptoms and prevent future episodes of back pain. A description of postoperative rehabilitation following total disc replacement has been provided by Keller.18 During the first 3 weeks after total disc replacement, activities are oriented toward symptom management and not stressing the area of the surgical incision. The patient is encouraged to walk frequently. Other activities are oriented toward gentle range of motion exercises, excluding extension. After 3 weeks, the patient is progressed to rotation and side-bending, as well as stabilization exercises. Controlled resistance training is also introduced at this time. After 6 weeks, the patient is progressed to more strenuous exercises, and activities involving extension of the spine are introduced.

Reported outcomes Charité Although total disc replacements have been used in Europe since the 1980s relatively little material has been published on these devices. Only recently have the results of prospective studies evaluating disc prostheses been reported. The device that has been in use the longest is the Charité. There were three generations of this device designed. The design introduced in 1987 is the model that remains in use today. The results for this device have been favorable. In 1988, Büttner-Janz et al. reported on the first 62 patients to receive the Charité implant.19 This group included patients receiving all three designs of the device. A high level of satisfaction was 1392

reported by 54% of patients with an additional 29% being classified as improved. There were device-related complications with the first two designs of the device, including migration and breakage of the metallic endplates. These problems have not been reported with the use of the third, and current, design of the implant. A retrospective review of 93 patients receiving the Charité device at several sites in Europe was reported with a mean follow-up of approximately 12 months.20 It reported significant improvement in visual analog scale ( VAS) scores assessing back and leg pain. Walking distance was also reported to have improved postoperatively. Cinotti et al. from Italy retrospectively reported results with a minimum 2-year follow-up after implantation of the Charité disc replacement in a series of 46 patients receiving 56 prostheses.16 The diagnoses in the group were symptomatic disc degeneration and pain in patients who had previously undergone a lumbar discectomy. Excellent or good results were noted in 63% of patients. Great benefit was reported by 67% of patients. The results followed a pattern similar to that frequently seen in lumbar fusion studies. Patient satisfaction was greater among those undergoing single-level implantation compared to those receiving prostheses at two levels (69% versus 40%). Also similar to fusion studies, patients with a history of previous spine surgery had less satisfactory results than did those with no previous spine surgery, 50% compared to 77%. Other authors have also reported favorable results in 70–75% of patients.21,22 Long-term follow-up after total disc replacement with the Charité device was reported by Lemaire et al.23 Their study included 100 patients with a minimum follow-up of 10 years. Single-level replacement was performed in 54 patients, two-level replacement in 45 patients, and one patient underwent a three-level replacement. They reported that 62% of patients had excellent results with an additional 28% having good results. The return to work rate was 91.5%. Zeegars et al. reported on a series of 50 patients with a minimum of 2-year follow-ups.24 The authors found that 70% of patients had satisfactory outcomes, and surgery at multiple levels was not associated with a less desirable outcome compared to patients receiving single-level replacement. However, they did find that patients with previous surgery or other lumbar degenerative pathology had less desirable results than those without such factors present (81% versus 66% satisfactory outcomes). Recently, Blumenthal et al. reported the results of a multicenter FDA trial.25 They found that at most of the follow-up periods the results of Charité artificial disc were superior to anterior lumbar interbody fusion based on Oswestry and VAS scores. A significantly greater percentage of patients in the Charité group indicated that they would choose the same treatment again compared to the fusion group.

ProDisc The device in use for the second longest period of time is the ProDisc, invented in France by Marnay.26 It is composed of three components: two cobalt chromium alloy endplates and a domed polyethylene core. Motion occurs through articulation between the domed core and the concave superior metallic endplate. Each metallic endplate is anchored to the vertebral body by a keel in the center of the device. Marnay implanted the devices into 64 patients and has reported the 7–11-year follow-up of 58 of these patients (three died for unrelated reasons).27 All of the devices were functioning with no cases of device fracture. The back pain scores improved significantly from a preoperative mean of 8.5 to 3.0 postoperatively. The leg pain scores also improved significantly. At follow-up, 65% of the patients reported themselves to be ‘entirely satisfied,’ 28% ‘satisfied,’ and only 7% ‘not satisfied.’ Mayer et al. in Germany reported their early results on a series of 34 patients.28 With a mean follow-up of 5.8 months, the pain VAS scores improved from 6.3 to 3.9. The change in Oswestry scores was

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much less, improving from 19.1 to 11.5. Patient satisfaction was high with 82.6% of patients reporting that they were either satisfied or completed satisfied with the results of their surgery. In a study with highly variable length of follow-up of 3–24 months, Bertagnoli and Kumar reported on 108 patients.13 Excellent results were noted in 90.8% of patients. Zigler et al. presented the results of one center’s experience with the ProDisc implant with 24 month (n=116) to 36 month (n=40) followup.29 In this prospective, randomized study, arthroplasty was compared to combined anteroposterior lumbar fusion. There were significant improvements in pain (measured by VAS), and function, measured by the Oswestry Disability Questionnaire. At some follow-up periods the ProDisc scores were significantly less than the fusion scores. Tropiano et al. reported their experience with 53 patients with a minimum follow-up of one year.12 They reported significant improvements in the VAS and Oswestry scores. Although they had only 13 patients receiving the device at multiple levels, these patients’ outcomes were similar to patients undergoing implantation at a single level.

Motion of the operated segment Two of the early Charité studies reported on the motion at the operated level. The results in the two studies were similar. Cinotti et al. reported 16° at a replaced L4–5 level and 9° at L5–S1.16 Lemaire et al. reported very similar results with 14° at a replaced L4–5 disc level and 9.5° at L5–S1.17 The study by Cinotti et al. was the first to carefully analyze the motion at the implanted disc levels.16 They found that motion was significantly greater at levels in which the prosthesis was implanted centrally or slightly posterior to central. The motion among such levels was 12° compared to only 5° measured at levels with the device implanted more anteriorly. The authors also noted the great influence of postoperative activities following implantation in future motion of the prosthesis. Patients who began exercising 1 week after surgery had 11° of motion at the implanted level compared to only 6° among those who wore a corset for 3 months. These authors also noted that patients in whom the metallic endplates covered 80% or more of the vertebral body endplate had significantly greater motion than patients with less coverage (13° versus 6°). In a recent prospective study, Guyer et al. reported that at the L4–5 and L5–S1 levels, at 24-month follow-up, the range of motion was the same as, or slightly greater than, the preoperative range of motion.30 These authors reported values that were less that those from the European studies, with range of motion of the implanted L4–5 level being 6.5° degrees and 3.9° at L5–S1. However, it should be noted that these patients also had less motion preoperatively than what was reported in the European studies. Data from the FDA IDE clinical trial evaluating Charité provided information on the motion of the implants.31 The range of motion at the operated level decreased at 3-month follow-up, but then increased at subsequent follow-up periods and exceeded the preoperative value. The range of motion, as well as clinical outcome ( VAS and Oswestry), were significantly better among patients in whom the device was ideally positioned compared to those in whom it was suboptimally or poorly positioned. With respect to the ProDisc implant, little has been published on the range of motion achieved with the device. Huang et al. reported that the mean motion of disc levels receiving the ProDisc implant was 3.8° at a mean follow-up of 104 months.32 These authors found that female gender was related to having less than 2° of motion at the operated segment. An interesting finding in that study was regarding degeneration of the segment adjacent to the replaced disc level. Among nondegenerated adjacent segments, the range of motion of the implanted level was 4.7°. This was significantly greater than the 1.6° of motion noted at the operated level below a degenerated adjacent segment. Although this does not prove a causal relationship

between motion and deterioration of an adjacent segment, it does provide support for a protective property of the prosthesis. Tropiano et al. reported that at a replaced L4–5 level, the segmental motion was 10° and at L5–S1 was 8°. The authors did not provide data on the preoperative segmental motion at these levels.12

Complication of total disc replacement A variety of complications have been reported with total disc replacement procedures. Many of these are similar in scope to those encountered with anterior lumbar interbody fusion, considering that the approach to the spine is the same. Lemaire reported a 10% complication rate with four of eleven complications being vascular. Other problems were endplate failure or heterotopic ossification. David reported 10 complications in a series of 96 patients.21 These included one device removal and fusion, one secondary bone migration with fusion, and eight patients who underwent posterior fusion. Five patients had complete ossification around the prosthesis. While this compromised the function of the prosthesis, it basically produced a fusion and did not necessarily compromise the patient’s clinical outcome. In a series of only 14 patients reported by Sott and Harrison, five patients had a warm foot postoperatively due to interference with the left paravertebral sympathetic nerves.22 In one patient, 3 mm of subsidence was noted at 6 months; the patient’s follow-up at 30 months indicated no further subsidence, and the patient had a good clinical result. Zeegars reported 24 reoperations in his series of the first 50 patients.24 There were 11 reoperations at levels other than the one with a prosthesis, six at the level of the prosthesis, and seven reoperations in three patients for the treatment of complications. Sachs et al. reported on a group of 147 patients with a minimum 2-year follow-up enrolled in randomized studies comparing total disc replacement to fusion.33 Overall occurrence of complications were similar in the disc replacement group and the fusion group. The most frequent complication was radiculopathy. Prosthesis subsidence occurred in 7% of disc replacement cases. There were no cases of deep infection or device failure. In a study of 53 ProDisc patients, Tropiano et al. reported five complications (9%).12 The complications were one case of postoperative vertebral body fracture occurring 3 weeks after surgery, one due to implantation into a patient with osteopenia, two cases with malpositioned implants, and two cases of patients with ongoing radicular pain in the absence of neural compression. The patient with the fractured vertebra required reoperation for removal of the device and an anterior fusion. Both patients with malpositioned devices were reoperated 6–8 weeks after surgery. The patients with radicular pain were managed successfully with medication. van Ooij et al. reported on 27 patients seen over a period of 8 years, presenting with various complications following total disc replacement.34 The authors did not provide a complication rate because the initial surgeries were performed at another center. However, the type of complications that arose is notable. In two patients, the prosthesis dislocated anteriorly. Disc degeneration at another level was seen in 12 patients. In seven of these patients, disc degeneration could be seen on radiographs made prior to the disc prosthesis surgery. In 11 patients, facet joint arthrosis was identified at the level of the prosthesis or an adjacent segment. In the eight patients who underwent a posterior fusion, a hypertrophic facet joint was visualized. Device subsidence was seen in 18 patients. In 10 of these cases, a prosthesis that was too small had been implanted. In one patient, the polyethylene core subluxed anteriorly. In two patients, there was slow anterior migration of the implant. One of these patients experienced good results for 10 years and then began having symptoms. Removal of the device revealed that it was loose in fibrotic tissue and had adhered onto the great vessels. The patient underwent anterior interbody 1393

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fusion followed later by posterior fusion. In one patient, CT imaging revealed cysts, as well as sclerosis and fragmentation of bone around the prosthesis. The authors associated these findings with wear; however, this could not be confirmed as the patient refused further surgery. In two patients, the wire around the polyethylene core was broken. In three patients, there was hyperlordosis of the implanted segment, resulting in opening of the facet joints. To date, there has been one case of possible wear debris reported by van Ooji et al.; however, there was no tissue confirmation of this.34

Reported results of reoperation following arthroplasty Results following any spine surgery are not perfect and not all patients will do well after surgery. Thus, one factor to consider when evaluating spinal implants is whether there is a viable salvage procedure available for patients who fail the initial treatment. With respect to total disc replacements, there has been little published on this topic. Cinotti et al. reported that among 17 patients who had unsatisfactory results following total disc replacement with the Charité device, seven underwent reoperation.16 Salvage surgery consisted of posterior spinal fusion, leaving the prosthesis in place. Only three of the seven had satisfactory results following the posterior fusion.

Other lumbar total disc replacements There have been a few reports on the use of other total disc replacements used in small numbers of patients. In 1993, Enker et al. reported on a series of six patients in whom an Acroflex disc (Acromed Corp; Cleveland, OH) was implanted.35 This device had a polyolefin rubber core vulcanized to two titanium endplates. The rubber core fractured in one patient, requiring reoperation. Three patients had good to excellent results, one had a fair outcome, and two patients had poor outcomes. Modifications of this device are still being pursued. Currently, two other total lumbar disc replacement devices that have not yet been approved in the US are the Maverick and the FlexiCore. Clinical results from the FDA IDE trials are not available for these devices at the time of this writing.

TOTAL CERVICAL DISC REPLACEMENTS As in the lumbar spine, total cervical disc replacements are designed with the concept to allow motion of the spine. Although the end goal is the same, the motion patterns and loads borne by the cervical spine are very different than in the lumbar region. These differences may allow for significantly different designs of implants. However, there is benefit in using the technology that has been applied and tested in lumbar total disc replacements. Several cervical total disc replacement devices (Bryant Cervical Disc, Prestige, ProDisc-C (Fig. 131.3), PCM, and Mobi-C) are currently being evaluated in FDA-regulated clinical trials, and others are near beginning their trials.

these devices are initially stable. The extremes of motion should be avoided for the first 6 weeks, however, while bony ingrowth to the endplates is taking place.

Clinical outcomes Unlike lumbar total disc replacement, cervical disc replacement is a new treatment and very little has been published on its results. However, there have been a few reports with various devices. As in the lumbar spine, the first cervical disc replacements were metallic spheres implanted by Fernström.2 However, in his publication he did not report the results of these devices since the follow-up was less than 12 months. In 1998, Cummins et al. reported on the use of a two-piece stainless steel metal-on-metal device, allowing motion through articulation of concave and convex surfaces.36 The device is anchored by screws attaching the device to the anterior surface of the vertebral bodies adjacent to the implanted level. This implant has been called the Cummins device. They used the device in 20 patients between 1991 and 1996. The Cummins device was redesigned and the name changed to the Frenchay implant.37 In 2002, Wigfield et al. reported on a series of 15 patients receiving this implant.37 At 24-month follow-up, the implanted disc levels demonstrated a mean of 6.5° of motion in flexion–extension. Pain scores improved 45% and scores on a disability questionnaire improved by 31%. Pointillart published on what he termed the first failures of cervical disc prosthesis.38 The implant uses a one-piece L-shaped titanium device with a carbon convex surface upon which the vertebral body superior to the implant can glide. Good clinical results were achieved initially in all ten patients. In eight of the ten patients, a spontaneous fusion occurred at the operated segment. The remaining two patients later reported the onset of neck pain. In one of these patients, the device was removed and a fusion performed. The results of the Bryan Cervical Disc prosthesis have been reported.39 This device has a polyurethane nucleus encased by, and articulated within, a shell made of titanium plates. There is a flexible membrane between the perimeters of the plates. The device has been implanted into 97 patients, of whom 49 had reached 12-month follow-up and 10 had reached 24-month follow-up. At 12 months, 70% of patients were classified as having an excellent outcome and 4% as having a good outcome.

Complications of cervical disc replacement In the Wigfield study using the Frenchay device, 10 patients experience adverse events postoperatively.37 These included the following:

Indications and contraindications Indications for cervical disc replacements are similar to those for lumbar total disc replacement. The patient should have failed a course of appropriate nonoperative care including mediations, activity modification, active rehabilitation, and possibly injections. There should be correlation between clinical examination findings and imaging studies. The patient should have no significant psychological problems. Vertebral body fracture is a contraindication. Patients may wear a soft collar for approximately two weeks after surgery. As in the lumbar spine, no time needs to be lost advancing to an active rehabilitation program waiting for bone to incorporate, as 1394

A Fig. 131.3 Model and radiographic images of the ProDisc-C cervical device (A) Cont’d.

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recurrence of brachialgia 2 months after surgery requiring foraminotomy at the adjacent level; two screws broke in one patient by the 6-month follow-up period with the patient developing pain on full extension; pain on extension (2 patients, one occurring after a car collision); progression of myelopathy; transient hoarseness in two patients (resolved in 3 and 6 months); recurrent brachialgia at 6 months after surgery (resolved by 12 months after surgery); and in one patient the device was removed and a fusion performed due to pain during extension; however, the patient’s pain persisted. Complications in the study of 97 patients reported by Bryan included: one patient with temporary dysphonia, one patient with pain related to an osteophyte that was not addressed during the device implantation (this was removed during a foraminotomy, with no negative effects on the disc prosthesis), two patients had pain in the shoulder region not requiring further surgical intervention, and one patient required drainage of a hematoma that formed due to the loosening of a postoperative drain.39 There were no device failures in the series.

CONCLUSIONS

B

Total lumbar disc replacements have been performed since the 1980s. The devices allow motion through articulation between concave and convex surfaces. These devices appear to be safe and the clinical results are favorable. Results from the Charité trial and preliminary results from the ProDisc trial show that patients are more satisfied with their artificial discs compared to their fusion counterparts. Although VAS and Oswestry outcomes are similar at some time periods for the disc and fusion groups, rehabilitation for the disc patients can be much faster and the morbidity of the surgery is less. Further analysis is needed to determine if the devices actually reduce the rate of deterioration of the adjacent segment that has been noted with spinal fusion. There is no doubt that the future will bring new designs, perhaps incorporating new materials. There will also likely be a progression away from metal and mechanical devices to those that incorporate properties of tissue regeneration. Such implants may be combined with the emerging world of microelectronics to enhance tissue healing and function. While the future is bright for spinal arthroplasty, the enthusiasm must be tempered with caution. Only with rigorous evaluation of new technologies can the outcomes of treatment be improved. Surgeons taking on these procedures must be appropriately trained in surgical technique. As always, patient selection for total disc replacement procedures is the key to achieving good results.

References 1. van Steenbrugghe H. Perfectionnements aux prothèses articulaires. French Patent FR1122634, 1956. 2. Fernström U. Arthroplasty with intercorporal endoprostheses in herniated disc and in painful disc. Acta Chir Scand 1966; 357:S154–S159. 3. Reitz H, Joubert MJ. Intractable headache and cervicobrachialgia treated by complete replacement of cervical intervertebral disc with a metal prosthesis. S Afr Med J 1964; 38:881–889. 4. Fernström U. Disk replacement with maintenance of mobility. Presented at the 7th working session of the Association for Spinal Column Research. Nov., 1971; Bad Homberg, Germany. 5. McKenzie AH. Fernström intervertebral disc arthroplasty: A long-term evaluation. Orthop International 1995; 3:313–324.

C Fig. 131.3 Cont’d Motion at the implanted level can be seen when comparing the flexion (B) and extension (C) views.

6. Büttner-Janz K. History. In: Büttner-Janz K, Hochschuler SH, McAfee PC, eds. The artificial disc. Berlin: Springer Verlag; 2003:1–10. 7. Boos N, Rieder R, Schade V, et al. The diagnostic accuracy of magnetic resonance imaging, work perception, and psychological factors in identifying symptomatic disc herniations. Spine 1995; 20:2613–2625. 8. Spengler DM, Ouelette EA, Battie M, et al. Elective discectomy for herniation of a lumbar disc. J Bone Joint Surg [Am] 1990; 72:230–237.

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Part 7: New Frontiers 9. Block AR, Ohnmeiss DD, Guyer RD, et al. The use of presurgical psychological screening to predict the outcome of spine surgery. Spine J 2001; 1:274–282. 10. Block AR, Gatchel RJ, Deardorff WW, et al. The psychology of spine surgery. Washington, DC: American Psychological Association; 2003. 11. Sachs BL, Clawson JJ. Indications and contra-indications for total disc replacement. In: Guyer RD, Zigler JE, eds. Spinal arthroplasty: a new era in spine care. St. Louis, MO: Quality Medical Publishers; 2005:39–46.

26. Marnay T. L’arthroplasty intervertebrale lombaire. Med Orthop 1991; 25:48–55.

12. Tropiano PJ, Huang R, Marnay T. Lumbar disc replacement: Preliminary results with ProDisc II after a minimum follow-up of one year. J Spin Disord Tech 2003; 16:362–368.

28. Mayer HM, Wiechert K, Korge A, et al. Minimally invasive total disc replacement: surgical technique and preliminary clinical results. Eur Spine J 2002; 11(Suppl 2): S124–S130.

13. Bertagnoli R, Kumar S. Indications for full prosthetic disc arthroplasty: a correlation of clinical outcome against a variety of indications. Eur Spine J 2002; 11(Suppl 2): S131–S136.

29. Zigler JE, Sachs BL, Rashbaum RF, et al. Lumbar disc replacement with ProDisc: 24 to 36-month results of a prospective randomized comparison to fusion. Presented at the 3rd Trans Atlantic Spine Congress. November, 2005; Dallas, Texas.

14. Büttner-Janz K. Surgical Approach. In: Büttner-Janz K, Hochschuler SH, McAfee PC, eds. The artificial disc. Berlin: Springer Verlag; 2003:103–114.

30. Guyer RD, Sohn JM, Blumenthal SL, et al. Range of motion analysis of the lumbar spine after total disc replacement: a prospective two-year follow-up study. Presented at the annual meeting of the Spinal Arthroplasty Society. May, 2004; Vienna, Austria.

15. Brau SA. Mini-open approach to the lumbar spine for anterior lumbar interbody fusion: description of the procedure, results and complications. Spine J 2002; 2:216–223. 16. Cinotti G, David T, Postacchini F. Results of disc prosthesis after a minimum followup of 2 years. Spine 1996; 21:995–1000. 17. Lemaire JP, Skalli W, Lavaste F, et al. Intervertebral disc prosthesis – Results and prospects for the year 2000. Clin Orthop 1997; 337:64–76. 18. Keller J. Rehabilitation following total disc replacement surgery. In: Büttner-Janz K, Hochschuler SH, McAfee PC, eds. The artificial disc. Berlin: Springer Verlag; 2003:175–182. 19. Büttner-Janz K, Schellnack K, Zippel H, et al. Experience and results with the SB Charité lumbar intervertebral endoprostheses. Z Klin Med 1988; 43:1785–1789. 20. Griffith SL, Shelokov AP, Büttner-Janz K, et al. A multicenter retrospective study of the clinical results of the LINK SB Charité intervertebral prosthesis – The initial European experience. Spine 1994; 19:1842–1849. 21. David TJ. Lumbar disc prosthesis: five years follow-up study on 96 patients. Presented at the annual meeting of the North American Spine Society. 2000. 22. Sott AH, Harrison DJ. Increasing age does not affect good outcome after lumbar disc replacement. Int Orthop 2000; 24:50–53. 23. Lemaire JP, Carrier H, Sari E-H, et al. Clinical and radiological outcomes with the Chariteé™ Artificial Disc: A 10-year minimum follow-up. J Spinal Disord Tech 2005; 18:353–359. 24. Zeegers WS, Bohnen LM, Laaper M, et al. Artificial disc replacement with the modular type SB Charité III: 2-year results in 50 prospectively studied patients. Eur Spine J 1999; 8:210–217.

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25. Blumenthal S, McAfee P, Guyer R, et al. A prospective, randomized, multicenter Food and Drug Administration Investigational Device Exemptions study of lumbar total disc replacement with the Chariteé™ Artificial Disc versus lumbar fusion. Part I: Evaluation of clinical outcomes. Spine 2005; 30:1565–1575. 27. Marnay T. Lumbar disc replacement: 7 to 11-year results with Prodisc. Spine J 2002; 2:94S.

31. McAfee PC, Cunningham B, Holtsapple G, et al. A prospective, randomized, multicenter FDA IDE study of the Charité™ Artificial Disc: A radiographic outcomes analysis, correlation of surgical technique accuracy with clinical outcomes, and evaluation of the learning curve. Spine 2005; 30:1576–1583. 32. Huang R, Girardi F, Cammisa F Jr, et al. Long-term flexion–extension range of motion of the ProDisc total disc replacement. J Spinal Disord Tech 2003; 16: 435–440. 33. Sachs BL, Gottlieb J, Guyer RD, et al. Comparison of complications associated with total disc replacement versus lumbar fusion at two-year follow-up. Presented at the annual meeting of the Spinal Arthroplasty Society. May, 2004; Vienna, Austria. 34. van Ooij A, Oner FC, Verbout AJ. Complications of artificial disc replacement: a report of 27 patients with the SB Charité disc. J Spinal Disord Tech 2003; 16:369–383. 35. Enker P, Steffee A, McMillin C, et al. Artificial disc replacement – Preliminary report with a 3-year minimum follow-up. Spine 1993; 18:1061–1070. 36. Cummins BH, Robertson JT, Gill SS. Surgical experience with an improved artificial cervical joint. J Neurosurg 1998; 88:943–948. 37. Wigfield CC, Gill SS, Nelson RJ, et al. The new Frenchay artificial cervical joint: Results from a two-year pilot study. Spine 2002; 27:2446–2452. 38. Pointillart V. Cervical disc prosthesis in humans: First failure. Spine 2001; 26: E90–E92. 39. Bryan VE Jr. Cervical motion segment replacement. Eur Spine J 2002; 11(Suppl 2): S92–S97.

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Fusion – Minimally Invasive Techniques Hoang Le, Issada Thongtrangan and Daniel H. Kim

INTRODUCTION Minimally invasive spinal surgery strives to achieve the goals of surgery while minimizing the iatrogenic injury incurred during the exposure process. The development of the microscope, laser technology, endoscopy, video and image guidance systems provided the foundation for minimally invasive spinal surgery. Minimally invasive treatments have been made in all areas of the spinal axis since the twentieth century. Lumbar disc disease has been treated by using chemonucleolysis, percutaneous discectomy, laser discectomy, intradiscal thermoablation, and minimally invasive microdiscectomy techniques. The use of thoracoscopy initially for thoracic discs and tumor biopsies has expanded to include deformity correction, sympathectomies, resection of paraspinal tumors, and vertebrectomy with reconstruction and instrumentation. Laparoscopic techniques as used for appendectomies or cholecystectomies by general surgeons have evolved into use by spinal surgeons for anterior lumbar discectomy and fusion. Image-guided systems have been adapted to facilitate pedicle screw placement with increased accuracy. Over the past decade, minimally invasive treatment of cervical spinal disorders has become feasible using similar technologies as developed for the thoracic and lumbar spine. Endoscopically assisted transoral surgery, cervical decompression, and instrumentation all represent the continual evolution of minimally invasive spinal surgery. Further improvement in optics and imaging resources, development of new biological agents such as recombinant human bone morphogenetic protein (rhBMP), and the introduction of innovative instrumentation systems designed for minimally invasive procedures have expanded significantly over the past decade to make minimally invasive fusion possible. The authors will discuss different techniques of minimally invasive fusion as it pertains to each segment of the spinal column.

LUMBAR SPINE Minimally invasive PLIF and TLIF The concept of lumbar interbody fusion as initially described by Cloward in 1951 offers several advantages over the traditional posterolateral arthrodesis including a rich blood supply from the cancellous fusion bed, a load-bearing force occurring through the fusion bed, the ability to distract the disc space and neuroforamina, and the ability to restore segmental lordosis. Traditional open posterior lumbar interbody fusion (PLIF) procedures have been reported to yield successful outcomes in approximately 80% of patients with fusion rates near 90%. Since 2000, minimally invasive PLIF (MI-PLIF) procedures have been utilized to reduce iatrogenic injury incurred during the exposure process of the open procedure. Long-term follow-up data are lacking, but retrospective reviews of MI-PLIF performed with the microscope, premachined bone graft or cages,

virtual fluoroscope, and percutaneous pedicle screw system at greater than 1-year follow-up were reported to yield clinical improvement comparable to the open procedure.1,2

Minimally invasive TLIF using the METRx system Transforaminal lumbar interbody fusion (TLIF), a unilateral posterior approach for achieving an interbody arthrodesis, has gained recent popularity. The disc interspace is accessed by performing a unilateral facetectomy. As such, retraction of the nerve root is kept to a minimum, allowing for safer placement of the interbody graft. The METRx system (Medtronic Sofamor Danek, Memphis, TN) can be used for exposure of the disc space and completion of the facetectomy. Placement of premachined bone graft or cage supplemented with bone morphogenic protein can obviate the need for local autograft harvesting. Supplemental percutaneous pedicle fixation is added for completion of the TLIF procedure. The unilateral TLIF approach for interbody fusion offers several advantages over the PLIF technique. Nerve root and dural retraction are minimized because of the lateral entry point, reducing the risk of neural injury. This lateral entry point to the disc space also makes revision surgeries less difficult, as there is less need to mobilize nerve roots that may be surrounded by epidural scar tissue. A potential disadvantage of a unilateral TLIF is that direct nerve root decompression can only be performed unilaterally. However, with increasing use of the tubular retractor system, bilateral foraminal decompression and even laminectomy can be achieved via a unilateral approach.

Surgical technique An expandable tubular retractor (X-Tube, Medtronic Sofamor Danek, Memphis, TN) (Fig. 132.1) can be used to accomplish a minimally invasive TLIF. The tube is inserted at a diameter of 26 mm and is expanded in situ to a final working diameter of 44 mm (which can span from pedicle to pedicle). Use of an endoscope or the operating microscope is possible through this tubular retractor (Fig. 132.2A). The basic surgical set is essentially the same as a standard laminectomy/fusion set. It is important to have a high-speed telescoping drill (Midas Rex, Ft. Worth, TX) available as an aid for removing bone. Instruments should be bayoneted so that visualization of the operative field is not occluded down the barrel of the tubular retractor. The tools for disc space preparation prior to graft placement consist of distractors (7–14 mm), rotating cutters, endplate scrapers, and chisel. Many options exist for interbody graft material and can include bone or cages (with autologous bone or BMP-2 [Medtronic Sofamor Danek, Memphis, TN]). The operating room is arranged such that the operating table is in the center of the room, anesthesia at the head and fluoroscopy monitor at the foot. The C-arm base is placed on the side opposite of the

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Fig. 132.1 Expandable tubular retractors. The tube is inserted at a diameter of 26 mm and is expanded in situ to a final working diameter of 44 mm (which can span from pedicle to pedicle). Decompression, interbody fusion, and instrumentation are possible through the tube.

A

B

C

D

Fig. 132.2 (A) The use of the microscope is possible through the tube instead of an endoscope, reducing the learning curve necessary for performing minimally invasive procedures. (B) An interbody allograft is placed directly under visualization through the tubular retractor (C) Pedicle screw instrumentation can also be placed directly through the tube. (D) The ATAVI Flexposure cannula (Endius) system. 1398

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TLIF as is the video monitor. Equipment tables are kept behind the surgeon on the operative side and a Mayo stand is situated over the feet to pass instruments in active use. The patient is positioned prone on a radiolucent Wilson frame over a Jackson table.

Localization and exposure The region of pathology is localized with aid of fluoroscopy and a Steinman pin. Once marked, a stab incision is made 3 cm from midline, and the Steinman pin is inserted until it rests on bone. Ideally, the pin should be on the facet complex of the affected level and the skin incision extended to a length of 3 cm. Sequential tubular dilators are passed over one another and fluoroscopy is used to confirm adequate insertion. The appropriate-length working channel ( X-tube) is introduced over all the dilators, brought into line with disc space in a medial orientation and secured to the operating table with a flexible arm clamp. The X-tube working channel is opened to its full capacity, which should span the distance from pedicle to pedicle at the level of interest. Muscle and soft tissue are cleared from the lamina and facet with monopolar cautery. Next, the working channel is angled laterally, and the transverse processes are exposed. The tubular retractor is turned medially to begin the laminotomy and facetectomy. The decompression should extend from pedicle to pedicle in a rostral–caudal direction. Laterally, a total facetectomy is done to provide adequate space for graft placement and to minimize root retraction. Next, the ligamentum flavum is removed. Epidural veins are coagulated with bipolar cautery and divided if necessary. The lateral edge of the dura, the nerve root, and the disc space should be clearly visualized. The anulus is cut and disc material is removed with pituitary rongeurs. A down-angled curette is helpful to ensure that subligamentous disc fragments and the contralateral disc are properly removed. The disc space is sequentially dilated until disc space height is similar to adjacent levels. The maximum insertable dilator translates into the width of the interbody graft used. Next, the rotating cutter is introduced parallel with the disc space and rotated to start preparing the vertebral body endplates. The endplates are scraped, and debris is removed with a pituitary rongeur. A disc space chisel can be used to better prepare the endplates. A graft of surgeon’s preference can now be placed (see Fig. 132.2B). Medial angulation of the tube will allow for midline graft placement. One should also pack autologous laminofacet bone removed during the decompression, anteriorly into the disc space prior to graft placement. The X-tube can also be repositioned laterally if a unilateral intertransverse fusion is desired.

Instrumentation with sextant In conjunction with the use of the X-tube, pedicle screw placement can be performed percutaneously with use of the sextant instrumentation set (Medtronic Sofamor Danek, Memphis, TN). For use of a single fluoroscopy machine, the ‘bull’s eye’ technique for percutaneous pedicle screw placement is adequate and more straightforward. On the other hand, if triangulation of the pedicle screws is desired, biplanar fluoroscopy is used for placement in a manner similar to a vertebroplasty procedure. Alternatively, image-guided systems can be used depending on surgeon’s comfort and preference. For the ‘bull’s eye’ pedicle screw placement, the C-arm is rotated 90° for a true anteroposterior (AP) view parallel with the disc space. The bone biopsy needle is localized over the pedicle and passed through the soft tissue onto the pedicle so that the needle will appear as a single spot (‘bull’s eye’) in this orientation. The needle is taped into the pedicle with a mallet and position is confirmed by fluoroscopy. Then, with the needle held firmly in the correct orientation, the stylet is removed and a K-wire is drilled approximately 1 cm into the pedicle. The bone needle is removed and fluoroscopy is used to confirm that the K-wire is in the center of the

pedicle. The process is repeated for the contralateral pedicle and then for both pedicles at the adjacent affected level. The C-arm is brought to the lateral position for advancement of the K-wires to approximately two-thirds the length of the vertebral body parallel with the endplate. Soft tissue over the K-wires is dilated, the pedicles are taped, and cannulated screws are inserted. Attention is paid to the K-wire as accidental removal or advancement would be undesirable. The sextant device is attached to the screw extenders and pushed through the soft tissue to create a tract for the rod. The rod size is calculated by placing templates on the sextant at this point. The tip of the sextant is replaced with the rod, which is pushed through the soft tissue and both screw heads. The C-arm is brought to the AP orientation to confirm the rod has passed through both screw heads before tightening. The screws are then compressed, tightened, and broken off with a torque wrench. The sextant is disconnected from the rod and removed. The process is repeated on the opposite side. In essence, if percutaneous pedicle screw placement is not desired, surgical instruments and fixation can all be applied directly through the retractor port (see Fig. 132.2C). Examples of commercial access systems in addition to the METRx Minimal Access System (Medtronic Sofamor Danek; Memphis, TN), include the Access Port (Spinal Concepts; Austin, TX), the Nuvasive system (Nuvasive; San Diego, CA) and the ATAVI System (Endius; Plainville, MA). The central mechanism of each of these systems is fundamentally that of tubular dilation and a cylindrical working portal. Like the METRx Xpand system, the ATAVI Flexposure cannula (Endius) (see Fig. 132.2D) can expand its ultimate working diameter up to 40–60 mm for direct pedicle screw placement.

Laparoscopic anterior lumbar interbody fusion Prior to the 1980s, laparoscopic procedures were mainly used in the field of gynecology and urology. The transition into general surgery began in the 1980s when the first laparoscopic appendectomy was performed in Germany. In 1987, the first human laparoscopic cholecystectomy was performed in France.3 The widespread acceptance of this minimally invasive approach can best be appreciated by noting the fact that within only 3 years after its introduction, more than 90% of all cholecystectomies were being performed laparoscopically. The significant advantages of transperitoneal laparoscopic surgical treatment include marked reductions in postoperative pain, early hospital discharges, and reduced incidences of postoperative ileus. Anterior lumbar interbody fusion (ALIF) was initially described by Burns in 1933 for the treatment of spondylolisthesis.4 In 1995, Mathews et al.5 and Zucherman et al.6 described the technique in detail and published preliminary outcome data for laparoscopic anterior lumbar fusion. In 2000, Regan et al.7 published a prospective comparative study of open versus laparoscopic anterior lumbar fusion. They demonstrated that the laparoscopy group had a shorter hospital stay and reduced blood loss but had increased operative time. Operative time improved in the laparoscopy group as surgeons’ experience increased. Operative complications were comparable in both groups, with an occurrence of 4.2% in the open approach and 4.9% in the laparoscopic approach. Overall, the device-related reoperation rate was higher in the laparoscopy group (4.7% versus 2.3%). Conversion to open procedure in the laparoscopy group was 10%. A more recent study did not favor the video-assisted techniques and laparoscopic approach. Escobar et al.8 published a comparative analysis focusing on the complications of three techniques (a ‘minilaparotomy’ open extraperitoneal approach through a small midline incision, a transperitoneal video-assisted insufflation technique, and a video-assisted gasless) for anterior lumbar interbody fusion in 135 patients. The study revealed the highest incidence of complications in video-assisted 1399

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techniques and the laparoscopic approach. Complications are primarily related to surgical exposure of the anterior spine, which can include damage to important vascular structures, the sympathetic plexus, or the abdominal viscera. The main disadvantage of the laparoscopic approach is the steep initial learning curve of the surgical team. Additionally, the anterior approach to cage placement is limited in being able to directly decompress the spinal canal. However, with care in patient selection, a standalone interbody cage fusion has been successfully demonstrated. In order to evolve to the laparoscopic placement technique of interbody cages, the access surgeon and spine surgeon should work as a team using the open approach but practice placing the particular instrumentation system they plan to use laparoscopically. Lastly, in terms of initial case selection, begin with nondeformity L5–S1 cases, as this represents the ideal case for ALIF (both open and laparoscopic).

Surgical technique Preprocedural preparation is important in ensuring a neutral orientation of the spine and for obtaining intraoperative fluoroscopic images. Whether performed via an open or a laparoscopic approach, every millimeter of exposure will be essential for graft placement. The patient is positioned supine on a radiolucent operating table. The patient’s pelvis and lumbar spine are preferentially elevated from the surface of the operating table with folded blankets. This permits the arms to then be positioned along the patient’s side (tucked and padded) without obscuring the lateral fluoroscopic visualization of the symptomatic motion segment. The spine should not be placed into a position of lordosis by way of positioning. The ability to maneuver the C-arm into position, when visualizing the pathologic motion segment, must be assessed (especially in the Trendelenburg position used during the procedure). The AP view must also show a neutral motion segment rotation prior to proceeding. The bladder is decompressed with a Foley catheter, and the stomach with an orogastric tube so that they do not interfere with operative visualization and retraction. Positioning checks (i.e. padding of neurovascular structures/bony prominences, etc.) are also rechecked (recall that the laparoscopic procedure requires up to 30° of Trendelenburg position throughout its duration, as opposed to the open anterior application of the interbody cages).

Exposure For L4–5 and L5–S1 the standard portal placement includes a periumbilical laparoscopic portal, a 5 mm right and left-lower abdominal quadrant dissection/retraction portals, and a suprapubic working portal. The initial portals placed include the camera and right-left lower quadrant sites. Using these portals, the dissection is performed and the desired level exposed. Once the level is verified, the suprapubic working portal is then created. This portal should allow a colinear approach to the disc space, representing the orientation of the interbody cage within the disc space at final placement. The autonomic plexus rests in the retroperitoneal fat layer. The posterior retroperitoneum should be opened with laparoscopic scissors rather than with cautery so that the risk of retrograde ejaculation is minimized. Incise the posterior peritoneum to the right of the midline. Middle sacral vessels can be ligated and divided for both L4–5 and L5–S1 procedures. The iliolumbar vessel is ligated and divided mainly for L4–5 procedures. The entire width of the disc space should be exposed as much as possible. Depending on the specific cage system being used, the sequence of cage placement may vary. However, there are several aspects that are not system dependent. Throughout the procedure, the surgeon must verify the midline and the lateral margins of the entry sites 1400

for the cages. This will help ensure correct cage placement. Debris should be cleared following each step with pituitary rongeurs so that the anatomy is clearly visualized. Fluoroscopy will confirm the depth of rongeur insertion. The medial edge of the working cannula should approximate the midline disc mark. If a gap exists, the cannula has worked itself laterally. If the midline mark is covered by the cannula, the cages may impinge on one another. Carefully verify appropriate endplate preparation and engagement of the cages with the endplate using fluoroscopy so that placement of undersized cages can be avoided. Proceed with each step only after verifying adequacy of the laparoscopic exposure and retraction. Harvest iliac cancellous bone graft if a rhBMP-2 product such as InFuse (Medtronic Sofamor Danek, Memphis, TN) is not utilized.

Lumbothoracic cage insertion The midline of the disc space should be marked using AP fluoroscopy. Keep this midline mark in view throughout the procedure. The medial edge of the spinal working cannula should approximate this midline mark throughout the procedure. Open the right and left discal entry sites using the starting guide appropriate for the templated implant size. The largest size trephine that will fit in the disc space should be used. Clear the discal entry sites using the pituitary rongeurs. Disc space distraction is initiated on the right discal entry site using the distractor size appropriate for the templated cage size. Firm annular tensioning should be noted. If not, determine if a larger implant should be used. Seat the spinal working cannula over the distraction plug and remove the distractor. Ream the adjacent endplates through the right discal entry site at a parallel angle. Next, move to the left discal entry site and repeat the sequence of disc space preparation, distraction and endplate reaming on the left. Prepare the graft for implantation. Pack cancellous bone firmly within the cage; if rhBMP-2 is placed within the implants, do not use suction over the implants. The saved image of reaming depth should be noted to avoid trying to insert the device further and stripping the implant. Slightly recess the cage from the anterior vertebral margin on both sides, but maintain contact with the ring apophysis. Use the adjuster instrument to fine tune cage rotation and obtain final AP and lateral fluoroscopic images for assessment of cage placement. Closing the posterior peritoneum is preferred and may help avoid the risk of adhesions to the surgical site but is optional. Fascial openings are closed along with skin. Oral postoperative analgesics are typically sufficient and patient can be discharged when ambulatory, voiding, and tolerating oral intake.

Minimally invasive retroperitoneal lumbar fusion The retroperitoneal approach to the lumbar spine was first described by Iwahara in 1963 and is now being increasingly used for treatment of spondylolisthesis,9–11 degenerative disc disease,11 internal disc derangement,4,12 instability,14 and for reoperations.14,15 Endoscopic approaches to the retroperitoneal space, called ‘retroperitoneoscopy,’ were initially described by urological surgeons in the 1990s. Gaur16 and McDougall et al.17 first used balloon dissection of the retroperitoneal space to enable laparoscopic visualization of the surrounding anatomy. This eventually gave rise to applications for treatment of lumbar disease. The balloon-assisted endoscopic retroperitoneal gasless (BERG) procedure is a minimally invasive retroperitoneal approach to the anterior lumbar spine. A gasless retroperitoneal approach has further advantages. This procedure is similar to an open spinal procedure, and conventional instruments may be implemented. Valved trocars are not required and the complications involved with carbon dioxide insufflation are avoided. Advances in interbody cage technology and artificial discs have generated a great deal of interest in anterior

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lumbar fusion. Minimal access techniques to the anterior lumbar spine will be important in optimizing clinical outcomes in addition to preserving posterior load-bearing elements.

Gasless endoscopic ALIF (the BERG approach) The BERG approach utilizes a balloon to perform the initial dissection followed by a combination of a mechanical lifting arm and fan retractor to distend the abdomen without the use of gas insufflation. This is a true retroperitoneal approach to the anterior lumbar column, which allows for access up to L1. Because there are no pressurized ports with this approach, the surgeon can utilize standard anterior instruments for lumbar fusion surgery. There is no pneumoperitoneum to maintain so loss of exposure due to suction is not a problem. Vascular and bowel retraction are similar to an open anterior retroperitoneal approach.

Surgical technique The following instruments and equipment are used for the BERG approach to ALIF: clear-ended endoscopic dissecting port, 3 cm flexible nonvalved ports, dissecting balloon and inflator, laprolift mechanical arm, fan retractor, peritoneal balloon retractor, 0° endoscope, two video monitors, and standard set of instruments for anterior lumbar surgery. The patient is positioned supine. Fluoroscopy is used to find the landmarks of the appropriate lumbar level and the skin marked. These are drawn on the lateral aspect of the left abdomen, marking the angles of the appropriate disc spaces. A transverse, 2 cm left flank incision is made approximately 1 cm above the left iliac crest in the midaxillary line. The dissection is taken down through the external oblique, internal oblique, and transversus muscles under direct vision to the preperitoneal fat layer using a clear-ended, endoscopic dissecting port. As the preperitoneal fat layer is penetrated by the clear-ended dissecting port, there is a color change to yellow. The retroperitoneal space is then gently insufflated with a bulb syringe and digitally dissected into the iliac fossa to allow for balloon insertion. An elliptical-shaped preperitoneal balloon is advanced through the incision until the entire balloon is within the retroperitoneal space. A 0° angle endoscope is placed through the lumen of the dissection cannula and the balloon is expanded to an approximate volume of one liter. The endoscope is directed toward the anterior abdominal wall for the identification of the peritoneal reflection. The peritoneal reflection is used as a landmark for the anterior working port which is located lateral to the peritoneal reflection on the rectus sheath. A 2–3 cm paramedian incision is made through the anterior abdominal wall and carried down through the fascia, lateral to the peritoneal reflection so that the peritoneal sac is avoided. The balloon is removed after a 1 cm malleable retractor is placed between the two ports under direct endoscopic vision. There are three levels of retraction necessary to access the anterior lumbar spine. The first of these is distraction of the anterior abdominal wall. This is accomplished by the insertion of a fan retractor into the initial flank port. The fan retractor is expanded under direct endoscopic vision. Once expanded, the fan retractor is attached to a mechanical lifting arm. The abdominal wall is elevated by this combination, creating the retroperitoneal space and replacing the need for gas. A flexible nonvalved port, utilized for lateral visualization and retraction, is placed directly below the legs of the fan retractor to provide a clear path for the endoscope. The second level of retraction is necessary to displace the peritoneal contents past the midline to provide access to the lumbar spine and vascular anatomy. A long retractor with an inflatable end is inserted through the newly created lateral working port in the initial left flank incision to push the peritoneal sac and intra-abdominal contents aside, creating the working space (Fig. 132.3). Once the retractor is in place,

the technician stands with his or her abdomen against the retractor handle, leaving two hands free for endoscope operation. The remaining level of retraction is vascular. The L5–S1 vascular retraction begins by identifying the right iliac vein and utilizing a vascular retractor to retract the fascia and presacral veins thereby exposing the anterior aspect of the L5–S1 interspace. Through the visualization/retraction port, a standard vein retractor is passed and is used to retract the iliac vein laterally. The L4–5 exposure is more complex. It begins by utilizing an anterior vessel retractor and displacing the vena cava or left iliac vein. This is placed on tension and the iliolumbar vein is identified. If necessary, the iliolumbar vein is ligated using corporeal knot tying. Once the iliolumbar vein is ligated, gentle soft dissection is used to retract the left iliac vein, exposing the L4–5 interspace past the midline. The vascular retraction for L3–4 is performed in a similar way but does not require ligation of the iliolumbar vein. Following psoas dissection and vessel retraction, fluoroscopy is used to confirm the operative level. The anterior working port allows for both vascular retraction and the introduction of standard spinal instruments such as dissectors, rongeurs, curettes, and endplate elevators. The technique for ALIF is essentially the same as with an open anterior retroperitoneal approach.

THORACIC SPINE Video-assisted thoracoscopic surgery The history of thoracoscopy dates back to 1910 when Jacobaeus performed the first thoracoscopic and laparoscopic procedure.18 In 1990, the introduction of video imaging to standard endoscopy marked the modern era of thoracoscopic surgery. The technique of video-assisted thoracic surgery was first reported in 1993 by Mack et al.19 Video-assisted thoracic surgery has since played a major role in the treatment of thoracic disc herniations, treatment of spinal deformities requiring anterior release, and corpectomies for the treatment of vertebral body tumors.20–22 Several published reports demonstrated the efficacy of video-assisted thoracoscopic surgery for excision of thoracic disc herniations.23,24 Thoracoscopic spine surgery has also made treatment of hyperhidrosis possible in a minimally invasive way. Picetti et al.25 performed corrective surgeries with the thoracoscope in 50 patients who were diagnosed with thoracic scoliosis. Postoperative pain was less, as well as a shorter duration of postoperative analgesic use, in patients treated thorascopically as compared with patients treated with formal open procedures. In the trauma series reported by Khoo et al,26 371 patients with fractures of the thoracic and thoracolumbar spine (T3–L3) were treated with a thoracoscopically assisted procedure. Seventy-three percent of the fractures were located at the thoracolumbar junction. In 49% of patients, mobilization of the diaphragm was performed thoracoscopically to expose the fracture site. The severe complication rate was low (1.3%), with one case each of aortic injury, splenic contusion, neurological deterioration, Peritoneal contents

Balloon retractor

Fig. 132.3 Balloon retractor of the peritoneal contents used for the BERG ALIF procedure. 1401

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cerebrospinal fluid leak, and severe wound infection. Compared with a group of 30 patients treated with open thoracotomy, thoracoscopically treated patients required 42% less narcotics for pain treatment after the operation. A thoracoscopic approach can only access the anterior and anterolateral aspects of the vertebrae and spinal canal. It cannot adequately expose the posterior elements, the contralateral pedicle, or the transverse process. Thoracoscopic surgery, like endoscopic surgery, will require a steep learning curve but has the advantages of reducing post-thoracotomy pain syndromes and exposure-related morbidity.

Thoracoscopic decompression and fixation As an alternative approach to thoracotomy or thoracoabdominal approach, thoracoscopic technique can be used to perform thoracic corpectomy to decompress the spinal canal, to reconstruct and fixate the segments affected by destructive disease and trauma. Within the thoracic cavity, thoracoscopic access to the thoracic vertebrae T4–12 can be easily accomplished. By thoracoscopically detaching the diaphragm, L1–3 can be reached so that it is possible to expose the entire thoracolumbar area for a minimally invasive endoscopic procedure (Fig. 132.4A). Thus, the thoracic spine as well as upper lumbar spine from T4 to L3 is accessible endoscopically using the thoracoscopic technique.

preferred for the treatment of pathologies from T4 to T8. A rightsided approach is preferred for exposing the thoracolumbar junction (T9–L3). The upper arm is abducted and elevated so that it does not interfere with the placement and manipulation of the endoscope. The surgeon stands behind the patient. The surgical technique of thoracoscopic spine surgery is described in detail by various authors.26–28 Early on in the authors’ experience, they often reserved the thoracoscopic approaches for thoracic pathologies involving the T4 to T10 vertebrae. With increasing experience, the authors extended the indications to pathologies involving the thoracolumbar junction.

Localization The target area is projected onto the skin level under fluoroscopic control. The borders of the involved vertebra are marked on the skin. The working channel is centered over the target vertebra (12.5 mm). The optical channel (10 mm) is placed between two and three intercostal spaces cranial to the target vertebra in the spinal axis. For approaching upper and middle thoracic spine, the optical channel is placed caudal to the target vertebra. The approach for suction/irrigation (5 mm) and retractor (10 mm) is placed approximately 5–10 cm anterior to the working and optical channels.

Surgical technique

Placement of portals

Lung isolation with double lumen endotracheal intubation will be required for the thoracoscopic procedure. The patient is placed in a lateral position on a Jackson spinal table. A left-sided approach is

The position of the portals in relation to one another and to the operating site on the spine influences the entire course of the operation. The operating portal is the first position to be marked exactly over the target

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Fig. 132.4 (A) Thoracoscopic detachment of the diaphragm allows exposure of the thoracolumbar junction down to L2–3, making stabilization of this area possible in a minimally invasive manner. (B) Thirty degree endoscope used for thoracoscopic procedures. 1402

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C

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Fig. 132.4 Cont’d (C) Thoracoscopic instrumentation of the thoracolumbar junction using the MACS-TL system. (D) Thoracoscopic incisions seen at 2 weeks postoperatively.

area, and then, corresponding to this, the portal for the optic is drawn in over the spine, two or three intercostals spaces above the mark for the operating portal, for thoracolumbar access, or underneath it for access to the central or upper thoracic spine. Portal for the suction and irrigation instrument is about four fingerbreadths from the operating portal in a ventral and cranial direction. The portal for the diaphragm or lung retractor should be placed as far as possible ventrally to avoid instruments coming into conflict. Lung isolation should start prior to incision. Subsequently, the most cranial portal (optical channel) should be placed first. Through a 1.5 cm skin incision above the intercostal space, a muscle-splitting technique is used to bluntly open into the intercostal space. A 10 mm trocar is inserted into the thoracic cavity. A 30° endoscope is inserted at a flat angle in the direction of the second trocar (see Fig. 132.4B). Perforation of the thoracic wall to insert the remaining trocars is performed under direct intrathoracic visualization through the scope.

Prevertebral dissection and diaphragm detachment A fan retractor inserted through the anterior port can retract the diaphragm and exposes the insertion of the diaphragm onto the spine. Total detachment of the diaphragm is not necessary for exposure of the thoracolumbar junction. A diaphragmatic opening of about 6–10 cm can expose the entire L2 vertebral body. The anterior circumference of the motion segment can be palpated with a blunt probe. The line of dissection for the diaphragm is ‘marked’ with monopolar cauterization. The diaphragm is then incised using endo-scissors. A rim of 1 cm is left on the spine to facilitate closure of the diaphragm at the end of the procedure. Retroperitoneal fat tissue is now exposed and mobilized from the anterior surface of the psoas insertions. The psoas muscle is dissected very carefully from the vertebral bodies in order not to damage the segmental blood vessels ‘hidden’ underneath. The retractor is now placed into the diaphragmal gap.

Corpectomy and decompression of the spinal canal The extent of the planned partial vertebrectomy is defined with an osteotome. The disc spaces are opened to define the borders. After resection of the intervertebral disc(s), the fragmented parts of the vertebra(e) are removed carefully with rongeurs. Resection close to the spinal canal is facilitated with the use of high-speed burrs. If decompression of the spinal canal is necessary, the lower border of the pedicle should first be identified with a blunt hook. The base of the pedicle is then resected in a cranial direction with a Kerrison rongeur and the thecal sac can be identified. Finally, the posterior fragment that occupies the spinal canal can be removed.

Bone grafting/cage placement Preparation of the graft bed is then completed and the length and the depth of the bone graft are measured with a caliper. A tricortical bone is taken from the iliac crest. The bone graft is prepared for insertion and mounted on a graft holder. The working portal is removed and a speculum is inserted. This allows the insertion of a bone graft up to 1.5 cm in length into the thoracic cavity. If the bone grafts are longer, they are inserted without the use of the speculum, but with the help of Langenbeck hooks. In these cases, they are mounted on the graft holder inside the thoracic cavity. The bone graft is inserted by press-fit into the graft bed. If slight reduction maneuvers are necessary, this can be achieved by manual pressure on the spinous processes of the involved segment, thus creating a segmental lordosis.

Screw/plate/rod placement Thoracoscopic instrumentation can be performed via available systems (i.e. MACS-TL, Frontier) and invariably involves the use of 1403

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cannulated top loading screws. Plates or rods can be used to interlink the screws for final stabilization (see Fig. 132.4C).

expandable access portals (e.g. FlexPosure (Endius; Plainville, MA) and Xpand (Medtronic Sofamor Danek; Memphis, TN), up to three lateral masses can be instrumented through a single exposure.

Closure The gap in the diaphragm is closed with staples or adaptive sutures using endoscopic technique. The thoracic cavity is irrigated, blood clots are removed, and a chest tube is inserted with the end placed in the costodiaphragmatic recess. The portals are closed with sutures after removal of the trocars (see Fig. 132.4D).

CERVICAL SPINE Percutaneous endoscopic cervical discectomy and stabilization Percutaneous endoscopic cervical discectomy (PECD) is a new surgical method for treating soft cervical disc herniations. Specially designed expandable holders can be used as interbody spacers to achieve stability without open discectomy fusion, thus avoiding many approach-related complications seen with open techniques. The goal of the procedure is decompression of the spinal nerve root by percutaneous removal of the herniated mass and shrinkage of the nucleus pulposus under local anesthesia. The minimally invasive PECD under local anesthesia offers an alternative to open therapeutic methods in cervicobrachial neuralgia or radiculopathy due to soft cervical disc herniation. In cases of failure, PECD does not impede conventional surgical approaches, and it offers numerous advantages such as the absence of risk of epidural bleeding and periradicular fibrosis, maintenance of stability of the intervertebral mobile segment, and reduced risk for recurrence after performing an anterior discal window. The procedure provides an excellent cosmetic effect, and the reduced operation time and hospital stay allows the patient to recover to normal daily activity more rapidly. Although PECD provides an effective and attractive alternative to open discectomy and fusion, it has limitations. For example, PECD is ineffective in the presence of segmental instability or cervical discogenic pain syndromes. Spinal stabilization performed by conventional open procedures, however, often requires an extended pathway through the neck to insert the fusion/spacer devices into the disc space.

Minimally invasive cervical lateral mass screw fixation Although not without its limitations, posterior cervical instrumentation can also be accomplished via a minimally invasive approach. A ‘novel’ surgical technique of lateral mass screw fixation through a special tunnel retractor has recently been described (Fig. 132.5A). The procedure is performed in the prone position with the use of tubular retractors introduced at two or three levels below the area of pathology at an angle used for placement of the lateral mass screws. Dorsal elevation of the retractor system will provide room for placement of the rod. This technique can be applied to three contiguous cervical levels. Newer lateral mass instrumentation systems utilize two rods and variable polyaxial screw islets at each level. These include the CerviFix system (Synthes; Paoli, PA), StarLock System (Synthes; Paoli, PA), Summit System (Depuy Acromed), and Vertex (Medtronic Sofamor Danek; Minneapolis, MN). These systems vary by the angulation of their screws as well as in the degree of the constraint placed at the screw–rod interface. The polyaxial connectors of the screws are able to angle medially, laterally, and straight with varying degrees of rotational freedom in each direction. As such, segmental fixation is more easily achieved via a top-loading approach, thereby making minimally invasive posterior cervical fixation possible (see Fig. 132.5B). With the advent of some of the newer types of 1404

VERTEBROPLASTY/KYPHOPLASTY Although not a fusion procedure in itself, vertebroplasty/kyphoplasty may obviate the need for a stabilization procedure via a minimally invasive way. Developed in France in the late 1980s, minimally invasive vertebroplasty involves the percutaneous injection of polymethyl methacrylate (PMMA) into a fractured vertebral body.30 Although this does not reexpand a collapsed vertebra, reinforcing and stabilizing the fracture seems to alleviate pain. The procedure was first used to treat aggressive vertebral hemangiomas30 and was later applied to other lesions that weaken the vertebral body, including osteolytic metastases31–34 and osteoporotic vertebral collapse. Although the European experience with vertebroplasty in the setting of spinal metastases and myeloma is more extensive, the indications for treatment in North America are currently heavily weighted toward osteoporotic bone disease. Percutaneous balloon

A

B

T1 – T3

Fig. 132.5 (A) Lateral mass screws placed through a tubular retractor for unilateral jumped facets. (B) Top-loading polyaxial screw design facilitates placement via a minimally invasive technique.

New Frontiers

kyphoplasty is a recent modification of the vertebroplasty technique and involves inflation of a balloon within a collapsed vertebral body to restore height and reduce kyphotic deformity followed by stabilization with PMMA. The risk of cement extravasation is theoretically reduced because the balloon creates a void within the vertebral body into which cement can be injected under relatively low pressure. In addition to PMMA and bone mineral cement, several alternative biological materials have been used in attempts to augment compromised vertebral bodies. The efficacy of osteoinductive growth factors (transforming growth factor-γ, bone morphogenetic protein-2, and bone morphogenetic protein7) in enhancing arthrodesis is currently being studied among patients undergoing spinal instrumentation.

IMAGING GUIDANCE-ASSISTED SURGERY Since its introduction, transpedicular screw fixation has been extensively utilized in various spinal disorders to promote fusion and stabilization. Screw misplacement can lead to undesirable neurovascular complications. Pedicle screw placement in patients with deformities carries an even greater risk of serious complications. Weinstein et al.35 reported pedicle cortex violation in close to 20% of these cases. To increase the accuracy of screw placement, various methods have been used to better target the pedicle with respect to the trajectory and depth of screw placement. Image-guided systems are widely used in intracranial surgery and have been adapted to assist with screw placement since the middle 1990s.36,37 The use of image-guided systems for pedicle screw placement has improved the accuracy of placement. The system relies on precise localization of the pedicles with computed tomography. Furthermore, by replacing direct visualization with radiographic visualization, it has enabled a reduction in surgical exposure, duration, and blood loss. Foley et al.1 described ‘virtual fluoroscopy’ and its successful use in various spinal procedures including pedicle screw insertion, interbody cage placement, odontoid screw insertion, and atlantoaxial transarticular screw fixation. Nolte et al.37 described the principles of computer-assisted pedicle screw fixation. An infrared camera (Optotrak; Northern Digital, Waterloo, Canada) tracked specific instruments (pedicle probe, awl, and space pointer) equipped with light-emitting diodes. The dynamic reference was fixed to the spinous process of the vertebra to be instrumented. Normal bony landmarks and their correlations with the images confirmed the calibration accuracy. Using that computerized system, Nolte et al.37 reported a pedicle screw misplacement rate of 4.3% under clinical conditions. In contrast, Choi et al.38 reported the use of computer-assisted fluoroscopic targeting for pedicle screw fixation. The authors compared the accuracy of pedicle screw placement with the fluoroscopy-guided system versus the image-guided system and observed no significant differences. Recent development of isocentric C-arm fluoroscopy, which generates CT images using an intraoperative fluoroscope, may offer another means of three-dimensional navigation using a two-dimensional intraoperative imaging source. With increasing familiarity, image-guided surgery will be a very useful adjunct to the further development of minimally invasive surgery.

CONCLUSION Rapid technological advancements of the last two decades have made minimal-access surgery possible. Virtually, all aspects of the spinal axis can be approached and treated in a minimally invasive approach. Core to the concept of minimally invasive surgery is the reduction of iatrogenically induced injury while achieving the goals of the performed surgery. With the innovation of better optics and video equipments, retractor and instrumentation systems, image guidance systems, and new biologic agents, the majority of traditional ‘open’ spinal procedures

can now be performed with minimal invasion. For most minimally invasive surgery procedures, however, long-term prospective, controlled data are still lacking. In addition, the use of new technology will require a new learning curve that may be initially discomforting for many surgeons. Nevertheless, proper patient selection for minimally invasive procedures remains paramount for optimizing clinical outcomes.

References 1. Foley KT, Gupta SK. Percutaneous pedicle screw fixation of the lumbar spine: Preliminary clinical results. J Neurosurgery (Spine 1) 2002; 97:7–12. 2. Foley KT, Holly LT, Schwender JD. Minimally invasive lumbar fusion. Spine 2003; 28:S26–S35. 3. Dubois F, Icard P, Berthelot G, et al. Coelioscopic cholecystectomy: Preliminary report of 36 cases. Ann Surg 1990; 211:60–62. 4. Burns BH. An operation for spondylolisthesis. Lancet 1933; 1:1233. 5. Mathews HH, Evans MT, Molligan HJ, et al. Laparoscopic discectomy with anterior lumbar interbody fusion: A preliminary review. Spine 1995; 20:1797–1802. 6. Zucherman JF, Zdeblick TA, Bailey SA, et al. Instrumented laparoscopic spinal fusion: Preliminary results. Spine 1995; 20:2029–2034. 7. Regan JJ, Yeun H, McAfee PC. Laparoscopic fusion of the lumbar spine: minimally invasive spine surger. a prospective multicenter study evaluating open and laparoscopic lumbar fusion. Spine 2000; 25:509–515. 8. Escobar E, Transfeldt E, Garvey T, et al. Video-assisted versus open anterior lumbar spine fusion surgery: A comparison of four techniques and complications in 135 patients. Spine 2003; 28:729–732. 9. Kim SS, Denis F, Lonstein JE, et al. Factors affecting fusion rate in spondylolisthesis. Spine 1990; 15:977–984. 10. Sacks S. Anterior interbody fusion of the lumbar spine: Indications and results in 200 cases. Clin Orthop 1966; 44:163–170. 11. Stauffer RW, Coventry MB. Anterior interbody lumbar spine fusion. J Bone Joint Surg [Am] 1972; 54A:756–768. 12. Calandruccio RA, Benton BF. Anterior lumbar fusion. Clin Orthop 1964; 35:63–68. 13. Harmon PH. Anterior extraperitoneal lumbar disk excision and vertebral fusion. Clin Orthop 1960; 18:169–198. 14. Sorensen KH. Anterior interbody lumbar spine fusion for incapacitating disc degeneration and spondylolisthesis. Acta Orthop Scand 1978; 49:269–277. 15. Takahashi K, Kitahara H, Yamagata M. Long-term results of anterior interbody fusion for treatment of degenerative spondylolisthesis. Spine 1990; 15:1211–1215. 16. Gaur DD. Laparoscopic operative retroperitoneoscopy: Use of a new device. J Urol 1992; 148:1137–1139. 17. McDougall EM, Clayman RV, Fadden PT. Retroperitoneoscopy: The Washington University Medical School experience. Urology 1994; 43:446–452. 18. Savitz MH, Chiu JC, Yeung AT. The practice of minimally invasive spinal technique. Richmond: AAMISMS Education Press; 2000. 19. Mack MJ, Regan JJ, Bobechko WP, et al. Application of thoracoscopy for diseases of the spine. Ann Thorac Surg 1993; 56:736–738. 20. McAfee PC, Regan JJ, Zdeblick T, et al. The incidence of complications in endoscopic anterior thoracolumbar spinal reconstructive surgery. A prospective multicenter study comprising the first 100 consecutive cases. Spine 1995; 20:1624–1632. 21. Nymberg SM, Crawford AH. Video-assisted thoracoscopic releases of scoliotic anterior spines. AORN J 1996; 63:561–576. 22. Regan JJ, Mack MJ, Picetti G. A technical report of video-assisted thoracoscopy ( VATS) in thoracic spinal surgery: Preliminary description. Spine 1995; 20: 831–837. 23. Horowitz MB, Moossy JJ, Julian T, et al. Thoracic discectomy using video assisted thoracoscopy. Spine 1994; 19:1082–1086. 24. Rosenthal D, Rosenthal R, De Simone A. Removal of a protruded thoracic disc using microsurgical endoscopy. Spine 1994; 19:1087–1091. 25. Picetti GD, Pang D, Bueff HU. Thoracoscopic techniques for the treatment of scoliosis: early results in procedure development. Neurosurgery 2002; 51:978–984. 26. Khoo LT, Beisse R, Potulski M. Thoracoscopic-assisted treatment of thoracic and lumbar fractures: a series of 371 consecutive cases. Neurosurgery 2002; 51(5 Suppl):104–117. 27. Beisse R, Potalski M, Temme C, et al. Endoscopically controlled division of the diaphragm. A minimally invasive approach to ventral management of thoracolumbar fractures of the spine. Unfallchirurg 1998; 101:619–627.

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Part 7: New Frontiers 28. Beisse R, Potulski M, Buhren V. Endoscopic techniques for the management of spinal trauma. Eur J Trauma 2001; 27:275–291.

33. Martin JB, Jean B, Sugiu K, et al. Vertebroplasty: Clinical experience and follow-up results. Bone 1999; 25(Suppl 2):11S–15S.

29. Wang MY, Prusmack CJ, Green BA, et al. Minimally invasive lateral mass screw in the treatment of cervical facet dislocations: technical note. Neurosurgery 2003; 52:444–447.

34. Weill A, Chiras J, Simon JM, et al. Spinal metastases: Indications for and results of percutaneous injection of acrylic surgical cement. Radiology 1996; 199:241–247.

30. Deramond H, Depriester C, Galibert P, et al. Percutaneous vertebroplasty with polymethylmethacrylate: Technique, indications, and results. Radiol Clin North Am 1998; 36:533–546. 31. Barr JD, Barr MS, Lemley TJ, et al. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine 2000; 25:923–928. 32. Cotten A, Dewatre F, Cortet B, et al. Percutaneous vertebroplasty for osteolytic metastases and myeloma: Effects of the percentage of lesion filling and the leakage of methyl methacrylate at clinical follow-up. Radiology 1996; 200:525–530.

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35. Weinstein JN, Spratt KF, Spengler D, et al. Spinal pedicle fixation: Reliability and validity of roentgenogram-based assessment and surgical factors on successful screw placement. Spine 1988; 13:1012–1018. 36. Glossop ND, Hu RW, Randle JA. Computer-aided pedicle screw placement using frameless stereotaxis. Spine 1996; 21:2026–2034. 37. Nolte LP, Zamorano LJ, Jiang Z, et al. Image-guided insertion of transpedicular screws: A laboratory set-up. Spine 1995; 20:497–500. 38. Choi WW, Green BA, Levi AD. Computer-assisted fluoroscopic targeting system for pedicle screw insertion. Neurosurgery 2000; 47:872–878.

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Endoscopic Discectomy and Foraminal Decompression Anthony T. Yeung and Christopher Alan Yeung

INTRODUCTION Endoscopic disc surgery is evolving rapidly because of improvements in surgical technique, endoscope design, adjunctive surgical tools, and instrumentation. New endoscopes and complementary surgical devices enhance the endoscopic spine surgeon’s ability also to probe spinal anatomy in a conscious patient. The surgeon can then evolve his or her diagnostic and surgical skills with this newly found ability to evaluate pathologic, anatomic, and physiologic processes causing the patient’s pain. Now that diagnostic spinal endoscopy can be performed, conditions previously not even considered for surgery may be probed, evaluated, and surgically treated, and perhaps with greater accuracy. We believe that our understanding of discogenic back pain is enhanced by this ability to endoscopically visualize lesions not previously seen intradiscally and in the ‘hidden’ extra-foraminal zone.1 Spinal endoscopy is poised to parallel the development and evolution of knee, shoulder, and ankle arthroscopy.2 Without endoscopy, spine surgeons must depend heavily on imaging systems that, while extremely sensitive in identifying pathologic conditions, do not always correlate that condition with the patient’s pain.

Interventional pain management complementing endoscopic surgery Foraminal epidurography and foraminal therapeutic injections can be performed using a needle technique that mimics the surgical approach to the foramen and spinal canal.3 The approach differs from traditional interventional pain management ‘down the tunnel’ approaches because it is the same far lateral approach used by endoscopic spinal surgeons to access the foramen for endoscopic surgery. The tip of the needle is directed into Kambin’s triangle between the exiting and traversing nerve root, rather than at the shoulder of the exiting nerve root. If non-ionic contrast agent (i.e. Isovue 300) is injected to outline the foramen, it should be able to identify the location and position of the traversing and exiting nerves that cross each spinal level (Fig. 133.1). Anomalous configurations such as conjoined nerves or furcal nerves provide additional information regarding the anatomy of the lumbar spine. In fact, these anomalies are rarely observed with magnetic resonance imaging (MRI) but are routinely visualized with spinal endoscopy in the ‘hidden zone’ or far lateral zone of the foramen.1,18,19 Diagnostic and therapeutic information gleaned from these modified injection procedures can be used by the surgeon to better select patients for surgical intervention. Patients with symptomatic disc protrusions, annular tears, and foraminal stenosis may first be diagnosed by discography followed by foramino-epidurography, then get relief with the therapeutic foraminal injection. If the response is favorable but short lived, the diagnostic and therapeutic process will help the surgeon with patient selection. As a bonus, the epidurogram will help determine the ease and feasibility of endoscopic surgery because it allows for a trial needle placement into the foramen before surgical intervention.

Fig. 133.1 This foraminal epidurogram outlines the traversing nerve and exiting nerve. Needle placement is at the axilla of the exiting nerve root, between the exiting and traversing nerve root. The exiting nerve is partially obstructed by a foraminal osteophyte causing lateral recess stenosis.

Endoscopic surgery following injection therapy Patients who experience temporary relief with injection procedures directed toward the pain generator may realize definitive relief with endoscopic or surgical correction of the pathoanatomy. Our treatment process entails directing a needle to the pain generator, desensitizing or anesthetizing it, dilating a path that will allow a tubular retractor to be inserted, followed by an operating endoscope. Evocative discography™ is helpful in identifying the disc as a pain generator in axial back pain and sciatica.4 When spinal endoscopy and probing complements discography performed with the patient in an aware state, the pathoanatomy and normal anatomy can be visually correlated with imaging studies. In the authors’ experience, new information or information different from the MRI interpretation occurs 30% of the time.4

INDICATIONS In general, the indications for diagnostic and/or therapeutic endoscopy require a pathologic lesion that is accessible, visible, treatable, or requires endoscopic confirmation through the foramen.5 Limitations of the surgeon’s skill and/or experience with the endoscopy or difficult spinal anatomic are the primary contraindications, exclusive of comorbidities such as infection or uncontrolled coagulopathy.6 For herniations from T10 to L4, the foraminal approach provides excellent access to the disc and epidural space (Fig.133.2). At L5–S1, anatomic restrictions may cause the surgeon to opt for the posterior transcanal approach. As surgeon experience increases, anatomy that previously precluded spinal endoscopy is no longer a barrier.7 1407

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Traditional surgical approaches to far lateral, extraforaminal disc herniations are more difficult, requiring a paramedian incision through the vascular intertransverse ligament. This surgical area is often termed the ‘hidden zone.’1 Although the lateral zone of the disc can be accessed with a paramedian incision, in our view, it is easier to access the extraforaminal zone endoscopically via the posterolateral portal. A typical foraminal view of nucleus pulposus extruded past the posterior annulus is shown (Fig. 133.4). In our experience, this is the preferred approach for disc herniations in the upper lumbar and lower thoracic spine since the transcanal approach will require more extensive laminectomy that may destabilize the spinal segment if the herniation is above L3–4.

Discitis

Fig. 133.2 Anatomy of the posterolateral foraminal portal from L2 to S1. Only in the L5–S1disc space is access to the spinal canal restricted due to the pelvis and the relatively wide facet (gray hubbed needle in the L5–S1 disc). High lumbar disc herniations from L1 to L3 are easier to reach endoscopically through the posterolateral foraminal portal. L4–5 provides ample room for either approach. Note the furcal nerve branches entering the psoas muscle.

Anatomic structures within reach of the spine endoscope transforaminally are illustrated in Figure 133.3.

Disc herniation Symptomatic disc herniation is the most common indication, with surgical decompression limited only by the accessibility of endoscopic instruments to the herniated fragment.8,9 The posterolateral foraminal approach is ideal for a far lateral, extraforaminal disc herniation.

Fig. 133.3 The dome. Spinal structures in the foramen accessible to visualization and surgical intervention and probing via the posterolateral approach. 1408

Endoscopic excisional biopsy and disc space debridement is ideal for surgically debriding infectious discitis (Fig. 133.5).10 With this technique the surgeon will not have to be overly concerned about creating dead space for the inflamed or infected disc material to spread into the dead space created by a posterior approach. The clinical results are dramatic and, we believe, tissue biopsy is more accurate than needle aspiration in identifying the cause of discitis. In our experience, even sterile discitis will benefit from intradiscal debridement and irrigation.

Lateral recess and central stenosis Endoscopic foraminoplasty by endoscopic techniques can be accomplished by experienced endoscopic surgeons.6,11,12 Although trephines, rasps, and burrs can be utilized, the Ho:YAG laser has enhanced the procedure technically, as laser is a very precise cutting tool for visually controlled soft tissue and bone ablation. Endoscopic laser foraminoplasty (ELF) has an inherent advantage over classic surgery as it will not produce further instability (Fig. 133.6).13 With endoscopy, the foramen can be enlarged up to 45.5% versus the 34.2% attainable with the standard posterior technique of removing only the medial one-third of the facet. As well, posterior decompression of the lamina with removal of the medial one-third of the facet will produce increased extension and axial rotation postoperatively.13 In comparison, endoscopic foraminoplasty has not been shown to

Fig. 133.4 Foraminal view of the decompressed traversing nerve after extraction of a large extruded subligamentous disc herniation through the posterior annulus at L5–S1. The indigo carmine dye stained the nucleus pulposus and disc fragment for easier identification and extraction. The fragment clearly extruded through the posterior annulus and was extracted from the ventral portion of the traversing nerve.

New Frontiers

usually due to impingement on the exiting nerve by the pars pseudoarthrosis defect. The goal in this instance is to decompress the compromised exiting nerve by elevating the dome formed by the undersurface of the superior articular facet and lamina without further destabilizing the spinal segment (Fig. 133.7).

Recurrent disc herniation

Fig. 133.5 Intradiscal view of discitis after partial debridement. Inflammatory tissue and loose endplate cartilage are usually visualized and readily removed from the disc space with pituitary rongeurs and automated shavers. Pain relief is immediate, and abundant tissue is available for laboratory analysis. Discitis is often sterile, or nonsuppurative, even when sufficient inflammatory tissue is removed for culture. The incidence of discitis following endoscopic disc surgery is about 0.3%.

We have observed that patients with recurrent pain following a discectomy may have a small and seemingly trivial recurrent disc herniation. In these cases, the recurrent disc herniation may cause pain out of proportion to the size of the herniation. This is, we suspect, due to either direct contact of the inflammation producing nucleus pulposus to the nerve or the traversing nerve being tethered to the epidural scar, resulting in the inability of the nerve to give way to the disc fragment. Posterolateral endoscopic discectomy avoids dissecting through scar tissue from the previous trans-canal posterior approach. The surgeon is also able to access the disc through virgin tissue and grab the herniated nucleus from the ventral side and remove it. In endoscopic discectomy, especially with indigo carmine staining, the fragment is readily visible for extraction through the foramen. The results of endoscopic decompression for previous transcanal or endoscopic discectomy is as good as the original index procedure.12,14

CURRENT IMAGING METHODS In the authors’ experience, our imaging studies are only about 70% accurate and specific for predicting pain.5,12,14–17 Conditions such as lateral annular tears, rim tears, endplate separation, small subligamentous disc herniations, anomalous nerves in the foramen, and miscellaneous discogenic conditions are cumulatively missed about 30% of the time. These conditions are diagnosable and often treatable with spinal endoscopy. Tears that are in the lateral and ventral aspect of the disc are sometimes missed by MRI studies. Very small disc herniations that protrude past the outer

Fig. 133.6 The technique of endoscopic foraminal decompression. The superior articular process can be decompressed by rotating the open face of the cannula against the base of the facet while the ventral half of the cannula protects the exiting nerve. The decompression continues cephalad toward the tip of the facet and the exiting nerve, resecting the ligamentum flavum attachment that can impinge on the axilla, causing symptomatic lateral recess stenosis. Just resecting the capsule and releasing the ligamentum flavum may be enough to enlarge the foramen and free the traversing as well as the exiting nerve. This foraminal endoscopic view at L5–S1 demonstrates how a diamond burr is used to decompress the ventral surface of the superior facet. The exiting nerve is at 9 o’clock.

cause increased instability, even in spondylolisthesis.12 The technique is most useful for lateral recess stenosis. In central spinal stenosis, when there is concomitant posterior disc protrusion, decompression of the spinal canal can be effectively accomplished by resecting the bulging annulus in a collapsed disc, thus lowering the floor of the foramen without destabilizing the spinal segment. In isthmic spondylolisthesis, when there is more leg pain than back pain, this is

Fig. 133.7 Illustration of side firing laser ablating bone under the superior articular process. 1409

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fibers of the annulus are also missed, since the fragment may be flattened against the posterior longitudinal ligament or nerve, appearing on the MRI as a thickened or bulged annulus, but really containing a subligamentous herniation. In rare circumstances, when the nerve root appears ‘swollen’ or enlarged, the MRI may not be capable of distinguishing a swollen nerve from a conjoined nerve or a nerve with an adherent fragment of disc. Endoscopy allows for direct visualization of such a ‘swollen root,’ thereby enhancing our ability to diagnose and subsequently treat this entity. We have observed that when the disc tissue is in direct contact with a nerve, the nerve can be irritated and a painful inflammatory membrane forms. When an inflammatory membrane is present, the pain pattern can be confusing. Diagnostic spinal endoscopy has confirmed ‘nondermatomal’ pain in scores of patients with proximal thigh, buttock, and groin pain at levels distal to the root origin of the anatomic area. Removal of the source of irritation can diminish or abate painful symptoms.

The role of intraoperative Evocative Chromodiscography™

A

If a vital dye is used to effect differential staining in the disc and epidural space intraoperatively, it is easier to recognize degenerative nucleus pulpolsus from normal nucleus, and the anulus and from facet capsule.4 The epidural space with its epidural vessels and fat become easy to differentiate and recognize. I trademarked evocative chromodiscography™ as an integral part of spinal endoscopy. The process of removing the indigo carmine dye-labeled nucleus was trademarked selective endoscopic discectomy™ to describe the technique (see Fig. 133.5).12

Future considerations It is conceivable that the spine scope will eventually be used for all conditions where endoscopic visual inspection is desired. The authors have utilized spinal endoscopy to inspect a spinal nerve suspected to be irritated by orthopedic hardware adjacent to the pedicle, to remove suspected recurrent or residual disc herniations that do not show up on imaging studies, to decompress the lateral recess by endoscopic laser foraminoplasty, to remove osteophytes and facet cysts that cause unrelenting sciatica, and to locate painful lateral annular tears or small disc herniations not evident on physical examination or on MRI. Some of these correctable lesions are responsible for failed back surgery syndrome (FBSS), especially with recurrent disc herniations and with lateral recess stenosis. The lateral ‘hidden zone’ is rarely visualized by surgeons. It has been demonstrated that, with endoscopy, it is possible to do isolated disc and annulus surgery using a visualized thermal modulation procedure (Fig. 133.8), challenging the old concept that disc surgery is merely nerve decompressive surgery. For example, discogenic pain from annular tears is currently being evaluated and correlated with the pathoanatomic conditions visualized.18,22–32

Nonoperative treatment Nonoperative medical rehabilitation and interventional spine treatments are a large component in the treatment of painful spinal disorders. Physicians specializing in spinal medicine, rehabilitation, and pain management are becoming more sophisticated in their ability to identify the tissue source of back pain. Once the source is identified, physical therapy and diagnostic and therapeutic injection methods are used for pain relief. These techniques, such as foraminal epidural blocks and selective nerve blocks, are therapeutically beneficial, but they may also be limited in their ability to ultimately correct the painful condition. These interventions are typically exhausted in an attempt to avoid classic spine surgery due to the inherent morbidity with dissecting and approaching the spine. Truly minimally invasive spine surgery with posterolateral selective endoscopic discectomyTM has no approach related morbidity, making this an attractive next step in the treatment algorithm. 1410

B Fig. 133.8 (A) Annular tears. Grade V annular tears open into the epidural space, extraforaminal zone, or psoas muscle, sensitizing the nerve and forming an inflammatory membrane that allow the ingrowth of nerves and capillaries. An inflammatory membrane next to the dorsal root ganglion of the exiting nerve, psoas muscle, or traversing nerve can cause nondermatomal pain out of proportion to the MRI study. If patients with annular tears get relief from foraminal epidural blocks after a painful positive discogram, more lasting relief is probable with selective endoscopic discectomy and thermal annuloplasty. The procedure removes degenerative nuclear material keeping the tear open, thermally closes the tear, and allows for ablation of the inflammatory tissue. (B) Grade IV annular tear. Degenerative interpositional disc tissue is embedded in the annulus. The annulus is contracted by a bipolar radiofrequency flexible probe or laser, removing the interpositional disc tissue that is preventing the annular tear from healing. Intraoperative chromo-discography will stain the degenerative disc and annulus.

TECHNIQUE Endoscopic spine surgery: the posterolateral approach The current technique utilized by the authors has evolved over a 13year period beginning in 1991 after learning arthroscopic microdiscectomy from Parviz Kambin. Previously, the authors had experience in the use of chymopapain, automated percutaneous discectomy, laser discectomy, and discography. The current technique combines the

New Frontiers

PROBLEMS AND COMPLICATIONS

C

D Fig. 133.8 Cont’d (C) This is intradiscal view of a large grade V annular tear. Inflammatory and granulation tissue surrounds the tear extending into the epidural space. The presence of inflammatory and granulation tissue is what makes annular tears painful. Ablation of the inflammatory membrane with radiofrequency may provide relief of varying periods, and may depend on the size and location of the tear. (D) Ellman bipolar radiofrequency trigger-flex probe thermal modulating a grade IV annular tear that has stained the outer fibers of the annulus. The more annular layers remain, the better the prognosis. If a radial tear or annular defect is large, thermal contraction sometimes causes the tear to enlarge, especially if there is an associated disc herniation. These large tears associated with large disc herniations do not create the chronic lumbar discogenic pain syndrome, which is still not completely understood.

best features of each percutaneous procedure into a visualized endoscopic method that is described as selective endoscopic discectomy™, thermal discoplasty, and annuloplasty. It continues by incorporating endoscopic foraminoplasty techniques for degenerative conditions of the lumbar spine. The foraminal approach is refined further by a standardized surgical protocol that helps decrease the learning curve.

As with arthroscopic knee surgery, the risks of serious complications or nerve injury are low, about 1–3% in the authors’ experience.33 The usual risks of infection, nerve injury, dural tears, bleeding, and scar tissue formation are always present, as with any spinal surgery. Fenestration past the anterior annulus is a potential hazard, creating a bowel or vascular injury. Although this is a rare complication because the thickness of the anterior annulus will usually prevent fenestration, it must be recognized as a potential risk if the annulus is weakened or fenestrated by an anterior disc herniation. This risk is also present with the posterior approach. One limitation of the endoscopic technique is the need to use some instruments in a ‘blind’ fashion. This occurs because the size of shavers, pituitary rongeurs, and basket forceps are too large to fit into the working channel of the endoscope. Of course, their placement and use must be monitored with fluoroscopy. The cannulae are designed to protect vital structures by utilizing windows as surgical portals. Spinal nerves may be adherent to the disc and annulus, and can be extracted along with the disc or annulus by shavers or cutting instruments. In addition, the authors have identified anomalous autonomic and peripheral nerves in the foramen (furcal nerves), buried in the annular fat, that connect with the sacral plexus or the traversing nerve. These nerves are described in the medical literature and can be symptomatic but are typically small and not appreciated during open surgery. These furcal nerves are readily visualized endoscopically and probing them can produce pain in the awake patient. (Fig. 133.9). The inflammatory membrane may contain tiny nerves and blood vessels that contribute to severe discogenic pain (Fig. 133.10). Dysesthesia, the most common postoperative complaint, occurs about 5–15% of the time, but is almost always transient. Its cause is still incompletely understood and may be related to manipulation of furcal nerves or the anulus. Another possibility is simply delayed nerve recovery as the symptoms typically occur days or weeks after surgery. Finally, this side effect may be due to irritation of the dorsal root ganglion from manipulation or postoperative bleeding. This condition cannot be completely avoided, as neuromonitoring with dermatomal SEP and continuous EMG, the most sensitive means of monitoring, has not identified intraoperative irritation as the major cause of dysesthesia.34 In some cases the symptoms can be severe and similar to complex regional pain syndrome (CRPS), but usually without the skin changes that accompany CRPS. Stimulation of the dorsal root ganglion of the exiting spinal nerve can also result in dysesthesia when foraminoplasty is performed, even when the exiting nerve was clearly identified and protected during endoscopy. The endoscopic technique, because of its approach, may be accompanied by risk for iatrogenic injury. We suspect spinal endoscopy is safer than traditional surgery, as the patient is awake and able to provide immediate input to the surgeon when pain is generated. Since the authors prefer patients to be reasonably alert, we never use propofol for ‘sedation.’ Neuromonitoring techniques can warn the surgeon of nerve irritation. About 66% of the time, there is EMG activity recorded that warns the surgeon that there is nerve irritation.34 Neuromonitoring may give the surgeon more intraoperative feedback, but in a subsequent study comparing surgical cases without neuromonitoring, it has been demonstrated to be just as safe using of dilute local anesthetic and conscious sedation. As previously stated, the patient’s ability to feel pain provides the surgeon with a safety net. Consequently, the authors only use a dilute solution of local anesthetic (0.5% Xylocaine or its equivalent) to minimize the risk of deeply anesthetizing the spinal nerve. As well, the ability of the patient to report pain during the probing component of the procedure will enable the recognition of pain generators in the spine. When there is documented postoperative improvement in 1411

Part 7: New Frontiers

A

C

B

Fig. 133.9 Anomalous nerves (A) Furcal nerve. (B) Autonomic nerve. (C) Biopsy of autonomic nerve shown in (B). Anomalous nerves are seen in the annular fat in the ‘hidden’ foraminal zone. When found in the foramen, it is considered an anomalous branch, but furcal nerves are common branches from the exiting nerve entering the psoas muscle. These communicating branches are described as furcal nerves in the anatomy and literature. Small sympathetic nerves are occasionally seen. Ablation or resection of these nerves may be associated with dysesthesia, but removal may also decrease chronic discogenic lumbar pain.

nerve conduction velocities and improvement of abnormal preoperative EMGs immediately postoperatively, this is clear, objective evidence of clinical improvement.34 If a patient is not improved following surgery when electrodiagnostic studies show an improvement, it is likely due to the progression of the disease process itself.

NEW HORIZONS There will soon be an explosion of new imaging systems, endoscopes, and endoscopic instruments. These new devices will enhance the precision of the endoscopic surgeon. As well, with more physicians performing these techniques there will necessarily be a refinement in the techniques used. This will culminate in improved outcomes and ultimately result in the universal acceptance of this method of treatment.

KEY POINTS Fig. 133.10 Neoangiogenesis and neoneurogenesis is commonly present in the inflammatory membrane adjacent to annular tears in patients who have severe discogenic pain and sciatica, but a rather benign MRI. 1412

1. The endoscopic foraminal posterolateral surgical approach to the lumbar disc offers the least trauma to normal anatomy. 2. Spinal endoscopy offers expanded diagnostic as well as therapeutic benefits not possible with traditional surgery.

New Frontiers

3. Spinal endoscopy is a complement to interventional spine management. 4. New terminology and concepts, evocative discography™, evocative chromo-discography™, selective endoscopic discectomy™, and thermal anuloplasty, are introduced and explained in the text. 5. The learning curve is steep, but once mastered, this approach will revolutionize the surgical treatment of the lumbar disc, and provide a delivery system for emerging technology in tissue repair and regeneration.

References

15. Yeung AT. The evolution of percutaneous spinal endoscopy and discectomy: state of the art. Mt Sinai J Med 2000; 67(4):327–332. 16. Yeung AT. Selective discectomy with the Yeung endoscopic spine system. In: The practice of minimally invasive spinal technique. Savitz MH, Chiu J, Yeung AT, eds. AAMISMS Education LLC; 2000:115–122. 17. Yeung AT. Transforaminal endoscopic selective nuclectomy and annuloplasty for chronic lumbar discogenic pain: an alternative to fusion. In: Spine Arthroplasty II Spine Arthroplasty Society 2002; Montpellier, France, May 5–8. 18. Yeung AT. Macro-and micro-anatomy of degenerative conditions of the lumbar spine (Best Paper Presentation Award). In: International Intradiscal Therapy Society 16th Annual Meeting. 2003; Chicago, Illinois, April 2–5. 19. Yeung AT. Rauschning’s anatomy for minimally invasive spine surgery. In: Spine across the sea. 2003; July 27–31.

1. Macnab I. Negative disc exploration. An analysis of the causes of nerve-root involvement in sixty-eight patients. J Bone Joint Surg [Am] 1971; 53(5):891–903.

20. Carragee EJ, et al. The rates of false-positive lumbar discography in select patients without low back symptoms. Spine 2000; 25(11):1373–1380; discussion 1381.

2. Yeung AT. Endoscopic spinal surgery: what future role? J Musculoskeletal Med 2001; 18(11):518–528.

21. Carragee EJ, et al. False-positive findings on lumbar discography. Reliability of subjective concordance assessment during provocative disc injection. Spine 1999; 24(23):2542–2547.

3. Yeung A.T. Discography, foraminal epidurography and therapeutic foraminal injections: its role in endoscopic spine surgery. In: International 22nd course for Percutaneous Endoscopic Spinal Surgery and Complementary Techniques. 2004; Zurich, Switzerland, January 20–30.

22. Tsou PM, Yeung AT, Yeung CA. Posterolateral transforaminal selective endoscopic discectomy and thermal annuloplasty for chronic lumbar discogenic pain. Spine J 2004;

4. Yeung AT. The role of provocative discography in endoscopic disc surgery. In: Savitz MH, Chiu J, Yeung AT, eds. The practice of minimally invasive spinal technique. AAMISMS Education LLC; 2000:231–236.

23. Yeung AT. Arthroscopic electro-thermal surgery for discogenic low back pain: a preliminary report. In: International Intradiscal Therapy Society Annual Meeting. 1998; San Antonio, Texas.

5. Yeung AT, Porter J. Minimally invasive endoscopic surgery for the treatment of lumbar discogenic pain. In: Pain management: a practical guide for clinicians. Lyon: CRC Press; 2002: 1073–1078.

24. Yeung AT. Classification and electro-thermal treatment of annular tears. In: American Back Society Annual Meeting. 1998; Las Vegas, Nevada, December 12.

6. Yeung AT Endoscopic decompressive approaches to the disc. In: North American Spine Society Annual Meeting Symposium: Minimally invasive surgical treatments of spinal pathhologies: a rational approach. 2003; San Diego California, October 21–25. 7. Yeung AT, Gore SA. Evolving methodology in treating discogenic back pain by selective endoscopic discectomy (SED). J Minimally Invasive Spinal Technique 2001; 1:8–16. 8. Tsou PM, Yeung AT. Transforaminal endoscopic decompression for radiculopathy secondary to intracanal noncontained lumbar disc herniations: outcome and technique. Spine J 2002; 2(1):41–48. 9. Yeung AT, Tsou PM. Posterolateral endoscopic excision for lumbar disc herniation: Surgical technique, outcome, and complications in 307 consecutive cases. Spine 2002; 27(7):722–731. 10. Savitz SI, Savitz MH, Yeung AT. Antibiotic prophylaxis for percutaneous discectomy. J Minimally Invasive Spinal Technique 2001; 1(Inaugural): 49–51. 11. Yeung AT. Endoscopic access for degenerative disorders of the lumbar spine. In: International Society for Minimal Intervention In Spinal Surgery, 19th course for Percutaneous Spinal Surgery and Complementary Techniques. 2001; Zurich, Switzerland, January 25–26. 12. Yeung AT, Yeung CA. Advances in endoscopic disc and spine surgery: foraminal approach. Surg Technol Int 2003; 11:253–261. 13. Osman SG et al. Transforaminal and posterior decompressions of the lumbar spine. A comparative study of stability and intervertebral foramen area. Spine 1997; 22(15):1690–1695. 14. Yeung AT. Minimal invasive techniques in the lumbar spine: evolving methodology since 1991 (Magistral speaker). In: International 20th Jubilee course for Percutaneous Endoscopic Spinal Surgery and Complementary Techniques. 2002; Zurich, Switzerland.

25. Yeung AT. Annular tears: correlating discogram and endoscopic findings with electrothermal response. In: International Intradiscal Therapy Society and International Society for Minimally Invasive Spine Surgery Annual Meeting. 1999; Cambridge, England, August 1–5. 26. Yeung AT. Endoscopic thermal modulation as an alternative to fusion for discogenic pain. In: International Meeting for Advanced Spine Technologies. 1999; Vancouver, British Columbia, Canada, July 8–10. 27. Yeung AT. Patho-anatomy of discogenic pain. In: Minimally Invasive Spine Update. 1999; Disney Magic Cruise, Nov 5–8. 28. Yeung AT. Thermal modulation of disc pathology. In: 1st World Congress American Academy of Minimally Invasive Spinal Medicine and Surgery. 2000; Las Vegas, Nevada, Dec 7–10. 29. Yeung AT. Thermal modulation: SED versus IDET. In: 1st World Congress American Academy of Minimally Invasive Spinal Medicine and Surgery. 2000; Las Vegas, Nevada, Dec 7–10. 30. Yeung AT, et al. Intradiscal thermal therapy for discogenic low back pain. In: Savitz MH, Chiu J, Yeung AT, eds.The practice of minimally invasive spinal technique. AAMISMS Education LLC; 2000. 31. Yeung AT, Savitz MH. Treatment of multi-level lumbar disc disease by selective endoscopic discectomy and thermal annuloplasty: case report. J Minimally Invasive Spinal Technique 2002; 2(Spring):36 AAMISMS Education LLC; 200038. 32. Yeung AT, Yeung CA. Microtherapy in low back pain. In: Mayer M, ed. Minimally invasive spine surgery. New York: Springer Verlag; 2004. 33. Yeung AT, Savitz MH. Complications of percutaneous spinal surgery. In: Vacarro A, ed. Complications in adult and pediatric spine surgery. 2004. 34. Yeung AT, Porter J, Merican C. SEP as a sensory integrity check in selective endoscopic discectomy using the Yeung endoscopic spine system. In: 2nd World Congress American Academy of Minimally Invasive Spinal Medicine and Surgery. 2001; Las Vegas, Nevada, December.

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Index

Figures and tables are comprehensively referred to from the text. Therefore, significant material in figures and tables has generally only been given a page reference in the absence of their concomitant mention in the text referring to that figure. ‘vs’ indicates the differentiation of two or more conditions.

A A fibers, 30, 30–1, 32, 40, 46 A-beta fibers, 30, 30–1 and gate control theory, 1166–7 wind-up and, 43, 44 AAPM&R (American Academy of Physical Medicine and Rehabilitation), history, 2, 3 ABC assessment, on-field athletic spinal injuries, 1345, 1359 abdomen, radio receiver/pulse generator implantation in, 348 abdominal muscles anatomy, 774, 862–3 and sports activity, 1333 examination in pregnancy, 1314, 1323 spinal stabilizing role, 1110 abdominal rectus plication, wide, 1068 abductors, hip, examination, 844–5 ablative techniques in chronic pain, 1191–9 abscesses epidural see epidural infections intradiscal, laser decompression and nucleotomy complicated by, 336 intramedullary, neck, 535 subdural, neck, 535 absorbed dose see dose acceleration injuries to cervical spine, 601, 603 accessory ligament, 520 AccRx pain pump, 353 acetabular labral tears, 1277, 1278 acetaminophen (paracetamol) lumbar radiculopathy due to herniated disc, 874 postoperative pain, 116 pregnancy-related back pain, 1325 achondroplastic lumbar spinal stenosis, 953 Acroflex disc, 1394 acromioclavicular joint anatomy, 548 action potentials evoked compound muscle, in lumbosacral radiculopathy, 897 nerve impulse, 194 active release therapy, sacroiliac joint syndrome, 1251–2 active spinal stability subsystem, 1110–11 activities of daily living (ADL) in lumbar disc surgery rehabilitation, 970, 971

activities (Continued) in lumbar radiculopathy due to disc herniation, 872, 873–4 modification and/or limitation in lumbar radiculopathy due to disc herniation, 872 in sacral insufficiency fractures, 1286 predisposing to lumbar disc degeneration, 819–21 see also bed rest; disuse; exercise; immobilization; sport acupressure, lumbar radiculopathy due to herniated disc, 872 acupuncture lumbar radiculopathy due to herniated disc, 885 neck pain, 699 pregnancy-related back pain, 1327 acute phase of rehabilitation, 993 axial back pain, 994–5 adalimumab ankylosing spondylitis, 397 lumbar radicular pain, 916 Adamkiewicz’s great radicular artery, 768 ADCON-L, 1144 addiction benzodiazepines, 182 opioid/narcotic, 165 cervical radicular pain and, 658 see also dependence adenosine, intrathecal infusion, 359 adherence with treatment see compliance adhesiolysis, epidural, 1155–64 complications, 1160 indications/contraindications, 1156 minimally invasive/endoscopic, 1143, 1161 outcomes, 1160–1 physical therapy, 1161 preprocedural matters, 1156 technique, 1156–60 adhesion of polymorphonucleocytes and local anesthetics, 141 adhesive arachnoiditis, 1138–9 adjuvant drugs with analgesics (=coanalgesics), 1205 intrathecal infusion, 356–9, 1183 in radicular pain, 129–36, 635 in sacroiliac joint syndrome, 1249 with local anesthetics, 150

adolescents/teenagers disc degeneration, 25 discitis, 401 herniated lumbar nuclear pulposus, 947 idiopathic scoliosis, pregnancy and, 1309 spondylolisthesis, surgical indications, 1099 sports injuries and back pain in, 1350–1 adrenal gland physiology, 153 α2-adrenergic receptor, pain and, 49 α2-adrenergic receptor agonists anxiolytic effects, 180, 181 intrathecal, as adjuvant analgesics, 356, 357–8 β-adrenergic receptor blockers as anxiolytics, 180, 181 Adson’s maneuver, 544 Advanced Bionics spinal cord stimulator, 341, 343, 1167 Advanced Neuromodulation Systems spinal cord stimulator, 341, 1167–8, 1169 aerobic exercises in spondylolysis, 1377 aerobic fitness of deconditioned subjects, 1215 affective disorders comorbid with chronic pain, assessment for, 108 pain pathways and, 44 afferent nerve/nerve fibers in pain, 30, 43 primary, 29 see also deafferentiation age back/spinal pain and, 13 sports injuries and, 1350–1 bone changes with, 428–9, 435 disc changes (incl. degeneration), 25, 304 lumbar, 813, 992 fusion surgery and, 1125 lumbar spinal stenosis surgery and, 955, 956 agoraphobia, panic disorder with, screening questions, 178 airway assessment on-field athletic spinal injuries, 1345, 1359 for sedation and analgesia, 240 ala, sacral, fractures, 1281, 1282 alar ligaments, 520 alarms, Synchromed pain pumps, 1179 aldosterone, 153 alendronate osteoporosis, 443 Paget’s disease, 449 1415

Index alimentary tract see gastrointestinal tract alkaline phosphatase, Paget’s disease, 447, 533 allergic reactions see hypersensitivity reactions allografts of bone cervical myelopathy surgery, 756 for fusion surgery in anterior cervical discectomy for foraminal stenosis, 670, 671 influence on outcome, 1125–6 alpha blockers see α2-adrenergic receptor agonists alprazolam, acute anxiety, 180 alternative therapies see complementary/ alternative therapy AMA (American Medical Association), 1, 2 American Academy of Physical Medicine and Rehabilitation (AAPM&R), history, 2, 3 American Association of Electrodiagnostic Medicine guidelines for radiculopathy evaluation, 96–7 American football cervical spine injuries, 1334, 1335, 1340, 1353, 1354 spear-tackler’s spine see spear-tackler’s spine stingers/burners see stingers helmets see helmets lumbar disc pathology, 1337 American Medical Association (AMA), 1, 2 American Pain Society, acute and cancer pain management guidelines, 113, 114 American Society of Anesthesiologists, sedation guidelines, 240 amide-type local anesthetics, 141–2, 142–5, 196 pharmacology, 139 amine neurotransmitters, anxiety and, 176 amino acid(s), excitatory, and pain, 33, 47 amino acid neurotransmitters, anxiety and, 176–7 Amor criteria, 393 AMPA receptors and pain, 33 amygdala, fear and anxiety and the, 174–5 amyotrophic lateral sclerosis vs compression myelopathy, 569 analgesia airway assessment for, 240 care following, 242–3 definitions, 239 emergency equipment, 241 spinal see spinal analgesia analgesic discography see discography (analgesic) analgesic drugs, 113–70, 241–2, 1205–6 adjuvant see adjuvant drugs axial back pain, 994, 995 cervical radicular pain, 635 coccydynia, 1296 as component in pain rehabilitation, 1205–6 failed back surgery syndrome, 1142 lumbar radiculopathy due to disc herniation, 872, 874–7, 888 placebo response, 204 postoperative pain, 113, 116–24 pregnancy-related back pain, 1325–7 sacral insufficiency fractures, 1286 sacroiliac joint syndrome, 1249 spondylolysis, 1377 whiplash injury, patient advice, 599 see also specific (classes of) drugs anaphylactic reactions with spinal injections, 213 steroids, 155

1416

androgens, fusion surgery and effects of, 1124 anesthesia and anesthetics see general anesthesia; local anesthesia; local anesthetics; spinal anesthesia aneurysm, subclavian artery, with thrombosis, 553 aneurysmal bone cyst, 459 cervical, 531–2 imaging, 80–1, 459 anger levels with chronic pain, assessment for, 109 angiography, magnetic resonance, primary tumors, 456 animal studies, whiplash injury, 602 anisotropy, 831 anulus fibrosus, 832 ankle dorsiflexion in modified straight leg raising test, 848 strength assessment, 845 plantar strength assessment, 845 ankylosing spondylitis, 392 case studies, 397–8 clinical features, 392 lumbar pain, 809 thoracic pain, 779, 780 genetics, 391 imaging, 73–4, 781 laboratory studies, 392 pharmacotherapy, 397 physical examination, 392, 780 provocative tests, 1246 systemic features, 396 treatment, 784 annuloplasty, intradiscal electrothermal see intradiscal electrothermal therapy an(n)ulus fibrosus, 17, 827, 832–3, 866 block, in whiplash injury, 590 degeneration, 821, 832, 866 imaging, 59 innervation, 867 intradiscal electrothermal therapy and the, 303 mechanics, 832–3 structure, 17, 827, 866, 1332 tears/fissures, 60 MRI, 61 anode (X-ray source), 229 Anrep, Vassily von, 137 anterior cord syndrome, and its symptoms, 618, 621 anterior elements in cervical myelopathy, surgical approach via, 755–6 lumbar spine, 992 fusion (with instability due to anterior lesions), 1121, 1122, 1123 infection, causing instability, 1112 inspection, 839 sports injuries in children and, 1350 anterior lumbar interbody fusion, 1068–9 gasless endoscopic, 1401 laparoscopic, 1399–400 posterior and, combined, 1069 anterior—posterior resection reduction in spondylolisthesis, 1103–4 anteroposterior (AP) glide, sacroiliac joint provocative testing in pregnancy, 1316 antibiotics opioid interactions with, 169 in spinal infection, 408, 534 childhood discitis, 409

antibiotics (Continued) discography complicated by discitis, 223 tuberculosis, 536 in spinal procedures, prophylactic, 411 cervical discography, 725–6 lumbar discography, effect on complication rates, 1044–5 vertebroplasty, 368 antibodies 99m Tc-labelled, 90 monoclonal see monoclonal antibodies anticoagulant drugs epidural adhesiolysis and, 1156 spinal/epidural injections and, 218, 1151 anticonvulsant drugs see antiepileptic drugs antidepressants as anxiolytics, 181 in lumbar radiculopathy due to herniated disc, 874, 876, 888 opioid interactions, 169 SSNRIs, lumbar radiculopathy due to herniated disc, 876 SSRIs see selective serotonin reuptake inhibitors tricyclic see tricyclic antidepressants antiepileptic (anticonvulsant) drugs, 129–36 drug interactions, 131–2, 132, 133, 134, 135, 169 in pregnancy-related back pain, 1326 in radicular pain, 129–36 lumbar radicular pain due to herniated disc, 876, 888 mechanisms of action, 130 newer, 129–34 older, 134–5 other, 135 in spondylolisthesis, 1087–8 vitamin D metabolism affected by, 436 antihistamines see histamine H1 antagonists anti-inflammatory drugs axial back pain, 994, 995 non-steroidal see non-steroidal antiinflammatory drugs anti-inflammatory effects local anesthetics, 141, 196 steroids, 154–5 antituberculous drugs in spinal tuberculosis, 536 anulus fibrosus see annulus fibrosus anxiety acute, pharmacotherapy, 180–1 biological basis, 174–5 clinical, evaluation, 178 effects on pain conditions and disorders, 174 injection procedure, 209 in low back pain patients, 1218 origin and definition, 173–4 anxiety disorders/syndromes, 173–85 chronic, 181–2 comorbid with chronic pain (incl. spinal pain), 173–85 assessment for, 108, 109 diagnosis, 177–8 treatment, 179–84 anxiolysis (minimal sedation), 239 anxiolytics, 180–4 acute anxiety, 180–1 AP (anteroposterior) glide, sacroiliac joint provocative testing in pregnancy, 1316 apophyseal glides, natural, 695

Index apoptosis and wind-up, 42 aquatic therapy in pregnancy, 1323 arachidonic acid metabolites in inflammation/ inflammatory pain, 21, 114–15 arachnoid (mater) cyst, 419 imaging, 83–4 lumbar, anatomy, 863–4 see also thecal sac arachnoiditis adhesive, 1138–9 in ankylosing spondylitis, 74 in failed back surgery syndrome, 1131 gabapentin for radicular pain, 131 imaging, 69, 74, 1141 arcuate system arteries (cervical vertebral bodies), 521–2 Aristocort®, spinal injection, 158–9 Aristopan®, spinal injection, 158–9 arm see upper limb arterial anatomy/supply cervical spine, 521–2 lumbar spine and cord, 861–2 shoulder, 552 thoracic spine/spinal cord, 768 arterial injury in cervical discography, 299, 727 in cervical epidural injection, 652–4 in cervical manual therapy, 697 in cervical zygapophyseal joint injection, 220–1, 652–3 in stellate ganglion block, 713 arteriovenous lesions (malformations/fistulas), 420 imaging, 84–5, 420 arthritis degenerative see osteoarthritis differential diagnosis of systemic causes, 394 enteropathic, 394 psoriatic see psoriatic arthritis reactive, 393 rheumatoid see rheumatoid arthritis Arthrocare spine wand, 925 arthrodesis see fusion arthrography, sacroiliac joint, 1266 arthroplasty (disc replacement), total, 1389–96 cervical disc, 1394–5 history, 1389 indications and evaluation, 1389–91 lumbar disc, 1071–3, 1390–4 articular processes cervical, 519 in epidural adhesiolysis, superior (SAP), 1158 lumbar, 859 ascending reticular activating system, 48–9 aseptic meningitis complicating spinal injection, 216–17 Asia, epidemiology Paget’s disease, 446 spinal pain, 11 Aspen orthosis, 486 Aspergillus, 413 aspiration nucleus pulposus see nucleotome seroma, 1152 synovial cyst, 267 aspirin (for low back pain) in breastfeeding mothers, 1327 in pregnancy, 1325–6

assessment/evaluation (and selection), patient for automated percutaneous lumbar discectomy, 323–5 in cervical axial neck pain see axial pain in cervical foraminal stenosis, 668 for cervical myelopathy surgery, 753 in cervical radiculopathy and radicular pain, 635, 636–7, 668 for disc replacement, 1389–91 for discography, 291 in hip—spine syndrome, 1278 for intradiscal electrothermal therapy/ annuloplasty/nucleoplasty of lumbar region, 304–5, 984 for kyphoplasty, 378 errors, 381–2 for laser decompression, 332–3 in lumbar instability, 1111–16, 1121, 1122 in lumbar pain, 1066 for neuraxial analgesia, 1178–82 for neuroablative therapy, 1192 for pain rehabilitation, 1202–3, 1203–4 for sacroiliac joint syndrome surgery, 1269–74 for sedation, 240 for spinal injection procedures, 207–11 new patient, 207 post-procedure, 209–10, 213 pre-procedure, 207–8, 213 sports injuries see sports activities for vertebroplasty, 367 in whiplash injury, 595–7 see also examination associative stage of rehabilitation in lumbar instability, 1117 astrocytes in injury and pain (incl. reactive gliosis), 34–5, 49 astrocytoma, 420 imaging, 76, 420 athetoid cerebral palsy, cervical myelopathy associated with, 764 athletic activities see sports atlantoaxial joint (AA; C1—C2), 709, 747–8 anatomic aspects, 520, 574, 584, 709, 747 sport and, 1331 function (incl. biomechanics), 518–19, 709 regarding orthoses, 485 regarding stability, 574 injection therapy, 260–1, 709, 710 cervicogenic headache, 709, 710, 747–8 technique, 260–1 instability assessment for, 575–6 in Down syndrome, 576–7 pain, clinical presentation, 707–9 pain referral maps, 679 rotation mobilization, 695 spinal cord stimulation in area of, 347 subluxation, 560 risk assessment in Down syndrome, 576–7 atlanto-occipital (AO/OA; C0—C1) joint, 707–10, 747–8 anatomic aspects, 520, 574, 584, 707, 747 biomechanics, 518, 574, 707 regarding orthoses, 485 regarding stability, 574 injections (incl. blocks), 260, 709, 710 head/axial neck pain, 709, 710, 747–8 steroid, 260, 709

atlanto-occipital (Continued) injury mechanisms, 707 pain referral maps, 679 atlas (C1) anatomy and function, 260, 518, 520, 707 spinal nerve, 526 postnatal development, 516–17, 857 ring fracture in sport, 1344 transverse ligament, 520 atlas-dental interval, 560 ATPase, Na+K+ (sodium ion—potassium ion pump), 194 Australia, whiplash injury incidence, 607 autografts of bone cervical myelopathy surgery, 756 for fusion surgery in anterior cervical discectomy for foraminal stenosis, 669–70 influence on outcome, 1125 automated percutaneous discectomy cervical, 930 lumbar (APLD), 321–30, 905, 906, 923–4, 925, 929–31, 1068 chemonucleolysis vs, 929 contraindications, 930 indications, 929–30, 1068 instrumentation, 322–3 L5—S1 level, 327–8 long-term results, 930–1 patient positioning and selection of entry route, 323–5 postoperative care, 328–9 safety/complications, 322, 930 autonomic dysreflexia, 772 autonomic nervous system embryological development, 856 lumbar disc, 867 thoracic spine, 772 pain and, 768, 773 autonomous stage of rehabilitation in lumbar instability, 1117 avoidance behavior with low back pain, 807, 1217–19, 1227 axial compression and tension, 834 axial loading and cervical spine injuries in sport, 1334–5, 1339–40, 1344, 1354 axial pain (incl. mechanical pain) cervical (=axial neck pain), 679–736 algorithmic methodology for non-surgical management, 679–84 algorithmic methodology for surgical management, 729 centralization see centralization clinical assessment, 680–1, 730 fusion surgery see fusion historical aspects of management, 679 imaging, 685, 730–1 injections, diagnostic, 679, 682, 685 injections, therapeutic, 682, 700, 707–12 natural history, 685 radiofrequency denervation see radiofrequency ablation rehabilitation see rehabilitation sources of acute vs chronic pain, 685–6 upper vs lower, 680 lumbar, 975–1076 algorithmic approach to management, 975–89 case studies, 985–6

1417

Index axial pain (Continued) clinical presentation, 992–3, 1065–7 epidemiology/risk factors, 991 medical rehabilitation see rehabilitation pathophysiology, 1013, 1015 surgery, 1065–75 thoracic, 793–5 clinical features, 793–4 radiofrequency denervation, 793–4 axillary artery, 552 axillary herniated lumbar herniated nucleus pulposus, 946–7 axillary nerves, 551 axillary vein, 552 axis (C2) anatomy and function, 260, 518, 709 spinal nerve, 526 postnatal development, 517, 857 axis of rotation, sports injury and, 1333–4 axolemma, 194 axonal injury and whiplash, 617

B Babinski sign, 545 primary tumors, 455 back pain see pain back school, 1022 lumbar radiculopathy due to herniated disc, 872, 878 back surgery see surgery baclofen intrathecal infusion, 358–9, 359 lumbar radiculopathy due to herniated disc, 876 bacterial infection, spinal meninges, 535 Bakody’s sign, 617 ball-in-bowel analogy of intervertebral motion— pain hypothesis, 1111 balloon-assisted endoscopic retroperitoneal gasless (BERG) approach in anterior lumbar interbody fusion, 1401 balloon (bone) tamp inflation for kyphoplasty, 377, 381, 508 ‘bamboo’ spine, 73 baseball, 1351–2 basketball, 1352 basophils, 20 battered nerve root syndrome, 1139 battery for spinal cord stimulation, 343 batting, fast-pitch softball, 1352 beam equilization filters, 229 Beatty test, 1302–3 Beck Depression Inventory, 107–9 Beck scale for suicide ideation, 109 bed rest axial back pain, 994 lumbar radiculopathy due to herniated disc, 873–4 sacral insufficiency fractures, 1286 behavior protective, with low back pain, 807 whiplash injury signs in, 596 behavioral effects of steroids, 156 behavioral management/therapy, 1204–5 anxiety disorders, 179 in pain rehabilitation, 1204–5, 1208 evaluation, 1204–5 stress, 1229 Behçet’s syndrome, 82

1418

Belgium, epidemiology of spinal pain, 10 belts lumbar see lumbar belts pelvic, pregnancy, 1324–5 sacroiliac joint see sacroiliac orthoses/belts bending moment, 828 bending motions, 835 bent needle (curved needle) technique, 246, 247 with L5—S1 foramen blockage, 257–9 bent spine syndrome, 387 benzocaine, 146 benzodiazepines, 180–1, 181–3, 241 acute anxiety, 180–1 chronic anxiety, 181–2 dosing chart, 184 GABA receptors and, 177 intrathecal infusion, 358 in lactating mothers, 1327 in pregnancy, 1326 problems with, 182–3 reversal (antagonists), 241, 243 tapering, 184 BERG approach in anterior lumbar interbody fusion, 1401 beta blockers (β-adrenergic receptor blockers) as anxiolytics, 180, 181 betamethasone, spinal injection, 157 bicarbonate addition to local anesthetics, 139–40 biceps (brachii) manual muscle testing, 630 reflex assessment, 544 tendinitis, Speed’s test, 625 biconcave fractures, osteoporosis, 778 bicycling see cycling Bier, August, 138 biochemical studies see laboratory studies biofeedback, EMG, in pain rehabilitation, 1208 biologics in discogenic lumbar axial pain, 1018–19 biomechanical disorders hip—spine syndrome and, 1277 lumbar spine, 803–1238 thoracic spine, 767–802 biomechanics bone, age-related changes in biomechanical properties, 428 cervical spine see cervical spine disc see disc fractures and, 439–40 lumbar spine see lumbar spine nociception/pain and, 33–5 orthoses, 485–6 in pain rehabilitation, interventions relating to, 1207 sacral insufficiency fractures, 1281–2 shoulder, 549–50 sports injuries, 1333–7, 1351–7 of stabilizing system of spine, 1109–11 terminology, 828–31 thoracic spine see thoracic spine biopsy and histology (predominantly percutaneous and of bone), 473–4 complications, 458–9, 474–5 CT-guided see computerized tomographyguided percutaneous biopsy in kyphoplasty, 510–11 lumbar disc degeneration, 821–2 metastatic tumors, 473–4, 481 sacral, 1283, 1286 primary tumors, 456

biopsy and histology (Continued) sacroiliac joint, 1239 solitary vs multiple lesions, 457, 473–4 success rate, 449, 456–7 types, 456, 473 in vertebroplasty, 371 biopsychosocial model of pain, 1231–2 tertiary pain management and, 1232, 1234 bisphosphonates metastatic disease, 477 osteoporosis, 440–2, 442–3, 443, 1286 Paget’s disease, 447–9 primary tumors of bone, 463 bleeding complications cervical discography due to carotid puncture, 299, 727 implantable pump surgery, 362 vertebroplasty, 374 blood patch, epidural, 219–20, 1148 blood supply/damage/disease see entries under vascular blunt injury, piriformis syndrome, 1301 BNDF and pain, 48 body jacket, plastic, 489–90 body mass index and coccydynia, 1290 body mechanics see biomechanics Bohlman’s fibular dowel technique, 1105 bone, 423–83 age-related changes, 428–9 aneurysmal cyst see aneurysmal bone cyst biology, 423–33, 435–6 biopsy see biopsy cellular elements, 423 disorders, 435–83 neck pain due to, 708 neoplastic see bone tumors drugs inhibiting, 440–3 formation see ossification fractures see fractures healing (incl. in spinal fusion surgery), factors affecting, 1123–7 NSAID (non- and COX-2-specific) effects on, 122–4, 1124–5 mass/density, 435, 436, 436–8 determination, 436–7 factors affecting, 436 see also dual-energy X-ray absorptiometry matrix demineralized, in spinal fusion, 1127 formation, 426 metabolic disease see metabolic bone disease metabolism/turnover, 435–6 organization, 423 in pregnancy in lower back, 1309 remodelling in spine, 427–8 and disease, 428 resorption, 426–7 coupling to formation, 427–8 markers, 437 mechanisms, 426–7 regulation, 428 steroid adverse effects, 156, 438, 1124 thoracic spine bony landmarks, 772–3 bone cement see cement bone graft in cervical myelopathy surgery, 756 in fusion surgery in anterior cervical discectomy for foraminal stenosis, 669–70, 671

Index bone graft (Continued) influence on outcome, 1125–6 in minimally invasive transforaminal lumbar interbody fusion, 1400 lower cervical spine, 579 in thoracoscopic surgery, 1403 bone morphogenetic proteins, 425 in fusion surgery (recombinant), 1070 influence on outcome, 1125, 1126 in lumbar axial pain, intradiscal injections, 1018–19 bone scan (scintigraphy) cervical foraminal stenosis, 668 cervical radicular pain and radiculopathy, 631 metastatic disease, 472 Paget’s disease, 447, 534 primary tumors, 455 sacral insufficiency fractures, 1283 sacroiliac joint syndrome, 977, 1265 spondyloarthropathies, 394 spondylolisthesis, 1082 thoracic spinal pain, 782 bone tamp (balloon tamp) inflation for kyphoplasty, 377, 381, 508 bone tumors, 453–83 imaging, 79–81 primary, 453–67 benign, 453, 457–61 clinical presentation, 453–4 diagnosis, 453 malignant, 453, 461–3 management, 463–6 physical examination, 454–5 treatment, 453 work-up, 455–7 secondary see metastases bone vibration test (vibration pain provocation) lumbar axial pain, 1033–5 thoracic pain, 794 Boston brace, modified, 492 bowel see intestine bowstring sign, 849 braces see orthoses brachial plexus anatomy, 527, 550–1 development, 516 transient neurapraxia in sport, 1341 brachioradialis manual muscle testing, 630 reflex assessment, 544 bradykinin and pain, 32 Braggard’s sign, 848 brain fear and anxiety and the, 174–6 injury in sport, 1339 pain and the, 43, 44 brain-derived neurotrophic factor (BNDF) and pain, 48 breast cancer, spinal metastases, 475 breastfeeding and medications for low back pain, 1326–7 breathing assessment, on-field athletic spinal injuries, 1345, 1359 bremsstrahlung, 230 Britain see United Kingdom and Britain Brown-Séquard syndrome and its symptoms, 618, 622 Bryan cervical disc, 1394 buckling (spinal), extent of, 1002

bupivacaine, 142, 143, 144 diagnostic selective nerve root injection, 199 intrathecal infusion, 356 with morphine, 359, 1183 toxicity, 144, 147, 148 burners see stingers burning hand syndrome, 1341 bursitis, trochanteric, 385–7 buspirone as anxiolytic, 181 butamben, 150

C C-arm CT, positioning, 236 fluoroscopy for kyphoplasty, 378 for vertebroplasty, 368 C fibers, 30, 31, 40, 46, 1165 wind-up and, 43, 44 C-reactive protein, infection, 408 C0—C1 see atlanto-occipital joint C1 see atlas C1—C2 see atlantoaxial joint C2 see axis C3 spinal nerves anatomy, 526 medial branch block, 266 C4 medial branch block, 265 C4—C8 radiculopathies, reflex/motor/sensory testing, 629 C5 nerve root palsy following cervical myelopathy surgery, 761 cadaveric studies of disc mechanics and degeneration, 834 cages see intervertebral cages calcification coccygeal, 1291 ligamentum flavum, 560 spinal (in general), steroid injection-induced, 1054 calcitonin, 427 administration osteoporosis, 442 Paget’s disease, 447 calcitonin gene-related peptide and pain, 32–3 calcium in bone turnover, 435–6 dietary supplementation, 436 with bisphosphonates, 440–2 drugs interfering with retention, 436 calcium ion(s) local anesthetic myotoxicity and, 149 local anesthetic neurotoxicity and, 148 pain and, 32 wind-up, 44 calcium ion channel blockers as intrathecal adjuvant analgesics, 356, 358, 1183–4 camptocormia, 387 Canada, epidemiology of spinal pain, 11 cancellous (trabecular) bone, 423 age-related changes, 428 strength, and vertebral body compression fracture risk, 496 Candida, 413 cannulas see catheters and cannulas capacitive coupling augmenting spinal fusion, 1126 capsaicin, topical, in lumbar radiculopathy due to herniated disc, 877

carbamazepine, 134–5 dosing and titration, 132, 135 in radicular pain, 134–5 carbonation, local anesthetics, 139 carcinoma see specific tissue of origin cardiopulmonary resuscitation, on-field, 1360 cardiovascular system, 1215–16 ankylosing spondylitis involving, 396 COX-2-specific inhibitor effects, 121–2, 874–6 fitness loss in chronic back pain, 1215–16 maintenance in prolonged sports injury, 1382 local anesthetic effects, 146–7, 214–15 measurement, 1215–16 steroid effects, 154 vertebroplasty-associated complications, 502–3 see also heart carotid artery damage in cervical discography, 299, 727 in stellate ganglion block, 713 carotid pulse, palpation, 543 carpal—metacarpal joint, osteoarthritis, 628 carpal tunnel syndrome, 627 cartilage formation see chondrification models/differentiation, 424 cartilaginous endplate see endplate Cash orthosis, 885 catabolic activity, lumbar disc degeneration, 822 cataracts, radiation-induced, 232 β-catenin and osteogenesis, 425–6 catheters and cannulas epidural adhesiolysis in caudal approach, 1156–7 in transforaminal approach, 1157, 1158 intradiscal electrothermal therapy, 309–12, 1059–60 kinking, 312 kyphoplasty, 380–1 local anesthetic infusion, 150 percutaneous (for intrathecal drug delivery), 1177 complications related to, 363, 363, 1187–8 implantable intrathecal pumps, 363, 363 cathode (X-ray source), 229 cauda equina, 30, 95, 863 surgery, 947, 955 cauda equina syndrome, 940 features, 940 local anesthetics, 148–9 surgery in, 873 percutaneous disc decompression contraindications, 333–4 caudal approach to epidural adhesiolysis, 1156–9 caudal epidural injections, 249, 250–1 complications, 222 lumbar, 1018 in spondylolisthesis, 1095 technique, 1018 causal factors (spinal pain), 12–13 cavernous malformation, 420 imaging, 76, 420 Cbfa1, 424 CD11b—CD18 and local anesthetics, 141 cefazolin prophylaxis, cervical discography, 726 celecoxib adverse effects, 121, 121–2

1419

Index celecoxib (Continued) bone healing and spinal fusion effects of, 124 indications, 117 postoperative setting, 118–19 Celestone®, spinal injection, 157, 158, 159 celiac nerves, 772 cell adhesion and local anesthetics, 141 cement (bone) kyphoplasty, 381 leakage, 382–3, 510 PMMA see polymethylmethacrylate vertebroplasty, 371–3 leakage, 373–4, 502 central canal stenosis endoscopic surgery, 1408–9 lumbar, 889, 911, 951–2, 953, 953–4, 956, 958, 964 MRI, 818 central cord syndrome, and its symptoms, 618, 622 central nervous system local anesthetic toxicity, 147–8, 214 opioid effects, 167, 361–2 in pain, 39–52, 804 anxiety and its effects on, 174 central sensitization, 114, 115–16 immune changes, 33, 40 low back pain and, 804 in whiplash-associated chronic pain, 604 spinal injections adversely affecting, 219 steroid effects, 154 centralization of low back pain in lumbar radiculopathy, treatment resulting in, 872, 878–81 of neck pain, 686–7 in radiculopathy, 636 in radiculopathy, treatment resulting in, 640 see also McKenzie method cephalic vein, 552 cephalosporin prophylaxis, cervical discography, 726 cord damage due to, 726 cerebral palsy, athetoid, cervical myelopathy associated with, 764 cerebrospinal fluid (CSF) dissemination of tumor to leptomeninges via, 78 flow, spinal stenosis and role of, 198 in meningitis, examination/cultures, 536 postoperative leak, 1147–9 with intrathecal drugs (incl. implanted pumps), 362–3, 1187 cerebrospinal fluid space width in spinal cord stimulation, 344 cerebrovascular accident see stroke cervical artery dissection in cervical manual therapy, 697 cervical disc(s) cervical spinal fusion-associated disease of adjacent discs, 559–60 excision see discectomy herniation, 1367–8 historical notes, 657 imaging, 62 myelopathy due to, 559 internal disc disruption syndrome, 682 laser decompression and nucleotomy complications, 335 technique, 334 normal, imaging, 59

1420

cervical disc(s) (Continued) pain and damage in whiplash injury, 610 pain referred from distal to elbow, 617, 619, 620 to head, 738, 747–8 provocative discography, 619, 620 replacement, 1394–5 sport-related disease, 1367–8 cervical discography, 295–7, 300–1, 721–8 axial pain, 731 clinical utility, 724–7 cervicogenic headache, 738 competing diagnostic tests, 722–3 complications, 221, 299, 724–7 historical aspects, 679, 721 pain referral patterns with cervical discogenic pain, 619, 620 sensitivity and specificity, 721–2 whiplash injury, 590 cervical facet (zygapophyseal) joints, 261, 276–8, 709–11 anatomy, 261, 276, 709–10 and sport, 1331 in cervicogenic headache etiology, 738, 744 injections (incl. blocks), 262–3, 682, 711 in axial pain, 731 in cervicogenic headache, 711, 745–7 complications, 221 historical aspects, 679 outcome, 711 in radicular pain, 632 in whiplash injury, 590, 711 injury mechanisms, 710–11 in sport, 1344 pain, 681–2, 717–18 presentation, 711, 717 prevalence, 711 referral patterns, 613, 614 syndrome of, 681–2 pain in whiplash injury, 589, 590, 609, 679 assessment by medial branch block, 590–1 radiofrequency denervation, 276–8, 682, 717–18 indications/contraindications, 717 outcomes, 682, 717–18 procedure, 276–7 side-effects/complications, 717 cervical instability, 573–81 definitions, 573 guidelines for diagnosis, 579–81 lower, 577–9 diagnosis, 578–9 management, 579 upper, 574–7 in congenital disease, 576–7 diagnosis, 574–6 management, 576–7 cervical lordosis, diminished, 540 cervical lysis of epidural adhesions, 1159 cervical medial branch block see medial branch block cervical musculature (paraspinal muscles), 523–5 defects and training, 687–8 examination, 100 in sporting activity, 1333 strains, 1341, 1368–9

cervical myelopathy, 557–72, 753–66 clinical presentation, 564 complications, 761–3 compressive differential diagnosis, 569–70 pathology, 557–64 diagnosis, 564–9 extrinsic and intrinsic causes, 557 radiculopathy and, simultaneous (=myeloradiculopathy), 617–18, 618, 623 surgery, 753–66 anterior, 753–6, 764 author’s preferred techniques, 765 indications, 753 outcomes, 763–5 postoperative care, 761 cervical nerve root(s), 613–78 anatomy, 525, 613–15 palsies following cervical myelopathy surgery, 761 pathology see cervical radiculopathy resection (rhizotomy) in occipital neuralgia, 748, 749 transient neurapraxia in sport, 1341 cervical nerve root pain, 613–78, 719–20 epidural steroid injections, 645–56 evaluation/diagnosis in, 615, 617–32, 635, 718, 748 algorithmic approach, 618–23 electrodiagnostic studies see electrodiagnostic studies historical notes, 657 pathophysiology, 615–17 patient assessment, 635, 636–7, 668 radiofrequency denervation (dorsal root ganglion), 278–80, 719, 748 rehabilitation methods, 635–44 surgery see surgery in whiplash injury, 609–10, 617 cervical orthosis (CO), 485, 486–8 indications, 491 cervical plexus, 527–8 cervical radicular pain see cervical nerve root pain cervical radiculopathy electrodiagnostic studies see electrodiagnostic studies manual muscle testing, 629 myelopathy and, simultaneous (=myeloradiculopathy), 617–18, 618, 623 radicular pain and radicular pain without radiculopathy, 613 radiculopathy without radicular pain, 613 cervical segmental nerve block in cervicogenic headache diagnostic, 738 therapeutic, 748 cervical spinal cord compression, 557–64 causes, 557–64 evoked potentials, 98 myelopathy due to see cervical myelopathy cordotomy, 1194–5 myelopathy see cervical myelopathy neurapraxia, in sport, 1341–2 stimulation, 347 cervical spinal cord injury in discography, 221, 299, 726–7 with epidural injections, 220 in sport, 1335, 1340–4, 1360–1, 1362–70

Index cervical spinal cord injury (Continued) epidemiology, 1362 evaluation and management, 1362 pathomechanics, 1362 return to play, 1362 soccer, 1356 variants, 1362 symptoms, 618 cervical spinal stenosis/narrowing (developmental/ congenital) athlete, 1339, 1342–3, 1363–4 return to play, 1364, 1384 imaging, 65 cervical spine, 515–766 anatomy, 515–30, 584 developmental, 515–17 relating to radicular pain, 613–14 relating to whiplash injury, 608, 609 anatomy, functional, 518–20 relating to lower cervical spine stability, 577 relating to sport, 1331, 1332 relating to upper cervical spine stability, 574 biomechanics lower cervical spine, 577 orthoses and, 485 upper cervical spine, 574, 707, 709 whiplash injury and, 583–8, 591, 607, 608, 710–11 examination, 539–46 scope and limitations, 539 fusion see spinal fusion headache relating to see cervicogenic headache imaging MRI technique, 54–5 vertebrae (normal), 56 injections complications, 219, 220–1 interlaminar see interlaminar space injections pathoanatomic considerations with epidural injections, 249 transforaminal see transforaminal epidural steroid injections injury (traumatic) facet joint, mechanisms, 710–11 sports see subheading below instability see cervical instability minimally invasive procedures, 1404 pain axial see axial pain classification, 539–40 referral from other areas, 623–8, 708 tertiary rehabilitation programs, 1225 primary tumors, surgery, 465 radiofrequency denervation see radiofrequency ablation reasons/goals, 539–40 sports injury, 1334–6, 1339–48, 1360–70 American football see American football baseball/softball, 1351–2 biomechanical etiologic factors, 1351 classification, 1360–2 cycling, return to competition after prolonged injury, 1385, 1386 functional anatomy relating to, 1331, 1332 mechanisms, 1334–6, 1340–1 on-field evaluation, 1344–7, 1359–60 return to play, 1360–2, 1383–4 secondary injury prevention, 1347 specific injuries, 1362–70

cervical spinal (Continued) syrinx, 421 cervical spondylosis, 557–9 evoked potentials, 98 foraminal stenosis with, 667 radicular pain in, 618–23, 667–78 atraumatic, 618–20 traumatic, 620–3 cervical synovial joints, anatomy and injection, 260–1 cervicocranial junction, dural attachments at, in cervicogenic headache etiology, 740 cervicogenic headache, 707–12, 737–51 clinical presentation and diagnostic criteria, 707–9, 740–5 differential diagnosis/similarities with other headaches, 740, 741 epidemiology, 737 historical aspects, 737 neuroanatomic basis and pathophysiologic mechanisms, 737–40 treatment, 745–8 injection therapy, 707–12, 745–8 radiofrequency denervation, 717–18, 746–7, 748 Cervicogenic Headache International Study Group diagnostic criteria, 740, 743 cervicortrigeminal interneuronal relay, 738 cervicothoracic (stellate ganglion) sympathetic block, 285–7 cervicothoracic ganglion see stellate ganglion CFU-Fs and bone formation, 425 Charité disc replacement, 1071–2, 1392–3, 1393 chemical mediators of inflammation see inflammatory mediators chemical radiculitis, 1140 chemoembolization, metastatic disease, 478 chemokines, 22 chemonucleolysis, lumbar disc, 315–19, 927–9, 1067–8 background/history, 315 complications, 315, 923, 928 indications/contraindications, 315–16, 928, 1067–8 long-term results, 928–9 technique, 316–19 chemoreceptor trigger zone and opioids, 167 chemotherapy metastatic disease, 477–8, 481 primary bone tumors, 464 see also chemoembolization chest see entries under thoracic children discitis, 401 clinical presentation, 401 management, 409 pathogenesis/etiology/natural history, 401 plain radiology, 404 sports injuries and back pain in, 1350–1 assessment/investigations, 1379 see also adolescents; children; infants; neonates chiropracty cervical axial pain, 693–4 lumbar axial/low back pain, 1001 in pregnancy, 1327 chlordiazepoxide, acute anxiety, 180 chlorprocaine, 142, 143, 144, 145–6 sodium bisulphite with, toxicity, 149

chondrification (vertebrae) embryological, 515, 855 fetal, 516, 856 chondrocytes differentiation, 424 disc degeneration and, 24 chondroitin sulfate, lumbar intradiscal injections, 1054, 1071 chondrosarcoma, 461–2 cervical, 533 imaging, 81, 461–2 chorda reticulum, 856 chordoma, 80, 461 cervical, 533 chromodiscography, evocative, 1410 chrondroclasts, 424 chrondrocytes, 423–4 chronic paroxysmal hemicrania vs cervicogenic headache, 741 chymopapain (in chemonucleolysis), 316, 319, 927 hazards, 315, 923 cineradiography lower cervical spine kinematics, 578 upper cervical spine kinematics, 575–6 circulation assessment, on-field athletic spinal injuries, 1345, 1359 clefts, intraosseous, vertebral fractures containing, 501 clinical examination see examination clinical trials see trials clonazepam, radicular pain, 135 clonidine acute anxiety, 180, 181 intrathecal infusion, 357, 359 with morphine, 357, 359, 1183 clorazepate, acute anxiety, 180 closed reduction in spondylolisthesis, 1102 clotting see coagulation Cloward technique (anterior cervical discectomy and fusion), 657, 669 cluster headache (CH) vs cervicogenic headache, 741 coagulation (clotting) system in inflammation, 19 spinal injection adversely affecting, 217 steroid adverse effects, 156 coanalgesics see adjuvant drugs coblation technology see nucleoplasty cocaine, 146 history, 137 Coccidioides, 413 coccygeal disc, 269–71 anatomy, 269, 1289 diagnostic injections, 269, 1294–5 therapeutic injections, 269–70, 1053–4, 1295–6 coccygectomy, 1296 coccyx, 269–71, 1289–97 anatomy, 269, 1289, 1296 examination see examination pain (coccydynia), 1289–97 acute vs chronic, 1290 historical assessment, 1289–90 physical examination, 1290 in pregnancy, 1312 radiographs, 1290–5 treatment, 269–70, 1295–6

1421

Index codeine, in pregnancy, 1326 Codman model 400 pump, 353 Codman paradox, 549 cognitive—behavioral therapy (CBT), anxiety disorders, 179 cognitive changes, opioids, 167 cognitive stage of rehabilitation in lumbar instability, 1116–17 cold treatment (incl. cryotherapy) lumbar radiculopathy due to herniated disc, 877 neck/cervical pain, 699 radicular pain, 638 thoracic spinal pain, 784 collagen in bone, 435 age-related decline in content, 428 breakdown products as bone resorption markers, 437 lumbar disc degeneration and, 822 nucleus pulposus, 865, 866 collagenase for chemonucleolysis, 927–8 collar hard, 486 soft see soft collar whiplash injury, 491, 599 collimation, 229 CT, 55, 236 colon, posteriorly placed, in automated percutaneous lumbar discectomy, 322 colony-forming unit-fibroblasts and bone formation, 425 colony-stimulating factor-1 see macrophage-colony stimulating factor colorectal cancer, spinal metastases, 476 combined magnetic fields augmenting spinal fusion, 1126 Commission for Accreditation of Rehabilitation Facilities (CARF), 1224 commissural myelotomy, 1195–6 comorbid conditions lumbar spinal stenosis, 956 musculoskeletal, in pregnancy, 1313–14 compact bone see cortical bone compensation for cervical radicular pain due to accident, 657–8 complement system in inflammation, 19, 21–2 complementary/alternative therapy ankylosing spondylitis, 397 axial back pain, 996 pregnancy-related back pain, 1327 complex regional pain syndrome (reflex sympathetic dystrophy) diagnostic blocks, 190 stellate ganglion block, 713–14 compliance/adherence chronic neck pain exercises, 692 orthoses, 491 compression soft tissue relating to intervertebral disc anulus fibrosus, 832 axial, 834 nerve root see nerve root nucleus pulposus, 831 testing, 829–30, 830 thecal sac, 951 spinal cord cervical see cervical spinal cord ischemia due to, 558–9 thoracic, 778

1422

compression (Continued) spine (in general) cervical nerve roots in sports, 1341 lumbar, damage caused by, 992 in sport, 1332 subclavian vessel see subclavian vessel see also decompression; maximal compression test compression fractures, 495–505 benign vs malignant, 69, 78 cervical sport-related, 1369 imaging, 67–9, 78 kyphoplasty, 377, 382, 440, 441, 507–13 failure of reduction, 383 malignant, 500 benign vs, 69, 78 management, 478, 512 multiple, 373, 382 osteoporotic see osteoporosis pathophysiology, 496–7 thoracic spine, 777–8 traditional treatment approaches, 495–6 vertebroplasty for see vertebroplasty compression test, sacroiliac joint assessment in pregnancy, 1316 Compton scatter, 229, 231 computerized tomography (non-contrast/in general), 55–6 abnormal spine, 60–85 advantages/disadvantages, 55 cervical injury in athletes, 1342, 1343 cervical myelopathy, 566–7 cervical radicular pain, 718–19 implanted pain pumps, 1189 kyphoplasty, multiple fractures, 382 lumbar disc before intradiscal electrothermal annuloplasty, 1059 degeneration, 823 lumbosacral radiculopathy, 896 metastatic disease, 472 with multiplanar reformations, in failed back surgery syndrome, 1132, 1133 normal spine, 56–9 primary bone tumors, 455–6 pyogenic spondylodiscitis, 404–5 roles, 55 sacral insufficiency fractures, 1283–4 spondyloarthropathies, 394 spondylolisthesis, 1082 spondylolysis, 1374 in treatment phase, 1375, 1377 staff radiation management during, 236–7 technique, 55–6 thoracic disc disease, 800 vertebroplasty, 368 whiplash injury, 596, 597, 603 see also single photon emission computerized tomography computerized tomography discography, 300 lumbar region, 294, 984, 1035–6 in intradiscal electrothermal therapy, 311 thoracic region, 298 computerized tomography-guided injections cervical region, tranforaminal epidural, 648–9 lumbar region, in selective nerve root block, 915 computerized tomography-guided percutaneous biopsy infection, 408 metastatic disease, 474

computerized tomography myelography, 56 cervical foraminal stenosis, 668 cervical myelopathy, 566 cervical radicular pain and radiculopathy, 631 neural scarring, 1141 pseudomeningocele, 1148 tumors metastatic, 472–3 primary osseous, 456–7 concept validity, 187 diagnostic blocks, 188 concomitant conditions see comorbid conditions concussion, sport, 1339 conditioning and placebo effect, 204 confirmation form, spinal injection procedure education, 207 congenital/developmental abnormalities and anomalies cervical spine causing instability, 576–7 causing myelopathy, 562 stenosis see cervical spinal stenosis disc, 60 low back pain due to, 808 lumbar spinal stenosis, 953 spondylolisthesis caused by see dysplastic spondylolisthesis conscious sedation, 239 consciousness level, on-field assessment with athletic spinal injuries, 1345, 1359 consent controlled substances, 165 intradiscal electrothermal therapy, 305 constipation with opioids, 167, 361 constitutional spinal stenosis, 953 construct validity, 187–8 diagnostic blocks, 189 consultation controlled substances, 166 new patient, 207 vertebroplasty referral, 367 contact pressure, 828 content validity, 187 diagnostic blocks, 188–9 continuous passive motion (CPM) in lumbar axial pain treatment, 1004, 1005, 1007, 1009 contrast-enhanced CT, 236–7 contrast-enhanced MRI (with gadolinium) advantages, 54 cervical spinal pain, 534 failed back syndrome, 66 neural scarring, 1141 infections, 405, 407, 534, 536 lumbar spine, 55 thoracic spinal pain, 781 contrast media in cervical discography, cord injury due to, 726–7 in chemonucleolysis, 318 in epidural injections, 250 in epidurogram for adhesiolysis, 1157 reactions, 215–16 controlled substances in pain management, model guidelines for use, 165–6 convergence theory, cervicogenic headache, 737–8 coping in chronic pain assessing ability, 110 whiplash injury patients, passive vs active, 598–9

Index coracohumeral ligaments, 549 cordectomy, 1196 cordotomy, 1194–5 core musculature strength lumbar disc degeneration and, 820–1 strengthening exercises, 881, 1332 core stability, examination in pregnancy, 1314 corpectomy in cervical myelopathy, 755 discectomy combined with, 756, 1403 thoracoscopic, 1402 corsets, lumbosacral, 490 in lumbar radiculopathy due to herniated disc, 885 in spondylolysis, 1375, 1376, 1377 cortical (compact) bone, 423 age-related changes, 428 corticosteroid(s), 153–60 absorption systemically, 155 actions, 154–5 complications/side-effects, 155–6, 215, 477 on bone, 156, 438, 1124 with prolonged use, 155–6 with systemic use, 155–6 complications/side-effects, with local injection, 155, 215, 220–1, 222–3 cervical injections, 651–4 fusion surgery and effects of, 1124 injectable (locally), 157–9, 248 ankylosing spondylitis, 397 coccydynia, 269–70, 1294–5 epidural see epidural injections neural scarring in failed back surgery, 1142, 1143 piriformis syndrome, 1305 sacroiliac joint, 977 side-effects, 155, 215, 220–1, 222–3 thoracic spinal pain, 782 injectable (locally), cervical axial pain/neck pain, 700, 709, 710 cervicogenic headache, 709, 710, 745–6 facet joint syndrome, 682 radicular pain, 645–56 injectable (locally), lumbar, 913–14, 982–3, 1014–18 intradiscal, 1019, 1049–56 in spondylolisthesis, 1089–95 zygapophyseal joint, 979–80, 1020, 1029 oral, in lumbar radiculopathy due to herniated disc, 876, 888 physiology, 153–4 therapeutic use in the spine, 157–9 local injection see injectable (subheading above) systemic/oral, 157 tumors of spine, 463–4, 477 withdrawal, rebound effects, 155–6 see also glucocorticoids; mineralocorticoids corticosteroid-binding globulin, 153 cortisol, 153 cost, economic and/or social kyphoplasty, 509–10 osteoporotic vertebral fractures, 495–6 of pain incl. spinal pain, 12, 29 assessment/evaluation, individuals with chronic pain, 1226–7 assessment/evaluation, as outcome measure in functional restoration, 1236

cost-effectiveness of pain management, 1236 costochondritis, 778 costoclavicular syndrome, 552 costotransverse foramen of Cruveilhier, 770 costotransverse joints, 773, 774 injection, 792 costotransversectomy, 801 costovertebral joints, 773, 774 injection, 791–2 coulomb, 230, 231 counseling see education counterstrain techniques, lumbar axial pain, 1004, 1005 coupled motion, upper cervical spine, 574 craniocervical flexion exercises acute nontraumatic neck pain, 688 acute traumatic neck pain, 690 craniocervical flexion test, 688 craniocervical junction, dural attachments at, in cervicogenic headache etiology, 740 Cranioplastic type 1 Slow Set cement, vertebroplasty, 372 creep, 831, 834 Crohn’s disease, arthritis associated with, 394 crossed femoral nerve stretch test, 849 crossed straight leg raising test, 848 cruciform ligament, 520 crush fractures, osteoporosis, 778 Cruveilhier’s costotransverse foramen, 770 cryotherapy see cold treatment cryptococcosis, 413 CSF-1 see macrophage-colony stimulating factor cultural phenomena, whiplash injury, 593–600 cultures, cerebrospinal fluid samples, 536 Cummins cervical disc, 1395 cumulative trauma disorders, 1223 curved needle see bent needle technique cushingoid effects of steroids, 156 Cushing’s syndrome (cushingoid features), steroids, 156, 215 cushions coccydynia, 1296 lumbar, in radiculopathy, 872, 886–7 cycling, 1356 return to competition after prolonged injury, 1385–6 cyclobenzaprine, lumbar radiculopathy due to herniated disc, 876 cyclooxygenase inhibitors (non-specific) see nonsteroidal anti-inflammatory drugs cyclooxygenase-1 (COX-1), 114–15 cyclooxygenase-2 (COX-2), 114–15 central sensitization and, 115–16 peripheral sensitization and, 115 cyclooxygenase-2 (COX-2)-specific inhibitors, 117–22, 1205 adverse effects, 120–2, 874–6 axial back pain, 994 bone healing and spinal fusion effects of, 122–4, 1125 central sensitization and, 115–16 cervical radicular pain, 635 lumbar radiculopathy due to herniated disc, 874–6 postoperative use, 117–20 analgesic efficacy, 117–20 drug interactions, 120 spondyloarthropathies, 397

Cyriax, James, 694 cysts, 83–4 aneurysmal bone see aneurysmal bone cyst arachnoid see arachnoid dermoid see dermoid cyst epidermoid see epidermoid cyst facet joint, lumbar see lumbar facet joints juxta-articular, 66 neurenteric/enterogenous see neurenteric/ enterogenous cyst perineural/Tarlov, 84 synovial see synovial cyst cytokines, 22–5 cervicogenic headache and, 740 chemotactic, 22 disc degeneration and, 22–5 inflammation and, 20, 21 pain and, 33 radicular, 615, 912, 916 see also inflammatory mediators; lymphokines

D daily activities in rehabilitation lumbar disc surgery, 970, 971 schedule of (in pain rehabilitation), 1203 DBC International equipment, cervical muscle strengthening programs, 691 de Quervain’s stenosing tenosynovitis, 628 dead man switch, fluoroscopy, 237 deafferentiation pain, 42 death, spondylodiscitis, 410 debridement childhood discitis and spondylodiscitis, 409–10 postoperative infections, 411 deceleration injuries to cervical spine, 601, 603 decompression cervical foraminal stenosis, 668–77 cervical myelopathy, anterior, 755–6 complications, 761–2 outcome, 764 cervical myelopathy, posterior, 756–61 cervical nerve root, posterior, 658–60 foraminal see foraminotomy laser see laser treatment lumbar/lumbosacral, 905, 906 in degenerative disc disease, 1067–8 in degenerative spondylolisthesis, 1106–7 for hematomas, 1151–2 inclusion criteria, 927 in isthmic and dysplastic spondylolisthesis, 1100 lumbar/lumbosacral, for herniated disc, 927–37, 940–8 indications, 940 lumbar/lumbosacral, for spinal stenosis, 955–65, 1106–7 definition of terms, 956–7 extent, 957 indications/contraindications, 955–6 planning, 957 previous, 956 results, 964–5 technique, 962–4 metastatic disease, 479, 479, 481 thoracic cord, 800 thoracoscopic, 1402, 1403 see also discectomy deconditioning, physical (in chronic pain patients), 1213–21

1423

Index deconditioning, physical (Continued) historical perspectives, 1214 physiologic approach to treatment, 1227 quantification, 1225–6 deep interosseous ligament see interosseous ligament deep venous thrombosis see thromboembolism degeneration/degenerative disease (disc), 17, 60–6, 813–26 anulus fibrosus in, 821, 832, 866 axial compression loading with, 834 biochemistry, 22–5 endplate see endplate imaging, 60–6 compared with infection, 407 thoracic spine, 781 lumbar see lumbar disc mechanisms/pathophysiology, 814–23, 1013 lumbar spine, 814–23, 1057, 1065 means of studying, 833–4 in sports injuries, 1349–50 nucleus pulposus in, 821, 832, 866 radicular pain associated with, 615 spinal stenosis associated with, 63 steroid injection-associated acceleration, 1054 temporal relationships, 25 total disc replacement, 1391 whiplash injury-associated risk of, 610 degeneration/degenerative disease (generally or other than discs) facet joints, 835 instability in, 1121 scoliosis see scoliosis spondylolisthesis see spondylolisthesis Dekompressor, lumbar, 905, 906, 925, 934–5 complications, 934 indications/contraindications, 934 outcomes, 934–5 technique, 934 deltoid muscle manual muscle testing, 629 pain and its evaluation, 624–5 demineralized bone matrix in spinal fusion, 1127 demyelinating disease imaging, 82 pain, 41–2 denervation, radiofrequency see radiofrequency ablation Denis classification, sacral fractures, 1281 dens (odontoid process), functional anatomy, 518, 520 dependence benzodiazepines, 182–3 management, 1208 opioid, 164–5 see also addiction Depo Medrol[O] see methylprednisolone depolarization, 194, 195 local anesthetic effects, 195 depression cervical radicular pain surgery and, 658 low back pain patients, 1218 self-report questionnaire, 107–9 treatment, 1208 see also antidepressants dermatomal somatosensory evoked potentials (DSEP), 98 dermoid cyst, 419 imaging, 84

1424

descending pathways and pain, 44 destructive spondyloarthropathy, cervical spine, 562–3 detoxification (in drug dependency), 1208–9 developing (low-income) countries, epidemiology of spinal pain, 11 development (incl. embryological and fetal) abnormalities see congenital/developmental abnormalities cervical spine, 515–17 lumbar spine, 855–9 thoracic spine, 767 vertebrae, 424, 515, 855–6 diabetes type 1, osteoporosis associated with, 438 diagnostic techniques, 53–112 injections see injection (intraspinal) placebo effect, 205 diaphragm detachment in thoracoscopic spinal surgery, 1403 sporting activity and the, 1333 diary, anxiety disorders, 179 diazepam acute anxiety, 180 lactating mothers, 1327 in pregnancy-related back pain, 1326 as sedative, 242 diffuse idiopathic (interstitial) skeletal hyperostosis (DISH; Forestier’s disease), 74, 392 Paget’s disease and, 447 diffuse noxious inhibitory control (DNIC), 204 digestive tract see gastrointestinal tract 1,25-dihydroxyvitamin D3 and bone metabolism, 435–6 diode laser for disc decompression and nucleotomy, 337 direct current electrical stimulation as spinal fusion adjunct, 1126, 1127 disability, 13 assessment questionnaires, 1234–5 disc (intervertebral), 17–18, 827–38 biomechanics, 17–18, 828–35 cervical spine, 577, 578 substructures, 831–3 terminology relating to, 828–31 cervical see cervical discs coccygeal see coccygeal disc decompression see decompression degeneration see degeneration development fetal, 516, 856–7 postnatal, 517, 858 dysfunction leading to degeneration, 814 herniation see herniation, disc imaging (normal discs), 59 internal disruption see internal disc disruption lumbar see lumbar disc motion segment see motion segment pain relating to see pain (spinal/back), discogenic puncture (for discography) cervical, 295–6 lumbar, 292–3 thoracic, 297–8 radicular pain and role of, 197–8 replacement see arthroplasty ruptured/slipped see herniation, disc sacrococcygeal, anatomy and injection, 269–71

disc (Continued) sport-related functional anatomy, 1332 structure/anatomy, 17, 827–8, 865–7 cervical spine, 577 thoracic see thoracic disc see also entries under intradiscal discectomy (disc resection), 321–30, 331, 939–40 cervical, anterior, with fusion, 661–3, 664–5, 675–7 cervical, anterior, without fusion, 664 biomechanical effects, 577, 578 in cervical myelopathy, 755 in cervical myelopathy, combined with corpectomy, 756, 1403 cervical, percutaneous, 930, 1404 endoscopic see endoscopic procedures laser see laser treatment lumbar, 930–2, 939–50 contraindications, 940–1 in decompressive surgery for spinal stenosis, 958–9, 963, 964 microscopic see microsurgery percutaneous see percutaneous procedures thoracic, thoracoscopic, 800–1 discharge criteria, sedation and analgesia, 242–3 disciplinary action, opioids and fear of, 165 discitis, 409–11, 534 cervical, 534 discography complicated by, 724–5, 725–6 chemonucleolysis complicated by, 318 children see children imaging, 70, 534 postoperative discitis, 67 lumbar discography complicated by, 299, 1043 intradiscal electrothermal annuloplasty complicated by, 1062 pain, 813 management, 409–11 endoscopic, 1408 postoperative imaging, 67 with microscopic discectomy, 948 prevention, 411–12 pyogenic see pyogenic discitis spinal injection complicated by, 217 in cervical discography, 724–5, 725–6 in lumbar discography, 223, 299 thoracic examination, 779–80 treatment, 783 discography (analgesic), 297 cervical, 723 lumbar, 1044 discography (provocative), 210–11, 291–302, 721–8 axial neck pain, 685 cervical see cervical discography clinical trials, 299–300 complications, 221, 223, 299 CT following see computerized tomography discography indications/contraindications, 291 lumbar see lumbar discography postprocedural care, 298 preprocedural evaluation and patient preparation, 291–2 risks and complications, 299 thoracic, 297–8, 299, 301, 790–1, 794

Index discography (Continued) in total disc replacement, preoperative evaluation using, 1390 disease vs illness, definition, 1231–2 dislocations, cervical sports-related, 1334–5, 1344 displacement, 829 Distinguished Clinician Award, 7 Distinguished PASSOR Member Award, 7 distraction test, 543–4 distress in chronic low back pain, 1218 disuse, neuromuscular effects, 1213–14 diving accidents, 1334–5, 1353 dizziness, opioid-induced, 361 doorbell sign, 543 dopamine anxiety and, 176 pain and, 48, 49 dorsal columns of spinal cord, electrical stimulation, 344 dorsal horn electrical stimulation, 344 pain and, 30, 40, 41, 43 dorsal nerve plexus, thoracic disc and vertebral bodies innervated by, 790 dorsal rami anatomy cervical, 525–6 lateral branches see lateral branches lumbar, 863–4, 1259 sacral, 1259 thoracic, 768, 770–1, 788 dorsal root(s) cervical, 525 electrical stimulation, 344 lumbar, 863 section (rhizotomy), 1192–3 dorsal root entry zone anatomy, 1193 electrical stimulation, 344 lesioning (drezotomy), 1193–4 dorsal root ganglion (DRG), 29, 46, 193 cervical, 278–80, 748 anatomy, 278, 525 injury in whiplash, 617 radiofrequency denervation, 278–80, 719, 748 excision (ganglionectomy), 1192–3 lumbar, 284–5, 804 anatomy, 284, 863–4 pain and the, 804, 911–12 radiofrequency denervation, 284–5 mechanical deformation, 718 radicular pain and, 197 thoracic, 281–2 anatomy, 281 radiofrequency denervation, 281–2, 795–6 dorsal sacral plexus, 1259 dose, radiation absorbed, 230, 231 quantities and units for biologic risk quantitation, 232 management for radiology staff, 233–6 measurement (dosimetry), 231, 234–5 dose equivalent (radiation), 230, 231, 232 to fetus/embryo, 238 Down’s syndrome, atlantoaxial instability, 576–7 drainage, wound, 412 spinal hematomas and, 1151 draping, vertebroplasty, 368 drezotomy (dorsal root entry zone lesioning), 1193–4

dropped head syndrome, 387 drug abuse, opioids and previous history of, 166 drug adverse effects on bone, 436 fusion surgery and, 1124–5 drug dependency see dependence drug—drug interactions antiepileptics, 131–2, 132, 133, 134, 135, 169 COX-2-specific inhibitors in surgical setting, 120 opioids, 169 drug therapy/medication (pharmacotherapy) anxiety see anxiolytics cervicogenic headache, 746 complications of spinal injections, 213–16 for emergencies (incl. resuscitation), 241 failed back surgery syndrome, 1142 lumbar axial pain, 994 lumbar radiculopathy due to herniated disc, 874–7, 888 osteoporosis, 440–3, 1286 Paget’s disease, 447–8 pain see analgesia; analgesic drugs sacroiliac joint syndrome, 1249 spondyloarthropathies, 396–7 spondylolisthesis, 1087–8 thoracic inflammatory disorders, 784 in vertebroplasty patients, preoperative considerations, 367–8 dual-energy X-ray absorptiometry (DEXA) in bone density determination, 436–7, 1285 duloxetine lumbar radiculopathy due to herniated disc, 876 side-effects, 183 DuPen catheter, 1177 dura (mater) arteriovenous lesions, 84–5 attachments in cervicogenic headache etiology, 740 ectasia in ankylosing spondylitis, 74 imaging, 69–70, 74 lumbar anatomy, 863, 864 puncture, 219–20 caudal injections, 222 cervical injections, 220 tear/injury in microscopic discectomy, 948 pseudomeningocele due to, 1147 tension tests lower limb, 894, 900 upper limb see upper limb, neural/dural tension tests see also intradural; thecal sac and entries under epidural; transdural dynamic radiographs, coccydynia, 1291–5 dynanometers, handheld, for isometric testing of lower extremity muscles, 845 dynatomal maps for cervical nerve roots, 615, 616, 647 dysesthesia complicating endoscopic surgery, 1411 dysplastic (congenital) spondylolisthesis, 1077, 1080 surgery, 1100

E economic cost; see cost edema, leg/pedal, opioid-induced, 361

education (American football), tackling technique, 1347 education (patient) and information/advice/ counseling back pain axial, rehabilitation, 994–5, 1022 failed back surgery syndrome, 1143 in lumbar radiculopathy due to herniated disc, 878 in pregnancy, 1321 cervical problems exercise in neck pain, 692–3 radicular pain, 642 whiplash injury, 599–600 functional restoration programs in chronic pain patients, 1208, 1229 spinal injection procedures, 207–11, 213 education (professional) and training manual therapy, 694 PASSOR and, 5–6 efferent pathways and pain, 43–4 Ehlers—Danlos syndrome and pregnancy, 1309 elbow pain, tendinopathies causing, 627 elderly see age; older adults electrical stimulation see electrotherapy; functional electrical stimulation; nerves, electrical stimulation electroacupuncture and TENS, neck pain, 699 electrodes spinal cord stimulation, 341–3, 345–7, 1167–8 X-ray source, 229 electrodiagnostic studies in radiculopathy, 95–104, 388 in cervical radiculopathy and radicular pain, 100, 618, 631–2 EMG sensitivity, 99 implications of confirmed radiculopathy, 103 lumbosacral radiculopathy see lumbosacral radiculopathy nonspinal causes of radiculopathy, 388 purpose, 98 usefulness, 98 electrodiagnostic studies in shoulder pain, 555 electrolyte disturbances, steroid-associated, 156 electromagnetic therapy, pulsed, 699 electromyography (EMG), 95, 96, 96–7, 99–103 cervical radiculopathy/radicular pain, 631–2, 719 failed back surgery syndrome, 1144 hip—spine syndrome, 1278 limitations, 102 purpose, 98 sensitivity, 99 stingers, 1366 thoracic spinal pain, 781 usefulness, 98 whiplash injury studies, 603 electromyography—biofeedback in pain rehabilitation, 1208 electrophysiology cardiac, local anesthetic effects, 147 nerve conduction, 194–5 electrotherapy (incl. electrical stimulation) lumbar axial pain, 995 radiculopathy due to herniated disc, 877 as spinal fusion adjunct, 1126–7 neck/cervical pain, 699

1425

Index electrotherapy (Continued) radicular pain, 638 nerves see nerves, electrical stimulation spinal cord see spinal cord, stimulation electrothermal therapy, intradiscal see intradiscal electrothermal therapy Elvey’s upper limb neural tension tests see upper limb Ely test, 843, 1278 embolism, pulmonary, vertebroplasty-associated risk, 502 see also thromboembolism embolization metastatic disease, 478 primary tumors of bone, 464 embryological development see development emergency equipment, sedation/analgesia, 241 emergency response, on-field cervical spine injuries, 1344–5, 1359–60 emesis (vomiting) with opioids, 167, 361 EMLA cream, 146 encephalomyelitis, acute disseminated, imaging, 82 endocrinopathies diagnosis, 438 opioid-induced, 361 see also hormones endoneurium dorsal root ganglion, 193 peripheral nerve, 194 endoscopic procedures, 1407–13 anterior lumbar interbody fusion, 1399–400 gasless, 1401 discectomy, 1407–13 cervical, 1404 epidural adhesiolysis, 1143, 1161 foraminotomy and foraminoplasty, 1408–9 posterior cervical, 673, 674–5 indications, 1407–9 laminectomy, cervical partial, 759 problems and complications, 1411–12 technique, 1410–11 see also minimally invasive procedures; thoracoscopic surgery endothelium in acute inflammation, 18 polymorphonucleocyte adhesion to, local anesthetic effects, 141 endplate, cartilaginous/vertebral, 827–8, 833, 866 anatomy/structure, 303–4, 827–8, 866 degeneration, 827–8, 833 MRI, 1038 see also Modic changes function incl. mechanics, 833, 866 imaging, 59 in laser decompression and nucleotomy, damage, 337 endurance strategies in coping with low back pain, 1217 endurance training, cervical muscles in chronic pain, 691, 692 enterogenous cyst see neurenteric/enterogenous cyst enteropathic arthritis, 394 enthesopathy in spondyloarthropathy, 391 entrapment neuropathies, forearm, 627–8 eosinophil(s), 20 eosinophilic granuloma, 457 ependymoma, 420 imaging, 75–6, 420

1426

epicondylitis, lateral and medial, 627 epidemiology of spinal pain, 9–16 epidermoid cyst, 419 imaging, 84 epidural (extradural) adhesiolysis see adhesiolysis epidural (extradural) blood patch, 219–20, 1148 epidural (extradural) infections incl. abscesses, 404, 417, 534–5 cervical, 534–5 complicating discography, 221, 725 clinical presentation, 404 compression myelopathy, 562 complicating spinal injection, 216 in cervical discography, 221, 725 imaging, 70–1 management, 411 pathogenesis/etiology/natural history, 404 epidural (extradural) infusion of analgesics (opioids) for intractable pain, 1177, 1178, 1181, 1182, 1183 efficacy, 1185 epidural (extradural) injections, 220–1, 248–59 anatomic/pathoanatomic considerations, 248–9 anesthesia, local anesthetics used, 144 dural puncture see dura, puncture face validity of diagnostic blocks, 189 steroids, 220–1, 248–9, 248–59 side-effects/complications, 215, 220–1, 651–4 steroids, in cervical region, 220–1 in cervicogenic headache, 747–8 in radicular pain, 645–56 steroids, in lumbar region, 913–14, 982–3, 1014–18 case study, 1022 efficacy, 913 safety, 913–14 in spondylolisthesis, 99, 1089–90, 1090, 1091–5 technical procedure, 913, 1017–18, 1018 thoracic, 792 types, 249–59 epidural (extradural) lesions abscess see abscess arachnoid cyst, 84 fibrosis see fibrosis, epidural hematoma, 1149–52 clinical features, 1150–1 complicating intrathecal infusion pump implantation, 362 complicating spinal injection, 217, 1150 in pregnancy, 1328 other causes, 1150 lipomatosis, associated with spinal steroid injection, 155 neoplasms, 417 imaging, 77–81 scar, postoperative, 66 epidural (extradural) mapping, 1160 epidural (extradural) venous stasis, 805 epidurography in epidural fibrosis, 1155 in adhesiolysis procedure, 1157 epimeres, 767 epineurium, 1137 dorsal root ganglion, 193 peripheral nerve, 194 erector spinae muscles, anatomy and function, 524–5, 774, 862, 992, 1110 ergonomic restoration, 1207 in cervical radicular pain, 642

erythrocyte sedimentation rate (ESR), infection, 407, 408, 535 ester-type local anesthetics, 145–6, 196 pharmacology, 139 estrogen fusion surgery and effects of, 1124 osteoclast effects of, 427 in osteoporosis, 442 estrogen receptor modulators, selective, in osteoporosis, 442 etanercept ankylosing spondylitis, 397 lumbar radicular pain, 916, 917 etidronate, Paget’s disease, 449 etiological/causal factors (spinal pain), 12–13 Europe, epidemiology of spinal pain, 10 European Spondyloarthropathy Study Group criteria, 393 evaluation see assessment evocative chromodiscography, 1410 evoked potentials radiculopathy/radicular pain, 98 cervical, 719 lumbosacral, 897 somatosensory see somatosensory evoked potentials Ewing sarcoma, 81, 461 cervical, 533 examination, physical/clinical ankylosing spondylitis, 392, 780 axial neck pain, 685 in back pain, 387–8, 1033–5 nonspinal causes of pain, 387–8 in pregnancy, 1314–17 structuring of electrodiagnostic studies following, 95–6 cervical axial neck pain, 730 cervical myelopathy, 565 cervical radiculopathy/radicular pain, 628–9 cervical spine see cervical spine coccyx in pain (coccydynia), 1290 in pregnancy, 1316 lumbar spine, 839–53 in axial pain, 1066 disc herniation, 939 in spondylolisthesis, 1079–80 lumbosacral radiculopathy, 894–5, 900–1 case report, 906 sacroiliac joint, 1241–7 in pregnancy, 1315–16, 1323 shoulder pain, 554 thoracic spinal pain, 779–80 tumors metastatic, 472 primary, 454–5 see also assessment excitatory amino acids and pain, 33, 47 exercises/physical activities (and training), 1206 epidural adhesiolysis patients, 1161, 1162 in functional restoration program, 1206, 1227–9 intradiscal electrothermal therapy patients, postprocedure, 312–13 lumbar disc surgery rehabilitation, 971, 972 lumbar pain/low back pain rehabilitation axial, 994, 1022 in pregnancy, 1321–4

Index exercises/physical activities (Continued) lumbar radiculopathy due to herniated disc, 874, 881–2 neck pain rehabilitation acute non-traumatic, 686–8 acute traumatic (incl. whiplash injury), 599, 688–90 chronic/recurrent, 690–2 radiculopathy, 641 piriformis syndrome, 1304 sacral insufficiency fractures, 1286 spondylolysis, 1375–7 see also activities; inactivity; sports expectation and placebo effect, 204 experimental (animal) studies, whiplash injury, 602 extension cervical examination, 541 lower cervical spine, 577 retraction and, with traction and rotation, 694 upper cervical spine, 574 lumbar, injury due to, 992 thoracolumbosacral and lumbosacral orthosis in control of, 488 see also flexion—extension bending; flexion— extension radiographs; hyperextension extension-biased exercise, axial back pain, 995 extension-pattern microinstability, 1115 extensors cervical, in chronic neck pain, strengthening, 687–8 hip, examination, 844 lumbar, 862, 863 external rotation sign in sacroiliac joint syndrome, 1242 extracellular matrix bone see bone, matrix metalloproteinases, 22–4 nucleus pulposus, 866 extradural analgesia/blood patch/lesions etc. see entries under epidural extramedullary intradural neoplasms, 76–7, 417–19 cervical myelopathy, 561 imaging, 76–7 extremities see lower limb; upper limb extrusion (disc), 60 lumbar, 940 MRI, 818 eye absorbed radiation dose to, 232 spondyloarthropathies involving, 396 steroid adverse effects, 156

F F-reflexes, 97 FABERS and forced FABERS test, 1244, 1247, 1315 face mask (American football helmets), removal, 1345–6 face validity, 187 diagnostic blocks, 189 facet joints (zygapophyseal joints), 260–8, 276–8, 282–4, 979–81, 1019–21, 1197 cervical see cervical facet joints imaging, 59 synovitis, 70–1 infection, 404

facet joints (Continued) management, 411 postprocedural, 404 injections, 260–8 cervical facet joints see cervical facet joints lumbar see lumbar facet joints rehabilitation technique, 262–8, 1020 lumbar see lumbar facet joints pain, 979–81, 1019–21 diagnostic injections, 199, 979, 1028–9 radiofrequency ablation see radiofrequency ablation therapeutic local anesthetic injections see local anesthetics therapeutic steroid injections, 979–80, 1020 thoracic, 787–90 in whiplash injury see cervical facet joints pain, lumbar see lumbar facet joints pain, lumbar, pathophysiology, 1027–8 resection in microscopic discectomy, 944 in sports injuries cervical, 1344 degenerative cascade involving, 1350 thoracic see thoracic facet joints in torsional loading, damage/degeneration, 835 failed back (surgery) syndrome (FBSS; residual symptoms/pain following lumbar disc surgery), 967–8, 1129–36 cause/etiology, 1129–32 establishing, 1133–4 neural scarring see neural scarring pre-/intra-/postoperative factors underlying, 967–8 pseudomeningocele, 1147–9 psychological factors, 1132 structural factors, 1129–30 technical failure and complications, 1131–2, 1134 definition, 967, 1129 history-taking, 1133 imaging, 66–7, 1130, 1132–3 rating of pain, 1129 treatments, 1142–4 intrathecal opioids, 1143, 1184–6 fall and fractures, 439 false-negative (in tests), lumbar provocation discography, 1043 false-positive (in tests), 188 diagnostic blocks, 189 lumbar provocation discography, 1040–3, 1043 familial factors, Paget’s disease, 445 family group in pain rehabilitation, 1208 fascia, thoracolumbar see thoracolumbar fascia fast MRI lumbar spine, 55, 58 pregnant patient with low back pain, 1317 fasting, preprocedure, ASA guidelines, 240 fat graft, neural scarring in failed back surgery, 1144 fatigue fractures, 1281 fear biological basis, 174–5 in low back pain, 1225 protective/avoidance behavior, 807, 1217–18, 1227 see also anxiety females see women femoral cutaneous neuropathy, lateral, in pregnancy, 1313

femoral nerve stretch test, 849 crossed, 849 fentanyl, 242, 355 intrathecal infusion, 355 in pregnancy, 1326 transdermal patch, 168–9 fetus analgesic drug hazards, 1325–7 development see development exercise causing harm to, 1321 radiation exposure, 238 FGFs and osteogenesis, 426 fibrillations, paraspinal muscle, 99, 100, 103 fibrinolytic system in inflammation, 19 fibroblast growth factors and osteogenesis, 426 fibroblastic phase, whiplash injury, 689 fibrosis, epidural, 1139–40 diagnosis/imaging, 1141–2, 1144, 1155 in failed back surgery syndrome, 1131 pathophysiology, 1139–40, 1155 treatment, 1142–4 gabapentin, 131, 1142 surgical see adhesiolysis see also scarring fibrosis, intraneural, 1139–40 treatment, 1142–3 fibrous bands, lumbar nerve root, 865 fibrous dysplasia, cervical spine, 532 fibrous histiocytoma, malignant, cervical, 533 fibular dowel technique, Bohlman’s, 1105 figure-4 (Patrick’s) test, 1244, 1247, 1315 filament circuit (X-ray tube), 232 filtration of X-rays, 229 fingertip to floor test, 840–1 Finland, epidemiology of spinal pain, 10, 12 fistulas, arteriovenous, 84–5 fixation, internal see internal fixation fixed-rate (non-programmable) pain pumps, 353, 363, 1177–8 flexibility (spine) lumbar spine, assessment, 843–4 in prolonged sports injury, increasing, 1380–1 rectus femoris (Ely test), 843, 1278 in spondylolysis, increasing, 1375, 1377 Flexicore replacement disk, 1394 flexion cervical examination, 541 lower cervical spine, 577 upper cervical spine, 574, 688 lumbar injury due to, 992 lateral, 862, 863 relaxation phenomenon, absence, 807 in sacroiliac joint syndrome, tests of, 1242 sports-related, 1332 thoracolumbosacral and lumbosacral orthosis in control of, 488–90 see also hyperflexion; lateral flexion flexion-biased exercise, axial back pain, 995 flexion—distraction techniques in lumbar axial pain treatment, 1004, 1005 flexion—extension bending, 835 flexion—extension radiographs, lumbar segmental instability, 1112–13 flexion-pattern microinstability, 1114–15 flexor(s) cervical, 523

1427

Index flexor(s) (Continued) in acute neck pain, defects and strengthening, 687–8 lumbar, 862 flexor carpi radialis, manual muscle testing, 631 fluid disturbances, steroid-associated, 156 fluid pressure, 828–9 flumazenil, 241, 243 fluorodeoxyglucose (FDG) for PET, 89, 90, 91–2 infections, 91 tumors metastatic, 473 primary, 456 fluoroscopic procedures, 229 biopsy guidance for suspected metastatic lesions, 473 cervical injections (for guidance), 679 epidural steroids, 645–6 intra-articular (facet joint) steroids, 682 chemonucleolysis, 317 complications, 652 contrast media reactions, 215–16 kyphoplasty, 378–9 radiation protection patient, 237–8 staff, 236 sacroiliac joint injections, 1253 views, 246–8 fluoroscopy table, discography, 210 fluoxetine as anxiolytic, 181, 182 fluvoxamine as anxiolytic, 181, 182 food prior to vertebroplasty, 367–8 football see American football; soccer footdrop with laser decompression and nucleotomy, 336 foramina (intervertebral) cervical, stenosis, 667–78 clinical presentation and patient evaluation, 668 etiology, 667 surgical decompression, 668–78 lumbar/lumbosacral anatomy, 863, 864, 865, 1138 disc herniation into, 887–9, 946 interbody fusion via see transforaminal lumbar interbody fusion stenosis, 889, 952, 953, 955, 1093–4 removal of part of wall see foraminotomy steroid injections through see transforaminal epidural steroid injections foraminotomy endoscopic see endoscopic procedures posterior cervical, 659, 660, 672–6 and/or discectomy, 661–2, 662, 663–4 posterior lumbar, 957 force, 828 force-couple concept, shoulder motion, 550 forced FABERS test, 1315 forearm pain, evaluation, 625, 627–8 Forestier disease see diffuse idiopathic skeletal hyperostosis fractures (especially vertebral) biomechanics and, 439–40 cervical sports-related, 1334–5, 1344, 1369–70 coccygeal, 1290–1 compression see compression fractures epidemiology, 439–40 healing, NSAID (non- and COX-2-specific) effects on, 122–4

1428

fractures (Continued) insufficiency see insufficiency fractures lumbar low back pain, 809 sport-related, 1336 nomenclature, 1281 pars, Z-joint injection with, 267–8 pathological, 1281 osteoporosis see osteoporosis pagetoid bone, 447 risk/incidence of aging and, 428 factors increasing, 437–8 post-kyphoplasty, adjacent and remote sites, 511–12 post-vertebroplasty, adjacent and remote sites, 503, 511–12 sacral see sacrum stress see stress fractures thoracic diagnosis, 780 examination, 780 pain, 777–8, 780 treatment, 782, 783 vertebroplasty for see vertebroplasty free radicals in inflammation, 20–1 Freiberg test, 1302–3 functional assessment/tests cervical radicular pain, 632 lumbosacral radiculopathy, 897–900 in rehabilitation, 1203–4 spondyloarthropathies, 396 functional deficits in lumbar radiculopathy due to disc herniation, 872, 873 functional electrical stimulation, 1206 functional independence with sacral insufficiency fractures, maintenance, 1286 functional MRI, upper cervical spine, 575 functional pain, 162 Functional Rating Index, 1235 functional restoration (maintenance phase of rehabilitation), 993, 1201–38 axial back pain, 996 chronic pain patients, 1223–30, 1232 socioeconomic outcome measures in evaluation of effectiveness, 1236 fungal infections, 403, 413 fusion (arthrodesis) cervical axial neck pain, 729–36 indications/patient selection, 729–30 office evaluation, 730 for specific anatomic diagnoses, 731–3 sacroiliac joint, 979, 1269–74 anterior, 1270–1 posterior, 1269–70 spinal see spinal fusion

G G-protein-coupled receptors and local anesthetics, 141 GABA (and GABA receptors) anxiety and, 176–7 GABA-alpha agonists see benzodiazepines GABA-alpha and beta agonists for intrathecal adjuvant analgesia, 358–9 pain and, 47 gabapentin pregnancy-related back pain, 1326 radicular pain, 129–32, 1142

gabapentin (Continued) lumbar, due to herniated disc, 876 spondylolisthesis, 1087–8 gadolinium-enhanced MRI see contrast-enhanced MRI Gaenselen’s sacroiliac joint operation, 1269 Gaenselen’s test, 1244, 1396 Gaines procedure, 1105 gait abnormalities piriformis syndrome, 1301 spondylolisthesis, 1080 gallium nitrate, Paget’s disease, 450 gallium-67 citrate imaging, 90 infections, 405 gangliocytoma, 76 ganglioglioma, 76 ganglion (ganglia) cervical, 527–8 dorsal root see dorsal root ganglion (DRG) stellate/cervicothoracic see stellate ganglion thoracic, 772 ganglionectomy, 1192–3 upper thoracic, 1196 ganglioneuroblastoma, 81–2 ganglioneuroma, 81–2 gastric cancer, spinal metastases, 475–6 gastrointestinal tract adverse effects COX-2-specific inhibitors NSAIDs, 120–1 non-specific NSAIDs, 117 opioids, 167, 361 cancer, spinal metastases, 475–6 low back pain relating to disorders of, 808 spondyloarthropathies involving, 396 gate control theory, 804, 1165, 1166–7, 1191 spinal cord stimulation and, 1166–7 gelatin-derived products, neural scarring in failed back surgery, 1144 general anesthesia chemonucleolysis, 317 definitions, 239 implants for spinal cord stimulation, 345 kyphoplasty, 378 generalized anxiety disorder (GAD) buspirone, 181 pharmacotherapy, 181, 182 screening questions, 178 genetics lumbar disc degeneration, 822–3 ossification of posterior longitudinal ligament, 559 Paget’s disease, 445 spondyloarthropathies, 391 genitourinary disorders as complications in ankylosing spondylitis, 396 of spinal injections, 220 in pregnancy, low back pain due to, 1311 geriatric patients see older adults Germany, chronic whiplash syndrome, 593 giant cell tumor, 460–1 cervical, 532 imaging, 80, 460 Gillet’s test, 1242, 1315 gla proteins, 426 Glasgow coma scale, on-field athletic cervical spine injuries, 1345 glenohumeral joint anatomy, 548–9

Index glenohumeral joint (Continued) biomechanics, 549–50 innervation, 552 glia and pain, 34, 49, 50 gliosis, reactive (astrocytic response to injury), 34, 49 glucocorticoids, 153 in bone metabolism, 424, 427 see also corticosteroids glucosamine, lumbar intradiscal injections, 1054, 1071 glutamate local anesthetic neurotoxicity, 148 pain and, 33, 45, 47 wind-up, 44 gluteal region musculature, 1300 glycine, biology, 176 glycoproteins, bone matrix formation, 426 glycosaminoglycans, nucleus pulposus, 866 Goldenhar’s syndrome, cervical malformations and instability, 577 golf, spinal/back injury, 1354–5 return to competition after prolonged injury, 1384–5 golfer’s elbow, 627 gonadal effects, opioids, 167 goniometer, 842 gonococcal arthritis, differential diagnosis, 394 gout, 83 graft bone see bone graft fat, for neural scarring in failed back surgery, 1144 granuloma catheter tip, 363, 1187–8 eosinophilic, 457 gravity lumbar traction, 877 gray (Gy), 230, 231 gray rami communicantes lumbar, 864 thoracic, 768, 772 Greece, chronic whiplash syndrome, 593 group counseling, functional restoration programs in chronic pain patients, 1229 growth retardation, steroid-associated, 156 spurts, postnatal and pubertal, 517, 858 growth factors, osteogenic, 425–6 growth hormone age-related decline (=somatopause), and bone, 428–9 fusion surgery and effects of, 1124 gymnastics, 1355 gynecologic disorders in pregnancy, low back pain due to, 1311

H H-reflexes piriformis syndrome, 1303 S1 radiculopathy, 97 half-value layer, 231 halo vest orthosis, 487 hamstring flexibility assessment, 843 strength assessment, 845 exercises increasing, 1250–1 hangman’s fracture, sport, 1344 hard collar, 486

Hawkin’s maneuver, 625 Hawthorne effect and lumbar spinal manipulation, 1009 head injury in sport, 1339 restraint systems in vehicles, 586 head cervical orthosis, 486–7 head cervical thoracic orthosis, 487 headache, 740, 1209 cervicogenic see cervicogenic headache comorbid in chronic pain, management, 1209 non-cervicogenic, differences from/similarities to cervicogenic headache, 740, 741 post-dural puncture, 219, 1147–8 management, 219–20, 1148 heading balls in soccer, 1356 healing see repair heart chest pain relating to, 628 valve disease, ankylosing spondylitis, 396 heat (thermal energy) in cervical/neck pain treatment, 698–9 radicular pain, 638 in intradiscal electrothermal annuloplasty, 1057–8 in lumbar radiculopathy treatment, 877 in radiofrequency nerve lesioning, importance, 276 in radiofrequency nucleoplasty, injury to disc from, 932 heating protocol, intradiscal electrothermal therapy, 310, 311–12 helical CT see spiral CT helix—loop—helix proteins, osteoblastogenesis, 424 helmets (American football etc.), 1340, 1345–6, 1359–60 necessary removal, 1360 hemangioblastoma, 420 imaging, 76 hemangioma, vertebral body, 459 cervical region, 531 compression fracture, 500–1 imaging, 78–9, 459 hematogenous seeding/spread of infection in spinal instrumentation, 403 of metastases, 470 hematologic complications of spinal injection, 217 hematolymphopoietic tumors imaging, 81 metastatic, 476 hematoma cervical discography complicated by, 299, 727 as laser decompression and nucleotomy complication, 336 piriformis syndrome associated with, 1301 spinal, 1149–52 clinical features, 1150–1 complicating intrathecal infusion pump implantation, 362 epidural see epidural lesions etiology, 217, 1150 investigations, 1151 management, 1151–2 hematomyelia, 569 hemicrania, chronic paroxysmal (CPH), vs cervicogenic headache, 741

hemicrania continua vs cervicogenic headache, 741 hemorrhage see bleeding hemostasis, surgical, in lumbar spinal stenosis surgery, 962 heparinized patients and spinal hematomas, 1151–2 herniation, disc (slipped/ruptured disc), 60, 61–3 biochemistry, 24 cervical see cervical disc decompression see decompression endoscopic surgery, 1408 for recurrent herniation, 1409 imaging, 61–3 recurrent (postoperative) herniation, 66 lumbar see lumbar disc herniation natural history, 63 piriformis syndrome vs, 1303 thoracic see thoracic disc herniation herniation, spinal cord, transdural, 84 high-intensity zone in lumbar disc MRI, 1037–8 high-velocity low-amplitude (HVLA) manipulation lumbar axial pain, 1005, 1006, 1007, 1009 sacroiliac joint syndrome, 1252, 1253 hip abductors/extensors/flexors, examination, 844–5 osteoarthritis, 1277 in pregnancy examination, 1314 pathology, 1313 range of motion assessment in sacroiliac joint syndrome, 1245 sciatic nerve course, 1301 hip joint examination, 1278 pathology diagnostic injections, 899–900, 1278–9 lumbosacral radiculopathy vs, 893 restriction, and lumbar disc degeneration, 820 hip—spine syndrome, 1277–9 clinical presentation, 1278 diagnostic aids, 1278–9 types, 1278–9 hippocampus, fear and anxiety and the, 175 histamine, 19 histamine H1 antagonists (antihistamines) acute anxiety, 180, 181 chemonucleolysis, pretreatment, 316 histamine H2 antagonists, chemonucleolysis, pretreatment, 316 histiocytoma, malignant fibrous, cervical, 533 histiocytosis, Langerhans cell, 457 histology see biopsy Histoplasma spondylodiscitis, 413 history (historical background) cervical discography, 679, 721 chemonucleolysis, 315 deconditioning syndrome, 1214 disc replacement, 1389 interventional physiatry, 1–3 local anesthetics, 137–8 manual therapy, 693–4 opioids, 168 orthoses, 485 pain (and its management), 10, 1191, 1201 cervical axial neck pain, 679 cervical radicular pain, 657

1429

Index history (Continued) cervicogenic headache, 737 lumbar axial pain, 1014, 1192, 1193, 1194, 1195, 1196, 1197 sacroiliac joint syndrome surgery, 1269–70 sciatica and radiculopathy, 385, 389 radiofrequency denervation, 275, 679 history-taking cervical axial neck pain, 730 cervical radicular pain, 617–18 coccydynia, 1289 failed back surgery syndrome, 1133 low back pain, 808, 809, 1033–5 shoulder pain, 553–4 HIV-associated myelopathy, 569 HLA-B27 in spondyloarthropathies, 391 ankylosing spondylitis, 391, 392 Hoffman reflex, 545 primary tumors, 455 Hoffmann ligaments, 1138 holmium:YAG laser (for disc decompression and nucleotomy), 332 Hoover test, 850 hormones adrenal, 153 bone metabolism and, 424, 427 fusion surgery and effects of, 1124 opioid effects on, 167 in osteoporosis, therapeutic, 442 see also endocrinopathies Horner’s syndrome in laser decompression and nucleotomy, 337 thoracic ganglia and, 772 HTLV-I-associated myelopathy, 569 human immunodeficiency virus (HIV)-associated myelopathy, 569 human T-cell lymphotrophic virus-1-associated myelopathy, 569 humeral head (in relation to glenohumeral articulation) biomechanical aspects, 549–50 maximum diameter, 548–9 hydrocortisone, 153 hydromorphone, intrathecal infusion, 354–5, 359 hydromyelia, imaging, 83 hydrostatic pressure, 828–9 hydrotherapy (aquatic therapy) in pregnancy, 1323 hydroxyethylene diphosphonate (HDP), 99m Tc-labelled, 89–90 5-hydroxytryptamine see serotonin hydroxyzine, acute anxiety, 180, 181 hyperalgesia molecular mechanisms, 48 opioid-induced, 164 primary, 114 secondary, 114 hyperextension diving, 1353 whiplash injury, 607, 608 hyperextension brace see Jewitt orthosis hyperflexion in whiplash injury, 607, 608 hypermobility coccygeal, 1292–3 sacroiliac joint see sacroiliac joint hyperostosis, diffuse idiopathic skeletal see diffuse idiopathic skeletal hyperostosis hyperparathryoidism primary, 438

1430

hyperparathryoidism (Continued) secondary, age-related, 428–9 hyperreflexia, cervical myelopathy, 565 hypersensitivity caused by inflammation, 114 hypersensitivity reactions (allergic reactions) acute inflammation caused by, 18 spinal injections, 213 with steroids, 155 hyperthyroidism, bone turnover increase, 438 hypomeres, 767 hyporeflexia, cervical myelopathy, 565 hypothalamic—pituitary axis, opioid effects on, 167, 354 hypothalamus, fear and anxiety and the, 175 hypoxia and low back pain, 803 hysteresis, 831

I IASP see International Association for the Study of Pain iatrogenic complications endoscopic surgery, 1411–12 of intrathecal infusion pumps, 363 lumbar provocation discography, 1044 see also safety issues IDET see intradiscal electrothermal therapy ileum, perforation in laser decompression and nucleotomy, 336 iliac compression test, side-lying, 1242, 1244, 1246 iliac crest autografts, in anterior cervical discectomy and fusion, 669–70 height assessment, 839 palpation in sacroiliac joint syndrome, sitting/ standing, 1242 transforaminal injections and L5—S1 foramen blocked by, 257 iliac gapping test, supine, 1242, 1244 iliac spine palpation, sitting/standing posterior superior, 1242 iliacus, 862 see also iliopsoas iliocostalis, 524, 774, 862 innervation, 864 iliolumbar ligaments, 861 iliopsoas flexibility assessment, 843 lumbar disc degeneration and the, 820 in sacroiliac joint rehabilitation, 1251, 1252 see also iliacus; psoas ilium/iliac bones crest of see iliac crest osteitis condensans, 1273–4, 1309 in pregnancy crest and spine, assessment, 1315 ligament insertions, 1309 radio receiver/pulse generator implantation in posterior iliac area, 347–8 rotated, 1250–1, 1252 illness vs disease, definition, 1231–2 image guidance-assisted surgery, 1405 image intensifier, 229 imaging see radiology immobilization athlete with spinal injuries, on-field, 1346–7, 1359 sacral insufficiency fractures, adverse effects, 1286

immobilization (Continued) see also activities, modification; bed rest immune changes, CNS, and pain, 33, 40 immune system, steroid effects, 154 immunocompromised patients, thoracic pain (due to infection), 777 examination, 779–80 laboratory tests, 781 treatment, 783 immunoscintigraphy (99mTc-labelled antibodies), 90 impingement syndromes, shoulder, 625 implanted devices in cervical myelopathy surgery, 756 failure, 761 for cord stimulation see spinal cord, stimulation pain pumps, 351–65, 1177–8 compounding of drugs for, 359–61 in failed back surgery, 1143 indications, 351–2 long term use, 359–60 non-opioids (adjuvants), 356–9 opioids see opioid analgesics radiology, 1189 side effects/complications, 361–3, 1187–8 systems available, 353–4, 1177–8 trials for, 352–3, 1182 see also arthroplasty; sacral nerve roots inactivity/disuse, neuromuscular effects, 1213–14 incidence (angle), coccygeal, 1292 incidence (frequency of occurrence), spinal pain, 9 inclinometer, 842 indometacin and breastfeeding, 1327 infants, discitis, 401 infarction, spinal, 569 infection (generally or extraspinal) anterior column, causing instability, 1112 lumbar disc degeneration associated with, 823 lumbar discography complicated by, 299, 1043 neck pain due to, 534–6, 708 in Paget’s disease etiology, 445 postoperative see postoperative problems sacroiliac joint, in pregnancy, 1329 sciatica-like pain due to, 386 spinal injection complicated by, 216–17 steroid prolonged use and risk of, 156 infection (spinal/vertebral), 401–15 cervical discography complicated by, 724–5 prevention/diagnosis/treatment, 725–6 compressive myelopathy vs, 569 diagnosis (other than imaging), 407–8 imaging, 70, 404–7 neck, 534, 535 nuclear studies, 90–1, 405 postoperative infections, 67 tuberculosis, 412 intrathecal infusion pump implantation complicated by, 362 kyphoplasty-associated risk, 510 laser decompression and nucleotomy complicated by, 336 lumbar discography complicated by, 299 lumbar intradiscal electrothermal annuloplasty complicated by, 1062 management, 408–11 neck pain due to, 534, 708 prevention, 411 thoracic pain due to, 777

Index infection (Continued) diagnosis, 780, 781 examination, 779–80 treatment, 782, 783 see also discitis; osteomyelitis; spondylodiscitis inflammation, 18–22, 114–15 acute, 18 principal effects, 18 in whiplash injury, 689 cells, 20–1 cervicogenic headache and, 740 low back pain and, 803, 1013–14 mediators see inflammatory mediators process, 19–20 radicular pain and role of, 197–8, 615 cervical, 615, 645 lumbar, in failed back surgery syndrome, 1140 sterile, following spinal surgery, 403 see also anti-inflammatory effects inflammatory bowel disease, arthritis associated with, 394 inflammatory disorders, thoracic pain diagnosis, 780, 781–2 treatment, 782, 784 inflammatory mediators, 19, 21–2 lumbar disc degeneration and, 822 pain and, 32, 46, 114–15 cervicogenic headache, 740 discogenic lumbar, 1014 radicular, 615, 645, 912, 1140 inflammatory pain, 114–15, 162 inflexibilities, spinal, in prolonged sports injury, correction, 1380–1 infliximab ankylosing spondylitis, 397 radiculopathy due to herniated disc, 876–7, 916, 917 information, patient see education informed consent controlled substances, 165 intradiscal electrothermal therapy, 305 infraclavicular area, implants for spinal cord stimulation, 349 infraspinatus testing, 629, 630 Infusaid, 353 inhomogeneitiy, 831 anulus fibrosus, 832 injection (intraspinal/intrathecal), 187–202, 213–27, 245–73, 351–65 cervical spine see cervical spine complications and side-effects, 213–27 in general, 213–20 hematoma, 217, 1150 specific to injection site, 220–3 steroids see corticosteroids diagnostic, 187–202, 248 axial back pain, 977, 979–81, 982–3, 985 axial neck pain, 679, 682, 685 cervicogenic headache, 738–9, 745 coccydynia, 269, 1294–5 control blocks, 189–90 failed back surgery syndrome, 1130 with local anesthetics see local anesthetics lumbar facet joint, 1028–9 nerve roots see nerve root block piriformis syndrome, 899, 1303 premise, 193 principles, 187–91

injection (Continued) technique (in general), 248 thoracic facet joint, 789–90 for local anesthesia see spinal anesthesia lumbar spine see lumbar spine needle see needle patient assessment see assessment patient education, 207–11, 213 procedure, 209 steroids see corticosteroid therapeutic, 248–9 cervicogenic headache, 707–12 coccydynia, 269–70, 1294–5 endoscopic surgery following, 1407 lumbar axial pain (in general), 1013–25 lumbar disc pain, 982–3, 985, 1018–19, 1049–54 lumbar facet joint pain, 979–80, 1020, 1029 lumbar radiculopathy due to herniated disc, indications, 887 neck pain, 682, 700, 707–12 piriformis syndrome, 1305 pregnancy-related back pain, 1328 sacroiliac joint, 268–9, 1253, 1262 spondylolisthesis, 1089–95 with steroids see corticosteroids technique (in general), 248–9 thoracic spinal pain, 782, 783 zygapophyseal joint pain, 199, 979–80, 1020 thoracic spine see thoracic spine injection (other than intraspinal), 187–273 epidural see epidural injections hip joint, 899, 1278–9 intravenous see intravenous injection joints see joint injections in lumbar radicular pain/radiculopathy diagnostic, 899–900 therapeutic (trigger points), 872 injury (traumatic - generally or non-spinal) acute, cervical radiography, 630 fetal, exercise causing, 1321 iatrogenic see iatrogenic complications nerve see nerves nociception/pain and, 33–5 injury (traumatic - spinal/spinal region) atlanto-occipital joint, mechanisms, 707 cervical/neck clinical assessment of axial neck pain due to, 680 facet joint, mechanisms, 710–11 in sport see sports whiplash see whiplash injury cervical radicular pain in patients with history of, 617 cervical stability assessment with neurologic deficits referable to, 581 coccygeal, 1290 disc degeneration following, 60 dural see dura neck pain due to, 708 rehabilitation, 599, 688–90, 696–7, 702 piriformis syndrome following, 1301 sacroiliac joint pain associated with, treatment, 1254 spondylolisthesis associated with, 1077, 1079 spondylotic cervical radicular pain associated with, 620–3 sports see sports thoracic, pain, 779

injury (Continued) torsion, lumbar discogenic pain, 813 see also cumulative trauma disorders; fractures; spinal cord injury innervation see nerve supply innominate bones see pelvis inspection/visualization (in back pain) cervical spine, 539 lumbar spine, 839–40 sacroiliac joint, 1242 instability, 573–81, 1109–19, 1121 causes, 1111–12, 1121, 1122 postoperative, in spinal fusion patients, 1132 cervical see cervical instability clinical manifestations and assessment, 1111–16, 1121, 1122 definitions, 573, 1109 fusion surgery see spinal fusion lumbar, 1109–19 in degenerative disease, 814–17, 1112 rehabilitation, 1116–17 see also microinstability instantaneous axis of rotation (IAR), 1333–4 instrumentation cervical spine fusion surgery in foraminal stenosis, 670 in myelopathy, 759–60 in lumbar surgery in automated percutaneous discectomy, 322–3 fusion surgery, 1121, 1125 for gradual reduction in spondylolisthesis, 1103–5 sacroiliac joint with fusion, 1271 without fusion, 1270 see also internal fixation insufficiency fractures in pelvic region in pregnancy, 1312 sacral see sacrum insulin-like growth factor-1 and osteogenesis, 425 interbody fusion, 1123 complications, 1132 posterior lumbar, 960–1, 1123 intercoccygeal joint, 1289 intercostal nerves, 770 freezing, 784 intercostobrachial nerve, 770 Interdisciplinary Pain Rehabilitation programs, 1224–5 interlaminar space exposure in microscopic discectomy, 943 interlaminar space injections of epidural steroids, 249, 251 cervical, 251, 645, 646 complications, 651 disadvantage compared to transforaminal injections, 250 lumbar, 251, 1018 complications, 222 indications and efficacy, 1018 in spondylolisthesis, 1095 technique, 1018 thoracic, 251 interleukin-1 (IL-1) cervicogenic headache and, 740 disc degeneration and, 23 inflammation and, 22

1431

Index interleukin-1 (Continued) local anesthetics and, 141 radicular pain and, 198 interleukin-1 receptor antagonist, recombinant, in lumbar radicular pain, 916, 917 interleukin-6 (IL-6) and radicular pain, 912 internal disc disruption (syndrome) cervical, 682 lumbar, 813 internal fixation cervical region in cervical myelopathy, 756, 760–1 lower, 579 upper (C0—C1—C2), 576 lumbar/lumbosacral region, in spondylolisthesis, 960, 1102–3, 1105 screws see screws thoracic spine, thoracoscopic, 1402 see also instrumentation internal pulse generator for spinal cord stimulation, 1168 International Association for the Study of Pain (IASP) cervicogenic headache classification scheme, 740, 743 positive discography criteria, 1042 radicular pain vs radiculopathy classification scheme, 718 International Headache Society diagnostic criteria for cervicogenic headache, 707, 737, 742 International Spine Intervention Society (ISIS), discography criteria, 1046 interosseous (sacroiliac) ligament, deep anatomy, 1261 injections diagnostic, 1262 therapeutic, 1262 pain arising from, 1259 interscapular pain, 680–1 interspinales muscles, 525, 863 interspinous ligaments, 860 intertransversarius, 863, 992 intertransverse space, 770 intertransversi muscles, 774 interventional physiatry, history, 1–3 intervertebral cages, 1126 lumbothoracic, 1400 misplacement, 1132 thoracoscopic placement, 1403 intervertebral disc see disc intervertebral foramina see foramina intervertebral motion related to low back pain, 1111 intervertebral osteochondrosis, 61 intestine cancer (colorectal), spinal metastases, 476 in laser decompression and nucleotomy, perforation, 336 posteriorly placed colon in automated percutaneous lumbar discectomy, 322 intra-articular injections see joint injections intradiscal antibiotics in cervical discography, 726 intradiscal electrothermal therapy/annuloplasty/ nucleoplasty (IDET), 303–14, 1057–63 clinical data review, 1061–2 lumbar, 223, 303–14, 984, 1057–63, 1068, 1070–1 anatomy relating to, 303–4 anesthesia, 307

1432

intradiscal electrothermal (Continued) case histories, 313, 986 complications, 223, 1062 patient positioning and skin markings, 306–7 patient preparation, 305–6, 307 patient selection/indications, 304–5, 984, 1058–9 postprocedure care, 312–13 prolotherapy compared to or after failed response to, 1054–5 repeat, 305 sedation, 307 lumbar, technique, 1059–61 catheter, 309–12, 1059–60 introducer placement, 308–9 thoracic, 795 intradiscal injections in lumbar discogenic pain, 1018–19 steroids, 1019, 1049–56 intradiscal pressure lumbar, evaluation, 878 thoracic, evaluation, 794 thoracolumbosacral and lumbosacral orthosis effects on, 488 intradiscal prolotherapy, 1054–5 intradural lesions arachnoid cyst, 83–4 neoplasms, 75–7, 417–21 compression myelopathy, 561 intramedullary abscess, cervical, 535 intramedullary arteriovenous malformations, 85 intramedullary neoplasms, 75–6, 419–21 compression myelopathy vs, 569 imaging, 75–6 intraneural fibrosis see fibrosis, intraneural intraosseous clefts, vertebral fractures containing, 501 intrathecal analgesia and anesthesia see spinal analgesia; spinal anesthesia intravenous injection antibiotics in cervical discography, prophylactic, 726 local anesthetics, inadvertent prevention and recognition, 148 toxicity, 147 treatment, 147 introducer placement for intradiscal electrothermal therapy, 308–9 inversion traction, 877 ion channels (nerves), 194–5 local anesthetics and, 138–9, 140, 141, 195–6 see also specific ions ionic contrast media, 237 ipriflavone, Paget’s disease, 450 irradiation-associated problems see radiationassociated problems ischemia lumbar disc degeneration and, 823 spinal cord, due to compression, 558–9 ISIS (International Spine Intervention Society), discography criteria, 1046 Isomed pain pump, 353 isometric testing of lower extremity muscles in lumbar spine examination, 845 isotonic exercises, 1227 isthmic spondylolisthesis (IS), 1077, 1079, 1086 management, 1106 facet joint injection, 1095

isthmic spondylolisthesis (Continued) surgical, 1100 itching (pruritus), opioid-induced, 167, 361

J Jackson’s sacral fixation technique, 1105 Japanese Orthopaedic Association score, cervical myelopathy, 567–9 Jefferson’s fracture, sport, 1344 Jendrassik maneuver, 846 Jewitt orthosis (hyperextension brace), 486, 488 lumbar radiculopathy due to herniated disc, 885 job see entries under occupational joint fusion see fusion joint injections (intra-articular injections) incl. blocks atlantoaxial see atlantoaxial joint atlanto-occipital joint see atlanto-occipital joint facet/zygapophyseal joint see facet joint hip joint, 899, 1278–9 sacroiliac see sacroiliac joint thoracic facet joint, 789–90 joint position error, cervical, measurement, 690 juxta-articular cysts, 66

K kainate receptors and pain, 33 Kaltenborn, Freddy, 696–7 Kenalog®, spinal injection, 158–9 kerma (kinetic energy released per unit mass), 230 ketamine, 150, 241 ketoprofen, postoperative pain, 116 ketorolac, postoperative pain, 116 kidney see entries under renal kilovoltage peak, 230, 232 kinetic and kinematic parameters, sacroiliac joint, 1239–40 kinetic chain dysfunction in sports injuries, 1350 kinetic energy released per unit mass (kerma), 230 kinins, 19 knee flexion test, prone, in sacroiliac joint syndrome, 1242 Knight orthosis, 489 Knight-Taylor orthosis, 489 Koller, Carl, 137 KTP laser treatment (for disc decompression and nucleotomy), 332, 337 lumbar, 931, 932 kyphoplasty, percutaneous, 377–84, 440, 441, 507–13, 1404–5 anatomical considerations, 378 biopsy during, results, 510–11 complications and their prevention, 381–2, 510 compression fractures see compression fractures contraindications, 509 controversies, 509 evidence-based outcomes, 509–10 fractures at adjacent and remote sites following, 511–12 indications, 508–9 for metastases, 512 metastatic disease, 478–9 for multiple myeloma, 512 osteoporosis, 783 patient selection, 377–8 errors, 381–2 primary tumors of bone, 464 technique, 378–81

Index kyphosis post-laminectomy, 762 Scheuermann see Scheuermann disease thoracic diagnosis, 780 examination, 780 loss, 773 normal, 767 pregnancy-related changes, 1309 treatment options, 782 vertebral fractures causing, 440

L L1-L2 staphylococcal spondylodiscitis, 406 L4 radiculopathies in L4—L5 spondylolisthesis, 1092 L4—L5 disc degeneration, MRI, 815–17 disc puncture (for discography), 292–3 laparoscopic anterior interbody fusion, 1400 spondylolisthesis management, 889, 1091–3, 1094 MRI, 818 L5 deficits in lumbar radiculopathy, 873 L5—S1 disc automated percutaneous discectomy, 327–8 chemonucleolysis, 317–18 puncture (for discography), 293 foramen in transforaminal epidural steroid injections, 1017–18 blocked, 257–9 laparoscopic anterior interbody fusion, 1400 radiculopathy, evoked potentials, 98 spondylolisthesis, management, 889, 1091–3, 1094 Z-joint, lumbar medial branch block for, 266 L5 vertebrectomy in spondyloptosis, 1105 labor, TENS in, 1324 laboratory studies (incl. biochemistry) ankylosing spondylitis, 392 bone tumors primary, 455 secondary, 472 epidural adhesiolysis, preprocedural, 1156 infection, 407–8, 535 neck pain, 535 osteoporosis, 437–8 Paget’s disease, 447, 533 thoracic spinal pain, 780–1 labral tear, superior or posterior, 626 lactation and medications for low back pain, 1326–7 lamellae of anulus fibrosus, anatomy relevant to intradiscal electrothermal therapy, 303 of bone, structure, 423 lamina (dorsal horn), pain and, 30 wind-up, 43 see also interlaminar space injections lamina (vertebral), lumbar, 859 laminectomy, 756–7, 956 cervical, 756, 756–7 kyphosis following, 762 outcome, 764 for hematoma, 1151–2 for implanting spinal cord stimulation electrodes, 1165, 1170, 1171 instability following, 1132 partial see laminotomy

laminectomy (Continued) thoracic, 800 total/bilateral/complete, 956, 957, 962–3 in degenerative scoliosis, 961 in degenerative spondylolisthesis, 959 technique, 962–3 laminoforaminotomy, posterior cervical, 672 case study, 675–6 see also foraminotomy laminoplasty in cervical myelopathy, 756, 757–9 neck pain following, 762 outcome, 764 laminotomy (partial laminectomy), 956, 957, 963–4 in cervical myelopathy, 756–7 endoscopic, 759 in degenerative spondylolisthesis, 959 technique, 963–4 ‘laminotomy’ implants for spinal cord stimulation, 342 Lamitrode 4/44/88 electrodes, 1167 lamotrigine, 132 adverse effects, 131, 132 radicular pain, 132 lumbar, due to herniated disc, 876 Langerhans cell histiocytosis, 457 laparoscopic anterior lumbar interbody fusion, 1399–400 large bowel (colorectal) cancer, spinal metastases, 476 laryngeal nerve, recurrent, injury, 220, 221 in stellate ganglion block, 713 Lase device, 925 laser treatment endoscopic foraminoplasty, 1408–9 neck pain, 698–9 percutaneous discectomy and nucleotomy, 331–9, 931–2 clinical experience, 335 complications, 335–6 indication and patient selection, 332–3 lumbar, 931–2, 1068 principles, 331–2 safety, 332 selection of laser, 337 technique, 334–5 thoracic, 783 lateral bending, 835 lateral branches (of dorsal rami) sacral, 1259 injection therapy, 1262 sensory stimulation-guided radiofrequency neurotomy, 1262–6 thoracic, 770, 771 lateral canal (lumbar spine) disc herniation into, 887–9 stenosis endoscopic surgery, 1408–9 lumbar spine see lumbar spinal stenosis, lateral lateral epicondylitis, 627 lateral femoral cutaneous neuropathy in pregnancy, 1313 lateral flexion lumbar spine, 862, 863 mobilization, 694 lateral inspection of lumbar spine, 840 lateral mass screws, cervical, 760 minimally invasive placement, 1404

lateral rotation, cervical, examination, 541 lateral shift pattern of microinstability, 1115–16 latissimus dorsi, 774 law and legislation compensation for cervical radicular pain due to accident, 657–8 controlled substances, 166 leads (electrodes), spinal cord stimulation, 341–3, 345–7, 1167–8 leg see lower limb legal issues see law leptomeninges, metastases, imaging, 78 leukemia, 81 leukocytes (white cells) counts in cervical discitis and vertebral osteomyelitis, 534 polymorphonuclear see neutrophils radiolabelled, 90 leukotrienes in inflammation, 19, 21 local anesthetics and, 141 levator ani muscles, pain originating from, 1295 levator scapular weakness testing, 629 levetiracetam, 134 adverse effects, 131, 134 dosing and titration, 132, 134 in radicular pain, 134 levobupivacaine, 142, 143, 144 L’hermitte’s sign/phenomenon, 545, 726 lidocaine (Xylocaine), 142–3, 245 development, 138 neutrophils and effects of, 196 patch (Lidoderm), 146 lumbar radiculopathy due to herniated disc, 877 trigger point injections in lumbar radiculopathy due to herniated disc, 886–7 lifestyle rehabilitation, 1204 lifting in ante-/postpartum low back pain, technique, 1255 lumbar and cervical function evaluation, 1226 ligament(s) cervical region, 520–1 anatomy, 520–1 sprains in sport, 1341, 1368–9 whiplash-associated injury, 601–3 glenohumeral joint, 548–9 lumbar region, 860–1 nerve fibers, 867 pain relating to, 804 in pregnancy in lower back, 1309 in sport, anatomy and injury, 1332 ligamentum flavum, 521, 860 anatomy, 521, 860 calcification, 560 release/detachment in microscopic discectomy, 944 in partial laminectomy (=laminotomy), 964 in total laminectomy, 963 retraction, in microscopic discectomy, 944–5 ligamentum nuchae, 520 limbs see lower limb; upper limb Linder maneuver, 848 line-1/2/3/4/5/6 approaches to long-term intrathecal infusion, 359–60 linear attenuation coefficient, 231 lipid mediators in inflammation, 21

1433

Index lipoma, intramedullary, 420 lipomatosis, epidural, associated with spinal steroid injection, 155 liposomal preparations of local anesthetics, 150 lithium battery for spinal cord stimulation, 343 Lithuania, chronic whiplash syndrome, 593, 594 litigation for cervical radicular pain due to injury, 658 load-sharing classification system, instability determination, 1121, 1122 loading axial, and cervical spine injuries in sport, 1334–5, 1339–40, 1344, 1354 lumbar disc degeneration related to, 819–21 mismatch between appropriate local intersegmental stiffness and demand of, 1002 provider (doctor)-induced, in lumbar axial pain treatment, 1004–6 soft tissue, 829–30 anulus fibrosus, 832 bending load, 835 cadaveric studies, 834 compression loading, 834 nucleus pulposus, 831 torsional loading, 835 vertebral body fracture related to, 496–7 local anesthesia chemonucleolysis, 316–17 implant insertion for spinal cord stimulation, 345 intradiscal electrothermal therapy, 307 vertebroplasty, 368 see also spinal anesthesia local anesthetics, 137–52, 213–15 as adjuvant analgesics in intrathecal infusions, 356–7 classification, 141–2, 196 complications/side-effects/toxicity, 146–9, 213–15 in lumbar sympathetic block, 223 current development, 149–50 diagnostic injections cervicogenic headache, 745 hip joint, 899, 1278–9 sacroiliac joint, 199–200, 899, 977, 1261–2 selective nerve root see nerve root blocks zygapophyseal joint pain, 199, 979, 1028–9 history, 137–8 long-acting and pain-selective, 149–50 mechanism of action, 138–41, 195–7 ion channels, 138–9, 140, 141, 195–6 mixtures, 146 tachyphylaxis, 150 therapeutic injections coccydynia, 269–70, 1295–6 neck pain and cervicogenic headache, 709, 710 neural scarring in failed back surgery, 1142, 1143 piriformis syndrome, 1305 sacroiliac joint complex pain, 1262 zygapophyseal joint pain, 199 topical see topical anesthetics see also nerve block log-roll injured athlete on-field, 1359 technique, 1346–7

1434

longissimus, 524, 774, 862, 992 innervation, 864 longitudinal ligaments anterior, 520 anatomy, 520, 860 imaging, 59 posterior, 304, 520–1 anatomic aspects, 304, 520–1, 577, 860 biomechanical aspects, 577 imaging, 59, 74 innervation, 867 ossification see ossification longus capitis, anatomy, 523 longus colli, anatomy, 523 lorazepam, acute anxiety, 180 lordosis cervical, diminished, 540 lumbar, pregnancy-related changes, 1309 loupes (in discectomy), advantages of microscope over, 942 Low Back Outcome Score, 1235 low back pain (lumbar pain), 803–11, 871–1128 in automated percutaneous lumbar discectomy, increased, 329 axial see axial pain biological and dysfunctional aspects of chronic pain, 806–7 biological causes, 803–5 classification/differential diagnosis, 808 in coccydynia, 1290, 1295 disability questionnaires, 1234, 1235 in failed back surgery syndrome, 1133 full syndrome and individual predominance, 807 intervertebral motion related to, 1111 mechanisms, 804–5 medical causes, 803–11 non-mechanical, 808 orthoses see orthoses in Paget’s disease, 446–7 pathophysiology, 1013 percutaneous discectomy for herniations, 925 in piriformis syndrome, 1299 in pregnancy see pregnancy with radiating lower extremity complaints, differential diagnosis, 939–40 risk factors for chronic pain, 805 sacral insufficiency fractures, 1283 secondary, 807–9 sports injuries, 1336, 1349 tertiary rehabilitation programs, 1225 in vertebroplasty, exacerbation, 374 low-density lipoprotein receptor-related protein 5 and osteogenesis, 425–6 low-income countries, epidemiology of spinal pain, 11 lower limb/leg assessment in hip—spine syndrome, 1278 edema, opioid-induced, 361 flexibility, and lumbar disc degeneration, 820–1 length discrepancy assessment, 844 sacroiliac joint syndrome and its management in, 1253 single-leg stance with triplanar motion, pregnant patient, 1314 lower limb/leg pain causes, 893

lower limb/leg pain (Continued) in failed back surgery syndrome, 1133 see also sciatica diagnosing cause, 1277 algorithmic approach, 900–6 low back pain radiating to, differential diagnosis, 939–40 selective nerve root injections, 897–9 mechanical causes, 808 sciatic see sciatica see also straight leg raising test lumbar arteries, 861–2 lumbar belts in pregnancy, 1324–5 in radiculopathy due to herniated disc, 885 lumbar disc(s), 981–5 bulging, definition, 940 categories, 60–1 degeneration, 60–1, 813–26, 1057 chemical inflammatory properties, 822 epidemiology, 813 histology, 821–2 instability associated with, 814–23, 1112 medical and genetic risk factors, 822–3 pathophysiology, 814–23, 1057, 1065 radiology, 823–4 treatment, 1067–73 exploration in lumbar spinal stenosis surgery, 963 extrusion see extrusion herniation see lumbar disc herniation intradiscal electrothermal therapy see intradiscal electrothermal therapy laser decompression and nucleotomy complications, 335 technique, 334–5 MRI of various pathologies, 815–18 normal, imaging, 59 pain relating to, 804, 813, 911, 981–5, 1015 in failed back surgery syndrome, 1130 inflammatory mechanisms, 1013–14 management, 981–5, 1018–19, 1049–63, 1130 pathophysiology, 813, 1015 sequestration, 889 definition, 940 space, irrigation in discectomy, 945 sport-related pathology, 1336–7 surgery, 1065–75 excision see discectomy rehabilitation see rehabilitation residual symptoms see failed back (surgery) syndrome total disc replacement, 1071–3, 1390–4 lumbar disc herniation (rupture/slip), 866, 939–50 definition, 939, 951 diagnosis, 939–40 algorithm, 901 differential, 939–40 in failed back surgery syndrome, 1131 high lumbar level (L2/3/4), 387, 947 imaging, 62 lumbosacral radiculopathy due to, 893–4 natural history, 912–13 of paramedian herniation, 871–3 pathophysiology, 911, 912, 939, 1015 in pregnancy, 1313 radicular pain with, 911, 912 recurrent, 947, 948

Index lumbar disc herniation (Continued) treatment, 871–87, 887–8, 906, 927–50, 1015 chemonucleolysis see chemonucleolysis conservative methods, 871–87, 887–8, 940 discectomy see discectomy lateral or foraminal herniation, 887–9 paramedian herniation, 871–87 pathoanatomic considerations with epidural injections, 249 sequestered herniated disc, 889 unusual situations, 946–8 lumbar discography, 292–5, 300, 983–4, 1033–47, 1066–7 case study, 986 complications, 223, 299, 1043, 1044–5 controversies, 1043–6 CT following see computerized tomography discography data guiding treatment, 1045–6 in failed back surgery syndrome, 1130 false-positives, 1040–3, 1043 history and physical examination correlations with, 1033–5 MRI correlations with, 1036–8 predictive value for treatment and prognosis, 1038–40 technique, 292–5, 983–4 validity, 1040–3 lumbar facet (zygapophyseal) joints, 262, 282–4, 804, 979–81, 986 anatomy, 262, 282–3, 992, 1027, 1197 biomechanics, 992 orthoses and, 485–6 cysts MRI, 816 spinal stenosis due to, 906, 955 degeneration, MRI, 815 in failed back surgery syndrome, 1131 injections, 263–4, 979–81, 986, 1020, 1028–9 case study, 1023 complications, 223 in spondylolisthesis, 1095 pain and the, 804, 979–81, 986, 993, 1019–21, 1027–32, 1131 diagnosis, 1028–9 patterns of pain, 1028–9, 1277 radiofrequency denervation, 282–4, 980, 981, 986, 1029–30, 1197 clinical effectiveness/outcomes, 1029–30, 1197 complications, 223 procedure, 283, 1197 in spondylolisthesis, 1095 lumbar flexion relaxation phenomenon, absence, 807 lumbar medial branch block see medial branch block lumbar nerve roots anatomy, 863, 864, 1137–8 blocks (diagnostic selective), 632 exploration in lumbar spinal stenosis surgery, 963 in failed back surgery syndrome (damage etc.), 1131, 1138, 1139 pathophysiology, 1139–40 herniated nucleus pulposus involving multiple roots, 947 pain (radicular pain) and radiculopathy, 804, 871–974, 911–21, 1014–15

lumbar nerve roots (Continued) algorithms for diagnosis and treatment, 914, 917–18 epidural fibrosis as cause of, 1155 inflammatory mediators and, 615 lower extremity symptoms, 1277 medical management, 871–92 motor and sensory examination, 845 natural course, 912–13 pathophysiology, 911–13 surgery see surgery transforaminal epidural steroid injections, 1014–15 pain (radicular pain) and radiculopathy, spinal injections, 913–17 indications, 887 retraction in microscopic discectomy, 944–5 stimulation, 1173 lumbar pain see low back pain lumbar paraspinal muscles, 862–3 anatomy, 862–3 disinsertion in partial laminectomy (laminotomy), 963 in total laminectomy, 962–3 examination, 100 functions, 992 innervation, 864 pain relating to, 804–5 selective weakness in low back pain patients, 807 strengthening exercises in sports-injured, 1381 lumbar peritoneal shunting, 1149 lumbar radiculopathy see lumbar nerve roots, pain; lumbosacral radiculopathy lumbar spinal cord stimulation, 347 lumbar spinal stenosis, 63–4, 911, 951–65 central see central canal stenosis classification, 951–5 definition, 951 diagnostic algorithm, 902–3 disc rupture into stenotic canal, 947 electrodiagnostic studies, 101 facet joint cysts causing, 906 foraminal, 889, 952, 953, 955, 1093–4 lateral, 889, 911, 952, 953, 954–5, 956, 958–9, 964 failed back surgery syndrome due to, 1130 lower limb pain, 1277 medical therapy, 875, 889 spondylolisthesis with see spondylolisthesis, degenerative surgical decompression see decompression types, 952–5, 956 combined, 955 primary, 953 secondary, 953–4 surgical management related to, 958–61 see also lumbosacral spinal stenosis lumbar spine, 803–1238 anatomy, 859–67, 991–2 predisposing to degeneration, 820 predisposing to spondylolysis, 1373 biomechanical disorders, 803–1238 biomechanics, 991–2 degenerative disease, 818–20, 819–20 orthoses and, 485 development, 855–9 facet joints see facet joints

lumbar spine (Continued) hip pathology and/or pathology of, 1277–9 injections, 913–17 complications, 222–3 interlaminar epidural, 251 in radicular pain see lumbar nerve roots, pain transforaminal epidural see transforaminal epidural steroid injections injury of/in region of, pathophysiology, 992 injury of/in region of, sports-related American football, 1336–7, 1353–4, 1354 baseball/softball, 1352 biomechanical etiologic factors, 1351 cycling incl. mountain biking, 1351, 1356, 1386 golf, 1354 return to competition after prolonged injury, 1384 running sports, 1384 soccer, 1355–6 tennis, 1356 instability see instability interbody fusion see spinal fusion lordosis, pregnancy-related changes, 1309 mechanics and pathomechanics, 1109–11 minimally invasive techniques, 1397–401 MRI technique, 54–5 pain see axial pain; lumbar nerve roots physical examination, 839–53 in pregnancy, examination, 1314 primary tumors, surgery, 465 radiofrequency denervation see radiofrequency ablation vertebrae see lumbar vertebrae see also entries under L lumbar spondylosis, 267–8 athlete returning to competition after prolonged injury, 1384 orthoses, 492 Z-joint injection, 267–8 lumbar sympathetic chain anatomy, 287, 864–5 block, 287–8, 714–15 complications, 223, 715 face validity, 189 indications and contraindications, 715 outcomes, 715 radiofrequency thermolesion, 715 surgical excision, 1196–7 lumbar traction in radiculopathy, 872, 877–8 lumbar vertebrae normal, imaging, 56–7 vertebroplasty, approach, 369 lumbosacral ligaments, 861 lumbosacral orthosis (LSO), 485 pregnancy, 1324 see also thoracolumbosacral orthosis lumbosacral radiculopathy, 893–909 algorithmic approach, 900–5 case report, 906–7 clinical approach, 894–5 definition, 893 diagnostic evaluation, 895–900 electrodiagnostic studies, 100–1, 895–6 EMG sensitivity, 99 evoked potentials, 98 etiologies, 893 failed back surgery syndrome, 1131 imitators, 893

1435

Index lumbosacral radiculopathy (Continued) management, 903–6, 907 pathophysiology, 893–4 piriformis syndrome associated with, 1301 see also lumbar nerve roots, pain lumbosacral spinal stenosis EMG sensitivity, 99 surgical decompression see decompression see also lumbar spinal stenosis lumbosacral stiffness, coccyydynia due to, 1295 lumbothoracic cage insertion, 1400 lung cancer/carcinoma, spinal metastases, 475 see also respiratory complications lupus erythematosus, systemic, 82 luxation, posterior coccygeal, 1292 lymph nodes, cervical, palpation, 543 lymphokines, 19 lymphoma, 81 extradural, 81, 417 imaging, 81 metastases, 476 solitary, 463 lymphoproliferative tumors see hematolymphopoietic tumors lysosomal compounds, 19

M McCulloch, John, 319 Mckenzie method of mechanical diagnosis and therapy, 694 lumbar axial pain, 995, 1033 lumbar radiculopathy due to herniated disc, 878–81 neck pain acute nontraumatic, 686 chronic, 691 macrophage(s) disc herniation and, 24 in inflammation, 21 macrophage-colony stimulating factor (M-CSF; CSF-1) osteoclast activity and, 427 osteoclast differentiation, 426 magnetic evoked potentials, 98, 98 magnetic fields, combined, augmenting spinal fusion, 1126 magnetic resonance angiography, primary tumors, 456 magnetic resonance imaging, 53–5, 60–85, 1409–10 abnormal spine, 60–85 advantages and disadvantages, 53–4, 1409–10 cervical spine, 722–3 axial pain, 731 cervical myelopathy, 567, 763 cervical radiculopathy and axial neck pain, 630–1, 718, 719 cervicogenic headache, 738, 745 discography vs, 722–3 infections, 534, 535, 536 in sports-related injury, 1335, 1342, 1343–4, 1363–4, 1367, 1368 stenosis, 668, 1363–4 whiplash injury, 596, 597, 603, 610 discogenic pain source identification discography vs, 296, 299 lumbar, 981 failed back surgery syndrome, 1132 neural scarring, 1141

1436

magnetic resonance imaging (Continued) pseudomeningocele, 1148 seroma, 1152 functional, upper cervical spine, 575 hematoma, 1151 hip—spine syndrome, 1278 implanted pain pumps, 1189 infections, 405–6 cervical, 534, 535, 536 kyphoplasty, multiple fractures, 382 lumbar disc, 981, 1066 degeneration, 815–18, 823 herniation before chemonucleolysis, 315–16 in intradiscal electrothermal annuloplasty, pre-procedural, 1058 provocation discography correlations, 1036–8 in lumbar nerve root infiltration (for guidance), 915 lumbosacral radiculopathy, 896, 903 normal spine, 56–9 Paget’s disease, 447 piriformis syndrome, 1303 pregnant patient with low back pain, 1317 roles, 53 sacral insufficiency fractures, 1284–5 sacroiliac joint syndrome, 977 shoulder pain, 555 spondyloarthropathies, 394–5 spondylolisthesis, 1082 spondylolysis, 1374 in sports-related injury, 1361 cervical spine, 1335, 1342, 1343–4, 1363–4, 1367, 1368 technique, 54–5 thoracic spine disc disease, 799, 800 fractures, 781 infections, 781 inflammatory diseases, 781 total disc replacement, preoperative assessment, 1389–90 tumors metastatic, 473 primary, 456 magnification control, CT, 236 Maigne’s syndrome, 774 maintenance phase of rehabilitation see functional restoration Maitland concept, 694–5, 694 malignant tumors (cancer) compression fractures due to see compression fractures imaging, 81 of associated compression fractures, 69, 78 pain with in general see pain (cancer) low back pain, 809 neck pain, 532–3 shoulder, 554 primary, 453, 461–3 secondary see metastases malnutrition and spinal fusion surgery, 1124 manipulation see manual therapy manual muscle testing in lumbar spine examination and low back pain, 844–5 in neck/cervical/upper limb pain, 544, 545, 629

manual therapy (manipulation and mobilization), 693–8, 1001–12 basis, 1002–3 cervical (for neck pain), 693–8 evidence for, 696–7 radicular pain, 639–40 risks, 697–8 coccydynia, 1296 history, 693–4 influential therapists and their concepts, 694–6 lumbar axial pain, 995, 1001–12 case examples, 1009 diagnostic findings, 1003 diagnostic independence, 1008–9 effectiveness, 1009 in pregnancy, 1327 safety and contraindications, 1009–10 lumbar disc surgery rehabilitation, 971 lumbar radiculopathy due to herniated disc, 872, 884–5 methods, 1004–7 see also specific methods sacroiliac joint syndrome, 1249–50, 1251–2 in pregnancy, 1255 skill and control factors, 1003 thoracic spinal pain, 782 massage, 1206 low back pain (axial), 995 in pregnancy, 1327 neck pain (axial), 698 mast cells, 20 matrix metalloproteinases (MMPs), 22–4 see also extracellular matrix Maverick replacement disk, 1394 maximal compression test, 543 MCP-1 and disc herniation and degeneration, 24 meaning model and the placebo effect, 204 measles virus and Paget’s disease, 445 mechanical factors bone mass affected by, 436 cervical myelopathy, 557–8 lumbar nerve root compression, 1139–40 see also biomechanics mechanical pain see axial pain mechanoreceptors, facet joints, 199 thoracic, 787 medial branch (of thoracic dorsal rami), anatomy, 770–1, 788 medial branch block, 265–7 cervical, 265–6 in axial pain, 731 complications, 221 in radiculopathy/radicular pain, 632 in whiplash injury, 590–1 lumbar, 266–7, 980–1, 1020–1, 1028 complications, 223 efficacy, 1020–1 face validity, 189 in spondylolisthesis, 1095 technique, 1021 in spondylolysis, 1377 thoracic, 266, 771, 772, 788–9 see also radiofrequency ablation medial epicondylitis, 627 median nerve bias dural glide, 640 median nerve entrapment, 627 medical disorders distinction of illness vs disease, 1231–2

Index medical disorders (Continued) predisposing to lumbar disc degeneration, 822–3 medical records, controlled substances in, 166 medico-legal issues, compensation for cervical radicular pain due to accident, 657–8 see also law Medtronic pain pumps, 353, 353–4 spinal cord stimulator, 1167 MedX equipment, cervical muscle strengthening programs, 691 membrane, formation in vertebral development, 855 membrane stabilizers, epidural and intraneural fibrosis, 1142 memory problems, opioid-induced, 361 Menell’s test, 1316 meningeal nerve, recurrent see sinuvertebral nerve meninges (incl. leptomeninges) development, 516, 856 metastases, imaging, 78 meningioma, intradural extramedullary, 418–19 compression myelopathy, 561 imaging, 76–7 meningitis, 535–6 complicating spinal injection, 216–17 menopause and bone loss, 428–9, 435 menstrual status, bone mass and, 436 meperidine, 242, 355 intrathecal infusion, 355, 1182 mepivacaine, 142, 143, 144 meralgia paresthetica in pregnancy, 1313 mesenchyme/mesenchymal cells, condensation, 424 metabolic bone disease neck pain, 533–4 work-up, 438–9 metabolism in disc degeneration, 822 steroid effects, 154 metalloproteinases, matrix (MMPs), 22–4 metastases (secondary tumors), 419, 469–83 anatomic distribution, 469–70 thoracic spine, 768 clinical presentation, 470–1 compression fractures, 500 compression myelopathy, 561–2 diagnosis, 469 imaging, 472–3 extramedullary metastases, 77–8 intramedullary metastases, 76 intradural extramedullary, 419 imaging, 77–8 kyphoplasty, 512 management, 477–9 algorithmic approach, 480–1 origin of primary tumors, 474–7, 1283, 1286 physical examination, 471–2 sacral, 1283, 1286 biopsy, 1283, 1286 sacral insufficiency fractures vs, 1283 thoracic spine, 778, 783–4 treatment, 469–70, 783–4 work-up, 472–5 algorithmic approach, 474

methadone, 168, 355 intrathecal infusion, 355 methotrexate, spondyloarthropathies, 397 methylene diphosphonate (MDP), 99mTc-labelled, 89–90 methylprednisolone locally-injectable (incl. Depo-Medrol), 157–8, 159 adverse effects, 1054 lumbar discogenic pain, 1051, 1052, 1053 neural scarring in failed back surgery, 1142 oral, 157 METRx system, minimally invasive-transforaminal lumbar interbody fusion, 1397–9 Mexico, epidemiology of spinal pain, 11 Miami J orthosis, 486 microendoscopic posterior cervical foraminotomy, 673, 674–5 microglia and injury and pain, 34 microinstability clinical syndromes of, 1114–16 MRI, 816 microscope, operating, for lumbar herniated disc decompression, 942 see also microsurgery microsphere preparations of local anesthetics, 150 microsurgery (microscopic surgery) discectomy (microdiscectomy), lumbar, 924, 925, 942–8 complications, 948 technique, 942–8 laminotomy, 964 midazolam for intrathecal analgesia, 358, 359 for sedation, discography, 292 midline herniated nucleus pulposus, 947 midline myelotomy, 1195–6 migraine (M) vs cervicogenic headache, 741 milliamperage (mA), 230, 232 Million visual analog scale, 1234–5 mineralization, bone, 426 mineralocorticoids, 153 see also corticosteroids Minerva orthosis, 487, 488 Mini-Finland Health Survey, 10, 12 minimally invasive procedures, 1397–406 cervical spine, 1404 epidural adhesiolysis, 1143, 1161 lumbar spine, 1397–401 metastatic disease, 478–9 primary tumors of bone, 464 sacroiliac joint syndrome, 977–9, 1253–4, 1259–67 thoracic spine, 1401–4 see also endoscopic procedures; percutaneous procedures mithramycin, Paget’s disease, 450 mitochondria and local anesthetic neurotoxicity, 148 mobilization chronic pain patients, 1227 lumbar disc surgery rehabilitation, 971, 971–2 lumbar radiculopathy due to herniated disc, 872, 882–3 neural see neural mobilization sacral insufficiency fractures, 1286 whiplash injury, 689 see also manual therapy; motion modalities see physical therapy

Modic changes (in disc degeneration), 1038, 1066 intradiscal steroid injection effects, 1053 osteochondrosis, 61 molecular mechanisms disc degeneration, 822 pain, 44–50 moment, bending, 828 monkeys, whiplash injury, 602 monoamine neurotransmitters, anxiety and, 176 monoclonal antibodies 99m Tc-labelled, 90 to TNF-α see tumor necrosis factor α monocyte chemoattractant protein-1 and disc herniation and degeneration, 24 mood, whiplash injury-associated symptoms and, 598 morphine, 168, 242 intrathecal (incl. implantable pumps), 354, 359, 360, 1182–3 with clonidine, 357, 1183 efficacy, 1184–6 in failed back surgery, 1143, 1184, 1185 morphologic variant of unknown significance, 61 mortality, spondylodiscitis, 410 motion (movement/mobility) in cervical radicular pain, repeated as test, 636 as treatment, 639–40 coccygeal, assessment, 1291, 1292 intervertebral, related to low back pain, 1111 lower cervical spine, 577 assessment, 578 range of see range of motion sacroiliac joint in pregnancy, assessment, 1315 in total disc replacement of operated segment, 1393 upper cervical spine, 574 assessment, 575 see also mobilization motion segment, 833–5 non-linearity in, 830 sports injuries and degeneration in, 1349–50 structural mechanics, 833–5 motor function/control evaluation in cervical myelopathy, 565, 568 in cervical/neck/upper limb pain and suspected cervical disorders, 544–5 in deconditioned subjects, 1216 in lumbar spine examination, 844–5, 1216 in lumbosacral radiculopathy, 895 with primary bone tumors, 455 in rehabilitation, 1203–4 exercises acute neck pain (incl. whiplash injury), 689–90 chronic neck pain, 691 learning model, in phases/stages of rehabilitation, 1116, 1117 low back pain patients deficits, 807 examination, 844–5, 1216 treatment strategies, 1206–7 motor nerve conduction studies, radiculopathy, 97 embryological development, 515, 856 motor neuron disease vs compression myelopathy, 569 motor neuron lesions, upper, tests for, 545

1437

Index motor system (anterior cord) syndrome, and its symptoms, 618, 621 motor testing of implanted spinal cord stimulation system, 349 motor vehicle accident rear-end collision, 586–7 biomechanics, 584–6 muscle tension, 586 whiplash injury, 586–7, 607 mountain biking, 1356 movement see mobilization; motion Mulligan, Brian, 695 multiaxial inventories, 106–7 multidirectional-pattern microinstability, 1116 multidisciplinary team, pain rehabilitation, 1203 multifidus, 525, 774–5, 862–3 innervation, 864 in lumbar disc surgery rehabilitation, 971 stabilizing role, 1110 multiple myeloma, 476–7 compression fractures, 500 kyphoplasty, 512 diagnosis, 438 multiple sclerosis (MS), 82, 82 compression myelopathy vs, 570 muscle(s) (skeletal) adverse effects on (myotoxicity) local anesthetics, 149 opioids, 167 steroid, 156 cervical, evaluation/testing, 540 in neck/cervical/upper limb pain, 544, 545, 629 core, examination in pregnancy, 1314 disorders causing neck pain, 708 see also myopathy evoked compound muscle action potentials, in lumbosacral radiculopathy, 897 functional decline (and atrophy/wasting) in deconditioned subjects, 1216 examination for, 540 in lumbar axial pain treatment, activation, 1004, 1007 in lumbar disc surgery rehabilitation, 971 in lumbar instability rehabilitation, activation, 1116–17 in lumbar spine examination and low back pain, evaluation testing, 844–5, 1115 pain see myofascial pain paraspinal see paraspinal muscles pelvic girdle, flexibility assessment, 843–4 in posterior pelvic pain treatment, activation, 1250–2 with shared nerve root shared but different nerves, 388 shoulder, strength, 550 strength see strength; strengthening exercises stretch reflexes see stretch reflexes tension, in rear-end collisions, 586 weakness see weakness whiplash-associated injury, 601–3, 605 muscle energy techniques lumbar axial pain, 1004, 1005 sacroiliac joint syndrome, 1251 muscle fibers of deconditioned subjects, 1216 muscle relaxants axial back pain, 994 failed back surgery syndrome, 1142

1438

muscle relaxants (Continued) lumbar radiculopathy due to herniated disc, 876, 888 pregnancy-related back pain, 1326 musculocutaneous nerve, 551 musculoskeletal conditions low back pain in pregnancy due to, 1313–14 sciatica due to, 385–6 physical examination for, 387, 388 musculoskeletal inspection of spine, 455 musculoskeletal system disordered, initiating pain-related phenomena, 1202 exercises in pregnancy causing injury to, 1321 musculoskeletal ultrasound, spondyloarthropathies, 395 Mycobacterium tuberculosis/M. bovis/ M. africanum see tuberculosis myelography, 56 cervical myelopathy, 565–7 CT following, 56 lumbosacral radiculopathy, 896 metastatic tumors, 472 neoplasms, 75 primary bone tumors, 456 pseudomeningocele, 1148 roles/advantages/disadvantages/technique, 56 spinal stenosis, 63–5 myeloma multiple see multiple myeloma solitary see plasmacytoma myelopathy (spinal cord), 557–62 cervical see cervical myelopathy differential diagnosis, 569–70 in metastatic disease, 471 MRI, 66 radiation see radiation-associated problems myeloradiculopathy, cervical, 617–18, 618, 623 myeloscopy, epidural adhesiolysis with, 1143 myelotomy, midline/comissural, 1195–6 myocardial contractility, local anesthetics affecting, 146–7 myoclonus, opioid-induced, 167 myofascial pain (muscle pain) pelvic floor in pregnancy, 1312 syndromes of, 779, 1202 diagnosis, 780 physical examination, 780 treatment, 782 trigger points with see trigger points myofascial therapy/myofascial release lumbar axial pain, 1022 radiculopathy due to herniated disc, 872, 883–4 neck pain, 698 myopathy drug-induced see muscle paraspinal muscle, 387 myotome development, 767

N nalmefene, 243 naloxone, 243 narcotics see opioid analgesics National Health and Nutrition Examination Surveys (NHANES), 10, 385 Paget’s disease, 445 natural apophyseal glides, 695 nausea with opioids, 167, 361

Nd:YAG laser see neodymium:YAG laser neck dysfunction vs shoulder dysfunction, 545 injury see injury neck pain, 679–736 axial see axial pain centralization see centralization in cervical myelopathy surgery, postoperative, 762 cervical orthoses, 491 cervical stability assessment in patient with, 579–81 common and uncommon causes, 708 injection treatment, 682, 699–700, 707–12 medical causes, 531–7 neurologic examination, 544–5 posterior, referred from other sites, 623–4 in whiplash injury, 593–600, 604, 607 needle, spinal, 245–6 automated percutaneous lumbar discectomy, 323, 325 in cervical discography, microbial contamination of tip, 724 in epidural adhesiolysis, 1156, 1157, 1158, 1159 in lumbar discography, insertion damage due to, 1044 site related to results, 1044 vertebroplasty insertion, 369–71 removal, 373 neodymium:YAG laser treatment (for disc decompression and nucleotomy), 331, 331–2, 332, 333, 334, 337 lumbar, 931, 932 thoracic, 783 neonates, discitis, 401 neoplasm see tumor neostigmine, intrathecal infusion, 359 neovascularization, 21 nerve(s) electrical stimulation percutaneous, in lumbar radiculopathy, 877 peripheral, 1173–4 transcutaneous see transcutaneous electrical nerve stimulation entrapment syndromes, forearm, 627–8 injury in endoscopic surgery, 1411 in failed back surgery syndrome, 1131 in pregnancy, 1313 response, 1138 in sport, 1341 see also neurologic complications injury, spinal injections, 218–19, 220 cervical, 221 lumbar, 222 radiofrequency ablation see radiofrequency ablation see also entries under neural nerve block with local anesthetics, 195–6 cervical axial neck pain, 731 major, 143 minor, 143 miscellaneous, 145 use-dependent, 140–1 nerve conduction electrophysiology, 194–5 radiculopathies, 97 cervical, 631–2

Index nerve fiber, structure, 1137–8 nerve plexus see plexus nerve root(s) anatomy, 193–4, 1192 variations, 95 cervical see cervical nerve roots compression, 951 fibrosis in response to, 1139–40 imaging, 63–5 total disc replacement and evaluation of, 1391 lumbar see lumbar nerve roots muscles sharing same root, but different nerves, 388 normal, imaging, 56–7 pseudomeningocele formation and, 1148 resection see rhizotomy sacral see sacral nerve roots thoracic, dysfunction, 779 see also radiculopathy nerve root blocks, selective (injection with local anesthetic), 197–9, 914–16 diagnostic, 197–9, 632 cervical, 632, 646–7, 723 lumbosacral, 897–9, 900, 914 therapeutic in lumbar radicular pain, 914–16 neural scarring in failed back surgery, 1142–3 nerve root pain (radicular pain), 129–36 adjuvant analgesics, 129–36, 635 algorithms for diagnosis and treatment, 914, 957–8 anatomical aspects, 193–4 cervical see cervical nerve root pain lumbar see lumbar nerve roots mechanisms, 129 radiculopathy and, definitions and distinction, 718 in whiplash injury, 609–10, 617 nerve sheath, structure, 194 nerve sheath tumors, intradural extramedullary, 418 imaging, 77 nerve supply (innervation), 856 cervical spine, 525–8 lumbar spine, 863–5 anatomy, 863–5 embryological development, 856 lumbar disc, 804, 866–7, 981 sacroiliac joint, 1241, 1259–61 shoulder, 550–2 thoracic spine region, 767–72 nerve tissue, radiofrequency current effects, 276 nervous system autonomic see autonomic nervous system central see central nervous system in pain, 29–52 anatomical aspects, 29–30 Netherlands, epidemiology of spinal pain, 10 neural aspects of pain see nervous system neural control subsystem in spinal stability, 1111 neural mobilization cervical radicular pain, 639–40 lumbar disc surgery rehabilitation, 971 lumbar radiculopathy due to herniated disc, 872, 884 neural prosthesis, sacral root see sacral nerve roots neural scarring (following spinal surgery), 1137–46

neural scarring (Continued) anatomy relating to, 1137–8 diagnosis, 1141–2 prevention, 1144 treatment, 1142–4 neural tension tests, upper limb see upper limb neural tests see neurologic examination neural tube development and differentiation, 767 neuralgia occipital, 739, 748–9 post-herpetic see post-herpetic neuralgia trigeminal, oxcarbazepine, 133 neurapraxia in cervical region, sports-related, 1335, 1341–2 return to play after, 1343–4 transient, 1335, 1341 neuraxial analgesia and anesthesia see spinal analgesia; spinal anesthesia neurenteric/enterogenous cyst, imaging, 83, 419 neuroablative techniques in chronic pain, 1191–9 neuroblastoma, 81–2 neurofibroma, intradural extramedullary, 418 compression myelopathy, 561 imaging, 77 neurofibromatosis type 1 (von Recklinghausen’s disease) dural ectasia, 71 neurofibroma, 77 compression myelopathy, 561 neurofibromatosis type 2, schwannoma, 77 neurogenic muscle wasting and atrophy in, 540 neurogenic pain cervical, examination, 539 neuropathic pain vs, 1131 neurokinin-1 receptors (NK-1R), 40, 41, 47–8 neurologic complications bone tumors primary, 454 secondary, 471 cervical myelopathy surgery, 761 cervical stability assessment in spinal injury patients with, 581 drugs (incl. neurotoxicity) corticosteroids, 215 local anesthetics, 147–9, 214 hematomas, 1150 injections, 218–19, 220 cervical, 221, 652–3, 653–4 lumbar, 222 laser decompression and nucleotomy, 336–7 lumbar discography, 299 sacral insufficiency fractures, 1283 see also central nervous system neurologic disorders in cervical radicular pain, surgical management, 663 in cervical spondylosis, 667 low back pain in pregnancy due to, 1313 neck pain due to, 708 shoulder pain due to, 552–3 neurologic examination (incl. neural tests) cervical axial neck pain, 730 with cervical spinal disorders, 543–5 foraminal stenosis, 668 myelopathy, 565 radicular pain, 636, 718 in lumbar spine (and low back pain) assessment, 844–7 in pregnancy-associated back pain, 1314

neurologic examination (Continued) primary bone tumors, 455 neuromodulation therapy, percutaneous, 699 neuromuscular causes of sciatica, 386, 386 physical examination for, 388 neuromuscular therapy, lumbar axial pain, 1004, 1005, 1007 neuronal toxicity of local anesthetics, 148–9 neuropathic pain, 162, 1165 anxiety effects on, 174 with cervical epidurals, 221 coanalgesics, 1206 in failed back surgery syndrome, 1131, 1137–46 neurogenic pain vs, 1131 neuropathies, focal forearm due to entrapment, 627–8 physical examination for, 388–9 sciatica-like pain, 386–7 neuropeptide(s), disc pathology and role of, 198 neuropeptide Y in anulus fibrosus, 866 neurophysiological basis of pain rehabilitation, 1201–2 neuroplasticity and pain, 39–40, 46, 114 neuroprosthesis, sacral root see sacral nerve roots neurotomy, radiofrequency see radiofrequency ablation neurotoxicity see neurologic complications neurotransmitters anxiety and, 176–7 pain and, 32, 44, 47, 49–50 neutral zone concept, 1109–11 neutrophils (polymorphonuclear leukocytes), 20–1 in acute inflammation, 18, 19 local anesthetic effects, 141, 196 newborns see neonates NHANES see National Health and Nutrition Examination Surveys night-time aggravation of neck pain, mechanical factors, management, 692 nimesulide, 115–16 nitric oxide (NO) cervicogenic headache and, 740 disc degeneration and, 23, 24–5 inflammation and, 20–1, 24–5 pain transmission and, 32, 33 NMDA receptors, 163–4 antagonists, 164 local anesthetic neurotoxicity and, 148 pain and, 33, 41, 46, 47, 48 wind-up, 42, 43 Nocardia asteroides, 413 nociception, 29–52, 1165–6 facet joint, 787 injury and biomechanical factors modulating, 33–5 low back pain and, 803 molecules involved, 46 placebo effect and, 204 nociceptive pain, 162, 1177 anxiety effects on, 174 nocturnal aggravation of neck pain, mechanical factors, management, 692 non-Hodgkin’s lymphoma, 81 non-linearity of materials, 830–1 anulus fibrosus, 832 non-specific cervical spinal pain, 539–40

1439

Index non-steroidal anti-inflammatory drugs (NSAIDs), 113–27, 1205, 1206 axial back pain, 994 cervical radicular pain, 635 as component in pain rehabilitation, 1205, 1206 COX-2-specific see cyclooxygenase-2 inhibitors failed back surgery syndrome, 1142 intradiscal electrothermal therapy and discontinuance of, 305 lumbar radiculopathy due to herniated disc, 874–6, 888 metastatic disease, 477 non-specific, 116–17 adverse effects, 117, 1325–6 bone healing and spinal fusion effects of, 122–4, 1124–5 postoperative pain, 116–17 pregnancy-related back pain, 1325–6 spondyloarthropathies, 397 spondylolisthesis, 1087 norepinephrine anxiety and, 176 pain and, 48, 49 North America, epidemiology of spinal pain, 10 see also United States North American Spine Society’s Compendium of Outcome Instruments for Assessment and Research in Spinal Disorders, 1234, 1235 notochord, 855, 856 nuchal tubercle, palpation, 543 nuclear medicine imaging, 89–93 bone see bone scan infections of the spine, 90–1, 405 piriformis syndrome, 1303 radiopharmaceuticals and methodology, 89–90 spondylolisthesis, 1082 nucleoplasty (coblation by radiofrequency) intradiscal electrothermal therapy and see intradiscal electrothermal therapy lumbar, 905, 906, 932–5 Arthrocare spine wand, 925 nucleotome (Nucleotome®), 923 automated percutaneous lumbar discectomy, 322–3 placement, 325–7 laser see laser treatment nucleus pulposus, 17, 827, 832, 865–6 aspiration see nucleotome degeneration, 821, 832, 866 herniated see herniation, disc imaging, 59 innervation, 867 in intradiscal electrothermal therapy, anatomy, 303 mechanics, 832 hydrostatic pressure, 828–9 prosthetic replacement, lumbar region, 1072–3 radicular pain and role of, 197–8 lumbar, in failed back surgery syndrome, 1140 structure, 17, 828, 865–6 numerical rating score, failed back surgery syndrome, 1129 Nurick score, 567, 568 nursing in pain rehabilitation, 1209 nutrition spinal fusion surgery and effects of, 1124 vertebral endplate function in, 866 see also food

1440

nutritional myelopathy vs compression myelopathy, 570

O obesity in deconditioned subjects, 1216–17 total disc replacement and, 1391 oblique abdominal muscles external, 856 internal, 774, 856 spinal stabilizing role, 1110 sporting activity and, 1333 obliquus capitis inferior, 525 O’Brien’s test, 625–6 obsessive—compulsive disorder (OCD) and obsessive—compulsive spectrum disorder (OCSD), 177–8 clinical vignette, 177–8 comorbid with chronic pain, assessment for, 109 pharmacotherapy, 182 psychotherapy, 179 occipital nerves, 739–40, 748–9 greater, 739–40 cervicogenic headache and the, 740 interventional techniques, 748–9 lesser, 739 interventional techniques, 748–9 third, 711 anatomy, 711 blocks, 711 cervicogenic headache and the, 740 lesioning, complications, 221 occipital neuralgia, 739, 748–9 occipitoatlantal joint see atlanto-occipital joint occipitocervical angle, 574 occipitocervical distance, 574 occupation (job; vocation; work) lumbar disc degeneration with heavy physical work, 819 in lumbar disc surgery rehabilitation, 969–70 in pain rehabilitation, 1204, 1205 job simulation and work readiness, 1207 neck pain, 692 workplace design, 1207–8 spinal pain related to, 12 compensation for cervical radicular pain due to accident, 657–8 pregnancy-related low back pain, 1308 Occupational Safety and Health Administration (OSHA), 237 Occupational Stress Inventory, 109 occupational therapy, 1207 evaluation, 1204 octreotide, intrathecal infusion, 359 Octrode, 1167 ocular problems see eye Odom criteria, 567, 568 odontoid process (dens), functional anatomy, 518, 520 older adults/geriatic patients back pain/injuries, 13 sports-related, 1351 rehabilitation in chronic pain, 1209 see also age ominous cervical spinal spine, 539 Omnipaque, 56 on-field evaluation of sports injuries, 1344–7, 1359–60

operating microscope for lumbar herniated disc decompression, 942 ophthalmologic problems see eye opioid(s), 49, 241 endogenous, 49 receptors, 49, 163, 351, 1177 opioid analgesics (narcotics), 161–71, 242, 1205 addiction see addiction back pain, axial, 994 back pain, chronic, 161–3 lactating mothers, 1327 pregnancy, 1326 back pain, chronic, intrathecal (incl. implantable pumps), 354–6, 1178–81, 1184–6 in failed back surgery, 1143, 1184–6 indications and contraindications, 1178–9 back pain, due to radiculopathy from herniated disc, 874, 888 cervical radicular pain, 635 as component in pain rehabilitation, 1205 discontinuing/tapering off, 169 efficacy, 167 guidelines for use, 165–6 history, 168 long-term use, clinical concerns, 164–5 mechanisms of action, 163–4 postoperative pain, 116 with NSAIDs, 116–17 practical aspects of use, 166–7 recommendations for safe and effective in spine care, 166 reversal of effects, 243 routes of administration and doses, 166–7 short- vs long-acting, 166 side-effects, 167, 361–2 specific, 167–9 time- vs pain-contingent dosing, 166 opponens pollicis, manual muscle testing, 629, 631 optical coupling device, 230 orbitofrontal cortex and fear and anxiety, 175–6 orthoses (incl. braces), 485–93 biomechanics, 485–6 cervical radicular pain, 635 classification, 485 compliance, 491 contraindications, 491 indications, 491–2 sacroiliac joint syndrome, 1253, 1324 low back pain, 491–2, 997 lumbar radiculopathy due to herniated disc, 885–6 in pregnancy, 1324–5 material/manufacturing/fit, 490–1 potential functions, 485 spondylolisthesis, 1089 spondylolysis, 1375, 1376, 1377 tumors metastatic disease, 477 primary tumors of bone, 464 ossification/osteogenesis (bone formation) biochemical markers, 437 normal (in spine), 423–4, 424–6 cervical spine, 515, 516, 517 growth factors, 425–6 lumbar spine, 856, 857 postnatal, 857 regulation, 428 thoracic spine, 767

Index ossification/osteogenesis (Continued) posterior longitudinal ligaments (OPLL), 74, 559 surgery, 753, 755, 764 resorption and, coupling, 427–8 secondary ossification centres, 856, 857 steroid injection-induced, 1054 osteitis condensans ilii, 1273–4, 1309 osteitis deformans see Paget’s disease osteitis pubis in pregnancy, 1313 osteoarthritis carpal—metacarpal joint, 628 hip, 1277 in Paget’s disease, 446–7 osteoblast(s), 423, 424–6, 426–7 defects/lesions, 428 age-related (senescence), 429 differentiation, 424–6 regulation of activity, 426–7 osteoblastoma, 458 cervical, 532 imaging, 80, 458 osteocalcin, 426 osteochondroma, 458 cervical, 532 imaging, 79–80, 458 osteochondrosis, intervertebral, 61 osteoclasts, 423 activity excessive, 428 regulation, 426–7, 428 differentiation, 426 in ossification, 424 osteoconductive bone grafts for fusion surgery, 1125 osteocytes, 423 osteodiscitis, nuclear imaging, 90 osteogenesis see ossification osteogenesis imperfecta and pregnancy, 1309 osteogenic bone grafts for fusion surgery, 1125 osteogenic protein-1, intradiscal infusion, 1019 osteoid osteoma, 458 cervical, 532 imaging, 80, 458 osteoinductive bone grafts for fusion surgery, 1125 osteoma, osteoid see osteoid osteoma osteomalacia, 438 osteomyelitis, 90–1 acute, nuclear imaging, 90 chronic, nuclear imaging, 90–1 fungal, 413 neck pain, 534 postoperative, imaging, 67 spinal injection complicated by, 217 thoracic pain, 777 osteonecrosis hip, in pregnancy, 1313 steroid-associated, 156 osteonectin, 426 osteopathy, 693–4 pregnancy-related back pain, 1327 sacroiliac joint syndrome, 1251 osteophytes, 615, 671, 1106 lumbar herniated nucleus pulposus and, 948 osteoporosis, 435–44 fractures/compression fractures associated with, 67–8, 69, 435 epidemiology/cost, 495–6

osteoporosis (Continued) kyphoplasty, 507–8 pathophysiology, 496–7 sacral, 1281, 1282, 1285, 1286 thoracic, 778, 780, 781, 783 vertebroplasty, 68, 69, 499–500, 783 vertebroplasty complications, 502 investigations, 436–8 lumbar disc degeneration and, 823 orthoses, 492 physical examination, 780 in pregnancy, transient, 1313, 1328–9 management, 1328–9 steroid-associated, 156, 438 total disc replacement contraindicated in, 1391 treatment, 783 pharmacotherapy, 440–3, 1286 work-up, 438–9 osteoprogenitor cells, 424–5 osteoprotegerin, 426–7 osteosarcoma, 461 cervical, 533 imaging, 81, 461 secondary, 461 Osterix, 424 Oswestry Low Back Pain Disability Questionnaire, 1234 overpressure, patient or therapist-applied, in cervical radicular pain, 639 overuse syndrome and spondylolysis, 1373 oxazepam, acute anxiety, 180 oxcarbazepine, 132–3 adverse effects, 131, 133 radicular pain, 132–3 oxycodone, controlled-release (Oxycontin®), 168 oxygen consumption (VO2), deconditioned subjects, 1215 reactive species, in inflammation, 20–1 Ozzlo pillow, 1325

P Paget’s disease (osteitis deformans), 445–51, 533–4 anatomic distribution, 446 diagnosis, 447 epidemiology, 445–6 etiology, 445 histopathology, 446 presentation and complications, 446–7 neck pain, 533–4 spinal stenosis, 954 treatment, 447 pain (cancer) American Pain Society management guidelines, 113, 114 primary bone tumors, 454 management, 464 referred to neck, 708 secondary bone tumors, 470–1 management, 477 pain (generally) acute, 40–1, 1231 American Pain Society management guidelines, 113, 114 distinction from chronic pain, 1191 anatomic aspects, 29–30, 193–4, 1165–6 biochemical mediators, 32–3, 114

pain (generally) (Continued) biopsychosocial model see biopsychosocial model coping see coping definitions, 39–40 drawings, in lumbar axial pain, 1034 drug therapy see analgesia; analgesic drugs endoscopic surgery complementing interventional management of, 1407 inflammation and see inflammation; inflammatory pain local anesthetics for see local anesthetics management/control cost-effectiveness, 1236 diagnosis as key to, 1177, 1191–2 historical aspects see pain with sacral insufficiency fractures, 1286 sports injuries (severe/prolonged), 1380 see also analgesia; analgesic drugs; rehabilitation mechanisms/pathways, 29–52, 114, 1165–6 central see central nervous system in low back pain, 803–4 molecular, 44–50 in radicular pain, 129, 130 spinal cord stimulation and its effects on, 1166–7 neurogenic see neurogenic pain neuropathic see neuropathic pain perception, injury and biomechanical factors modulating, 33–5 persistent and chronic, 32, 41, 1231 anxiety disorders comorbid with see anxiety disorders deconditioning in see deconditioning distinction from acute pain, 1191 psychiatric and psychological comorbidity see psychiatric disorders; psychological comorbidity somatic comorbidity, 105–6 whiplash injury, 604 post-thoracotomy see thoracotomy provocation (for discography), 210 cervical region, 296–7 lumbar region, 294 thoracic region, 298 recurrent, 13, 1231 referral to cervical spine, 623–8, 708 referral from cervical spine assessment, 617–18 in cervical radiculopathy, centralization see centralization from zygapophyseal joints, 613, 614 see also somatic referred pain referral from lumbosacral area to coccyx, 1295 referral from lumbosacral nerve roots, 897–8 referral from sacroiliac joint, 977, 1240–1 referral from thoracic facet joints, 787–8 segmentation see segmentation sensitization see hyperalgesia; sensitization sympathetically-mediated, 713 as symptom vs disease, 39 transduction, 30–1 transmission, 31–2 types, 162 in whiplash injury, 593–600, 604, 617 epidemiology, 609–10 wind-up, 40, 42–4 see also nociception pain (postoperative), 113–27

1441

Index pain (postoperative) (Continued) epidemiology, 113 undertreatment, 113 pain (sites/tissues other than spine or back) leg see lower limb myofascial see myofascial pain piriformis see piriformis syndrome shoulder see shoulder pain (spinal/back) in cancer see pain (cancer) cervical, classification, 539–40 chronic/persistent, 161–3, 690–2 ablative techniques, 1191–9 anxiety disorders comorbid with see anxiety disorders deconditioning in see deconditioning implantable pumps see implanted devices opioids see opioid analgesics rehabilitation see rehabilitation spinal cord stimulation see spinal cord coccygeal see coccyx continuing/recurring after surgery see failed back syndrome discogenic basketball, 1352 cervical see cervical discs lumbar see lumbar discs provocative discography see discography thoracic, 777, 779 epidemiology, 9–16 historical aspects see history in intradiscal electrothermal therapy, monitoring, 311 lumbar see low back pain nonspinal causes of back pain, 385–90 pre-injection procedure assessment, 207–8, 213 radicular see nerve root pain sacroiliac joint see sacroiliac joint sports-related see sports thoracic, 777–86 autonomic nervous system and, 768, 772 diagnosis, 780–2 etiology, 777–9 generators, 767–8 physical examination, 779–80 provocation (for discography), 298 types, 768 vertebral compression fracture, 497 reduction with vertebroplasty, 499 pain beliefs, 110 Pain Disability Questionnaire, 1235 pain pumps see implanted devices palpation cervical spine, 542–3 lumbar spine, 842–3 sacroiliac joint, 1242 in pregnancy, 1315 palsies see paralysis pamidronate ankylosing spondylitis, 397 metastatic disease, 477 osteoporosis, 443 Paget’s disease, 449 panic disorder pharmacotherapy, 182 psychotherapy, 179 screening questions, 178

1442

paper and pencil test for psychiatric and psychological comorbidity, 106–7 paracetamol see acetaminophen paralysis/palsies all four limbs see quadriplegia cervical nerve root, following cervical myelopathy surgery, 761 paramyxovirus and Paget’s disease, 445 paraspinal muscles cervical see cervical musculature examination/screening, 98–101, 103 which and how many to study, 100–1 lumbar see lumbar paraspinal muscles myopathy, 387 sports-related functional anatomy, 1332, 1333 as stability components, 1110–11 strengthening see strengthening exercises thoracic, 774–5 parathyroid hormone bone metabolism and, 427, 435–6 therapeutic, 440, 443 in hyperparathyroidism, 438 parecoxib adverse effects, 120, 120–1 drug interactions, 120 indications, 117 postoperative setting, 117–18 parietal pain, 768 Paris, Stanley, 695 parotid glands, palpation, 543 paroxetine as anxiolytic, 181, 182 pars interarticularis fracture, Z-joint infection with, 267–8 imaging, 59 defect (=spondylolysis), 74, 1373–4 repair, 1100 spondylolisthesis and defects in, 1077, 1100 spondylolysis and defects in, 1337, 1373–8 passive spinal stability subsystem, 1110 PASSOR see Physiatric Association of Spine, Sports and Occupational Rehabilitation patellar allograft in anterior cervical discectomy and fusion, 671 patient assessment see assessment education/information see education radiation protection, 237–8 Patrick’s maneuver, 1244, 1247, 1315 Pavlov ratio, 558 pectoral nerve, lateral, 551 pediatrics see adolescents; children; infants; neonates pedicle, 859 cervical, functional anatomy, 519 in kyphoplasty, cannulation, 380–1 in vertebroplasty, in surgical approach, 367 see also transpedicular approach pedicle screws in cervical myelopathy surgery, 760–1 in minimally invasive surgery image-guided insertion, 1405 transforaminal lumbar interbody fusion, 1399 misplaced, 1132, 1134 in spondylolisthesis surgery, 1102–3 pelvic belts, pregnancy, 1324–5 pelvic floor in pregnancy examination, 1316–17

pelvic floor (Continued) myofascial pain, 1312 in sporting activity, 1333 pelvic girdle muscles, flexibility assessment, 843–4 pelvic joints in biomechanics of sacral insufficiency fracture, 1282 in pregnancy, examination, 1315 pelvic muscles and low back function, 992 pelvic pain, posterior (PPP) physical therapy, 1250–3 in pregnancy, 1255, 1323, 1324 peripartum, 1324 provocation test, 1316 pelvic region/area insufficiency fractures see insufficiency fractures organ/tissues low back pain with disorders of, 808 neoplasm, vs sacral insufficiency fracture, 1283 pelvic ring see pelvis pelvic sagittal rotation, 1292 pelvis (pelvic ring/innominate bones) anatomy, 1311 fractures imaging, 1283 sacral insufficiency fractures associated with, 1281 in pregnancy, 1311–12 ligamentous and osseous support, 1309 obliquity, 1311–12 peptic ulcers, steroid-associated, 156 Perc-DC® Spine Wand, 932, 933–4 percutaneous procedures catheters for see catheters cervical cordotomy, 1194 cervical discectomy see discectomy CT-guided biopsy in infection, 408 disc decompression, 927–37 laser see laser treatment lumbar, 927–37, 1068 electrical nerve stimulation in lumbar radiculopathy, 877 epidural adhesiolysis, 1143, 1161 kyphoplasty see kyphoplasty lumbar discectomy, 321–30, 905, 906, 923–6, 930–2, 1068 automated see automated percutaneous discectomy evolution, 923–4 future directions, 925 indications, 925, 1068 selective vs nonselective, 923 neuromodulation therapy, 699 pedicle screw placement for minimally-invasive transforaminal lumbar interbody fusion, 1399 radiofrequency denervation see radiofrequency ablation sacroplasty, 1286–7 sedation see sedation seroma aspiration, 1152 spinal cord stimulation electrode placement, 342, 343, 345–6, 1165, 1170, 1171 retrograde, 1173 vertebroplasty see vertebroplasty perineural cysts, 84

Index perineural nerve block see nerve block perineurium, 1137 dorsal root ganglion, 193 peripheral nerve stimulation, 1173–4 see also nerve peripheral sensitization to pain, 114 peripheral vascular disease assessment, 1278 signs and symptoms, 1277 periscapular muscles, 774 periscapular pain, 680–1 permeability, 830 personality tests, chronic pain patients, 106–7, 110–11 pH, local anesthetics and, 139, 195–6 pharmacodynamics, local anesthetics, 138 pharmacokinetics, local anesthetics, 138 pharmacotherapy see drug therapy phenytoin, radicular pain, 135 Philadelphia orthosis (HCO), 486 phobias (specific) psychotherapy, 179 screening questions, 178 phospholipase A2 and radicular pain, 615, 912 in failed back surgery syndrome, 1140 Physiatric Association of Spine, Sports and Occupational Rehabilitation (PASSOR), 1–8 Charter Members, 4 Distinguished Clinician Award, 7 Distinguished PASSOR Member Award, 7 Founding Members, 4 future, 7–8 history, 1–3 influences to become members of, 2 present, 3–7 Presidents, 4 physiatry, interventional see interventional physiatry physical abuse in chronic pain patients, screening, 109–10 physical activity see activities; exercise; sports physical deconditioning see deconditioning physical examination see examination Physical Medicine and Rehabilitation (American Academy of), history, 2, 3 physical therapy (physical modalities), 1206 cervical radicular pain, 636, 638 chronic pain patients, 1227–9 epidural adhesiolysis patients, 1161 evaluation, 1204 failed back surgery syndrome, 1142 lumbar axial pain rehabilitation, 995 lumbar disc surgery rehabilitation, 971 lumbar radiculopathy due to herniated disc, 877 lumbosacral radiculopathy, 903 neck pain, 693–849 piriformis syndrome, 1304 sacral insufficiency fractures, 1286 sacroiliac joint syndrome, 1250–3 in pregnancy, 1255, 1323–4 shoulder pain, 554 spondyloarthropathies, 396 spondylolisthesis, 1088 spondylolysis, 1377 thoracic spinal pain, 784 see also specific methods pillows lumbar radiculopathy due to herniated disc, 886 in pregnancy-related back pain, 1325

pilonidal sinus and coccygeal spicule, 1294 piriformis muscle anatomy, 1299–300 piriformis syndrome, 893, 1299–306 causes, 894, 1300–1 primary, 1300, 1301 secondary, 1300, 1301 clinical presentation, 1302–3 sciatica-like pain, 386, 1299, 1302 diagnosis, 899 differential, 1303 injections, 899, 1303 epidemiology, 1299 treatment, 1304–5 Pisces Quad Compact and Plus, 1167 pit, skin, coccygeal spicule and, 1294 pitching injuries (in baseball/softball), 1352 placebo, as control block, 189 cervical facet joint injections, 682 placebo response, 203–5 fake, 203 in lumbar spinal manipulation, 1009 magnitude, 204–5 mechanism, 203–4 not in clinical practice, 203 rate, 203 plain films see radiographs plasmacytoma (solitary myeloma), 461 cervical, 533 plastic body jacket, 489–90 plate electrodes for spinal cord stimulation, 342 placement, 346–7 plate fixation cervical myelopathy surgery, 756 complications, 762 thoracoscopic, 1403–4 platelet effects of NSAIDs, 117 COX-2-specific inhibitors, 120 plating, lower cervical spine, 579 plexopathy, radiation, 386 plexus(es) (blood vessel), vertebral venous, 522–3 plexus(es) (nerve) brachial see brachial plexus cervical, 527–8 lumbar, 864 sacral, dorsal, 1259 of thoracic disc and vertebral bodies, 790 plexus block, 143 plicamcin, Paget’s disease, 450 PMMA see polymethylmethacrylate pneumothorax with spinal injections, 220 in cervical discography, 221 Polyanalgesic Consensus Conference guideline and amended guidelines, 359, 360, 360–1 polyethylene glycol (in steroid preparations), neurotoxicity, 215 polymethylmethacrylate (PMMA) kyphoplasty, 377, 381 extravasation, 382–3 metastases, 478 primary tumors of bone, 464 operative stabilization, metastases, 479 sacroplasty, 1286 vertebroplasty, 371, 497 leakage, 502 metastases, 478 occupational exposure to vapour, 374 polymorphonuclear leukocytes see neutrophils popliteal angle measurement, 843

portals for video-assisted thoracoscopic surgery, 1402–3 positometric relaxation, sacroiliac joint rehabilitation, 1251 positron emission tomography (PET), 89, 91–2 infections, 90, 91 tumors metastatic, 473 primary, 456 posterior—anterior lower cervical mobilization, 695 posterior elements of spine in cervical myelopathy, surgical approach via, 756–61 imaging, 59 lumbar, 992 fusion (with instability due to posterior lesion), 1121, 1122 inspection, 839–40 sports injuries in children and, 1350 posterior lumbar interbody fusion, 960–1, 1069–70, 1123, 1397–9 anterior and, combined, 1069 minimally invasive, 1397–9 posterior shear test, 1244, 1246 posterolateral approach endoscopic surgery, 1410–11 in situ fusion, 1100–2 post-herpetic neuralgia (PHN) diagnosis, 780 Lidoderm patch, 146 physical examination, 780 thoracic pain, 778, 780 treatment, 782, 784 postnatal spinal development, 516–17, 857–9 postoperative care/rehabilitation automated percutaneous lumbar discectomy, 328–9 cervical myelopathy surgery, 761 kyphoplasty, 381 lumbar disc surgery see rehabilitation lumbar percutaneous nucleoplasty, 933 sacroiliac joint complex instrumented arthrodesis, 1272 radiofrequency neurotomy, 1265–6 vertebroplasty, 373 postoperative course, surgical decompression of lumbar herniated nucleus pulposus, 946 postoperative problems (incl. complications) infections deep wound see wound in microscopic discectomy, 948 prophylaxis, 411 lumbosacral radiculopathy diagnostic algorithm, 905 indications, 940 pain (acute) see pain (postoperative) post-traumatic stress disorder (PTSD) chronic pain in whiplash injury and, 690 neurobiology, 175 pharmacotherapy, 182 psychotherapy, 179 screening questions, 178 posture cervical radicular pain correction of abnormalities, 638 examination, 636 correction, 1207 with neck pain, 692

1443

Index posture (Continued) examination (in general), 540 low back pain, control abnormalities and difficulties, 807 thoracic postural curve development, 767 potassium ion channels (peripheral nerve), 194, 195 potassium-titanyl-phosphate laser see KTP laser predictive validity, 188 prednisolone, coccygeal intradiscal therapeutic injections, 1053–4 prefrontal cortex, dorsolateral, fear and anxiety and the, 175–6 pregabalin, 134 adverse effects, 131, 134 dosing and titration, 132, 134 in radicular pain, 134 pregnancy, 1307–30 back pain, 1255, 1307–30 causes, 1311–14 diagnostic work-up, 1317–18 epidemiology, 1307–10 examination, 1314–17 prevention, 1322 treatment, 1321–30 radiation exposure considerations, 238 sacroiliac joint, 1240 dysfunction/syndrome, 1255, 1312 pressure, 828–9 intradiscal see intradiscal pressure swelling see swelling pressure see also overpressure pressure manometry for provocative cervical discography, 294–5 prevalence of spinal pain, 9 pregnancy-related low back pain, 1307, 1308 prilocaine, 142, 143, 144 primary treatment, 1224, 1231 procaine, 137, 142, 145 ProDisc total disc prosthesis, 1072, 1392–3, 1394 Productive Rehabilitation Institute of Dallas for Ergonomics (PRIDE), 1227, 1234 progenitor cells, bone-forming, 424–5 programmable pain pumps, 353, 354, 363, 1178, 1179–81 future prospects, 1189 progressive inertial lifting evaluation (PILE), 1226 prolotherapy intradiscal, 1054–5 sacroiliac joint, 1054 pronator teres manual muscle testing, 629, 630 reflex assessment, 544 prone knee flexion test in sacroiliac joint syndrome, 1242 lumbar spine examination, 843 lumbar traction, 878 propofol (for sedation), 241 discography, 292 implants for spinal cord stimulation, 345 propoxyphene in pregnancy, 1326 propranolol, acute anxiety, 180, 181 proprioceptive exercises, chronic neck pain, 691 prostaglandins, 114–16 inflammation and, 19, 21 pain and, 32, 48, 114–16

1444

prostaglandins (Continued) radicular, 198 prostanoids, 114–15 biosynthesis, 114, 115 pain and, 32, 48, 114–15 prostate cancer, spinal metastases, 474–5 prosthesis see arthroplasty; implanted devices; sacral nerve roots protective (avoidance) behavior with low back pain, 807, 1217–19, 1227 protective apparel, radiology staff, 234 protective equipment used by athletes, 1370 management with cervical spine injuries, 1345–6 protective phase in lumbar disc surgery rehabilitation, 970 protein(s), structural, in disc degeneration, 822 protein kinase C and pain, 48 proteoglycans, nucleus pulposus, 865–6 protrusion (disc), 60 lumbar, 817 provocation of pain for discography see pain (generally) lumbar spine examination, 846–50 sacroiliac joint, 1246–8 in pregnancy, 1315–16 by vibration see bone vibration test pruritus, opioid-induced, 167, 361 pseudoarthrosis (intravertebral), 501 lumbar, 1131–2 diagnosis, 1134 pseudomeningocele, 1147–9 pseudoradicular syndrome, 385 pseudotolerance, opioids, 164 psoas muscles, 862 innervation, 864 posteriorly placed colon behind, in automated percutaneous lumbar discectomy, 322 see also iliopsoas psoriatic arthritis, 393–4 differential diagnosis, 394 spondyloarthropathy, 391, 393–4 psychiatric disorders comorbid in chronic pain, 105–12 assessment for, 107–9 in pain rehabilitation, 1209 sciatica-like pain, 386 psychoactive substance use disorders comorbid with chronic pain, assessment for, 108, 109 psychological comorbidity in chronic pain, 105–12 assessment for, 109–11 psychological effects laser decompression and nucleotomy, 337 steroids, 156 psychosocial assessment (incl. psychometric tests) in chronic pain and its rehabilitation, 1204, 1207, 1226–7 in lumbar discography, pre-procedural, 1045 in total disc replacement, preoperative, 1390 psychosocial factors in spinal pain, 12–13, 1217–19 in low back/lumbar pain, 805–6, 993, 1217–19 in facet joint pain, 1028 in failed back surgery syndrome, 1132 in whiplash injury, 690 see also biopsychosocial model

psychosocial issues incl. intervention (in functional restoration in prolonged/ chronic pain), 1229 pregnancy-related back pain, 1327–8 prolonged sports injury, 1382 psychotherapy, anxiety disorders, 179 pubertal growth spurts, 517, 858 pubic bone fractures, 1282 imaging, 1283 sacral insufficiency fractures associated with, 1281 symphysis see symphysis pulmonary embolism risk, vertebroplasty, 502 pulmonary non-vascular disorders/complications see lung; respiratory complications pulse generators for spinal cord stimulation, 343, 347–8, 1168 pulsed electromagnetic therapy cervical axial pain, 699 lumbar spinal fusion adjunct, 1126–7 pulsed radiofrequency current, nerve tissue effects, 276 pumps, pain see implanted devices pyogenic discitis, 402–3 clinical presentation, 402–3 management, 409–10 pathogenesis/etiology/natural history, 402 plain radiology, 404 pyogenic spondylodiscitis, 401–2 clinical presentation, 402 computerized tomography, 404–5 pathogenesis/etiology/natural history, 401–2

Q quadratus lumborum, 774, 863, 992, 1333 quadriceps, strength testing, 845 quadriplegia (tetraplegia) post-cervical discography, 725 transient, sports-related, 1335, 1341–2, 1362–3 epidemiology, 1362 evaluation, 1363 management, 1361, 1363 pathomechanics, 1362–3 return to play, 1363 quality improvement, sedation/analgesia, 243 Quebec Back Pain Disability Scale, 1235 Quebec Headache Group diagnostic criteria for cervicogenic headache, 740, 743 Quebec Task Force on Whiplash-Associated Disorders, 593, 594

R racquet sports, 1356–7 rad, 230, 231 radial nerve bias testing, 544 radial neuropathy, 627–8 radiation, 229–38 safety, 229–38 patient, 237–8 philosophy, 232–3 radiology staff see radiology staff terminology, 229–30 radiation-associated problems fetal harm, 1317 myelopathy, 83 compression myelopathy vs, 570 osteosarcoma, 461 plexopathy, 386

Index radiation-associated problems (Continued) sacral insufficiency fractures, 1282 radiation therapy metastatic disease, 478, 481 thoracic spine, 783–4 primary tumors of bone, 464 radicular arteries cervical, anatomy, 522 lumbar, anatomy, 862 penetration with cervical epidural injection, 652–4 thoracic, anatomy, 768 radicular veins cervical, 522 lumbar, 862 radiculitis, chemical, 1140 radiculopathy, 95–104, 385–90 cervical see cervical radiculopathy chronic, antiepileptics in, 131, 132, 132–3, 133, 133–4, 134, 135 differential diagnosis, 385–7 electrodiagnostic approach see electrodiagnostic studies history and epidemiology, 385 lumbosacral see lumbosacral radiculopathy myelography in lumbar radiculopathy, 63–5 nonspinal causes, 385–90 radicular pain and, definitions and distinction, 718 see also nerve roots radiofrequency ablation/denervation/neurotomy/ thermocoagulation, 275–89, 1027–32 cervical, 276–80, 679, 717–18, 719 cervicogenic headache, 717–18, 746–7, 748 complications, 221, 278, 280, 717, 719 dorsal root ganglion (in radicular pain), 276–8, 719, 748 facet joint see cervical facet (zygapophyseal) joints indications and contraindications, 717, 719 outcomes, 717–18, 719 history, 275, 679 lesion size, 275 lumbar, 282–5, 1029–30 complications, 223, 284 facet joint see lumbar facet joints sympathetic chain, 715 physics/equipment, 275–6 sacroiliac joint pain, 977–9, 1253, 1262–5 case study, 1266 thoracic, 280–2 facet joint, 280–1, 782, 788, 788–9, 793–4 segmental pain syndromes, 795–6 side-effects and complications, 795–6 tumors metastatic, 478 primary tumors of bone, 464 radiofrequency-controlled implanted receiver for spinal cord stimulation, 343, 347–8, 1168 radiofrequency nucleoplasty see nucleoplasty radiographs, conventional/standard (plain films; X-rays), 53 cervical axial neck pain, 730–1 cervical foraminal stenosis, 668 cervical infection-related pain, 534, 536 cervical instability assessment, 581 lower, 578 upper, 575

radiographs, conventional/standard (Continued) cervical myelopathy, 565 cervical radicular pain, 718 cervicogenic headache, 744–5 coccydynia, 1290–5 head and neck acute trauma cases, 630 hip—spine syndrome, 1278 infections, 404, 534 tuberculosis, 536 lumbar axial pain, 1066 lumbar segmental instability, 1112–13 lumbosacral radiculopathy, 895–6, 903 metastatic disease, 472 Paget’s disease, 446, 447, 534 sacral insufficiency fractures, 1283 sacroiliac joint syndrome, 1265 shoulder pain, 554, 555 spondyloarthropathy, 394 spondylolisthesis, 1082, 1090 thoracic spinal pain, 781 whiplash injury, 596 radiology (imaging), 53–93, 1409–10 abnormal spine, 60–85 cervical injury athletes, 1342, 1343, 1363–4, 1366–7, 1379 whiplash-related, 596–7, 603, 689 cervical instability, 581 lower cervical spine, 575–6 upper cervical spine, 575–6 cervical myelopathy, 565–6 cervical pain axial neck pain, 685, 730–1 radicular pain, 630–1, 718–19 cervical stenosis, 1363–4 foraminal, 668 cervicogenic headache, 744–5 coccydynia, 1290–5 diagnostic (in general), 53–105 correlation with clinical evaluation, 66 epidural fibrosis, 1141–2, 1144, 1155 failed back surgery syndrome, 1130, 1132–3 neural scarring, 1141, 1144 pseudomeningocele, 1148 seroma, 1152 hematoma, 1151 hip—spine syndrome, 1278 implanted pain pumps, 1189 implanted spinal cord stimulation systems, intraoperative, 349 infections see infection lumbar disc degeneration, 823–4 herniation, 939 in intradiscal electrothermal annuloplasty, pre-procedural, 1058, 1059 lumbosacral radiculopathy, 895–6, 903 metastases see metastases modalities, 53–6 see also specific modalities normal spine, 56–9 Paget’s disease, 446, 447 piriformis syndrome, 1303 pregnant patient with low back pain, 1317 sacral insufficiency fractures, 1283–5 sacroiliac joint syndrome, 977 case study, 1265 shoulder pain, 555 spondyloarthropathies, 394–5 spondylolisthesis, 74–5, 1081–2

radiology (imaging) (Continued) spondylolysis, 74, 1373–4 in treatment phase, 1375, 1377 thoracic disc disease, 799, 800 thoracic spinal pain, 781 radiology staff, occupational radiation exposure management, 233–7 in vertebroplasty, 374 radionuclide studies see nuclear medicine imaging radiotherapy see radiation therapy raloxifene, osteoporosis, 442 rami see dorsal rami; ventral rami rami communicantes gray see gray rami communicantes white, 768, 772 Ramsay Level of Sedation Scale, 240 Ranawat’s 4-grade criteria in rheumatoid arthritis, 561 randomized controlled trials, postoperative rehabilitation in lumbar disc surgery, 968–70 Raney flexion lumbosacral orthosis, 489 range of motion (assessment) cervical spinal, 539, 541–2 upper region (C0—C2), 574 coccygeal, 1291 hip, in sacroiliac joint syndrome, 1245 lumbar spinal, 840–2 shoulder joint, 554 range of motion (therapeutic improvement), 1206 RANK and RANK ligand osteoclast activity and, 426–7 osteoclast differentiation, 426 Paget’s disease and RANK mutations, 445 rating scales, psychiatric, 106–7 reaction times, slow, low back pain patients, 807 reactive arthritis, 393 reactive gliosis (astrocytic response to injury), 34, 49 reactive species of oxygen in inflammation, 20–1 rear-end collision see motor vehicle accident reconstructive surgery in cervical myelopathy, 756 outcome, 764 records, medical, controlled substances in, 166 recovery from sedation and analgesia, 242–3 recovery phase in rehabilitation see subacute/recovery phase recreational activities see sports activities rectal examination of pelvic floor musculature in pregnancy, 1316 rectus abdominis anatomy, 862 integrity assessment in pregnancy, 1314 rectus capitis anterior, anatomy, 523 rectus capitis lateralis, anatomy, 523 rectus capitis posterior major and minor, 525 rectus femoris flexibility assessment (Ely test), 843, 1278 recurrent laryngeal nerve see laryngeal nerve red cell (erythrocyte) sedimentation rate (ESR), infection, 407, 408, 535 red flags coccydynia, 1290 low back pain, 809 whiplash-associated disorder, indicating poor prognosis, 596 reduction in kyphoplasty for compression fractures, failure, 383 in spondylolisthesis, 1102–5

1445

Index reflex testing cervical/neck problems compression myelopathy, 565 in neck/cervical/upper limb pain, 544, 544–5 radiculopathy, 629 lumbar spine disorders, 845–6 primary bone tumors, 455 shoulder pain diagnosis, 555 regeneration, 19 regulations, controlled substances, 166 rehabilitation, 1201–11 admission criteria, 1202–3 algorithm for, 1202–4, 1209 axial back pain, 991–1012, 1022 factors influencing, 991–3 manual therapy see manual therapy phases, 994–7 axial neck pain, 685–705 acute nontraumatic pain, 686–8, 696, 701 acute traumatic pain, 599, 688–90, 696–7, 702 cervical radiculopathy, 635–44 chronic/recurrent pain, 690–2, 697, 702 basic concepts in, 993–4 components, 1205–9 functional restoration in see functional restoration goals, 993 lumbar disc surgery, 967–74 evidence, 968–70 protocol, 970–2 lumbar instability, 1116–17 lumbar radiculopathy due to herniated disc, 871–92 neurophysiological basis, 1201–2 outcome evaluation, 1209 piriformis syndrome, 1304 sacroiliac joint, 1249–57 sports injuries, 1380–3 three levels of non-surgical care, 1224–5 tertiary level see tertiary rehabilitation Reiter’s syndrome, 393 differential diagnosis, 393 relaxation training, 1207–8 anxiety disorders, 179 rem, 231 remodelling phase in whiplash injury, 689 renal adverse effects of NSAIDs COX-2-specific inhibitors, 121 non-specific NSAIDs, 117 renal cell carcinoma, spinal metastases, 475 repair/healing (in tissue damage), 19 bone see bone whiplash injury, 688–9 repetitive motion disorders, 1223 research, PASSOR and, 6–7 resistance training in pregnancy-related back pain, 1322–3 resolution (in inflammation), 19 respiratory (pulmonary/lung) complications spinal injections, 220 in spondyloarthropathies, 396 vertebral fractures, 440 see also lung cancer rest axial back pain, 1022 in bed see bed rest

1446

‘restorative’ lumbar intradiscal injections (incl. glucosamine and chondroitin), 1054–5, 1071 Resume electrodes, 1167, 1168 resuscitation, cardiopulmonary, on-field, 1360 reticular activating system, ascending, 48–9 reticular formation, fear and anxiety and the, 175 retraction and extension with traction and rotation, 694 retroperitoneal lumbar interbody fusion, minimally invasive, 1400–1 rheumatoid arthritis, 560–1 cervical myelopathy in, 560–1 cervical spine assessment in, 575 differential diagnosis, 394 imaging, 71–3, 781 physical examination, 780 thoracic pain, 779, 780, 784 treatment, 784 rheumatologic disorders neck pain, 708 thoracic pain diagnosis, 780 treatment, 782 rhizotomy, 1192–3 historical background, 1192 in occipital neuralgia, 748, 749 rhomboid weakness testing, 629 rigid (hard) collar, 486 risedronate osteoporosis, 443 Paget’s disease, 450 risk stratification for sedation, ASA guidelines, 240 road vehicle accident see motor vehicle accident Robinson—Smith technique (anterior cervical discectomy and fusion), 657, 669 rod placement, thoracoscopic, 1403–4 Roentgen unit, 230, 231 rofecoxib, 874–6 bone healing and spinal fusion effects of, 124 cardiovascular effects, 121, 874–6 lumbar radiculopathy due to herniated disc, 874–6 renal effects, 121 Roland—Morris Disability Questionnaire, 1234 Roman chair, 1227 Roos’ test, 544 ropivacaine, 142, 143, 144, 145 Rosenthal Foundation awards and lecturers, 3, 6 rotation axis of, sports injury and, 1333–4 cervical spine lower, 577 in manual therapy, 694, 695, 696 upper, 574 iliac, 1250–1, 1252 pelvic, sagittal, 1292 thoracolumbosacral orthoses controlling, 489–90 see also external rotation sign; lateral rotation rotator cuff, strength tests, 554–5 rotator muscles cervical, 525 lumbar, 863, 992 thoracic, 774, 775 rowing, return to competition after prolonged injury, 1386 running sports, return to competition after prolonged injury, 1384 Runx2, 424

S S1 deficits in lumbar radiculopathy, 873 S1 radiculopathy, H-reflexes, 96–7 Saal brothers, 3 sacral nerve roots accidental anesthetization, 222 anatomy, 863 stimulation, 1173 third, neuroprosthesis, 1254 in posterior sacroiliac arthrodesis, 1274 see also lumbosacral radiculopathy; S1 radiculopathy sacral paraspinal muscle examination, 100 sacral plexus, dorsal, 1259 sacral spinal region, 1277–306 sports injuries, biomechanical etiologic factors, 1351 sports-related functional anatomy, 1331–2 transforaminal epidural steroid injections, 257 sacral spinal stenosis see lumbosacral spinal stenosis sacral sulcus pressure (test), 1244 sacral thrust, 1244, 1246 sacrococcygeal disc anatomy and injection, 269–71 sacrococcygeal joint, 1289 sacroiliac joint (pain/syndrome relating to), 268–9, 894, 977–9, 1239–75 anatomy, 268, 1239, 1259–61 diagnostic algorithm, 1259, 1260 diagnostic injections, 199–200, 899, 977, 1241, 1246–7, 1261–2 in pregnancy, 1317–18 epidemiology, 1239–41 in failed back surgery syndrome, 1131 hypermobility/laxity, 1241, 1254 in pregnancy, 1255, 1323 injections, 268–9, 1253, 1261–2 diagnostic see subheading above technique, 268–9 therapeutic, 268–9, 1253, 1262 management, 977–9, 1249–75, 1324 adjunct therapy, 1253–4 medical/conservative, 1249–57 minimally-invasive, 977–9, 1253–4, 1259–67 scenarios, 1254–5 surgery see surgery physical examination see examination physiology, 1239–40 in pregnancy, 1255, 1312, 1323 examination, 1315–16, 1323 sacroiliac joint infection in pregnancy, 1329 sacroiliac orthoses/belts, 490, 1253 pregnancy, 1324 sacroiliitis in spondyloarthropathy, 391–2 sacroplasty, 1286–7 sacrum, 1277–306 fixation, 1105 fractures, 1281–8 insufficiency see subheading below nomenclature/types, 1281 insufficiency fractures, 1281–8 clinical presentation, 1283 complications, 1287 definition, 1281 diagnosis, 1283–6 differential diagnosis, 1283

Index sacrum (Continued) epidemiology, 1281 etiology and biomechanics, 1281–2 preventing complications, 1286 treatment, 1286–7 in pregnancy, ligament insertions, 1309 primary tumors, surgery, 465 thrust maneuvers, 1252–3 see also trans-sacral transvertebral interbody fixation safety issues anti-TNF-α drugs, 917 automated percutaneous lumbar discectomy, 322, 930 epidural steroid injections cervical transforaminal, 254–5 lumbar, 913–14 laser disc decompression and nucleotomy, 332 lumbar spinal manipulation, 1009–10 nerve root blocks (selective), 916 radiation see radiation see also iatrogenic complications ‘safety’ view (fluoroscopy), 246, 247 sagittal rotation, pelvic, 1292 sagittal trunk strength, assessment, 1226 salicylates and breastfeeding, 1327 sarcoidosis, 82 sarcoma, 461–2 cervical spine, 533 imaging, 81, 461, 462 pagetoid bone, 447 Saskatchewan, epidemiology of spinal pain, 11, 12 scalene muscles anatomy, 524 subclavian artery compression by, 553 scaption test, 625 scapulae, pain in region of or between, 680–1 scapular muscles exercises in neck pain, 688 pain, 624, 626–7 scapulothoracic joint anatomy, 549 scapulothoracic rhythm, 549 scarring epidural, postoperative, 66 neural see neural scarring see also fibrosis scatter radiation, 230–1 Scheuermann disease/kyphosis, 767, 1350 lumbar disc degeneration and, 823 Schmorl’s nodes, 767 children, 1350 gymnasts, 1355 Schober test, and modifications, 392, 841 Schwann cells, 194 schwannoma, intradural extramedullary, 418 imaging, 77 sciatic nerve anatomy, 1299–300 lesions in pregnancy, 1313 in piriformis syndrome surgery, 1305 sciatica electrodiagnostic testing, 98 epidemiology and nonspinal causes, 385–9 historical accounts, 385, 389 lumbar disc herniation causing, percutaneous discectomy, 925 in piriformis syndrome, 386, 1299, 1302 see also lower limb/leg pain scintigraphy see nuclear medicine imaging

sclerotome development, 515, 767, 855 pain referral see somatic referred pain scoliosis degenerative lumbar, 954 radiographic progression, 1113 surgical management, 961 in pregnancy adolescent idiopathic, 1309 bracing, 1325 thoracic, 767 diagnosis, 780 pain, 778 treatment, 782 scottie dog image, 53, 307, 1373 screws cervical surgery in cervical myelopathy, 756, 760–1 minimally invasive placement, 1404 sacroiliac joint with arthrodesis, 1271 without arthrodesis, 1270 in spondylolisthesis, 1102–3 thoracoscopic placement, 1403–4 vertebral pedicle, misplaced, 1132, 1134 second messenger systems see signal transduction secondary care/treatment, 1224, 1231 secondary gain, 12 screening and measurement, 108 sedation, 239–44 common drugs, 241–2 complications, 242 discography, 292 emergency equipment, 241 intradiscal electrothermal therapy, 307 levels and definitions, 239 opioids, 167, 361 post-procedural care, 242–3 preparation for, 240 reversal, 241, 243 segmental motion of lumbar spine, examination, 841 segmental nerves cervical see cervical segmental nerve block thoracic, anatomy, 768–70 segmental pain syndromes, thoracic, 795–6 segmental stability, 1109–19 conditions affecting, 1112 exercises in acute nontraumatic axial neck pain for, 687–8 neutral zone concept, 1109–11 see also instability segmentation of pain cervical axial neck pain, 680 thoracic segmental pain syndromes, 795–6 seizures with spinal injections, 219 selective estrogen receptor modulators in osteoporosis, 442 selective serotonin and norepinephrine reuptake inhibitors (SSNRIs), lumbar radiculopathy due to herniated disc, 876 selective serotonin reuptake inhibitors (SSRIs) anxiolytic effects, 181 in lumbar radiculopathy due to herniated disc, 876 side-effects, 183 self-reporting of spinal pain, 9 semispinalis, 525, 774 sensitivity (of test), 188

sensitivity (Continued) cervical discography, 721–2 stretch reflexes, 846–7 sensitization to pain, 114 see also hyperalgesia sensory function, evaluation in cervical myelopathy, 558–9, 565 in cervical radiculopathy, 629 in cervical/neck/upper limb pain and suspected cervical disorders, 544–5 in lumbar spine examination, 845 with primary bone tumors, 455 sensory nerves conduction studies in radiculopathy, 97 embryological development, 516, 856 lumbar disc supply, 867 pain and, 30 sensory neurone-specific sodium ion channel block by local anesthetics, 150 sensory stimulation-guided lateral branch radiofrequency neurotomy in sacroiliac joint syndrome, 1262–6 septic discitis, thoracic examination, 779–80 treatment, 783 sequestration (free fragment), 60 lumbar disc see lumbar disc seroma, postoperative, 1152 with intrathecal infusion pump implantation, 362, 1188 seronegative spondyloarthropathies, 391 serotonin (5-hydroxytryptamine; 5-HT) anxiety and, 176 pain and, 48 see also selective serotonin and norepinephrine reuptake inhibitors; selective serotonin reuptake inhibitors serotonin syndrome, 874 sertraline as anxiolytic, 181, 182 sex hormones, osteoclast effects of, 427 sextant instrumentation, percutaneous pedicle screw placement for transforaminal lumbar interbody fusion, 1399 sexual abuse in chronic pain patients, screening, 109–10 sexual dysfunction, opioid-induced, 361 SF-36, 1235 sham-treatment and placebo effect, 204–5 shear loading test, soft tissue, 830 shear properties of soft tissue, 830 anulus fibrosus, 833 nucleus pulposus, 832 shear test, posterior, 1244, 1246 shielding, radiation, 234 Short Form Health Survey (SF-36), 1235 shoulder, 547–56, 624–7 anatomy, 547–9 biomechanics, 549–50 dysfunction, differentiation from neck dysfunction, 545 height, assessment, 839 pain, 547–56, 624–7 evaluation, 553–5, 624–7 shoulder blocks, face validity, 189 shoulder pads (American football), removal, 1346 SIBLING family, 426 side-lying iliac compression test, 1242, 1244, 1246

1447

Index sievert (Sv), 230, 231 signal transduction (second messenger systems) G-protein-coupled receptors and, local anesthetic effects, 141 pain and, 48 single photon emission computerized tomography (SPECT), 89 cervical radicular pain and radiculopathy, 631 sacroiliac joint syndrome, 1265 spondyloarthropathies, 394 spondylolysis, 1374 in treatment phase, 1375, 1377 single-leg stance with triplanar motion, pregnant patient, 1314 sinuvertebral (recurrent meningeal) nerve anatomy cervical, 528 lumbar, 864 thoracic, 768, 771 sitting position cervical traction in, 638 flexion test in sacroiliac joint syndrome, 1242 pain in failed back surgery syndrome in, 1133 transition to standing see standing see also supine, long sitting test Sitting Workplace Analysis and Design (SWAD), 1207 skeletal muscle see muscle skiing, cautions following lumbar radiculopathy due to herniated disc, 887 skin ankylosing spondylitis involving, 396 closure see wound incision in discectomy, 943 in lumbar spinal stenosis surgery, 962 see also wound skin markings, intradiscal electrothermal therapy, 306–7 skin pit, coccygeal spicule and, 1294 sleep and pain, 47, 49 slip reduction, 1102 see also spondylolisthesis slipped disc see herniation, disc slouch/overcorrect procedure, 692, 693 slump test, 849 in lumbar radiculopathy due to herniated disc, 884 small cell lung carcinoma, spinal metastases, 475 Smith—Robinson technique (anterior cervical discectomy and fusion), 657, 669 smoking spinal fusion surgery outcome and, 1124 spinal pain and, 13 soccer, 1355–6 social anxiety, pharmacotherapy, 182 Social Security Disability Insurance, 1223–4 sociocultural phenomena, whiplash injury, 593–600 socioeconomic cost see cost sodium bisulphite with chlorprocaine, toxicity, 149 sodium ion channels (peripheral nerve), 194, 195 block by local anesthetics, 138, 140, 195–6 sensory neurone-specific, 150 sodium ion—potassium ion pump (ATPase), 194 soft collar, 486 indications, 491 soft tissue

1448

soft tissue (Continued) biomechanical behavior, 829–31 disorders causing neck pain, 708 manual therapy/mobilization in neck pain, 698 in sacroiliac joint syndrome, 1251–2 sports-related injury cervical region, 1341, 1368–9 children, 1350 whiplash-associated damage, 601–6 softball, 1351–2 fast-pitch, 1352 Soluspan®, spinal injection, 157, 158, 159 somatic comorbidity in chronic pain, 105–6 somatic referred pain (sclerotomal pain) cervical disc, 617 thoracic, 768 somatoform and somatization disorders comorbid with chronic pain, assessment for, 108, 109 somatopause and bone, 428–9 somatosensory evoked potentials, 98 implanted spinal cord stimulation system, 349 somatostatin analog, intrathecal infusion, 359 Spain, epidemiology of spinal pain, 10 spear-tackler’s spine, 1336, 1344, 1347, 1353, 1364–5, 1384 epidemiology, 1364–5 pathomechanics, 1365 evaluation and management, 1365 return to play, 1365 specificity (of test), 188 cervical discography, 721–2 stretch reflexes, 846–7 SPECT see single photon emission computerized tomography Speed’s test, bicipital tendinitis, 625 spicules, coccygeal, 1293–4 spin echo images of lumbar spine, fast (FSE), 55, 58 spina bifida and spondylolisthesis, 1080 spinal analgesia (intrathecal/neuraxial administration), 351–65, 1177–90 complications, 1186–8 compounding of drugs for, 360–1 delivery systems, 1177–8 implantable pumps see implanted devices efficacy, 1184–6 troubleshooting for lack of, 1188 patient selection and screening trials, 1178–82 selection of drugs, 1182–6 side effects, 361–3 spinal anesthesia (intrathecal/neuraxial injection), local anesthetics inadvertent prevention and recognition, 148 toxicity, 147–8 treatment, 148 types used and doses, 144 spinal arteries cervical, 522 thoracic, 768 spinal canal entry/opening in lumbar spinal stenosis surgery, 963 in microscopic discectomy, 943–4 stenosis see spinal stenosis spinal column (vertebral column) anterior elements see anterior elements injury see injury

spinal column (Continued) posterior elements see posterior elements thoracic, anatomy, 773 spinal cord anatomy pain-related, 29–30, 193–4 thoracic region, 768–72 variations, 95 arteriovenous malformations and fistulas, 85 compression see compression; compression fractures ischemia due to compression, 558–9 normal cord, imaging, 56–7 pain and the, 29–30, 40, 41 wind-up, 42–3 placebo effect and, 204 see also entries under intramedullary; myelo-stimulation, 341–50, 1165–76 clinical outcomes, 1170–2 complications, 1172–3 equipment, 341–3, 1167–8 future prospects, 1173–4 mechanism of action and structures stimulated, 343–5, 1166–7 operative technique, 345–9 patient selection/indications, 1170 surgical divisions and incisions see cordectomy; cordotomy; myelotomy transdural herniation, 84 spinal cord injury cervical see cervical spinal cord injury high rates, 173 pain following, 42 pediatric, 1350 sports, 1335, 1360–2 classification, 1360–1 diving, 1353 without radiographic abnormalities (SCIWORA), 1361 spinal fusion (arthrodesis), 1121–8 cervical anterior, adjacent disc disease after, 559–60 anterior, anterior discectomy and, 661–3, 664–5, 675–7 discography in selecting level of, 724 in myelopathy, 759–60 upper (C0—C1—C2) region, 576 in discogenic low back pain, discography aiding, 300 factors affecting outcome, 1123–7 NSAIDs (non- and COX-2-specific), 122–4, 1124–5 intradiscal electrothermal therapy with prior history of, 305 lumbar, 1068–70, 1121–8 complications, 1131–2 in discogenic pain, 984–5, 1068–70 indications, 1121 intradiscal electrothermal annuloplasty combined with, 1059 minimally invasive, 1397–401 in spondylolisthesis, 959–61, 1099–100, 1100–5 technique, 1068–70, 1121–3 lumbar, in spinal stenosis (with surgical decompression), 956, 958 in degenerative spondylolisthesis, 959–61 see also internal fixation

Index spinal injection see injection spinal injury see injury spinal nerve(s) cervical anatomy, 525, 526 developmental anatomy, 515 lumbar anatomy, 863–4 blood supply, 862 meningeal branch see sinuvertebral nerve thoracic, 773 spinal nerve roots see nerve roots spinal segmental nerves see segmental nerves spinal stenosis, 63–6, 951–65 causes, 63, 65, 198 Paget’s disease, 447 cervical see cervical spinal stenosis electrodiagnostic studies, 99, 101 endoscopic surgery, 1408–9 imaging, 63–6 lumbosacral see lumbar spinal stenosis; lumbosacral spinal stenosis thoracic diagnosis, 779 pain, 777 treatment, 782 spinal veins, cervical, 522 spinalis capitis, 524 spinalis cervicalis, 524 spinalis thoracis, 774 SpineCATH, 308, 309 spinothalamic tracts anatomy, 1194, 1195 in cordotomy, 1194 in myelotomy, 1195 in spinal cord stimulation, 1167 spinous processes cervical, 519 fractures, 1370 lumbar, 859 fractures, 1336 thoracic, 772–3 spiral CT pyogenic spondylodiscitis, 404–5 technique, 55 splanchnic nerves, 772 surgical resection, 1197 splenius muscle, anatomy, 524 spondylitis, ankylosing see ankylosing spondylitis spondyloarthropathies, 391–400 case studies, 397–8 clinical features, 391 definition and classification, 391 destructive, cervical spine, 562–3 diagnosis, 392–6 differential, 392 epidemiology, 391 genetics, 391 imaging, 394–5 management, 396–7 pathology, 391–2 prognostic indicators, 396 undifferentiated, 393 spondylodiscitis cervical, 534 fungal, 413 management, 409–10 MRI, 405, 406 Nocardia asteroides, 413

spondylodiscitis (Continued) nuclear imaging, 90 pyogenic see pyogenic spondylodiscitis spondylolisthesis, 889, 1077–108 associated conditions, 1080 classification and causes, 1077, 1085, 1099 degenerative (causing spinal stenosis), 953–4, 1077–9, 1085–6, 1089 management and results, 959–60, 964–5, 1090, 1092, 1093–4, 1095, 1106–7 MRI, 818 radiographic progression, 1113 diagnosis, 1079–80, 1081–2 disc rupture at level of, 947 imaging, 74–5, 1081–2 incidence, 1077–8 instability associated with, 1112 interventional techniques, 1089–95 rationale for use, 1089 medical/conservative management, 875, 889, 1081, 1087–9 in pregnancy, 1314 progression, 1080–1 spondylolytic see spondylolytic spondylolisthesis sports activities and, 1079, 1337 surgery, 1099–108 indications, 1099 options, 1099–100 spondylolysis, 1100, 1373–8 anatomic considerations, 1373 diagnosis, 1373–4 imaging see radiology pars repair, 1100 sports and, 1337, 1373–8 treatment, 1375–7 spondylolytic spondylolisthesis, 1079, 1080 lumbar disc rupture at slip level of, 947 spondyloptosis, 1105 spondylosis cervical see cervical spondylosis gymnasts, 1355 lumbar see lumbar spondylosis spondylosis deformans, 60–1, 61 imaging, 61 sports activities (and athletics and recreation), 1331–87 back/spinal injury and pain due to, 887, 991, 993, 1079, 1333–7, 1349–58 advice, 887 assessment (off-field), 1379–80 assessment (on-field), 1344–7, 1359–60 biomechanical factors, 1333–7, 1351–7 cervical region see cervical spine epidemiology, 1351–7, 1379 etiological factors, 1349–51 general management principles, 1380–3 prevention, 1370 re-integration in sports-specific activity, 1382–3 brain injury and concussion, 1339 functional anatomy, 1331–3 in lumbar disc surgery rehabilitation, 972 return to play/competition, 1360–1, 1362, 1363, 1364, 1366, 1368 after prolonged injury, 1383–4 spondylolisthesis associated with, 1079, 1337 sports medicine, concepts, 1227–9 spring test in sacroiliac joint syndrome, 1242 spur, traction, 1112 Spurling’s maneuver/test, 543, 628, 629

Spurling’s maneuver/test (Continued) modified, 628 stability, 1109–11 concepts, 1109–11 core, examination in pregnancy, 1314 in low back pain, inefficient control, 807 see also instability stabilization cervical spine exercises, in radicular pain, 641 on-field athlete with injuries, 1346 percutaneous endoscopic, 1404 lumbar spine, exercises, 1022 in radiculopathy, 881 lumbar spine, as final phase of degenerative disease, 819 operative metastatic disease, 479, 479–80, 481 primary tumors of bone, 465–6 segmental, exercises, in acute nontraumatic axial neck pain, 687–8 standing position lumbar spine examination, 843 pain in failed back surgery syndrome in, 1133 in sacroiliac joint syndrome, various tests in, 1242 from sitting coccydynia during move to, 1290 failed back surgery syndrome and pain during move to, 1133 staphylococcal spondylodiscitis, 406 State and Trait measurement, 107, 109 statistics, 10–11 stellate (cervicothoracic) ganglion anatomy, 285–6, 772 block, 285–7, 713–14 control blocks, 190 indications and contraindications, 713 outcomes, 713–14 side effects and complications, 714 stem cells, mesenchymal, bone formation and, 424–5 stenosing tenosynovitis, de Quervain’s, 628 stenosis foraminal see foramina spinal canal see spinal stenosis sterile inflammation following spinal surgery, 403 sterility, cervical discography, 725 sternal occipital mandibular immobilizer, 487 sternoclavicular joint anatomy, 548 sternocleidomastoid muscles, anatomy, 523 steroids see corticosteroids stiffness in lumbar disc degeneration, 819 nucleus pulposus, 832 stingers/burners, 1336, 1341, 1353, 1354, 1365–6 epidemiology, 1365 evaluation, 1365–6, 1366 management, 1365–6 pathomechanics, 1365 return to play, 1366 stomach (gastric) cancer, spinal metastases, 475–6 straight back syndrome, 773 straight leg raising test (SLR), 847–8 crossed, 848 in lumbosacral radiculopathy, 894, 900, 918 reverse, 894–5 modifications, 848–9 sacroiliac joint assessment in pregnancy, 1316

1449

Index strain (biomechanical term), 829 strain (injury), cervical soft tissues in sport, 1341, 1368–9 strain—counterstrain, sacroiliac joint rehabilitation, 1251, 1253 strength lower extremities, testing, 844–5 in hip—spine syndrome, 1278 shoulder muscles, 550 testing, 554–5 strengthening exercises axial back pain, 996 axial neck pain acute nontraumatic, 688 chronic, 691, 692 chronic pain patients, 1227 core, 881, 1332 hamstrings, 1250–1 lumbar radiculopathy due to herniated disc, 881–2 pregnancy-related back pain, 1322–3 spondylolysis, 1375, 1377 sports injuries (prolonged), 1381 stress, 828 see also distress stress fractures pelvic area in pregnancy, 1312–13 sacral, 1281 thoracic, 778 treatment, 782, 783 stress management training, 1229 stress-relaxation test, 831 stretch reflexes, muscle in lumbar spine examination, 845–7 in shoulder pain diagnosis, 555 stretching exercises lumbar radiculopathy due to herniated disc, 881 piriformis syndrome, 1304 stroke (cerebrovascular accident) pain following, 41 risk with cervical manual therapy, 697 subacute/recovery phase of rehabilitation, 993 axial back pain, 995–6 sacroiliac joint pain associated with trauma, 1254 subarachnoid region anatomy, 193–4 contrast installation with epidural injections, 250 subclavian vessel/artery aneurysm with thrombosis, 553 compression, 553 examination for, 544 subcostal nerve, 770 subdural cavity abscess, 535 hematoma, 1150 subluxation, cervical in Down syndrome, 576–7 in rheumatoid arthritis, 560 suboccipital regions, musculature, 525 subscapular nerves, 551 substance abuse, opioids and previous history of, 166 substance P, 32–3, 40–1, 41, 45, 46, 47–8 in anulus fibrosus, 866 wind-up and, 44 suction drains and spinal hematomas, 1151 sufentanil, intrathecal infusion, 355–6 1450

suicide ideation comorbid with chronic pain, assessment for, 108, 109 sulfasalazine, spondyloarthropathies, 397 supine cervical traction while, 638–9 iliac gapping test in sacroiliac joint syndrome, 1242, 1244 long sitting test in sacroiliac joint syndrome, 1242 supine bridging, pregnant patient, 1314 suprascapular nerve, 551–2 supraspinous ligaments, 861 surgery ankylosing spondylitis, 397 cauda equina syndrome see cauda equina syndrome cervical axial neck pain see fusion cervical discitis and vertebral osteomyelitis, 534 cervical instability lower, 579 upper, 576 cervical myelopathy see cervical myelopathy cervical nerve root pain, 657–78 contraindications, 657–8 historical notes, 657 indications, 657 techniques, 658–63, 669–75 cervicogenic headache, 746 coccydynia, 1296 decompressive see decompression for failed back surgery syndrome (=reoperation), 1144 fusion see spinal fusion for implantable pain pump location, complications, 362 infections childhood discitis and spondylodiscitis, 409–10 epidural abscess, 411 for postoperative infections, 411 tuberculosis, 412–13 lumbar/back (in general) minimally invasive, 1397–401 in pregnancy, 1328 symptoms (incl. pain) continuing/recurring after see failed back syndrome lumbar axial pain, 1065–71 lumbar disc see lumbar disc lumbar herniated nucleus pulposus, 939–50 indications, 873, 940 lumbar radiculopathy due to, 873, 887 microscopic see microsurgery minimally invasive see endoscopic procedures; minimally invasive procedures; thoracoscopic surgery piriformis syndrome, 1305 sacral insufficiency fractures, 1286 sacroiliac joint syndrome, 1269–75 case studies, 1272–4 complications, 1272 patients selection, 1269–74 postoperative care, 1272 technique in various procedures, 1269–72 spondylolysis, 1377 thoracic disc disease, 799–802 contraindications, 800 indications, 799–800 technique, 800–2 tumors

surgery (Continued) metastatic, 479, 481 primary, of bone, 464–6 see also minimally invasive procedures; postoperative course; postoperative problems and specific procedures Survivor of Violence scale, 109–10 sustained natural apophyseal glides, 695 Sweden, epidemiology of spinal pain, 10 swelling pressure, 830 anulus fibrosus, 832 nucleus pulposus, 832 swing, golfer’s, 1354–5, 1385 Symmix electrodes, 1167–8 sympathetic trunk, 713–16, 1196–7 anatomy, 1196 blocks, 285–8, 713–16 face validity, 189 lumbar see lumbar sympathetic chain stellate ganglion see stellate ganglion thoracic, 287, 714 cervical, 527–8 surgery (sympathectomy), 1196–7 thoracic, 768, 771–2 symphysis (pubic) in pregnancy pain, 1313 palpation, 1315 symptom control (in chronic pain patients), 1224 synaptophysin, anulus fibrosus, 866 Synchromed pain pumps, 353–4, 1178 comparisons, 1179–80 Syncromed EL, 1178, 1179–80 Syncromed II, 1178, 1179–80 syndesmophytes, 73 synovial cyst, 889 treatment, 889 aspiration, 267 medical, 875 synovial joints, cervical, anatomy and injection, 260–1 synovitis facet joint, imaging, 70–1 in spondyloarthropathy, 391 syringohydromyelia, imaging, 83 syringomyelia compression myelopathy vs, 570 pain, 42 syrinx, cervical, 421 systemic disorders lumbar radicular pain as, 912 sciatica caused by, 386–7, 387 in spondyloarthropathies, 395–6 systemic lupus erythematosus, 82

T T4 syndrome, 779 treatment, 784 T12—L1 disc puncture (discography), 292–3 tachyphylaxis and tolerance benzodiazepines, 182 local anesthetics, 150 opioids, 164, 361 tamoxifen, osteoporosis, 442 taping lumbar radiculopathy due to herniated disc, 885 neck pain rehabilitation, 692 Tarlov cysts, 84

Index Task Force on The Standardization of Prosthetic Orthotic Terminology Committee, 485 Taylor orthosis, 489 ‘teardrop’ fracture, 1335, 1344 technetium-99m scans infections, 405 labelled compounds monoclonal antibodies, 90 organic analogs of pyrophosphate, 89–90 spondylolisthesis, 1082 tectorial ligament, 520 teenagers see adolescents tegmental area, ventral (VTA), fear and anxiety and the, 175, 176 telomerase and osteoblast senescence, 429 temazepam, acute anxiety, 180 tendinitis, bicipital, Speed’s test, 625 tendinopathy, forearm and hand pain due to, 627, 628 tendon(s), cervical, sports-related strains, 1341 tendon reflex assessment in lumbar spine examination, 846 tennis, 1337, 1356–7 tennis elbow, 627 TENS see transcutaneous electrical nerve stimulation tension cervical nerve roots in sports, overload, 1341 muscle, in rear-end collisions, 586 soft tissue anulus fibrosus, 832–3 axial, 834 testing, 829 tension-type headache vs cervicogenic headache, 741 tertiary rehabilitation/treatment, 1223–30 biopsychosocial approach, 1232, 1234 definition, 1224–5 outcomes, 1231–8 measurement and its review, 1234–6 tetracaine, 142, 146 tetraplegia see quadriplegia TGF-β see transforming growth factor-β thalidomide, ankylosing spondylitis, 397 thecal sac compression, 951 see also arachnoid; dura thermal energy and thermotherapy see heat thermocoagulation, radiofrequency see radiofrequency ablation Thomas test, 843 thoracic cord compression, 778 thoracic disc(s), 773 anatomy, 773, 790 disease/lesions (in general), 794–5, 799–802 clinical syndrome, 794 diagnosis, 780, 781 differential diagnosis, 782 examination, 779 pain, 777 treatment, 782, 794–5, 799–802 herniation see thoracic disc herniation laser decompression, technique, 334 thoracic disc herniation differential diagnosis, 782 imaging, 62, 781 pain, 777, 779 physical examination, 779 surgery, 799 thoracic discectomy, thoracoscopic, 800–1

thoracic discography, 297–8, 299, 301, 790–1, 794 thoracic facet (zygapophyseal) joints, 261–2, 263, 280–1, 773–4, 787–90 anatomy, 261–2, 280, 773–4, 787–8 injections, 263 manipulative therapy, 782 orientation, 775, 789 orthoses and biomechanics of, 485 pain, 787–90 radiofrequency denervation, 280–1, 782, 788, 788–9, 793–4 thoracic ganglionectomy, upper, 1196 thoracic lysis of epidural adhesions, 1159 thoracic medial branch block, 266, 771, 772, 788–9 thoracic nerve, long, 551 thoracic nerve root dysfunction, 779 injections with osteoporotic fractures, 783 thoracic outlet syndrome, 552–3 sciatica-like pain, 386–7 testing for/diagnosis, 544 thoracic pain (chest pain) evaluation, 625, 627–8 referred to neck, 625, 627–8, 708 syndromes of, 793–7 nonspinal causes, 793 spinal causes see pain (spinal/back) thoracic spinal cord anatomy, 768–72 decompression see decompression stimulation, 347 thoracic spine, 767–802 anatomy, 767–76, 1193 biomechanical disorders, 767–802 biomechanics, 775 orthoses and, 485 injections, 787–92 complications, 221–2 interlaminar epidural, 251 intra-articular facet joint, 789–90 transforaminal epidural, 255 kyphosis see kyphosis minimally invasive surgery, 1401–4 pain see pain (spinal/back) primary tumors, surgery, 465 radiofrequency denervation, 280–2 sports injuries in region of baseball/softball, 1352 biomechanical etiologic factors, 1351 functional anatomy relevant to, 1331–2 golf, 1354 thoracic sympathetic chain anatomy, 287 block, 287, 714 thoracic vertebrae imaging (normal vertebrae), 56 vertebroplasty, approach, 369 thoracic wall (chest wall), lateral, radio receiver/pulse generator implantation in, 349 thoracolumbar fascia anatomy, 774, 1332–3 incision in laminotomy, 963 thoracolumbar junction exposure in thoracoscopic surgery, 1403 thoracolumbosacral orthosis (TLSO), 485, 486, 488–90 indications, 491–2 spondylolysis, 1375

thoracolumbosacral orthosis (Continued) see also head cervical thoracic orthosis; lumbosacral orthosis thoracoscopic surgery of thoracic spine discectomy, 800–1 video-assisted, 1401–4 thoracotomy, pain following, 770, 778 diagnosis, 780 physical examination, 780 treatment, 782, 784 thorascopic surgery, video-assisted, thoracic disc disease, 795 3-D technique of cervical lysis of adhesions, 1159 thromboembolism (incl. deep venous thrombosis) laser decompression and nucleotomy complicated by, 336 with spinal tumors, prophylaxis, 463, 477 see also pulmonary embolism thrombosis, subclavian artery aneurysm with, 553 throwing (pitching) injuries in baseball/softball, 1352 thyroid hormone effects on fusion surgery, 1124 tibial nerve sign, posterior, 849 Tietze’s syndrome, 778 bone scan, 782 tissue inhibitors of metalloproteinases (TIMPs), 22, 23 tissue plasminogen activator and chronic low back pain, 198 tizanidine intrathecal infusion, 357–8 lumbar radiculopathy due to herniated disc, 876 TNF-α see tumor necrosis factor α tolerance see tachyphylaxis and tolerance tonic block, local anesthetics, 140 tophi, 83 topical anesthetics and analgesics, 146 lumbar radiculopathy due to herniated disc, 877, 888 topiramate, 133 adverse effects, 131, 133 dosing and titration, 132, 133 in radicular pain, 133 due to lumbar herniated disc, 876 Torg ratio, 1342, 1363 torque, 828 torsion, 835 lumbar, 820 injury due to, and lumbar discogenic pain, 813 torso see trunk trabecular bone see cancellous bone traction, 1206 cervical, 699 in radicular pain, 637–8 retraction and extension with, and rotation, 694 lumbar, in radicular pain, 872, 877–8 traction spur, 1112 Trainer’s Angel, 1345, 1346 training (physical) see exercises training (professional) see education trajectory view, 246 tramadol, radicular pain, 131 lumbar, due to herniated disc, 874 transcutaneous electrical nerve stimulation (TENS), 1206

1451

Index transcutaneous electrical nerve stimulation (Continued) in cervical axial pain, electroacupuncture and, 699 in lumbar radiculopathy due to herniated disc, 877 in pregnancy, 1324 transdermal patch fentanyl, 168–9 lidocaine see lidocaine transdural spinal cord herniation, 84 transforaminal epidural adhesiolysis, 1158–9 transforaminal epidural steroid injections, 249, 250, 251–9 advantages over interlaminar injections, 250 cervical, 251–5, 645–6, 648–51 cervicogenic headache, 747–8 complications, 651–4 lumbar, 255–6, 914, 915, 982, 982–3, 1014–18 case study, 1023 complications, 222–31 in degenerative disc disease, 1019 efficacy, 1014–15, 1015–18 with neural scarring in failed back surgery, 1142–3 in spondylolisthesis, 1091–4 technique, 1017–18 sacral, 257 thoracic, 255 transforaminal lumbar interbody fusion, 1070, 1123 minimally invasive, 1397–9 transforaminal nerve root injections vs cervical discography, diagnostic value, 723 transforming growth factor-β (TGF-β) inflammation and, 22 osteoblast activity and, 435 osteogenesis and, 425, 440 transient neurologic symptoms (TNS), local anesthetics, 148–9 transition syndrome, cervical myelopathy surgery, 762–3 translaminar epidural steroid injections see interlaminar space transpedicular approach to thoracic disc lesions, 801 transportation, athlete with cervical spine injuries, 1346–7 trans-sacral transvertebral interbody fixation, 1105–6 transthoracic approach to thoracic cord decompression, 800 transverse lesion syndrome, and symptoms, 618, 621 transverse ligament of atlas, 520 transverse processes atlas, 707 cervical anatomy, 519 palpation, 543 lumbar, 859 fractures, 1336 L5, transforaminal injections and L5—S1 foramen blocked by, 257 thoracic, 770, 773 see also costotransversectomy transversospinalis, 774 transversus abdominis, 774 in lumbar disc surgery rehabilitation, 971 sporting activity and, 1333

1452

trapezius muscle anatomy, 524, 774 pain, 623–4 trauma see injury travel, cautions following lumbar radiculopathy due to herniated disc, 887 treatment outcomes and their measurement, 1232–6 primary, 1224, 1231 secondary, 1224, 1231 tertiary see tertiary rehabilitation see also rehabilitation and specific disorders trials/studies, clinical discography, 299–300 postoperative rehabilitation in lumbar disc surgery, 968–70 triamcinolone, spinal injection, 158–9 lumbar discogenic pain, 1051–3 triazolam, acute anxiety, 180 triceps manual muscle testing, 629, 631 reflex assessment, 545 tricyclic antidepressants opioid interactions, 169 radicular pain, 131 trigeminal nerve and cervicogenic headache, 737–8 trigeminal neuralgia, oxcarbazepine, 133 trigger points in lumbar radiculopathy, 883–4 injections, 872, 886–7 in pregnancy-related back pain, injections, 1328 in spondylolisthesis, injections, 1091 see also myofascial therapy trocar, automated percutaneous lumbar discectomy, 323–8 trochanteric bursitis, 385–6 tropical spastic paraparesis, 569 trunk/torso muscle strengthening exercises, 881–2 rotation strength device, 1227, 1228 sagittal trunk strength assessment, 1226 tuberculosis (Mycobacterium tuberculosis/ M. bovis/M. africanum), 412–13, 536 clinical features, 412 neck pain, 536 sciatica-like pain, 386 thoracic pain, 777 pathogenesis and natural history, 412 radiology, 412 treatment, 783 tumor(s) (neoplasms), 75–81, 453–83, 561–2 compression myelopathy vs, 569 compression myelopathy with, 561 disc degeneration associated with, 61 epidemiology, 453 imaging, 75–81, 455–6, 472–3 technique, 75 lumbar instability caused by, 1112 neck pain caused by, 531–3 pelvic, vs sacral insufficiency fracture, 1283 primary, 417–22, 453–67 benign, 453, 457–61, 783 clinical presentation, 453–4 diagnosis, 453 malignant, 453, 461–3 management, 463–6, 783 non-osseous, 417–22

tumor(s) (neoplasms) (Continued) physical examination, 454–5 treatment, 453 work-up, 455–7 secondary see metastases shoulder pain caused by, 554 thoracic spinal pain caused by, 783–4 tumor necrosis factor α (TNF-α) cervicogenic headache and, 740 disc degeneration and, 24 drugs targeting (antagonists incl. monoclonals), 24, 916–17 ankylosing spondylitis, 397 lumbar radiculopathy (incl. radiculopathy due to herniated disc), 876–7, 888, 916–17 inflammation and, 22 radicular pain and, 912 two-handed technique (fluoroscopy), 247

U UK see United Kingdom and Britain ulcer(s), peptic, steroid-associated, 156 ulcerative colitis, arthritis associated with, 394 ulnar nerve bias testing, 544 ulnar neuropathy, 627 ultrasound imaging, pregnant patient with low back pain, 1317 ultrasound therapy, neck pain, 698 uncinate process cervical, 519–20 lumbar, 859 uncovertebral joints, biomechanics and anatomy, 577, 578 United Kingdom and Britain causes of spinal pain, 12 COX-2-specific inhibitors available in, 117 epidemiology of spinal pain, 10 of whiplash injury, 607 Paget’s disease epidemiology, 607–8 United States (USA) controlled substances in, model guidelines for use, 165–6 COX-2-specific inhibitors available in, 117 epidemiology of spinal pain, 10 upper limb neural/dural tension tests, 544 in cervical radiculopathy and radicular pain, 628, 629 pain, evaluation, 625, 627–8 in complex regional pain syndromes, 190 neurologic examination, 544–5 upper motor neuron lesions, tests for, 545 urinary retention with opioids, 361 urological disorders see genitourinary disorders USA see United States use-dependent block, local anesthetics, 140–1

V vaginal manual examination of pelvic floor musculature in pregnancy, 1316 valdecoxib adverse effects, 120, 122 drug interactions, 120 indications, 117 postoperative setting, 119–20 validity, 187 diagnostic blocks, 188–9 lumbar provocation discography, 1040–3

Index valproic acid, radicular pain, 135 vaporization of disc, laser, 331 vascular damage with cervical discography, 299, 727 with cervical epidural steroid injections, 220–1, 652–4 with cervical manual therapy, 697 with lumbar microscopic discectomy, 948 in stellate ganglion block, 713 vascular disease compression myelopathy vs, 569 peripheral see peripheral vascular disease vascular endothelium see endothelium vascular flow, chronic low back pain and role of, 198 vascular lesions compression fractures due to, 500–1 neck pain due to, 708 spinal, 84–5 vascular malformations, 420 imaging, 84–5, 420 vascular permeability in acute inflammation, 18 see also neovascularization vascular supply cervical spine and cord, 521–3 lumbar spine and cord, 861–2 in failed back surgery syndrome etiology, 1140 shoulder, 552–3 thoracic spine and cord, 768 vasoconstrictor effects, local anesthetics, 147, 148 vasodilator effects, local anesthetics, 147 vasovagal reactions, laser decompression and nucleotomy, 336 venlafaxine as anxiolytic, 181, 183 lumbar radiculopathy due to herniated disc, 876 side-effects, 183 venography in vertebroplasty, 371 venous drainage/systems cervical spine, 522–3 lumbar spine, 862 shoulder, 552 venous stasis, epidural, 805 venous thrombosis, deep see thromboembolism ventral nerve plexus, thoracic disc and vertebral bodies innervated by, 790 ventral rami cervical, anatomy, 526–7 lumbar anatomy, 863, 864 discography-associated trauma, 299 thoracic, anatomy, 768–70 ventral roots, lumbar, 863 ventral tegmental area (VTA), fear and anxiety and the, 175, 176 versican, 426 vertebra(e) body of see vertebral body bracing preventing collapse (with tumors) see orthoses development and morphogenesis cervical spine, 515, 516–17 embryological, 424, 515, 855–6 fetal, 516, 856 postnatal, 516–17, 857, 858–9 fractures see fractures functional anatomy in cervical spine, 518–20

vertebra(e) (Continued) fusion surgery see interbody fusion; spinal fusion imaging, 74–5 normal vertebrae, 57–8 infections see infection metastases see metastases vertebra prominens, palpation, 543 vertebral artery anatomy, 519, 521 damage in cervical manual therapy, 697 cervical zygapophyseal joint injection, 221 in stellate ganglion block, 713 vertebral body compression fractures see compression fractures fusion between see interbody fusion hemangioma see hemangioma in kyphoplasty access, 379 access complications, 382 preparation, 381 in vertebroplasty, approaches, 368 vertebral canal see spinal canal vertebral column see spinal column vertebral endplate see endplate vertebral plexuses, external/internal, 522–3 vertebrectomy, L5, in spondyloptosis, 1105 vertebroplasty, percutaneous, 367–75, 495–505, 1404–5 clinical utility and future directions, 503 complications and their avoidance, 373–4, 501–3 compression fractures, 68, 69, 367, 373, 377, 495–505 osteoporotic see osteoporosis risk of future fractures, 503, 511–12 consultation, 367 efficacy, 499–501 fractures at adjacent and remote sites following, 511–12 historical overview, 496 indications and contraindications, 497–9 mechanism of action, 497 at multiple levels, 373, 509 repeat, 373, 501 screening of referred patients, 367 technique, 367–73 tumors metastatic, 478–9 primary, of bone, 464 vibration pain provocation see bone vibration test (vibration pain provocation) video-assisted thorascopic surgery, thoracic disc disease, 795 viral agent compression myelopathy vs, 569 in Paget’s disease etiology, 445 visceral causes of low back pain, 808 in pregnancy, 1311 visceral pain anxiety effects on, 174 thoracic region, 768 viscoelasticity, 831, 834 nucleus pulposus, 831 visual analog scale (VAS) cervical radicular pain, 632 failed back surgery syndrome, 1129

visual analog scale (Continued) lumbar discectomy with Dekompressor, 934–5 lumbar nucleoplasty with Perc-DC® Spine Wand, 933 Million VAS, 1234–5 post-injection procedure, 210 pre-injection procedure, 208 vertebroplasty efficacy measured via, 499 whiplash-associated chronic pain, 604 visual inspection see inspection vitamin B12 deficiency-associated myelopathy, 570 vitamin D3 bone metabolism and, 424, 427, 435–6 dietary supplementation, 436, 442 low levels, 438 vocation see entries under occupational voltage (kilovoltage) peak, 230, 232 vomiting with opioids, 167, 361 von Anrep, Vassily, 137 von Recklinghausen’s disease see neurofibromatosis type 1 von Willebrand’s disease, 217

W Waddell Disability Index, 1235 Waddell signs, 596, 849–50 warfarin and spinal injections, 218 water therapy in pregnancy, 1323 weakness (muscle) in cervical radiculopathy, 629 in low back pain patients, selective, 807 wedge fractures, osteoporosis, 778 weight (body), 12 weight training, cautions following lumbar radiculopathy due to herniated disc, 887 West Haven—Yale Multidimensional Pain Inventory, 109 whiplash injury, 583–612 acute, and associated disorders, 597, 601 advice for acute whiplash patient, 599–600 biomechanics, 583–8, 591, 607, 608, 710–11 collars, 491, 599 definition, 583–4 epidemiology, 607–11 of pain, 609–10 facet joint pain see facet joints pathophysiology, 589–90 patient assessment, 595–7 patterns, 587 postmortem/cadaveric studies, 589, 602–3 prognostic/outcome, and factors affecting, 595–6, 607–9 repair/healing processes, 688–9 sociocultural phenomena, 593–600 soft tissue damage, 601–6 symptom amplification, 597–8 treatment/management, 599, 711 exercises, 599, 688–90 white rami communicantes, 768, 772 wide abdominal rectus plication, 1068 Williams flexion orthosis, 489 wind-up, 40, 42–4 wiring, lower cervical spine, 579 withdrawal syndrome/symptoms, opioids, 169 Wnts and osteogenesis, 425–6 women (females) in physiatry, 8 pregnancy see pregnancy whiplash injury predisposition, 587

1453

Index

1454

work see entries under occupational wound (of spinal surgery) closure in discectomy, 945 in total laminectomy, 963 debridement see debridement deep infection, 403–4 clinical presentation, 403–4 pathogenesis/etiology/natural history, 403 drainage see drainage irrigation and protection, 412 Wright’s test, 544

X-rays (Continued) source/beam, 229 for CT, 55 terminology, 229–30 concerning safety, 230–1 see also dual-energy X-ray absorptiometry; radiation X-Tube for minimally invasive-transforaminal lumbar interbody fusion, 1397, 1399 xenografts of bone for fusion surgery, influence on outcome, 1126 Xylocaine see lidocaine

X

Y

X-rays generation, fundamentals, 231–6 plain see radiographs

Yergason’s test, 625 young adult athlete, spinal/back injury, 1351

Z Z-values, dual-energy X-ray absorptiometry, 437 ziconotide, intrathecal infusion, 356, 358, 360, 1183–4 zolendronate, 443 zona fasciculata, 153 zona glomerulosa, 153 zona reticularis, 153 zonisamide, 133–4 adverse effects, 131, 134 dosing and titration, 132, 133 in radicular pain, 133–4 zygapophyseal joints see facet joints